PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 27862504-7 2017 This procedure allowed us to establish the dissociation pattern for steviol glycosides, and thus the sugar arrangement in the branched oligosaccharide portion linked at position C-13 of steviol, and also infer the sugar arrangement at C-19. Oligosaccharides 135-150 homeobox C13 Homo sapiens 178-182 19657284-0 2009 Blocking the salt-inducible kinase 1 network prevents the increases in cell sodium transport caused by a hypertension-linked mutation in human alpha-adducin. Sodium 76-82 adducin 1 Homo sapiens 143-156 19657284-1 2009 OBJECTIVES: Because a newly described salt-inducible kinase 1 (SIK1) network is responsible for increases in active cell sodium transport in response to elevated intracellular sodium, we hypothesized that this network could mediate the effects of the mutant (hypertensive) form of alpha-adducin on Na,K-ATPase activity. Sodium 121-127 adducin 1 Homo sapiens 281-294 19657284-1 2009 OBJECTIVES: Because a newly described salt-inducible kinase 1 (SIK1) network is responsible for increases in active cell sodium transport in response to elevated intracellular sodium, we hypothesized that this network could mediate the effects of the mutant (hypertensive) form of alpha-adducin on Na,K-ATPase activity. Sodium 176-182 adducin 1 Homo sapiens 281-294 19657284-7 2009 CONCLUSION: The SIK1 network may constitute an alternative target by which agents can modulate active sodium transport in renal epithelia and avoid the increases in systemic blood pressure that are associated with genetic mutations in the human alpha-adducin molecule. Sodium 102-108 adducin 1 Homo sapiens 245-258 19726542-2 2009 The present study tested the hypothesis that the microtubule- rather than the clathrin-dependent endocytic pathway regulates AT1-mediated uptake of ANG II and ANG II-induced sodium and hydrogen exchanger-3 (NHE-3) expression in PT cells. Sodium 174-180 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 159-165 19675531-1 2009 Because dopamine D(1) receptors (DRD1) influence renal sodium transport and vascular hemodynamics, we examined whether genetic polymorphisms play a role in renal function. Sodium 55-61 dopamine receptor D1 Homo sapiens 33-37 19455045-2 2009 Hepatocellular carcinoma (HCC) and low serum sodium (SNa) are manifestations of end-stage liver disease and are associated with poor survival in decompensated cirrhosis patients. Sodium 45-51 snail family transcriptional repressor 1 Homo sapiens 53-56 19858959-8 2009 Construct validity testing revealed a small but significant correlation between higher patient and FM knowledge on sodium restriction questions and lower ingested sodium, r = -0.17, P = .05 and r = -0.19, P = .04, respectively, and between patient knowledge and number of days that medications were taken correctly (diuretics: r = 0.173, P < .05, and angiotensin-converting enzyme: r = 0.223, P = .01). Sodium 115-121 angiotensin I converting enzyme Homo sapiens 354-383 19549694-12 2009 CONCLUSIONS: Our data suggest that not only vasopressin (possibly via its V1a receptor), but also the CaSR (which is sensitive to high sodium concentrations) may play a role in osmomediated natriuresis. Sodium 135-141 calcium sensing receptor Homo sapiens 102-106 19638349-1 2009 Aldosterone and endothelin-1 (ET-1) act on collecting duct cells of the kidney and are important regulators of renal sodium transport and cardiovascular physiology. Sodium 117-123 endothelin 1 Rattus norvegicus 16-28 19638349-1 2009 Aldosterone and endothelin-1 (ET-1) act on collecting duct cells of the kidney and are important regulators of renal sodium transport and cardiovascular physiology. Sodium 117-123 endothelin 1 Rattus norvegicus 30-34 19572987-5 2009 5-HT is selectively transported into neurons through the serotonin transporter (SERT), which is a member of the sodium- and chloride-dependent neurotransmitter transporter (SLC6) family. Sodium 112-118 solute carrier family 6 member 4 Homo sapiens 57-78 19572987-5 2009 5-HT is selectively transported into neurons through the serotonin transporter (SERT), which is a member of the sodium- and chloride-dependent neurotransmitter transporter (SLC6) family. Sodium 112-118 solute carrier family 6 member 4 Homo sapiens 80-84 19809188-0 2009 Crystal structures of sodium-bound annexin A4. Sodium 22-28 annexin A4 Homo sapiens 35-45 19635986-1 2009 Experiments in Cushing patients and healthy control subjects receiving adrenocorticotropic hormone (ACTH) indicate that transient renal sodium retention may contribute to the generation of hypertension. Sodium 136-142 proopiomelanocortin Homo sapiens 71-98 19635986-1 2009 Experiments in Cushing patients and healthy control subjects receiving adrenocorticotropic hormone (ACTH) indicate that transient renal sodium retention may contribute to the generation of hypertension. Sodium 136-142 proopiomelanocortin Homo sapiens 100-104 19593208-10 2009 CONCLUSION: The CYP2C9*3 allele was associated with lower activity of the renin-angiotensin-aldosterone system in hypertensive men, which may reflect a more efficient sodium reabsorption capacity. Sodium 167-173 renin Homo sapiens 74-79 19790137-6 2009 In the group without diuretics, the mean serum sodium was 124 mmol/L 1 day before and on the day of conivaptan initiation, but the serum sodium rose to a mean of 127.7 mmol/L by day 1 and further increased to 128.6 mmol/L by the second day of the infusion. Sodium 47-53 immunoglobulin kappa variable 1-16 Homo sapiens 67-70 19706515-9 2009 Both with wild-type EAAC1 and EAAC1-D455N, not only sodium but also lithium could support radioactive acidic amino acid uptake. Sodium 52-58 solute carrier family 1 member 1 Homo sapiens 20-25 19572935-9 2009 RBF decreased and GFR, filtration fraction, sodium reabsorption, RVO2, RO2Ex and renal vascular resistance increased dose-dependently with vasopressin. Sodium 44-50 arginine vasopressin Homo sapiens 139-150 19563532-0 2009 Pals-associated tight junction protein functionally links dopamine and angiotensin II to the regulation of sodium transport in renal epithelial cells. Sodium 107-113 PATJ crumbs cell polarity complex component Homo sapiens 0-38 19563532-0 2009 Pals-associated tight junction protein functionally links dopamine and angiotensin II to the regulation of sodium transport in renal epithelial cells. Sodium 107-113 angiotensinogen Homo sapiens 71-85 19542911-7 2009 This hyperactivation of the renin-angiotensin-aldosterone system was associated with hyponatremia and hyperkalemia in the newborn infants, and high urinary sodium loss, consistent with a partial aldosterone resistance at birth. Sodium 156-162 renin Homo sapiens 28-33 19785774-1 2009 The epithelial sodium channel [ENaC] is critical for the maintenance of sodium balance, extracellular fluid volume and long term blood pressure control. Sodium 15-21 sodium channel epithelial 1 subunit gamma Rattus norvegicus 31-35 19574959-4 2009 RESULTS: We identified a significant association between a rare ADD1 variant rs17833172 and SBP, DBP, and MAP responses to high sodium (P values <0.0001) and DBP response to low sodium (P value = 0.002). Sodium 128-134 adducin 1 Homo sapiens 64-68 19574959-4 2009 RESULTS: We identified a significant association between a rare ADD1 variant rs17833172 and SBP, DBP, and MAP responses to high sodium (P values <0.0001) and DBP response to low sodium (P value = 0.002). Sodium 181-187 adducin 1 Homo sapiens 64-68 19574959-4 2009 RESULTS: We identified a significant association between a rare ADD1 variant rs17833172 and SBP, DBP, and MAP responses to high sodium (P values <0.0001) and DBP response to low sodium (P value = 0.002). Sodium 181-187 D-box binding PAR bZIP transcription factor Homo sapiens 161-164 19282825-6 2009 Furthermore, in response to HS, a higher BMI was associated to a higher rise in filtered load of sodium (FL(Na(+)) = [Na(+)] x GFR, r = 0.281, P < 0.05). Sodium 97-103 filamin A Homo sapiens 105-116 19706515-9 2009 Both with wild-type EAAC1 and EAAC1-D455N, not only sodium but also lithium could support radioactive acidic amino acid uptake. Sodium 52-58 solute carrier family 1 member 1 Homo sapiens 30-35 19575010-3 2009 This current is primarily permeant to sodium ions, independent of intracellular calcium stores and G proteins but dependent on Src activation, and resistant to TTX. Sodium 38-44 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 127-130 19549517-7 2009 Heterologous expression of the two cDNAs in mammalian cells resulted in saturable, sodium-dependent serotonin transport activity with an apparent affinity for serotonin comparable to that of the human serotonin transporter. Sodium 83-89 solute carrier family 6 member 4 Homo sapiens 201-222 19131642-2 2009 Sodium hyperabsorption by the airways, profound lung inflammation, and dysregulation of calcium homeostasis, are presumably causally related to loss of CFTR-dependent chloride function in patients with CF. Sodium 0-6 CF transmembrane conductance regulator Homo sapiens 152-156 19694742-0 2009 Variation in the CYP2D6 gene is associated with a lower serum sodium concentration in patients on antidepressants. Sodium 62-68 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 17-23 19694742-1 2009 AIM: To study the effect of the CYP2D6*4 polymorphism on serum sodium concentration in users of antidepressants [selective serotonin reuptake inhibitors and tricyclic antidepressants (TCAs)]. Sodium 63-69 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 32-38 19694742-3 2009 Multivariate linear regression was used to study the association between CYP2D6*4 and serum sodium concentration. Sodium 92-98 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 73-79 19694742-4 2009 RESULTS: CYP2D6 poor metabolizers (PMs) (*4/*4) had a significantly lower mean serum sodium concentration in comparison with CYP2D6 extensive metabolizers (EMs) (*1/*1) [difference -3.9 mmol l(-1); 95% confidence interval (CI) -0.86, -7.03; P= 0.013]. Sodium 85-91 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 9-15 19671928-5 2009 Characterization of dkf-2 null mutants and transgenic animals expressing DKF-2B, DKF-2A, or both isoforms revealed that PKDs couple DAG signals to regulation of sodium ion (Na+)-induced learning. Sodium 161-167 Serine/threonine-protein kinase dkf-2 Caenorhabditis elegans 20-25 19694742-5 2009 In CYP2D6*4 heterozygotes (*1/*4) serum sodium concentration was 1.7 mmol l(-1) (95% CI -3.48, 0.18) lower compared with CYP2D6 EMs, but this difference was not statistically significant (P= 0.077). Sodium 40-46 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 3-9 19255824-1 2009 BACKGROUND: The inhibition of the renin-angiotensin system in the diabetic condition was reported to enhance the sodium sensitivity of blood pressure. Sodium 113-119 renin Homo sapiens 34-39 19464262-2 2009 A member of the family of potassium-dependent sodium/calcium exchangers, NCKX3 (SLC24A3) plays a critical role in the transport of an intracellular calcium and potassium ion in exchange for four extracellular sodium ions. Sodium 46-52 solute carrier family 24 (sodium/potassium/calcium exchanger), member 3 Mus musculus 73-78 19464262-2 2009 A member of the family of potassium-dependent sodium/calcium exchangers, NCKX3 (SLC24A3) plays a critical role in the transport of an intracellular calcium and potassium ion in exchange for four extracellular sodium ions. Sodium 46-52 solute carrier family 24 (sodium/potassium/calcium exchanger), member 3 Mus musculus 80-87 19464262-2 2009 A member of the family of potassium-dependent sodium/calcium exchangers, NCKX3 (SLC24A3) plays a critical role in the transport of an intracellular calcium and potassium ion in exchange for four extracellular sodium ions. Sodium 209-215 solute carrier family 24 (sodium/potassium/calcium exchanger), member 3 Mus musculus 73-78 19464262-2 2009 A member of the family of potassium-dependent sodium/calcium exchangers, NCKX3 (SLC24A3) plays a critical role in the transport of an intracellular calcium and potassium ion in exchange for four extracellular sodium ions. Sodium 209-215 solute carrier family 24 (sodium/potassium/calcium exchanger), member 3 Mus musculus 80-87 19373217-10 2009 CONCLUSIONS: Insulin and D(5) receptors interact to regulate renal sodium transport; an aberrant interaction between insulin and D(5) receptor may participate in the pathogenesis of hypertension. Sodium 67-73 insulin Homo sapiens 13-20 19487301-3 2009 RESULTS: Of the 4 single nucleotide polymorphisms (SNPs) on the sodium bicarbonate cotransporter gene (SLC4A5), rs8179526 had a statistically significant interaction with cytosine/thymine (C/T) genotype by sodium status on systolic BP (SBP; p=.0077). Sodium 64-70 solute carrier family 4 member 5 Homo sapiens 103-109 19373217-10 2009 CONCLUSIONS: Insulin and D(5) receptors interact to regulate renal sodium transport; an aberrant interaction between insulin and D(5) receptor may participate in the pathogenesis of hypertension. Sodium 67-73 insulin Homo sapiens 117-124 19487583-0 2009 Enhanced distal nephron sodium reabsorption in chronic angiotensin II-infused mice. Sodium 24-30 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 55-69 19303743-6 2009 The verapamil vVg-CCB, which crosses the blood-brain barrier (BBB): (a) inhibits the P-glycoprotein, an active efflux transporter protein expressed in normal tissue, including the brain, which is believed to contribute to the in situ phenomenon of multidrug resistance; and (b) may regulate membrane depolarization induced by abnormal sodium channels functions by modulating the abnormal Ca++ influxes into neurons with subsequent cell resting. Sodium 335-341 ATP binding cassette subfamily B member 1 Homo sapiens 85-99 19487583-2 2009 To assess whether chronic Ang II infusions (15 ng/min for 2 weeks) enhance distal nephron sodium reabsorption, we compared sodium excretion before and after blockade of the 2 main distal nephron sodium transporters by IV amiloride (5 mg/kg of body weight) plus bendroflumethiazide (12 mg/kg of body weight) in male C57/BL6 anesthetized control mice (n=10) and in chronic Ang II-infused mice (n=8). Sodium 90-96 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 26-32 19487583-7 2009 In chronic Ang II-infused mice treated with spironolactone (n=5), fractional reabsorption of distal sodium delivery was similarly augmented as in chronic Ang II-infused mice (94.6+/-1.7%; P<0.01). Sodium 100-106 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 11-17 19563686-7 2009 CONCLUSION: These data suggest that activation of NK-1 receptor potentiates Na(v)1.8 sodium current via PKCepsilon-dependent signaling pathway, probably participating in the generation of inflammatory hyperalgesia. Sodium 85-91 sodium voltage-gated channel alpha subunit 10 Rattus norvegicus 76-84 19542465-9 2009 High sodium concentrations also liberate LL-37 in CF BAL fluid in vitro. Sodium 5-11 cathelicidin antimicrobial peptide Homo sapiens 41-46 19400583-3 2009 Here, we report that changing the cations associated with an N-acetyl-enriched heparin polysaccharide, from sodium to copper(II), converted it from supporting signaling through the fibroblast growth factor receptor (FGF-1-FGFR1c) tyrosine kinase signaling system to being inhibitory in a cell-based BaF3 assay. Sodium 108-114 fibroblast growth factor 1 Homo sapiens 216-221 19297450-0 2009 Inhibition of insulin-stimulated hydrogen peroxide production prevents stimulation of sodium transport in A6 cell monolayers. Sodium 86-92 insulin Homo sapiens 14-21 19297450-1 2009 Insulin-stimulated sodium transport across A6 cell (derived from amphibian distal nephron) monolayers involves the activation of a phosphatidylinositol (PI) 3-kinase. Sodium 19-25 insulin Homo sapiens 0-7 19386745-6 2009 In the basic model adjusted for age, sex, and smoking, higher levels of 24-h sodium excretion were directly associated with serum CRP, with an increase in serum CRP of 1.20 mg/L per 100-mmol increment in sodium excretion (95% CI: 1.11, 1.30). Sodium 77-83 C-reactive protein Homo sapiens 130-133 19386745-6 2009 In the basic model adjusted for age, sex, and smoking, higher levels of 24-h sodium excretion were directly associated with serum CRP, with an increase in serum CRP of 1.20 mg/L per 100-mmol increment in sodium excretion (95% CI: 1.11, 1.30). Sodium 77-83 C-reactive protein Homo sapiens 161-164 19386745-6 2009 In the basic model adjusted for age, sex, and smoking, higher levels of 24-h sodium excretion were directly associated with serum CRP, with an increase in serum CRP of 1.20 mg/L per 100-mmol increment in sodium excretion (95% CI: 1.11, 1.30). Sodium 204-210 C-reactive protein Homo sapiens 130-133 19386745-6 2009 In the basic model adjusted for age, sex, and smoking, higher levels of 24-h sodium excretion were directly associated with serum CRP, with an increase in serum CRP of 1.20 mg/L per 100-mmol increment in sodium excretion (95% CI: 1.11, 1.30). Sodium 204-210 C-reactive protein Homo sapiens 161-164 19386745-7 2009 However, this association was reduced after adjustment for body mass index, with an increase in serum CRP of 1.06 mg/L per 100-mmol increment in sodium excretion (95% CI: -1.02, 1.15). Sodium 145-151 C-reactive protein Homo sapiens 102-105 19386745-8 2009 CONCLUSIONS: We observed a linear association between an objective measure of sodium intake and serum CRP that may be influenced by confounding by body mass index. Sodium 78-84 C-reactive protein Homo sapiens 102-105 19297450-3 2009 We therefore questioned whether insulin would produce an intracellular burst of H2O2 leading to PI 3-kinase activation and subsequent increase in sodium transport. Sodium 146-152 insulin Homo sapiens 32-39 19297450-5 2009 This fluorescent signal and the increase in sodium transport were completely inhibited in monolayers incubated with peggylated catalase, indicating that H2O2 is the main intracellular ROS produced upon insulin stimulation. Sodium 44-50 insulin Homo sapiens 202-209 19297450-8 2009 In contrast, PI-103, an inhibitor of class IA PI 3-kinase, inhibited insulin-stimulated sodium transport but did not significantly reduce insulin-stimulated H2O2 production. Sodium 88-94 insulin Homo sapiens 69-76 19297450-9 2009 Taken together, our data suggest that insulin induces an acute burst of H2O2production which participates in an increase in phosphatidylinositol 3,4,5-trisphosphate production and subsequently stimulation of sodium transport. Sodium 208-214 insulin Homo sapiens 38-45 19380724-1 2009 Hormonal control of transepithelial sodium (Na(+)) transport utilizes phosphatidylinositide 3"-kinase (PI3K) and Raf-MAPK/ERK kinase (MEK)-ERK-dependent signaling pathways, which impact numerous cell functions. Sodium 36-42 mitogen-activated protein kinase 1 Homo sapiens 117-121 19329540-4 2009 According to a different hypothesis, CFTR mutation hyperacidifies organelles by an indirect mechanism involving unregulated sodium efflux through epithelial sodium channels. Sodium 124-130 CF transmembrane conductance regulator Homo sapiens 37-41 19345287-1 2009 The tescalcin gene (Tesc) encodes an EF-hand calcium-binding protein that interacts with the sodium/hydrogen exchanger, NHE1. Sodium 93-99 tescalcin Mus musculus 4-13 19345287-1 2009 The tescalcin gene (Tesc) encodes an EF-hand calcium-binding protein that interacts with the sodium/hydrogen exchanger, NHE1. Sodium 93-99 tescalcin Mus musculus 20-24 19345287-1 2009 The tescalcin gene (Tesc) encodes an EF-hand calcium-binding protein that interacts with the sodium/hydrogen exchanger, NHE1. Sodium 93-99 solute carrier family 9 (sodium/hydrogen exchanger), member 1 Mus musculus 120-124 19380724-1 2009 Hormonal control of transepithelial sodium (Na(+)) transport utilizes phosphatidylinositide 3"-kinase (PI3K) and Raf-MAPK/ERK kinase (MEK)-ERK-dependent signaling pathways, which impact numerous cell functions. Sodium 36-42 mitogen-activated protein kinase 1 Homo sapiens 122-125 19380724-1 2009 Hormonal control of transepithelial sodium (Na(+)) transport utilizes phosphatidylinositide 3"-kinase (PI3K) and Raf-MAPK/ERK kinase (MEK)-ERK-dependent signaling pathways, which impact numerous cell functions. Sodium 36-42 mitogen-activated protein kinase 1 Homo sapiens 139-142 19017867-1 2009 BACKGROUND: The defect in chloride and sodium transport in cystic fibrosis (CF) patients is a consequence of CF transmembrane conductance regulator (CFTR) loss of function and an abnormal interaction between CFTR and the epithelial sodium channel (ENaC). Sodium 39-45 CF transmembrane conductance regulator Homo sapiens 109-147 19017867-1 2009 BACKGROUND: The defect in chloride and sodium transport in cystic fibrosis (CF) patients is a consequence of CF transmembrane conductance regulator (CFTR) loss of function and an abnormal interaction between CFTR and the epithelial sodium channel (ENaC). Sodium 39-45 CF transmembrane conductance regulator Homo sapiens 149-153 19017867-1 2009 BACKGROUND: The defect in chloride and sodium transport in cystic fibrosis (CF) patients is a consequence of CF transmembrane conductance regulator (CFTR) loss of function and an abnormal interaction between CFTR and the epithelial sodium channel (ENaC). Sodium 39-45 CF transmembrane conductance regulator Homo sapiens 208-212 19224431-3 2009 The epithelial sodium channel (ENaC) modulates sodium reabsorption in the kidney, but little is known about sex-specific regulation of ENaC subunit expression. Sodium 15-21 sodium channel epithelial 1 subunit gamma Rattus norvegicus 31-35 19106216-4 2009 To overcome this complexity, we used a transgenic mouse model allowing conditional GR overexpression (doxycycline inducible TetON system, Hoxb7 promoter) in the renal collecting duct (CD) to identify GR-regulated genes involved in sodium transport in the CD. Sodium 231-237 nuclear receptor subfamily 3, group C, member 1 Mus musculus 200-202 19106216-11 2009 These results suggest that enhanced GR expression may contribute to enhanced sodium retention in some pathological situations. Sodium 77-83 nuclear receptor subfamily 3, group C, member 1 Mus musculus 36-38 19237446-8 2009 Identification of SLC4A5, SLC5A10 and LDOC1 indicated that sodium/bicarbonate transport, sodium/glucose transport and cell-proliferation regulation may play important upstream roles and identification of BNIP1, APOBEC3F and LDOC1 suggested that apoptosis, innate immune response and cell-proliferation regulation may play important downstream roles in hypertension. Sodium 59-65 solute carrier family 4 member 5 Homo sapiens 18-24 19490286-3 2009 Obesity-induced hypertension has multiple potential etiologic pathways, the most well established being increased renal sodium reabsorption with impaired pressure natriuresis via (1) activation of the renin-angiotensin system, (2) stimulation of the sympathetic nervous system, and (3) altered intrarenal physical forces. Sodium 120-126 renin Homo sapiens 201-206 19237446-8 2009 Identification of SLC4A5, SLC5A10 and LDOC1 indicated that sodium/bicarbonate transport, sodium/glucose transport and cell-proliferation regulation may play important upstream roles and identification of BNIP1, APOBEC3F and LDOC1 suggested that apoptosis, innate immune response and cell-proliferation regulation may play important downstream roles in hypertension. Sodium 59-65 LDOC1 regulator of NFKB signaling Homo sapiens 38-43 19237446-8 2009 Identification of SLC4A5, SLC5A10 and LDOC1 indicated that sodium/bicarbonate transport, sodium/glucose transport and cell-proliferation regulation may play important upstream roles and identification of BNIP1, APOBEC3F and LDOC1 suggested that apoptosis, innate immune response and cell-proliferation regulation may play important downstream roles in hypertension. Sodium 59-65 LDOC1 regulator of NFKB signaling Homo sapiens 224-229 19237446-8 2009 Identification of SLC4A5, SLC5A10 and LDOC1 indicated that sodium/bicarbonate transport, sodium/glucose transport and cell-proliferation regulation may play important upstream roles and identification of BNIP1, APOBEC3F and LDOC1 suggested that apoptosis, innate immune response and cell-proliferation regulation may play important downstream roles in hypertension. Sodium 89-95 solute carrier family 4 member 5 Homo sapiens 18-24 19237446-8 2009 Identification of SLC4A5, SLC5A10 and LDOC1 indicated that sodium/bicarbonate transport, sodium/glucose transport and cell-proliferation regulation may play important upstream roles and identification of BNIP1, APOBEC3F and LDOC1 suggested that apoptosis, innate immune response and cell-proliferation regulation may play important downstream roles in hypertension. Sodium 89-95 LDOC1 regulator of NFKB signaling Homo sapiens 38-43 19358945-6 2009 RESULTS: With systemic BNP at this clinically used dose (without the bolus), urine flow increased, but there was only a trend for an increase in urinary sodium excretion and glomerular filtration rate (GFR). Sodium 153-159 natriuretic peptide B Canis lupus familiaris 23-26 19357275-1 2009 Neuronal activity largely depends on two key components on the membrane: the Na,K-ATPase (NKA) that maintains the ion gradients and sets the foundation of excitability, and the ionotropic glutamatergic AMPA receptors (AMPARs) through which sodium influx forms the driving force for excitation. Sodium 240-246 tachykinin precursor 1 Homo sapiens 77-88 19201752-1 2009 GAT-1 is a sodium- and chloride-coupled gamma-aminobutyric acid (GABA) transporter, which fulfills an essential role in the synaptic transmission by this neurotransmitter. Sodium 11-17 solute carrier family 6 member 1 Homo sapiens 0-5 19176702-9 2009 This work demonstrates that AMPK activation in macula densa-like cells occurs via isosmolar changes in sodium or chloride concentration, leading to phosphorylation of ACC and NKCC2. Sodium 103-109 solute carrier family 12, member 1 Mus musculus 175-180 19357275-1 2009 Neuronal activity largely depends on two key components on the membrane: the Na,K-ATPase (NKA) that maintains the ion gradients and sets the foundation of excitability, and the ionotropic glutamatergic AMPA receptors (AMPARs) through which sodium influx forms the driving force for excitation. Sodium 240-246 tachykinin precursor 1 Homo sapiens 90-93 19357275-2 2009 Because the frequent sodium transients from glutamate receptor activity need to be efficiently extruded, a functional coupling between NKA and AMPARs should be a necessary cellular device for synapse physiology. Sodium 21-27 tachykinin precursor 1 Homo sapiens 135-138 19330810-4 2009 Serum PON1 and sodium-stimulated PON1 activities (p < 0.05) and ARE activity (p < 0.01) were found significantly higher in the patients than in the controls. Sodium 15-21 paraoxonase 1 Homo sapiens 33-37 19444964-5 2009 We have recently shown that PPARg agonists upregulate sodium and water transport channels in human proximal tubule cells and that Sgk-1 is involved. Sodium 54-60 peroxisome proliferator activated receptor gamma Homo sapiens 28-33 19355940-9 2009 CaSR also mediates the acute adverse renal effects of hypercalcemia, which include a reduced sodium, potassium and water reabsorption. Sodium 93-99 calcium sensing receptor Homo sapiens 0-4 19337901-1 2009 Beta2-agonists have been shown to increase alveolar fluid reabsorption, and at least part of their effect depends on active sodium transport from the alveolus into the epithelial cell by the amiloride-sensitive epithelial sodium channel (ENaC). Sodium 124-130 sodium channel epithelial 1 subunit gamma Rattus norvegicus 238-242 19292883-1 2009 BACKGROUND: Tumour necrosis factor alpha (TNF-alpha) has been implicated in the development of diabetic nephropathy and the accompanying increase in sodium retention. Sodium 149-155 tumor necrosis factor Homo sapiens 42-51 19150416-7 2009 These data suggest that TNF-alpha may affect the pathophysiology of acute lung injury and pulmonary edema through the inhibition of alveolar liquid clearance and sodium transport. Sodium 162-168 tumor necrosis factor Rattus norvegicus 24-33 19284629-12 2009 SCN2A, SCN3A and SCN9A gene products likely account for the tetrodotoxin-sensitive sodium currents in taste receptor cells. Sodium 83-89 sodium channel, voltage-gated, type III, alpha Mus musculus 7-12 19273719-0 2009 Early-life sodium exposure unmasks susceptibility to stroke in hyperlipidemic, hypertensive heterozygous Tg25 rats transgenic for human cholesteryl ester transfer protein. Sodium 11-17 cholesteryl ester transfer protein Homo sapiens 136-170 19284629-12 2009 SCN2A, SCN3A and SCN9A gene products likely account for the tetrodotoxin-sensitive sodium currents in taste receptor cells. Sodium 83-89 sodium channel, voltage-gated, type IX, alpha Mus musculus 17-22 18581270-1 2009 The serotonin transporter (SERT) belongs to a family of sodium- and chloride-dependent neurotransmitter transporters that are responsible for the active re-uptake of the neurotransmitter serotonin from the synapse. Sodium 56-62 solute carrier family 6 member 4 Homo sapiens 27-31 19317814-0 2009 Insulin sensitivity increase after calcium supplementation and change in intraplatelet calcium and sodium-hydrogen exchange in hypertensive patients with Type 2 diabetes. Sodium 99-105 insulin Homo sapiens 0-7 19066294-1 2009 CONTEXT: Calcium binding to the Ca-sensing receptor (CASR) expressed in thick ascending limb inhibits the Na,K,2Cl cotransporter, which decreases sodium reabsorption and secondarily decreases Ca reabsorption. Sodium 146-152 calcium sensing receptor Homo sapiens 32-51 19066294-1 2009 CONTEXT: Calcium binding to the Ca-sensing receptor (CASR) expressed in thick ascending limb inhibits the Na,K,2Cl cotransporter, which decreases sodium reabsorption and secondarily decreases Ca reabsorption. Sodium 146-152 calcium sensing receptor Homo sapiens 53-57 18581270-1 2009 The serotonin transporter (SERT) belongs to a family of sodium- and chloride-dependent neurotransmitter transporters that are responsible for the active re-uptake of the neurotransmitter serotonin from the synapse. Sodium 56-62 solute carrier family 6 member 4 Homo sapiens 4-25 19223069-1 2009 BACKGROUND: Since insulin resistance is thought to be the underlying mechanism for metabolic syndrome, affected individuals might be sensitive to a dietary sodium intervention. Sodium 156-162 insulin Homo sapiens 18-25 19185581-4 2009 METHODS: ENaC-mediated sodium transport in glucocorticoid receptor (GR)-expressing HT-29/B6 cells and rat distal colon, under the influence of the synthetic glucocorticoid dexamethasone and TNF-alpha, was quantified in Ussing chambers. Sodium 23-29 nuclear receptor subfamily 3 group C member 1 Homo sapiens 43-66 19185581-4 2009 METHODS: ENaC-mediated sodium transport in glucocorticoid receptor (GR)-expressing HT-29/B6 cells and rat distal colon, under the influence of the synthetic glucocorticoid dexamethasone and TNF-alpha, was quantified in Ussing chambers. Sodium 23-29 nuclear receptor subfamily 3 group C member 1 Homo sapiens 68-70 19185581-12 2009 p38 Mitogen-activated protein kinase is required for this synergistic effect: p38 inhibition blocked the increase in GR protein expression and ENaC-dependent sodium absorption. Sodium 158-164 mitogen-activated protein kinase 14 Homo sapiens 0-3 19185581-12 2009 p38 Mitogen-activated protein kinase is required for this synergistic effect: p38 inhibition blocked the increase in GR protein expression and ENaC-dependent sodium absorption. Sodium 158-164 mitogen-activated protein kinase 14 Homo sapiens 78-81 20046983-4 2009 This brief review is focused on recent evidence that inappropriate activation of renin in distal nephron segments, by acting on angiotensinogen generated in the proximal tubule cells and delivered to the distal nephron may contribute to increased distal intrarenal angiotensin II formation, sodium retention and development and progression of hypertension. Sodium 291-297 renin Homo sapiens 81-86 19286753-1 2009 INTRODUCTION: Central administration of angiotensin II (Ang II) is known to reduce urinary volume and to increase sodium and potassium excretion. Sodium 114-120 angiotensinogen Rattus norvegicus 40-54 19286753-1 2009 INTRODUCTION: Central administration of angiotensin II (Ang II) is known to reduce urinary volume and to increase sodium and potassium excretion. Sodium 114-120 angiotensinogen Rattus norvegicus 56-62 19286753-6 2009 RESULTS: ICV administration of Ang II to conscious hydrated rats resulted in a significant decrease in urinary volume in the first hour, and an increased sodium and potassium excretion during the 6-hour period of urine collection, which was most effective during the 3 and 6 h. Interference with the NAD(P)H oxidase signalling by central administration of apocynin, tempol or chelerythrine, blunted the natriuretic and kaliuretic effect induced by central administration of Ang II, without affecting its antidiuretic action. Sodium 154-160 angiotensinogen Rattus norvegicus 31-37 19286753-7 2009 CONCLUSION: This study demonstrates that increases of urinary sodium and potassium excretion elicited by central administration of Ang II are mediated by NAD(P)H oxidase- dependent production of superoxide and protein kinase C activation in conscious hydrated rats. Sodium 62-68 angiotensinogen Rattus norvegicus 131-137 19290794-2 2009 The RAAS--involved primarily in blood pressure and sodium homeostasis--is activated in many renal and cardiovascular diseases, and therapy with ACE inhibitors and other blockers of the RAAS has proven to be clinically beneficial. Sodium 51-57 angiotensin I converting enzyme Homo sapiens 144-147 19176751-2 2009 In this study, we used 3 independent assays to determine whether such a small increase in sodium concentrations per se alters endothelial nitric oxide synthase (eNOS) function and contributes to hypertension. Sodium 90-96 nitric oxide synthase 3 Homo sapiens 126-159 19176751-2 2009 In this study, we used 3 independent assays to determine whether such a small increase in sodium concentrations per se alters endothelial nitric oxide synthase (eNOS) function and contributes to hypertension. Sodium 90-96 nitric oxide synthase 3 Homo sapiens 161-165 19129479-1 2009 The newly described yeast endosomal sorting complexes required for transport (ESCRT) protein increased sodium tolerance-1 (Ist1p) binds the late-acting ESCRT proteins Did2p/charged MVB protein (CHMP) 1 and Vps4p and exhibits synthetic vacuolar protein sorting defects when combined with mutations in the Vta1p/LIP5-Vps60p/CHMP5 complex. Sodium 103-109 Vta1p Saccharomyces cerevisiae S288C 304-309 19143560-10 2009 With sodium fluoride (NaF) as the subphase electrolyte, it is demonstrated that sodium exhibits a weak complexation-type interaction with the zwitterionic lipids. Sodium 5-11 C-X-C motif chemokine ligand 8 Homo sapiens 22-25 19143561-7 2009 In the present paper, we first prove that the experimental results for sodium fluoride (NaF) can be fitted by a model that is based on simultaneous complexation of sodium ions with up to three lipid molecules, as suggested by recent molecular dynamics simulations. Sodium 71-77 C-X-C motif chemokine ligand 8 Homo sapiens 88-91 19073901-12 2009 The results are compatible with the notion that at constant arterial pressure, a volume receptor elicited reduction in RSNA via receptors other than beta1-adrenoceptors, decreases renal tubular sodium reabsorption proximal to the macula densa leading to increased NaCl concentration at the macula densa, and subsequent inhibition of renin secretion. Sodium 194-200 renin Homo sapiens 333-338 18547339-12 2009 A thorough clinical investigation of the heterozygote SCNN1A mutation carriers revealed increased sweat sodium and chloride levels consistent with a dominant effect of the mutant S562P allele. Sodium 104-110 sodium channel epithelial 1 subunit alpha Homo sapiens 54-60 18704622-1 2009 Interactions between the renin-angiotensin-aldosterone system and other mechanisms determining sodium balance are important in the pathophysiology of hypertension. Sodium 95-101 renin Homo sapiens 25-30 18704622-2 2009 Low-renin hypertension is a common type of resistant hypertension and is often associated with increased sodium retention. Sodium 105-111 renin Homo sapiens 4-9 19146798-8 2009 Furthermore, research using this technique indicates the effectiveness of renin-angiotensin-aldosterone system blockers in correcting impaired sodium regulation and consequent hypertension in these individuals. Sodium 143-149 renin Homo sapiens 74-79 18996841-5 2009 NHE1 and NCX1 within such protein complex are functionally coupled, such that a local increase of sodium concentration caused by NHE1 can drive NCX1 to generate sodium efflux in exchange for calcium influx. Sodium 98-104 solute carrier family 9 member A1 Homo sapiens 0-4 18996841-5 2009 NHE1 and NCX1 within such protein complex are functionally coupled, such that a local increase of sodium concentration caused by NHE1 can drive NCX1 to generate sodium efflux in exchange for calcium influx. Sodium 98-104 solute carrier family 8 member A1 Homo sapiens 9-13 18996841-5 2009 NHE1 and NCX1 within such protein complex are functionally coupled, such that a local increase of sodium concentration caused by NHE1 can drive NCX1 to generate sodium efflux in exchange for calcium influx. Sodium 98-104 solute carrier family 9 member A1 Homo sapiens 129-133 18996841-5 2009 NHE1 and NCX1 within such protein complex are functionally coupled, such that a local increase of sodium concentration caused by NHE1 can drive NCX1 to generate sodium efflux in exchange for calcium influx. Sodium 98-104 solute carrier family 8 member A1 Homo sapiens 144-148 18996841-5 2009 NHE1 and NCX1 within such protein complex are functionally coupled, such that a local increase of sodium concentration caused by NHE1 can drive NCX1 to generate sodium efflux in exchange for calcium influx. Sodium 161-167 solute carrier family 9 member A1 Homo sapiens 0-4 18996841-5 2009 NHE1 and NCX1 within such protein complex are functionally coupled, such that a local increase of sodium concentration caused by NHE1 can drive NCX1 to generate sodium efflux in exchange for calcium influx. Sodium 161-167 solute carrier family 8 member A1 Homo sapiens 9-13 18996841-5 2009 NHE1 and NCX1 within such protein complex are functionally coupled, such that a local increase of sodium concentration caused by NHE1 can drive NCX1 to generate sodium efflux in exchange for calcium influx. Sodium 161-167 solute carrier family 9 member A1 Homo sapiens 129-133 18996841-5 2009 NHE1 and NCX1 within such protein complex are functionally coupled, such that a local increase of sodium concentration caused by NHE1 can drive NCX1 to generate sodium efflux in exchange for calcium influx. Sodium 161-167 solute carrier family 8 member A1 Homo sapiens 144-148 19132338-5 2009 Vasopressin infusion was associated with an 8 mmol/L fall in serum sodium concentration (p < 0.01) and with higher incidence of hyponatraemia (8 vs. 66%, p < 0.01). Sodium 67-73 arginine vasopressin Homo sapiens 0-11 19132338-8 2009 CONCLUSION: Low-dose vasopressin infusion in haemodynamically stable, but critically ill, children is associated with reduction in urine output and decreased serum sodium level, yielding a high incidence of hyponatraemia. Sodium 164-170 arginine vasopressin Homo sapiens 21-32 19076265-4 2009 Administration of AVP increased sodium excretion. Sodium 32-38 arginine vasopressin Rattus norvegicus 18-21 19104001-4 2009 Infusion of endothelin 1 (ET-1) significantly increased sodium excretion (U(Na)V) in female, but not male, wt rats (Delta U(Na)V: 0.41+/-0.07 versus -0.04+/-0.06 micromol/min, respectively). Sodium 56-62 endothelin 1 Rattus norvegicus 12-24 19104001-4 2009 Infusion of endothelin 1 (ET-1) significantly increased sodium excretion (U(Na)V) in female, but not male, wt rats (Delta U(Na)V: 0.41+/-0.07 versus -0.04+/-0.06 micromol/min, respectively). Sodium 56-62 endothelin 1 Rattus norvegicus 26-30 19076265-5 2009 Pretreatment with V(2) or V(1a) antagonists decreased, and Conivaptan abolished, the sodium excretion induced by AVP. Sodium 85-91 arginine vasopressin Rattus norvegicus 113-116 18940794-1 2009 Copper metabolism Murr1 domain 1 (COMMD1) is a 21-kDa protein involved in copper export from the liver, NF-kappaB signaling, HIV infection, and sodium transport. Sodium 144-150 copper metabolism domain containing 1 Homo sapiens 34-40 19199261-1 2009 OBJECTIVE: To investigate the association of the polymorphisms of rs4961 in alpha-adducin (ADD1) and rs28933400 in Na+/K+ -ATPase a2 (ATP1A2) genes, the products of which are important for sodium transport, with essential hypertension. Sodium 189-195 ATPase Na+/K+ transporting subunit alpha 2 Homo sapiens 134-140 18984663-6 2009 In controls, a close correlation between plasma copeptin and serum sodium (r(2) = 0.62, P < 0.001) or urine osmolality (r(2) = 0.39, P = 0.001) was observed. Sodium 67-73 arginine vasopressin Homo sapiens 48-56 18983442-9 2009 Plasma renin is log-linearly related to salt intake, and normally, decreases in renin secretion are a precondition of natriuresis after increases in total body sodium. Sodium 160-166 renin Homo sapiens 7-12 18983442-9 2009 Plasma renin is log-linearly related to salt intake, and normally, decreases in renin secretion are a precondition of natriuresis after increases in total body sodium. Sodium 160-166 renin Homo sapiens 80-85 18983442-12 2009 Recent results indicate that renal denervation reduces ABP and renin activity, and that sodium loading may decrease renin without changes in ABP, glomerular filtration rate or beta(1)-mediated nerve activity. Sodium 88-94 renin Homo sapiens 116-121 18983445-4 2009 In this article, we focus on our studies that have uncovered the intricate signalling mechanisms downstream of EGFr that regulate both chloride secretion and sodium absorption by colonocytes. Sodium 158-164 epidermal growth factor receptor Homo sapiens 111-115 19071883-9 2009 In addition to the clinical pharmacokinetic analysis, the ability of mipomersen sodium to inhibit the major CYP isoform enzymes (namely CYP1A2, CYP2C9, CYP2C19, CYP2D6 and CYP3A4) was evaluated in cryo-preserved human hepatocytes in vitro. Sodium 80-86 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 161-167 19071883-9 2009 In addition to the clinical pharmacokinetic analysis, the ability of mipomersen sodium to inhibit the major CYP isoform enzymes (namely CYP1A2, CYP2C9, CYP2C19, CYP2D6 and CYP3A4) was evaluated in cryo-preserved human hepatocytes in vitro. Sodium 80-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 172-178 18637833-10 2009 Hippocampal CA3 neurons also showed increased persistent sodium current in kindled animals compared to sham-kindled controls. Sodium 57-63 carbonic anhydrase 3 Mus musculus 12-15 19412798-0 2009 Plasma vasopressin, oxytocin, estradiol, and progesterone related to water and sodium excretion in normal pregnancy and gestational hypertension. Sodium 79-85 arginine vasopressin Homo sapiens 7-18 18753604-4 2009 This study determined the effects of the estrous cycle, pregnancy, progesterone (P4), and interferon tau (IFNT) on expression of both facilitative (SLC2A1, SLC2A3, and SLC2A4) and sodium-dependent (SLC5A1 and SLC5A11) glucose transporters in ovine uterine endometria from Days 10 to 16 of the estrous cycle and Days 10 to 20 of pregnancy, as well as in conceptuses from Days 10 to 20 of pregnancy. Sodium 180-186 solute carrier family 5 member 1 Homo sapiens 198-204 19077666-1 2009 OBJECTIVE: Sodium-dependent and chloride-dependent gamma-aminobutyric acid (GABA) transporter 1 (SLC6A1) is the target of a number of drugs of clinical importance and is a major determinant of synaptic GABA concentrations. Sodium 11-17 solute carrier family 6 member 1 Homo sapiens 97-103 19145783-2 2009 Sodium reabsorption through ENaC in distal nephron segments is a rate-limiting step in transepithelial sodium transport. Sodium 0-6 sodium channel epithelial 1 subunit gamma Rattus norvegicus 28-32 19145783-2 2009 Sodium reabsorption through ENaC in distal nephron segments is a rate-limiting step in transepithelial sodium transport. Sodium 103-109 sodium channel epithelial 1 subunit gamma Rattus norvegicus 28-32 19546583-1 2009 BACKGROUND/AIMS: Angiotensin II promotes sodium retention and influences the central regulation of fluid intake. Sodium 41-47 angiotensinogen Homo sapiens 17-31 19164256-5 2009 METHODS: Theoretical investigations of possible causes of the improved fluid and sodium removal during PD with the combination solution (CIG) were carried out using the three-pore model. Sodium 81-87 fibronectin 1 Homo sapiens 137-140 19164256-10 2009 RESULTS: The simulations described well clinical data that showed a dramatic increase in ultrafiltration and sodium removal with the CIG fluid in comparison with the two other dialysis fluids. Sodium 109-115 fibronectin 1 Homo sapiens 133-136 19816037-0 2009 Sodium load combined with low doses of exogenous angiotensin II upregulate intrarenal angiotensin II. Sodium 0-6 angiotensinogen Rattus norvegicus 86-100 19816037-5 2009 RESULTS: Ang II levels in glomeruli and vessels were exacerbated when sodium load and Ang II were given simultaneously, independently of MAP elevation. Sodium 70-76 angiotensinogen Rattus norvegicus 9-15 19816037-6 2009 In tubules, Ang II staining in the presence of sodium overload was greater in the Ang 0.1 groups than in the Ang 5 groups. Sodium 47-53 angiotensinogen Rattus norvegicus 12-18 19816037-9 2009 CONCLUSION: We conclude that local renal Ang II levels were upregulated when acute sodium overload and nonhypertensive Ang II doses were administered simultaneously in normal rats, independently from blood pressure and glomerular function changes. Sodium 83-89 angiotensinogen Rattus norvegicus 41-47 19713718-5 2009 Expression of the sodium-hydrogen exchanger 3 (NHE3), the predominant transporter responsible for sodium transport in this segment, was measured by immunoblot. Sodium 18-24 solute carrier family 9 (sodium/hydrogen exchanger), member 3 Mus musculus 47-51 18986164-1 2008 The excitatory amino acid carrier EAAC1 belongs to a family of glutamate transporters that use the electrochemical transmembrane gradients of sodium and potassium to mediate uphill transport of glutamate into the cell. Sodium 142-148 solute carrier family 1 member 1 Homo sapiens 34-39 19006386-2 2008 When 4 equiv of sodium were added, complex Na(2)(Et(2)O)(4)[Co(II)(L(Red))(2)] (4) was isolated, which included some crystals of a minor (<2%) product Na(Et(2)O)(2)[Co(III)(L(Red))(2)] (3). Sodium 16-22 mitochondrially encoded cytochrome c oxidase II Homo sapiens 60-66 19688648-1 2009 We report a trigger finger of the right index finger in a 28-year-old man with acromegaly, in which condition growth hormone increases extracellular volume by stimulating sodium reabsorption in the distal nephron. Sodium 171-177 growth hormone 1 Homo sapiens 110-124 18922887-7 2008 TNF-alpha alone (n = 7) caused decreases in RBF (7.9 +/- 0.3 to 6.4 +/- 0.3 ml.min(-1).g(-1)) and GFR (1.04 +/- 0.06 to 0.62 +/- 0.08 ml.min(-1).g(-1)) as well as increases in absolute (0.8 +/- 0.3 to 1.4 +/- 0.3 micromol.min(-1).g(-1)) and fractional excretion of sodium (0.5 +/- 0.2 to 1.5 +/- 0.4%) without affecting arterial pressure. Sodium 265-271 tumor necrosis factor Mus musculus 0-9 18922887-13 2008 The natriuretic response to TNF-alpha is related to its direct effects on tubular sodium reabsorption. Sodium 82-88 tumor necrosis factor Mus musculus 28-37 18202829-7 2008 The two P. yezoensis UTs had 56% AA identity to each other, and showed the closest relationship to higher plant and yeast DUR3 proteins which formed a subfamily of the sodium-solute symporter protein family. Sodium 168-174 Dur3p Saccharomyces cerevisiae S288C 122-126 18955661-2 2008 Ang II affects blood pressure via maintenance of sodium homeostasis by regulating renal Na(+) absorption through its effects on Na/K-ATPase (NKA). Sodium 49-55 angiotensinogen Rattus norvegicus 0-6 18622631-6 2008 Our results indicate that NSIAD is already present during the neonatal period and that molecular analysis of the V2R receptor should therefore be carried out, in all newborns with prolonged euvolemic hyponatremia with hypo-osmolarity, high urinary sodium and normal/low or undetectable AVP levels. Sodium 248-254 arginine vasopressin receptor 2 Homo sapiens 113-116 24692821-20 2008 Blockade of the renin-angiotensin system restored the normal pattern of renal response to high sodium intake in these women. Sodium 95-101 renin Homo sapiens 16-21 18851690-0 2008 Renin-angiotensin-aldosterone responsiveness to low sodium and blood pressure reactivity to angiotensin-II are unrelated to cholesteryl ester transfer protein mass in healthy subjects. Sodium 52-58 renin Homo sapiens 0-5 18818245-1 2008 Angiotensin II (ANGII) plays a central role in the enhanced sodium reabsorption in early type 1 diabetes in man and in streptozotocin-induced (STZ) diabetic rats. Sodium 60-66 angiotensinogen Homo sapiens 0-14 18818245-1 2008 Angiotensin II (ANGII) plays a central role in the enhanced sodium reabsorption in early type 1 diabetes in man and in streptozotocin-induced (STZ) diabetic rats. Sodium 60-66 angiotensinogen Homo sapiens 16-21 18753266-3 2008 Here our goal was to examine the water and sodium intake in this model under basal conditions and in response to increased ANG II levels. Sodium 43-49 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 123-129 18753266-5 2008 Activation of endogenous ANG II production by sodium depletion (10 days low-sodium diet followed by furosemide, 1 mg sc) enhanced NaCl intake in NSE-AT(1A) mice compared with wild types. Sodium 46-52 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 25-31 18753266-5 2008 Activation of endogenous ANG II production by sodium depletion (10 days low-sodium diet followed by furosemide, 1 mg sc) enhanced NaCl intake in NSE-AT(1A) mice compared with wild types. Sodium 76-82 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 25-31 18753266-6 2008 Fos immunohistochemistry, used to assess neuronal activation, demonstrated sodium depletion-enhanced activity in the anteroventral third ventricle region of the brain in NSE-AT(1A) mice compared with control animals. Sodium 75-81 angiotensin II receptor, type 1a Mus musculus 174-179 18851690-4 2008 Blood pressure response to incremental angiotensin-II infusion was assessed in 34 subjects during liberal sodium diet. Sodium 106-112 angiotensinogen Homo sapiens 39-53 18851690-7 2008 No significant differences in (changes) in mean arterial pressure, aldosterone and active plasma renin concentration in response to low sodium were observed between the lowest and highest tertiles of CETP mass, HDL-C and apolipoprotein A-I. Sodium 136-142 renin Homo sapiens 97-102 18701624-1 2008 Sodium excretion is bidirectionally regulated by dopamine, acting on D1-like receptors (D1R) and angiotensin II, acting on AT1 receptors (AT1R). Sodium 0-6 angiotensinogen Rattus norvegicus 97-111 18708479-1 2008 The sodium/iodide symporter (SLC5A5; also known as NIS), a transmembrane glycoprotein principally in the thyroid gland, is responsible for the accumulation of iodide necessary for thyroid hormones. Sodium 4-10 solute carrier family 5 member 5 Homo sapiens 29-35 18708479-1 2008 The sodium/iodide symporter (SLC5A5; also known as NIS), a transmembrane glycoprotein principally in the thyroid gland, is responsible for the accumulation of iodide necessary for thyroid hormones. Sodium 4-10 solute carrier family 5 member 5 Homo sapiens 51-54 18701625-3 2008 We have previously demonstrated that the level of intracellular sodium concentration modulates the regulation of Na-K-ATPase activity by angiotensin II and dopamine. Sodium 64-70 angiotensinogen Homo sapiens 137-151 18986218-1 2008 INTRODUCTION: We conducted a molecular imaging and gene therapy method in alpha-fetoprotein (AFP)-producing hepatocellular carcinoma (HCC) by tumor-specific expression of the human sodium/iodide symporter (hNIS) using an AFP promoter. Sodium 181-187 alpha fetoprotein Homo sapiens 74-91 18986218-1 2008 INTRODUCTION: We conducted a molecular imaging and gene therapy method in alpha-fetoprotein (AFP)-producing hepatocellular carcinoma (HCC) by tumor-specific expression of the human sodium/iodide symporter (hNIS) using an AFP promoter. Sodium 181-187 alpha fetoprotein Homo sapiens 93-96 18986218-1 2008 INTRODUCTION: We conducted a molecular imaging and gene therapy method in alpha-fetoprotein (AFP)-producing hepatocellular carcinoma (HCC) by tumor-specific expression of the human sodium/iodide symporter (hNIS) using an AFP promoter. Sodium 181-187 solute carrier family 5 member 5 Homo sapiens 206-210 18855635-7 2008 The most important sodium transport mechanisms that may underlie increased [Na+]i are: Na+/H(+)-exchanger (NHE-1), Na+-HCO(3)(-) co-transporter (NBC), Na(+)-K(+)-Cl(-) co-transporter (NKCC), Na(+)-channel, Na+/K(+)-ATPase and Na+/Ca(2+)-exchanger (NCX). Sodium 19-25 solute carrier family 9 member A1 Homo sapiens 107-112 18986218-1 2008 INTRODUCTION: We conducted a molecular imaging and gene therapy method in alpha-fetoprotein (AFP)-producing hepatocellular carcinoma (HCC) by tumor-specific expression of the human sodium/iodide symporter (hNIS) using an AFP promoter. Sodium 181-187 alpha fetoprotein Homo sapiens 221-224 18855635-7 2008 The most important sodium transport mechanisms that may underlie increased [Na+]i are: Na+/H(+)-exchanger (NHE-1), Na+-HCO(3)(-) co-transporter (NBC), Na(+)-K(+)-Cl(-) co-transporter (NKCC), Na(+)-channel, Na+/K(+)-ATPase and Na+/Ca(2+)-exchanger (NCX). Sodium 19-25 solute carrier family 8 member A1 Homo sapiens 226-246 18855635-7 2008 The most important sodium transport mechanisms that may underlie increased [Na+]i are: Na+/H(+)-exchanger (NHE-1), Na+-HCO(3)(-) co-transporter (NBC), Na(+)-K(+)-Cl(-) co-transporter (NKCC), Na(+)-channel, Na+/K(+)-ATPase and Na+/Ca(2+)-exchanger (NCX). Sodium 19-25 solute carrier family 8 member A1 Homo sapiens 248-251 18572207-5 2008 Therefore, we hypothesised that renin-angiotensin system (RAS) function is altered by changes in sodium intake during pregnancy. Sodium 97-103 renin Homo sapiens 32-37 18711008-1 2008 The G protein-coupled receptor kinase 4 is involved in renal sodium handling and blood pressure regulation. Sodium 61-67 G protein-coupled receptor kinase 4 Homo sapiens 4-39 18596730-7 2008 Our results show that PPAR alpha pathway induces renal tubular 20-HETE production which affects sodium retention and blood pressure regulation in DOCA-salt-treated mice. Sodium 96-102 peroxisome proliferator activated receptor alpha Mus musculus 22-32 18506424-10 2008 Stimulation of NHE1-stimulated sodium ion uptake might also trigger uptake of chloride ions and osmotically obliged water. Sodium 31-37 solute carrier family 9 member A1 Homo sapiens 15-19 18653476-0 2008 Activity of the p110-alpha subunit of phosphatidylinositol-3-kinase is required for activation of epithelial sodium transport. Sodium 109-115 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 16-26 18653476-0 2008 Activity of the p110-alpha subunit of phosphatidylinositol-3-kinase is required for activation of epithelial sodium transport. Sodium 109-115 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 38-67 18596120-0 2008 Sodium excretion in response to vasopressin and selective vasopressin receptor antagonists. Sodium 0-6 arginine vasopressin Homo sapiens 32-43 18621856-6 2008 However, CN/Tg-iNOS(-/-) mice had improved systolic performance (P < 0.001) and less heart block (P < 0.0001); larger sodium current density and lower serum TNF-alpha levels (P < 0.03); and less apoptosis (P < 0.01) resulting in improved survival (P < 0.0003). Sodium 124-130 nitric oxide synthase 2, inducible Mus musculus 15-19 18985840-1 2008 The syndrome of inappropriate antidiuretic hormone secretion (SIADH) is a disorder of sodium and water balance characterized by hypotonic hyponatremia and impaired water excretion in the absence of renal insufficiency , adrenal insufficiency or any recognized stimulus for the antidiuretic hormone (ADH). Sodium 86-92 arginine vasopressin Homo sapiens 30-50 18985840-1 2008 The syndrome of inappropriate antidiuretic hormone secretion (SIADH) is a disorder of sodium and water balance characterized by hypotonic hyponatremia and impaired water excretion in the absence of renal insufficiency , adrenal insufficiency or any recognized stimulus for the antidiuretic hormone (ADH). Sodium 86-92 arginine vasopressin Homo sapiens 64-67 18596120-0 2008 Sodium excretion in response to vasopressin and selective vasopressin receptor antagonists. Sodium 0-6 arginine vasopressin Homo sapiens 58-69 18596120-1 2008 The mechanisms by which arginine vasopressin (AVP) exerts its antidiuretic and pressor effects, via activation of V2 and V1a receptors, respectively, are relatively well understood, but the possible associated effects on sodium handling are a matter of controversy. Sodium 221-227 arginine vasopressin Homo sapiens 33-44 18596120-6 2008 Vasopressin reduced sodium excretion at 1 mug/kg but increased it at doses >5 umg/kg,an effect that was abolished by the V1a antagonist. Sodium 20-26 arginine vasopressin Homo sapiens 0-11 18596120-8 2008 In the usual range of regulation, antidiuretic effects of vasopressin may be associated with variable sodium retention. Sodium 102-108 arginine vasopressin Homo sapiens 58-69 18689375-0 2008 Blood pressure and interactions between the angiotensin polymorphism AGT M235T and sodium intake: a cross-sectional population study. Sodium 83-89 angiotensinogen Homo sapiens 69-72 18524856-1 2008 Genetic variation in alpha-adducin cytoskeletal protein is implicated in the polymerization and bundling of actin and alteration of the Na/K pump, resulting in abnormal renal sodium transport and hypertension in Milan hypertensive rats and humans. Sodium 175-181 adducin 1 Homo sapiens 21-34 18604476-7 2008 In addition, CK2 also regulates a critical cancer-relevant and CFTR-regulated cation channel (ENaC) that mediates the cellular accumulation of sodium ions within epithelia such as the colon and lung. Sodium 143-149 CF transmembrane conductance regulator Homo sapiens 63-67 18552167-0 2008 Molecular identity of the late sodium current in adult dog cardiomyocytes identified by Nav1.5 antisense inhibition. Sodium 31-37 sodium voltage-gated channel alpha subunit 5 Canis lupus familiaris 88-94 18689375-1 2008 BACKGROUND: Intervention studies have indicated an interaction between the blood pressure response to a low-sodium or a low-fat and high-fruit and -vegetable diet and the angiotensinogen gene (AGT) polymorphisms G-6A and M235T. Sodium 108-114 angiotensinogen Homo sapiens 171-186 18689375-1 2008 BACKGROUND: Intervention studies have indicated an interaction between the blood pressure response to a low-sodium or a low-fat and high-fruit and -vegetable diet and the angiotensinogen gene (AGT) polymorphisms G-6A and M235T. Sodium 108-114 angiotensinogen Homo sapiens 193-196 18700548-3 2008 Insulin increased in association with insulin resistant in MS increases sodium reabsorption in the kidney leading to sodium retention. Sodium 72-78 insulin Homo sapiens 0-7 18470848-0 2008 Enhanced iodide sequestration by 3-biphenyl-5,6-dihydroimidazo[2,1-b]thiazole in sodium/iodide symporter (NIS)-expressing cells. Sodium 81-88 solute carrier family 5 member 5 Homo sapiens 106-109 18503006-4 2008 Expression of GRX6 is modestly upregulated by several stresses (calcium, sodium, and peroxides) in a manner dependent on the Crz1-calcineurin pathway. Sodium 73-79 glutathione-disulfide reductase GRX6 Saccharomyces cerevisiae S288C 14-18 18719325-2 2008 Endocrinopathy had well been controlled by hormone replacement therapy and administration of 1-amino-8-d-arginine-vasopressin with serum sodium concentration within the normal range. Sodium 137-143 arginine vasopressin Homo sapiens 114-125 18700548-3 2008 Insulin increased in association with insulin resistant in MS increases sodium reabsorption in the kidney leading to sodium retention. Sodium 72-78 insulin Homo sapiens 38-45 18700548-3 2008 Insulin increased in association with insulin resistant in MS increases sodium reabsorption in the kidney leading to sodium retention. Sodium 117-123 insulin Homo sapiens 0-7 18700548-3 2008 Insulin increased in association with insulin resistant in MS increases sodium reabsorption in the kidney leading to sodium retention. Sodium 117-123 insulin Homo sapiens 38-45 18700548-4 2008 Increased intra-cranial sodium ions are known to augment sympathetic nervous system activity via stimulation of epithelial sodium channels, mineralocorticoid receptors, the renin-angiotensin-aldosterone system and endogenous digitalislike factors in the brain. Sodium 24-30 renin Homo sapiens 173-178 20641953-3 2004 Angiotensin II also stimulates the production of aldosterone from the adrenal glands, which promotes retention of sodium and water. Sodium 114-120 angiotensinogen Homo sapiens 0-14 18547722-2 2008 Here, we demonstrate that the activation of ERK MAPK pathway by sodium selenite can inhibit endogenous gamma-secretase activity. Sodium 64-70 mitogen-activated protein kinase 1 Homo sapiens 44-47 18547722-2 2008 Here, we demonstrate that the activation of ERK MAPK pathway by sodium selenite can inhibit endogenous gamma-secretase activity. Sodium 64-70 mitogen-activated protein kinase 3 Homo sapiens 48-52 18621678-3 2008 Only L263V and Q1489K generated quantifiable sodium currents when coexpressed in tsA201 cells with the human beta(1) and beta(2) accessory subunits. Sodium 45-51 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 109-116 18591455-2 2008 In previous studies, variants in the genes for alpha-adducin (ADD1), WNK1, and NEDD4L, which all regulate renal sodium absorption, have been associated with increased BP. Sodium 112-118 adducin 1 Homo sapiens 47-60 18591455-2 2008 In previous studies, variants in the genes for alpha-adducin (ADD1), WNK1, and NEDD4L, which all regulate renal sodium absorption, have been associated with increased BP. Sodium 112-118 adducin 1 Homo sapiens 62-66 18591455-9 2008 Physiological interaction between the ADD1 and WNK1-NEDD4L pathways influences the effects of variants in these genes on sodium-related BP regulation. Sodium 121-127 adducin 1 Homo sapiens 38-42 18591455-10 2008 Relatively common alleles in the ADD1, WNK1, and NEDD4L genes when present in combination may have significant effects on renal sodium handling, BP, and antihypertensive response to thiazides. Sodium 128-134 adducin 1 Homo sapiens 33-37 18605990-2 2008 Atrial natriuretic peptide (ANP) is an important regulator of the sodium and volume homeostasis. Sodium 66-72 natriuretic peptide A Homo sapiens 0-26 18605990-2 2008 Atrial natriuretic peptide (ANP) is an important regulator of the sodium and volume homeostasis. Sodium 66-72 natriuretic peptide A Homo sapiens 28-31 18448589-8 2008 These observations suggest that PLZF is a negative regulator of ENaC in renal epithelial cells and might be part of a negative feedback loop that limits aldosterone"s stimulatory effects on sodium reabsorption. Sodium 190-196 zinc finger and BTB domain containing 16 Mus musculus 32-36 18509682-8 2008 Although insulin raised the sodium [35S]sulfate uptake significantly, different concentrations of daidzein, genistein, or 17beta-estradiol showed no significant effects. Sodium 28-34 insulin Homo sapiens 9-16 18591664-7 2008 A390V-SNTA1 expressed with SCN5A, nNOS, and PMCA4b in heterologous cells increased peak and late sodium current compared with WT-SNTA1, and the increase was partially inhibited by NOS blockers. Sodium 97-103 syntrophin alpha 1 Homo sapiens 6-11 18591664-8 2008 Expression of A390V-SNTA1 in cardiac myocytes also increased late sodium current. Sodium 66-72 syntrophin alpha 1 Homo sapiens 20-25 18591664-10 2008 These results establish an SNTA1-based nNOS complex attached to SCN5A as a key regulator of sodium current and suggest that SNTA1 be considered a rare LQTS-susceptibility gene. Sodium 92-98 syntrophin alpha 1 Homo sapiens 27-32 18591664-10 2008 These results establish an SNTA1-based nNOS complex attached to SCN5A as a key regulator of sodium current and suggest that SNTA1 be considered a rare LQTS-susceptibility gene. Sodium 92-98 syntrophin alpha 1 Homo sapiens 124-129 18504321-0 2008 Acute angiotensin II infusions elicit pressure natriuresis in mice and reduce distal fractional sodium reabsorption. Sodium 96-102 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 6-20 18504321-9 2008 These data indicate that Ang II-mediated pressure natriuresis involves an increase in distal sodium delivery combined with a reduced distal nephron fractional sodium reabsorption, suggesting that increased AP prevents the distal nephron transport mechanisms from accommodating the increased distal delivery. Sodium 93-99 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 25-31 18504321-9 2008 These data indicate that Ang II-mediated pressure natriuresis involves an increase in distal sodium delivery combined with a reduced distal nephron fractional sodium reabsorption, suggesting that increased AP prevents the distal nephron transport mechanisms from accommodating the increased distal delivery. Sodium 159-165 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 25-31 18399542-5 2008 Compared with more common VGSCs, Na(v)1.8 and Na(v)1.9 have unusual biophysical and pharmacological properties, including persistent sodium currents and resistance to the canonical sodium channel blocker tetrodotoxin (TTX). Sodium 133-139 sodium channel, voltage-gated, type X, alpha Mus musculus 33-41 18551010-4 2008 DESIGN AND METHODS: Three hundred fifteen participants had renal plasma flow response to subpressor doses of angiotensin II (3 ng/kg/min) measured by para-aminohippuric acid clearance in high-sodium balance. Sodium 192-198 angiotensinogen Homo sapiens 109-123 18668439-2 2008 Sodium (Na(+))-dependent bile acid uptake from portal blood into the liver is mediated primarily by the Na(+) taurocholate co-transporting polypeptide (NTCP), while secretion across the canalicular membrane into the bile is carried out by the bile salt export pump (BSEP). Sodium 0-6 solute carrier family 10 member 1 Homo sapiens 104-150 18668439-2 2008 Sodium (Na(+))-dependent bile acid uptake from portal blood into the liver is mediated primarily by the Na(+) taurocholate co-transporting polypeptide (NTCP), while secretion across the canalicular membrane into the bile is carried out by the bile salt export pump (BSEP). Sodium 0-6 solute carrier family 10 member 1 Homo sapiens 152-156 18560669-4 2008 Hormonal mechanisms including the renin-angiotensin system, aldosterone, and vasopressin are involved in modifying fetal renal excretion, reabsorption of sodium and water, and regulation of vascular volume. Sodium 154-160 renin Homo sapiens 34-39 18560669-4 2008 Hormonal mechanisms including the renin-angiotensin system, aldosterone, and vasopressin are involved in modifying fetal renal excretion, reabsorption of sodium and water, and regulation of vascular volume. Sodium 154-160 arginine vasopressin Homo sapiens 77-88 18426992-8 2008 Upregulation of distal tubular renin helps to explain how sustained intrarenal angiotensin II formation occurs even during juxtaglomerular renin suppression, thus allowing maintained effects on tubular sodium reabsorption that contribute to the hypertension. Sodium 202-208 angiotensinogen Rattus norvegicus 79-93 18413491-0 2008 Blood pressure and renal sodium handling in relation to genetic variation in the DRD1 promoter and GRK4. Sodium 25-31 dopamine receptor D1 Homo sapiens 81-85 18177483-13 2008 We conclude that noradrenaline-induced increases in the expression of NHE-3, NBC-1, BSC-1 and aquaporin-2 are likely to play an important role in the regulation of salt and water transport by noradrenaline in the kidney and may explain, at least in part, the altered renal sodium and water handling associated with overactivation of the sympathetic system. Sodium 273-279 solute carrier family 4 member 4 Rattus norvegicus 77-82 18413491-0 2008 Blood pressure and renal sodium handling in relation to genetic variation in the DRD1 promoter and GRK4. Sodium 25-31 G protein-coupled receptor kinase 4 Homo sapiens 99-103 18413491-1 2008 Activation of type-1 dopamine receptors (DRD1) reduces renal sodium reabsorption. Sodium 61-67 dopamine receptor D1 Homo sapiens 41-45 18413491-6 2008 While standardizing to mean sodium excretion (8.7 mmol/h) and adjusting for covariates and relatedness, RNa(dist) was lower in DRD1 -94GG homozygotes than -94A allele carriers (effect size, -0.94%; P=0.005) with opposite findings for FE(Na) (+0.084%; P=0.014). Sodium 28-34 dopamine receptor D1 Homo sapiens 127-131 18413491-13 2008 In conclusion, renal sodium handling and BP were associated with genetic variation in the DRD1 promoter. Sodium 21-27 dopamine receptor D1 Homo sapiens 90-94 18238849-0 2008 The role of SGK-1 in angiotensin II-mediated sodium reabsorption in human proximal tubular cells. Sodium 45-51 angiotensinogen Homo sapiens 21-35 18238849-1 2008 BACKGROUND: The role of angiotensin II (Ang II) in mediating excessive sodium reabsorption in diabetic nephropathy is recognized. Sodium 71-77 angiotensinogen Homo sapiens 24-38 18238849-1 2008 BACKGROUND: The role of angiotensin II (Ang II) in mediating excessive sodium reabsorption in diabetic nephropathy is recognized. Sodium 71-77 angiotensinogen Homo sapiens 40-46 18238849-8 2008 SGK-1 was silenced in the PTCs using small interfering RNA to determine the role of SGK-1 in mediating Ang II-induced increases in NHE3-mediated sodium uptake. Sodium 145-151 angiotensinogen Homo sapiens 103-109 18238849-13 2008 CONCLUSION: These data suggest that increased sodium reabsorption in renal proximal tubular cells considered to be due to Ang II in diabetes mellitus is mediated through SGK-1 expression. Sodium 46-52 angiotensinogen Homo sapiens 122-128 18381286-1 2008 The sodium- and chloride-coupled gamma-aminobutyric acid (GABA) transporter GAT-1 is essential for efficient synaptic transmission by this neurotransmitter. Sodium 4-10 solute carrier family 6 member 1 Homo sapiens 76-81 18353901-8 2008 In addition, PRL markedly increased paracellular sodium permeability and the permeability ratio of sodium to chloride, which are indicators of the paracellular charge-selective property and are known to be associated with the enhanced paracellular calcium transport. Sodium 49-55 prolactin Rattus norvegicus 13-16 18353901-8 2008 In addition, PRL markedly increased paracellular sodium permeability and the permeability ratio of sodium to chloride, which are indicators of the paracellular charge-selective property and are known to be associated with the enhanced paracellular calcium transport. Sodium 99-105 prolactin Rattus norvegicus 13-16 18458162-1 2008 The Gly460Trp variant of the alpha-adducin gene has been associated with renal sodium retention and salt-sensitive hypertension. Sodium 79-85 adducin 1 Homo sapiens 29-42 18464934-8 2008 Sodium current was lower when NaV1.5 was coexpressed with mutant beta1 or beta1B subunits than when it was coexpressed with WT subunits. Sodium 0-6 BCL2 related protein A1 Homo sapiens 65-70 18354055-10 2008 Finally, the hSERT mutant A169D displayed altered kinetics for sodium binding, indicating that this residue may lie near the putative sodium binding site. Sodium 63-69 solute carrier family 6 member 4 Homo sapiens 13-18 18354055-10 2008 Finally, the hSERT mutant A169D displayed altered kinetics for sodium binding, indicating that this residue may lie near the putative sodium binding site. Sodium 134-140 solute carrier family 6 member 4 Homo sapiens 13-18 18326052-0 2008 Protease-activated receptor-1 mediates thrombin-induced persistent sodium current in human cardiomyocytes. Sodium 67-73 coagulation factor II thrombin receptor Homo sapiens 0-29 18326052-0 2008 Protease-activated receptor-1 mediates thrombin-induced persistent sodium current in human cardiomyocytes. Sodium 67-73 coagulation factor II, thrombin Homo sapiens 39-47 18326052-2 2008 The role of PAR1 was investigated in the thrombin effect on sodium current (I(Na)). Sodium 60-66 coagulation factor II thrombin receptor Homo sapiens 12-16 18326052-2 2008 The role of PAR1 was investigated in the thrombin effect on sodium current (I(Na)). Sodium 60-66 coagulation factor II, thrombin Homo sapiens 41-49 18326052-5 2008 Thrombin-activated PAR1 induced a tetrodotoxin-blocked persistent sodium current, I(NaP), in a concentration-dependent manner with an apparent EC(50) of 28 U/ml. Sodium 66-72 coagulation factor II, thrombin Homo sapiens 0-8 18326052-5 2008 Thrombin-activated PAR1 induced a tetrodotoxin-blocked persistent sodium current, I(NaP), in a concentration-dependent manner with an apparent EC(50) of 28 U/ml. Sodium 66-72 coagulation factor II thrombin receptor Homo sapiens 19-23 18326052-8 2008 Thrombin, through PAR1 activation, increases persistent component of the Na(+) current resulting in an uncontrolled sodium influx into the cardiomyocyte, which can contribute to cellular injuries observed during cardiac ischemia. Sodium 116-122 coagulation factor II, thrombin Homo sapiens 0-8 18326052-8 2008 Thrombin, through PAR1 activation, increases persistent component of the Na(+) current resulting in an uncontrolled sodium influx into the cardiomyocyte, which can contribute to cellular injuries observed during cardiac ischemia. Sodium 116-122 coagulation factor II thrombin receptor Homo sapiens 18-22 18436727-7 2008 Because of their effects on sodium, vasopressin antagonists need to be carefully monitored to ensure that serum sodium levels do not increase too quickly and put the patient at risk for overcorrection or osmotic demyelination syndrome. Sodium 112-118 arginine vasopressin Homo sapiens 36-47 18291093-7 2008 These results reveal a new mechanism by which BK can modulate renal sodium excretion: coupling between B2 receptor and activation of membrane-associated iPLA2. Sodium 68-74 kininogen 1 Homo sapiens 46-48 18291093-7 2008 These results reveal a new mechanism by which BK can modulate renal sodium excretion: coupling between B2 receptor and activation of membrane-associated iPLA2. Sodium 68-74 phospholipase A2 group VI Homo sapiens 153-158 18355814-0 2008 Altered ENaC expression leads to impaired sodium absorption in the noninflamed intestine in Crohn"s disease. Sodium 42-48 sodium channel epithelial 1 subunit gamma Rattus norvegicus 8-12 18355814-7 2008 RESULTS: Electrogenic sodium absorption via ENaC was strongly impaired in the macroscopically noninflamed CD colon because of reduced gamma-ENaC transcription, whereas subcellular localization of ENaC was not changed. Sodium 22-28 sodium channel epithelial 1 subunit gamma Rattus norvegicus 134-144 18192334-5 2008 During vehicle treatment, low sodium reduced renal ACE mRNA and activity without affecting ACE2 mRNA or activity and plasma Ang(1-7) and Ang II balance. Sodium 30-36 angiotensin I converting enzyme Rattus norvegicus 51-54 18192334-7 2008 During ACE inhibition, low sodium reduced both ACE and ACE2 mRNA without affecting ACE2 activity or further reducing ACE activity. Sodium 27-33 angiotensin I converting enzyme Rattus norvegicus 7-10 18192334-7 2008 During ACE inhibition, low sodium reduced both ACE and ACE2 mRNA without affecting ACE2 activity or further reducing ACE activity. Sodium 27-33 angiotensin I converting enzyme Rattus norvegicus 47-50 18192334-7 2008 During ACE inhibition, low sodium reduced both ACE and ACE2 mRNA without affecting ACE2 activity or further reducing ACE activity. Sodium 27-33 angiotensin I converting enzyme Rattus norvegicus 47-50 18192334-9 2008 Plasma Ang(1-7) and Ang II balance is positively shifted towards the beneficial vasopeptide Ang(1-7) by the ACE inhibitor lisinopril, especially during a low sodium intake. Sodium 158-164 angiotensin I converting enzyme Rattus norvegicus 108-111 18355814-7 2008 RESULTS: Electrogenic sodium absorption via ENaC was strongly impaired in the macroscopically noninflamed CD colon because of reduced gamma-ENaC transcription, whereas subcellular localization of ENaC was not changed. Sodium 22-28 sodium channel epithelial 1 subunit gamma Rattus norvegicus 140-144 18355814-9 2008 Exposure of rat distal colon to tumor necrosis factor alpha led to reduced electrogenic sodium absorption because of impaired transcriptional gamma-ENaC induction, which resembled the changes found in CD. Sodium 88-94 tumor necrosis factor Rattus norvegicus 32-59 18355814-2 2008 In this study, we have investigated sodium absorption via epithelial sodium channels (ENaC) in the macroscopically noninflamed colon in active CD. Sodium 36-42 sodium channel epithelial 1 subunit gamma Rattus norvegicus 86-90 18355814-12 2008 CONCLUSIONS: In CD, macroscopically noninflamed colon contributes to diarrhea via impaired ENaC-mediated sodium absorption. Sodium 105-111 sodium channel epithelial 1 subunit gamma Rattus norvegicus 91-95 18355814-3 2008 METHODS: Sodium transport via ENaC was investigated in Ussing chambers using biopsy specimens of sigmoid colon from controls and active CD limited to the small intestine. Sodium 9-15 sodium channel epithelial 1 subunit gamma Rattus norvegicus 30-34 18355814-7 2008 RESULTS: Electrogenic sodium absorption via ENaC was strongly impaired in the macroscopically noninflamed CD colon because of reduced gamma-ENaC transcription, whereas subcellular localization of ENaC was not changed. Sodium 22-28 sodium channel epithelial 1 subunit gamma Rattus norvegicus 44-48 18633183-0 2008 Angiotensin II increases intrarenal transforming growth factor-beta1 in rats submitted to sodium overload independently of blood pressure. Sodium 90-96 angiotensinogen Rattus norvegicus 0-14 17940875-1 2008 Arginine vasopressin (AVP) is known to a neuropeptide that plays important roles in water conservation, sodium homeostasis, and in the regulation of serum osmolality. Sodium 104-110 arginine vasopressin Rattus norvegicus 9-20 17940875-1 2008 Arginine vasopressin (AVP) is known to a neuropeptide that plays important roles in water conservation, sodium homeostasis, and in the regulation of serum osmolality. Sodium 104-110 arginine vasopressin Rattus norvegicus 22-25 18420307-2 2008 Bolus U-II injection (15 nmol kg(-1)) caused a transient decrease in glomerular filtration rate (GFR), urine flow rate (UV), urinary sodium (UNaV) and potassium excretion (U(K)V) that corresponded with a committed decrease in mean arterial pressure (MAP) and renal blood flow (RBF) during the first 30 min. Sodium 133-139 urotensin 2 Rattus norvegicus 6-10 18256274-10 2008 Because these transcriptional effects of ANG II in isolated nuclei were induced by ANG II in the absence of cell surface receptor-mediated signaling and completely blocked by losartan, we concluded that ANG II may directly stimulate nuclear AT(1a) receptors to induce transcriptional responses that are associated with tubular epithelial sodium transport, cellular growth and hypertrophy, and proinflammatory cytokines. Sodium 338-344 angiotensinogen Rattus norvegicus 41-47 18318439-15 2008 CONCLUSION: In BDL rats, U-II is a mediator of splanchnic vasodilation, portal hypertension and renal sodium retention. Sodium 102-108 urotensin 2 Rattus norvegicus 25-29 18633183-13 2008 In conclusion, the interaction of Ang II with acute-sodium overload exacerbated intrarenal TGF-beta1, alpha-SMA and NF-kappaB expression, independently from changes in blood pressure levels, in normal rats. Sodium 52-58 transforming growth factor, beta 1 Rattus norvegicus 91-100 18319322-0 2008 Retinoic acid stimulation of the sodium/iodide symporter in MCF-7 breast cancer cells is mediated by the insulin growth factor-I/phosphatidylinositol 3-kinase and p38 mitogen-activated protein kinase signaling pathways. Sodium 33-39 mitogen-activated protein kinase 14 Homo sapiens 163-166 18256274-7 2008 ANG II markedly increased in vitro transcription of mRNAs for transforming growth factor-beta1 by 143% (P < 0.01), macrophage chemoattractant protein-1 by 89% (P < 0.01), and the sodium and hydrogen exchanger-3 by 110% (P < 0.01). Sodium 185-191 angiotensinogen Rattus norvegicus 0-6 18332863-0 2008 Sodium/hydrogen exchange inhibition with cariporide reduces leukocyte adhesion via P-selectin suppression during inflammation. Sodium 0-6 selectin P Rattus norvegicus 83-93 18259039-10 2008 This study shows that the reduction of angiotensin II effects during the nephrogenic period modifies renal function and induces the development of an angiotensin II-dependent hypertension that becomes sodium sensitive during aging. Sodium 201-207 angiotensinogen Rattus norvegicus 39-53 18259039-10 2008 This study shows that the reduction of angiotensin II effects during the nephrogenic period modifies renal function and induces the development of an angiotensin II-dependent hypertension that becomes sodium sensitive during aging. Sodium 201-207 angiotensinogen Rattus norvegicus 150-164 18633183-0 2008 Angiotensin II increases intrarenal transforming growth factor-beta1 in rats submitted to sodium overload independently of blood pressure. Sodium 90-96 transforming growth factor, beta 1 Rattus norvegicus 36-68 18633183-1 2008 Angiotensin II (Ang II) promotes sodium-retention, cell growth and fibrosis in addition to its classical effects on blood pressure and fluid homeostasis. Sodium 33-39 angiotensinogen Rattus norvegicus 0-22 18633183-2 2008 In this study we examined whether low and non-hypertensive doses of exogenous Ang II could enhance the intrarenal expression of transforming growth factor-beta1 (TGF-beta1) observed in rats submitted to sodium overload. Sodium 203-209 angiotensinogen Rattus norvegicus 78-84 18633183-2 2008 In this study we examined whether low and non-hypertensive doses of exogenous Ang II could enhance the intrarenal expression of transforming growth factor-beta1 (TGF-beta1) observed in rats submitted to sodium overload. Sodium 203-209 transforming growth factor, beta 1 Rattus norvegicus 162-171 18633183-12 2008 Moreover, Ang II and sodium overload induced additional changes in TGF-beta1, alpha-SMA and NF-kappaB immunostanding in glomeruli, medullary tubules and renal vessels. Sodium 21-27 transforming growth factor, beta 1 Rattus norvegicus 67-76 18304838-2 2008 In the present work we sought to develop a simplified protocol for measuring the acute activity of MR antagonists on urinary excretion of sodium and potassium in rats based on the original studies of mineralocorticoids in adrenalectomized rats reported by Kagawa et al. Sodium 138-144 nuclear receptor subfamily 3, group C, member 2 Rattus norvegicus 99-101 18536434-1 2008 The mechanism of interaction mechanism of barbital sodium with bovine serum albumin (BSA) was studied by fluorescence spectroscopy. Sodium 51-57 albumin Homo sapiens 70-83 18184654-5 2008 Co-expression of MOG1 with Nav1.5 in HEK293 cells increased sodium current densities. Sodium 60-66 RAN guanine nucleotide release factor Homo sapiens 17-21 18184654-7 2008 Western blot analysis revealed that MOG1 increased cell surface expression of Nav1.5, which may be the underlying mechanism by which MOG1 increased sodium current densities. Sodium 148-154 RAN guanine nucleotide release factor Homo sapiens 36-40 18184654-7 2008 Western blot analysis revealed that MOG1 increased cell surface expression of Nav1.5, which may be the underlying mechanism by which MOG1 increased sodium current densities. Sodium 148-154 RAN guanine nucleotide release factor Homo sapiens 133-137 18219299-0 2008 Renal response to angiotensin II is blunted in sodium-sensitive normotensive men. Sodium 47-53 angiotensinogen Homo sapiens 18-32 18398972-6 2008 Elevated breast milk sodium concentration (> or =13 mmol/L) at 4 months was associated with HIV transmission, low maternal CD4 cell count, and high maternal plasma viral load. Sodium 21-27 CD4 molecule Homo sapiens 126-129 18270170-1 2008 Calmodulin (CaM) regulates steady-state inactivation of sodium currents (Na(V)1.4) in skeletal muscle. Sodium 56-62 calmodulin 1 Homo sapiens 0-10 18270170-1 2008 Calmodulin (CaM) regulates steady-state inactivation of sodium currents (Na(V)1.4) in skeletal muscle. Sodium 56-62 calmodulin 1 Homo sapiens 12-15 18304838-7 2008 RESULTS: Aldosterone had no significant effect on sodium or potassium excretion and MR antagonists dose-dependently increased the ratio of sodium to potassium. Sodium 139-145 nuclear receptor subfamily 3, group C, member 2 Rattus norvegicus 84-86 17971421-2 2008 In this study, we investigated mechanisms by which acute exposure to peroxynitrite impairs function of the sodium-dependent hemicholinium-3 (HC-3)-sensitive choline transporter (CHT) that provides substrate for acetylcholine synthesis. Sodium 107-113 solute carrier family 6 member 8 Rattus norvegicus 157-176 17971421-2 2008 In this study, we investigated mechanisms by which acute exposure to peroxynitrite impairs function of the sodium-dependent hemicholinium-3 (HC-3)-sensitive choline transporter (CHT) that provides substrate for acetylcholine synthesis. Sodium 107-113 solute carrier family 6 member 8 Rattus norvegicus 178-181 18305244-0 2008 Pumilio binds para mRNA and requires Nanos and Brat to regulate sodium current in Drosophila motoneurons. Sodium 64-70 nanos Drosophila melanogaster 37-42 18305244-0 2008 Pumilio binds para mRNA and requires Nanos and Brat to regulate sodium current in Drosophila motoneurons. Sodium 64-70 brain tumor Drosophila melanogaster 47-51 18060773-3 2008 Intracellular delivery of dipalmitoyl PtdIns(3,4,5)PT(3)-mimicked insulin in activating sodium transport in A6 cells. Sodium 88-94 insulin Homo sapiens 66-73 18297608-8 2008 These findings suggest that iNOS-derived NO does not produce a harmful effect but rather protects the ADR-treated kidney against sodium excretion. Sodium 129-135 nitric oxide synthase 2 Homo sapiens 28-32 17947299-0 2008 Sodium-potassium ATPase 1 subunit is a molecular partner of Wolframin, an endoplasmic reticulum protein involved in ER stress. Sodium 0-6 wolframin ER transmembrane glycoprotein Homo sapiens 60-69 18024548-11 2008 These data suggest that dietary sodium regulates ENaC expression and the quantitative importance of the vascular ENaC signaling pathway contributing to myogenic constriction. Sodium 32-38 sodium channel epithelial 1 subunit gamma Rattus norvegicus 49-53 20641324-3 2004 Angiotensin II also stimulates the production of aldosterone from the adrenal glands that promotes sodium and water retention. Sodium 99-105 angiotensinogen Homo sapiens 0-14 18404603-1 2008 INTRODUCTION: We have previously demonstrated a profound hypotensive response to the angiotensin II type 1 (AT1)-receptor antagonist losartan in rats consuming a normal salt diet that is not seen in salt-loaded rats, presumably due to a suppression of the renin-angiotensin system (RAS) by high sodium levels. Sodium 295-301 angiotensin II receptor, type 1b Rattus norvegicus 85-121 18568693-2 2008 We hypothesize that PPARalpha modulation of ion transport defines the capacity for sodium excretion (U(Na)V). Sodium 83-89 peroxisome proliferator activated receptor alpha Mus musculus 20-29 18182798-9 2008 For kidney disease in the metabolic syndrome it is relevant that insulin resistance is linked to salt sensitivity and increased tubular reabsorption of sodium. Sodium 152-158 insulin Homo sapiens 65-72 18090672-5 2008 Medullary cyclooxygenase-2 metabolites modulate salt and water excretion, and cyclooxygenase-2 inhibitors lead to sodium and volume retention and may raise blood pressure. Sodium 114-120 prostaglandin-endoperoxide synthase 2 Homo sapiens 78-94 18209477-8 2008 The NHE8 cDNA transfected cells exhibited a sodium-dependent proton exchanger activity having a Km for pH(i) of approximately pH 6.5, and a Km for sodium of approximately 23 mM. Sodium 44-50 solute carrier family 9 (sodium/hydrogen exchanger), member 8 Mus musculus 4-8 17989136-0 2008 Chronic activation of plasma renin is log-linearly related to dietary sodium and eliminates natriuresis in response to a pulse change in total body sodium. Sodium 70-76 renin Homo sapiens 29-34 17989136-0 2008 Chronic activation of plasma renin is log-linearly related to dietary sodium and eliminates natriuresis in response to a pulse change in total body sodium. Sodium 148-154 renin Homo sapiens 29-34 18661333-3 2008 This ubiquitously expressed sodium/hydrogen exchanger (NHE-1) plays a central housekeeping role in all cells regulating cell volume and internal pH (pHi). Sodium 28-34 solute carrier family 9 member A1 Homo sapiens 55-60 20021424-9 2008 (2) In diabetic neuropathy, the activation of the polyol pathway mediated by an enzyme, aldose reductase, leads to reduced Na(+)/K(+) pump activity, and intra-axonal sodium accumulation; sodium currents are reduced presumably due to decreased trans-axonal sodium gradient. Sodium 166-172 aldo-keto reductase family 1 member B Homo sapiens 88-104 20021424-9 2008 (2) In diabetic neuropathy, the activation of the polyol pathway mediated by an enzyme, aldose reductase, leads to reduced Na(+)/K(+) pump activity, and intra-axonal sodium accumulation; sodium currents are reduced presumably due to decreased trans-axonal sodium gradient. Sodium 187-193 aldo-keto reductase family 1 member B Homo sapiens 88-104 20021424-9 2008 (2) In diabetic neuropathy, the activation of the polyol pathway mediated by an enzyme, aldose reductase, leads to reduced Na(+)/K(+) pump activity, and intra-axonal sodium accumulation; sodium currents are reduced presumably due to decreased trans-axonal sodium gradient. Sodium 187-193 aldo-keto reductase family 1 member B Homo sapiens 88-104 20021424-10 2008 Aldose reductase inhibitiors improve nodal sodium currents, as well as nerve conduction, and this can be objectively assessed by threshold tracking. Sodium 43-49 aldo-keto reductase family 1 member B Homo sapiens 0-16 18509500-4 2008 The tubular function is also concerned as diabetic animals supplemented with C-peptide exhibit better renal function resulting in reduced urinary sodium waste and protein excretion together with the reduction of the diabetes-induced glomerular hyperfiltration. Sodium 146-152 insulin Homo sapiens 77-86 18047633-12 2008 Levels of IL-1beta, IL-6 and AngII were all significantly increased (P < 0.05) in the sodium-loaded rats. Sodium 89-95 interleukin 1 beta Rattus norvegicus 10-18 18047633-12 2008 Levels of IL-1beta, IL-6 and AngII were all significantly increased (P < 0.05) in the sodium-loaded rats. Sodium 89-95 interleukin 6 Rattus norvegicus 20-24 18047633-12 2008 Levels of IL-1beta, IL-6 and AngII were all significantly increased (P < 0.05) in the sodium-loaded rats. Sodium 89-95 angiotensinogen Rattus norvegicus 29-34 18600398-7 2008 Alkaline phosphatase (ALP) activity and mineralization ability increased in cells treated at 10(-8) to 10(-5) M with sodium versus the controls, but decreased at 5.0 x 10(-4) to 10(-3) M dosage. Sodium 117-123 alkaline phosphatase, placental Homo sapiens 0-20 30743782-9 2008 Treatment with vasopressin analogues is almost always effective in controlling renal water excretion and normalizing plasma sodium concentrations. Sodium 124-130 arginine vasopressin Homo sapiens 15-26 19169968-5 2008 Since both vasopressin and oestrogen have been reported to inhibit ion fluxes essential for the adaptation of the brain to the lowering of serum sodium concentration, we sought to study the effect of acute and chronic hyponatraemia or hyponatraemia associated with vasopressin on brain morphology in male and female rats. Sodium 145-151 arginine vasopressin Rattus norvegicus 11-22 18600398-7 2008 Alkaline phosphatase (ALP) activity and mineralization ability increased in cells treated at 10(-8) to 10(-5) M with sodium versus the controls, but decreased at 5.0 x 10(-4) to 10(-3) M dosage. Sodium 117-123 alkaline phosphatase, placental Homo sapiens 22-25 18191075-5 2008 In 148 episodes of DH corrected with insulin only, the mean increase in serum sodium per 100-mg/dl decrease in serum glucose (Delta[Na]/Delta[Glu]) was -1.61 mmol/l. Sodium 78-84 insulin Homo sapiens 37-44 18460877-12 2008 It is hypothesized that this is caused by sodium retention during the day mediated by renal nerve sympathetic activity which together with angiotensin II acts on the kidney to increase tubular sodium reabsorption either directly or by reducing daytime glomerular filtration rate. Sodium 193-199 angiotensinogen Homo sapiens 139-153 18600297-7 2008 Moderate but significant increases in plasma AGT (40%, p = 0.01) and systolic blood pressure (4-6 mmHg, p ranging from 0.01 to <0.001) were observed in the sodium-sensitive background, but not in the sodium-resistant animals. Sodium 159-165 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 45-48 18600297-7 2008 Moderate but significant increases in plasma AGT (40%, p = 0.01) and systolic blood pressure (4-6 mmHg, p ranging from 0.01 to <0.001) were observed in the sodium-sensitive background, but not in the sodium-resistant animals. Sodium 203-209 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 45-48 19283081-5 2008 This unwanted effect is due to the activation of PPARgamma in the mesonephric distal collecting system, where PPARgamma positively regulates sodium and water resorbtion leading to the expansion of interstitial fluid volume. Sodium 141-147 peroxisome proliferator activated receptor gamma Homo sapiens 49-58 19283081-5 2008 This unwanted effect is due to the activation of PPARgamma in the mesonephric distal collecting system, where PPARgamma positively regulates sodium and water resorbtion leading to the expansion of interstitial fluid volume. Sodium 141-147 peroxisome proliferator activated receptor gamma Homo sapiens 110-119 18814578-0 2008 Comparative equilibrium studies of sorption of Pb(II) ions by sodium and calcium alginate. Sodium 62-68 submaxillary gland androgen regulated protein 3B Homo sapiens 47-53 17931588-2 2007 High levels of angiotensin II may be responsible for hypertension and heart failure because they increase systemic vascular resistance, arterial pressure, and sodium and fluid retention. Sodium 159-165 angiotensinogen Homo sapiens 15-29 17895315-7 2007 RESULTS: In low-sodium balance, the increases in systolic and diastolic BP in response to infused AngII were blunted with increased serum progesterone concentrations (P < 0.05). Sodium 16-22 angiotensinogen Homo sapiens 98-103 18056581-2 2007 For FHM, three genes have been identified encoding subunits of a calcium channel (CACNA1A), a sodium-potassium pump (ATP1A2), and a sodium channel (SCN1A). Sodium 94-100 ATPase Na+/K+ transporting subunit alpha 2 Homo sapiens 117-123 18221617-3 2007 There are conclusive data that vasopressin antagonists improve or normalize serum sodium in this patient population. Sodium 82-88 arginine vasopressin Homo sapiens 31-42 17895315-13 2007 CONCLUSIONS: In postmenopausal women in low-sodium balance, the pressor and renovascular responses to AngII are blunted with increased endogenous progesterone concentrations. Sodium 44-50 angiotensinogen Homo sapiens 102-107 18080921-10 2007 In the cirrhotic group, insulin like growth factor- 1 level was positively correlated with serum albumin and negatively correlated with serum creatinine and sodium levels and spleen size. Sodium 157-163 insulin like growth factor 1 Homo sapiens 24-53 17965845-1 2007 Non-steroidal antiphlogistics and COX-2 inhibitors routinely cause sodium retention and a blood pressure increase by about 5 mmHg, a decrease in renal function (by about 10 ml/min) and in 1-2% an acute renal failure. Sodium 67-73 mitochondrially encoded cytochrome c oxidase II Homo sapiens 34-39 17714972-11 2007 Urate monosodium crystals are specifically detected via the NALP3 inflammasome, which results in marked IL-1beta overproduction and initiation of an inflammatory response. Sodium 6-16 NLR family pyrin domain containing 3 Homo sapiens 60-65 17714972-11 2007 Urate monosodium crystals are specifically detected via the NALP3 inflammasome, which results in marked IL-1beta overproduction and initiation of an inflammatory response. Sodium 6-16 interleukin 1 beta Homo sapiens 104-112 17656065-5 2007 Moderate sodium restriction, possibly combined with diuretic therapy, helps to maximize the effect of renin-angiotensin inhibitors. Sodium 9-15 renin Homo sapiens 102-107 17554565-1 2007 Sodium retention and edema are common features of nephrotic syndrome that are classically attributed to hypovolemia and activation of the renin-angiotensin-aldosterone system. Sodium 0-6 renin Homo sapiens 138-143 17960916-0 2007 Sodium-dependent reorganization of the sugar-binding site of SGLT1. Sodium 0-6 solute carrier family 5 member 1 Homo sapiens 61-66 17629970-1 2007 alpha2-Adrenoceptor activation with moxonidine (alpha2-adrenergic/imidazoline receptor agonist) into the lateral parabrachial nucleus (LPBN) enhances angiotensin II/hypovolaemia-induced sodium intake and drives cell dehydrated rats to ingest hypertonic sodium solution besides water. Sodium 186-192 angiotensinogen Rattus norvegicus 150-164 17967976-9 2007 Compared with wild-type GPD1-L, GPD1-L mutations coexpressed with SCN5A in heterologous HEK cells produced a significantly reduced sodium current (P<0.01). Sodium 131-137 glycerol-3-phosphate dehydrogenase 1 like Homo sapiens 32-38 17967976-10 2007 Adenovirus-mediated gene transfer of the E83K-GPD1-L mutation into neonatal mouse myocytes markedly attenuated the sodium current (P<0.01). Sodium 115-121 glycerol-3-phosphate dehydrogenase 1 like Homo sapiens 46-52 17967976-12 2007 CONCLUSIONS: The present study is the first to report mutations in GPD1-L as a pathogenic cause for a small subset of sudden infant death syndrome via a secondary loss-of-function mechanism whereby perturbations in GPD1-L precipitate a marked decrease in the peak sodium current and a potentially lethal BrS-like proarrhythmic substrate. Sodium 264-270 glycerol-3-phosphate dehydrogenase 1 like Homo sapiens 67-73 17967976-12 2007 CONCLUSIONS: The present study is the first to report mutations in GPD1-L as a pathogenic cause for a small subset of sudden infant death syndrome via a secondary loss-of-function mechanism whereby perturbations in GPD1-L precipitate a marked decrease in the peak sodium current and a potentially lethal BrS-like proarrhythmic substrate. Sodium 264-270 glycerol-3-phosphate dehydrogenase 1 like Homo sapiens 215-221 17928448-0 2007 Reduced sodium current in Purkinje neurons from Nav1.1 mutant mice: implications for ataxia in severe myoclonic epilepsy in infancy. Sodium 8-14 sodium channel, voltage-gated, type I, alpha Mus musculus 48-54 17939993-3 2007 Increases in intracellular sodium are paralleled by elevations in intracellular calcium through the reversible Na(+)/Ca(2+) exchanger, leading to the activation of SIK1 (Thr-322 phosphorylation) by a calcium calmodulin-dependent kinase. Sodium 27-33 solute carrier family 8 member A1 Homo sapiens 111-133 17692454-7 2007 Furthermore, EGFR signaling may serve as a negative feedback loop to limit sodium retention. Sodium 75-81 epidermal growth factor receptor Homo sapiens 13-17 17704762-6 2007 Here we show that introduction of a negatively charged amino acid at or near one of the two putative sodium-binding sites of the GABA (gamma-aminobutyric acid) transporter GAT-1 from rat brain (also called SLC6A1) renders both net flux and exchange of GABA largely chloride independent. Sodium 101-107 solute carrier family 6 member 1 Homo sapiens 172-177 17928448-8 2007 Our results show that Na(V)1.1 channels play a crucial role in the excitability of cerebellar Purkinje neurons, with major contributions to peak, persistent, and resurgent forms of sodium current and to sustained action potential firing. Sodium 181-187 sodium channel, voltage-gated, type I, alpha Mus musculus 22-30 17286173-12 2007 Snow on the trail was significantly denser and significantly more acidic with significantly higher concentrations of sodium, ammonium, calcium, magnesium, fluoride, and sulfate than in snow off the trail. Sodium 117-123 TNF superfamily member 10 Homo sapiens 12-17 17693541-8 2007 Four weeks on a low-sodium diet (0.08%) to raise PRA reduced reactivity to ANG II in OZR back to normal levels without effect on LZR. Sodium 20-26 angiotensinogen Rattus norvegicus 75-81 17485228-0 2007 Abnormal expression of ENaC and SGK1 mRNA induced by dietary sodium in Dahl salt-sensitively hypertensive rats. Sodium 61-67 sodium channel epithelial 1 subunit gamma Rattus norvegicus 23-27 17485228-1 2007 Epithelial sodium channel (ENaC) plays a crucial role in controlling sodium reabsorption in the kidney keeping the normal blood pressure. Sodium 11-17 sodium channel epithelial 1 subunit gamma Rattus norvegicus 27-31 17485228-3 2007 In the present study, we investigated whether dietary sodium abnormally affects the expression of ENaC and SGK1 mRNA in DS rats. Sodium 54-60 sodium channel epithelial 1 subunit gamma Rattus norvegicus 98-102 17485228-7 2007 The expression of beta- and gamma-ENaC mRNA in DS rats was also abnormally increased by high sodium diet unlike DR rats. Sodium 93-99 sodium channel epithelial 1 subunit gamma Rattus norvegicus 34-38 17686957-0 2007 Insulin"s impact on renal sodium transport and blood pressure in health, obesity, and diabetes. Sodium 26-32 insulin Homo sapiens 0-7 17560155-6 2007 During chronic GH-exposure an initial sodium retaining state often occurs, followed by a normalization of the urinary sodium excretion, although extracellular volume expansion still persists. Sodium 38-44 growth hormone 1 Homo sapiens 15-17 17560155-6 2007 During chronic GH-exposure an initial sodium retaining state often occurs, followed by a normalization of the urinary sodium excretion, although extracellular volume expansion still persists. Sodium 118-124 growth hormone 1 Homo sapiens 15-17 17560155-9 2007 We propose, that the GH-induced increase in NKCC2 activity may explain the initial water and sodium retention seen in a number of studies. Sodium 93-99 growth hormone 1 Homo sapiens 21-23 17560155-9 2007 We propose, that the GH-induced increase in NKCC2 activity may explain the initial water and sodium retention seen in a number of studies. Sodium 93-99 solute carrier family 12 member 1 Homo sapiens 44-49 17845533-9 2007 These results indicate that sodium-independent transport of bile salts may be mediated by Oatp2 and 4 during biliary obstruction, because its expression remains unaffected and may compensate for loss of Oatp1 expression and function in cholestatic hepatocytes. Sodium 28-34 solute carrier organic anion transporter family, member 1a1 Rattus norvegicus 203-208 17485228-9 2007 These observations indicate that the expression of ENaC and SGK1 mRNA is abnormally regulated by dietary sodium in salt-sensitively hypertensive rats, and that this abnormal expression would be one of the factors causing salt-sensitive hypertension. Sodium 105-111 sodium channel epithelial 1 subunit gamma Rattus norvegicus 51-55 17683784-1 2007 An enhanced sodium appetite is found in rats by the synergist interaction of peripheral mineralocorticoids, deoxycorticosterone acetate (DOCA), and central angiotensin II (AngII), the synergy theory. Sodium 12-18 angiotensinogen Rattus norvegicus 156-170 17573101-0 2007 Vasopressin and angiotensin receptors of the medial septal area of the brain in the control of thirst and salt appetite induced by vasopressin in water-deprived and sodium-depleted rats. Sodium 165-171 arginine vasopressin Rattus norvegicus 0-11 17573101-2 2007 A stainless steel cannula was implanted into the medial septal area (MSA) of male Holtzman rats AVP injection enhanced water and sodium intake in a dose-dependent manner. Sodium 129-135 arginine vasopressin Rattus norvegicus 96-99 17573101-3 2007 Pretreatment with V(1) antagonist injected into the MSA produced a dose-dependent reduction, whereas prior injection of V(2) antagonist increased, in a dose-dependent manner, the water and sodium responses elicited by the administration of AVP. Sodium 189-195 arginine vasopressin Rattus norvegicus 240-243 17573101-4 2007 Both AT(1) and AT(2) antagonists administered into the MSA elicited a concentration-dependent decrease in water and sodium intake induced by AVP, while simultaneous injection of the two antagonists was more effective in decreasing AVP responses. Sodium 116-122 arginine vasopressin Rattus norvegicus 141-144 17573101-5 2007 These results also indicate that the increase in water and sodium intake induced by AVP was mediated primarily by MSA AT(1) receptors. Sodium 59-65 arginine vasopressin Rattus norvegicus 84-87 17683784-1 2007 An enhanced sodium appetite is found in rats by the synergist interaction of peripheral mineralocorticoids, deoxycorticosterone acetate (DOCA), and central angiotensin II (AngII), the synergy theory. Sodium 12-18 angiotensinogen Rattus norvegicus 172-177 17472579-1 2007 The alpha-adducin Gly460Trp polymorphism alters renal sodium transport and is associated with hypertension. Sodium 54-60 adducin 1 Homo sapiens 4-17 17567721-8 2007 In experiment 2, the hypothesis that prior experience with central VP would cross-sensitize rats to drinking hypertonic sodium (NaCl) solutions was tested. Sodium 120-126 arginine vasopressin Rattus norvegicus 67-69 17567721-12 2007 This pattern of cross-sensitization links central VP signaling, amphetamine, and sodium deficiency, and therefore it may play a role in the cross-sensitization between sodium appetite and amphetamines. Sodium 81-87 arginine vasopressin Rattus norvegicus 50-52 17513344-7 2007 Injections of L-NAME or Ang II produced an increase in plasma levels of AVP, OT and ANP, a reduction in urinary volume and an increase in sodium excretion. Sodium 138-144 angiotensinogen Rattus norvegicus 14-30 17786049-1 2007 COMMD1 is a protein which is associated with multiple cellular pathways, including NFkappaB signaling, copper homeostasis and sodium transport. Sodium 126-132 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 83-91 17404832-9 2007 These results suggest that the enhancement of TTX-sensitive sodium current density in differentiated NG108-15 cells is mainly due to the increase in the expression of the TTX-sensitive voltage-gated Na+ channel, NaV1.7. Sodium 60-66 sodium channel, voltage-gated, type IX, alpha Mus musculus 212-218 17970536-0 2007 Does bicarbonated mineral water rich in sodium change insulin sensitivity of postmenopausal women? Sodium 40-46 insulin Homo sapiens 54-61 17404832-0 2007 Enhancement of sodium current in NG108-15 cells during neural differentiation is mainly due to an increase in NaV1.7 expression. Sodium 15-21 sodium channel, voltage-gated, type IX, alpha Mus musculus 110-116 17970536-1 2007 AIM: To study the effects of drinking 0.5 L of two sodium-rich bicarbonated mineral waters (BMW-1 and 2), with a standard meal, on postprandial insulin and glucose changes. Sodium 51-57 insulin Homo sapiens 144-151 17544362-8 2007 These results support and extend the role of GRK2 in sodium transport regulation. Sodium 53-59 G protein-coupled receptor kinase 2 Homo sapiens 45-49 17687025-4 2007 The signaling toward the degenerative phenotype involved suppression of the extracellular signal-regulated kinase 1/2 (ERK1/2) pathway, and electrophysiological recording showed that the neurodegeneration is accompanied by reduced NMDAR current and Ca2+ influx, as well as reduced voltage-gated sodium currents, consistent with compromised neurite integrity. Sodium 295-301 mitogen-activated protein kinase 1 Homo sapiens 76-117 17687025-4 2007 The signaling toward the degenerative phenotype involved suppression of the extracellular signal-regulated kinase 1/2 (ERK1/2) pathway, and electrophysiological recording showed that the neurodegeneration is accompanied by reduced NMDAR current and Ca2+ influx, as well as reduced voltage-gated sodium currents, consistent with compromised neurite integrity. Sodium 295-301 mitogen-activated protein kinase 3 Homo sapiens 119-125 17475897-11 2007 These results suggest that altered expression of alpha-, beta-, and gamma-ENaC may contribute to impaired renal sodium and water handling in response to ureteral obstruction. Sodium 112-118 sodium channel epithelial 1 subunit gamma Rattus norvegicus 68-78 17537986-6 2007 In contrast, Agtr1a-/- mice had lower basal systolic pressures (P < 0.001), smaller kidneys with much fewer AT(1b) receptors (P < 0.001), higher basal 24-h urinary sodium excretion (P < 0.01), as well as basal plasma and whole kidney ANG II levels (P < 0.01). Sodium 170-176 angiotensin II receptor, type 1a Mus musculus 13-19 17425514-1 2007 The literature on salt intake and insulin sensitivity presents a mixed picture, as some studies have shown an increase, whereas others have shown a decrease, in insulin action as sodium intake is enhanced. Sodium 179-185 insulin Homo sapiens 161-168 17667056-1 2007 BACKGROUND: The model for end-stage liver disease (MELD), hepatic venous pressure gradient (HVPG), and serum sodium (SNa) are important prognostic markers for patients with liver cirrhosis. Sodium 109-115 snail family transcriptional repressor 1 Homo sapiens 117-120 17665974-4 2007 Tubular NADPH oxidase stimulated by angiotensin II or aldosterone contributes to sodium retention and to tubulointerstitial damage. Sodium 81-87 angiotensinogen Homo sapiens 36-50 17412768-2 2007 Murine PCT cells grown on a transwell dish showed endogenous CNT3 activity at their apical membrane that was responsible for the sodium-dependent transepithelial flux of both purine and pyrimidine nucleosides. Sodium 129-135 solute carrier family 28 (sodium-coupled nucleoside transporter), member 3 Mus musculus 61-65 17412768-6 2007 Apical-to-basolateral transepithelial flux was present in all cells expressing a functional CNT3 transporter and was significantly higher than that found either in PCT cells in absence of sodium or in mock-transfected MDCK cells. Sodium 188-194 concentrative Na+-nucleoside cotransporter Canis lupus familiaris 92-96 17587492-2 2007 Angiotensin II (Ang II) is a potent growth factor for glomerulosa cells, appearing as a proliferative factor in vivo, under sodium-deficient diet conditions, as well as in vitro, in studies conducted with whole zona glomerulosa. Sodium 124-130 angiotensinogen Homo sapiens 0-14 17587492-2 2007 Angiotensin II (Ang II) is a potent growth factor for glomerulosa cells, appearing as a proliferative factor in vivo, under sodium-deficient diet conditions, as well as in vitro, in studies conducted with whole zona glomerulosa. Sodium 124-130 angiotensinogen Homo sapiens 16-22 17488805-10 2007 To investigate whether the PRL-enhanced paracellular transport was linked to changes in the epithelial charge selectivity, the permeability ratio of sodium and chloride (P(Na)/P(Cl)) was determined. Sodium 149-155 prolactin Rattus norvegicus 27-30 17344192-0 2007 Hypotonicity stimulates renal epithelial sodium transport by activating JNK via receptor tyrosine kinases. Sodium 41-47 mitogen-activated protein kinase 8 Homo sapiens 72-75 17586409-0 2007 High sodium intake strengthens the association of ACE I/D polymorphism with blood pressure in a community. Sodium 5-11 angiotensin I converting enzyme Homo sapiens 50-53 17586409-2 2007 We hypothesized that persons with the I allele of the ACE gene have elevated BP levels in response to a higher sodium intake, and thus the association of ACE I/D polymorphism with BP levels was stronger among persons with a higher sodium intake than those with a lower sodium intake. Sodium 111-117 angiotensin I converting enzyme Homo sapiens 54-57 17586409-2 2007 We hypothesized that persons with the I allele of the ACE gene have elevated BP levels in response to a higher sodium intake, and thus the association of ACE I/D polymorphism with BP levels was stronger among persons with a higher sodium intake than those with a lower sodium intake. Sodium 111-117 angiotensin I converting enzyme Homo sapiens 154-157 17586409-2 2007 We hypothesized that persons with the I allele of the ACE gene have elevated BP levels in response to a higher sodium intake, and thus the association of ACE I/D polymorphism with BP levels was stronger among persons with a higher sodium intake than those with a lower sodium intake. Sodium 231-237 angiotensin I converting enzyme Homo sapiens 54-57 17586409-2 2007 We hypothesized that persons with the I allele of the ACE gene have elevated BP levels in response to a higher sodium intake, and thus the association of ACE I/D polymorphism with BP levels was stronger among persons with a higher sodium intake than those with a lower sodium intake. Sodium 231-237 angiotensin I converting enzyme Homo sapiens 154-157 17586409-2 2007 We hypothesized that persons with the I allele of the ACE gene have elevated BP levels in response to a higher sodium intake, and thus the association of ACE I/D polymorphism with BP levels was stronger among persons with a higher sodium intake than those with a lower sodium intake. Sodium 231-237 angiotensin I converting enzyme Homo sapiens 54-57 17586409-2 2007 We hypothesized that persons with the I allele of the ACE gene have elevated BP levels in response to a higher sodium intake, and thus the association of ACE I/D polymorphism with BP levels was stronger among persons with a higher sodium intake than those with a lower sodium intake. Sodium 231-237 angiotensin I converting enzyme Homo sapiens 154-157 17586409-7 2007 CONCLUSIONS: A high sodium intake strengthens the association of ACE I/D polymorphism with BP levels in community-based samples. Sodium 20-26 angiotensin I converting enzyme Homo sapiens 65-68 17712057-3 2007 Arginine vasopressin-receptor antagonists, a novel class of agents that block the action of arginine vasopressin on V2 receptors in the renal collecting ducts, may provide specific correction of sodium and water imbalance in hyponatremia by promoting free water clearance while sparing electrolytes (aquaresis). Sodium 195-201 arginine vasopressin Homo sapiens 9-20 17663307-1 2007 Hyponatraemia often complicates the treatment of underlying conditions in patients who are seriously ill. Arginine vasopressin receptor antagonists block the action of arginine vasopressin and correct sodium and water imbalance in patients with euvolaemic or hypervolaemic hyponatraemia. Sodium 201-207 arginine vasopressin Homo sapiens 115-126 17565280-1 2007 PURPOSE OF REVIEW: The sodium-hydrogen exchanger isoform-1 (NHE1) functions in intracellular pH and cell volume homeostasis by catalyzing an electroneutral exchange of extracellular sodium and intracellular hydrogen. Sodium 23-29 solute carrier family 9 member A1 Homo sapiens 60-64 17356845-5 2007 Expression analysis of NaDC3 in Xenopus laevis oocytes by the two-electrode-voltage-clamp technique demonstrated the sodium-dependent translocation of 3OH-GA with a K (M) value of 0.95 mM. Sodium 117-123 solute carrier family 13 (sodium-dependent dicarboxylate transporter), member 3 L homeolog Xenopus laevis 23-28 17635698-3 2007 RESULTS: Residues around the active site (Tyr50 and Glu202) and the sodium-binding site (Glu229 and Arg233) were required for thrombin inhibition by PCI with and without cofactors. Sodium 68-74 coagulation factor II, thrombin Homo sapiens 126-134 17587386-9 2007 Future research should therefore be directed at better understanding PPARgamma-related mechanisms of renal sodium retention and endothelial vascular permeability of the periphery, as well as development of newer compounds without this side-effect. Sodium 107-113 peroxisome proliferator activated receptor gamma Homo sapiens 69-78 17712057-3 2007 Arginine vasopressin-receptor antagonists, a novel class of agents that block the action of arginine vasopressin on V2 receptors in the renal collecting ducts, may provide specific correction of sodium and water imbalance in hyponatremia by promoting free water clearance while sparing electrolytes (aquaresis). Sodium 195-201 arginine vasopressin Homo sapiens 101-112 17572013-2 2007 Mutations in the CFTR gene result in defective sodium, chloride, and water transport in the epithelial cells of the respiratory, hepatobiliary, gastrointestinal, and reproductive tracts, the pancreas, and the eye. Sodium 47-53 CF transmembrane conductance regulator Homo sapiens 17-21 17452328-4 2007 However, sodium currents measured in the Orai3-expressing HEK293 cells were significantly larger in current density than Stim1-expressing cells. Sodium 9-15 ORAI calcium release-activated calcium modulator 3 Homo sapiens 41-46 17452328-4 2007 However, sodium currents measured in the Orai3-expressing HEK293 cells were significantly larger in current density than Stim1-expressing cells. Sodium 9-15 stromal interaction molecule 1 Homo sapiens 121-126 17418447-6 2007 SIADH in patients with ectopic ACTH syndrome may be underdiagnosed due to the antagonistic hormone actions of cortisol and ADH on renal sodium excretion. Sodium 136-142 proopiomelanocortin Homo sapiens 31-35 17576410-0 2007 BACE1 regulates voltage-gated sodium channels and neuronal activity. Sodium 30-36 beta-secretase 1 Homo sapiens 0-5 17576410-2 2007 The voltage-gated sodium channel (Na(v)1) beta2-subunit (beta2), a type I membrane protein that covalently binds to Na(v)1 alpha-subunits, is a substrate for BACE1 and gamma-secretase. Sodium 18-24 glycoprotein hormone subunit alpha 2 Homo sapiens 42-47 17576410-2 2007 The voltage-gated sodium channel (Na(v)1) beta2-subunit (beta2), a type I membrane protein that covalently binds to Na(v)1 alpha-subunits, is a substrate for BACE1 and gamma-secretase. Sodium 18-24 beta-secretase 1 Homo sapiens 158-163 17576410-6 2007 BACE1, by cleaving beta2, thus regulates Na(v)1 alpha-subunit levels and controls cell-surface sodium current densities. Sodium 95-101 ST3 beta-galactoside alpha-2,3-sialyltransferase 5 Mus musculus 19-24 17519130-4 2007 Ang II signaling is integrated with sodium-sensitive neurons in the SFO and/or organum vasculosum of the lamina terminalis (OVLT) and drives sympathetic premotor neurons in the rostral ventrolateral medulla (RVLM) via the paraventricular nucleus (PVN). Sodium 36-42 angiotensinogen Homo sapiens 0-6 17317768-7 2007 Low extracellular sodium ([Na(+)](o)) solution increases the intracellular Ca(2+) concentration via NCX transporter in fura-2-loaded osteoclasts. Sodium 18-24 solute carrier family 8 member A1 Rattus norvegicus 100-103 17485169-9 2007 These results showed that acute osmotic stimulus-induced GALP gene expression in the pituicyte of the PP, but not in the neurons in the Arc, and the gene expression in the pituicyte might be regulated by plasma osmolality and/or plasma sodium concentration. Sodium 236-242 galanin-like peptide Rattus norvegicus 57-61 17443257-1 2007 Reaction of [18]aneO(5)S with the aminating agent MSH results in the {[18]aneO(5)SNH(2)}+ cation which may be converted through to the linked crown system [({[18]aneO(5)S}(2)N)]+ via deprotonation, bromination and reaction with the parent crown; significantly, despite their positive charge, both systems can coordinate sodium cations to the ether linkages. Sodium 320-326 msh homeobox 2 Homo sapiens 50-53 17430903-0 2007 Expression of allosteric linkage between the sodium ion binding site and exosite I of thrombin during prothrombin activation. Sodium 45-51 coagulation factor II, thrombin Homo sapiens 86-94 17430903-0 2007 Expression of allosteric linkage between the sodium ion binding site and exosite I of thrombin during prothrombin activation. Sodium 45-51 coagulation factor II, thrombin Homo sapiens 102-113 17218419-3 2007 Endothelin-1 (ET-1) is a potent vasoconstrictor that alters both sodium transport and hydrogen ion secretion in the kidney. Sodium 65-71 endothelin 1 Rattus norvegicus 0-12 17403190-1 2007 BACKGROUND: The models for end-stage liver disease (MELD) and serum sodium (SNa) are important prognostic markers in cirrhosis. Sodium 68-74 snail family transcriptional repressor 1 Homo sapiens 76-79 17372036-5 2007 The ABCB1 and CYP3A5 genes interact with urinary sodium excretion in their effect on ambulatory blood pressure (daytime systolic: P=0.05; nighttime systolic and diastolic: P<0.01), suggesting a gene-gene-environment interaction. Sodium 49-55 ATP binding cassette subfamily B member 1 Homo sapiens 4-9 17372036-5 2007 The ABCB1 and CYP3A5 genes interact with urinary sodium excretion in their effect on ambulatory blood pressure (daytime systolic: P=0.05; nighttime systolic and diastolic: P<0.01), suggesting a gene-gene-environment interaction. Sodium 49-55 cytochrome P450 family 3 subfamily A member 5 Homo sapiens 14-20 17341566-0 2007 Low dietary sodium and exogenous angiotensin II infusion decrease plasma adiponectin concentrations in healthy men. Sodium 12-18 adiponectin, C1Q and collagen domain containing Homo sapiens 73-84 17292670-3 2007 Arginine vasopressin (AVP) is etiologically critical for hyponatremia, and it has been proven that AVP receptor (AVP-R) antagonists normalize serum sodium levels in hyponatremic patients. Sodium 148-154 arginine vasopressin Homo sapiens 0-20 17218419-3 2007 Endothelin-1 (ET-1) is a potent vasoconstrictor that alters both sodium transport and hydrogen ion secretion in the kidney. Sodium 65-71 endothelin 1 Rattus norvegicus 14-18 17684472-2 2007 Moreover, the acute sodium-retaining action of insulin at the kidney level has been proposed to participate in the development of salt sensitivity in essential hypertension. Sodium 20-26 insulin Homo sapiens 47-54 17288452-3 2007 In the transport studies with hSGLT1, significant sodium-independent phlorizin inhibitable alpha-methyl d-glucopyranoside (alpha-MDG) uptake was observed which amounted to approximately 20% of the uptake observed in the presence of a sodium gradient. Sodium 50-56 solute carrier family 5 member 1 Homo sapiens 30-36 17188293-0 2007 Regulation of voltage-gated cardiac sodium current by epidermal growth factor receptor kinase in guinea pig ventricular myocytes. Sodium 36-42 epidermal growth factor receptor Cavia porcellus 54-86 17389890-3 2007 Kinins (bradykinin and lys-bradykinin) are endogenous vasodilators and natriuretic peptides known best for their ability to antagonize angiotensin-induced vasoconstriction and sodium retention. Sodium 176-182 kininogen 1 Homo sapiens 8-18 17389890-3 2007 Kinins (bradykinin and lys-bradykinin) are endogenous vasodilators and natriuretic peptides known best for their ability to antagonize angiotensin-induced vasoconstriction and sodium retention. Sodium 176-182 kininogen 1 Homo sapiens 27-37 17394769-6 2007 Taken together, our findings suggest that ERK plays an active role in mediating sodium seleniteinduced apoptosis in NB4 cells. Sodium 80-86 mitogen-activated protein kinase 1 Homo sapiens 42-45 17447595-4 2007 Sodium retention leads to severe low renin hypertension. Sodium 0-6 renin Homo sapiens 37-42 17288452-11 2007 If all these data are taken into consideration, it seems that Trp-561 in hSGLT1 forms part of a low-affinity sodium-independent binding and/or translocation site for d-glucose. Sodium 109-115 solute carrier family 5 member 1 Homo sapiens 73-79 17288452-12 2007 The rate of sodium-independent translocation via hSGLT1 seems, however, to be tightly regulated in the intact cell by yet unknown factors. Sodium 12-18 solute carrier family 5 member 1 Homo sapiens 49-55 17050615-7 2007 FXYD1 was completely replaced with FXYD2a in cells adapted to 700 mosmol/kgH(2)O and showed a significantly decreased sodium affinity. Sodium 118-124 FXYD domain containing ion transport regulator 1 Homo sapiens 0-5 17050615-7 2007 FXYD1 was completely replaced with FXYD2a in cells adapted to 700 mosmol/kgH(2)O and showed a significantly decreased sodium affinity. Sodium 118-124 FXYD domain containing ion transport regulator 2 Homo sapiens 35-40 17699429-2 2007 Vasopressin administration has been shown in healthy humans to delay sodium excretion along with its antidiuretic action. Sodium 69-75 arginine vasopressin Homo sapiens 0-11 17487823-1 2007 Angiotensin II (Ang II) has powerful sodium-retaining, growth-promoting and pro- inflammatory properties in addition to its physiological role in maintaining body salt and fluid balance and blood pressure homeostasis. Sodium 37-43 angiotensinogen Homo sapiens 0-22 17214984-7 2007 Furthermore, Fos-Li IR in the MnPO was increased following AngII infusion in rats consuming a high sodium diet, but not in animals drinking Tap. Sodium 99-105 angiotensinogen Rattus norvegicus 59-64 17214984-8 2007 These data suggest that increased dietary sodium sensitizes the MnPO neurons to excitatory input from brain areas responding to circulating AngII. Sodium 42-48 angiotensinogen Rattus norvegicus 140-145 17214984-0 2007 Increased dietary sodium alters Fos expression in the lamina terminalis during intravenous angiotensin II infusion. Sodium 18-24 angiotensinogen Rattus norvegicus 91-105 17223989-9 2007 CONCLUSIONS: MC2R mutations should be considered in children who have primary adrenal failure with apparent mild disturbances in renin-sodium homeostasis. Sodium 135-141 renin Homo sapiens 129-134 17242746-2 2007 The archaeal lipid bilayer shows minor changes in their physical properties, indicating the unusual high stability of the membrane against salt, though small reductions of molecular area and lateral diffusion of the lipid are detected at the highest electrolyte concentration of 4 M. Sodium ions penetrate to the ether-rich region, where the ions are likely bound to the ether oxygen in the sn-1 chain rather than to that in the sn-2 chain. Sodium 284-290 solute carrier family 38 member 3 Homo sapiens 391-395 17242746-2 2007 The archaeal lipid bilayer shows minor changes in their physical properties, indicating the unusual high stability of the membrane against salt, though small reductions of molecular area and lateral diffusion of the lipid are detected at the highest electrolyte concentration of 4 M. Sodium ions penetrate to the ether-rich region, where the ions are likely bound to the ether oxygen in the sn-1 chain rather than to that in the sn-2 chain. Sodium 284-290 solute carrier family 38 member 5 Homo sapiens 429-433 17331207-7 2007 Intracellular sodium depletion and its successive ionophoretic restoration moved the neuron from a stable low-conductance state to maximum gCl sensitization, pointing to a link between gCl sensitization and [Na+]i. Sodium 14-20 germ cell-less 1, spermatogenesis associated Rattus norvegicus 139-142 17305665-4 2007 The present case report describes the mechanism of severe hyponatraemia in a patient taking deamino arginine vasopressin, and the subsequent development of both central pontine and extrapontine myelinolysis after rapid correction of sodium levels. Sodium 233-239 arginine vasopressin Homo sapiens 109-120 17331207-7 2007 Intracellular sodium depletion and its successive ionophoretic restoration moved the neuron from a stable low-conductance state to maximum gCl sensitization, pointing to a link between gCl sensitization and [Na+]i. Sodium 14-20 germ cell-less 1, spermatogenesis associated Rattus norvegicus 185-188 17214873-15 2007 These results do not support the working hypothesis but could be interpreted as evidence for the existence of two separately modulated central Ang II systems: one responding to mineralocorticoids with increased neuronal activity and the other responsible for the Ang II-induced sodium appetite in conscious rats. Sodium 278-284 angiotensinogen Rattus norvegicus 143-149 17202415-10 2007 This was associated with reduced expression of active sodium transporters-sodium/potassium/chloride transporter type 2 (NKCC2), sodium/chloride transporter, and Na(+),K(+)-ATPase-along with increased sodium excretion and reduced urinary concentration. Sodium 54-60 solute carrier family 12 member 1 Homo sapiens 120-125 17214873-15 2007 These results do not support the working hypothesis but could be interpreted as evidence for the existence of two separately modulated central Ang II systems: one responding to mineralocorticoids with increased neuronal activity and the other responsible for the Ang II-induced sodium appetite in conscious rats. Sodium 278-284 angiotensinogen Rattus norvegicus 263-269 17241128-0 2007 Critical role of sodium in cytosolic [Ca2+] elevations in cultured hippocampal CA1 neurons during anoxic depolarization. Sodium 17-23 carbonic anhydrase 2 Rattus norvegicus 38-41 17097678-1 2007 COMMD1 is the prototype of a new protein family that plays a role in several important cellular processes, including NF-kappaB signaling, sodium transport, and copper metabolism. Sodium 138-144 copper metabolism domain containing 1 Homo sapiens 0-6 17301693-11 2007 CONCLUSION: The present study demonstrates that the ABCB1 3435 genotype affects angiotensin II-stimulated serum aldosterone levels and salt-stimulated urinary sodium excretion. Sodium 159-165 ATP binding cassette subfamily B member 1 Homo sapiens 52-57 17005263-17 2007 This mechanism demonstrates a DA-ANF relationship involved in the modulation of both decreased sodium reabsorption and increased natriuresis. Sodium 95-101 natriuretic peptide A Homo sapiens 33-36 17664863-1 2007 BACKGROUND: Most cases of hyponatremia--serum sodium concentration ([Na+]) < 135 mEq/l (< 135 mM)--are associated with an elevated plasma arginine vasopressin level. Sodium 46-52 arginine vasopressin Homo sapiens 153-164 16917017-0 2007 Renal sodium retention in cirrhotic rats depends on glucocorticoid-mediated activation of mineralocorticoid receptor due to decreased renal 11beta-HSD-2 activity. Sodium 6-12 nuclear receptor subfamily 3, group C, member 2 Rattus norvegicus 90-116 16917017-1 2007 Downregulation of the renal glucocorticoid-metabolizing enzyme 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD-2) during liver cirrhosis may allow activation of the mineralocorticoid receptor (MR) by glucocorticoids and contribute to sodium retention. Sodium 241-247 nuclear receptor subfamily 3, group C, member 2 Rattus norvegicus 172-198 17002597-3 2007 ET(A) receptors function to promote vasoconstriction, growth, and inflammation, whereas ET(B) receptors produce vasodilation, increases in sodium excretion, and inhibit growth and inflammation. Sodium 139-145 endothelin receptor type B Homo sapiens 88-93 16980346-2 2007 It has recently been proposed, however, that elevated sodium levels may exacerbate the hypertensive effects of ANG II, which by itself dramatically affects salt sensitivity, by acting at sodium-sensing neurons in certain circumventricular organs of the brain. Sodium 54-60 angiotensinogen Rattus norvegicus 111-117 16980346-2 2007 It has recently been proposed, however, that elevated sodium levels may exacerbate the hypertensive effects of ANG II, which by itself dramatically affects salt sensitivity, by acting at sodium-sensing neurons in certain circumventricular organs of the brain. Sodium 187-193 angiotensinogen Rattus norvegicus 111-117 17245074-2 2007 Previous data suggested that insulin promotes sodium retention from the kidney, and thus research efforts focused on this action among several other possible pathways connecting insulin resistance and hyperinsulinemia with hypertension. Sodium 46-52 insulin Homo sapiens 29-36 16965835-1 2007 Circulating angiotensin II is crucial for the activation of salt appetite after sodium depletion. Sodium 80-86 angiotensinogen Rattus norvegicus 12-26 16965835-10 2007 Thus, an overnight infusion of ANG II is sufficient to mimic the robust expression of salt appetite as observed after furosemide and overnight sodium depletion. Sodium 143-149 angiotensinogen Rattus norvegicus 31-37 17241874-0 2007 Butyrate induces intestinal sodium absorption via Sp3-mediated transcriptional up-regulation of epithelial sodium channels. Sodium 28-34 Sp3 transcription factor Homo sapiens 50-53 17164836-0 2007 IGF-1 vs insulin: respective roles in modulating sodium transport via the PI-3 kinase/Sgk1 pathway in a cortical collecting duct cell line. Sodium 49-55 insulin like growth factor 1 Homo sapiens 0-5 22477329-10 2007 A change in renal treatment of sodium caused by insulin may be one of several possible explanations of the results, but further studies are warranted to confirm the findings. Sodium 31-37 insulin Homo sapiens 48-55 17032723-4 2007 OBJECTIVES: This study examined the ratio of serum aldosterone to plasma renin activity as an index of sodium wasting in patients with 21 OHD CAH, heterozygotes, and normal individuals. Sodium 103-109 renin Homo sapiens 73-78 17164836-9 2007 IGF-1 could play an important physiological role in regulating basal sodium transport via the PI3-K/Sgk1 pathway in ASDN. Sodium 69-75 insulin like growth factor 1 Homo sapiens 0-5 17164836-0 2007 IGF-1 vs insulin: respective roles in modulating sodium transport via the PI-3 kinase/Sgk1 pathway in a cortical collecting duct cell line. Sodium 49-55 insulin Homo sapiens 9-16 17164836-1 2007 Insulin and insulin-like growth factor 1 (IGF-1) may play a role in the regulation of sodium balance by increasing basal and aldosterone-stimulated transepithelial sodium transport in the aldosterone-sensitive distal nephron (ASDN). Sodium 86-92 insulin Homo sapiens 0-7 17164836-1 2007 Insulin and insulin-like growth factor 1 (IGF-1) may play a role in the regulation of sodium balance by increasing basal and aldosterone-stimulated transepithelial sodium transport in the aldosterone-sensitive distal nephron (ASDN). Sodium 86-92 insulin like growth factor 1 Homo sapiens 12-40 17164836-1 2007 Insulin and insulin-like growth factor 1 (IGF-1) may play a role in the regulation of sodium balance by increasing basal and aldosterone-stimulated transepithelial sodium transport in the aldosterone-sensitive distal nephron (ASDN). Sodium 86-92 insulin like growth factor 1 Homo sapiens 42-47 16925467-0 2007 A preliminary study on T-786C endothelial nitric oxide synthase gene and renal hemodynamic and blood pressure responses to dietary sodium. Sodium 131-137 nitric oxide synthase 3 Homo sapiens 30-63 17596722-7 2007 Serum sodium (sNa) fell by 5.7 and 2.7 mmol/l (p < 0.01) in patients with and without ARF, respectively. Sodium 6-12 snail family transcriptional repressor 1 Homo sapiens 14-17 17356196-1 2007 Hyponatremia, defined as a serum sodium concentration ([Na+]) less than 135 mEq/L, is commonly caused by elevated levels of the hormone arginine vasopressin (AVP), which causes water retention. Sodium 33-39 arginine vasopressin Homo sapiens 145-156 17363184-1 2007 The antisense drug G3139 (oblimersen sodium, Genta, Inc.) is a phosphorothioate oligodeoxynucleotide (ODN) containing unmethylated CpG units, which is targeted to suppress Bcl-2. Sodium 37-43 BCL2 apoptosis regulator Homo sapiens 172-177 17622738-10 2007 Angiotensin II synthesis, proliferation, and apoptosis were exaggerated in mesangial cell cultures from Sprague-Dawley rats and, more so, spontaneously hypertensive rats fed the high-sodium diet, but were inhibited in cultures from rosiglitazone-treated animals. Sodium 183-189 angiotensinogen Rattus norvegicus 0-14 17969373-2 2007 The effect of angiotensin II is mediated via the angiotensin type I receptor (AT1 ) resulting in vasoconstriction, sodium retention and myocyte growth changes. Sodium 115-121 angiotensinogen Homo sapiens 14-28 17645932-10 2007 In particular, calcium content increased both in HS- and febrile-animals, while CSF sodium decreased significantly only under IL-1beta-injected treatment. Sodium 84-90 interleukin-1 beta Oryctolagus cuniculus 126-134 16788141-1 2006 The kidney responds to high levels of ANG II, as may occur during malignant hypertension, by increasing sodium and water excretion. Sodium 104-110 angiotensinogen Rattus norvegicus 38-44 17060507-1 2006 We tested the hypothesis that changes in sodium intake modulate adipose-tissue renin-angiotensin and natriuretic peptide system gene expression in humans. Sodium 41-47 renin Homo sapiens 79-84 17060507-6 2006 With high-sodium intake, systemic renin activity and aldosterone levels were suppressed, angiotensin-converting enzyme activity did not change, and systemic levels of the atrial natriuretic peptide increased. Sodium 10-16 renin Homo sapiens 34-39 18030731-0 2007 [Sodium ions as the effector of catalytic action of alpha-thrombin]. Sodium 1-7 coagulation factor II, thrombin Homo sapiens 58-66 17082469-1 2006 BACKGROUND AND PURPOSE: Carriers of the 460Trp allele of the alpha-adducin gene (ADD1) show higher rates of sodium reabsorption compared with homozygous carriers of the Gly460 allele and were found to have an increased risk of hypertension and cardiovascular disease. Sodium 108-114 adducin 1 Homo sapiens 61-74 17082469-1 2006 BACKGROUND AND PURPOSE: Carriers of the 460Trp allele of the alpha-adducin gene (ADD1) show higher rates of sodium reabsorption compared with homozygous carriers of the Gly460 allele and were found to have an increased risk of hypertension and cardiovascular disease. Sodium 108-114 adducin 1 Homo sapiens 81-85 17042919-13 2006 Replacing extracellular sodium or chloride significantly decreased the hSERT currents by 89 and 45%, respectively (P < 0.05, n = 7 each). Sodium 24-30 solute carrier family 6 member 4 Homo sapiens 71-76 17042919-16 2006 These results demonstrate that hSERT activity is not only voltage dependent, but is also affected by intracellular calcium and extracellular sodium and chloride. Sodium 141-147 solute carrier family 6 member 4 Homo sapiens 31-36 17027026-0 2006 How does endothelin-1 cause a sustained increase in intracellular sodium and calcium which lead to hypertrophy? Sodium 66-72 endothelin 1 Homo sapiens 9-21 17066056-4 2006 This Review focuses on the counter-regulation between the dopaminergic and renin-angiotensin systems in the renal proximal tubule, which is the site of about 70% of total renal sodium reabsorption. Sodium 177-183 renin Homo sapiens 75-80 17469342-8 2006 The glucose-insulin-potassium solution provides the glucose needed by the myocardium in reperfusion conditions and protects the cellular membrane"s integrity as well as pumps and ionic channels, it allows maintaining the action potential probably because ATP-depended channels block and prevent potassium loss, it reduces the cytosol calcium overload and prevent cardiac arrhythmias, preserves the sodium ATPasa pump avoiding the rise in cytosolic sodium; glucose prevents the production of free oxygen radicals. Sodium 398-404 insulin Homo sapiens 12-19 16690903-9 2006 Colonic surface cells from wild-type mice demonstrated S1611- and HOE694-sensitive pH(i) recovery in response to luminal sodium, confirming a functional role for both NHE3 and NHE2 at this site. Sodium 121-127 solute carrier family 9 (sodium/hydrogen exchanger), member 3 Mus musculus 167-171 16868049-7 2006 RESULTS: In high-sodium balance, urinary aldosterone, basal serum aldosterone, and serum aldosterone response to infused AngII were significantly greater (P < 0.05) in the luteal vs. follicular phase. Sodium 17-23 angiotensinogen Homo sapiens 121-126 16984231-9 2006 Testosterone amplifies GH stimulation of IGF-I, sodium retention, substrate metabolism and protein anabolism while exhibiting similar but independent actions of its own. Sodium 48-54 growth hormone 1 Homo sapiens 23-25 16831195-3 2006 In the neuronal glutamate transporter EAAC1, lithium can replace sodium. Sodium 65-71 solute carrier family 1 member 1 Homo sapiens 38-43 16966578-6 2006 In women as well as in men, a 1-SD increment in fractional proximal sodium reabsorption was associated with decreases in femoral and brachial diameter, amounting to 111.6 mum (95% CI: 38.2 to 185.1; P=0.003) and 52.5 mum (95% CI: 10.0 to 94.9; P=0.016), respectively. Sodium 68-74 latexin Homo sapiens 171-174 16966578-6 2006 In women as well as in men, a 1-SD increment in fractional proximal sodium reabsorption was associated with decreases in femoral and brachial diameter, amounting to 111.6 mum (95% CI: 38.2 to 185.1; P=0.003) and 52.5 mum (95% CI: 10.0 to 94.9; P=0.016), respectively. Sodium 68-74 latexin Homo sapiens 217-220 16940246-0 2006 The G protein-coupled receptor kinase 4 gene modulates stress-induced sodium excretion in black normotensive adolescents. Sodium 70-76 G protein-coupled receptor kinase 4 Homo sapiens 4-39 16940246-10 2006 The 65L allele of the GRK4 gene is associated with stress-induced U(Na)V reduction, suggesting impaired sodium handling in affected black youth. Sodium 104-110 G protein-coupled receptor kinase 4 Homo sapiens 22-26 16831195-4 2006 To address the question of whether the coupling ion interacts with the "driven" substrate during co-transport, the kinetic parameters of transport of the three substrates, L-glutamate and D- and L-aspartate by EAAC-1 in sodium- and lithium-containing media were compared. Sodium 220-226 solute carrier family 1 member 1 Homo sapiens 210-216 16825309-7 2006 LIL-6 males and IL-6 females showed decreased urinary flow rate and urinary sodium and potassium excretion. Sodium 76-82 interleukin 6 Rattus norvegicus 1-5 16982943-2 2006 The aim of the present study was to investigate the effects of ET-1 antagonism on pulmonary hypertension, renal water, and sodium balance under acute and prolonged exposure to high-altitude-associated hypoxia. Sodium 123-129 endothelin 1 Homo sapiens 63-67 17040873-1 2006 Cystic fibrosis is caused by mutations in the CFTR gene (Cystic Fibrosis Transmembrane conductance Regulator) encodes a protein mainly functioning as a chloride channel that regulates chloride and sodium transport in secretory epithelial cells. Sodium 197-203 CF transmembrane conductance regulator Homo sapiens 46-50 17040873-1 2006 Cystic fibrosis is caused by mutations in the CFTR gene (Cystic Fibrosis Transmembrane conductance Regulator) encodes a protein mainly functioning as a chloride channel that regulates chloride and sodium transport in secretory epithelial cells. Sodium 197-203 CF transmembrane conductance regulator Homo sapiens 57-108 16919017-2 2006 ET-1 exerts a wide variety of biological effects, including constriction of cortical and medullary vessels, mesangial cell contraction, stimulation of extracellular matrix production, and inhibition of sodium and water reabsorption along the collecting duct, effects that are primarily mediated in an autocrine/paracrine manner. Sodium 202-208 endothelin 1 Homo sapiens 0-4 16954431-1 2006 The sodium/iodide symporter (NIS) mediates iodide uptake in the thyroid gland and lactating breast. Sodium 4-10 solute carrier family 5 member 5 Homo sapiens 29-32 16597605-13 2006 This impairment may involve increased sodium reabsorption via NKCC2 or ENaC, decreased glomerular filtration rate, and/or nitric oxide bioavailability. Sodium 38-44 sodium channel epithelial 1 subunit gamma Rattus norvegicus 71-75 16970147-7 2006 New agents that antagonize arginine vasopressin at the V2 receptor or both the V(1A) and V2 receptors show promise for treating hypervolemic and euvolemic hyponatremia, as they induce desired free water diuresis without inducing sodium excretion. Sodium 229-235 arginine vasopressin Homo sapiens 36-47 16921370-6 2006 The sodium current density was, however, substantially reduced in inhibitory interneurons of Scn1a+/- and Scn1a-/- mice but not in their excitatory pyramidal neurons. Sodium 4-10 sodium channel, voltage-gated, type I, alpha Mus musculus 93-98 16921370-6 2006 The sodium current density was, however, substantially reduced in inhibitory interneurons of Scn1a+/- and Scn1a-/- mice but not in their excitatory pyramidal neurons. Sodium 4-10 sodium channel, voltage-gated, type I, alpha Mus musculus 106-111 16757479-1 2006 The sodium- and chloride-dependent electrogenic gamma-aminobutyric acid (GABA) transporter GAT-1, which transports two sodium ions together with GABA, is essential for synaptic transmission by this neurotransmitter. Sodium 4-10 solute carrier family 6 member 1 Homo sapiens 91-96 16973514-9 2006 CONCLUSION: In CRF patients there is a negative correlation between FR(Na) and EPO dose, which supports the hypothesis that EPO deficiency may be related to the decreased renal oxygen-consuming work of sodium reabsorption. Sodium 202-208 erythropoietin Homo sapiens 79-82 16973514-9 2006 CONCLUSION: In CRF patients there is a negative correlation between FR(Na) and EPO dose, which supports the hypothesis that EPO deficiency may be related to the decreased renal oxygen-consuming work of sodium reabsorption. Sodium 202-208 erythropoietin Homo sapiens 124-127 16973514-0 2006 Correlation between fractional reabsorption of sodium and erythropoietin dose in peritoneal dialysis patients. Sodium 47-53 erythropoietin Homo sapiens 58-72 16973514-1 2006 BACKGROUND: Erythropoietin (EPO) deficiency of chronic renal failure (CRF) may be a functional consequence of decreased glomerular filtration rate and fractional reabsorption of sodium (FR(Na)). Sodium 178-184 erythropoietin Homo sapiens 12-26 16973514-1 2006 BACKGROUND: Erythropoietin (EPO) deficiency of chronic renal failure (CRF) may be a functional consequence of decreased glomerular filtration rate and fractional reabsorption of sodium (FR(Na)). Sodium 178-184 erythropoietin Homo sapiens 28-31 16757479-1 2006 The sodium- and chloride-dependent electrogenic gamma-aminobutyric acid (GABA) transporter GAT-1, which transports two sodium ions together with GABA, is essential for synaptic transmission by this neurotransmitter. Sodium 119-125 solute carrier family 6 member 1 Homo sapiens 91-96 16757479-3 2006 To identify putative lithium selectivity determinants, we have mutated the five GAT-1 residues corresponding to those whose side chains participate in the sodium binding sites Na1 and Na2 of the bacterial leucine-transporting homologue LeuT(Aa). Sodium 155-161 solute carrier family 6 member 1 Homo sapiens 80-85 16879429-1 2006 There are three different sodium transport systems (Ena1-4p, Nha1p, Nhx1p) in Saccharomyces cerevisiae. Sodium 26-32 Nha1p Saccharomyces cerevisiae S288C 61-66 17111037-7 2006 PC2 and its homologue, polycystin-L (PCL), are nonselective cation channels permeable to potassium, sodium, and calcium. Sodium 100-106 polycystin 2, transient receptor potential cation channel Homo sapiens 0-3 16774642-6 2006 Only the dianisidine derivative, redoxal, and the biphenyl quinoline-carboxylic acid derivative, brequinar sodium, which are known to be potent inhibitors of mammalian DHODH, markedly reduced C. albicans DHODH activity. Sodium 107-113 dihydroorotate dehydrogenase (quinone) Homo sapiens 168-173 16807543-8 2006 Infusion in rats produced conflicting results: exogenous UII has been shown to increase glomerular filtration rate (GFR) and excretion of water and sodium, but also to reduce the same variables. Sodium 148-154 urotensin 2 Rattus norvegicus 57-60 16890144-0 2006 Dietary sodium intake modulates myocardial relaxation responsiveness to angiotensin II. Sodium 8-14 angiotensinogen Homo sapiens 72-86 16890144-1 2006 Dietary sodium alters renovascular responsiveness to angiotensin II (Ang II) in normal subjects. Sodium 8-14 angiotensinogen Homo sapiens 53-67 16890144-1 2006 Dietary sodium alters renovascular responsiveness to angiotensin II (Ang II) in normal subjects. Sodium 8-14 angiotensinogen Homo sapiens 69-75 16890144-7 2006 Dietary sodium significantly modulated E" and RBF responsiveness to Ang II infusion in like manner. Sodium 8-14 angiotensinogen Homo sapiens 68-74 16890144-9 2006 The authors describe for the first time that dietary sodium modulates myocardial relaxation and responsiveness to Ang II. Sodium 53-59 angiotensinogen Homo sapiens 114-120 16890144-11 2006 Ang II may play a role in the interaction between dietary sodium and myocardial relaxation. Sodium 58-64 angiotensinogen Homo sapiens 0-6 16774642-6 2006 Only the dianisidine derivative, redoxal, and the biphenyl quinoline-carboxylic acid derivative, brequinar sodium, which are known to be potent inhibitors of mammalian DHODH, markedly reduced C. albicans DHODH activity. Sodium 107-113 dihydroorotate dehydrogenase (quinone) Homo sapiens 204-209 16545521-3 2006 Consistent with earlier reports, chronic intrathecal Nav 1.8 AS, but not mismatch (MM), ODN decreased TTX-resistant sodium current density (by 60.5+/-10.2% relative to MM; p<0.05) in neurons from L4 to L5 dorsal root ganglia and significantly attenuated mechanical allodynia following intraplantar complete Freund"s adjuvant. Sodium 116-122 sodium voltage-gated channel alpha subunit 10 Rattus norvegicus 53-60 17048213-2 2006 It has been attributed to the inhibition exerted by CaSR activity on sodium transport in the thick ascending limb of the loop of Henle (TALH). Sodium 69-75 calcium sensing receptor Homo sapiens 52-56 16937603-9 2006 Sodium excretion significantly increased after exercise training in the ACE II (114 +/- 22 vs 169 +/- 39 mEq/day, P=.04), but not in the ID (100 +/- 8 vs 133 +/- 17 mEq/day, P=.12) or DD (113 +/- 18 vs 138 +/- 11 mEq/day, P=.13) genotype groups. Sodium 0-6 angiotensin I converting enzyme Homo sapiens 72-75 16937603-9 2006 Sodium excretion significantly increased after exercise training in the ACE II (114 +/- 22 vs 169 +/- 39 mEq/day, P=.04), but not in the ID (100 +/- 8 vs 133 +/- 17 mEq/day, P=.12) or DD (113 +/- 18 vs 138 +/- 11 mEq/day, P=.13) genotype groups. Sodium 0-6 DNA polymerase epsilon 4, accessory subunit Homo sapiens 174-179 16716756-7 2006 The occurrence of both these apparently opposite effects on the renal water and sodium handling suggests a complex role of PPARgamma in the kidney that is likely related to the metabolic state. Sodium 80-86 peroxisome proliferator activated receptor gamma Homo sapiens 123-132 16759088-3 2006 Because inhibition of related enzymes such as 11beta-HSD2 and 17beta-HSDs causes sodium retention and hypertension or interferes with sex steroid hormone metabolism, respectively, highly selective 11beta-HSD1 inhibitors are required for successful therapy. Sodium 81-87 hydroxysteroid 11-beta dehydrogenase 1 Homo sapiens 197-208 16643970-9 2006 Evidence shows that a deficiency of Ang AT1a receptors results in an enhancement in sodium sensitivity along with a disruption of the normal light/dark BP rhythm. Sodium 84-90 angiotensin II receptor, type 1a Mus musculus 40-44 16643970-4 2006 The major finding was that the Ang AT1a -/- mice showed enhanced sodium sensitivity. Sodium 65-71 angiotensin II receptor, type 1a Mus musculus 35-39 16733240-2 2006 Several possible mechanisms linking insulin resistance and compensatory hyperinsulinemia with hypertension have been described, such as renal sodium reabsorption enhancement, sympathetic nervous system activation, and blunted insulin-mediated vasodilation caused by endothelial dysfunction. Sodium 142-148 insulin Homo sapiens 36-43 16449355-2 2006 In advanced cirrhosis, sodium retention is accompanied by elevated plasma ANP levels, and infusion of ANP causes hypotension, but in normal humans increasing the concentration of ANP through the inhibition of neutral endopeptidase, localized in renal proximal tubule cells, causes natriuresis without any arterial pressure drop. Sodium 23-29 natriuretic peptide A Homo sapiens 74-77 16733240-2 2006 Several possible mechanisms linking insulin resistance and compensatory hyperinsulinemia with hypertension have been described, such as renal sodium reabsorption enhancement, sympathetic nervous system activation, and blunted insulin-mediated vasodilation caused by endothelial dysfunction. Sodium 142-148 insulin Homo sapiens 77-84 16787194-12 2006 COX-2 expression increases in high renin states and in response to a high-sodium diet or water deprivation. Sodium 74-80 mitochondrially encoded cytochrome c oxidase II Homo sapiens 0-5 16532430-0 2006 ACE inhibition has adverse renal effects during dietary sodium restriction in proteinuric and healthy rats. Sodium 56-62 angiotensin I converting enzyme Rattus norvegicus 0-3 16432696-8 2006 These data are in agreement with the hypothesis of a modulation of the sodium current by the expression of the highly sialylated beta1-subunit, which would alter the channel gating by increasing the density of surface negative charges in the vicinity of the sodium channel voltage sensing machinery. Sodium 71-77 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 129-134 16741004-0 2006 Chronic high-sodium diet increases aortic wall endothelin-1 expression in a blood pressure-independent fashion in rats. Sodium 13-19 endothelin 1 Rattus norvegicus 47-59 16741004-3 2006 We hypothesized that a high-sodium diet (HNa) increases vascular ET-1 production independent of arterial blood pressure changes. Sodium 28-34 endothelin 1 Rattus norvegicus 65-69 16741004-5 2006 Comparing WKY rats fed a low-sodium diet (LNa) with those fed HNa for 3 weeks, aortic wall ET-1 protein is significantly increased in response to HNa (331 +/- 43 pg/g tissue for LNa vs. 557 +/- 34 pg/gm tissue for HNa). Sodium 29-35 endothelin 1 Rattus norvegicus 91-95 16741004-11 2006 Therefore, the expression of ET-1 mRNA by the aortic wall is increased in response to chronic high dietary sodium in WKY rats in the absence of changes in arterial blood pressure. Sodium 107-113 endothelin 1 Rattus norvegicus 29-33 16772637-4 2006 In addition, sodium restriction generates other, sometimes undesirable effects, including increased insulin resistance, activation of the renin-angiotensin system, and increased sympathetic nerve activity. Sodium 13-19 insulin Homo sapiens 100-107 16772637-4 2006 In addition, sodium restriction generates other, sometimes undesirable effects, including increased insulin resistance, activation of the renin-angiotensin system, and increased sympathetic nerve activity. Sodium 13-19 renin Homo sapiens 138-143 16611713-8 2006 These data highlight the critical role of MR in the maintenance of salt homeostasis early in life and illuminate the sodium dependence of pathologic effects of renin and angiotensin II. Sodium 117-123 angiotensinogen Homo sapiens 170-184 16786909-3 2006 Selective antagonism of the vasopressin 2 (V2) receptor may facilitate a safe diuresis and normalize low serum sodium levels, as demonstrated in preliminary clinical trials. Sodium 111-117 arginine vasopressin Homo sapiens 28-39 16732371-1 2006 Sodium plays an important role in modulating both the amidolytic and proteolytic activities of thrombin. Sodium 0-6 coagulation factor II, thrombin Homo sapiens 95-103 16612255-4 2006 We analyzed the association between the CYP3A5 alleles (*1, *3, *6 and *7) and ABP, GFR and renal sodium handling (fractional excretion of lithium), from pedigree data, allowing for other covariates and familial correlations. Sodium 98-104 cytochrome P450 family 3 subfamily A member 5 Homo sapiens 40-46 16612255-7 2006 For night-time ABP, the effect of CYP3A5*1 was modified by urinary sodium excretion, not by age. Sodium 67-73 cytochrome P450 family 3 subfamily A member 5 Homo sapiens 34-40 16612255-10 2006 CONCLUSIONS: These data demonstrate that CYP3A5 polymorphisms are associated with ambulatory BP, CYP3A5*1 carriers showing a higher age- and sodium- related increase in ABP than non-carriers. Sodium 141-147 cytochrome P450 family 3 subfamily A member 5 Homo sapiens 41-47 16612255-10 2006 CONCLUSIONS: These data demonstrate that CYP3A5 polymorphisms are associated with ambulatory BP, CYP3A5*1 carriers showing a higher age- and sodium- related increase in ABP than non-carriers. Sodium 141-147 cytochrome P450 family 3 subfamily A member 5 Homo sapiens 97-103 16612255-11 2006 The age effect may be due, in part, to the action of CYP3A5 on renal sodium handling. Sodium 69-75 cytochrome P450 family 3 subfamily A member 5 Homo sapiens 53-59 16263808-0 2006 Effects of ACE inhibition on proximal tubule sodium transport. Sodium 45-51 angiotensin I converting enzyme Homo sapiens 11-14 16141358-1 2006 Angiotensin II (Ang II) activates a wide spectrum of signaling responses via the AT1 receptor (AT1R) that mediate its physiological control of blood pressure, thirst, and sodium balance and its diverse pathological actions in cardiovascular, renal, and other cell types. Sodium 171-177 angiotensinogen Homo sapiens 0-14 16141358-1 2006 Angiotensin II (Ang II) activates a wide spectrum of signaling responses via the AT1 receptor (AT1R) that mediate its physiological control of blood pressure, thirst, and sodium balance and its diverse pathological actions in cardiovascular, renal, and other cell types. Sodium 171-177 angiotensinogen Homo sapiens 16-22 16478724-1 2006 Substrate transport by the plasma membrane glutamate transporter EAAC1 is coupled to cotransport of three sodium ions. Sodium 106-112 solute carrier family 1 member 1 Homo sapiens 65-70 16571019-1 2006 The distribution of sodium, choline, sulfate, and chloride ions around two proteins, horseradish peroxidase (HRP) and bovine pancreatic trypsin inhibitor (BPTI), is investigated by means of molecular dynamics simulations with the aim to elucidate ion adsorption at the protein surface. Sodium 20-26 trophoblast Kunitz domain protein 1 Bos taurus 136-153 16406318-2 2006 Furthermore, we have demonstrated that intracerebroventricular injection of hypertonic saline increases the firing rate of AHA angiotensin II-sensitive neurons via angiotensins and that the central sodium-induced activation of AHA neurons is enhanced in spontaneously hypertensive rats (SHR) and Dahl salt-sensitive (Dahl S) rats. Sodium 198-204 angiotensinogen Rattus norvegicus 127-141 16283205-5 2006 Incubation of WT slices with 100 nM VIP or RO 25-1553 resulted in inhibition of fast tetrodotoxin-sensitive sodium currents and delayed rectifier K(+) currents in most of the cells tested. Sodium 108-114 vasoactive intestinal polypeptide Mus musculus 36-39 16107787-2 2006 Three gene products of the sodium-calcium exchanger family NCX1, NCX2, and NCX3 couple, in a bidirectional way, the movement of these ions across the cell membrane during cerebral ischemia. Sodium 27-33 solute carrier family 8 member A1 Rattus norvegicus 59-63 16357101-0 2006 Corticotropin-releasing hormone in the lateral parabrachial nucleus inhibits sodium appetite in rats. Sodium 77-83 corticotropin releasing hormone Rattus norvegicus 0-31 16357101-5 2006 Conversely, in sodium-depleted animals, bilateral injections of CRH inhibited sodium chloride intake. Sodium 15-21 corticotropin releasing hormone Rattus norvegicus 64-67 16357101-6 2006 These results suggest that there is an endogenous CRH inhibitory mechanism operating in the LPBN to modulate the intake of sodium (salt appetite). Sodium 123-129 corticotropin releasing hormone Rattus norvegicus 50-53 16585956-2 2006 In the kidney, renin secretion is tightly linked to sodium intake and renal perfusion pressure, reflecting the important role of the renin-angiotensin system (RAS) in controlling body fluid volume and blood pressure. Sodium 52-58 renin Homo sapiens 15-20 16531985-12 2006 Endogenous UII appears to contribute to the regulation of GFR and renal sodium and water handling in the rat. Sodium 72-78 urotensin 2 Rattus norvegicus 11-14 16613704-11 2006 The serum sodium level was negatively correlated with the umbilical ANP level (r=-0.99, P < 0.01). Sodium 10-16 natriuretic peptide A Homo sapiens 68-71 16051293-2 2006 This paper describes the action of 11 structurally diverse commercial pyrethroid insecticides on the rat Na v 1.8 sodium channel isoform, the principal carrier of the tetrodotoxin-resistant, pyrethroid-sensitive sodium current of sensory neurons, expressed in Xenopus laevis oocytes. Sodium 114-120 sodium voltage-gated channel alpha subunit 10 Rattus norvegicus 105-113 16673263-5 2006 It cleaves fibrinogen, factors XI (FXI) and FXIII, cofactors V and VIII, and the thrombin receptors; uses thrombomodulin to activate protein C and thrombin-activatable-fibrinolysis inhibitor; is inhibited by heparin cofactor II and antithrombin III with the help of acidic carbohydrates; and its activity/specificity is modulated by sodium ions. Sodium 333-339 coagulation factor II, thrombin Homo sapiens 81-89 16673263-5 2006 It cleaves fibrinogen, factors XI (FXI) and FXIII, cofactors V and VIII, and the thrombin receptors; uses thrombomodulin to activate protein C and thrombin-activatable-fibrinolysis inhibitor; is inhibited by heparin cofactor II and antithrombin III with the help of acidic carbohydrates; and its activity/specificity is modulated by sodium ions. Sodium 333-339 coagulation factor II, thrombin Homo sapiens 147-155 16303259-8 2006 The sodium and potassium transport activity of Nha1 antiporters from both D. hansenii strains was almost identical, indicating that plasma membrane antiporter activity is not one of the factors determining the different levels of halotolerance in the two strains. Sodium 4-10 Nha1p Saccharomyces cerevisiae S288C 47-51 16439609-3 2006 METHODS: In Japanese patients with newly diagnosed, untreated hypertension (n = 184), we studied polymorphisms in 10 genes, including G protein-coupled receptor kinase type 4 (GRK4), some variations of which are associated with hypertension and impair D1 receptor (D1R)-inhibited renal sodium transport. Sodium 286-292 G protein-coupled receptor kinase 4 Homo sapiens 134-174 16406782-1 2006 Therapeutic agents brequinar sodium and leflunomide (Arava) work by binding in a hydrophobic tunnel formed by a highly variable N-terminus of family 2 dihydroorotate dehydrogenase (DHODH). Sodium 29-35 dihydroorotate dehydrogenase (quinone) Homo sapiens 151-179 16406782-1 2006 Therapeutic agents brequinar sodium and leflunomide (Arava) work by binding in a hydrophobic tunnel formed by a highly variable N-terminus of family 2 dihydroorotate dehydrogenase (DHODH). Sodium 29-35 dihydroorotate dehydrogenase (quinone) Homo sapiens 181-186 16487178-4 2006 Amino acid 552 has been reported to be involved in the allosteric transition, which is induced by sodium binding to thrombin. Sodium 98-104 coagulation factor II, thrombin Homo sapiens 116-124 16439609-3 2006 METHODS: In Japanese patients with newly diagnosed, untreated hypertension (n = 184), we studied polymorphisms in 10 genes, including G protein-coupled receptor kinase type 4 (GRK4), some variations of which are associated with hypertension and impair D1 receptor (D1R)-inhibited renal sodium transport. Sodium 286-292 G protein-coupled receptor kinase 4 Homo sapiens 176-180 16439609-7 2006 Sodium excretion was inversely related to the number of GRK4 variants in hypertensive persons, and the natriuretic response to dopaminergic stimulation was impaired in normotensive persons having > or =3 GRK4 gene variants. Sodium 0-6 G protein-coupled receptor kinase 4 Homo sapiens 56-60 16467655-11 2006 Sodium restriction did not alter BP and resulted in a marked increase in ANG II levels in HanSD, but caused a significant decrease in BP in TGR without altering plasma or tissue ANG II concentrations. Sodium 0-6 angiotensinogen Rattus norvegicus 73-79 24459482-6 2006 An increased apical targeting of alpha-, beta-, and gamma-ENaC subunits in connecting tubule, and cortical and medullary collecting duct segments in sodium retaining phase of liver cirhosis but not in escape phase of sodium retention. Sodium 149-155 sodium channel epithelial 1 subunit gamma Rattus norvegicus 58-62 24459482-8 2006 These observations therefore strongly support the view that the renal sodium retention associated with nephrotic syndrome and liver cirrhosis is caused by increased sodium reabsorption in the aldosterone sensitive distal nephron including the connecting tubule and collecting duct, and increased apical targeting of ENaC subunits plays a role in the development of sodium retention in nephrotic syndrome and liver cirrhosis. Sodium 70-76 sodium channel epithelial 1 subunit gamma Rattus norvegicus 316-320 16365189-1 2006 The NaHCO3 cotransporter gene (SLC4A5) on chromosome 2 encodes a protein that transports sodium and bicarbonate across the cell membrane and regulates cellular pH. Sodium 89-95 solute carrier family 4 member 5 Homo sapiens 31-37 16633090-1 2006 This study investigated whether intrarenal endothelin-1(ET-1) contributes to sodium excretion in aged rats. Sodium 77-83 endothelin 1 Rattus norvegicus 43-55 16467655-0 2006 Effects of changes in sodium balance on plasma and kidney angiotensin II levels in anesthetized and conscious Ren-2 transgenic rats. Sodium 22-28 angiotensinogen Rattus norvegicus 58-72 17699212-4 2006 COX-2 metabolites have been implicated in mediation of renin release, regulation of sodium excretion, and maintenance of renal blood flow. Sodium 84-90 prostaglandin-endoperoxide synthase 2 Homo sapiens 0-5 16528252-6 2006 The apical immunostaining of ENaC increased in response to sodium restriction, as expected, but dDAVP did not further enhance this apical labelling. Sodium 59-65 sodium channel epithelial 1 subunit gamma Rattus norvegicus 29-33 16601568-2 2006 RESULTS: AT1-receptor activation by angiotensin II is not only involved in the regulation of blood pressure, water and sodium homeostasis, and control of other neurohumoral systems, but also leads to excessive production of reactive oxygen species and to hypertrophy, proliferation, migration, and apoptosis of vascular cells. Sodium 119-125 angiotensinogen Homo sapiens 36-50 16319216-0 2006 Chronic IL-1beta signaling potentiates voltage-dependent sodium currents in trigeminal nociceptive neurons. Sodium 57-63 interleukin 1 beta Homo sapiens 8-16 16319216-2 2006 To better understand such molecular and cellular mechanisms, we investigated how IL-1beta modulates the total voltage-dependent sodium currents (INa) and its tetrodotoxin-resistant (TTX-R) component in capsaicin-sensitive trigeminal nociceptive neurons, both after a brief (5-min) and after a chronic exposure (24-h) of 20 ng/ml IL-1beta. Sodium 128-134 interleukin 1 beta Homo sapiens 81-89 16528252-8 2006 These findings suggest that the previously reported increase in sodium transport induced by sustained stimulation of vasopressin V2 receptor is probably mediated by other mechanism than an increase in the apical density of ENaC. Sodium 64-70 arginine vasopressin receptor 2 Rattus norvegicus 117-140 16528252-8 2006 These findings suggest that the previously reported increase in sodium transport induced by sustained stimulation of vasopressin V2 receptor is probably mediated by other mechanism than an increase in the apical density of ENaC. Sodium 64-70 sodium channel epithelial 1 subunit gamma Rattus norvegicus 223-227 16288954-4 2006 We have characterized the structure, topography and lipophilicity of this channel in the ligand-free fast (sodium-bound) and slow (sodium-free) forms of thrombin, in the sole available structure of activated protein C and in several structures of the coagulation factors VIIa, IXa and Xa, differing in the nature of the bound inhibitor and in the occupancy of exosite-I as well as the Ca2+ and Na+ binding sites. Sodium 131-137 coagulation factor II, thrombin Homo sapiens 153-161 16174867-11 2006 The increased targeting of ENaC and AQP2 likely represents direct or compensatory effects to increase sodium and water reabsorption and to prevent volume depletion in response to prolonged ANP infusion. Sodium 102-108 sodium channel epithelial 1 subunit gamma Rattus norvegicus 27-31 16288954-7 2006 We also disclosed major topographical changes on the thrombin"s surface upon sodium release and transition to the slow form that culminate in the narrowing of the S1 subsite entrance and, strikingly, in the loss of communication between the primary specificity pocket and the exosite-I. Sodium 77-83 coagulation factor II, thrombin Homo sapiens 53-61 16467103-7 2006 All three patients who presented with hyponatremia and elevated ANP showed a decline in serum sodium following fluid restriction, whereas two patients with SCLC and elevated AVP had normalized serum sodium levels. Sodium 94-100 natriuretic peptide A Homo sapiens 64-67 16322117-1 2006 PURPOSE: To assess the feasibility and antitumor activity of oblimersen sodium, an antisense oligonucleotide directed to the Bcl-2 mRNA, combined with irinotecan in patients with advanced colorectal carcinoma, characterize the pharmacokinetic behavior of both oblimersen sodium and irinotecan, and examine Bcl-2 protein inhibition in peripheral blood mononuclear cells (PBMC). Sodium 72-78 BCL2 apoptosis regulator Homo sapiens 125-130 16467103-8 2006 The combination of hyponatremia and elevated ANP was associated with a persistent natriuresis and inappropriately low aldosterone levels despite sodium restriction, suggesting ANP suppression of the aldosterone axis. Sodium 145-151 natriuretic peptide A Homo sapiens 45-48 16514431-1 2006 The renin-angiotensin system in the kidney plays a critical role in the regulation of renal hemodynamics and sodium handling through the activation of vascular, glomerular and tubular angiotensin II type 1 (AT1) receptor-mediated signaling. Sodium 109-115 angiotensin II receptor, type 1a Mus musculus 207-210 16826914-1 2006 The fluorescence spectrum of bovine serum albumin (BSA) influenced by copper ion, sodium ion and molybdenum ion is studied. Sodium 82-88 albumin Homo sapiens 36-49 16452726-0 2006 Remodeling and angiotensin II responses of the uterine arcuate arteries of pregnant rats are altered by low- and high-sodium intake. Sodium 118-124 angiotensinogen Rattus norvegicus 15-29 16554088-2 2006 Central administration of IL-1beta significantly reduced water and salt intake in fluid-deprived animals and decreased salt intake in sodium-depleted rats. Sodium 134-140 interleukin 1 beta Rattus norvegicus 26-34 16554088-3 2006 The antidipsogenic and antinatriorexic effects elicited by the central administration of IL-1beta were suppressed by pretreatment with central injections of the non-selective opioid antagonist naloxone (10 mug) in the two different experimental protocols used here (water deprivation and sodium depletion). Sodium 288-294 interleukin 1 beta Rattus norvegicus 89-97 16554088-5 2006 The present results suggest that the activation of the central interleukinergic component by IL-1beta impairs the increase in water and salt intake induced by water deprivation and the enhancement in sodium appetite that follows sodium depletion. Sodium 200-206 interleukin 1 beta Rattus norvegicus 93-101 16554088-5 2006 The present results suggest that the activation of the central interleukinergic component by IL-1beta impairs the increase in water and salt intake induced by water deprivation and the enhancement in sodium appetite that follows sodium depletion. Sodium 229-235 interleukin 1 beta Rattus norvegicus 93-101 16452726-8 2006 The arcuate arteries of non-pregnant rats on the low-sodium diet showed markedly increased responses to AngII and phenylephrine (Phe). Sodium 53-59 angiotensinogen Rattus norvegicus 104-109 16452726-9 2006 Pregnancy also resulted in heightened responses to AngII and Phe that were significantly reduced for the former agent in rats on the low-sodium diet. Sodium 137-143 angiotensinogen Rattus norvegicus 51-56 16461192-1 2006 BACKGROUND: G protein-coupled receptor kinase 4 (GRK4) is involved in activity of dopamine receptors in renal proximal tubules and thus mediates sodium reabsorption and blood pressure (BP) regulation. Sodium 145-151 G protein-coupled receptor kinase 4 Homo sapiens 12-47 16377440-12 2006 These findings indicate that central sodium-induced activation of AHA angiotensin II-sensitive neurons is enhanced in SHR and Dahl S rats. Sodium 37-43 angiotensinogen Rattus norvegicus 70-84 16837788-2 2006 Serum osmolality and sodium concentration [Na+] are regulated by thirst, the hormone arginine vasopressin (AVP), and renal water and sodium handling. Sodium 21-27 arginine vasopressin Homo sapiens 94-105 16441255-4 2006 With this in mind we analyzed genetic variation in the G protein-coupled receptor kinase 4 (GRK4) gene, a gene whose product has recently been shown to inhibit the dopamine receptor D1 (DRD1) from increasing sodium excretion. Sodium 208-214 G protein-coupled receptor kinase 4 Homo sapiens 55-90 16441255-4 2006 With this in mind we analyzed genetic variation in the G protein-coupled receptor kinase 4 (GRK4) gene, a gene whose product has recently been shown to inhibit the dopamine receptor D1 (DRD1) from increasing sodium excretion. Sodium 208-214 G protein-coupled receptor kinase 4 Homo sapiens 92-96 16441255-4 2006 With this in mind we analyzed genetic variation in the G protein-coupled receptor kinase 4 (GRK4) gene, a gene whose product has recently been shown to inhibit the dopamine receptor D1 (DRD1) from increasing sodium excretion. Sodium 208-214 dopamine receptor D1 Homo sapiens 164-184 16441255-4 2006 With this in mind we analyzed genetic variation in the G protein-coupled receptor kinase 4 (GRK4) gene, a gene whose product has recently been shown to inhibit the dopamine receptor D1 (DRD1) from increasing sodium excretion. Sodium 208-214 dopamine receptor D1 Homo sapiens 186-190 16461192-1 2006 BACKGROUND: G protein-coupled receptor kinase 4 (GRK4) is involved in activity of dopamine receptors in renal proximal tubules and thus mediates sodium reabsorption and blood pressure (BP) regulation. Sodium 145-151 G protein-coupled receptor kinase 4 Homo sapiens 49-53 19789728-1 2006 It is well recognized that the renin-angiotensin system plays an important role in the regulation of arterial pressure and sodium homeostasis. Sodium 123-129 renin Homo sapiens 31-36 17121069-8 2006 CONCLUSIONS: Short-term COX-2 inhibition in patients with moderate renal impairment was associated with significant decrease of tubular transport of sodium, without changing GFR and water excretion. Sodium 149-155 mitochondrially encoded cytochrome c oxidase II Homo sapiens 24-29 17183188-8 2006 Sodium overload increased the expression of: RANTES (38.4.3 +/- 0.8 vs. 2.9 +/- 0.6%, p < 0.001), transforming-growth-factor-beta(1) (35.3 +/- 1.0 vs. 5.0 +/- 0.7%, p < 0.001), alpha-smooth muscle actin (15.6 +/- 0.7 vs. 3.1 +/- 0.3%, p < 0.001), NF-kappaB (9.4 +/- 1.3 to 2.2 +/- 0.5 cells/mm(2), p < 0.001), HIF-1alpha (38.2 +/- 1.7 to 8.4 +/- 0.8 cells/mm(2), p < 0.001) and angiotensin II (35.9 +/- 1.3 to 8.2 +/- 0.5%, p < 0.001). Sodium 0-6 transforming growth factor, beta 1 Rattus norvegicus 101-135 17183188-8 2006 Sodium overload increased the expression of: RANTES (38.4.3 +/- 0.8 vs. 2.9 +/- 0.6%, p < 0.001), transforming-growth-factor-beta(1) (35.3 +/- 1.0 vs. 5.0 +/- 0.7%, p < 0.001), alpha-smooth muscle actin (15.6 +/- 0.7 vs. 3.1 +/- 0.3%, p < 0.001), NF-kappaB (9.4 +/- 1.3 to 2.2 +/- 0.5 cells/mm(2), p < 0.001), HIF-1alpha (38.2 +/- 1.7 to 8.4 +/- 0.8 cells/mm(2), p < 0.001) and angiotensin II (35.9 +/- 1.3 to 8.2 +/- 0.5%, p < 0.001). Sodium 0-6 angiotensinogen Rattus norvegicus 393-407 16809911-0 2006 Glucagon-like peptide-1 is involved in sodium and water homeostasis in humans. Sodium 39-45 glucagon Homo sapiens 0-23 16443562-1 2006 Renal angiotensin II (AII) is suggested to play a role in the enhanced sodium reabsorption that causes a shift in pressure natriuresis in obesity related hypertension; however, the mechanism is not known. Sodium 71-77 angiotensinogen Rattus norvegicus 6-20 16443562-1 2006 Renal angiotensin II (AII) is suggested to play a role in the enhanced sodium reabsorption that causes a shift in pressure natriuresis in obesity related hypertension; however, the mechanism is not known. Sodium 71-77 angiotensinogen Rattus norvegicus 22-25 16472174-8 2006 Because NHE-1 exchanges intracellular H(+) for extracellular Na(+) in a one by one stoichiometry, the intracellular ionic changes resulting from increased activity, will be a increased pH(i) and intracellular sodium ([Na(+)](i)). Sodium 209-215 solute carrier family 9 member A1 Homo sapiens 8-13 16166603-6 2006 Under chronic low sodium diet, Gal 3-/- mice had lower extracellular fluid (ECF) volume than WT mice (p < 0.05). Sodium 18-24 lectin, galactose binding, soluble 3 Mus musculus 31-36 16166603-8 2006 Chronic high sodium diet resulted paradoxically in lower blood pressure (p < 0.01) in Gal 3-/- than in WT. Sodium 13-19 lectin, galactose binding, soluble 3 Mus musculus 89-94 16809911-1 2006 UNLABELLED: In previous studies with glucagon-like peptide-1 (GLP-1) we have observed that this peptide modulates fluid intake and increases renal sodium excretion in healthy volunteers and in patients with diabetes mellitus type 2. Sodium 147-153 glucagon Homo sapiens 37-60 16344378-1 2006 NO produced by endothelial NO synthase (NOS3) decreases sodium transport by the thick ascending limb (THAL). Sodium 56-62 nitric oxide synthase 3 Homo sapiens 40-44 16809911-1 2006 UNLABELLED: In previous studies with glucagon-like peptide-1 (GLP-1) we have observed that this peptide modulates fluid intake and increases renal sodium excretion in healthy volunteers and in patients with diabetes mellitus type 2. Sodium 147-153 glucagon Homo sapiens 62-67 16809911-9 2006 RESULTS: In study part A, an increase in renal sodium excretion was demonstrated: FeNa rose from 1.6 +/- 0.3 (placebo) to 2.7 +/- 0.2% (GLP-1; p = 0.0005). Sodium 47-53 glucagon Homo sapiens 136-141 16809911-11 2006 In part B, an oral salt challenge of 27.7 +/- 0.5 g led to an increased renal excretion of sodium during GLP-1: FeNa increased from 1.6 +/- 0.2% (placebo) to 2.0 +/- 0.2% (GLP-1; p = 0.012). Sodium 91-97 glucagon Homo sapiens 105-110 16809911-15 2006 CONCLUSIONS: GLP-1 acts on renal tissue reducing sodium absorption, probably via similar sodium transporters, which also may be localized in the gastrointestinal tract. Sodium 49-55 glucagon Homo sapiens 13-18 16785827-6 2006 COX-2 metabolites have been implicated in the mediation of renin release, regulation of sodium excretion, and maintenance of renal blood flow. Sodium 88-94 mitochondrially encoded cytochrome c oxidase II Homo sapiens 0-5 16864980-8 2006 CONCLUSION: Since renal papillary endothelin-1 appears to counteract the fluid and sodium retaining effects of renal nerve activity, an impaired renal endothelin-1 synthesis in SHR may contribute to excessive sodium retention and thus to the pathogenesis of hypertension in SHR. Sodium 209-215 endothelin 1 Rattus norvegicus 151-163 16354689-8 2006 In the pyramidal cell layer of the hippocampal CA3 region, where AE3 is strongly expressed, disruption of AE3 abolished sodium-independent chloride-bicarbonate exchange. Sodium 120-126 carbonic anhydrase 3 Mus musculus 47-50 17057415-6 2006 However, a subgroup of 6 volunteers - showing an increase in sodium excretion after ACE-I - also demonstrated lower AII levels at 13:00 h, a higher cumulative urine flow, and a higher urinary NTproBNP/creatinine excretion in comparison with control (all: p < 0.05). Sodium 61-67 angiotensinogen Homo sapiens 116-119 16785747-2 2006 The cloning and identification of sodium transporting genes and proteins like NHE3, NKCC2, ROMK, CLCNKB, NCC, and EnaC has considerably improved our understanding of renal salt handling. Sodium 34-40 solute carrier family 12 member 1 Homo sapiens 84-89 16198010-0 2005 Interaction between arginine vasopressin and angiotensin II receptors in the central regulation of sodium balance. Sodium 99-105 arginine vasopressin Homo sapiens 29-69 17003572-1 2006 BACKGROUND/AIMS: Angiotensin II (ANG II) and dopamine (DA) are both important regulators of sodium and water transport across renal proximal tubules. Sodium 92-98 angiotensinogen Rattus norvegicus 17-31 17003572-1 2006 BACKGROUND/AIMS: Angiotensin II (ANG II) and dopamine (DA) are both important regulators of sodium and water transport across renal proximal tubules. Sodium 92-98 angiotensinogen Rattus norvegicus 33-39 16198010-8 2005 AVP injection into the LPO increased sodium renal excretion, but this was reduced by prior AAVP administration. Sodium 37-43 arginine vasopressin Homo sapiens 0-3 16352916-0 2006 Sodium intake modifies the negative prognostic value of renal damage prior to treatment with ACE inhibitors on proteinuria induced by adriamycin. Sodium 0-6 angiotensin I converting enzyme Rattus norvegicus 93-96 16464787-11 2006 This is most likely a compensatory phenomenon in addition to the increase in the renin-angiotensin system to prevent excess loss of sodium and water. Sodium 132-138 renin Homo sapiens 81-86 16198010-1 2005 We speculated that the influence of lateral preoptic area (LPO) in sodium balance, involves arginine8-vasopressin (AVP) and angiotensin (ANG II) on Na+ uptake in LPO. Sodium 67-73 arginine vasopressin Homo sapiens 92-113 16198010-1 2005 We speculated that the influence of lateral preoptic area (LPO) in sodium balance, involves arginine8-vasopressin (AVP) and angiotensin (ANG II) on Na+ uptake in LPO. Sodium 67-73 arginine vasopressin Homo sapiens 115-118 16326361-1 2005 BACKGROUND: The antihypertensive and renoprotective effects of ACE inhibitor (ACEi) therapy are enhanced by inducing a negative sodium balance. Sodium 128-134 angiotensin I converting enzyme Rattus norvegicus 63-66 16216878-9 2005 These observations suggest a novel link between GILZ and regulation of epithelial sodium transport through modulation of ERK signaling and could represent an important pathway for mediating aldosterone actions in health and disease. Sodium 82-88 mitogen-activated protein kinase 1 Homo sapiens 121-124 16141309-1 2005 Epithelial sodium channels (ENaC) are important for regulating sodium transport across epithelia. Sodium 11-17 sodium channel epithelial 1 subunit gamma Rattus norvegicus 28-32 16150593-5 2005 Estrone sulfate uptake by mOAT5 displayed a time-dependent and sodium-independent manner. Sodium 63-69 solute carrier family 22 (organic anion transporter), member 19 Mus musculus 26-31 16267158-5 2005 The mechanism of ENaC activation was similar in CCD from nephrotic and sodium-depleted rats, as demonstrated by (1) increased number of active ENaC evaluated by patch clamp, (2) recruitment of ENaC to the apical membrane determined by immunohistochemistry, (3) shift in the electrophoretic profile of gamma-ENaC, and (4) increased abundance of beta-ENaC mRNA. Sodium 71-77 sodium channel epithelial 1 subunit gamma Rattus norvegicus 17-21 16257484-3 2005 Since earlier morphological studies showed that some phthalates induced thyroid hyperactivity, we thought it important to investigate possible effects of six major phthalates on the transcriptional activity of sodium/iodide symporter (NIS). Sodium 210-216 solute carrier family 5 member 5 Homo sapiens 235-238 16267597-2 2005 Fluorescence melting experiments show that this intramolecular quadruplex, which is more stable in potassium- than sodium-containing buffers, shows considerable hysteresis between the melting and annealing profiles, even when heated at a rate of 0.05 degrees C min(-1). Sodium 115-121 CD59 molecule (CD59 blood group) Homo sapiens 261-267 16169866-5 2005 RESULTS: Our major findings are as follows: (1) Urinary sodium excretion significantly increased during the early phases of NH4Cl-induced acidosis, (2) This occurrence is associated with sustained renal hypertrophy, and (3) sustained basal phosphorylation of IRS-1, Shc, and MAPK/ERKs in acidotic kidneys. Sodium 56-62 insulin receptor substrate 1 Rattus norvegicus 259-264 16210348-4 2005 With Kv1 channels blocked, dendritic calcium spikes drive bursts of somatic sodium spikes and prevent the cell from faithfully encoding motor timing signals. Sodium 76-82 potassium voltage-gated channel subfamily A member 5 Rattus norvegicus 5-8 16272955-2 2005 The CYP3A5 isoenzyme is also expressed in the kidney and has been implicated in renal sodium reabsorption and blood pressure regulation. Sodium 86-92 cytochrome P450 family 3 subfamily A member 5 Homo sapiens 4-10 16358319-1 2005 The functional expression of the mouse Kir2.1 potassium channel in yeast cells lacking transport systems for potassium and sodium efflux (ena1-4delta nha1delta) resulted in increased cell sensitivity to high external concentrations of potassium. Sodium 123-129 potassium inwardly-rectifying channel, subfamily J, member 2 Mus musculus 39-45 16300400-6 2005 Kinetic analysis of hSGLT1 in proteoliposomes revealed sodium-dependent, secondary active, phlorizin-sensitive, and stereospecific alpha-methyl-d-glucopyranoside transport, demonstrating its full catalytic activity. Sodium 55-61 solute carrier family 5 member 1 Homo sapiens 20-26 15956775-12 2005 These results suggest that the increased protein abundance of ENaC subunits as well as the increased apical targeting of AQP2 may contribute to renal sodium and water retention observed during the development of hypertension in SHR. Sodium 150-156 sodium channel epithelial 1 subunit gamma Rattus norvegicus 62-66 15972388-5 2005 Complexin II mRNA coexpressed with alpha-, beta-, and gamma-ENaC subunits in Xenopus laevis oocytes reduced sodium currents to 16 +/- 3% (n = 19) of control values. Sodium 108-114 sodium channel, non voltage gated 1 gamma subunit S homeolog Xenopus laevis 54-64 15944208-6 2005 The transport of succinate by xNaDC-3 is dependent on sodium, with sigmoidal activation kinetics, and lithium can partially substitute for sodium. Sodium 54-60 high-affinity Na/dicarboxylate cotransporter Xenopus laevis 30-37 15944208-6 2005 The transport of succinate by xNaDC-3 is dependent on sodium, with sigmoidal activation kinetics, and lithium can partially substitute for sodium. Sodium 139-145 high-affinity Na/dicarboxylate cotransporter Xenopus laevis 30-37 15944208-7 2005 As with other members of the family, xNaDC-3 is electrogenic and exhibits inward substrate-dependent currents in the presence of sodium. Sodium 129-135 high-affinity Na/dicarboxylate cotransporter Xenopus laevis 37-44 15944208-8 2005 However, other electrophysiological properties of xNaDC-3 are unique and involve large leak currents, possibly mediated by anions, that are activated by binding of sodium or lithium to a single site. Sodium 164-170 high-affinity Na/dicarboxylate cotransporter Xenopus laevis 50-57 16006463-2 2005 The renin-angiotensin system (RAS) is directly concerned with sodium and water homeostasis. Sodium 62-68 renin Homo sapiens 4-9 16420073-6 2005 The dose of urea was increased if morning serum sodium level (SNa) was lower than 132 mmol/L. Sodium 48-54 snail family transcriptional repressor 1 Homo sapiens 62-65 16186597-0 2005 Phase I to II multicenter study of oblimersen sodium, a Bcl-2 antisense oligonucleotide, in patients with advanced chronic lymphocytic leukemia. Sodium 46-52 BCL2 apoptosis regulator Homo sapiens 56-61 16185723-4 2005 Efflux via SERT depends on this sodium flux that is believed to be a prerequisite for outward transport. Sodium 32-38 solute carrier family 6 member 4 Homo sapiens 11-15 16133044-8 2005 The association of renal ET-1 and AVP activity with sodium excretion in premature infants treated with indomethacin and ibuprofen supports the hypothesis that these factors may play a role in the physiologic changes in sodium excretion. Sodium 52-58 endothelin 1 Homo sapiens 25-29 16133044-8 2005 The association of renal ET-1 and AVP activity with sodium excretion in premature infants treated with indomethacin and ibuprofen supports the hypothesis that these factors may play a role in the physiologic changes in sodium excretion. Sodium 219-225 endothelin 1 Homo sapiens 25-29 16126183-1 2005 Electrospray-ionization MSn mass spectrometry (ESI-MSn) with low-energy, collision-induced dissociation (CID) was used to establish the fragmentation behavior of sodium ion adducts of higher-carbon amino spiro-sugar derivatives. Sodium 162-168 moesin Homo sapiens 24-27 16126183-1 2005 Electrospray-ionization MSn mass spectrometry (ESI-MSn) with low-energy, collision-induced dissociation (CID) was used to establish the fragmentation behavior of sodium ion adducts of higher-carbon amino spiro-sugar derivatives. Sodium 162-168 moesin Homo sapiens 51-54 15898956-2 2005 In the present study, we report that deletion of AQP3 is also associated with an increased urinary sodium excretion. Sodium 99-105 aquaporin 3 Mus musculus 49-53 16168010-2 2005 AIMS: The interplay between natriuretic dopamine and antinatriuretic angiotensin II represents an important mechanism for the regulation of renal sodium and water excretion. Sodium 146-152 angiotensinogen Rattus norvegicus 69-83 15898956-4 2005 RESULTS: The present study confirms that AQP3 null mice exhibit severe polyuria and polydipsia and demonstrated that they exhibit increased urinary sodium excretion. Sodium 148-154 aquaporin 3 Mus musculus 41-45 15898956-12 2005 CONCLUSIONS: The results improve the possibility that the severe urinary concentrating defect in AQP3 null mice may in part be caused by the decreased expression of AQP2, p-AQP2 and AQP4 in CNT and CCD, whereas the increased urinary sodium excretion may in part be accounted for by Na,K-ATPase in CCD in AQP3 null mice. Sodium 233-239 aquaporin 3 Mus musculus 97-101 15961410-5 2005 Ucn-I enhanced urinary sodium excretion (5.3-fold, P=0.0001) and creatinine clearance (1.3-fold, P=0.0055) long-term, and tended to increase urine output (P=0.0748). Sodium 23-29 urocortin Ovis aries 0-3 16169319-1 2005 BACKGROUND: Sodium retention and volume expansion, mediated in part by aldosterone, are prominent features in low-renin hypertension. Sodium 12-18 renin Homo sapiens 114-119 16164646-1 2005 BACKGROUND: Although prolactin affects sodium and water transport across the plasma membrane and interacts with dopamine in the brain, its role in the kidney is unclear. Sodium 39-45 prolactin Rattus norvegicus 21-30 16164646-9 2005 In rats, prolactin infusion resulted in an increase in urinary sodium, potassium, and water excretion. Sodium 63-69 prolactin Rattus norvegicus 9-18 16207143-2 2005 In rats and humans, mutation of the alpha-adducin subunit leads to the stimulation of the sodium (Na(+)), potassium (K(+))-adenosine triphosphate (ATP)-ase activity in renal tubular cells, increased renal Na(+) reabsorption, and, subsequently, hypertension. Sodium 90-96 adducin 1 Homo sapiens 36-49 16173949-12 2005 In conclusion, neonatal ACE inhibition in rats induces pronounced alterations in renal haemodynamics and function, characterized by reductions in ERPF and GFR, increased RVR and impaired tubular sodium and water reabsorption, which are evident at weaning. Sodium 195-201 angiotensin I converting enzyme Rattus norvegicus 24-27 16093448-3 2005 Patients who have congenital NDI and bear mutations in the AVPR2 or AQP2 genes have a "pure" NDI phenotype with loss of water but normal conservation of sodium, potassium, chloride, and calcium. Sodium 153-159 arginine vasopressin receptor 2 Homo sapiens 59-64 16092068-1 2005 Sodium-iodide-symporter (NIS), an integral plasma membrane glycoprotein, mediates the sodium-dependent active uptake of iodide (I(-)) into the thyroid gland, which is a fundamental step in thyroid hormone synthesis. Sodium 86-92 solute carrier family 5 member 5 Rattus norvegicus 0-23 16092068-1 2005 Sodium-iodide-symporter (NIS), an integral plasma membrane glycoprotein, mediates the sodium-dependent active uptake of iodide (I(-)) into the thyroid gland, which is a fundamental step in thyroid hormone synthesis. Sodium 86-92 solute carrier family 5 member 5 Rattus norvegicus 25-28 15849242-1 2005 The GABA transporter GAT1 removes the neurotransmitter GABA from the synaptic cleft by coupling of GABA uptake to the co-transport of two sodium ions and one chloride ion. Sodium 138-144 solute carrier family 6 member 1 Homo sapiens 21-25 16099717-7 2005 The elevated nighttime excretion, with values similar to those in the daytime, hint at a possibly elevated fluid, sodium, and chloride intake during daytime. Sodium 114-120 histidine triad nucleotide binding protein 1 Homo sapiens 79-83 16098822-3 2005 Recent studies establish a role for PPARgamma in renal sodium reabsorption, providing a mechanism for the plasma volume expansion induced by these drugs. Sodium 55-61 peroxisome proliferator activated receptor gamma Homo sapiens 36-45 16014042-1 2005 BACKGROUND: System x(-) (c) is a heterodimeric transporter, comprised of a light chain, xCT, and heavy chain, 4F2hc, which mediates the sodium-independent exchange of cystine and glutamate at the plasma membrane. Sodium 136-142 solute carrier family 7 member 11 Canis lupus familiaris 88-91 16014042-1 2005 BACKGROUND: System x(-) (c) is a heterodimeric transporter, comprised of a light chain, xCT, and heavy chain, 4F2hc, which mediates the sodium-independent exchange of cystine and glutamate at the plasma membrane. Sodium 136-142 solute carrier family 3 member 2 Canis lupus familiaris 110-115 16142301-1 2005 Angiotensin II, a potent vasoconstrictor, also participates in the regulation of renal sodium and water excretion, not only via a myriad of effects on renal hemodynamics, glomerular filtration rate, and regulation of aldosterone secretion, but also via direct effects on renal tubule transport. Sodium 87-93 angiotensinogen Homo sapiens 0-14 16142301-8 2005 Interestingly, in this part of the nephron, the effects of aldosterone and angiotensin II are not sodium dependent, whereas in the cortical collecting duct, both aldosterone and angiotensin II, by contrast, affect H+ secretion by sodium-dependent mechanisms. Sodium 230-236 angiotensinogen Homo sapiens 178-192 15840770-12 2005 These data indicate that COX-2 may be an important factor contributing to the impaired renal water and sodium handling in response to BUO. Sodium 103-109 mitochondrially encoded cytochrome c oxidase II Homo sapiens 25-30 15905165-1 2005 GAT-1 is a sodium- and chloride-dependent gamma-aminobutyric acid transporter and is the first identified member of a family of transporters that maintain low synaptic neurotransmitter levels and thereby enable efficient synaptic transmission. Sodium 11-17 solute carrier family 6 member 1 Homo sapiens 0-5 15734879-1 2005 The subfornical organ (SFO), one of the brain circumventricular organs, is known to mediate some of the central effects of angiotensin II related to sodium and water homeostasis. Sodium 149-155 angiotensinogen Rattus norvegicus 123-137 15888562-0 2005 Vasopressin-V2 receptor stimulation reduces sodium excretion in healthy humans. Sodium 44-50 arginine vasopressin receptor 2 Homo sapiens 0-23 15888562-9 2005 The possibility that an inappropriate stimulation of ENaC by vasopressin might lead to significant sodium retention in chronic situations remains to be determined. Sodium 99-105 arginine vasopressin Homo sapiens 61-72 15893844-0 2005 A novel sodium overload test predicting ascites decompensation in rats with CCl4-induced cirrhosis. Sodium 8-14 C-C motif chemokine ligand 4 Rattus norvegicus 76-80 16202699-4 2005 At some point, angiotensin II activates additional mechanisms responsible for sustained increased blood pressure including sodium retention, endothelial dysfunction, and vasoconstriction related to production of reactive oxygen species. Sodium 123-129 angiotensinogen Homo sapiens 15-29 15950597-6 2005 Nha1p activity is associated with a net charge movement across the membrane, transporting more protons per single sodium ion (i.e., electrogenic). Sodium 114-120 Nha1p Saccharomyces cerevisiae S288C 0-5 15970963-6 2005 A semi-quantitative, absolute detection limit of 17 nmol s(-1) was obtained for sodium with a sample flow rate of 100 microL min(-1) and an integration time of 100 ms in air at atmospheric pressure. Sodium 80-86 CD59 molecule (CD59 blood group) Homo sapiens 125-131 15893443-2 2005 Are reported and analyzed molecular mechanisms about sodium retention in collecting duct cells regarding activation and surface expression of epithelial sodium channels (ENaC) and sodium-potassium-ATPase (Na,K-ATPase) by aldosterone, vasopressin, natriuretic peptide system (underfill theory): is necessary a better understanding about the dysregulation of ENaC and Na,K-ATPase surface expression and the resistance to natriuretic peptide system. Sodium 53-59 arginine vasopressin Homo sapiens 234-245 15831538-10 2005 These results suggest that, in skeletal muscle, CNTF can rapidly decrease sodium currents by altering inactivation gating, probably through an intracellular PKC-dependent mechanism that could lead to decreased membrane excitability. Sodium 74-80 ciliary neurotrophic factor Rattus norvegicus 48-52 15671346-1 2005 Activation of phosphatidylinositol 3-kinase (PI 3-kinase) is required for insulin stimulation of sodium transport in A6 cell monolayers. Sodium 97-103 insulin Homo sapiens 74-81 15671346-6 2005 Since the mitogen-activated protein kinase (MAPK) pathway has also been implicated in the regulation of sodium transport, we also investigated whether this pathway is turned on by insulin, H2O2, or EGF. Sodium 104-110 mitogen-activated protein kinase 3 Homo sapiens 44-48 15671346-9 2005 The latter effect was associated with an increase in PKB phosphorylation, thus suggesting that the stimulation of the MAPK pathway prevents, in part, the stimulation of the PI 3-kinase pathway in the transport of sodium stimulated by EGF. Sodium 213-219 mitogen-activated protein kinase 3 Homo sapiens 118-122 15827364-15 2005 Mean daily urine sodium dropped from baseline to day 2 (194 +/- 43 vs 43 +/- 38 mmol x L-1), remaining lower on days 3, 4, and 6 (40 +/- 39, 39 +/- 39, and 68 +/- 40 mmol x L-1, respectively). Sodium 17-23 immunoglobulin kappa variable 1-16 Homo sapiens 87-90 15863001-1 2005 Design, synthesis, and structure-activity relationships of 3,4-dihydro-2(1H)-quinazolinone derivatives as inhibitors of the sodium/calcium (Na(+)/Ca(2+)) exchanger are discussed. Sodium 124-130 solute carrier family 8 member A1 Homo sapiens 140-163 15863236-2 2005 In this study, uptake of L-[14C]cystine by three of the high affinity sodium-dependent mammalian glutamate transporters (GLT1, GLAST and EAAC1) individually expressed in HEK cells has been determined. Sodium 70-76 solute carrier family 1 member 2 Homo sapiens 121-125 15955065-1 2005 The mammalian members of the inorganic phosphate (P(i)) transporter (PiT) family, the type III sodium-dependent phosphate (NaP(i)) transporters PiT1 and PiT2, have been assigned housekeeping P(i) transport functions and are suggested to be involved in chondroblastic and osteoblastic mineralization and ectopic calcification. Sodium 95-101 POU class 1 homeobox 1 Homo sapiens 144-148 16075377-9 2005 Classical, well-defined actions of Angiotensin II in the brain include the regulation of hormone formation and release, the control of the central and peripheral sympathoadrenal systems, and the regulation of water and sodium intake. Sodium 219-225 angiotensinogen Rattus norvegicus 35-49 15883230-4 2005 Under anesthesia with moderate sodium loading, COX-1(-/-) had higher MAP (109+/-5 versus 124+/-4 mm Hg; P<0.05), renal vascular resistance (23.5+/-1.6 versus 30.7+/-1.7 mm Hg . Sodium 31-37 cytochrome c oxidase I, mitochondrial Mus musculus 47-52 15863236-2 2005 In this study, uptake of L-[14C]cystine by three of the high affinity sodium-dependent mammalian glutamate transporters (GLT1, GLAST and EAAC1) individually expressed in HEK cells has been determined. Sodium 70-76 solute carrier family 1 member 3 Homo sapiens 127-132 15863236-2 2005 In this study, uptake of L-[14C]cystine by three of the high affinity sodium-dependent mammalian glutamate transporters (GLT1, GLAST and EAAC1) individually expressed in HEK cells has been determined. Sodium 70-76 solute carrier family 1 member 1 Homo sapiens 137-142 15863236-4 2005 L-glutamate and L-homocysteate are potent inhibitors of sodium-dependent L-[14C]cystine uptake in HEK(GLAST), HEK(GLT1) and HEK(EAAC1) cells. Sodium 56-62 solute carrier family 1 member 3 Homo sapiens 102-107 15863236-4 2005 L-glutamate and L-homocysteate are potent inhibitors of sodium-dependent L-[14C]cystine uptake in HEK(GLAST), HEK(GLT1) and HEK(EAAC1) cells. Sodium 56-62 solute carrier family 1 member 2 Homo sapiens 114-118 15863236-4 2005 L-glutamate and L-homocysteate are potent inhibitors of sodium-dependent L-[14C]cystine uptake in HEK(GLAST), HEK(GLT1) and HEK(EAAC1) cells. Sodium 56-62 solute carrier family 1 member 1 Homo sapiens 128-133 15914973-10 2005 The treatment of hyponatremia may be facilitated by emerging therapies that block the actions of arginine vasopressin at V2 and V1a receptors to promote aquaresis, the electrolyte-sparing elimination of free water, and elevate serum sodium concentrations. Sodium 233-239 arginine vasopressin Homo sapiens 106-117 15755725-9 2005 These results indicate that IL-1beta may contribute to alveolar edema in ALI by reducing distal lung epithelial sodium absorption. Sodium 112-118 interleukin 1 beta Homo sapiens 28-36 15946459-14 2005 The high basal levels of insulin and the high rate of HD and diabetes in patients with central obesity seem to indicate that they suffer a metabolic syndrome with significant hormonal imbalances and sodium retention. Sodium 199-205 insulin Homo sapiens 25-32 15613622-0 2005 Inhibition of cGMP-specific phosphodiesterase type 5 reduces sodium excretion and arterial blood pressure in patients with NaCl retention and ascites. Sodium 61-67 phosphodiesterase 5A Homo sapiens 28-52 15613622-1 2005 In the present study, we tested the hypothesis that inhibition of renal phosphodiesterase type 5 (PDE5) in patients with liver cirrhosis and ascites increases sodium excretion. Sodium 159-165 phosphodiesterase 5A Homo sapiens 72-96 15613622-1 2005 In the present study, we tested the hypothesis that inhibition of renal phosphodiesterase type 5 (PDE5) in patients with liver cirrhosis and ascites increases sodium excretion. Sodium 159-165 phosphodiesterase 5A Homo sapiens 98-102 15854151-4 2005 In renal failure, a defect in renal sodium excretory function leads to an abnormal pressure natriuresis relationship and activation of the renin-angiotensin-aldosterone system, contributing to the development of hypertension and progression of kidney disease. Sodium 36-42 renin Homo sapiens 139-144 15726118-0 2005 Repeated cocaine administration decreases calcineurin (PP2B) but enhances DARPP-32 modulation of sodium currents in rat nucleus accumbens neurons. Sodium 97-103 protein phosphatase 1, regulatory (inhibitor) subunit 1B Rattus norvegicus 74-82 15627648-6 2005 BNP resulted in increases in urinary sodium excretion (U(Na)V) (2.2+/-0.7 to 164+/-76 microeq/min, P<0.05) and glomerular filtration rate (GFR) (27+/-4 to 52+/-11 ml/min, P<0.05) that were greater than those with Uro (P<0.05), whereas ANP did not result in increases in U(Na)V or GFR. Sodium 37-43 natriuretic peptide B Canis lupus familiaris 0-3 15922564-5 2005 Whole cell sodium currents in Chinese hamster ovary (CHO) cells coexpressing human Na(v)1.3 sodium channels and C121Wbeta1 exhibited altered gating properties, compared to currents in cells coexpressing Na(v)1.3 and wild type beta1. Sodium 11-17 immunoglobulin lambda variable 2-11 Homo sapiens 83-91 15922564-5 2005 Whole cell sodium currents in Chinese hamster ovary (CHO) cells coexpressing human Na(v)1.3 sodium channels and C121Wbeta1 exhibited altered gating properties, compared to currents in cells coexpressing Na(v)1.3 and wild type beta1. Sodium 11-17 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 117-122 15808917-1 2005 Involvement of Angiotensin II (Ang II) in the regulation of sodium levels by modulating the Na+/H+ exchangers is demonstrated in many tissues. Sodium 60-66 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 15-29 15808917-1 2005 Involvement of Angiotensin II (Ang II) in the regulation of sodium levels by modulating the Na+/H+ exchangers is demonstrated in many tissues. Sodium 60-66 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 31-37 15585668-1 2005 Vasopressin and ANG II, which are known to play a major role in renal water and sodium reabsorption, are mainly coupled to the cAMP/PKA and phosphoinositide pathways, respectively. Sodium 80-86 arginine vasopressin Rattus norvegicus 0-11 15618459-7 2005 However, after the prior inhibition of sodium transport using amiloride, there was an increased PD in the non-CF group alone, suggesting CFTR-mediated chloride secretion in response to luminal hypertonicity. Sodium 39-45 CF transmembrane conductance regulator Homo sapiens 137-141 15585668-1 2005 Vasopressin and ANG II, which are known to play a major role in renal water and sodium reabsorption, are mainly coupled to the cAMP/PKA and phosphoinositide pathways, respectively. Sodium 80-86 angiotensinogen Rattus norvegicus 16-22 15634721-0 2005 Adiponectin, leptin, and erythrocyte sodium/lithium countertransport activity, but not resistin, are related to glucose metabolism in growth hormone-deficient adults. Sodium 37-43 growth hormone 1 Homo sapiens 134-148 15780066-0 2005 Cyclic AMP-phosphodiesterases inhibitor improves sodium excretion in rats with cirrhosis and ascites. Sodium 49-55 cathelicidin antimicrobial peptide Rattus norvegicus 0-10 15780097-11 2005 In contrast, under conditions of endogenous RAS activation due to clipping of the renal artery or to sodium restriction, Ang-(1-7) serves as opponent of the vasoconstrictor actions of Ang II. Sodium 101-107 angiotensinogen Rattus norvegicus 184-190 15743993-0 2005 Mineralocorticoid versus glucocorticoid receptor occupancy mediating aldosterone-stimulated sodium transport in a novel renal cell line. Sodium 92-98 nuclear receptor subfamily 3, group C, member 1 Mus musculus 25-48 15780066-7 2005 RESULTS: In control and in non-ascitic cirrhotic rats, cAMP administration significantly increased sodium and phosphate excretions, but did not change these excretions in cirrhotic rats with ascites. Sodium 99-105 cathelicidin antimicrobial peptide Rattus norvegicus 55-59 15716695-5 2005 RESULTS: Relative to carriers of the wild type (Gly/Gly) ADD1 gene, patients carrying the mutated Trp ADD1 allele had higher blood pressure (systolic blood pressure (SBP) 143.2 +/- 1.0 versus 140.6 +/- 0.6 mmHg P = 0.027 and diastolic blood pressure (DBP) 94.2 +/- 0.77 versus 92.3 +/- 0.5 mmHg, P = 0.03), lower PRA and EO, consistent with the hypothesis of the renal sodium retaining effect of the Trp allele. Sodium 369-375 adducin 1 Homo sapiens 102-106 15804404-2 2005 We investigated the expression of the sodium-dependent high-affinity glutamate transporters EAAT1, EAAT2, and EAAT3 in 11 human autopsied cases without neurological disorders and in four cases with type II lissencephaly including Walker Warburg"s syndrome (WWS) and Fukuyama-type congenital muscular dystrophy (FCMD), both of which are classified as migration disorders of the human brain. Sodium 38-44 solute carrier family 1 member 3 Homo sapiens 92-97 15804404-2 2005 We investigated the expression of the sodium-dependent high-affinity glutamate transporters EAAT1, EAAT2, and EAAT3 in 11 human autopsied cases without neurological disorders and in four cases with type II lissencephaly including Walker Warburg"s syndrome (WWS) and Fukuyama-type congenital muscular dystrophy (FCMD), both of which are classified as migration disorders of the human brain. Sodium 38-44 solute carrier family 1 member 2 Homo sapiens 99-104 15804404-2 2005 We investigated the expression of the sodium-dependent high-affinity glutamate transporters EAAT1, EAAT2, and EAAT3 in 11 human autopsied cases without neurological disorders and in four cases with type II lissencephaly including Walker Warburg"s syndrome (WWS) and Fukuyama-type congenital muscular dystrophy (FCMD), both of which are classified as migration disorders of the human brain. Sodium 38-44 solute carrier family 1 member 1 Homo sapiens 110-115 15743391-3 2005 RESULTS: Increasing sodium intake led to suppression of circulating renin, angiotensin II, and aldosterone in rats and mice in the absence of alterations in arterial blood pressure. Sodium 20-26 angiotensinogen Rattus norvegicus 75-89 15743391-4 2005 Additional experiments demonstrated that continuous intravenous infusion of angiotensin II (20 ng kg(-1) min(-1)) significantly increased arterial blood pressure by approximately 35 mmHg in conscious rats at all levels of sodium intake (n = 6). Sodium 222-228 angiotensinogen Rattus norvegicus 76-90 15528393-10 2005 These data indicate that endogenous production of ANG II and action at forebrain receptors is critically involved in depletion-related sodium appetite in mice. Sodium 135-141 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 50-56 15900896-2 2005 The milk from cows infected with subclinical mastitis revealed a significant decrease in potassium (P < 0.001) and a significant increase in sodium and phosphorus content (P < 0.01). Sodium 144-150 Weaning weight-maternal milk Bos taurus 4-8 15900896-3 2005 Similarly, the milk from cows with the clinical form of the disease showed a significant increase in sodium (P < 0.001) and a significant decrease in potassium, magnesium (P < 0.001) and calcium (P < 0.01). Sodium 101-107 Weaning weight-maternal milk Bos taurus 15-19 15900896-4 2005 Comparison of healthy cow"s milk with that from cows with subclinical mastitis revealed a highly significant increase in sodium (P < 0.001). Sodium 121-127 Weaning weight-maternal milk Bos taurus 28-32 15794866-1 2005 Oblimersen sodium is an antisense oligonucleotide to the first 6 codons of the B-cell leukemia gene 2 (bcl-2) open reading frame. Sodium 11-17 BCL2 apoptosis regulator Homo sapiens 79-101 15794866-1 2005 Oblimersen sodium is an antisense oligonucleotide to the first 6 codons of the B-cell leukemia gene 2 (bcl-2) open reading frame. Sodium 11-17 BCL2 apoptosis regulator Homo sapiens 103-108 15732067-7 2005 DISCUSSION: Although the pathophysiology of refeeding edema is not entirely understood, it is well known that insulin induces sodium retention by increasing distal tubular sodium reabsorption. Sodium 126-132 insulin Homo sapiens 110-117 15716702-4 2005 A shift in sodium status modifies the activity of the renin-angiotensin-aldosterone system and the effects of ACEi, but its effects on angiotensin-(1-7) are unknown. Sodium 11-17 renin Homo sapiens 54-59 15361890-9 2005 Thus, reduced modulation of renin activity in response to sodium restriction and an increased aldosterone on a high sodium diet appear to identify characteristics of hypertensive patients predisposed to abnormal cardiac remodelling. Sodium 58-64 renin Homo sapiens 28-33 15667315-6 2005 This fine mapping facilitated a candidate gene approach within the interval, which resulted in the cloning and characterization of a novel member of the sodium-dependent neurotransmitter transporter family (B(0)AT1, SLC6A19) from mouse and human kidney, which shows all properties of system B(0). Sodium 153-159 solute carrier family 6 (neurotransmitter transporter), member 19 Mus musculus 207-214 15667315-6 2005 This fine mapping facilitated a candidate gene approach within the interval, which resulted in the cloning and characterization of a novel member of the sodium-dependent neurotransmitter transporter family (B(0)AT1, SLC6A19) from mouse and human kidney, which shows all properties of system B(0). Sodium 153-159 solute carrier family 6 (neurotransmitter transporter), member 19 Mus musculus 216-223 15745085-6 2005 Results showed that VIP but not saline infusion induced netjejunal sodium secretion, watery diarrhea, and cardiovascular effects (P < 0.04). Sodium 67-73 vasoactive intestinal peptide Homo sapiens 20-23 15361890-0 2005 Influence of dietary sodium on the renin-angiotensin-aldosterone system and prevalence of left ventricular hypertrophy by EKG criteria. Sodium 21-27 renin Homo sapiens 35-40 15498826-2 2005 Congestive heart failure (CHF) is characterized by excessive sodium retention, attributed to both an excessive effect of angiotensin II and diminished responsiveness to natriuretic peptides. Sodium 61-67 angiotensinogen Rattus norvegicus 121-135 15669052-2 2005 A-II functions by binding its type 1 (AT1) receptors to cause vasoconstriction and retention of sodium and fluid. Sodium 96-102 angiotensinogen Homo sapiens 0-4 15694820-7 2005 The induction of three subunits of ENaC and prostasin mRNA was observed in proctocolectomized, aldosterone-infused rats but not in dietary sodium-depleted rats. Sodium 139-145 sodium channel epithelial 1 subunit gamma Rattus norvegicus 35-39 15652409-6 2005 Consistent with expression of a functional SERT, specific uptake of (3)H-serotonin in macrophages was sodium dependent and inhibited by fluoxetine (IC(50) 6.9 nM) and desipramine (IC(50) 32 nM) but not by nisoxetine or reserpine. Sodium 102-108 solute carrier family 6 (neurotransmitter transporter, serotonin), member 4 Mus musculus 43-47 15695791-2 2005 Referring to the knowledge about epigenetic modulation, we succeeded in reversing the silencing of sodium/sodide symporter (hNIS) transgenes transfected into human neural stem (HB1.F3) cells. Sodium 99-105 solute carrier family 5 member 5 Homo sapiens 124-128 15695791-2 2005 Referring to the knowledge about epigenetic modulation, we succeeded in reversing the silencing of sodium/sodide symporter (hNIS) transgenes transfected into human neural stem (HB1.F3) cells. Sodium 99-105 histocompatibility minor HB-1 Homo sapiens 177-180 15641067-4 2005 This study was undertaken to test the hypothesis that IL-8 promotes chondrocyte hypertrophy by modulating chondrocyte PiT-1 expression and sodium-dependent Pi uptake, and to assess differential roles in this activity. Sodium 139-145 C-X-C motif chemokine ligand 8 Homo sapiens 54-58 21290760-4 2005 This shift in activity is caused by an increase in intracellular sodium due to stimulation of the sarcolemmal Na(+)/H(+) exchanger-1 (NHE1). Sodium 65-71 solute carrier family 9 member A1 Homo sapiens 110-132 21290760-4 2005 This shift in activity is caused by an increase in intracellular sodium due to stimulation of the sarcolemmal Na(+)/H(+) exchanger-1 (NHE1). Sodium 65-71 solute carrier family 9 member A1 Homo sapiens 134-138 21290775-1 2005 The mammalian MEC/DEG/ENaC gene superfamily encodes membrane proteins which are involved in diverse functions including acid sensing, maintenance of sodium homeostasis and transduction of mechanical stimuli and nociceptive pain. Sodium 149-155 C-C motif chemokine ligand 28 Homo sapiens 14-17 15960298-0 2005 Enhanced pressor response to centrally administered vasopressin in WKY rats on high sodium diet. Sodium 84-90 arginine vasopressin Rattus norvegicus 52-63 15513953-4 2005 Northern and Western blot analyses and immunohistochemistry were used to determine the abundance of sodium-independent glucose and fructose transporters (GLUT)2 and GLUT5. Sodium 100-106 solute carrier family 2 member 5 Rattus norvegicus 165-170 15641067-8 2005 IL-8, but not IL-1 or the CXCR2 ligand growth-related oncogene alpha, induced PiT-1 expression and increased sodium-dependent Pi uptake by >40% in chondrocytes. Sodium 109-115 C-X-C motif chemokine ligand 8 Homo sapiens 0-4 15641067-12 2005 CONCLUSION: Our results link low-grade IL-8-mediated cartilaginous inflammation in OA to altered chondrocyte differentiation and disease progression through PiT-1 expression and sodium-dependent Pi uptake mediated by CXCR1 signaling. Sodium 178-184 C-X-C motif chemokine ligand 8 Homo sapiens 39-43 16502970-1 2005 We have demonstrated that insulin stimulates sodium reabsorption in the distal nephron by stimulating the phosphatidylinositol 3-kinase (PI 3-kinase) pathway and that any stimulation of this enzyme (e.g. by EGF, by H2O2 or by exogenous PIP3, added apically) leads to a parallel increase in sodium reabsorption. Sodium 45-51 insulin Homo sapiens 26-33 15586010-8 2005 This hypothesis is supported by recent data showing that sodium retention and hypertension can develop when the balance of production of these free radicals is tipped towards O2*-, such as in diabetes, atherosclerosis and renin-angiotensin-system activation. Sodium 57-63 renin Homo sapiens 222-227 15638741-12 2005 Dual inhibitors of ACE and endopeptidase 24.11 may be of value where there is both sodium retention and increased angiotensin II. Sodium 83-89 angiotensin I converting enzyme Homo sapiens 19-22 15892676-5 2005 COX-2 metabolites have been implicated in mediation of renin release, regulation of sodium excretion and maintenance of renal blood flow. Sodium 84-90 mitochondrially encoded cytochrome c oxidase II Homo sapiens 0-5 15383399-1 2005 Epoxyeicosatrienoic acids (EETs), which belong to cytochrome P-450 (CYP)-derived eicosanoids, have been implicated to vasodilate renal arterioles, inhibit sodium transport in the nephron, and regulate blood pressure in several animal models. Sodium 155-161 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 50-66 15383399-1 2005 Epoxyeicosatrienoic acids (EETs), which belong to cytochrome P-450 (CYP)-derived eicosanoids, have been implicated to vasodilate renal arterioles, inhibit sodium transport in the nephron, and regulate blood pressure in several animal models. Sodium 155-161 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 68-71 16403686-6 2005 The diuretic-induced decrease in total body sodium activates the renin-angiotensin system, thus rendering blood pressure maintenance angiotensin II-dependent. Sodium 44-50 renin Homo sapiens 65-70 16403686-6 2005 The diuretic-induced decrease in total body sodium activates the renin-angiotensin system, thus rendering blood pressure maintenance angiotensin II-dependent. Sodium 44-50 angiotensinogen Homo sapiens 133-147 16403692-5 2005 Endothelium-dependent vascular relaxation in response to acetylcholine was almost maximally impaired in ApoE(-)/(-) mice during a normal sodium diet. Sodium 137-143 apolipoprotein E Mus musculus 104-108 15586018-1 2005 PURPOSE OF REVIEW: The renin-angiotensin system is a coordinated hormonal cascade important to the regulation of the renal sodium excretion and blood pressure. Sodium 123-129 renin Homo sapiens 23-28 16502970-1 2005 We have demonstrated that insulin stimulates sodium reabsorption in the distal nephron by stimulating the phosphatidylinositol 3-kinase (PI 3-kinase) pathway and that any stimulation of this enzyme (e.g. by EGF, by H2O2 or by exogenous PIP3, added apically) leads to a parallel increase in sodium reabsorption. Sodium 290-296 insulin Homo sapiens 26-33 15534073-4 2005 Renal interstitial Ang II increased by 47-fold in response to LS and increased further in response to valsartan or PD by 67-fold and 61-fold from normal sodium diet (NS) and by 41% and 29% from LS, respectively. Sodium 153-159 angiotensinogen Rattus norvegicus 19-25 15610243-1 2005 BACKGROUND: Prostasin has been shown to be involved in the regulation of sodium handling in the kidney. Sodium 73-79 serine protease 8 Rattus norvegicus 12-21 15623826-0 2005 Growth hormone and epidermal growth factor upregulate specific sodium-dependent glutamine uptake systems in human intestinal C2BBe1 cells. Sodium 63-69 growth hormone 1 Homo sapiens 0-14 15610243-9 2005 CONCLUSION: Our findings indicate the possibility that TGF-beta1 transcriptionally inhibits prostasin expression by the induction of IkappaBalpha and the subsequent inhibition of NF-kappaB/Rel activity in M-1 cells, and also suggest the possibility that TGF-beta1 might inhibit sodium reabsorption through a reduction in prostasin expression and subsequent inhibition of ENaC activity. Sodium 278-284 transforming growth factor, beta 1 Rattus norvegicus 55-64 15610243-9 2005 CONCLUSION: Our findings indicate the possibility that TGF-beta1 transcriptionally inhibits prostasin expression by the induction of IkappaBalpha and the subsequent inhibition of NF-kappaB/Rel activity in M-1 cells, and also suggest the possibility that TGF-beta1 might inhibit sodium reabsorption through a reduction in prostasin expression and subsequent inhibition of ENaC activity. Sodium 278-284 serine protease 8 Rattus norvegicus 92-101 15610243-2 2005 TGF-beta1 has been demonstrated to suppress alphaENaC expression and sodium uptake. Sodium 69-75 transforming growth factor, beta 1 Rattus norvegicus 0-9 15610243-3 2005 Therefore, we hypothesized that TGF-beta1 may regulate prostasin expression to modulate sodium reabsorption in the kidney. Sodium 88-94 transforming growth factor, beta 1 Rattus norvegicus 32-41 15610243-3 2005 Therefore, we hypothesized that TGF-beta1 may regulate prostasin expression to modulate sodium reabsorption in the kidney. Sodium 88-94 serine protease 8 Rattus norvegicus 55-64 15675318-1 2005 Clinical and laboratory experiments have demonstrated that arginine vasopressin (AVP), renin-aldosterone system and catecholamines play a crucial role in water and sodium retention in edematous diseases, including congestive heart failure, nephrotic syndrome and liver cirrhosis. Sodium 164-170 arginine vasopressin Homo sapiens 68-79 16050265-5 2005 hERG and APD/QT liabilities may be dissociated when hERG block is offset by block of calcium or sodium currents. Sodium 96-102 ETS transcription factor ERG Homo sapiens 0-4 15675318-1 2005 Clinical and laboratory experiments have demonstrated that arginine vasopressin (AVP), renin-aldosterone system and catecholamines play a crucial role in water and sodium retention in edematous diseases, including congestive heart failure, nephrotic syndrome and liver cirrhosis. Sodium 164-170 arginine vasopressin Homo sapiens 81-84 16050265-5 2005 hERG and APD/QT liabilities may be dissociated when hERG block is offset by block of calcium or sodium currents. Sodium 96-102 ETS transcription factor ERG Homo sapiens 52-56 15675318-1 2005 Clinical and laboratory experiments have demonstrated that arginine vasopressin (AVP), renin-aldosterone system and catecholamines play a crucial role in water and sodium retention in edematous diseases, including congestive heart failure, nephrotic syndrome and liver cirrhosis. Sodium 164-170 renin Homo sapiens 87-92 15675318-6 2005 Also, norepinephrine increases sodium reabsorption in proximal tubules, and in part augments renin-aldosterone system that increases sodium reabsorption in distal nephron. Sodium 133-139 renin Homo sapiens 93-98 15684587-0 2005 Involvement of drinking and intestinal sodium absorption in hyponatremic effect of atrial natriuretic peptide in seawater eels. Sodium 39-45 natriuretic peptide A Homo sapiens 83-109 15717837-6 2005 Low sodium intake also prevented proteinuria and cardiac hypertrophy in TGR. Sodium 4-10 thioredoxin reductase 3 Mus musculus 72-75 15850610-11 2005 The increase of the decline in pHi elicited by preexposure to thrombin was still observed in the presence of an inhibitor of the Na+/H+ exchange or in sodium-free solutions. Sodium 151-157 coagulation factor II, thrombin Homo sapiens 62-70 15579501-10 2004 These results suggest that regulation of the basolateral Cl(-)/HCO(3)(-) exchanger AE2 plays an important role in the adaptation of bicarbonate absorption in the TAL during chronic acid-base disturbances and high sodium intake. Sodium 213-219 solute carrier family 4 member 2 Rattus norvegicus 83-86 15451889-8 2004 The decrease of the electrochemical gradient of sodium caused inversion of the Na-Ca exchanger that provided an additional mean of entry for calcium. Sodium 48-54 nascent polypeptide associated complex subunit alpha Homo sapiens 79-84 15579501-0 2004 Regulation of the Cl-/HCO3- exchanger AE2 in rat thick ascending limb of Henle"s loop in response to changes in acid-base and sodium balance. Sodium 126-132 solute carrier family 4 member 2 Rattus norvegicus 38-41 15579773-0 2004 Forskolin, 8-Br-3",5"-cyclic adenosine 5"-monophosphate, and catalytic protein kinase A expression in the nucleus increase radioiodide uptake and sodium/iodide symporter protein levels in RET/PTC1-expressing cells. Sodium 146-152 ret proto-oncogene Rattus norvegicus 188-191 15579501-2 2004 The purpose of this study was to test whether chronic changes in acid-base status and sodium intake regulate AE2 polypeptide abundance in the TAL of the rat. Sodium 86-92 solute carrier family 4 member 2 Rattus norvegicus 109-112 15614030-0 2004 Low sodium diet inhibits the local counter-regulator effect of angiotensin-(1-7) on angiotensin II. Sodium 4-10 angiotensinogen Rattus norvegicus 84-98 15614025-1 2004 OBJECTIVE: Angiotensin II and aldosterone, generated by the angiotensin-converting enzyme (ACE) and aldosterone synthase (CYP11B2), respectively, not only regulate sodium and water homeostasis, but also influence vascular remodeling in response to high blood pressure. Sodium 164-170 angiotensinogen Homo sapiens 11-25 15614025-1 2004 OBJECTIVE: Angiotensin II and aldosterone, generated by the angiotensin-converting enzyme (ACE) and aldosterone synthase (CYP11B2), respectively, not only regulate sodium and water homeostasis, but also influence vascular remodeling in response to high blood pressure. Sodium 164-170 angiotensin I converting enzyme Homo sapiens 60-89 15614030-11 2004 This non-competitive antagonism of Ang-(1-7) is abolished by a low sodium intake in normotensive rats, suggesting that it serves as a negative feedback towards Ang II in response to an altered sodium intake. Sodium 67-73 angiotensinogen Rattus norvegicus 160-166 15614025-1 2004 OBJECTIVE: Angiotensin II and aldosterone, generated by the angiotensin-converting enzyme (ACE) and aldosterone synthase (CYP11B2), respectively, not only regulate sodium and water homeostasis, but also influence vascular remodeling in response to high blood pressure. Sodium 164-170 angiotensin I converting enzyme Homo sapiens 91-94 15614030-11 2004 This non-competitive antagonism of Ang-(1-7) is abolished by a low sodium intake in normotensive rats, suggesting that it serves as a negative feedback towards Ang II in response to an altered sodium intake. Sodium 193-199 angiotensinogen Rattus norvegicus 160-166 15803438-1 2004 INTRODUCTION: High-sodium intake blunts the renoprotective efficacy of angiotensin-converting enzyme (ACE) inhibitors. Sodium 19-25 angiotensin I converting enzyme Rattus norvegicus 71-100 15599092-1 2004 The candidate mechanisms for maintaining hypertension in a chronically angiotensin II (Ang II)-infused state include direct vasoconstriction of the vasculature, disturbance of renal water/sodium handling, and central/peripheral sympathetic nerve regulation of hemodynamics. Sodium 188-194 angiotensinogen Rattus norvegicus 71-85 15599092-1 2004 The candidate mechanisms for maintaining hypertension in a chronically angiotensin II (Ang II)-infused state include direct vasoconstriction of the vasculature, disturbance of renal water/sodium handling, and central/peripheral sympathetic nerve regulation of hemodynamics. Sodium 188-194 angiotensinogen Rattus norvegicus 87-93 15803438-1 2004 INTRODUCTION: High-sodium intake blunts the renoprotective efficacy of angiotensin-converting enzyme (ACE) inhibitors. Sodium 19-25 angiotensin I converting enzyme Rattus norvegicus 102-105 15806712-0 2004 Elevated dietary sodium intake exacerbates myocardial hypertrophy associated with cardiac-specific overproduction of angiotensin II. Sodium 17-23 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 117-131 15806712-10 2004 CONCLUSION: This study demonstrates that, where there is a pre-existing genetic condition of Ang II-dependent cardiac hypertrophy, the pro-growth effect of elevated dietary sodium is selectively augmented. Sodium 173-179 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 93-99 15569339-7 2004 An experimental rise in sodium concentration greater than 5 mmol/L induces pressor effects on the brain and on the renin-angiotensin system. Sodium 24-30 renin Homo sapiens 115-120 15806712-13 2004 The cellular mechanistic bases for this specific ANG II-dietary sodium interaction remain to be elucidated. Sodium 64-70 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 49-55 15962610-5 2004 In 73 patients with a history of hypertension plasma renin activity was estimated in basal conditions and after stimulation by sodium restriction and upright position. Sodium 127-133 renin Homo sapiens 53-58 15452715-2 2004 Incubation with high glucose concentrations caused an increase in NHE1 activity, as estimated by internal pH and sodium-uptake measurements. Sodium 113-119 solute carrier family 9 member A1 Homo sapiens 66-70 15328386-9 2004 Finally, ET-1 decreased sodium excretion by 58% and VML 588 reduced this decrease dose-independently by two-thirds. Sodium 24-30 endothelin 1 Homo sapiens 9-13 15528469-1 2004 Alpha-adducin polymorphism in humans is associated with abnormal renal sodium handling and high blood pressure. Sodium 71-77 adducin 1 Homo sapiens 0-13 15762045-5 2004 Following insulin treatment he developed marked insulin edema and a cluster of abnormalities, including decreased sodium excretion, hypokalemia, hypouricemia, proteinuria, hypoalbuminemia and anemia. Sodium 114-120 insulin Homo sapiens 10-17 15471576-0 2004 Modulation of renal CNG-A3 sodium channel in rats subjected to low- and high-sodium diets. Sodium 27-33 cyclic nucleotide gated channel subunit alpha 3 Rattus norvegicus 20-26 15492316-9 2004 The ACE D/I polymorphism, together with the ACE genotype-by-sodium interaction term, significantly and independently improved the models relating LVM index to the AGTR2 polymorphism and the AGTR2 genotype-by-sodium interaction. Sodium 60-66 angiotensin I converting enzyme Homo sapiens 44-47 15492316-9 2004 The ACE D/I polymorphism, together with the ACE genotype-by-sodium interaction term, significantly and independently improved the models relating LVM index to the AGTR2 polymorphism and the AGTR2 genotype-by-sodium interaction. Sodium 208-214 angiotensin I converting enzyme Homo sapiens 4-7 15492316-9 2004 The ACE D/I polymorphism, together with the ACE genotype-by-sodium interaction term, significantly and independently improved the models relating LVM index to the AGTR2 polymorphism and the AGTR2 genotype-by-sodium interaction. Sodium 208-214 angiotensin I converting enzyme Homo sapiens 44-47 15506212-1 2004 Addition of corrosion promoters, such as sodium and potassium chloride, accelerated TNT degradation during water treatment using zerovalent zinc and iron. Sodium 41-47 chromosome 16 open reading frame 82 Homo sapiens 84-87 15161602-2 2004 Specifically, we show that a 2-min exposure to 0.1 and 1 nM ANG II slowed the rate of intracellular sodium accumulation in response to an increase in extracellular sodium added in the presence of gramicidin D. From these data, we show that ANG II directly stimulates Na-K-ATPase activity at rate-limiting concentrations of intracellular sodium. Sodium 100-106 angiotensinogen Rattus norvegicus 60-66 15161602-2 2004 Specifically, we show that a 2-min exposure to 0.1 and 1 nM ANG II slowed the rate of intracellular sodium accumulation in response to an increase in extracellular sodium added in the presence of gramicidin D. From these data, we show that ANG II directly stimulates Na-K-ATPase activity at rate-limiting concentrations of intracellular sodium. Sodium 164-170 angiotensinogen Rattus norvegicus 60-66 15161602-2 2004 Specifically, we show that a 2-min exposure to 0.1 and 1 nM ANG II slowed the rate of intracellular sodium accumulation in response to an increase in extracellular sodium added in the presence of gramicidin D. From these data, we show that ANG II directly stimulates Na-K-ATPase activity at rate-limiting concentrations of intracellular sodium. Sodium 164-170 angiotensinogen Rattus norvegicus 60-66 15201142-4 2004 To elucidate the role of endosomal SGLT1 in the regulation of sodium-dependent d-glucose uptake into enterocytes, we compared SGLT1-mediated D-glucose uptake into Caco-2 cells with the subcellular distribution of SGLT1 after challenging the cells with different stimuli. Sodium 62-68 solute carrier family 5 member 1 Homo sapiens 35-40 15284836-3 2004 During a 12:12 light-dark cycle, as compared to control CHO cells, the implantation of encapsulated hANP-producing CHO cells was associated with an increase in the net excretion of water, sodium and potassium, and with a reversal of the advanced circadian phases related to renovascular hypertension in 2K1C rats. Sodium 188-194 natriuretic peptide A Homo sapiens 100-104 15500134-2 2004 All classic physiological effects of AII, such as vasoconstriction, aldosterone and vasopressin release, sodium and water retention and sympathetic facilitation, are mediated by the AT1 receptor. Sodium 105-111 angiotensinogen Homo sapiens 37-40 15549446-0 2004 In vivo induction of prostasin mRNA in colonic epithelial cells by dietary sodium depletion and aldosterone infusion in rats. Sodium 75-81 serine protease 8 Rattus norvegicus 21-30 15814461-6 2004 Functionally, sodium-free induced forward mode of NCX1 attenuated by Cav-1 antisense ODN. Sodium 14-20 solute carrier family 8 member A1 Rattus norvegicus 50-54 15814461-6 2004 Functionally, sodium-free induced forward mode of NCX1 attenuated by Cav-1 antisense ODN. Sodium 14-20 caveolin 1 Rattus norvegicus 69-74 15571230-1 2004 We have examined whether hyperuricemia in essential hypertension may be related to an increased insulin secretion thereby enhancing the tubular reabsorption of sodium and thus uric acid. Sodium 160-166 insulin Homo sapiens 96-103 15221289-1 2004 PURPOSE: We evaluated the feasibility of non-invasive imaging of recombinant adenovirus-mediated human sodium-iodide symporter (hNIS) gene expression by (99m)TcO(4)(-) scintigraphy in skeletal muscle of rats. Sodium 103-109 solute carrier family 5 member 5 Homo sapiens 128-132 15571230-5 2004 These results suggest that insulin may mediate uric acid underexcretion due to its tubular sodium retaining effect in essential hypertensive patients. Sodium 91-97 insulin Homo sapiens 27-34 15549446-10 2004 RESULTS: Treatment with sodium-depleted diet and aldosterone infusion resulted in an increase of plasma aldosterone and induction of prostasin mRNA in the left colon. Sodium 24-30 serine protease 8 Rattus norvegicus 133-142 15175418-0 2004 Low sodium modifies the vascular effects of angiotensin-converting enzyme inhibitor therapy in healthy rats. Sodium 4-10 angiotensin I converting enzyme Rattus norvegicus 44-73 15481860-0 2004 Sodium reduces calcium binding to albumin and fibrinogen. Sodium 0-6 fibrinogen beta chain Homo sapiens 46-56 15593031-0 2004 Central role of vasopressin in sodium/water retention in hypo- and hypervolemic nephrotic patients: a unifying hypothesis. Sodium 31-37 arginine vasopressin Homo sapiens 16-27 15593031-4 2004 In the transition, a central role is played by vasopressin, which is secreted in the two phases, respectively, by a volume and an osmotic stimulus; therefore, persistent sodium/water retention is maintained through the vascular and tubular effects of this peptide. Sodium 170-176 arginine vasopressin Homo sapiens 47-58 15593031-5 2004 In addition, we propose that vasodilation and sodium/water excretion could ensue when both stimuli for vasopressin release fade away, leading to the resolution of the syndrome. Sodium 46-52 arginine vasopressin Homo sapiens 103-114 15521214-4 2004 Treatment with insulin resulted in a decrease in serum glucose value from 913 +/- 197 mg/dL to 170 +/- 78 mg/dL, an increase in serum sodium level from 125 +/- 5 to 136 +/- 5 mmol/L, and a fall in calculated serum tonicity value from 300 +/- 13 to 282 +/- 11 mmol/kg (all at p < 0.001). Sodium 134-140 insulin Homo sapiens 15-22 15175418-1 2004 Low dietary sodium (LS) increases the effect of angiotensin-converting enzyme (ACE) inhibitor therapy in patients and experimental models, but mechanisms underlying this enhanced efficacy are largely unknown. Sodium 12-18 angiotensin I converting enzyme Homo sapiens 48-77 15175418-1 2004 Low dietary sodium (LS) increases the effect of angiotensin-converting enzyme (ACE) inhibitor therapy in patients and experimental models, but mechanisms underlying this enhanced efficacy are largely unknown. Sodium 12-18 angiotensin I converting enzyme Homo sapiens 79-82 15175418-9 2004 Whether cause or consequence of the enhanced blood pressure response, our data demonstrate a modifying effect of dietary sodium on vascular effects of ACE inhibition. Sodium 121-127 angiotensin I converting enzyme Rattus norvegicus 151-154 15272911-7 2004 MEASUREMENTS: Basal and angiotensin II stimulated plasma and 24-h urinary steroid excretion during low (60 mmol/day) and high (160 mmol/day) sodium intake and plasma steroids after ACTH stimulation were measured. Sodium 141-147 angiotensinogen Homo sapiens 24-38 15100098-0 2004 Phosphatidylinositol 3,4,5-trisphosphate: an early mediator of insulin-stimulated sodium transport in A6 cells. Sodium 82-88 insulin Homo sapiens 63-70 15100098-1 2004 Insulin stimulates sodium transport across A6 epithelial cell monolayers. Sodium 19-25 insulin Homo sapiens 0-7 15100098-2 2004 Activation of phosphatidylinositol 3-kinase (PI 3-kinase) was suggested as an early step in the insulin-stimulated sodium reabsorption (Ref. Sodium 115-121 insulin Homo sapiens 96-103 15100098-7 2004 To further establish that the stimulation of sodium transport induced by insulin is related to PIP(3) levels, we transfected A6 cells with human PTEN cDNA and observed a 30% decrease in the natriferic effect of insulin. Sodium 45-51 insulin Homo sapiens 73-80 15100098-7 2004 To further establish that the stimulation of sodium transport induced by insulin is related to PIP(3) levels, we transfected A6 cells with human PTEN cDNA and observed a 30% decrease in the natriferic effect of insulin. Sodium 45-51 insulin Homo sapiens 211-218 15554451-7 2004 After infusion of angiotensin II mean arterial blood pressure in cold-induced hypertensive rats on high sodium diet was significantly higher compared to cold-induced hypertensive rats on low sodium diet (p < 0.05). Sodium 104-110 angiotensinogen Rattus norvegicus 18-32 15554451-7 2004 After infusion of angiotensin II mean arterial blood pressure in cold-induced hypertensive rats on high sodium diet was significantly higher compared to cold-induced hypertensive rats on low sodium diet (p < 0.05). Sodium 191-197 angiotensinogen Rattus norvegicus 18-32 15554451-8 2004 Angiotensin II-induced contraction of aortic rings was significantly higher in cold-induced hypertensive rats on high sodium diet compared to cold-induced hypertensive rats on low sodium diet (2.39 +/- 0.03 g vs. 2.21 +/- 0.04 g, n = 12, p < 0.01). Sodium 118-124 angiotensinogen Rattus norvegicus 0-14 15554451-8 2004 Angiotensin II-induced contraction of aortic rings was significantly higher in cold-induced hypertensive rats on high sodium diet compared to cold-induced hypertensive rats on low sodium diet (2.39 +/- 0.03 g vs. 2.21 +/- 0.04 g, n = 12, p < 0.01). Sodium 180-186 angiotensinogen Rattus norvegicus 0-14 15150264-1 2004 Microsomal epoxide hydrolase (mEH) plays a central role in xenobiotic metabolism as well as mediating the sodium-dependent uptake of bile acids into the liver, where these compounds regulate numerous biological processes such as cholesterol metabolism and hepatocyte signaling pathways. Sodium 106-112 epoxide hydrolase 1, microsomal Mus musculus 30-33 15246823-0 2004 Dietary sodium regulates angiotensin AT1a and AT1b mRNA expression in mouse brain. Sodium 8-14 angiotensin II receptor, type 1a Mus musculus 37-41 15199296-8 2004 Renal sodium retention in liver cirrhosis, nephrotic syndrome and hypoxia have been linked to 11beta-HSD2 reduced activity. Sodium 6-12 hydroxysteroid 11-beta dehydrogenase 2 Mus musculus 94-105 15213008-8 2004 Thus, it seems that the sodium intake control is performed by MnPO neurons through the stimulatory action of angiotensin II on AT1 receptors under sodium depletion, but not water deprivation or salt overload neither of ad libitum water and salt intake condition. Sodium 24-30 angiotensinogen Rattus norvegicus 109-123 15213008-8 2004 Thus, it seems that the sodium intake control is performed by MnPO neurons through the stimulatory action of angiotensin II on AT1 receptors under sodium depletion, but not water deprivation or salt overload neither of ad libitum water and salt intake condition. Sodium 147-153 angiotensinogen Rattus norvegicus 109-123 15201536-8 2004 RESULTS AND CONCLUSIONS: Our analysis shows that the 460Trp variant of the alpha-adducin polymorphism is probably associated with a sodium-sensitive form of hypertension, while the polymorphisms of the angiotensin II type 1 receptor gene and the -344C/T variant of the aldosterone synthase gene are not associated with this phenotype. Sodium 132-138 adducin 1 Homo sapiens 75-88 15497505-12 2004 Hsp90alpha and Hsp90beta upregulation induced by a low-sodium diet together with redistribution in thick ascending limb cells suggests that Hsp90 plays a role in the modulation of sodium reabsorption under these circumstances. Sodium 55-61 heat shock protein 90 alpha family class A member 1 Rattus norvegicus 0-5 15497505-12 2004 Hsp90alpha and Hsp90beta upregulation induced by a low-sodium diet together with redistribution in thick ascending limb cells suggests that Hsp90 plays a role in the modulation of sodium reabsorption under these circumstances. Sodium 180-186 heat shock protein 90 alpha family class A member 1 Rattus norvegicus 0-5 15010500-1 2004 Previously, we demonstrated that malignant glioma cell lines have increased intracellular pH (pHi) as a result of increased activities of the type I sodium/hydrogen exchanger (NHE1). Sodium 149-155 solute carrier family 9 member A1 Homo sapiens 176-180 15252776-4 2004 NO antagonizes the effects of Ang II on vascular tone, cell growth, and renal sodium excretion, and also down-regulates the synthesis of angiotensin-converting enzyme (ACE) and Ang II type 1 receptors. Sodium 78-84 angiotensinogen Homo sapiens 30-36 15241786-6 2004 The implantation of encapsulated hANP-producing cells also caused significant increases in renal blood flow (RBF), glomerular filtration rate (GFR), sodium output, urine excretion, and urinary cGMP levels. Sodium 149-155 natriuretic peptide A Homo sapiens 33-37 15188166-9 2004 Inhibition of electrogenic sodium transport as well as beta- and gamma-ENaC mRNA expression could be mimicked in control colon by in vitro preexposure for 8 hours to tumor necrosis factor alpha and interferon gamma. Sodium 27-33 tumor necrosis factor Homo sapiens 166-193 15217967-2 2004 Oblimersen sodium is an antisense oligonucleotide compound designed to specifically bind to human bcl-2 mRNA, resulting in catalytic degradation of bcl-2 mRNA and subsequent decrease in bcl-2 protein translation. Sodium 11-17 BCL2 apoptosis regulator Homo sapiens 98-103 15217967-2 2004 Oblimersen sodium is an antisense oligonucleotide compound designed to specifically bind to human bcl-2 mRNA, resulting in catalytic degradation of bcl-2 mRNA and subsequent decrease in bcl-2 protein translation. Sodium 11-17 BCL2 apoptosis regulator Homo sapiens 148-153 15217967-2 2004 Oblimersen sodium is an antisense oligonucleotide compound designed to specifically bind to human bcl-2 mRNA, resulting in catalytic degradation of bcl-2 mRNA and subsequent decrease in bcl-2 protein translation. Sodium 11-17 BCL2 apoptosis regulator Homo sapiens 148-153 15232215-4 2004 Erythrocyte NHE-1 activity has been estimated by fluorometrical determination of the intracellular pH and quantification of sodium uptake using 22Na. Sodium 124-130 solute carrier family 9 member A1 Homo sapiens 12-17 15188166-9 2004 Inhibition of electrogenic sodium transport as well as beta- and gamma-ENaC mRNA expression could be mimicked in control colon by in vitro preexposure for 8 hours to tumor necrosis factor alpha and interferon gamma. Sodium 27-33 interferon gamma Homo sapiens 198-214 15206148-3 2004 Insulin resistance/hyperinsulinemia induces blood pressure elevation by sodium retention, activation of sympathetic nervous system and renin-angiotensin system(RAS) and promotion of vascular cell growth. Sodium 72-78 insulin Homo sapiens 0-7 15149328-1 2004 BACKGROUND: Proximal tubule (PT) angiotensinogen (AGT) is part of a tubular renin-angiotensin system (RAS) that participates in the regulation of sodium reabsorption along the entire nephron. Sodium 146-152 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 33-48 15149328-1 2004 BACKGROUND: Proximal tubule (PT) angiotensinogen (AGT) is part of a tubular renin-angiotensin system (RAS) that participates in the regulation of sodium reabsorption along the entire nephron. Sodium 146-152 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 50-53 15110895-7 2004 CONCLUSIONS: The alpha-adducin WW genotype was associated with higher systolic BP among men with a higher sodium intake. Sodium 106-112 adducin 1 Homo sapiens 17-30 15170065-6 2004 Two additional findings, namely, a lack of the ability to increase BSC1 expression leads to urinary concentrating defect and an enhanced BSC1 expression underlies the edema-forming condition, confirm the close association between sodium handling in TAL and body fluid accumulation. Sodium 230-236 solute carrier family 12 member 1 Homo sapiens 137-141 15160833-6 2004 Chronic exposure to excess angiotensin II produces eccentric ventricular hypertrophy, vasoconstriction, and sodium retention. Sodium 108-114 angiotensinogen Homo sapiens 27-41 15068965-2 2004 Sympathetic nervous and renin-angiotensin-aldosterone system activation appear to play an important role in the sodium and water retention, rightward shift in the pressure-natriuresis, and blood pressure elevation observed in obese individuals. Sodium 112-118 renin Homo sapiens 24-29 15071349-3 2004 The decline rate from the peak value of intracellular 45Ca2+ concentration ([Ca2+]i) mobilized by angiotensin II was decelerated by removal of extracellular sodium (Na+o) in SHR but not in WKY. Sodium 157-163 angiotensinogen Rattus norvegicus 98-112 15086906-8 2004 In sensitized distal tubule cells, TNF-stimulated sodium uptake was blocked by amiloride and PD098059, inhibitors of epithelial sodium channels and extracellular signal-related protein kinase (ERK) activation, respectively. Sodium 50-56 Eph receptor B1 Rattus norvegicus 148-191 15148385-3 2004 Using triple-labeled fluorescent immunocytochemistry, we also show that Nav1.6, which is known to produce a persistent sodium current, and the Na+/Ca2+ exchanger, which can be driven by persistent sodium current to import damaging levels of calcium into axons, are colocalized with beta-amyloid precursor protein, a marker of axonal injury, in acute MS lesions. Sodium 197-203 solute carrier family 8 member A1 Homo sapiens 143-161 15148385-3 2004 Using triple-labeled fluorescent immunocytochemistry, we also show that Nav1.6, which is known to produce a persistent sodium current, and the Na+/Ca2+ exchanger, which can be driven by persistent sodium current to import damaging levels of calcium into axons, are colocalized with beta-amyloid precursor protein, a marker of axonal injury, in acute MS lesions. Sodium 197-203 amyloid beta precursor protein Homo sapiens 282-312 15003832-0 2004 Effects of angiotensin and vasopressin V(1) receptors on water and sodium intake induced by injection of vasopressin into lateral septal area. Sodium 67-73 arginine vasopressin Rattus norvegicus 105-116 15003832-5 2004 Water and sodium intake were measured at 0.25, 0.5, 1.0 and 2.0 h. Injection of AVP reduced the water and sodium ingestion vs. control (0.15 M saline). Sodium 10-16 arginine vasopressin Rattus norvegicus 80-83 15003832-5 2004 Water and sodium intake were measured at 0.25, 0.5, 1.0 and 2.0 h. Injection of AVP reduced the water and sodium ingestion vs. control (0.15 M saline). Sodium 106-112 arginine vasopressin Rattus norvegicus 80-83 15086906-8 2004 In sensitized distal tubule cells, TNF-stimulated sodium uptake was blocked by amiloride and PD098059, inhibitors of epithelial sodium channels and extracellular signal-related protein kinase (ERK) activation, respectively. Sodium 50-56 Eph receptor B1 Rattus norvegicus 193-196 14993496-8 2004 CONCLUSIONS: COX-2 inhibitors may cause reversible ARF and hyperkalaemia in patients with oedematous conditions treated with low sodium diets and loop diuretics. Sodium 129-135 prostaglandin-endoperoxide synthase 2 Homo sapiens 13-18 15098812-12 2004 Careful monitoring of water and sodium balance is warranted in all patients treated with vasopressin for septic shock. Sodium 32-38 arginine vasopressin Homo sapiens 89-100 15023890-8 2004 Similarly, urinary sodium excretion was higher in the Fs+BNP group. Sodium 19-25 natriuretic peptide B Canis lupus familiaris 57-60 15126925-17 2004 CONCLUSIONS: The enhanced responses of RPF and sodium excretion to AT1 receptor blockade in TGR suggest that renal hemodynamics and sodium excretion in TGR are under strong ANG II influence. Sodium 47-53 angiotensinogen Rattus norvegicus 173-179 15126925-17 2004 CONCLUSIONS: The enhanced responses of RPF and sodium excretion to AT1 receptor blockade in TGR suggest that renal hemodynamics and sodium excretion in TGR are under strong ANG II influence. Sodium 132-138 angiotensinogen Rattus norvegicus 173-179 14993484-1 2004 BACKGROUND: Adenosine A(1) receptor blockade has been suggested as a treatment in conditions with sodium and fluid retention because it increases urinary Na(+) excretion and increases proximal tubular fluid output. Sodium 98-104 adenosine A1 receptor Rattus norvegicus 12-35 15063785-0 2004 IL-1beta and TNFalpha regulate sodium absorption in rat distal colon. Sodium 31-37 interleukin 1 beta Rattus norvegicus 0-8 15063785-0 2004 IL-1beta and TNFalpha regulate sodium absorption in rat distal colon. Sodium 31-37 tumor necrosis factor Rattus norvegicus 13-21 15063785-9 2004 We conclude that the pro-inflammatory cytokines IL-1beta and TNFalpha inhibit electrogenic sodium absorption in rat distal colon by mRNA expression regulation of the beta- and gamma-ENaC subunits. Sodium 91-97 interleukin 1 beta Rattus norvegicus 48-56 15063785-9 2004 We conclude that the pro-inflammatory cytokines IL-1beta and TNFalpha inhibit electrogenic sodium absorption in rat distal colon by mRNA expression regulation of the beta- and gamma-ENaC subunits. Sodium 91-97 tumor necrosis factor Rattus norvegicus 61-69 15063785-9 2004 We conclude that the pro-inflammatory cytokines IL-1beta and TNFalpha inhibit electrogenic sodium absorption in rat distal colon by mRNA expression regulation of the beta- and gamma-ENaC subunits. Sodium 91-97 sodium channel epithelial 1 subunit gamma Rattus norvegicus 176-186 14744863-1 2004 The sodium- and chloride-dependent gamma-aminobutyric acid (GABA) transporter GAT-1 is the first identified member of a family of transporters, which maintain low synaptic neurotransmitter levels and thereby enable efficient synaptic transmission. Sodium 4-10 solute carrier family 6 member 1 Homo sapiens 78-83 14660513-1 2004 Exposure to prolonged bed rest is known to induce changes in the renin-angiotensin-aldosterone system (RAAS) by way of posture, sodium and potassium balance, and stress, which may have serious consequences for patients. Sodium 128-134 renin Homo sapiens 65-70 15136971-0 2004 Dietary sodium restriction specifically potentiates left ventricular ACE inhibition by zofenopril, and is associated with attenuated hypertrophic response in rats with myocardial infarction. Sodium 8-14 angiotensin I converting enzyme Rattus norvegicus 69-72 15151474-4 2004 Mechanisms by which cyclooxygenase-2 inhibitors may increase cardiovascular risk are selective inhibition of prostaglandin I2 over thromboxane A2 within the eicosanoid pathway, which promotes thrombosis, and inhibition of prostaglandins E2 and I2 within the kidney, which leads to sodium and water retention and blood pressure elevation. Sodium 281-287 prostaglandin-endoperoxide synthase 2 Homo sapiens 20-36 15001366-6 2004 RESULTS: Microbiological evaluation of amniotic fluid PPROM revealed aerobic, anaerobic or mixed aerobic anaerobic infections PPROM was associated with significant elevation of both fetal serum and amniotic fluid prolactin concentrations, increased amniotic fluid osmolality, sodium, chlorides and calcium. Sodium 276-282 prolactin Homo sapiens 213-222 14761863-6 2004 In rodents, a high-sodium diet (HSD) increases the pituitary abundance of POMC mRNA and of gamma-MSH content and results in a doubling of plasma gamma-MSH concentration. Sodium 19-25 proopiomelanocortin Homo sapiens 74-78 14761863-6 2004 In rodents, a high-sodium diet (HSD) increases the pituitary abundance of POMC mRNA and of gamma-MSH content and results in a doubling of plasma gamma-MSH concentration. Sodium 19-25 proopiomelanocortin Homo sapiens 91-100 14761863-6 2004 In rodents, a high-sodium diet (HSD) increases the pituitary abundance of POMC mRNA and of gamma-MSH content and results in a doubling of plasma gamma-MSH concentration. Sodium 19-25 proopiomelanocortin Homo sapiens 145-154 14732722-3 2004 COX-2 metabolites have been implicated in maintenance of renal blood flow, mediation of renin release, and regulation of sodium excretion. Sodium 121-127 mitochondrially encoded cytochrome c oxidase II Homo sapiens 0-5 14732722-4 2004 COX-2 inhibition may transiently decrease urine sodium excretion in some subjects and induce mild to moderate elevation of blood pressure. Sodium 48-54 mitochondrially encoded cytochrome c oxidase II Homo sapiens 0-5 15136971-3 2004 The antihypertensive and renoprotective effects of ACE inhibitors (ACE-Is) can be substantially enhanced by dietary sodium restriction. Sodium 116-122 angiotensin I converting enzyme Homo sapiens 51-54 15136971-3 2004 The antihypertensive and renoprotective effects of ACE inhibitors (ACE-Is) can be substantially enhanced by dietary sodium restriction. Sodium 116-122 angiotensin I converting enzyme Homo sapiens 67-70 15136971-4 2004 In line with the latter, the aim of the present study was to explore whether dietary sodium restriction enhances the efficacy of ACE-I after MI. Sodium 85-91 angiotensin I converting enzyme Homo sapiens 129-132 15136971-10 2004 However, only when ACE-I therapy was combined with dietary sodium restriction was LV ACE activity significantly reduced. Sodium 59-65 angiotensin I converting enzyme Homo sapiens 85-88 15136971-14 2004 CONCLUSIONS: Effects of ACE inhibition with zofenopril can be potentiated by additional dietary sodium restriction. Sodium 96-102 angiotensin I converting enzyme Homo sapiens 24-27 15136971-15 2004 However, these effects were tissue-specific, since LV, but not kidney or plasma, ACE activity was affected by the additional dietary sodium restriction. Sodium 133-139 angiotensin I converting enzyme Homo sapiens 81-84 15136971-17 2004 Since the measured parameters did not indicate any adverse side-effects, dietary sodium restriction may provide a safe strategy to improve ACE-I efficacy in patients with infarction-induced LV dysfunction. Sodium 81-87 angiotensin I converting enzyme Homo sapiens 139-142 14645214-9 2004 Murr1 inhibited amiloride-sensitive sodium current in a dose-dependent manner. Sodium 36-42 copper metabolism domain containing 1 Homo sapiens 0-5 14718610-10 2004 With sodium restriction, the renal system is activated and counterbalances the increased sodium-retaining state induced by activation of the renin-angiotensin-aldosterone system. Sodium 5-11 renin Homo sapiens 141-146 14718610-10 2004 With sodium restriction, the renal system is activated and counterbalances the increased sodium-retaining state induced by activation of the renin-angiotensin-aldosterone system. Sodium 89-95 renin Homo sapiens 141-146 14984931-1 2004 Microsomal epoxide hydrolase (mEH) is a bifunctional protein that plays a crucial role in the metabolism of numerous xenobiotics as well as in mediating the hepatic sodium-dependent uptake of bile acids that are involved in numerous physiological processes including the regulation of cholesterol metabolism. Sodium 165-171 epoxide hydrolase 1, microsomal Mus musculus 30-33 14558883-1 2004 Treatment with PTH (parathyroid hormone) or a high-P(i) diet causes internalization of the type IIa sodium-dependent phosphate (Na/P(i) IIa) co-transporter from the apical membrane and its degradation in the lysosome. Sodium 100-106 parathyroid hormone Homo sapiens 15-18 14514522-2 2004 In this study, we tested whether tumor necrosis factor-alpha (TNF-alpha), a proinflammatory cytokine involved in several lung pathologies, could modulate sodium absorption in cultured alveolar epithelial cells. Sodium 154-160 tumor necrosis factor Homo sapiens 33-60 14514522-2 2004 In this study, we tested whether tumor necrosis factor-alpha (TNF-alpha), a proinflammatory cytokine involved in several lung pathologies, could modulate sodium absorption in cultured alveolar epithelial cells. Sodium 154-160 tumor necrosis factor Homo sapiens 62-71 14514522-7 2004 All these data show that TNF-alpha, a proinflammatory cytokine present during lung infection, has a profound influence on the capacity of alveolar epithelial cells to transport sodium. Sodium 177-183 tumor necrosis factor Homo sapiens 25-34 14558883-1 2004 Treatment with PTH (parathyroid hormone) or a high-P(i) diet causes internalization of the type IIa sodium-dependent phosphate (Na/P(i) IIa) co-transporter from the apical membrane and its degradation in the lysosome. Sodium 100-106 parathyroid hormone Homo sapiens 20-39 15168906-0 2004 Central AII evokes a normal sodium appetite in the Fischer rat, but its low spontaneous sodium intake may be related to reduced excitation and increased inhibition in septo-preoptic AII neurons. Sodium 28-34 angiotensinogen Rattus norvegicus 8-11 15168906-9 2004 The central AII system appears to be regulated differently in these two strains, and may be related to the differences in their spontaneous sodium intake, but not to AII aroused sodium appetite. Sodium 140-146 angiotensinogen Rattus norvegicus 12-15 14600156-4 2004 Inhibition of NHE-1 with pharmacological agents or by isotonic replacement of sodium in the perfusate with choline or tetramethylammonium greatly attenuated ERK activation by 5-HT or Ang II. Sodium 78-84 Eph receptor B1 Rattus norvegicus 157-160 15076186-8 2004 LVMI increased with higher sodium excretion in ACE II homozygous offspring of both Slavic and Italian extraction (+4.2 +/- 2.1 g/m2 per 100 mmol; P = 0.04) and in Slavic (+2.6 +/- 1.1 g/m2 per 100 mmol; P = 0.02), but not Italian (-3.3 +/- 3.2 g/m2 per 100 mmol; P = 0.29) D allele carriers. Sodium 27-33 angiotensin I converting enzyme Homo sapiens 47-50 12851823-4 2004 NTCP and ASBT are cotransporters that mediate sodium-dependent, electrogenic uptake of mainly bile salts into hepatocytes (NTCP), biliary epithelial cells, ileal enterocytes and renal proximal tubular cells (ASBT). Sodium 46-52 solute carrier family 10 member 1 Homo sapiens 0-4 12851823-4 2004 NTCP and ASBT are cotransporters that mediate sodium-dependent, electrogenic uptake of mainly bile salts into hepatocytes (NTCP), biliary epithelial cells, ileal enterocytes and renal proximal tubular cells (ASBT). Sodium 46-52 solute carrier family 10 member 1 Homo sapiens 123-127 14594797-2 2004 Here we present data indicating that, in the neuronal electrogenic sodium- and potassium-coupled glutamate transporter EAAC-1, the substrate-binding site and one of the gates, or a residue controlling the gating process, are in close physical proximity. Sodium 67-73 solute carrier family 1 member 1 Homo sapiens 119-125 14600156-4 2004 Inhibition of NHE-1 with pharmacological agents or by isotonic replacement of sodium in the perfusate with choline or tetramethylammonium greatly attenuated ERK activation by 5-HT or Ang II. Sodium 78-84 angiotensinogen Rattus norvegicus 183-189 14600156-7 2004 Receptor-independent activation of NHE-1 by acute acid loading of RASM cells resulted in the rapid phosphorylation of ERK, which could be blocked by pharmacological inhibitors of NHE-1 or by isotonic replacement of sodium, closely linking the proton transport function of NHE-1 to ERK activation. Sodium 215-221 Eph receptor B1 Rattus norvegicus 118-121 14600156-7 2004 Receptor-independent activation of NHE-1 by acute acid loading of RASM cells resulted in the rapid phosphorylation of ERK, which could be blocked by pharmacological inhibitors of NHE-1 or by isotonic replacement of sodium, closely linking the proton transport function of NHE-1 to ERK activation. Sodium 215-221 Eph receptor B1 Rattus norvegicus 281-284 14745661-2 2004 Approximately one third of these patients have elevated blood pressure due to increased sodium and water retention by the kidney resulting in suppressed plasma renin and aldosterone concentrations with high urinary potassium excretion and low plasma potassium levels. Sodium 88-94 renin Homo sapiens 160-165 14715935-6 2004 In med cells, the resurgent component of beta-PMTX-modified sodium currents could be selectively abolished by application of intracellular alkaline phosphatase, suggesting that, like in NaV1.6-expressing cells, the open-channel block of NaV1.1 and NaV1.2 subunits is regulated by constitutive phosphorylation. Sodium 60-66 sodium channel, voltage-gated, type I, alpha Mus musculus 237-243 14700507-6 2004 CONCLUSIONS: Increased AT1 receptor expression and angiotensin II-induced calcium increase are compensatory effects in sodium-induced hypertension. Sodium 119-125 angiotensinogen Rattus norvegicus 51-65 14974053-7 2004 MAIN RESULTS: In 57 trials of mainly Caucasians with normal blood pressure, low sodium intake reduced SBP by -1.27 mm Hg (CI: -1.76; -0.77)(p<0.0001) and DBP by -0.54 mm Hg (CI: -0.94; -0.14) (p = 0.009) as compared to high sodium intake. Sodium 80-86 D-box binding PAR bZIP transcription factor Homo sapiens 157-160 15366973-14 2004 Additionally, glitazones may potentiate the renal effects of insulin on sodium and water retention. Sodium 72-78 insulin Homo sapiens 61-68 14974053-8 2004 In 58 trials of mainly Caucasians with elevated blood pressure, low sodium intake reduced SBP by -4.18 mm Hg (CI: -5.08; - 3.27) (p < 0.0001) and DBP by -1.98 mm Hg (CI: -2.46; -1.32) (p < 0.0001) as compared to high sodium intake. Sodium 68-74 D-box binding PAR bZIP transcription factor Homo sapiens 149-152 14974053-11 2004 In 8 trials of blacks with normal or elevated blood pressure, low sodium intake reduced SBP by -6.44 mm Hg (CI: -9.13; -3.74) (p < 0.0001) and DBP by -1.98 mm Hg (CI: -4.75; 0.78) (p = 0.16) as compared to high sodium intake. Sodium 66-72 D-box binding PAR bZIP transcription factor Homo sapiens 146-149 14662412-2 2004 We have analyzed the expression of the sodium-dependent glucose co-transporters SGLT-1 and-2 in short-term cultures of squamous cell carcinomas of the head and neck (HNSCC) by RT-PCR. Sodium 39-45 solute carrier family 5 member 1 Homo sapiens 80-92 15055250-0 2004 Blunted response of the renin-angiotensin system and nitric oxide synthesis related to sodium sensitivity in immunoglobulin A nephropathy. Sodium 87-93 renin Homo sapiens 24-29 15055250-7 2004 Changes in plasma renin activity and serum aldosterone during sodium restriction were greater in the low-index group than in the high-index group. Sodium 62-68 renin Homo sapiens 18-23 15055250-9 2004 These results indicate that impairment of NO synthesis and a blunted response of the renin-angiotensin system are attributable to the altered sodium sensitivity of blood pressure in patients with immunoglobulin A nephropathy. Sodium 142-148 renin Homo sapiens 85-90 15055256-0 2004 High sodium intake strengthens the association between angiotensinogen T174M polymorphism and blood pressure levels among lean men and women: a community-based study. Sodium 5-11 angiotensinogen Homo sapiens 55-70 14675055-0 2004 Angiotensin II receptor blockade prevents acute renal sodium retention induced by low levels of orthostatic stress. Sodium 54-60 angiotensinogen Homo sapiens 0-14 14691350-6 2004 Renal COX-2 is regulated by for example sodium and volume intake, angiotensin II, glucocorticoids often involving specific COX-2 promotor response elements. Sodium 40-46 prostaglandin-endoperoxide synthase 2 Homo sapiens 6-11 14691350-6 2004 Renal COX-2 is regulated by for example sodium and volume intake, angiotensin II, glucocorticoids often involving specific COX-2 promotor response elements. Sodium 40-46 prostaglandin-endoperoxide synthase 2 Homo sapiens 123-128 14691350-7 2004 COX-2 derived prostanoids are required for preservation of renal blood flow and glomerular filtration especially in states of fluid deficit, they promote natriuresis, and furthermore may stimulate renin secretion during low-sodium intake/loop diuretic use. Sodium 224-230 prostaglandin-endoperoxide synthase 2 Homo sapiens 0-5 14691350-9 2004 In addition, COX-2 inhibitors cause sodium retention, edema formation, cardiac failure and hypertension. Sodium 36-42 prostaglandin-endoperoxide synthase 2 Homo sapiens 13-18 14618235-1 2004 AIM/HYPOTHESIS: Increased proximal renal sodium re-absorption is associated with central adiposity and insulin resistance in white men. Sodium 41-47 insulin Homo sapiens 103-110 15627797-0 2004 Effect of dietary sodium intake on the expression of endothelin-converting enzyme in the renal medulla. Sodium 18-24 endothelin converting enzyme 1 Rattus norvegicus 53-81 15627797-2 2004 Previous studies suggested that the ET-1 system is involved in the regulation of sodium excretion by the kidney. Sodium 81-87 endothelin 1 Rattus norvegicus 36-40 15627797-3 2004 In particular, ET-1 via the ET(B) receptor-mediated signaling has been shown to increase renal medullary blood flow and decrease sodium transport in the collecting duct, both acting to promote renal sodium excretion. Sodium 129-135 endothelin 1 Rattus norvegicus 15-19 15627797-3 2004 In particular, ET-1 via the ET(B) receptor-mediated signaling has been shown to increase renal medullary blood flow and decrease sodium transport in the collecting duct, both acting to promote renal sodium excretion. Sodium 199-205 endothelin 1 Rattus norvegicus 15-19 15627797-8 2004 CONCLUSION: The findings suggest that upregulation of ECE-1, leading to increased generation of ET-1 in the renal medulla, may be a compensatory mechanism promoting enhanced sodium excretion by the kidney in response to high salt intake. Sodium 174-180 endothelin converting enzyme 1 Rattus norvegicus 54-59 15627797-8 2004 CONCLUSION: The findings suggest that upregulation of ECE-1, leading to increased generation of ET-1 in the renal medulla, may be a compensatory mechanism promoting enhanced sodium excretion by the kidney in response to high salt intake. Sodium 174-180 endothelin 1 Rattus norvegicus 96-100 14581294-7 2003 The inverse correlation between angiotensin II and sodium excretion during stress approached significance (r=-0.17; P<0.06). Sodium 51-57 angiotensinogen Homo sapiens 32-46 15529607-10 2004 CONCLUSIONS: Octreotide in a short infusion treatment induces an inhibitory effect on renin aldosterone secretion which may be responsible for the benefical effects on sodium excretion. Sodium 168-174 renin Homo sapiens 86-91 15196885-3 2004 The first isoform to be characterized and cloned, NHE1, is present on the plasma membrane of cells and functions to remove one intracellular proton in exchange for one extracellular sodium ion. Sodium 182-188 solute carrier family 9 member A1 Homo sapiens 50-54 12928314-3 2003 The amiloride-sensitive sodium channel (ENaC) is expressed in the renal connecting tubule and collecting duct and is essential in renal regulation of body sodium balance and blood pressure. Sodium 24-30 sodium channel epithelial 1 subunit gamma Rattus norvegicus 40-44 12928314-4 2003 We hypothesized that dysregulation of ENaC subunits may be responsible for the increased sodium excretion associated with lithium treatment. Sodium 89-95 sodium channel epithelial 1 subunit gamma Rattus norvegicus 38-42 12928314-8 2003 In contrast, immunohistochemistry showed increased apical labeling of all ENaC subunits in the connecting tubule and inner medullary collecting duct in rats on a fixed sodium intake but not in rats with free access to sodium. Sodium 168-174 sodium channel epithelial 1 subunit gamma Rattus norvegicus 74-78 12928314-10 2003 These results identify a marked and highly segment-specific downregulation of beta-ENaC and gamma-ENaC in the cortical and outer medullary collecting duct, chief sites for collecting duct sodium reabsorption, in rats with a lithium-induced increase in fractional excretion of sodium. Sodium 188-194 sodium channel epithelial 1 subunit gamma Rattus norvegicus 92-102 12928314-10 2003 These results identify a marked and highly segment-specific downregulation of beta-ENaC and gamma-ENaC in the cortical and outer medullary collecting duct, chief sites for collecting duct sodium reabsorption, in rats with a lithium-induced increase in fractional excretion of sodium. Sodium 276-282 sodium channel epithelial 1 subunit gamma Rattus norvegicus 92-102 14656372-8 2003 Myocardial VIP concentration decreased with increasing dietary sodium (P < 0.025). Sodium 63-69 vasoactive intestinal peptide Rattus norvegicus 11-14 14597645-7 2003 Angiotensin II infusion reduced renal blood flow, glomerular filtration, sodium excretion, and NO levels in a dose-dependent manner. Sodium 73-79 angiotensinogen Homo sapiens 0-14 14871034-0 2003 Dopamine D2 receptor modulates sodium handling via local production of dopamine in the kidney. Sodium 31-37 dopamine receptor D2 Mus musculus 0-20 14871034-1 2003 We have recently demonstrated that a deletion of the dopamine D2 receptor gene caused suppression of urinary sodium excretion and salt-sensitive elevation of blood pressure in mice. Sodium 109-115 dopamine receptor D2 Mus musculus 53-73 14634667-2 2003 Two sodium-hydrogen exchangers (NHE1 and NHE5) are expressed in spermatozoa. Sodium 4-10 solute carrier family 9 member A1 Homo sapiens 32-36 12930837-7 2003 The inhibitory effect of TGF-beta1 on sodium uptake and alphaENaC expression in ATII cells was mediated by activation of the MAPK, ERK1/2. Sodium 38-44 transforming growth factor, beta 1 Rattus norvegicus 25-34 14568334-8 2003 The b.End3 cells actively accumulated D-glucose in a sodium-independent manner with characteristics consistant with that of GLUT-1. Sodium 53-59 Eph receptor A3 Mus musculus 6-10 12930837-9 2003 These data indicate that increased TGF-beta1 activity in the distal airspaces during ALI promotes alveolar edema by reducing distal airway epithelial sodium and fluid clearance. Sodium 150-156 transforming growth factor, beta 1 Rattus norvegicus 35-44 14569001-13 2003 These results demonstrate that, in nitric oxide-deficient rats fed a normal-sodium diet, ACE and vasopeptidase inhibitors exhibit a marked renoprotective effect, whereas these treatments are less efficient in rats fed a high-sodium diet. Sodium 76-82 angiotensin I converting enzyme Rattus norvegicus 89-92 12842853-5 2003 In addition, we assessed the capacity of an mTNF-alpha-derived peptide (mLtip), which activates sodium transport by a receptor-independent mechanism, to reduce lung water content in an isolated, ventilated, autologous blood-perfused rat lung model. Sodium 96-102 tumor necrosis factor Mus musculus 44-54 14569001-13 2003 These results demonstrate that, in nitric oxide-deficient rats fed a normal-sodium diet, ACE and vasopeptidase inhibitors exhibit a marked renoprotective effect, whereas these treatments are less efficient in rats fed a high-sodium diet. Sodium 225-231 angiotensin I converting enzyme Rattus norvegicus 89-92 12923212-10 2003 Sodium excretion fell during OE2 administration due to greater distal tubular sodium reabsorption. Sodium 0-6 EBF transcription factor 3 Homo sapiens 29-32 14563363-4 2003 Functional expression of recombinant AMIH in HEK293 cells gave unitary currents that were preferentially selective for potassium over sodium ions and were activated by hyperpolarizing voltage steps. Sodium 134-140 hyperpolarization-activated ion channel Apis mellifera 37-41 14576507-0 2003 High dietary sodium blunts affects of angiotensin-converting enzyme inhibition on vascular angiotensin I-to-angiotensin II conversion in rats. Sodium 13-19 angiotensinogen Rattus norvegicus 108-122 14576507-1 2003 High sodium intake blunts the efficacy of angiotensin (Ang)-converting enzyme (ACE) inhibition (ACEi), but the underlying mechanism is incompletely characterized. Sodium 5-11 angiotensin I converting enzyme Rattus norvegicus 79-82 14576507-2 2003 High sodium has been reported to increase vascular expression and vascular activity of ACE. Sodium 5-11 angiotensin I converting enzyme Rattus norvegicus 87-90 12923212-10 2003 Sodium excretion fell during OE2 administration due to greater distal tubular sodium reabsorption. Sodium 78-84 EBF transcription factor 3 Homo sapiens 29-32 14607044-7 2003 The patient responded well to nasal-spray-administered deamino D arginine vasopressin and increased intravenous fluid intake, with resolution of symptoms and gradual normalization of serum sodium levels. Sodium 189-195 arginine vasopressin Homo sapiens 74-85 14551679-10 2003 Patients with PAC/renin activity less than 2 had higher total volume of infused fluid, serum creatinine level, and fractional excretion of sodium values; aldosterone and serum creatinine were negatively correlated. Sodium 139-145 renin Homo sapiens 18-23 12824077-3 2003 However, by lowering transmural urea concentration gradients, UTB reduces water efflux from DVR through aquaporin-1 (AQP1) water channels, thereby decreasing plasma sodium concentration. Sodium 165-171 aquaporin 1 (Colton blood group) Homo sapiens 117-121 12923071-2 2003 Here we report for the first time that PPARgamma is expressed in human renal cortical collecting ducts (CCD), segments of the nephor involved in regulation of sodium and water homeostasis via action of the epithelial sodium channel (ENaC). Sodium 159-165 peroxisome proliferator activated receptor gamma Homo sapiens 39-48 12923071-6 2003 Our results identify SGK1 as a target for PPARgamma and suggest a novel role for PPARgamma in regulation of sodium re-absorption in the CCD via stimulation of ENaC activity. Sodium 108-114 peroxisome proliferator activated receptor gamma Homo sapiens 81-90 12923071-7 2003 This pathway may play a role in sodium retention caused by activation of PPARgamma in man. Sodium 32-38 peroxisome proliferator activated receptor gamma Homo sapiens 73-82 14508195-1 2003 BACKGROUND: The prevailing sodium intake and renin-angiotensin system status influence the blood pressure response to an angiotensin II type 1 (AT1) receptor antagonist or an angiotensin I converting enzyme inhibitor, which is known to be reinforced by a low sodium intake or administration of a diuretic. Sodium 259-265 renin Homo sapiens 45-50 14508196-10 2003 CONCLUSIONS: These data indicate that Ang II-infused rats develop increased renal interstitial fluid concentrations of Ang II, which may contribute to the increased vascular resistance and reduced sodium excretion. Sodium 197-203 angiotensinogen Rattus norvegicus 38-44 14508196-10 2003 CONCLUSIONS: These data indicate that Ang II-infused rats develop increased renal interstitial fluid concentrations of Ang II, which may contribute to the increased vascular resistance and reduced sodium excretion. Sodium 197-203 angiotensinogen Rattus norvegicus 119-125 14519796-9 2003 Reducing sodium from the high to the low level significantly decreased serum OC 0.6 microg/L in subjects that consumed the DASH diet, fasting serum PTH 2.66 ng/L in control subjects and urinary calcium 0.5 mmol/24 h in both groups. Sodium 9-15 bone gamma-carboxyglutamate protein Homo sapiens 77-79 14596364-1 2003 Angiotensin II, via activation of AT1 receptors in the kidney regulates sodium/fluid homeostasis and blood pressure. Sodium 72-78 angiotensinogen Rattus norvegicus 0-14 14596364-2 2003 An exaggerated action of angiotensin II mediated via activation of AT1 receptors has been implicated in the increased renal sodium retention and the resetting of the pressure natriuresis in obesity related hypertension. Sodium 124-130 angiotensinogen Rattus norvegicus 25-39 14519796-12 2003 A reduced sodium intake reduced calcium excretion in both diet groups and serum OC in the DASH group. Sodium 10-16 bone gamma-carboxyglutamate protein Homo sapiens 80-82 12927775-6 2003 This led to the discovery of aliskiren, a highly potent and selective inhibitor of human renin in vitro, and in vivo; once-daily oral doses of aliskiren inhibit renin and lower blood pressure in sodium-depleted marmosets and hypertensive human patients. Sodium 195-201 renin Homo sapiens 89-94 12925036-4 2003 It has been demonstrated that the activity of neutral endopeptidase (NEP) is increased in CHF, and that its inhibition enhances renal cGMP production and renal sodium excretion. Sodium 160-166 membrane metalloendopeptidase Homo sapiens 46-67 12887970-0 2003 Sodium-calcium exchange influences the response to endothelin-1 in lens epithelium. Sodium 0-6 endothelin 1 Homo sapiens 51-63 12887970-9 2003 The half-time for decay of the ET-1 and ATP calcium peak was increased several folds by bepridil, ouabain and low-sodium conditions. Sodium 114-120 endothelin 1 Homo sapiens 31-35 12887970-11 2003 Taken together findings suggest inhibition of sodium-calcium exchange increases the magnitude of the receptor-initiated store-release phase of the ET-1 calcium signaling response as the result of impaired calcium clearance from the cytoplasm. Sodium 46-52 endothelin 1 Homo sapiens 147-151 12925036-4 2003 It has been demonstrated that the activity of neutral endopeptidase (NEP) is increased in CHF, and that its inhibition enhances renal cGMP production and renal sodium excretion. Sodium 160-166 membrane metalloendopeptidase Homo sapiens 69-72 12925036-7 2003 Sodium-retaining systems likely contribute to renal hyporesponsiveness to ANP through different mechanisms. Sodium 0-6 natriuretic peptide A Homo sapiens 74-77 12925036-11 2003 New treatments designed to restore renal ANP efficiency should limit sodium retention in CHF patients and thus delay the progression to overt heart failure. Sodium 69-75 natriuretic peptide A Homo sapiens 41-44 12970284-10 2003 Changes in circulating cortisol might contribute to individual sodium-induced alterations in insulin sensitivity. Sodium 63-69 insulin Homo sapiens 93-100 14526263-9 2003 Because sodium is a very efficient stimulus for VP secretion, it may be assumed that the fall in P(Na) occurring during AA infusion should have reduced VP secretion and thus P(VP). Sodium 8-14 arginine vasopressin Homo sapiens 48-50 14526263-9 2003 Because sodium is a very efficient stimulus for VP secretion, it may be assumed that the fall in P(Na) occurring during AA infusion should have reduced VP secretion and thus P(VP). Sodium 8-14 arginine vasopressin Homo sapiens 152-154 14563190-3 2003 Albumin is the ideal plasma expander in this setting, since it ameliorates systemic and reneal haemodynamics, so reducing sodium retention, and increases oncotic pressure in the splanchnic compartment. Sodium 122-128 albumin Homo sapiens 0-7 12856080-6 2003 RESULTS: During low sodium, DD-homozygotes showed higher blood pressure sensitivity to angiotensin I ( DD 21+/-5% vs II 15+/-5%, p<0.01). Sodium 20-26 angiotensinogen Homo sapiens 87-100 12742089-3 2003 It was demonstrated that, as in several other transporters, sodium binding and release by GAT1, GAT3 and BGT-1, the canine homolog of GAT2, resulted in the appearance of presteady-state currents. Sodium 60-66 solute carrier family 6 member 12 Canis lupus familiaris 105-110 12754175-7 2003 We speculate whether a high CYP3A5 expressor allele frequency among African-Americans may contribute to a high prevalence of sodium-sensitive hypertension in this population. Sodium 125-131 cytochrome P450 family 3 subfamily A member 5 Homo sapiens 28-34 12691602-0 2003 Decreased insulin sensitivity during dietary sodium restriction is not mediated by effects of angiotensin II on insulin action. Sodium 45-51 insulin Homo sapiens 10-17 12691602-1 2003 We have previously reported that modest dietary sodium restriction, as advocated in management guidelines for diabetes, may reduce insulin sensitivity. Sodium 48-54 insulin Homo sapiens 131-138 12691602-5 2003 Insulin sensitivity (M) was reduced during dietary sodium restriction [median M value, 10.2 mg/kg per min (interquartile range 9.50-13.85) versus 12.8 mg/kg per min (interquartile range 9.60-14.30), P <0.05]. Sodium 51-57 insulin Homo sapiens 0-7 12691602-8 2003 In conclusion, despite the observation that dietary sodium restriction was associated with a median 15% reduction in insulin sensitivity, we found no evidence of a direct effect of AII on insulin action in human adipocytes. Sodium 52-58 insulin Homo sapiens 117-124 12754202-1 2003 The sodium-calcium exchanger, NCX1, is a ubiquitously expressed membrane protein essential in calcium homeostasis for many cells including those in mammalian heart and brain. Sodium 4-10 solute carrier family 8 member A1 Homo sapiens 30-34 12872049-2 2003 DESIGN: Different dietary sodium intakes were used to physiologically alter endogenous angiotensin II activity. Sodium 26-32 angiotensinogen Rattus norvegicus 87-101 12872049-11 2003 CONCLUSIONS: Increased endogenous angiotensin II in rats on a low dietary sodium intake attenuates the renal sympathoinhibitory response to activation of the cardiac and sinoaortic baroreflexes by standardized vagus and aortic depressor nerve stimulation, respectively. Sodium 74-80 angiotensinogen Rattus norvegicus 34-48 12953027-10 2003 The ratio between the total sodium concentration in the ultrafiltrate (NaF(uf)) and NaF(pw) (alpha) at the post-reinfusion site was 0.96 and decreased to 0.94 when NaF(pw) values at the pre-reinfusion site were considered. Sodium 28-34 C-X-C motif chemokine ligand 8 Homo sapiens 71-74 12953027-10 2003 The ratio between the total sodium concentration in the ultrafiltrate (NaF(uf)) and NaF(pw) (alpha) at the post-reinfusion site was 0.96 and decreased to 0.94 when NaF(pw) values at the pre-reinfusion site were considered. Sodium 28-34 C-X-C motif chemokine ligand 8 Homo sapiens 84-87 12953027-10 2003 The ratio between the total sodium concentration in the ultrafiltrate (NaF(uf)) and NaF(pw) (alpha) at the post-reinfusion site was 0.96 and decreased to 0.94 when NaF(pw) values at the pre-reinfusion site were considered. Sodium 28-34 C-X-C motif chemokine ligand 8 Homo sapiens 84-87 12878321-6 2003 These studies demonstrate that the expression of mEH is greatly reduced in a patient with hypercholanemia, suggesting that mEH participates in sodium-dependent bile acid uptake in human liver where its absence may contribute to the etiology of this disease. Sodium 143-149 epoxide hydrolase 1, microsomal Mus musculus 123-126 12924618-4 2003 The angiotensinogen gene (AGT) is a thrifty gene which increases the risk for common disease with growth of civilization via sodium and body fluid retention. Sodium 125-131 angiotensinogen Homo sapiens 4-19 12878321-1 2003 Microsomal epoxide hydrolase (mEH) is a bifunctional protein that plays a central role in carcinogen metabolism and is also able to mediate the sodium-dependent uptake of bile acids into hepatocytes. Sodium 144-150 epoxide hydrolase 1, microsomal Mus musculus 30-33 12878321-6 2003 These studies demonstrate that the expression of mEH is greatly reduced in a patient with hypercholanemia, suggesting that mEH participates in sodium-dependent bile acid uptake in human liver where its absence may contribute to the etiology of this disease. Sodium 143-149 epoxide hydrolase 1, microsomal Mus musculus 49-52 12801964-8 2003 There was a significant reduction in ANG II and PRA (p<0.05 for each) and the change in ammonia excretion correlated directly with the change in urinary sodium excretion (p<0.007), ANG II (p<0.002), and PRA (p<0.01). Sodium 156-162 angiotensinogen Homo sapiens 187-193 12924618-4 2003 The angiotensinogen gene (AGT) is a thrifty gene which increases the risk for common disease with growth of civilization via sodium and body fluid retention. Sodium 125-131 angiotensinogen Homo sapiens 26-29 12924618-6 2003 On the other hand, the Gly460Trp genotype of the alpha-adducin gene (ADD1) is associated with erythrocyte sodium transport and increases tubular sodium reabsorption and risk for hypertension. Sodium 106-112 adducin 1 Homo sapiens 69-73 12924618-6 2003 On the other hand, the Gly460Trp genotype of the alpha-adducin gene (ADD1) is associated with erythrocyte sodium transport and increases tubular sodium reabsorption and risk for hypertension. Sodium 145-151 adducin 1 Homo sapiens 69-73 12810195-4 2003 In addition, genetic studies have identified gain-of-function mutations in the CASR gene, leading to a greater understanding of the pathogenesis of Bartter"s syndrome, an inherited nephropathy that results in deficiency of sodium and chloride absorption. Sodium 223-229 calcium sensing receptor Homo sapiens 79-83 12877077-3 2003 Insulin resistance often accompanied hyperinsulinemia and it is thought to elevate blood pressure through stimulation of the sympathetic nervous system and renin-angiotensin system, promotion of sodium retention in the renal tubules, and proliferation of vascular smooth muscle cells via insulin-like growth factor. Sodium 195-201 insulin Homo sapiens 0-7 12881590-2 2003 In peripheral epithelial tissues, sodium and water transport is regulated by corticosteroids and the 11beta-hydroxysteroid dehydrogenase (11beta-HSD) isozymes (11beta-HSD1 activating cortisol from cortisone, 11beta-HSD2 inactivating cortisol to cortisone). Sodium 34-40 hydroxysteroid 11-beta dehydrogenase 1 Homo sapiens 160-171 12804783-3 2003 Here we show that a hybrid protein composed of the Sod2 antiporter fused to the carboxy-terminal half of Nha1 strongly increased sodium tolerance, but did not allow growth at high potassium nor did rescue growth of the sit4 hal3 conditional mutant strain. Sodium 129-135 Nha1p Saccharomyces cerevisiae S288C 105-109 14586732-7 2003 RESULTS: This new equation, unlike all previous qualitative and quantitative approaches, can account mathematically for the simultaneous effects of TBW, Na(e), K(e), EMB, VMB, and the plasma glucose on the plasma water sodium concentration. Sodium 219-225 embigin Homo sapiens 166-169 12746271-2 2003 Indeed, some of the properties of the physiologically active component of the RAS, angiotensin II, include vasoconstriction, regulation of renal sodium and water absorption, and increasing thirst. Sodium 145-151 angiotensinogen Homo sapiens 83-97 12595301-0 2003 Sodium restriction prevents cardiac hypertrophy and oxidative stress in angiotensin II hypertension. Sodium 0-6 angiotensinogen Rattus norvegicus 72-86 12676175-6 2003 Centrally administered AT(1) receptor antagonists or angiotensinogen antisense oligonucleotides inhibit sympathetic activity and reduce arterial blood pressure in certain physiological or pathophysiological conditions, as well as disrupting water drinking and sodium appetite, vasopressin secretion, sodium excretion, renin release and thermoregulation. Sodium 260-266 angiotensinogen Homo sapiens 53-68 12676175-6 2003 Centrally administered AT(1) receptor antagonists or angiotensinogen antisense oligonucleotides inhibit sympathetic activity and reduce arterial blood pressure in certain physiological or pathophysiological conditions, as well as disrupting water drinking and sodium appetite, vasopressin secretion, sodium excretion, renin release and thermoregulation. Sodium 300-306 angiotensinogen Homo sapiens 53-68 12929469-6 2003 For example, the compensatory increase in renin secretion induced by sodium depletion may become the predominant factor sustaining high blood pressure. Sodium 69-75 renin Homo sapiens 42-47 12929469-7 2003 Simultaneous blockade of the renin-angiotensin system, with either an ACE inhibitor or an AT1 receptor blocker, makes this compensatory hyper-reninaemia ineffective and allows maximum benefit from sodium depletion. Sodium 197-203 renin Homo sapiens 29-34 12929469-7 2003 Simultaneous blockade of the renin-angiotensin system, with either an ACE inhibitor or an AT1 receptor blocker, makes this compensatory hyper-reninaemia ineffective and allows maximum benefit from sodium depletion. Sodium 197-203 angiotensin I converting enzyme Homo sapiens 70-73 12745204-0 2003 Relevance of the plasma renin hormonal control system that regulates blood pressure and sodium balance for correctly treating hypertension and for evaluating ALLHAT. Sodium 88-94 renin Homo sapiens 24-29 12943727-2 2003 Aldosterone acts via the mineralocorticoid receptor (MR) to induce the expression of genes whose products are involved in sodium transport. Sodium 122-128 nuclear receptor subfamily 3, group C, member 2 Rattus norvegicus 25-51 12943727-2 2003 Aldosterone acts via the mineralocorticoid receptor (MR) to induce the expression of genes whose products are involved in sodium transport. Sodium 122-128 nuclear receptor subfamily 3, group C, member 2 Rattus norvegicus 53-55 12595301-7 2003 Although the final TCP was similar in LS and normal sodium (NS) rats infused with high and low doses of angiotensin II, respectively, the increase in HWI was prevented by the LS diet. Sodium 52-58 angiotensinogen Rattus norvegicus 104-118 12595301-11 2003 The beneficial influence of dietary sodium restriction on target organ damage induced by angiotensin II is independent of arterial pressure reduction and possibly related to attenuation of the prooxidant effect of the peptide. Sodium 36-42 angiotensinogen Rattus norvegicus 89-103 12654713-5 2003 In combination with other genetic or environmental factors (such as dietary sodium intake), we suggest that this might be responsible for the long-term development of a resetting of the aldosterone response to angiotensin II, giving rise to the phenotype of hypertension with a raised ratio. Sodium 76-82 angiotensinogen Homo sapiens 210-224 15030296-6 2003 For example, the compensatory rise in renin secretion induced by sodium depletion may become the predominant factor sustaining high blood pressure. Sodium 65-71 renin Homo sapiens 38-43 15030296-7 2003 Simultaneous blockade of the renin-angiotensin system, with either an ACE inhibitor or an AT1-receptor blocker, makes this compensatory hyper-reninemia ineffective and allows maximum benefit from sodium depletion. Sodium 196-202 renin Homo sapiens 29-34 15030296-7 2003 Simultaneous blockade of the renin-angiotensin system, with either an ACE inhibitor or an AT1-receptor blocker, makes this compensatory hyper-reninemia ineffective and allows maximum benefit from sodium depletion. Sodium 196-202 angiotensin I converting enzyme Homo sapiens 70-73 12648160-2 2003 Cyclooxygenase-2-derived metabolites play a very important role in regulating renal haemodynamics when sodium intake is low whereas it plays a minor role in the control of cortical blood flow when sodium intake is normal or elevated. Sodium 103-109 prostaglandin-endoperoxide synthase 2 Homo sapiens 0-16 12887132-1 2003 Angiotensin II plays important roles in renal vasoconstriction, sodium reabsorption in proximal tubules, and cell proliferation. Sodium 64-70 angiotensinogen Homo sapiens 0-14 12695530-1 2003 We examined the effects on allosteric modulation and ligand binding of the mutation of amino acid residues of the human A(3) adenosine receptor (A(3)AR) that are hypothesized to be near one of three loci: the putative sodium binding site, the putative ligand binding site, and the DRY motif in transmembrane helical domain 3. Sodium 218-224 adenosine A3 receptor Homo sapiens 145-151 12648160-2 2003 Cyclooxygenase-2-derived metabolites play a very important role in regulating renal haemodynamics when sodium intake is low whereas it plays a minor role in the control of cortical blood flow when sodium intake is normal or elevated. Sodium 197-203 prostaglandin-endoperoxide synthase 2 Homo sapiens 0-16 12653683-3 2003 The rate-limiting constituent of collecting duct sodium transport is the epithelial sodium channel (ENaC). Sodium 49-55 sodium channel epithelial 1 subunit gamma Rattus norvegicus 100-104 12591117-10 2003 Salt loading produced a specific increase in AT1a mRNA in osmosensitive regions, suggesting that this receptor subtype is regulated by sodium/osmolar input. Sodium 135-141 angiotensin II receptor, type 1a Mus musculus 45-49 12733703-11 2003 Moreover, administration of high sodium load to WFR augmented the expression of TGF-beta1. Sodium 33-39 transforming growth factor, beta 1 Rattus norvegicus 80-89 12727445-4 2003 Using whole-cell and outside-out patch-clamp techniques, we observed that IL-1 beta decreased both inward sodium current amplitudes and outward potassium current amplitudes. Sodium 106-112 interleukin 1 beta Homo sapiens 74-83 12679012-0 2003 Mechanism of thrombin"s enigmatic sodium switch revealed. Sodium 34-40 coagulation factor II, thrombin Homo sapiens 13-21 12642013-1 2003 Elevations in intrarenal angiotensin II (Ang II) cause reductions in renal function and sodium excretion that contribute to progressive hypertension and lead to renal and vascular injury. Sodium 88-94 angiotensinogen Homo sapiens 25-39 12642013-1 2003 Elevations in intrarenal angiotensin II (Ang II) cause reductions in renal function and sodium excretion that contribute to progressive hypertension and lead to renal and vascular injury. Sodium 88-94 angiotensinogen Homo sapiens 41-47 12642013-6 2003 The increased urinary AGT indicates spillover of AGT into distal nephron segments supporting enhanced distal Ang II formation and sodium reabsorption. Sodium 130-136 angiotensinogen Homo sapiens 22-25 12642013-6 2003 The increased urinary AGT indicates spillover of AGT into distal nephron segments supporting enhanced distal Ang II formation and sodium reabsorption. Sodium 130-136 angiotensinogen Homo sapiens 49-52 12642013-7 2003 The augmentation of intrarenal Ang II provides the basis for sustained actions on renal function, sodium excretion, and maintenance of hypertension. Sodium 98-104 angiotensinogen Homo sapiens 31-37 12642017-2 2003 Angiotensin II (Ang II) has stimulatory effects on sodium transport in multiple nephron segments via binding to plasma membrane AT(1) receptors. Sodium 51-57 angiotensinogen Homo sapiens 0-14 12642017-2 2003 Angiotensin II (Ang II) has stimulatory effects on sodium transport in multiple nephron segments via binding to plasma membrane AT(1) receptors. Sodium 51-57 angiotensinogen Homo sapiens 16-22 12642017-4 2003 The stimulatory effect of Ang II on proximal sodium transport is enhanced by renal nerves, and is associated with internalization of apical and basolateral receptors. Sodium 45-51 angiotensinogen Homo sapiens 26-32 12623987-1 2003 Dopamine and angiotensin II negatively interact to regulate sodium excretion and blood pressure. Sodium 60-66 angiotensinogen Rattus norvegicus 13-27 12608998-8 2003 CONCLUSION: Physiological changes in the activity of the RAS produced by alterations in dietary sodium intake regulate the contribution of endogenous angII of brain origin in the modulation of arterial baroreflex regulation of renal SNA. Sodium 96-102 angiotensinogen Rattus norvegicus 150-155 12737373-2 2003 In pre-ascites, the renal sodium retaining tendency leads to "overfilling" of total blood volume, with increased glomerular filtration rates (GFR), overcoming the renal sodium retaining tendency possibly due to renal accumulation of angiotensin II. Sodium 26-32 angiotensinogen Homo sapiens 233-247 12623964-10 2003 The results suggest that DS on HS have an inappropriate augmentation of intrarenal angiotensinogen, which may contribute to impaired sodium excretion during a high salt diet and the development of hypertension in this strain. Sodium 133-139 angiotensinogen Rattus norvegicus 83-98 12569273-0 2003 Reduced activity of the kallikrein-kinin system predominates over renin-angiotensin system overactivity in all conditions of sodium balance in essential hypertensives and family-related hypertension. Sodium 125-131 renin Homo sapiens 66-71 12399257-0 2003 Increased dietary sodium alters neural control of blood pressure during intravenous ANG II infusion. Sodium 18-24 angiotensinogen Rattus norvegicus 84-90 12399257-6 2003 These data suggest that in normal rats increased dietary sodium enhances sympathoinhibitory responses during intravenous ANG II. Sodium 57-63 angiotensinogen Rattus norvegicus 121-127 12589181-5 2003 Obesity increases renal sodium reabsorption by activating the renin-angiotensin and sympathetic nervous systems, and by altering intrarenal physical forces. Sodium 24-30 renin Homo sapiens 62-67 12530941-3 2003 COX-2 metabolites have been implicated in mediation of renin release, regulation of sodium excretion, and maintenance of renal blood flow. Sodium 84-90 mitochondrially encoded cytochrome c oxidase II Homo sapiens 0-5 12535156-6 2003 The enhancement of plasma vasopressin responses was independent of plasma sodium concentrations or changes in blood pressure. Sodium 74-80 arginine vasopressin Rattus norvegicus 26-37 12507762-11 2003 The moderate decline in expression of Oatp1, -2 and -4 may explain the unchanged sodium-independent transport of bile acids due to overlapping substrate specificity. Sodium 81-87 solute carrier organic anion transporter family, member 1a1 Rattus norvegicus 38-54 12527745-12 2003 The immediate renal response to sodium excess appears to be fading of ANGII-mediated tubular sodium reabsorption. Sodium 32-38 angiotensinogen Homo sapiens 70-75 12507762-2 2003 Impaired sodium-dependent uptake of bile acids has been associated with diminished expression of a basolateral Na(+)/bile acid cotransporter (Ntcp), whereas sodium-independent uptake is maintained despite a down-regulation of the organic anion transporter Oatp1. Sodium 9-15 solute carrier organic anion transporter family, member 1a1 Rattus norvegicus 256-261 12492779-1 2003 AIM: During heart failure (HF), excess sodium retention is triggered by increased plasma renin-angiotensin-aldosterone activity and increased basal sympathetic nerve discharge (SND). Sodium 39-45 renin Homo sapiens 89-94 12487621-14 2003 However, trials with the new COX-2 inhibitors offer the chance to address these open questions of highly selective COX-2 inhibition; that is, thrombogenic risk, sodium and water retention, and interference with tissue repair, in particular, healing of mucosal damage. Sodium 161-167 mitochondrially encoded cytochrome c oxidase II Homo sapiens 29-34 14713115-10 2003 Renal vasculature and nephron segment heterogeneity in sodium reabsorption likely provides the anatomical construct to generate the marginal tissue oxygen pressure required to trigger the production of erythropoietin. Sodium 55-61 erythropoietin Homo sapiens 202-216 14713115-13 2003 Factors that affect blood supply and sodium reabsorption in a discordant manner may modulate the critmeter, e.g. angiotensin II. Sodium 37-43 angiotensinogen Homo sapiens 113-127 12820491-4 2003 Moreover, the hypertensive effect of insulin is caused by sympathetic stimulation, sodium and water renal retention and protooncogene stimulation leading to myocardial and vascular fibrosis and hypertrophy. Sodium 83-89 insulin Homo sapiens 37-44 12500203-0 2003 A vasopressin receptor antagonist (VPA-985) improves serum sodium concentration in patients with hyponatremia: a multicenter, randomized, placebo-controlled trial. Sodium 59-65 arginine vasopressin Homo sapiens 2-13 12535503-7 2003 MAIN RESULTS: In 57 trials of mainly Caucasians with normal blood pressure, low sodium intake reduced SBP by -1.27 mm Hg (CI: -1.76; -0.77)(p<0.0001) and DBP by -0.54 mm Hg (CI: -0.94; -0.14) (p = 0.009) as compared to high sodium intake. Sodium 80-86 D-box binding PAR bZIP transcription factor Homo sapiens 157-160 12535503-8 2003 In 58 trials of mainly Caucasians with elevated blood pressure, low sodium intake reduced SBP by -4.18 mm Hg (CI: -5.08; - 3.27) (p < 0.0001) and DBP by -1.98 mm Hg (CI: -2.46; -1.32) (p < 0.0001) as compared to high sodium intake. Sodium 68-74 D-box binding PAR bZIP transcription factor Homo sapiens 149-152 12535503-11 2003 In 8 trials of blacks with normal or elevated blood pressure, low sodium intake reduced SBP by -6.44 mm Hg (CI: -9.13; -3.74) (p < 0.0001) and DBP by -1.98 mm Hg (CI: -4.75; 0.78) (p = 0.16) as compared to high sodium intake. Sodium 66-72 D-box binding PAR bZIP transcription factor Homo sapiens 146-149 12486163-1 2002 Generalized epilepsy with febrile seizures plus type 1 is an inherited human epileptic syndrome, associated with a cysteine-to-tryptophan (C121W) mutation in the extracellular immunoglobin domain of the auxiliary beta1 subunit of the voltage-gated sodium channel. Sodium 248-254 BCL2 related protein A1 Homo sapiens 213-218 12506133-9 2003 The results indicate an important role for prostasin in sodium reabsorption in the kidney under pathophysiologic conditions. Sodium 56-62 serine protease 8 Rattus norvegicus 43-52 12972712-3 2003 METHODS: We investigated the role played by the ET-1 system in sodium and water retention and in proteinuria in puromycin aminonucleoside induced nephrotic syndrome in rats using microdissected nephron segments, competitive polymerase chain reaction, and Western blot. Sodium 63-69 endothelin 1 Rattus norvegicus 48-52 12972712-10 2003 CONCLUSION: These data suggest that an activated ET-1-ET A receptor pathway in glomeruli and/or an increased ECE-1 mRNA expression in distal segments may participate in sodium and water retention, but not in the occurrence of nephrotic syndrome. Sodium 169-175 endothelin 1 Rattus norvegicus 49-53 12972712-10 2003 CONCLUSION: These data suggest that an activated ET-1-ET A receptor pathway in glomeruli and/or an increased ECE-1 mRNA expression in distal segments may participate in sodium and water retention, but not in the occurrence of nephrotic syndrome. Sodium 169-175 endothelin converting enzyme 1 Rattus norvegicus 109-114 12573139-1 2002 Angiotensin II has been shown to participate in both physiological processes, such as sodium and water homeostasis and vascular contraction, and pathophysiological processes, including atherosclerosis and hypertension. Sodium 86-92 angiotensinogen Homo sapiens 0-14 12401375-6 2002 It was expected that the sodium ion would act on the herbicide-HSA association process by modifying the surface tension of the bulk solvent and increase the K and n(c) values. Sodium 25-31 albumin Homo sapiens 63-66 12419174-4 2002 Moreover, sodium depletion has multiple other effects including activation of the renin-angiotensin system and the sympathetic nervous system, and increase in insulin resistance. Sodium 10-16 renin Homo sapiens 82-87 12419174-4 2002 Moreover, sodium depletion has multiple other effects including activation of the renin-angiotensin system and the sympathetic nervous system, and increase in insulin resistance. Sodium 10-16 insulin Homo sapiens 159-166 12444201-7 2002 The data suggest that KCNA10 may facilitate proximal tubular sodium absorption by stabilizing cell membrane voltage. Sodium 61-67 potassium voltage-gated channel subfamily A member 10 Rattus norvegicus 22-28 16352114-14 2003 Positive sodium balance and ensuing volume expansion may be due to increased renal tubular sodium reabsorption induced by sympathetic stimulation, insulin or by a hyperactive renin-angiotensin system. Sodium 9-15 insulin Homo sapiens 147-154 16352114-14 2003 Positive sodium balance and ensuing volume expansion may be due to increased renal tubular sodium reabsorption induced by sympathetic stimulation, insulin or by a hyperactive renin-angiotensin system. Sodium 91-97 insulin Homo sapiens 147-154 12429407-1 2002 Circumventricular organs such as the subfornical organ (SFO) may mediate the effects of circulating angiotensin (ANG) II on salt appetite under conditions of sodium depletion in the rat. Sodium 158-164 angiotensinogen Rattus norvegicus 100-120 12372775-2 2002 RA, ANG I, and ANG II levels increased in a manner inversely related to sodium content of the diet in both plasma and renal tissues. Sodium 72-78 angiotensinogen Rattus norvegicus 15-21 12502529-1 2002 The Na(+)/Ca(2+) exchanger (NCX1) catalyzes the counter-transport of sodium and calcium ions. Sodium 69-75 solute carrier family 8 member A1 Homo sapiens 4-26 12502529-1 2002 The Na(+)/Ca(2+) exchanger (NCX1) catalyzes the counter-transport of sodium and calcium ions. Sodium 69-75 solute carrier family 8 member A1 Homo sapiens 28-32 12372776-9 2002 Such elevated intrarenal ANG II levels could contribute to maintain sodium and fluid balance and arterial blood pressure during salt-deficiency states. Sodium 68-74 angiotensinogen Rattus norvegicus 25-31 12411460-5 2002 Adrenomedullin also significantly enhanced urinary sodium excretion (day 4, 3-fold; P<0.05), creatinine excretion (1.2-fold; P<0.001), and creatinine clearance (1.4-fold; P<0.001) over the 4 days of treatment, whereas urine volume and cAMP excretion tended to be elevated (both, 0.1>P>0.05). Sodium 51-57 pro-adrenomedullin Ovis aries 0-14 12390519-6 2002 This increase, which was directly correlated with the level of GS expression, was dependent on the presence of external sodium ions, and could be completely abolished by methionine sulfoximine, a specific inhibitor of GS activity. Sodium 120-126 glutamate-ammonia ligase Homo sapiens 63-65 12491807-2 2002 The molecular cloning of these transporters revealed that NET, DAT, and SERT are members of a sodium-dependent neurotransmitter transporter gene family, while VMATs arise from proton-dependent transporter gene family. Sodium 94-100 solute carrier family 6 member 4 Homo sapiens 72-76 12392842-11 2002 Urocortin produced dose-dependent, sustained increases in urine volume (twofold, p < 0.01), sodium excretion (>9-fold rise, p < 0.001), and creatinine clearance (p < 0.001) in HF sheep. Sodium 95-101 urocortin Ovis aries 0-9 12225981-0 2002 Amiloride-sensitive sodium current in everted Ambystoma initial collecting tubule: short-term insulin effects. Sodium 20-26 insulin Homo sapiens 94-101 12379580-0 2002 Thrombin facilitation of voltage-gated sodium channel activation in human cardiomyocytes: implications for ischemic sodium loading. Sodium 39-45 coagulation factor II, thrombin Homo sapiens 0-8 12379580-10 2002 CONCLUSIONS: Facilitation of VGSC activation causing large increases in window current is a major mechanism by which thrombin may promote ischemic sodium loading and injury. Sodium 147-153 coagulation factor II, thrombin Homo sapiens 117-125 12225981-2 2002 Accessibility to both the apical and basolateral membranes made this preparation ideal for studying the regulation of sodium transport by insulin. Sodium 118-124 insulin Homo sapiens 138-145 12225981-11 2002 Thus application of insulin enhanced sodium reabsorption by increasing the fraction of time the channel spent in the open state. Sodium 37-43 insulin Homo sapiens 20-27 12239234-8 2002 The simultaneous inhibition of ACE and NEP may be more effective in reducing BP than the inhibition of ACE alone and less dependent on sodium balance. Sodium 135-141 angiotensin I converting enzyme Homo sapiens 31-34 12239234-8 2002 The simultaneous inhibition of ACE and NEP may be more effective in reducing BP than the inhibition of ACE alone and less dependent on sodium balance. Sodium 135-141 membrane metalloendopeptidase Homo sapiens 39-42 12389882-4 2002 However, COX-2 is also constitutively expressed in the human kidney Clinical studies have reported a significant decrease in glomerular filtration rate in young and elderly sodium-depleted volunteers given COX-2 inhibitors. Sodium 173-179 mitochondrially encoded cytochrome c oxidase II Homo sapiens 9-14 12413503-0 2002 Serum to urinary sodium concentration ratio is an estimate of plasma renin activity in congestive heart failure. Sodium 17-23 renin Homo sapiens 69-74 12230479-22 2002 The metabolism of absorbed icodextrin and the resultant rise in plasma levels of small glucose polymers (DP2 to DP4) do not result in hyperglycemia or hyperinsulinemia, but may result in a small decrease in serum sodium and chloride. Sodium 213-219 transcription factor Dp family member 3 Homo sapiens 112-115 12389882-4 2002 However, COX-2 is also constitutively expressed in the human kidney Clinical studies have reported a significant decrease in glomerular filtration rate in young and elderly sodium-depleted volunteers given COX-2 inhibitors. Sodium 173-179 mitochondrially encoded cytochrome c oxidase II Homo sapiens 206-211 12167595-1 2002 The present study was performed to investigate the role of type 1A ANG II (AT(1A)) receptors in regulating sodium balance and blood pressure maintenance during chronic dietary sodium variations in AT(1A) receptor-deficient (-/-) mice. Sodium 107-113 angiotensin II receptor, type 1a Mus musculus 75-80 12231389-3 2002 Big endothelin-1 markedly increased urine flow, urinary excretion of sodium and fractional excretion of sodium in wild-type rats treated with the vehicle. Sodium 69-75 endothelin 1 Rattus norvegicus 4-16 12231389-3 2002 Big endothelin-1 markedly increased urine flow, urinary excretion of sodium and fractional excretion of sodium in wild-type rats treated with the vehicle. Sodium 104-110 endothelin 1 Rattus norvegicus 4-16 12167595-0 2002 Effects of AT(1A) receptor deletion on blood pressure and sodium excretion during altered dietary salt intake. Sodium 58-64 angiotensin II receptor, type 1a Mus musculus 11-16 12082097-3 2002 The endothelial and inducible nitric-oxide synthase (eNOS and iNOS respectively) genes are also expressed in this nephron segment and are thought to play a role in regulating urinary sodium concentration. Sodium 183-189 nitric oxide synthase 2 Homo sapiens 62-66 12167595-7 2002 These studies demonstrate that mice lacking the AT(1A) receptor have blood pressures sensitive to changes in dietary sodium, marked alterations of the pressure-natriuresis relationship, and compensatory mechanisms capable of maintaining normal sodium balance across a wide range of sodium intakes. Sodium 117-123 angiotensin II receptor, type 1a Mus musculus 48-53 12167595-7 2002 These studies demonstrate that mice lacking the AT(1A) receptor have blood pressures sensitive to changes in dietary sodium, marked alterations of the pressure-natriuresis relationship, and compensatory mechanisms capable of maintaining normal sodium balance across a wide range of sodium intakes. Sodium 244-250 angiotensin II receptor, type 1a Mus musculus 48-53 12167595-7 2002 These studies demonstrate that mice lacking the AT(1A) receptor have blood pressures sensitive to changes in dietary sodium, marked alterations of the pressure-natriuresis relationship, and compensatory mechanisms capable of maintaining normal sodium balance across a wide range of sodium intakes. Sodium 244-250 angiotensin II receptor, type 1a Mus musculus 48-53 12219182-3 2002 High sodium intake induced a significant increase in nitric oxide synthase (NOS) activity in the medial basal hypothalamus and neural lobe, while a low sodium diet decreased NOS activity in the neural lobe, suggesting that central NOS is involved in the control of sodium balance. Sodium 5-11 nitric oxide synthase 2 Homo sapiens 53-74 12181064-6 2002 A human IgAK anti-Pr autoantibody and a mouse anti-human glycophorin A antibody increased erythrocyte permeability to sodium. Sodium 118-124 glycophorin A (MNS blood group) Homo sapiens 57-70 12192104-4 2002 In the kidney, PDE5 is involved in the regulation of sodium excretion and renin secretion. Sodium 53-59 phosphodiesterase 5A Homo sapiens 15-19 12219173-3 2002 Pretreatment with losartan and [Sar1, Ala8] ANG II completely abolished the water and sodium intake, and the pressor increase (0.5 +/- 0.2, 1.1 +/- 0.2, 0.5 +/- 0.2, and 0.8 +/- 0.2 ml, and 1.2 +/- 3.9, 31 +/- 4.6 mmHg, respectively, N = 9-12), whereas losartan blunted the urinary and sodium excretion induced by ANG II (13.9 +/- 1.0 ml and 187 +/- 10 micro Eq/120 min, respectively, N = 9). Sodium 86-92 angiotensinogen Rattus norvegicus 44-50 12219173-3 2002 Pretreatment with losartan and [Sar1, Ala8] ANG II completely abolished the water and sodium intake, and the pressor increase (0.5 +/- 0.2, 1.1 +/- 0.2, 0.5 +/- 0.2, and 0.8 +/- 0.2 ml, and 1.2 +/- 3.9, 31 +/- 4.6 mmHg, respectively, N = 9-12), whereas losartan blunted the urinary and sodium excretion induced by ANG II (13.9 +/- 1.0 ml and 187 +/- 10 micro Eq/120 min, respectively, N = 9). Sodium 286-292 angiotensinogen Rattus norvegicus 44-50 12219173-4 2002 Pretreatment with PD 123319 and [Sar1, Ala8] ANG II blocked the urinary and sodium excretion (10.7 +/- 0.8, 9.8 +/- 0.7 ml, and 67 +/- 13 and 57 +/- 17 micro Eq/120 min, respectively, N = 9), whereas pretreatment with PD 123319 partially blocked the water and sodium intake, and the MAP induced by ANG II administration (2.3 +/- 0.3, 1.1 +/- 0.1 ml, and 12 +/- 3 mmHg, respectively, N = 9-10). Sodium 76-82 angiotensinogen Rattus norvegicus 45-51 12219173-4 2002 Pretreatment with PD 123319 and [Sar1, Ala8] ANG II blocked the urinary and sodium excretion (10.7 +/- 0.8, 9.8 +/- 0.7 ml, and 67 +/- 13 and 57 +/- 17 micro Eq/120 min, respectively, N = 9), whereas pretreatment with PD 123319 partially blocked the water and sodium intake, and the MAP induced by ANG II administration (2.3 +/- 0.3, 1.1 +/- 0.1 ml, and 12 +/- 3 mmHg, respectively, N = 9-10). Sodium 260-266 angiotensinogen Rattus norvegicus 45-51 12481928-5 2002 Myocardial VIP concentration decreased with increasing dietary sodium intake in the WKYs (P < 0.01) and in the SHRs (P < 0.01). Sodium 63-69 vasoactive intestinal peptide Rattus norvegicus 11-14 12481928-8 2002 Further, in early myocardial fibrosis resulting from increasing dietary sodium intake in both normotensive and hypertensive rats the concentration of VIP in the heart was negatively correlated with the degree of fibrosis. Sodium 72-78 vasoactive intestinal peptide Rattus norvegicus 150-153 12174326-10 2002 Finally, increased renal tubular reabsorption of sodium may also occur, caused by an increased renal sympathetic nerve activity, the direct effect of insulin, hyperactivity of the renin-angiotensin system and possibly by an alteration of intrarenal physical forces. Sodium 49-55 insulin Homo sapiens 150-157 12174326-10 2002 Finally, increased renal tubular reabsorption of sodium may also occur, caused by an increased renal sympathetic nerve activity, the direct effect of insulin, hyperactivity of the renin-angiotensin system and possibly by an alteration of intrarenal physical forces. Sodium 49-55 renin Homo sapiens 180-185 12455713-10 2002 COX-2 inhibitor drugs, such as NSAIDs, reduce sodium excretion, and may cause acute renal failure in patients in whom the maintenance of adequate renal perfusion is "prostaglandin-dependent". Sodium 46-52 mitochondrially encoded cytochrome c oxidase II Homo sapiens 0-5 12195126-0 2002 Influence of sodium intake on the cardiovascular and renal effects of brain mineralocorticoid receptor blockade in normotensive rats. Sodium 13-19 nuclear receptor subfamily 3, group C, member 2 Rattus norvegicus 76-102 12683421-8 2002 Decreased extracellular chloride increases COX-2 expression in cultured cTALH, an effect mediated by increased p38 MAP kinase activity and, in vivo, a sodium-deficient diet increases expression of activated p38 in MD/cTALH. Sodium 151-157 prostaglandin-endoperoxide synthase 2 Homo sapiens 43-48 12683421-8 2002 Decreased extracellular chloride increases COX-2 expression in cultured cTALH, an effect mediated by increased p38 MAP kinase activity and, in vivo, a sodium-deficient diet increases expression of activated p38 in MD/cTALH. Sodium 151-157 mitogen-activated protein kinase 14 Homo sapiens 207-210 12169661-1 2002 Na+/H+ exchanger regulatory factor (NHERF)-1 and NHERF-2, two structurally related protein adapters containing tandem PSD-95/Discs large/ZO-1 (PDZ) domains, were identified as essential factors for protein kinase A-mediated inhibition of the sodium-hydrogen exchanger, NHE3. Sodium 242-248 solute carrier family 9 (sodium/hydrogen exchanger), member 3 regulator 2 Mus musculus 49-56 12215953-5 2002 As a consequence, activation of sodium- and volume-retaining neurohumoral systems such as the renin-angiotensin-aldosterone system and the sympathetic nervous system and a non-osmotic release of arginine-vasopressin can be observed. Sodium 32-38 renin Homo sapiens 94-99 12072429-3 2002 NDRG2 mRNA was expressed in classical aldosterone target epithelia, and in the kidney, it was specifically located in the collecting duct, the site of aldosterone-regulated sodium absorption. Sodium 173-179 NDRG family member 2 Rattus norvegicus 0-5 12169661-1 2002 Na+/H+ exchanger regulatory factor (NHERF)-1 and NHERF-2, two structurally related protein adapters containing tandem PSD-95/Discs large/ZO-1 (PDZ) domains, were identified as essential factors for protein kinase A-mediated inhibition of the sodium-hydrogen exchanger, NHE3. Sodium 242-248 solute carrier family 9 (sodium/hydrogen exchanger), member 3 Mus musculus 269-273 12151509-0 2002 Endothelin-1 (ET-1) selectively enhances the activation gating of slowly inactivating tetrodotoxin-resistant sodium currents in rat sensory neurons: a mechanism for the pain-inducing actions of ET-1. Sodium 109-115 endothelin 1 Rattus norvegicus 0-12 12357279-7 2002 It is evident from experimental studies that an elevation in dietary sodium intake during the growing phase heightens neural control of blood pressure and the kidney partly due to an enhanced role of the brain renin-angiotensin system. Sodium 69-75 renin Homo sapiens 210-215 12154110-6 2002 In the renal cortex, low sodium diet caused a 194% increase in prepro-endothelin-1 mRNA (P<0.05), whereas endothelin-converting enzyme-1 type B and type A receptors remained unchanged. Sodium 25-31 endothelin 1 Homo sapiens 70-82 12154110-9 2002 In conclusion, during low sodium diet, renal prepro-endothelin-1 synthesis increases mainly in the renal cortex (where no changes in receptors occur), whereas type B receptor is selectively enhanced in the renal medulla. Sodium 26-32 endothelin 1 Homo sapiens 52-64 12177182-0 2002 Serotonin receptor activation inhibits sodium current and dendritic excitability in prefrontal cortex via a protein kinase C-dependent mechanism. Sodium 39-45 proline rich transmembrane protein 2 Homo sapiens 108-124 12193099-2 2002 Renal production of ET-1 increases in CHF and it is a significant independent predictor of sodium excretion. Sodium 91-97 endothelin 1 Canis lupus familiaris 20-24 12192542-1 2002 At the molecular level, the uptake of radioiodine and pertechnetate is proportional to the expression of the thyroidal sodium/iodine symporter (NIS). Sodium 119-125 solute carrier family 5 member 5 Homo sapiens 144-147 12154110-1 2002 Renal endothelin-1 participates in sodium and water handling, and its urinary excretion is increased in sodium-retentive states. Sodium 35-41 endothelin 1 Homo sapiens 6-18 12154110-1 2002 Renal endothelin-1 participates in sodium and water handling, and its urinary excretion is increased in sodium-retentive states. Sodium 104-110 endothelin 1 Homo sapiens 6-18 12151509-0 2002 Endothelin-1 (ET-1) selectively enhances the activation gating of slowly inactivating tetrodotoxin-resistant sodium currents in rat sensory neurons: a mechanism for the pain-inducing actions of ET-1. Sodium 109-115 endothelin 1 Rattus norvegicus 14-18 12151509-0 2002 Endothelin-1 (ET-1) selectively enhances the activation gating of slowly inactivating tetrodotoxin-resistant sodium currents in rat sensory neurons: a mechanism for the pain-inducing actions of ET-1. Sodium 109-115 endothelin 1 Rattus norvegicus 194-198 12208207-5 2002 We might hypothesize that putative melatonin deficiency in cases of neurofibromatosis 1 might play a role in the pathogenesis of hyperphosphaturea by decreasing sodium-phosphate cotransport, increasing the level of cAMP, the un-antagonized effect of dopamine on phosphate reabsorption and increasing glucocorticoid levels. Sodium 161-167 neurofibromin 1 Homo sapiens 68-87 12080034-2 2002 Recently, an organic cation transporter, OCTN2, was cloned from rat intestinal epithelium and shown to transport L-carnitine in a sodium-dependent manner. Sodium 130-136 solute carrier family 22 member 5 Rattus norvegicus 41-46 12182943-1 2002 The ability of sodium deficiency to stimulate vasopressin (VP) release was examined by determining if sodium deficiency sensitizes the animal to the behavioral disruption caused by intraventricular injections of VP. Sodium 102-108 arginine vasopressin Rattus norvegicus 59-61 12182943-2 2002 In sodium-replete rats, intraventricular injections of 50 ng VP on Day 1 had no effect on behavior, but this dose elicited abnormal behaviors (barrel rolls, hind-limb extensions) when administered on Day 2, indicating a sensitization phenomenon. Sodium 3-9 arginine vasopressin Rattus norvegicus 61-63 12182943-3 2002 In separate experiments, the first intraventricular injection of 50 ng VP in sodium-deficient but not in sodium-replete rats also elicited barrel rotations followed by hind-limb extension. Sodium 77-83 arginine vasopressin Rattus norvegicus 71-73 12182943-4 2002 Intraventricular injection of VP also disrupted motor behavior in sodium-replete rats that had multiple prior experiences with sodium deficiency but not in naive rats. Sodium 66-72 arginine vasopressin Rattus norvegicus 30-32 12182943-4 2002 Intraventricular injection of VP also disrupted motor behavior in sodium-replete rats that had multiple prior experiences with sodium deficiency but not in naive rats. Sodium 127-133 arginine vasopressin Rattus norvegicus 30-32 12182943-5 2002 These results show that sodium deficiency can mimic the effect of central injections of VP in sensitizing the brain to the behavioral effects of exogenous VP. Sodium 24-30 arginine vasopressin Rattus norvegicus 88-90 12182943-5 2002 These results show that sodium deficiency can mimic the effect of central injections of VP in sensitizing the brain to the behavioral effects of exogenous VP. Sodium 24-30 arginine vasopressin Rattus norvegicus 155-157 12182943-6 2002 This suggests that sodium deficiency induces the central release of VP. Sodium 19-25 arginine vasopressin Rattus norvegicus 68-70 11994293-4 2002 Here we used cysteine-scanning mutagenesis of the GLT-1 transporter to test the idea that this loop undergoes conformational changes following sodium and substrate binding. Sodium 143-149 solute carrier family 1 member 2 Homo sapiens 50-55 12182943-0 2002 Sodium deficiency enhances the behavioral responses to centrally administered vasopressin in rats. Sodium 0-6 arginine vasopressin Rattus norvegicus 78-89 12182943-1 2002 The ability of sodium deficiency to stimulate vasopressin (VP) release was examined by determining if sodium deficiency sensitizes the animal to the behavioral disruption caused by intraventricular injections of VP. Sodium 15-21 arginine vasopressin Rattus norvegicus 46-57 12182943-1 2002 The ability of sodium deficiency to stimulate vasopressin (VP) release was examined by determining if sodium deficiency sensitizes the animal to the behavioral disruption caused by intraventricular injections of VP. Sodium 15-21 arginine vasopressin Rattus norvegicus 59-61 12096047-8 2002 This result is shown to be robust and independent of whether the apical entrance mechanism for the sodium ion is a channel, a SGLT1 transporter driving inward uphill water flux, or an electroneutral Na+-K+-2Cl- cotransporter. Sodium 99-105 solute carrier family 5 member 1 Homo sapiens 126-131 12072411-1 2002 The present study was intended to determine whether the long-term V2 receptor-mediated effects of vasopressin on sodium reabsorption in the renal collecting duct is an aggravating factor in salt-sensitive hypertension. Sodium 113-119 arginine vasopressin Rattus norvegicus 98-109 12358141-6 2002 (b) After adjustment for age, SBP and DBP showed a significant positive association with body mass index, urinary sodium (Na) excretion, and total cholesterol (TC) to high-density lipoprotein (HDL) cholesterol ratio (TC/HDL). Sodium 114-120 D-box binding PAR bZIP transcription factor Homo sapiens 38-41 12119799-4 2002 The DASH-Sodium trial demonstrates significant increases in SBP and DBP, with sodium intake greater than 65 mmol/d (= 3.7 g NaCl--see equivalencies in Appendix A) and with the usual American diet (versus the DASH diet). Sodium 9-15 D-box binding PAR bZIP transcription factor Homo sapiens 68-71 12220285-5 2002 Rofecoxib is a selective COX-2 inhibitor that has been shown to increase sodium reabsorption in the kidney via effects on prostaglandin E2 and the renal vasculature. Sodium 73-79 mitochondrially encoded cytochrome c oxidase II Homo sapiens 25-30 12086636-3 2002 Here, we characterize the functional effects of three mutations in the human neuronal sodium channel alpha subunit SCN1A by heterologous expression with its known accessory subunits, beta1 and beta2, in cultured mammalian cells. Sodium 86-92 BCL2 related protein A1 Homo sapiens 183-188 12086636-3 2002 Here, we characterize the functional effects of three mutations in the human neuronal sodium channel alpha subunit SCN1A by heterologous expression with its known accessory subunits, beta1 and beta2, in cultured mammalian cells. Sodium 86-92 glycoprotein hormone subunit alpha 2 Homo sapiens 193-198 12032117-2 2002 In addition to high glucose, other factors implicated in renal fibrosis and increased TGF-beta synthesis include angiotensin II and high dietary sodium intake. Sodium 145-151 transforming growth factor beta 1 Homo sapiens 86-94 12032117-3 2002 The aim of this study was to examine the effect of angiotensin receptor blockade (ARB) and dietary sodium restriction on the plasma concentration and urinary excretion of TGF-beta in hypertensive patients with type 2 diabetes and elevated albumin excretion rate (AER). Sodium 99-105 transforming growth factor beta 1 Homo sapiens 171-179 12032117-9 2002 In the losartan group, urinary TGF-beta excretion decreased by 23.2% (-39.2 and 13.6) [median (interquartile range)] and 38.5% (-46.8 and -6.1) in the regular- and low-sodium phases, respectively (P < 0.05 for drug effect). Sodium 168-174 transforming growth factor beta 1 Homo sapiens 31-39 11891217-4 2002 When choline was substituted for sodium to transform thrombin to its slow form, the maximal levels of alpha-profibrin rose to those expected for independent release of the two FPA. Sodium 33-39 coagulation factor II, thrombin Homo sapiens 53-61 12136266-0 2002 Segmental variability of ENaC subunit expression in rat colon during dietary sodium depletion. Sodium 77-83 sodium channel epithelial 1 subunit gamma Rattus norvegicus 25-29 12090248-7 2002 whi2 and psr1 psr2 mutants had similar phenotypes, including reduced STRE-mediated gene expression, higher sensitivity to sodium ions and heat shock, and hyper-phosphorylation of Msn2. Sodium 122-128 putative phosphatase Saccharomyces cerevisiae S288C 14-18 12185990-11 2002 PPAR-gamma is involved in regulating renal hemodynamic and water and sodium transport. Sodium 69-75 peroxisome proliferator activated receptor gamma Homo sapiens 0-10 11967726-1 2002 A renin-angiotensin level that is inappropriately high for the systemic blood pressure and the state of sodium balance is now recognized to be one of the modifiable cardiovascular risk factors. Sodium 104-110 renin Homo sapiens 2-7 12019284-0 2002 Effects of dietary sodium and genetic background on angiotensinogen and Renin in mouse. Sodium 19-25 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 52-67 12019284-1 2002 Elements of a renin-angiotensin system expressed along the entire nephron, including angiotensinogen secreted by proximal tubule and renin expressed in connecting tubule, may participate in the regulation of sodium reabsorption at multiple sites of the nephron. Sodium 208-214 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 85-100 12019284-5 2002 Angiotensinogen and renin excretion were significantly higher under high sodium than under low sodium. Sodium 73-79 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 0-15 12019284-5 2002 Angiotensinogen and renin excretion were significantly higher under high sodium than under low sodium. Sodium 95-101 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 0-15 12019284-7 2002 C57BL/6 exhibited significantly higher urinary excretion of angiotensinogen than did CD1 animals under both conditions of sodium intake. Sodium 122-128 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 60-75 12045366-1 2002 The effect of dietary sodium restriction on insulin, lipids, and blood pressure has been controversial. Sodium 22-28 insulin Homo sapiens 44-51 11834730-1 2002 SAT1-3 comprise members of the recently cloned family of System A transporters that mediate the sodium-coupled uptake of short chain neutral amino acids, and their activity is regulated extensively by stimuli such as insulin, growth factors, and amino acid availability. Sodium 96-102 insulin Homo sapiens 217-224 18968607-4 2002 The electrodes based on the tripodal compound with o-NPOE and DBP as plasticizer gave good performance (slope, limits of detection) to lithium and sodium ions. Sodium 147-153 D-box binding PAR bZIP transcription factor Homo sapiens 62-65 11809765-5 2002 These observations implicate sodium efflux in the pH homeostasis of a subset of endocytic organelles and indicate that a dysfunctional CFTR in cystic fibrosis leads to organellar hyperacidification in lung epithelial cells because of a loss of CFTR inhibitory effects on sodium transport. Sodium 29-35 CF transmembrane conductance regulator Homo sapiens 135-139 11809765-5 2002 These observations implicate sodium efflux in the pH homeostasis of a subset of endocytic organelles and indicate that a dysfunctional CFTR in cystic fibrosis leads to organellar hyperacidification in lung epithelial cells because of a loss of CFTR inhibitory effects on sodium transport. Sodium 29-35 CF transmembrane conductance regulator Homo sapiens 244-248 11809765-5 2002 These observations implicate sodium efflux in the pH homeostasis of a subset of endocytic organelles and indicate that a dysfunctional CFTR in cystic fibrosis leads to organellar hyperacidification in lung epithelial cells because of a loss of CFTR inhibitory effects on sodium transport. Sodium 271-277 CF transmembrane conductance regulator Homo sapiens 135-139 11998688-0 2002 Integration of sodium and osmosensory signals in vasopressin neurons. Sodium 15-21 arginine vasopressin Rattus norvegicus 49-60 11926892-1 2002 CONTEXT: A genetic variant in alpha-adducin has been associated with renal sodium reabsorption and salt-sensitive hypertension. Sodium 75-81 adducin 1 Homo sapiens 30-43 11912262-6 2002 With liberal sodium intake, the increases in MAP, renal vascular resistance, and aldosterone levels during AngI infusion (8 ng/kg per min) were significantly higher for the DD genotype, compared with the ID and II genotypes (all parameters presented as percent changes +/- 95% confidence intervals), with mean MAP increases of 22 +/- 2% (DD genotype), 13 +/- 5% (ID genotype), and 12 +/- 6% (II genotype) (P < 0.05), mean increases in renal vascular resistance of 100.1 +/- 19.7% (DD genotype), 73.0 +/- 16.3% (ID genotype), and 63.2 +/- 16.9% (II genotype) (P < 0.05), and increases in aldosterone levels of 650 +/- 189% (DD genotype), 343 +/- 71% (ID genotype), and 254 +/- 99% (II genotype) (P < 0.05). Sodium 13-19 angiotensinogen Homo sapiens 107-111 11912262-9 2002 In contrast, with low sodium intake, the responses to AngI were similar for all genotypes. Sodium 22-28 angiotensinogen Homo sapiens 54-58 11912262-12 2002 These results support the presence of gene-environment interactions between ACE genotypes and dietary sodium intake. Sodium 102-108 angiotensin I converting enzyme Homo sapiens 76-79 11893630-2 2002 Lateral ventricular injections of 100 ng and 1 microg VP caused barrel rotations and a dramatic decrease in NaCl intake by sodium-deficient rats and suppressed sucrose intake. Sodium 123-129 arginine vasopressin Rattus norvegicus 54-56 11912262-0 2002 Enhanced responses of blood pressure, renal function, and aldosterone to angiotensin I in the DD genotype are blunted by low sodium intake. Sodium 125-131 angiotensinogen Homo sapiens 73-86 11912262-2 2002 Blunted responses of BP and proteinuria to ACE inhibition among DD renal patients during periods of high sodium intake were reported. Sodium 105-111 angiotensin I converting enzyme Homo sapiens 43-46 11912262-3 2002 It was therefore hypothesized that sodium status affects the phenotype in the ACE I/D polymorphism. Sodium 35-41 angiotensin I converting enzyme Homo sapiens 78-81 11832422-7 2002 In oocytes overexpressing grp58, sodium uptake was increased compared with control. Sodium 33-39 protein disulfide isomerase family A, member 3 Rattus norvegicus 26-31 11832422-9 2002 Sodium uptake was lower in oocytes injected with both antisense grp58 cRNA and sense NCC compared with sense NCC oocytes. Sodium 0-6 protein disulfide isomerase family A, member 3 Rattus norvegicus 64-69 11864932-8 2002 Urinary sodium excretion was also highest with VPI+SQ BNP, with the greatest increase in glomerular filtration rate. Sodium 8-14 natriuretic peptide B Canis lupus familiaris 54-57 11906319-1 2002 (1) Salt sensitive hypertension, which occurs as a result of treatment with nitric oxide synthase inhibitors, is associated with a loss of the usual down-regulatory effect of dietary sodium on angiotensin II (Ang II) synthesis. Sodium 183-189 angiotensinogen Rattus norvegicus 193-207 11906319-1 2002 (1) Salt sensitive hypertension, which occurs as a result of treatment with nitric oxide synthase inhibitors, is associated with a loss of the usual down-regulatory effect of dietary sodium on angiotensin II (Ang II) synthesis. Sodium 183-189 angiotensinogen Rattus norvegicus 209-215 11906319-3 2002 We sought to determine therefore whether the salt sensitive component to the hypertension was associated with a loss of the regulatory effect of dietary sodium on Ang II synthesis. Sodium 153-159 angiotensinogen Rattus norvegicus 163-169 11906319-9 2002 (4) We conclude that the hypertension in the SHR is in part salt sensitive and that this salt sensitive component is associated with a loss of the normal down-regulatory effect of dietary sodium on Ang II and angiotensinogen synthesis. Sodium 188-194 angiotensinogen Rattus norvegicus 198-204 11906319-9 2002 (4) We conclude that the hypertension in the SHR is in part salt sensitive and that this salt sensitive component is associated with a loss of the normal down-regulatory effect of dietary sodium on Ang II and angiotensinogen synthesis. Sodium 188-194 angiotensinogen Rattus norvegicus 209-224 11792666-8 2002 The changes in Fos expression and PRA are consistent with a proposed role for ANG II in the control of the sodium appetite produced by water deprivation followed by rehydration with only water. Sodium 107-113 angiotensinogen Rattus norvegicus 78-84 11847182-0 2002 Low-renin hypertension, altered sodium homeostasis, and an alpha-adducin polymorphism. Sodium 32-38 renin Homo sapiens 4-9 11937868-3 2002 The bone mineral idealized as calcium hydroxyapatite, Ca10 (PO4)(6)(OH)2, is a carbonatehydroxyapatite, approximated by the formula: (Ca,X)(10)(PO4,HPO4,CO3)(6)(OH,Y)2, where X are cations (magnesium, sodium, strontium ions) that can substitute for the calcium ions, and Y are anions (chloride or fluoride ions) that can substitute for the hydroxyl group. Sodium 201-207 carbonic anhydrase 10 Homo sapiens 54-58 11875587-2 2002 The ubiquitous involvement of the renin-angiotensin-aldosterone system, originally conceived as an axis of sodium and fluid metabolism in inflammation, thrombosis and cardiac and smooth muscle hypertrophy, is a major factor in disease progression for conditions as diverse as hypertension, heart failure, coronary artery disease and diabetes. Sodium 107-113 renin Homo sapiens 34-39 11847182-8 2002 Therefore, this study demonstrates a common genetic basis for altered cellular sodium homeostasis, impaired renal sodium handling, and salt-sensitivity of systolic blood pressure in individuals homozygous for the 460Trp polymorphism of the alpha-adducin gene. Sodium 79-85 adducin 1 Homo sapiens 240-253 11847182-8 2002 Therefore, this study demonstrates a common genetic basis for altered cellular sodium homeostasis, impaired renal sodium handling, and salt-sensitivity of systolic blood pressure in individuals homozygous for the 460Trp polymorphism of the alpha-adducin gene. Sodium 114-120 adducin 1 Homo sapiens 240-253 11799146-1 2002 Angiotensin II (Ang II) regulates water and sodium transport in renal tubules and gastrointestinal tract. Sodium 44-50 angiotensinogen Homo sapiens 0-14 11790293-3 2002 The importance of the renin-angiotensin system in controlling sodium homeostasis and vascular resistance is well established, however, in the past decade, much attention has been focused on the importance of angiotensin II as a regulator of microvessel density, acting through the AT1 and AT2 receptors. Sodium 62-68 renin Homo sapiens 22-27 11859295-5 2002 ANF stimulates natriuresis mainly by inhibiting sodium reabsorption in the inner medullary collecting duct. Sodium 48-54 natriuretic peptide A Homo sapiens 0-3 11882573-7 2002 Plasma renin activity and blood pressure response to diuretic treatment, on the other hand, showed a weaker association with the sodium transport rate. Sodium 129-135 renin Homo sapiens 7-12 11799146-1 2002 Angiotensin II (Ang II) regulates water and sodium transport in renal tubules and gastrointestinal tract. Sodium 44-50 angiotensinogen Homo sapiens 16-22 11824859-9 2002 In conclusion, our results show that in diabetic patients with AN, vasopressin participates in BP control by stimulating vascular and renal V1 receptors, which results in vasoconstriction and sodium reabsorption. Sodium 192-198 arginine vasopressin Homo sapiens 67-78 11809721-9 2002 These results support a role for CFTR in differentiation of the respiratory epithelium and suggest that its expression levels are not merely reflecting major changes in the sodium/chloride bulk flow close to term. Sodium 173-179 CF transmembrane conductance regulator Homo sapiens 33-37 11818508-2 2002 Using the Ca(2+) chelator 1,2- bis(o-aminophenoxy)ethane-N,N,N",N"-tetraacetic acid, sodium (BAPTA-AM), we find both augmentation and inhibition of insulin signaling phenomena. Sodium 85-91 insulin Homo sapiens 148-155 11963285-12 2002 CONCLUSIONS: Our results show that intensive vasodilator therapy in patients with severe HF improves hemodynamic parameters and causes activation of renin-angiotensin-aldosterone and adrenergic systems, resulting in sodium retention. Sodium 216-222 renin Homo sapiens 149-154 11824860-1 2002 Salt-sensitive persons have lower plasma renin activity than salt-resistant persons and their plasma renin activity increases less with a low sodium diet or volume depletion, compared to salt-resistant individuals. Sodium 142-148 renin Homo sapiens 101-106 11824860-12 2002 These findings point to an intrinsic difference in the regulation of renin release between salt-sensitive and salt-resistant subjects that may account for the different BP responses to changes in dietary sodium intake. Sodium 204-210 renin Homo sapiens 69-74 12036384-9 2002 The AT(1) receptor is responsible for the majority of the effects of angiotensin II: vasoconstriction, sodium re-absorption, cell proliferation, extracellular matrix formation, inflammatory response and oxidative stress. Sodium 103-109 angiotensinogen Homo sapiens 69-83 11945151-8 2002 During repeated dosage with the specific COX-2 inhibitors, the 24 hour urinary excretion of sodium is only inhibited for the first day of treatment while the excretion of sodium is still decreased over the first 3 hours after the individual doses. Sodium 92-98 mitochondrially encoded cytochrome c oxidase II Homo sapiens 41-46 11945151-8 2002 During repeated dosage with the specific COX-2 inhibitors, the 24 hour urinary excretion of sodium is only inhibited for the first day of treatment while the excretion of sodium is still decreased over the first 3 hours after the individual doses. Sodium 171-177 mitochondrially encoded cytochrome c oxidase II Homo sapiens 41-46 12036386-1 2002 The renin-angiotensin system exerts a cardinal role in the maintenance of blood pressure and in the regulation of water and sodium excretion through its multiple effects on the vasculature, the kidneys, the heart, the adrenal glands and the brain. Sodium 124-130 renin Homo sapiens 4-9 12036388-1 2002 The octapeptide angiotensin II (Ang II), the potent effector molecule of the renin-angiotensin-aldosterone system (RAAS), is involved in the control of blood pressure, cardiac and vascular function as well as sodium and water homeostasis. Sodium 209-215 angiotensinogen Homo sapiens 16-30 12036388-1 2002 The octapeptide angiotensin II (Ang II), the potent effector molecule of the renin-angiotensin-aldosterone system (RAAS), is involved in the control of blood pressure, cardiac and vascular function as well as sodium and water homeostasis. Sodium 209-215 angiotensinogen Homo sapiens 32-38 12036388-1 2002 The octapeptide angiotensin II (Ang II), the potent effector molecule of the renin-angiotensin-aldosterone system (RAAS), is involved in the control of blood pressure, cardiac and vascular function as well as sodium and water homeostasis. Sodium 209-215 renin Homo sapiens 77-82 12036388-4 2002 The AT(1 )receptor mediates all of the known actions of Ang II in the cardiovascular system, such as vasoconstriction, increasing cardiac contractility and renal tubular sodium reabsorption, as well as vascular and cardiac hypertrophy. Sodium 170-176 angiotensinogen Homo sapiens 56-62 11913598-9 2002 Change in urinary sodium-to-creatinine ratios of 3 consecutive pooled overnight 8-hour urine collections correlated with changes in 24-hour ambulatory SBP (r = 0.294, P<.001) and DBP (r = 0.193, P<.05); however, change in total urinary sodium content was uncorrelated. Sodium 18-24 D-box binding PAR bZIP transcription factor Homo sapiens 182-185 12220575-13 2002 The results of this study support the hypothesis that Na(v)1.3 may mediate this fast sodium current. Sodium 85-91 immunoglobulin lambda variable 2-11 Homo sapiens 54-62 11805851-2 2002 We postulated that nitric oxide synthase inhibition might induce a salt-sensitive form of hypertension and that this salt sensitivity might be linked to a loss of the regulatory effect of sodium ingestion on angiotensin II (Ang II) and angiotensinogen. Sodium 188-194 angiotensinogen Rattus norvegicus 208-222 11805851-2 2002 We postulated that nitric oxide synthase inhibition might induce a salt-sensitive form of hypertension and that this salt sensitivity might be linked to a loss of the regulatory effect of sodium ingestion on angiotensin II (Ang II) and angiotensinogen. Sodium 188-194 angiotensinogen Rattus norvegicus 224-230 11805851-2 2002 We postulated that nitric oxide synthase inhibition might induce a salt-sensitive form of hypertension and that this salt sensitivity might be linked to a loss of the regulatory effect of sodium ingestion on angiotensin II (Ang II) and angiotensinogen. Sodium 188-194 angiotensinogen Rattus norvegicus 236-251 11984003-0 2002 The dual AngII/AVP receptor gene N119S/C163R variant exhibits sodium-induced dysfunction and cosegregates with salt-sensitive hypertension in the Dahl salt-sensitive hypertensive rat model. Sodium 62-68 angiotensinogen Rattus norvegicus 9-14 11984003-5 2002 The functional properties and renal-specific expression of the recently characterized AngII/AVP receptor suggest a putative modulator role in tubular sodium and fluid reabsorption. Sodium 150-156 angiotensinogen Rattus norvegicus 86-91 11984003-13 2002 CONCLUSIONS: The observed molecular dysfunction in the Dahl S AngII/AVP receptor is consistent with increased tubular sodium and fluid reabsorption observed in Dahl S rats. Sodium 118-124 angiotensinogen Rattus norvegicus 62-67 11805851-9 2002 In contrast, the plasma concentration of Ang II and angiotensinogen increased with increasing dietary sodium (P < 0.05 and P < 0.005, respectively). Sodium 102-108 angiotensinogen Rattus norvegicus 41-47 11805851-9 2002 In contrast, the plasma concentration of Ang II and angiotensinogen increased with increasing dietary sodium (P < 0.05 and P < 0.005, respectively). Sodium 102-108 angiotensinogen Rattus norvegicus 52-67 11752024-10 2002 A lower level of SCNN1A subunit expression among subjects with the AA genotype might lead to lower levels of sodium reabsorption in the kidney and might provide protection against the development of hypertension. Sodium 109-115 sodium channel epithelial 1 subunit alpha Homo sapiens 17-23 11701449-0 2001 Effects of growth hormone on renal tubular handling of sodium in healthy humans. Sodium 55-61 growth hormone 1 Homo sapiens 11-25 12424421-2 2002 ANG II (6 ng/min, n = 14) decreased glomerular filtration rate (GFR), renal plasma flow (RPF), absolute and fractional sodium excretion by -24 +/- 5, -25 +/- 6, -44 +/- 6 and -28 +/- 7%, respectively (p < 0.05). Sodium 119-125 angiotensinogen Rattus norvegicus 0-6 12424421-10 2002 While exogenous ANG II during blockade of the Ang-(1-7) receptor and the AT(2) receptor (by PD 123319; 1 microg/min i.r., n = 9) resulted in the same decreases in absolute and fractional sodium excretion (-39 +/- 8 and -38 +/- 6%, respectively, p < 0.05) as did ANG II in the absence of Ang-(1-7) receptor blockade. Sodium 187-193 angiotensinogen Rattus norvegicus 16-22 11701449-4 2001 Treatment with GH increased C(Li) and changed the tubular handling of sodium and water. Sodium 70-76 growth hormone 1 Homo sapiens 15-17 12511180-7 2002 In contrast, intrarenal inhibition of nNOS by L-SMTC did not alter GFR, RPF or RVR and elicited a marked increase in sodium excretion in TGR. Sodium 117-123 thioredoxin reductase 3 Mus musculus 137-140 12511180-10 2002 In addition, the data indicate that nNOS-derived NO increases tubular sodium reabsorption in TGR and that the renal nerves play an important modulatory role in this process. Sodium 70-76 thioredoxin reductase 3 Mus musculus 93-96 11705774-6 2001 ADM maintained both urine flow (P < 0.001) and sodium excretion (P = 0.01) compared with falls observed with NP. Sodium 50-56 pro-adrenomedullin Ovis aries 0-3 11701449-6 2001 The data demonstrate that GH-induced activation of the RAAS can be blocked by concomitant PG synthesis inhibition and that the tubular effects of GH include increased distal nephron sodium and water reabsorption. Sodium 182-188 growth hormone 1 Homo sapiens 26-28 11701449-6 2001 The data demonstrate that GH-induced activation of the RAAS can be blocked by concomitant PG synthesis inhibition and that the tubular effects of GH include increased distal nephron sodium and water reabsorption. Sodium 182-188 growth hormone 1 Homo sapiens 146-148 11701449-1 2001 To investigate the mechanisms behind the water- and sodium-retaining effects of growth hormone (GH), we studied the effect of GH on 1) water and sodium homeostasis, 2) the renin-angiotensin-aldosterone system (RAAS), and 3) lithium clearance (C(Li)) with and without concomitant prostaglandin (PG) synthesis inhibition with ibuprofen. Sodium 52-58 growth hormone 1 Homo sapiens 80-94 11701449-1 2001 To investigate the mechanisms behind the water- and sodium-retaining effects of growth hormone (GH), we studied the effect of GH on 1) water and sodium homeostasis, 2) the renin-angiotensin-aldosterone system (RAAS), and 3) lithium clearance (C(Li)) with and without concomitant prostaglandin (PG) synthesis inhibition with ibuprofen. Sodium 52-58 growth hormone 1 Homo sapiens 96-98 11746424-1 2001 A previous study has shown that glutamine (Gln) uptake in C6 cells grown in a standard medium containing 2 mM Gln, is predominantly mediated by a sodium-dependent system that is inhibited by ASC system substrates alanine (Ala), serine (Ser), cysteine (Cys) and threonine (Thr), shows pH sensitivity and partial tolerance to substitution of Na+ by Li+, features compatible with system ASCT2 that is strongly expressed in cultured astrocytes. Sodium 146-152 PYD and CARD domain containing Homo sapiens 191-194 11775123-0 2001 Role of angiotensin converting enzyme genotype in sodium sensitivity in older hypertensives. Sodium 50-56 angiotensin I converting enzyme Homo sapiens 8-37 11775123-8 2001 CONCLUSIONS: Based on these data in older hypertensive individuals, we conclude that the ACE gene ID and DD genotypes are associated with an increase in BP during a high Na+ diet, which is consistent with the phenotypic characteristic of sodium sensitivity. Sodium 238-244 angiotensin I converting enzyme Homo sapiens 89-92 11903318-4 2001 Increased sodium intake and increased AngII causes cardiac hypertrophy, but decreased sodium intake regresses cardiac hypertrophy despite high AngII levels. Sodium 86-92 angiotensinogen Rattus norvegicus 143-148 11447308-4 2001 ET(B) receptors may mediate some critical processes in the kidney such as sodium and water excretion in addition to releasing vasodilator substances such as NO and prostacyclin from endothelial cells. Sodium 74-80 endothelin receptor type B Homo sapiens 0-4 11709521-6 2001 RESULTS: The daily diet of 200 mmol of sodium resulted in weight gain and a positive sodium balance for three weeks, associated with significant suppression of plasma renin activity and aldosterone levels, and a significant rise in plasma atrial natriuretic peptide levels (p<0.05). Sodium 39-45 renin Homo sapiens 167-172 11746424-8 2001 In C6 cells grown in the presence or absence of Gln alike, approximately 20% of the sodium-dependent Gln uptake was resistant to MeAiB+Thr, indicating contribution of system N. The N system-mediated uptake in C6 cells grown in the absence, but not in the presence of Gln was not inhibited by glutamate (Glu) that conforms to the characteristics of the glial N system variant, SN1. Sodium 84-90 solute carrier family 38 member 3 Homo sapiens 376-379 11737606-2 2001 Conventional non-steroidal anti-inflammatory drugs (NSAIDs), which inhibit both COX isoforms (COX-1 and -2), cause sodium retention, exacerbate hypertension, and interfere with the efficacy of certain anti-hypertensive agents such as angiotensin-converting enzyme (ACE) inhibitors. Sodium 115-121 cytochrome c oxidase I, mitochondrial Mus musculus 94-106 11881132-3 2001 Angiotensin II (Ang II) increases sodium reabsorption and hence oxygen consumption at any given bloodflow rate; therefore, it may affect the balance of renal oxygen supply vs. demand and hence Epo production. Sodium 34-40 angiotensinogen Homo sapiens 0-14 11881132-3 2001 Angiotensin II (Ang II) increases sodium reabsorption and hence oxygen consumption at any given bloodflow rate; therefore, it may affect the balance of renal oxygen supply vs. demand and hence Epo production. Sodium 34-40 angiotensinogen Homo sapiens 16-22 11731622-6 2001 Simultaneous sodium restriction and losartan treatment caused increases in plasma potassium (5.5 +/- 0.1 mEq/liter) and aldosterone (1.84 +/- 0.38 ng/ml), with both Agtr1a-/- and Agtr1a+/+ cells intensively expressing aldosterone synthase mRNA. Sodium 13-19 angiotensin II receptor, type 1a Mus musculus 165-171 11731622-6 2001 Simultaneous sodium restriction and losartan treatment caused increases in plasma potassium (5.5 +/- 0.1 mEq/liter) and aldosterone (1.84 +/- 0.38 ng/ml), with both Agtr1a-/- and Agtr1a+/+ cells intensively expressing aldosterone synthase mRNA. Sodium 13-19 angiotensin II receptor, type 1a Mus musculus 179-185 11735260-0 2001 Regulation of sodium-calcium exchange and mitochondrial energetics by Bcl-2 in the heart of transgenic mice. Sodium 14-20 B cell leukemia/lymphoma 2 Mus musculus 70-75 11737606-10 2001 Sodium sensitivity and BP lowering also were enhanced in mice with combined deficiency of COX-1 and AT1A receptor. Sodium 0-6 cytochrome c oxidase I, mitochondrial Mus musculus 90-95 11737606-11 2001 CONCLUSIONS: The absence of COX-1 is associated with sodium loss and enhanced sensitivity to ACE inhibition, suggesting that COX-1 inhibition does not cause hypertension and abnormal sodium handling associated with NSAID use. Sodium 53-59 cytochrome c oxidase I, mitochondrial Mus musculus 28-33 11711512-0 2001 Chronic exposure to vasopressin upregulates ENaC and sodium transport in the rat renal collecting duct and lung. Sodium 53-59 arginine vasopressin Rattus norvegicus 20-31 11717455-5 2001 Studies with pharmacological agents indicated a role for sodium conductance, modulated by CFTR regulatory function, in determining the pH of TGN. Sodium 57-63 CF transmembrane conductance regulator Homo sapiens 90-94 11479303-6 2001 Strikingly, the glutamate-dependent gating of the uncoupled conductance mediated by EAAC-1 has a strict requirement for sodium; lithium cannot substitute for it. Sodium 120-126 solute carrier family 1 member 1 Homo sapiens 84-90 11728007-8 2001 It is proposed that salt-dependent hypertension in Dahl salt-sensitive rats may be due to enhanced Ang-II mediated sodium retention. Sodium 115-121 angiotensinogen Rattus norvegicus 99-105 11828179-4 2001 The role of angiotensin II in controlling sodium balance, in both renal insufficiency states and congestive heart failure, is clearly recognized. Sodium 42-48 angiotensinogen Homo sapiens 12-26 11711512-1 2001 Vasopressin is known to acutely stimulate sodium transport in the renal collecting duct. Sodium 42-48 arginine vasopressin Rattus norvegicus 0-11 11711512-12 2001 This study shows that vasopressin increases sodium transport in the renal collecting duct and probably in the lung, through a differential transcriptional regulation of ENaC subunits. Sodium 44-50 arginine vasopressin Rattus norvegicus 22-33 11711512-12 2001 This study shows that vasopressin increases sodium transport in the renal collecting duct and probably in the lung, through a differential transcriptional regulation of ENaC subunits. Sodium 44-50 sodium channel epithelial 1 subunit gamma Rattus norvegicus 169-173 11602666-1 2001 Rat oatp1 (Slc21a1) and oatp2 (Slc21a5) transport many structurally unrelated endogenous and exogenous compounds across the sinusoidal membrane of hepatocytes in a sodium-independent manner. Sodium 164-170 solute carrier organic anion transporter family, member 1a1 Rattus norvegicus 4-9 11703600-0 2001 Coordinated down-regulation of NBC-1 and NHE-3 in sodium and bicarbonate loading. Sodium 50-56 solute carrier family 4 member 4 Rattus norvegicus 31-36 11604491-3 2001 We now observe that this novel alkalinization pathway is mediated by the pH regulator NHE1, as shown by the requirement for sodium, blocking by pharmacological inhibitors or use of an NHE1-deficient cell line, and the altered phosphorylation of NHE1. Sodium 124-130 solute carrier family 9 member A1 Homo sapiens 86-90 11719734-0 2001 Low sodium and furosemide-induced stimulation of the renin system in man is mediated by cyclooxygenase 2. Sodium 4-10 renin Homo sapiens 53-58 11719734-0 2001 Low sodium and furosemide-induced stimulation of the renin system in man is mediated by cyclooxygenase 2. Sodium 4-10 prostaglandin-endoperoxide synthase 2 Homo sapiens 88-104 11719734-3 2001 Plasma renin activity increased 2 to 3 times over baseline with a low-sodium diet and 5 times over baseline 30 minutes after intravenous furosemide; it was still elevated nearly 5 times on day 9. Sodium 70-76 renin Homo sapiens 7-12 11719734-7 2001 We have concluded that low-sodium and furosemide-stimulated renin and aldosterone secretion is completely blocked in healthy volunteers during COX-2 inhibition with rofecoxib, suggesting that intact COX-2 is of major importance for stimulation of the renin system under these conditions in man. Sodium 27-33 renin Homo sapiens 60-65 11719734-7 2001 We have concluded that low-sodium and furosemide-stimulated renin and aldosterone secretion is completely blocked in healthy volunteers during COX-2 inhibition with rofecoxib, suggesting that intact COX-2 is of major importance for stimulation of the renin system under these conditions in man. Sodium 27-33 prostaglandin-endoperoxide synthase 2 Homo sapiens 143-148 11811373-11 2001 There is some evidence for a role of ET-1 in blood pressure elevation in some experimental forms of hypertension, particularly severe, sodium-sensitive hypertension, in which it may play a role in accentuating rather than initiating blood pressure elevation. Sodium 135-141 endothelin 1 Homo sapiens 37-41 11602666-1 2001 Rat oatp1 (Slc21a1) and oatp2 (Slc21a5) transport many structurally unrelated endogenous and exogenous compounds across the sinusoidal membrane of hepatocytes in a sodium-independent manner. Sodium 164-170 solute carrier organic anion transporter family, member 1a1 Rattus norvegicus 11-18 11597606-1 2001 Reversal of the Na(+)/Ca(2+) exchanger (NCX) occurs during ischemia-reperfusion injury as a result of changes in intracellular pH and sodium concentration. Sodium 134-140 solute carrier family 8 member A1 Rattus norvegicus 16-38 11676542-10 2001 For thrombin, smaller negative DeltaC(p) values are observed for ligand binding in the presence of sodium ions compared to the other alkali ions, probably due to stabilising effects on the protein or changes in the bound water structure. Sodium 99-105 coagulation factor II, thrombin Homo sapiens 4-12 11790424-1 2001 A depletion of sodium may increase sodium intake by increasing the synthesis of angiotensin (ANG) II in the blood and by stimulating ANG II receptors in the subfornical organ (SFO) of the rat. Sodium 15-21 angiotensinogen Rattus norvegicus 133-139 11597606-1 2001 Reversal of the Na(+)/Ca(2+) exchanger (NCX) occurs during ischemia-reperfusion injury as a result of changes in intracellular pH and sodium concentration. Sodium 134-140 solute carrier family 8 member A1 Rattus norvegicus 40-43 11710777-5 2001 CONCLUSIONS: The association of renal ET-1 and NO activity with sodium excretion supports the hypothesis that these factors play a role in the physiologic response to acute changes in sodium intake, particularly in African Americans. Sodium 64-70 endothelin 1 Homo sapiens 38-42 11710777-5 2001 CONCLUSIONS: The association of renal ET-1 and NO activity with sodium excretion supports the hypothesis that these factors play a role in the physiologic response to acute changes in sodium intake, particularly in African Americans. Sodium 184-190 endothelin 1 Homo sapiens 38-42 11710792-13 2001 Also in hypothyroid patients the application of a low sodium diet led to a lower increase in plasma renin activity in subjects with salt-sensitive BP than in individuals with salt-resistant BP. Sodium 54-60 renin Homo sapiens 100-105 11641319-2 2001 A coherent picture is emerging, with the final pathway of these mechanisms converging on the renin-angiotensin system in the presence of a positive sodium balance and responsible for arteriolar resistance and responsiveness to pressor agents. Sodium 148-154 renin Homo sapiens 93-98 11573975-2 2001 Classic studies, utilizing isolated perfused tubules, have revealed that vasopressin increases sodium reabsorption in the kidney thick ascending limb and the collecting duct. Sodium 95-101 arginine vasopressin Rattus norvegicus 73-84 11677251-1 2001 The serotonin transporter (SERT) is a high-affinity sodium/chloride-dependent neurotransmitter transporter responsible for reuptake of serotonin from the extracellular space. Sodium 52-58 solute carrier family 6 member 4 Homo sapiens 4-25 11811363-9 2001 In conclusion, weight loss by low-calorie diet with a constant intake of sodium, reduced blood pressure in obese hypertensives by improvement of vagal nervous activity and insulin resistance. Sodium 73-79 insulin Homo sapiens 172-179 11677251-1 2001 The serotonin transporter (SERT) is a high-affinity sodium/chloride-dependent neurotransmitter transporter responsible for reuptake of serotonin from the extracellular space. Sodium 52-58 solute carrier family 6 member 4 Homo sapiens 27-31 11714488-8 2001 We speculate that disruption of the KCNE1 gene impairs sodium metabolism in female mice drinking high levels of 150 mM NaCl, which causes malaise that becomes associated with NaCl taste, and as a consequence, reduced preference for NaCl. Sodium 55-61 potassium voltage-gated channel, Isk-related subfamily, member 1 Mus musculus 36-41 11507017-6 2001 Consistent with the modulation of ANG II, plasma aldosterone significantly decreased from 41 +/- 8 to 8 +/- 3 ng/dl when sodium intake was elevated (n = 6). Sodium 121-127 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 34-40 11506985-0 2001 Circulating angiotensin II mediates sodium appetite in adrenalectomized rats. Sodium 36-42 angiotensinogen Rattus norvegicus 12-26 11507017-11 2001 These studies indicate that the physiological suppression of circulating ANG II may be required to maintain a constancy of arterial pressure during alterations in sodium intake in normal mice. Sodium 163-169 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 73-79 11506985-1 2001 We investigated the role of circulating ANG II in sodium appetite after adrenalectomy. Sodium 50-56 angiotensinogen Rattus norvegicus 40-46 11506985-5 2001 Intravenous infusion of ANG II (starting 10-15 min before 0.3 M NaCl became available) in adrenalectomized, captopril-treated rats restored both sodium intake and blood pressure to values seen in rats not treated with captopril. Sodium 145-151 angiotensinogen Rattus norvegicus 24-30 11514289-0 2001 ANG II in median preoptic nucleus and pressor responses to CSF sodium and high sodium intake in SHR. Sodium 63-69 angiotensinogen Rattus norvegicus 0-6 11506985-8 2001 These results indicate that most or all of the sodium appetite of adrenalectomized rats is mediated by circulating ANG II. Sodium 47-53 angiotensinogen Rattus norvegicus 115-121 11514289-0 2001 ANG II in median preoptic nucleus and pressor responses to CSF sodium and high sodium intake in SHR. Sodium 79-85 angiotensinogen Rattus norvegicus 0-6 11496053-2 2001 Cyclooxygenase-2 regulates renin-angiotensin secretion, and thereby glomerular filtration rate and sodium homeostasis. Sodium 99-105 prostaglandin-endoperoxide synthase 2 Homo sapiens 0-16 11496053-2 2001 Cyclooxygenase-2 regulates renin-angiotensin secretion, and thereby glomerular filtration rate and sodium homeostasis. Sodium 99-105 renin Homo sapiens 27-32 11578526-5 2001 Rats on a low sodium diet had a significantly increased capsular/zona glomerulosa immunoreactive VIP (irVIP) level, while rats on a high sodium diet had suppressed levels relative to controls. Sodium 14-20 vasoactive intestinal peptide Rattus norvegicus 97-100 11532707-8 2001 Sodium-retaining endocrine systems, such as renin-aldosterone and catecholamines, are much more activated during microG than on Earth. Sodium 0-6 renin Homo sapiens 44-49 11578526-8 2001 Analysis of mRNA encoding VIP revealed a large increase in expression of VIP in the sodium-deplete group compared with the control, with no change in VIP expression in the sodium-loaded group. Sodium 84-90 vasoactive intestinal peptide Rattus norvegicus 26-29 11578526-8 2001 Analysis of mRNA encoding VIP revealed a large increase in expression of VIP in the sodium-deplete group compared with the control, with no change in VIP expression in the sodium-loaded group. Sodium 84-90 vasoactive intestinal peptide Rattus norvegicus 73-76 11578526-8 2001 Analysis of mRNA encoding VIP revealed a large increase in expression of VIP in the sodium-deplete group compared with the control, with no change in VIP expression in the sodium-loaded group. Sodium 84-90 vasoactive intestinal peptide Rattus norvegicus 73-76 11479173-10 2001 Renal vasculature and nephron segment heterogeneity in sodium reabsorption generate the marginal tissue oxygen pressure required to trigger the production of erythropoietin. Sodium 55-61 erythropoietin Homo sapiens 158-172 11564984-1 2001 OBJECTIVE: It is well-known that insulin induces renal sodium retention. Sodium 55-61 insulin Homo sapiens 33-40 12501974-6 2001 Acromegaly is frequently associated with insulin resistance and hyperinsulinaemia which may induce hypertension by stimulating renal sodium absorption and sympathetic nervous activity. Sodium 133-139 insulin Homo sapiens 41-48 11382758-4 2001 Mutagenesis analysis revealed that the region near the carboxyl-terminal end of Nha1 comprising residues 800-948 is dispensable for sodium detoxification but necessary for transport of K(+) cations. Sodium 132-138 Nha1p Saccharomyces cerevisiae S288C 80-84 11479173-12 2001 Factors that affect blood supply and sodium reabsorption in a discordant manner may modulate the critmeter (eg, angiotensin II). Sodium 37-43 angiotensinogen Homo sapiens 112-126 11473492-10 2001 While an excess water load is excreted rapidly, an excess sodium load is excreted very slowly, even in normal subjects, and causes persistent dilution of haematocrit and serum albumin. Sodium 58-64 albumin Homo sapiens 170-183 11471048-3 2001 The effect of Ang II and Ang-(1-7) on renal sodium excretion has been associated, at least in part, with modulation of proximal tubule sodium reabsorption. Sodium 44-50 angiotensinogen Homo sapiens 14-20 11471048-3 2001 The effect of Ang II and Ang-(1-7) on renal sodium excretion has been associated, at least in part, with modulation of proximal tubule sodium reabsorption. Sodium 135-141 angiotensinogen Homo sapiens 14-20 11493618-10 2001 Results suggest a sodium-specific inhibitory effect on up-regulation of beta2-integrins of fMLP-stimulated PMNLs, which is unlikely to be caused by alterations of fMLP receptor binding, decrease in cytosolic calcium, attenuation of calcium or protein kinase C-dependent pathways, suppression of p38- or p44/42 MAP kinase-dependent pathways, or cellular ability to increase or decrease volumes. Sodium 18-24 formyl peptide receptor 1 Homo sapiens 91-95 11493618-10 2001 Results suggest a sodium-specific inhibitory effect on up-regulation of beta2-integrins of fMLP-stimulated PMNLs, which is unlikely to be caused by alterations of fMLP receptor binding, decrease in cytosolic calcium, attenuation of calcium or protein kinase C-dependent pathways, suppression of p38- or p44/42 MAP kinase-dependent pathways, or cellular ability to increase or decrease volumes. Sodium 18-24 mitogen-activated protein kinase 14 Homo sapiens 295-298 11518842-1 2001 BACKGROUND: The genes encoding angiotensin converting enzyme (ACE, I/D), alpha-adducin (ADD, Gly460Trp) and aldosterone synthase (AS, -344C/T) share the potential of influencing blood pressure (BP) via sodium homeostasis. Sodium 202-208 adducin 1 Homo sapiens 73-86 11481269-11 2001 CONCLUSIONS: These results suggest that the 11 beta-HSD1 isozyme may modulate steroid-regulated sodium transport across the NPE, thereby influencing IOP. Sodium 96-102 hydroxysteroid 11-beta dehydrogenase 1 Homo sapiens 44-56 11518842-1 2001 BACKGROUND: The genes encoding angiotensin converting enzyme (ACE, I/D), alpha-adducin (ADD, Gly460Trp) and aldosterone synthase (AS, -344C/T) share the potential of influencing blood pressure (BP) via sodium homeostasis. Sodium 202-208 angiotensin I converting enzyme Homo sapiens 31-60 11399641-7 2001 Decreased extracellular chloride increases COX-2 expression in cultured cTALH, an effect mediated by increased p38 mitogen-activated protein kinase activity, and, in vivo, a sodium-deficient diet increases expression of activated p38 in MD/cTALH. Sodium 174-180 mitogen-activated protein kinase 14 Homo sapiens 230-233 11474481-1 2001 Insulin resistance and hyperinsulinemia have been suggested to precede and promote hypertension, possibly by impairing sodium balance. Sodium 119-125 insulin Homo sapiens 0-7 11399655-1 2001 Recent evidence suggests that endothelin-1 (ET-1), perhaps through the ET(B) receptor, may participate in blood pressure regulation through the control of sodium excretion. Sodium 155-161 endothelin 1 Rattus norvegicus 30-42 11474481-11 2001 Acute hyperinsulinemia impairs the ability to excrete an acute sodium load in hypertensive patients, but not in offspring of hypertensives with normal insulin sensitivity. Sodium 63-69 insulin Homo sapiens 11-18 11465650-0 2001 The effect of sodium supplementation on glucose tolerance and insulin concentrations in patients with hypertension and diabetes mellitus. Sodium 14-20 insulin Homo sapiens 62-69 11465650-1 2001 Severe short-term sodium restriction or extreme sodium loading may alter glucose tolerance and insulin resistance in patients with hypertension, but it is unclear whether variations in sodium intake within the clinically observed range affect glucose tolerance. Sodium 18-24 insulin Homo sapiens 95-102 11465650-1 2001 Severe short-term sodium restriction or extreme sodium loading may alter glucose tolerance and insulin resistance in patients with hypertension, but it is unclear whether variations in sodium intake within the clinically observed range affect glucose tolerance. Sodium 48-54 insulin Homo sapiens 95-102 11465650-1 2001 Severe short-term sodium restriction or extreme sodium loading may alter glucose tolerance and insulin resistance in patients with hypertension, but it is unclear whether variations in sodium intake within the clinically observed range affect glucose tolerance. Sodium 48-54 insulin Homo sapiens 95-102 11465650-8 2001 Thus, an abundant sodium intake may improve glucose tolerance and insulin resistance, especially in diabetic, salt-sensitive, and or medicated essential hypertensive subjects. Sodium 18-24 insulin Homo sapiens 66-73 11399655-1 2001 Recent evidence suggests that endothelin-1 (ET-1), perhaps through the ET(B) receptor, may participate in blood pressure regulation through the control of sodium excretion. Sodium 155-161 endothelin 1 Rattus norvegicus 44-48 11458030-5 2001 Applying these insights to the far more common disorder of low renin hypertension may shed new light on the underlying pathophysiology of this common form of human hypertension, and more clearly define the interactions of dietary constituents such as sodium and potassium in the regulation of blood pressure. Sodium 251-257 renin Homo sapiens 63-68 11414310-2 2001 IGF-1 exerts important effects on renal hemodynamics and renal sodium handling. Sodium 63-69 insulin like growth factor 1 Homo sapiens 0-5 11382701-6 2001 This partial transection could permit vasopressin to be secreted in response to a larger rise in plasma sodium concentration. Sodium 104-110 arginine vasopressin Homo sapiens 38-49 11458695-8 2001 The responses to central administration of angiotensin II type AT1 receptor antagonists, into the ventricular system or microinjected into the rostral ventrolateral medulla, are modulated by changes in activity of the renin-angiotensin system produced by physiological changes in dietary sodium intake. Sodium 288-294 angiotensinogen Homo sapiens 43-57 11458695-8 2001 The responses to central administration of angiotensin II type AT1 receptor antagonists, into the ventricular system or microinjected into the rostral ventrolateral medulla, are modulated by changes in activity of the renin-angiotensin system produced by physiological changes in dietary sodium intake. Sodium 288-294 renin Homo sapiens 218-223 11414310-11 2001 Our findings support the hypothesis that the disturbance of the IGF-1/IGF-BP axis may be related to the degree of renal vasodilation and renal sodium retention in cirrhotic patients. Sodium 143-149 insulin like growth factor 1 Homo sapiens 64-69 11414310-10 2001 A negative correlation was found between IGF-1-IGF-BP index and fractional sodium excretion (P < 0.01) and between IGF-BP1 and urinary sodium excretion (P < 0.02). Sodium 75-81 insulin like growth factor 1 Homo sapiens 41-53 11373334-5 2001 Therefore, it was hypothesized that prostasin could activate sodium currents, and a rat prostasin cDNA clone was isolated to investigate its physiologic function. Sodium 61-67 serine protease 8 Rattus norvegicus 36-45 11382805-5 2001 Together with the determination of the sodium ion concentration and voltage dependence of the two-exponential charge movement and of the steady-state EAAC1 properties, we developed a kinetic model that is based on sequential binding of Na(+) and glutamate to their extracellular binding sites on EAAC1 explaining our results. Sodium 39-45 solute carrier family 1 member 1 Homo sapiens 150-155 11382805-6 2001 In this model, at least one Na(+) ion and thereafter glutamate rapidly bind to the transporter initiating a slower, electroneutral structural change that makes EAAC1 competent for further, voltage-dependent binding of additional sodium ion(s). Sodium 229-235 solute carrier family 1 member 1 Homo sapiens 160-165 11439314-6 2001 Insulin sensitivity (M-value) was correlated with PRA before euglycaemic hyperinsulinaemic clamping (r = 0.577, P < 0.05), and was also inversely correlated with fractional excretion of sodium (FE(Na)) before clamping (r = -0.51, P < 0.05). Sodium 189-195 insulin Homo sapiens 0-7 11408380-5 2001 ICV infusion of losartan (1 mg/h) significantly increased plasma renin in sodium-depleted sheep. Sodium 74-80 renin Ovis aries 65-70 11439314-0 2001 Correlation of sodium-related factors with insulin sensitivity in young, lean, male offspring of hypertensive and normotensive subjects. Sodium 15-21 insulin Homo sapiens 43-50 11373334-8 2001 Coexpression of rat prostasin and rat ENaC in Xenopus oocytes increased the amiloride-sensitive sodium current by twofold. Sodium 96-102 serine protease 8 Rattus norvegicus 20-29 11373334-8 2001 Coexpression of rat prostasin and rat ENaC in Xenopus oocytes increased the amiloride-sensitive sodium current by twofold. Sodium 96-102 sodium channel epithelial 1 subunit gamma Rattus norvegicus 38-42 11380824-8 2001 Moreover, on a normal and low sodium intake, these mice exhibited an increase in the number of AT1 receptors in renal tissues; their BP lowered markedly during the Ang II receptor blockade (P < 0.01) and there was a clear tendency for an increase in urinary aldosterone excretion. Sodium 30-36 angiotensin II receptor, type 1a Mus musculus 95-98 11412338-5 2001 Amplitudes of the angiotensin II-induced inward currents were decreased during perfusion with a low sodium medium. Sodium 100-106 angiotensinogen Rattus norvegicus 18-32 11350050-0 2001 Identification and characterization of a sodium/calcium exchanger, NCX-1, in osteoclasts and its role in bone resorption. Sodium 41-47 solute carrier family 8 member A1 Homo sapiens 67-72 11390024-2 2001 The infusion of AngII produced a significant elevation in mean arterial pressure (MAP) with an accompanying decrease in cortical blood flow, glomerular filtration rate (GFR), urine volume, and urine sodium excretion. Sodium 199-205 angiotensinogen Rattus norvegicus 16-21 11299228-0 2001 Endothelial function during stimulation of renin-angiotensin system by low-sodium diet in humans. Sodium 75-81 renin Homo sapiens 43-48 11299228-5 2001 The low-sodium diet resulted in significantly decreased urine sodium excretion (placebo: 146 +/- 64 vs. 10 +/- 9 meq/24 h, P < 0.001; losartan: 141 +/- 56 vs. 14 +/- 14 meq/24 h, P < 0.001) and increased plasma renin activity (placebo: 1.0 +/- 0.5 vs. 5.0 +/- 2.5 ng x ml(-1) x h(-1), P < 0.001; losartan: 3.8 +/- 7.2 vs. 19.1 +/- 11.2 ng x ml(-1) x h(-1), P = 0.006) in both the losartan and placebo groups. Sodium 8-14 renin Homo sapiens 217-222 11405245-12 2001 We propose that this prolactin-induced water secretion is probably mediated by recycling of luminal sodium in the vicinity of tight junctions. Sodium 100-106 prolactin Rattus norvegicus 21-30 11422008-9 2001 CONCLUSIONS: In CHF, ACE-inhibition attenuates the deterioration of pulmonary gas transfer produced by saline infusion, suggesting an ability to readjust the upregulated sodium transport across the pulmonary microvascular endothelium. Sodium 170-176 angiotensin I converting enzyme Homo sapiens 21-24 11411143-5 2001 County medium sodium concentrations ranged from 6-1170 mg L-1, with more than 90% of those values exceeding 20 mg L-1. Sodium 14-20 immunoglobulin kappa variable 1-16 Homo sapiens 58-61 11375422-0 2001 Regulated expression of claudin-4 decreases paracellular conductance through a selective decrease in sodium permeability. Sodium 101-107 claudin 4 Homo sapiens 24-33 11380518-17 2001 In conclusion, marked diuresis and natriuresis after AT1 receptor blockade and/or ACE inhibition suggest that the extent of endogenous AngII-mediated sodium transport under basal conditions is greatly augmented in OZR. Sodium 150-156 angiotensin I converting enzyme Rattus norvegicus 82-85 11380518-17 2001 In conclusion, marked diuresis and natriuresis after AT1 receptor blockade and/or ACE inhibition suggest that the extent of endogenous AngII-mediated sodium transport under basal conditions is greatly augmented in OZR. Sodium 150-156 angiotensinogen Rattus norvegicus 135-140 11294697-9 2001 After 5 days of ACE inhibition, urinary sodium returned to baseline values, while urinary dopamine was markedly reduced. Sodium 40-46 angiotensin I converting enzyme Homo sapiens 16-19 11318932-4 2001 The renin-angiotensin system plays a central role in this response and is balanced by developmental changes in the renal response to atrial natriuretic peptide, all of which contribute to sodium conservation. Sodium 188-194 renin Homo sapiens 4-9 11386017-4 2001 MATERIAL AND METHODS: AVP was measured under basal conditions and after stimulation with a low-sodium diet and upright position. Sodium 95-101 arginine vasopressin Homo sapiens 22-25 11287956-10 2001 Furthermore, we find that lim-6 is required for this functional asymmetry and for the ability to distinguish sodium from chloride. Sodium 109-115 LIM domain family Caenorhabditis elegans 26-31 11392001-4 2001 Insulin and leptin increase sympathetic tone which results in sodium retention and hyper-responsiveness of blood vessels. Sodium 62-68 insulin Homo sapiens 0-7 11358332-2 2001 Agonist binding affinities were regulated more robustly by sodium and guanine nucleotide in W284L/CHO than in hDOR/ CHO cell membranes. Sodium 59-65 tumor protein p53 inducible nuclear protein 2 Homo sapiens 110-114 11515306-2 2001 Six NHS, acting in CHF, have presently been identified: three of them induce vasoconstriction and sodium retention (sympathetic nervous systems, renin-angiotensin-aldosterone system and arginine-vasopressine system); the remaining three offset or balance the former ones, acting, therefore as "counterregulators" (prostaglandins--PGE2 and PGI2--, dopaminergic system and atrial natriuretic factor). Sodium 98-104 renin Homo sapiens 145-150 11321677-3 2001 We pointed out the crucial role of the insertion loop 186a-d and the I16-D194 ion pair in the stabilization of sodium binding pocket in thrombin. Sodium 111-117 coagulation factor II, thrombin Homo sapiens 136-144 11403985-2 2001 ANG II injection into the MSA induced water and sodium intake, diuresis, natriuresis, and pressor responses. Sodium 48-54 angiotensinogen Homo sapiens 0-6 11403985-4 2001 Previous injection of a nonselective alpha-adrenergic antagonist, regitin, into the PVN blocked the urinary excretion, and reduced the water and sodium intake, sodium intake, and pressor responses induced by ANG II injected into the MSA. Sodium 145-151 angiotensinogen Homo sapiens 208-214 11256986-1 2001 The activity of the erythrocyte transport system, sodium/lithium countertransport (SLC), has been linked to the metabolic syndrome characterized by insulin resistance and compensatory hyperinsulinaemia. Sodium 50-56 insulin Homo sapiens 148-155 11566009-2 2001 In the kidney, ET-1 not only produces vasoconstriction, but also vasodilation in the renal medulla, stimulation of sodium reabsorption in the proximal tubule, and inhibition of reabsorption in a variety of nephron segments. Sodium 115-121 endothelin 1 Homo sapiens 15-19 11274080-10 2001 Sodium content was detectably increased in lenses exposed to ET-1 for 24 hours. Sodium 0-6 endothelin 1 Homo sapiens 61-65 11284472-13 2001 Enhanced sodium-dependent brush border neutral amino acid transport with GH plus EGF administration is independent of increased ATB0 mRNA expression in rabbit small intestine after enterectomy. Sodium 9-15 somatotropin Oryctolagus cuniculus 73-75 11289956-1 2001 The conductance of sodium ions through a simplified channel-membrane system immersed in a reservoir of 1M NaCl in SPC/E water is examined by molecular dynamics simulation. Sodium 19-25 proline rich protein gene cluster Homo sapiens 114-117 11226092-0 2001 The release of antidiuretic hormone is appropriate in response to hypovolemia and/or sodium administration in children with severe head injury: a trial of lactated Ringer"s solution versus hypertonic saline. Sodium 85-91 arginine vasopressin Homo sapiens 15-35 11226092-10 2001 In a prospective, randomized, and controlled study in 31 children, we were able to show that the antidiuretic hormone levels are appropriate in response to hypovolemia, sodium load, or both. Sodium 169-175 arginine vasopressin Homo sapiens 97-117 11244019-1 2001 In hypertensive rats, environmental stress causes sodium retention by an exaggerated increase in renal sympathetic nerve activity, which is modulated by angiotensin II. Sodium 50-56 angiotensinogen Rattus norvegicus 153-167 11244019-5 2001 ACE inhibition corrected the natriuretic response to mental stress in subjects with mild essential hypertension (Deltaurinary sodium excretion, 0.05+/-0.14 mmol/min with placebo versus 0.13+/-0.19 mmol/min with ACE inhibition; P:<0.01); thus, after ACE inhibition, urinary sodium excretion increased similarly in all 3 groups. Sodium 126-132 angiotensin I converting enzyme Homo sapiens 0-3 11244019-5 2001 ACE inhibition corrected the natriuretic response to mental stress in subjects with mild essential hypertension (Deltaurinary sodium excretion, 0.05+/-0.14 mmol/min with placebo versus 0.13+/-0.19 mmol/min with ACE inhibition; P:<0.01); thus, after ACE inhibition, urinary sodium excretion increased similarly in all 3 groups. Sodium 276-282 angiotensin I converting enzyme Homo sapiens 0-3 11244019-7 2001 This abnormality in sodium handling during activation of the sympathetic nervous system appears to be mediated by angiotensin II. Sodium 20-26 angiotensinogen Homo sapiens 114-128 28095242-5 2001 In contrast, RAS blockade coupled with reduced sodium diet (0.2%) significantly regresses cardiac hypertrophy, impairs animal growth and is associated with elevated plasma renin and dramatically suppressed plasma angiotensinogen levels. Sodium 47-53 angiotensinogen Rattus norvegicus 213-228 11245677-11 2001 Rather, our results suggest that traumatic deformation of axons induces abnormal sodium influx through mechanically sensitive Na(+) channels, which subsequently triggers an increase in intra-axonal calcium via the opening of VGCCs and reversal of the Na(+)-Ca(2+) exchanger. Sodium 81-87 nascent polypeptide associated complex subunit alpha Homo sapiens 251-259 11248216-8 2001 These results indicate that cultures of human keratinocytes and melanocytes established from human skin and melanoma cells express the NHE-1 isoform of the sodium--hydrogen exchanger. Sodium 156-162 solute carrier family 9 member A1 Homo sapiens 135-140 11357900-3 2001 This review examines the role of the renal sodium pump (sodium, potassium-ATPase, NKA) in hypertension and its integration into mechanisms of body sodium balance. Sodium 43-49 tachykinin precursor 1 Homo sapiens 82-85 11325073-11 2001 4) Body mass index and the ratio of sodium to potassium excretion showed significant and positive associations with SBP and DBP in multiple linear regression analyses. Sodium 36-42 D-box binding PAR bZIP transcription factor Homo sapiens 124-127 11230513-9 2001 There is clear evidence that two systems contribute to basal membrane transport since BCH is (in sodium-free media) only a partial inhibitor whereas L-histidine and L-cysteine are fully effective. Sodium 97-103 NK2 homeobox 1 Homo sapiens 86-89 11230340-1 2001 Angiotensin (Ang) II is considered a regulatory hormone stimulating vascular smooth muscle cell constriction, aldosterone release from the adrenal gland, and sodium reabsorption in the renal tubule. Sodium 158-164 angiotensinogen Homo sapiens 0-20 11211621-0 2001 Influence of sodium intake on the reliability of active renin as a measure of the renin-angiotensin system in essential hypertension. Sodium 13-19 renin Homo sapiens 56-61 11239067-5 2001 RESULTS: AQP1 is located in the endothelium lining peritoneal capillaries, and its expression is remarkably stable in samples ranging from normal to highly inflamed peritoneum and even when transcellular water permeability is absent (loss of sodium sieving). Sodium 242-248 aquaporin 1 (Colton blood group) Homo sapiens 9-13 11292079-0 2001 The low-temperature- and salt-induced RCI2A gene of Arabidopsis complements the sodium sensitivity caused by a deletion of the homologous yeast gene SNA1. Sodium 80-86 Low temperature and salt responsive protein family Arabidopsis thaliana 38-43 11158268-6 2001 In NHE3 knockout mice three changes were identified which could compensate for the loss of NHE3-mediated sodium absorption. Sodium 105-111 solute carrier family 9 (sodium/hydrogen exchanger), member 3 Mus musculus 3-7 11158268-6 2001 In NHE3 knockout mice three changes were identified which could compensate for the loss of NHE3-mediated sodium absorption. Sodium 105-111 solute carrier family 9 (sodium/hydrogen exchanger), member 3 Mus musculus 91-95 11158268-13 2001 More extensive adaptation occurred in the case of the NHE3 knockout, presumably because NHE3 is responsible for much more sodium absorption in normal mice than in NCC knockout mice. Sodium 122-128 solute carrier family 9 (sodium/hydrogen exchanger), member 3 Mus musculus 54-58 11158268-13 2001 More extensive adaptation occurred in the case of the NHE3 knockout, presumably because NHE3 is responsible for much more sodium absorption in normal mice than in NCC knockout mice. Sodium 122-128 solute carrier family 9 (sodium/hydrogen exchanger), member 3 Mus musculus 88-92 11158210-3 2001 Thus, the hypothesis was that the abundance of one or more of the sodium transporters of the distal tubule (a site for fine tuning of sodium balance) would be altered during vasopressin escape. Sodium 66-72 arginine vasopressin Rattus norvegicus 174-185 11158210-13 2001 These data suggest that several distal sodium reabsorptive mechanisms are upregulated during vasopressin escape; this may help to attenuate the developing hyponatremia resulting from water loading when vasopressin levels are inappropriately elevated. Sodium 39-45 arginine vasopressin Rattus norvegicus 93-104 11158210-13 2001 These data suggest that several distal sodium reabsorptive mechanisms are upregulated during vasopressin escape; this may help to attenuate the developing hyponatremia resulting from water loading when vasopressin levels are inappropriately elevated. Sodium 39-45 arginine vasopressin Rattus norvegicus 202-213 11729869-7 2001 A persistent sodium current has been postulated to underlie the rhythm generating mechanism of pacemaker neurons within the pBc. Sodium 13-19 dihydrolipoamide S-acetyltransferase Homo sapiens 124-127 11729869-8 2001 In the present study, a substantial persistent sodium current was documented in many neurons from the pBc and adjacent respiratory regions. Sodium 47-53 dihydrolipoamide S-acetyltransferase Homo sapiens 102-105 11398906-6 2001 Low sodium diet and/or diuretic treatment may help to increase the antiproteinuric effect of ACE inhibitors by maximally activating the renin-angiotensin system. Sodium 4-10 angiotensin I converting enzyme Homo sapiens 93-96 11275626-7 2001 This assertion is borne out by recent clinical studies showing that the COX-2 inhibitors rofecoxib and celecoxib procedure qualitative changes in urinary prostaglandin excretion, glomerular filtration rate, sodium retention, and their consequences similar to nonselective NSAIDs. Sodium 207-213 mitochondrially encoded cytochrome c oxidase II Homo sapiens 72-77 11205704-3 2001 The renin-aldosterone system is a major determinant of sodium balance in pregnancy. Sodium 55-61 renin Homo sapiens 4-9 11136161-8 2001 Although glucocorticoids themselves produce no increase in sodium reabsorption in this segment, angiotensin II-stimulated sodium transport is significantly greater in proximal tubular cells pretreated with glucocorticoids. Sodium 122-128 angiotensinogen Homo sapiens 96-110 11333009-1 2001 Among the many roles that angiotensin II plays in the kidney, one of the most important is the direct and indirect regulation of sodium excretion. Sodium 129-135 angiotensinogen Homo sapiens 26-40 11333009-3 2001 High levels of angiotensin II subtype 1 receptors have been detected on the luminal side of the tubular cells in the proximal convoluted tubule, and these have been implicated in the regulation of sodium excretion. Sodium 197-203 angiotensinogen Homo sapiens 15-29 11333009-5 2001 It is, therefore, reasonable to assume that blockade of these receptors, using non-peptide angiotensin II receptor antagonists, will bring about an increase in renal excretion of sodium. Sodium 179-185 angiotensinogen Homo sapiens 91-105 11460589-14 2001 The genes coding for components of renin-angiotensin system have drawn special attention, due to the central role that this system plays in the regulation of blood pressure, sodium metabolism, and renal hemodynamics. Sodium 174-180 renin Homo sapiens 35-40 11223998-3 2001 Nevertheless, given the paramount importance of the renin-angiotensin system in the control of sodium balance, a most likely explanation is that the lower renin is a consequence of differences in renal sodium handling between blacks and whites. Sodium 95-101 renin Homo sapiens 52-57 11204290-1 2001 OBJECTIVE: Insulin-mediated vasodilation has been shown to be impaired with hypertension and aggravated by dietary sodium restriction. Sodium 115-121 insulin Homo sapiens 11-18 11204310-0 2001 Insulin resistance in hypertensives: effect of salt sensitivity, renin status and sodium intake. Sodium 82-88 insulin Homo sapiens 0-7 11327100-3 2001 It now appears clear that a central feature of obesity-associated hypertension is related to changes in sodium handling that may result from abnormalities in sympathetic nervous system activity, the renin-angiotensin-aldosterone system, natriuretic peptides, and kidney function. Sodium 104-110 renin Homo sapiens 199-204 11223998-3 2001 Nevertheless, given the paramount importance of the renin-angiotensin system in the control of sodium balance, a most likely explanation is that the lower renin is a consequence of differences in renal sodium handling between blacks and whites. Sodium 95-101 renin Homo sapiens 155-160 11223998-3 2001 Nevertheless, given the paramount importance of the renin-angiotensin system in the control of sodium balance, a most likely explanation is that the lower renin is a consequence of differences in renal sodium handling between blacks and whites. Sodium 202-208 renin Homo sapiens 155-160 11799919-6 2001 In contrast, the consensus site binding activity of AP-1 was inhibited only with sodium selenite, but not with p-XSC in vitro or in vivo. Sodium 81-87 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 52-56 21331734-2 2001 One major function is the reabsorption of sodium and other electrolytes which is caused, in part, by angiotensin II (Ang II), a peptide that is made up of eight amino acids. Sodium 42-48 angiotensinogen Homo sapiens 101-115 21331734-2 2001 One major function is the reabsorption of sodium and other electrolytes which is caused, in part, by angiotensin II (Ang II), a peptide that is made up of eight amino acids. Sodium 42-48 angiotensinogen Homo sapiens 117-123 11842872-3 2001 This review will discuss how the gustatory system is used by the rat to aid in the recovery from deficiencies of sodium, vitamin B, and individual essential amino acids. Sodium 113-119 activation-induced cytidine deaminase Rattus norvegicus 72-75 11315341-4 2001 Both non-selective Cox-inhibitors and selective Cox-2 inhibitors induce renal side effects including sodium retention and reduction of the glomerular filtration rate. Sodium 101-107 mitochondrially encoded cytochrome c oxidase II Homo sapiens 48-53 11517684-0 2001 [Effects of anti-atherosclerotic low-sodium diet on dynamics of natural antibodies to angiotensin II, bradykinin and vasopressin in blood of patients with hypertension and obesity]. Sodium 37-43 angiotensinogen Homo sapiens 86-100 11517684-0 2001 [Effects of anti-atherosclerotic low-sodium diet on dynamics of natural antibodies to angiotensin II, bradykinin and vasopressin in blood of patients with hypertension and obesity]. Sodium 37-43 kininogen 1 Homo sapiens 102-112 11517684-0 2001 [Effects of anti-atherosclerotic low-sodium diet on dynamics of natural antibodies to angiotensin II, bradykinin and vasopressin in blood of patients with hypertension and obesity]. Sodium 37-43 arginine vasopressin Homo sapiens 117-128 11162903-22 2000 In both types of homeostasis, the calcium and sodium overload is avoided by opening of K+ voltage- and Ca-dependent channels, and by increase in activities of Na+/K+ ATPase and forward mode of Na+/Ca2+ exchanger. Sodium 46-52 solute carrier family 8 member A1 Homo sapiens 193-211 11078175-3 2000 The effect of dihydropyridine calcium blocking drugs is relatively independent of sodium intake, whereas the angiotensin-converting enzyme (ACE) inhibitors" effects can be blunted by a high-sodium diet. Sodium 190-196 angiotensin I converting enzyme Homo sapiens 109-138 11130776-2 2000 This association causes the following changes: insulin and leptin resistance with a suppressed biologic activity of natriuretic peptide, which contributes to sodium retention with concomitant expanded cardiopulmonary volume and increased cardiac output. Sodium 158-164 insulin Homo sapiens 47-54 11116129-9 2000 The responses to central administration of angiotensin II-type AT(1)-receptor antagonists into the ventricular system or microinjected into the rostral ventrolateral medulla are modulated by changes in activity of the renin-angiotensin system produced by physiological changes in dietary sodium intake. Sodium 288-294 angiotensinogen Homo sapiens 43-57 11116129-9 2000 The responses to central administration of angiotensin II-type AT(1)-receptor antagonists into the ventricular system or microinjected into the rostral ventrolateral medulla are modulated by changes in activity of the renin-angiotensin system produced by physiological changes in dietary sodium intake. Sodium 288-294 renin Homo sapiens 218-223 11078175-3 2000 The effect of dihydropyridine calcium blocking drugs is relatively independent of sodium intake, whereas the angiotensin-converting enzyme (ACE) inhibitors" effects can be blunted by a high-sodium diet. Sodium 190-196 angiotensin I converting enzyme Homo sapiens 140-143 11078175-11 2000 In patients taking amlodipine, the fall in plasma renin ameliorates the effect of sodium retention on BP. Sodium 82-88 renin Homo sapiens 50-55 11082136-1 2000 In a previous study, by using a candidate gene approach, we detected in both Milan hypertensive rats and humans a polymorphism in the alpha-adducin gene (ADD1) that was associated with blood pressure and renal sodium handling. Sodium 210-216 adducin 1 Homo sapiens 134-147 11079680-5 2000 RESULTS: Plasma BNP and 3",5"-cyclic guanosine monophosphate rapidly increased and peaked at 30 min after acute SQBNP administration with increases in urinary sodium excretion, urine flow and renal blood flow in association with reductions in cardiac filling pressures. Sodium 159-165 natriuretic peptide B Canis lupus familiaris 16-19 11078386-5 2000 Both ET-1 and glucocorticoids exert direct effects in the kidney and are involved in vascular resistance and sodium balance. Sodium 109-115 endothelin 1 Rattus norvegicus 5-9 11078416-3 2000 Intravenous ET-1 infusion in the presence of enrasentan at 30 microg/kg/min, resulted in an increase in renal plasma flow and sodium excretion; however, at a higher infusion rate (100 microg/kg/min) no renal vasodilation or natriuresis was observed. Sodium 126-132 endothelin 1 Canis lupus familiaris 12-16 11102561-6 2000 Animal experiments and clinical trials with preferential and specific COX-2 inhibitors revealed that COX-2 is the critical enzyme for sodium excretion, renin release and likely antagonism of antidiuretic hormone. Sodium 134-140 mitochondrially encoded cytochrome c oxidase II Homo sapiens 70-75 11102561-6 2000 Animal experiments and clinical trials with preferential and specific COX-2 inhibitors revealed that COX-2 is the critical enzyme for sodium excretion, renin release and likely antagonism of antidiuretic hormone. Sodium 134-140 mitochondrially encoded cytochrome c oxidase II Homo sapiens 101-106 11102561-9 2000 In summary, the gain of renal safety by use of preferential or specific COX-2 inhibitors is small or negligible with respect to sodium retention, hyperkalemia and probably water intoxication. Sodium 128-134 mitochondrially encoded cytochrome c oxidase II Homo sapiens 72-77 11082136-1 2000 In a previous study, by using a candidate gene approach, we detected in both Milan hypertensive rats and humans a polymorphism in the alpha-adducin gene (ADD1) that was associated with blood pressure and renal sodium handling. Sodium 210-216 adducin 1 Homo sapiens 154-158 11082152-3 2000 To make that comparison, we studied healthy volunteers in balance on a 10-mmol sodium intake to activate the renin system. Sodium 79-85 renin Homo sapiens 109-114 11096291-7 2000 Urinary excretion levels of mAM significantly correlated with those of sodium (r = 0. Sodium 71-77 activating transcription factor 7 interacting protein Mus musculus 28-31 11081765-2 2000 A diminished capacity to excrete sodium secondary to increased proximal tubular re-absorption and loss of the renal functional reserve are the two most relevant initial alterations of renal function in which angiotensin II has been proven to act directly. Sodium 33-39 angiotensinogen Homo sapiens 208-222 11036156-0 2000 Effects of subtypes alpha- and beta-adrenoceptors of the lateral hypothalamus on the water and sodium intake induced by angiotensin II injected into the subfornical organ. Sodium 95-101 angiotensinogen Rattus norvegicus 120-134 11036156-3 2000 These data show that injection of 5-methylurapidil into the LH prior to ANG II into the SFO increased the water and sodium intake induced by the injection of ANG II. Sodium 116-122 angiotensinogen Rattus norvegicus 158-164 11036156-5 2000 Thus, the alpha(1)- and beta-adrenoceptors of the LH are possibly involved with central mechanisms dependent on ANG II and SFO that control water and sodium intake. Sodium 150-156 angiotensinogen Rattus norvegicus 112-118 11011335-1 2000 BACKGROUND: Recent studies have shown that endothelin-1 (ET-1) antagonists increase sodium excretion and improve renal blood flow in experimental heart failure (HF). Sodium 84-90 endothelin 1 Homo sapiens 43-55 11027237-7 2000 These findings suggest that the Na(v)2 channel plays an important role in the central sensing of body-fluid sodium level and regulation of salt intake behavior. Sodium 108-114 neuron navigator 2 Mus musculus 32-38 11011335-1 2000 BACKGROUND: Recent studies have shown that endothelin-1 (ET-1) antagonists increase sodium excretion and improve renal blood flow in experimental heart failure (HF). Sodium 84-90 endothelin 1 Homo sapiens 57-61 11011335-3 2000 Our aim was to investigate renal ET-1 formation and its relation to sodium excretion in patients with HF. Sodium 68-74 endothelin 1 Homo sapiens 33-37 11011335-8 2000 In the 71 subjects who were not receiving diuretic treatment, urinary ET-1 was selected as the strongest predictor of sodium excretion by multivariate stepwise analysis. Sodium 118-124 endothelin 1 Homo sapiens 70-74 11011335-9 2000 CONCLUSIONS: Urinary ET-1 excretion increases in an earlier phase of HF than plasma ET-1 and appears to be closely correlated with sodium excretion, indicating renal ET-1 is a target for ET-1 antagonists in patients with HF. Sodium 131-137 endothelin 1 Homo sapiens 21-25 11035341-0 2000 A simplified index of the plasma sodium threshold for arginine vasopressin secretion-morning fasting, euhydrated sodium levels. Sodium 33-39 arginine vasopressin Homo sapiens 63-74 11003597-6 2000 SIN-1 treatment resulted in a prolonged increase in cystine uptake beginning at 6-9 h. Increases in cystine uptake after SIN-1 were blocked by inhibitors of protein and RNA synthesis, by extracellular glutamate but not by extracellular sodium. Sodium 236-242 MAPK associated protein 1 Homo sapiens 0-5 11035341-16 2000 CONCLUSIONS: The morning fasting, euhydrated sodium level can be used as a simplified index for the plasma osmotic threshold for arginine vasopressin secretion. Sodium 45-51 arginine vasopressin Homo sapiens 138-149 11061347-3 2000 In short-term clinical studies, very low sodium intake (<50 mmol/d) has been associated with greater values for total and low-density lipoprotein cholesterol, fasting and post-glucose insulin, uric acid, plasminogen activator inhibitor-1, and activity of the renin-angiotensin system. Sodium 41-47 renin Homo sapiens 262-267 19003375-1 2000 Sodium-dependent uptake of bile acids from blood is aliver-specific function which is mediated by theNa(+)-taurocholate cotransporting polypeptide(Ntcp). Sodium 0-6 solute carrier family 10 member 1 Homo sapiens 147-151 11001247-0 2000 Low serum sodium concentrations during treatment with citalopram in elderly patients: relationship to serum citalopram levels and to platelet serotonin 5-HT2A receptor status. Sodium 10-16 5-hydroxytryptamine receptor 2A Homo sapiens 142-167 11040234-10 2000 These results indicate that activation of sensory nerves, either by Ang II or by other hormonal or hemodynamic factors, plays a compensatory role in promoting urine and sodium excretion and attenuating elevated blood pressure initiated by Ang II. Sodium 169-175 angiotensinogen Rattus norvegicus 68-74 11213538-3 2000 The second part reviews the four factors frequently cited as possible causes for this sodium retention: insulin resistance, alteration in the renin-angiotensin system, altered vascular responsiveness and alterations in the sympathetic nervous system. Sodium 86-92 insulin Homo sapiens 104-111 11350495-12 2000 These data show that in this sodium deficient renovascular model of hypertension, blockade of angiotensin II receptors normalizes blood pressure but causes renal failure, whereas the vasodepressor action of the clonidine analogue AL-12 occurs without detriment to renal function. Sodium 29-35 angiotensinogen Rattus norvegicus 94-108 11213538-3 2000 The second part reviews the four factors frequently cited as possible causes for this sodium retention: insulin resistance, alteration in the renin-angiotensin system, altered vascular responsiveness and alterations in the sympathetic nervous system. Sodium 86-92 renin Homo sapiens 142-147 11213538-5 2000 CONCLUSIONS: There is clearly a strong relationship between obesity hypertension, sodium sensitivity and insulin resistance. Sodium 82-88 insulin Homo sapiens 105-112 11175566-1 2000 OBJECTIVE: The aims of this article are to verify if there is any alteration in the secretion of natriuretic atrial factor (NAF) in children submitted to mechanical pulmonary ventilation and if these possible alterations would lead to modification in the urinary volume and in the urinary sodium excretion. Sodium 289-295 C-X-C motif chemokine ligand 8 Homo sapiens 97-122 11049696-1 2000 INTRODUCTION: Dietary sodium restriction results in activation of the renin-angiotensin-aldosterone-system. Sodium 22-28 renin Homo sapiens 70-75 11175566-1 2000 OBJECTIVE: The aims of this article are to verify if there is any alteration in the secretion of natriuretic atrial factor (NAF) in children submitted to mechanical pulmonary ventilation and if these possible alterations would lead to modification in the urinary volume and in the urinary sodium excretion. Sodium 289-295 C-X-C motif chemokine ligand 8 Homo sapiens 124-127 10842183-4 2000 The reversal potential of the ASIC2a+3 current (>/=+20 mV) reflected a cationic current mainly selective for sodium. Sodium 112-118 acid sensing ion channel subunit 2 Homo sapiens 30-36 11049696-2 2000 In the non-pregnant situation renin release in response to a low sodium diet is mediated by prostaglandins. Sodium 65-71 renin Homo sapiens 30-35 10973807-6 2000 moat1 transports prostaglandin D(2) (K(m); 35.5 nM), leukotriene C(4) (K(m); 3.2 microM) and taurocholate (K(m); 17.6 microM) in a sodium-independent manner. Sodium 131-137 solute carrier organic anion transporter family, member 2b1 Rattus norvegicus 0-5 10821834-6 2000 Whole cell macroscopic sodium currents revealed that wild type (wt) alphabetagamma-rENaC-induced Na(+) current was inhibited by co-expression of CFTR, and further inhibited when CFTR was activated with a cAMP-raising mixture (CKT). Sodium 23-29 sodium channel epithelial 1 subunit gamma Rattus norvegicus 83-88 10981548-1 2000 Angiotensin II regulates sodium homeostasis by modulating aldosterone secretion, renal vascular response, and tubular sodium reabsorption. Sodium 25-31 angiotensinogen Homo sapiens 0-14 10981548-1 2000 Angiotensin II regulates sodium homeostasis by modulating aldosterone secretion, renal vascular response, and tubular sodium reabsorption. Sodium 118-124 angiotensinogen Homo sapiens 0-14 10981548-6 2000 Sodium excretion in response to 3.0 ng/kg/min angiotensin II was diminished in both groups (P < .01). Sodium 0-6 angiotensinogen Homo sapiens 46-60 10981548-8 2000 We conclude that increased sodium retention in response to angiotensin II exists in subjects with essential hypertension, which is unrelated to changes in glomerular filtration rate and aldosterone concentration. Sodium 27-33 angiotensinogen Homo sapiens 59-73 10981548-9 2000 Our data suggest a hyperresponsiveness to angiotensin II in essential hypertension that could lead to increased sodium retention. Sodium 112-118 angiotensinogen Homo sapiens 42-56 10986156-10 2000 Furthermore, dietary sodium restriction and diuretic therapy raise PRA and improve the response to ACE inhibitors. Sodium 21-27 angiotensin I converting enzyme Homo sapiens 99-102 11787472-1 2000 Gastric sodium loading results in an increase in the portal venous concentration of vasoactive intestinal peptide (VIP) and down-regulation of both the intrahepatic and circulating renin-angiotensin systems. Sodium 8-14 vasoactive intestinal peptide Rattus norvegicus 115-118 11787472-10 2000 These changes are similar to those reported after gastric sodium loading, and we suggest, therefore, that the increase in portal venous VIP that occurs after gastric sodium is the means by which the gastric sodium sensor signals the liver to effect these changes in the renin-angiotensin system. Sodium 58-64 vasoactive intestinal peptide Rattus norvegicus 136-139 11787472-10 2000 These changes are similar to those reported after gastric sodium loading, and we suggest, therefore, that the increase in portal venous VIP that occurs after gastric sodium is the means by which the gastric sodium sensor signals the liver to effect these changes in the renin-angiotensin system. Sodium 166-172 vasoactive intestinal peptide Rattus norvegicus 136-139 11787472-10 2000 These changes are similar to those reported after gastric sodium loading, and we suggest, therefore, that the increase in portal venous VIP that occurs after gastric sodium is the means by which the gastric sodium sensor signals the liver to effect these changes in the renin-angiotensin system. Sodium 166-172 vasoactive intestinal peptide Rattus norvegicus 136-139 10975407-3 2000 In a medium of Sodium, Potassium, and Magnesium [NKM] that supported active sperm motility, pHi was 6.9. Sodium 15-21 glucose-6-phosphate isomerase Bos taurus 92-95 10988274-0 2000 Angiotensin II sensitivity is associated with the angiotensin II type 1 receptor A(1166)C polymorphism in essential hypertensives on a high sodium diet. Sodium 140-146 angiotensinogen Homo sapiens 0-14 10988274-0 2000 Angiotensin II sensitivity is associated with the angiotensin II type 1 receptor A(1166)C polymorphism in essential hypertensives on a high sodium diet. Sodium 140-146 angiotensinogen Homo sapiens 50-64 10999820-2 2000 Renin suppression is due to aldosterone-dependent sodium retention and mild extracellular volume expansion. Sodium 50-56 renin Homo sapiens 0-5 11881033-1 2000 We have documented, contrary to expectation, that the renin-angiotensin-aldosterone system (RAAS) is stimulated normally by restriction of sodium intake inpatients with Type 2 diabetes mellitus (DM) and hypertension. Sodium 139-145 renin Homo sapiens 54-59 10994750-1 2000 OBJECTIVE: To examine the interaction of sodium intake with genetic variations of the angiotensinogen gene and hypertension. Sodium 41-47 angiotensinogen Homo sapiens 86-101 10994750-12 2000 CONCLUSION: Angiotensinogen genotype may affect the development of early-onset hypertension among Japanese, particularly in those who have a high sodium intake. Sodium 146-152 angiotensinogen Homo sapiens 12-27 11108153-2 2000 Recent studies showed that changes in Ang II receptor expression occur and underlie changes in the function of proximal tubules during altered sodium intake. Sodium 143-149 angiotensinogen Rattus norvegicus 38-44 11108153-3 2000 The present experiment was designed to determine (1) whether expression of the type 1 Ang II (AT1) receptor in the MTAL is regulated by altered sodium intake, and (2) the specific pathway(s) mediating sodium-induced AT1 expression in the MTAL. Sodium 144-150 angiotensinogen Rattus norvegicus 86-92 11108153-3 2000 The present experiment was designed to determine (1) whether expression of the type 1 Ang II (AT1) receptor in the MTAL is regulated by altered sodium intake, and (2) the specific pathway(s) mediating sodium-induced AT1 expression in the MTAL. Sodium 201-207 angiotensinogen Rattus norvegicus 86-92 11108153-13 2000 We conclude that (1) sodium restriction but not sodium loading increases AT1 receptor expression in the MTAL, (2) low sodium-induced upregulation of the AT1 receptor in the MTAL is Ang II-dependent, and (3) Ang II-induced upregulation of the AT1 receptor in the MTAL is mediated, at least in part, by cytochrome P450 pathways. Sodium 21-27 angiotensinogen Rattus norvegicus 181-187 11022893-3 2000 Under physiologic conditions, angiotensin II (Ang II) is important in causing the long-term relationship between arterial pressure and sodium excretion to be very steep, so that minimal changes in arterial pressure are necessary to maintain sodium balance in response to variations in sodium intake. Sodium 135-141 angiotensinogen Homo sapiens 30-44 11022893-3 2000 Under physiologic conditions, angiotensin II (Ang II) is important in causing the long-term relationship between arterial pressure and sodium excretion to be very steep, so that minimal changes in arterial pressure are necessary to maintain sodium balance in response to variations in sodium intake. Sodium 135-141 angiotensinogen Homo sapiens 46-52 11022893-3 2000 Under physiologic conditions, angiotensin II (Ang II) is important in causing the long-term relationship between arterial pressure and sodium excretion to be very steep, so that minimal changes in arterial pressure are necessary to maintain sodium balance in response to variations in sodium intake. Sodium 241-247 angiotensinogen Homo sapiens 30-44 11022893-3 2000 Under physiologic conditions, angiotensin II (Ang II) is important in causing the long-term relationship between arterial pressure and sodium excretion to be very steep, so that minimal changes in arterial pressure are necessary to maintain sodium balance in response to variations in sodium intake. Sodium 241-247 angiotensinogen Homo sapiens 46-52 11022893-3 2000 Under physiologic conditions, angiotensin II (Ang II) is important in causing the long-term relationship between arterial pressure and sodium excretion to be very steep, so that minimal changes in arterial pressure are necessary to maintain sodium balance in response to variations in sodium intake. Sodium 241-247 angiotensinogen Homo sapiens 30-44 11022893-3 2000 Under physiologic conditions, angiotensin II (Ang II) is important in causing the long-term relationship between arterial pressure and sodium excretion to be very steep, so that minimal changes in arterial pressure are necessary to maintain sodium balance in response to variations in sodium intake. Sodium 241-247 angiotensinogen Homo sapiens 46-52 11022893-4 2000 An inability to suppress Ang II formation in response to increases in sodium intake can lead to salt-sensitive hypertension. Sodium 70-76 angiotensinogen Homo sapiens 25-31 11022893-5 2000 Excess formation of Ang II, such as in renovascular hypertension, causes the pressure natriuresis relationship to be shifted to higher arterial pressures so that higher arterial pressures are necessary to maintain sodium balance. Sodium 214-220 angiotensinogen Homo sapiens 20-26 11022893-7 2000 Because Ang II does not decrease glomerular filtration in most circumstances, the sodium retaining actions of Ang II are usually caused by increased tubular reabsorption. Sodium 82-88 angiotensinogen Homo sapiens 110-116 10919852-12 2000 These findings demonstrate that chronic ANG II infusion leads to marked impairment of sodium excretion and suppression of the pressure-natriuresis relationship, which may contribute to the progressive hypertension that occurs in this model. Sodium 86-92 angiotensinogen Rattus norvegicus 40-46 10919848-10 2000 These data support a substantive role for BK potentiation during ACE inhibitor-induced renal vasodilation in dogs maintained on a low-sodium diet, with a relatively greater effect on MBF compared to CBF. Sodium 134-140 kininogen 1 Canis lupus familiaris 42-44 10871427-11 2000 Sodium selenite at this dose increased the production of proinflammatory cytokines, tumor necrosis factor alpha and interleukin-1 beta, in lipopolysaccharide-stimulated splenic macrophages. Sodium 0-6 tumor necrosis factor Mus musculus 84-111 10871427-11 2000 Sodium selenite at this dose increased the production of proinflammatory cytokines, tumor necrosis factor alpha and interleukin-1 beta, in lipopolysaccharide-stimulated splenic macrophages. Sodium 0-6 interleukin 1 beta Mus musculus 116-134 10974488-0 2000 Participation of alpha-1 and alpha-2 adrenoceptors of the lateral hypothalamic area in water intake, and renal sodium, potassium and urinary volume excretion induced by central administration of angiotensin II. Sodium 111-117 angiotensinogen Rattus norvegicus 195-209 10971624-4 2000 LqhII strongly inhibits sodium current inactivation of brain rBII subtype expressed in HEK293 cells, whereas LqhIII is weakly active at 2 microM, suggesting that LqhIII affects sodium channel subtypes other than rBII in the brain. Sodium 24-30 calcium voltage-gated channel subunit alpha1 E Rattus norvegicus 61-65 10974488-8 2000 The injection of ANGII into the LV reduced the sodium, potassium and urinary volume. Sodium 47-53 angiotensinogen Rattus norvegicus 17-22 10974488-9 2000 Previous treatment with clonidine attenuated the action of ANGII in reducing the sodium, potassium and urinary volume, whereas previous treatment with yohimbine attenuated the effects of ANGII but with less intensity than that caused by clonidine. Sodium 81-87 angiotensinogen Rattus norvegicus 59-64 10948075-2 2000 The dopamine D1 receptor (DRD1) has been localized to the proximal tubules and is known to increase sodium excretion by inhibiting Na-H exchanger and Na,K-ATPase activity. Sodium 100-106 dopamine receptor D1 Homo sapiens 4-24 10948075-2 2000 The dopamine D1 receptor (DRD1) has been localized to the proximal tubules and is known to increase sodium excretion by inhibiting Na-H exchanger and Na,K-ATPase activity. Sodium 100-106 dopamine receptor D1 Homo sapiens 26-30 10906163-7 2000 Infusion of ET-1 significantly decreased effective renal plasma flow, GFR, sodium excretion, and urine flow. Sodium 75-81 endothelin 1 Homo sapiens 12-16 10954007-1 2000 BACKGROUND: Additive hemodynamic effects of combined blockade of the renin-angiotensin system by an angiotensin I converting enzyme inhibitor and an angiotensin II antagonist have been observed in sodium-depleted normotensive volunteers and in patients with congestive heart failure. Sodium 197-203 renin Homo sapiens 69-74 10954007-1 2000 BACKGROUND: Additive hemodynamic effects of combined blockade of the renin-angiotensin system by an angiotensin I converting enzyme inhibitor and an angiotensin II antagonist have been observed in sodium-depleted normotensive volunteers and in patients with congestive heart failure. Sodium 197-203 angiotensinogen Homo sapiens 100-113 10954002-7 2000 In the cortex (C) and inner stripe (IS), the high sodium diet decreased AT1A and AT1B mRNAs in SBH/y and SBN/y, with a higher magnitude for SBH/y, than for SBN/y (C, -28 versus -20%; IS, -42 versus -20%). Sodium 50-56 angiotensin II receptor, type 1b Rattus norvegicus 81-85 10954002-9 2000 CONCLUSION: A high sodium diet significantly decreases both AT1A and AT1B gene expression in two specific zones of the rat kidney containing the target cells of angiotensin II (C and IS). Sodium 19-25 angiotensin II receptor, type 1b Rattus norvegicus 69-73 10954002-9 2000 CONCLUSION: A high sodium diet significantly decreases both AT1A and AT1B gene expression in two specific zones of the rat kidney containing the target cells of angiotensin II (C and IS). Sodium 19-25 angiotensinogen Rattus norvegicus 161-175 10812199-4 2000 About 80% of the sodium-dependent uptake was mediated by system ASC, which differed from system ASC common to other CNS- and non-CNS tissues by its pH-dependence and partial lithium tolerance. Sodium 17-23 PYD and CARD domain containing Homo sapiens 64-67 10812199-7 2000 The sodium-independent glutamine uptake differed from the astrocytic or neuronal uptake in its relatively weak inhibition by system L substrates and a strong inhibition by system ASC substrates, indicating a possible contribution of a variant of the ASC system. Sodium 4-10 PYD and CARD domain containing Homo sapiens 179-182 10812199-7 2000 The sodium-independent glutamine uptake differed from the astrocytic or neuronal uptake in its relatively weak inhibition by system L substrates and a strong inhibition by system ASC substrates, indicating a possible contribution of a variant of the ASC system. Sodium 4-10 PYD and CARD domain containing Homo sapiens 250-253 10894793-5 2000 Urinary ET-1-like immunoreactivity significantly increased from the second day in the DOCA-Salt group and correlated well with the urinary sodium excretion rate (r = 0.81, P < 0.001). Sodium 139-145 endothelin 1 Rattus norvegicus 8-12 10894786-1 2000 Sodium transport is increased by vasopressin in the cortical collecting ducts of rats and rabbits. Sodium 0-6 arginine vasopressin Rattus norvegicus 33-44 10953327-7 2000 Only a minor degree of inhibition of melphalan transport was noted after sodium depletion (System ASC, which is sodium dependent and unaffected by BCH). Sodium 73-79 PYD and CARD domain containing Homo sapiens 98-101 10894786-6 2000 These changes are too slow to play a major role in the short-term action of vasopressin to stimulate sodium reabsorption in the collecting duct. Sodium 101-107 arginine vasopressin Rattus norvegicus 76-87 10953327-7 2000 Only a minor degree of inhibition of melphalan transport was noted after sodium depletion (System ASC, which is sodium dependent and unaffected by BCH). Sodium 112-118 PYD and CARD domain containing Homo sapiens 98-101 11174896-1 2000 Low-renin hypertension is common and usually implies increased retention of sodium (Na(+)). Sodium 76-82 renin Homo sapiens 4-9 10859154-2 2000 Transport of the angiotensin converting enzyme inhibitor enalapril (1-750 microM with [(3)H]enalapril), a substrate of Oatp1, the sodium-independent organic anion transporting polypeptide 1 cloned from rat liver, was studied in rat hepatocytes isolated from all zones of the liver (homogeneous) and from enriched periportal (PP) and perivenous (PV) hepatocytes prepared by collagenase perfusion and zone-selective destruction with digitonin, respectively. Sodium 130-136 solute carrier organic anion transporter family, member 1a1 Rattus norvegicus 149-189 10859154-2 2000 Transport of the angiotensin converting enzyme inhibitor enalapril (1-750 microM with [(3)H]enalapril), a substrate of Oatp1, the sodium-independent organic anion transporting polypeptide 1 cloned from rat liver, was studied in rat hepatocytes isolated from all zones of the liver (homogeneous) and from enriched periportal (PP) and perivenous (PV) hepatocytes prepared by collagenase perfusion and zone-selective destruction with digitonin, respectively. Sodium 130-136 solute carrier organic anion transporter family, member 1a1 Rattus norvegicus 119-124 10869292-5 2000 In contrast, sodium-independent taurocholate uptake mediated by the organic anion transporting polypeptides, Oatp1 and Oatp2, was already substantially inhibited by 10 micromol/L rifamycin SV. Sodium 13-19 solute carrier organic anion transporter family, member 1a1 Rattus norvegicus 109-114 10912764-8 2000 Functionally, ANG II infused rats demonstrate reduced sodium excretion and marked suppression of pressure natriuresis. Sodium 54-60 angiotensinogen Rattus norvegicus 14-20 10904025-8 2000 Our study indicates that the bradykinin B(2) receptor antagonist icatibant attenuates the short-term blood pressure-lowering effect of acute ACE inhibition in normal men on a normal sodium diet. Sodium 182-188 kininogen 1 Homo sapiens 29-39 10912764-16 2000 The augmented intrarenal ANG II coupled with sustained levels of AT1 receptors contribute to the continued ANG II dependent suppression of renal function and sodium excretion thereby maintaining the hypertension. Sodium 158-164 angiotensinogen Rattus norvegicus 25-31 10912764-16 2000 The augmented intrarenal ANG II coupled with sustained levels of AT1 receptors contribute to the continued ANG II dependent suppression of renal function and sodium excretion thereby maintaining the hypertension. Sodium 158-164 angiotensinogen Rattus norvegicus 107-113 10759607-1 2000 Changes in angiotensin-converting enzyme (ACE) activity appear to be important in mediating the natriuresis which ensues after administration of an oral or gastric sodium load. Sodium 164-170 angiotensin I converting enzyme Rattus norvegicus 11-40 11048827-4 2000 CONCLUSIONS: The lower resistance indices of the uterine artery during sodium restriction might reflect an increase in pulse pressure/impedance ratio as a result of activation of the renin-angiotensin system. Sodium 71-77 renin Homo sapiens 183-188 10777497-0 2000 Psr1p/Psr2p, two plasma membrane phosphatases with an essential DXDX(T/V) motif required for sodium stress response in yeast. Sodium 93-99 putative phosphatase Saccharomyces cerevisiae S288C 6-11 10777497-2 2000 In this study, we report the identification of two previously uncharacterized genes, PSR1 and PSR2, that perform an essential function under conditions of sodium ion stress in the yeast Saccharomyces cerevisiae. Sodium 155-161 putative phosphatase Saccharomyces cerevisiae S288C 94-98 10912749-0 2000 Molecular variations in the calcium-sensing receptor in relation to sodium balance and presence of hypertension in blacks and whites. Sodium 68-74 calcium sensing receptor Homo sapiens 28-52 10912758-6 2000 The alpha-adducin gene remained a significant independent predictor of hypertension in a multivariate logistic model even after correcting for other risk factors for hypertension, including gender, age, body mass index (BMI), smoking, LDL cholesterol, triglycerides, urine sodium (Na), and urine potassium (K), (OR = 1.55, 95% CI = 1.03, 2.34). Sodium 273-279 adducin 1 Homo sapiens 4-17 10886360-9 2000 This finding demonstrates that the mGluR1-mediated postsynaptic current leads to a significant influx of sodium into the dendritic cytoplasm of Purkinje cells and thereby provides a novel intracellular signalling mechanism that might be involved in mGluR1-dependent synaptic plasticity at this synapse. Sodium 105-111 glutamate metabotropic receptor 1 Rattus norvegicus 35-41 10886360-9 2000 This finding demonstrates that the mGluR1-mediated postsynaptic current leads to a significant influx of sodium into the dendritic cytoplasm of Purkinje cells and thereby provides a novel intracellular signalling mechanism that might be involved in mGluR1-dependent synaptic plasticity at this synapse. Sodium 105-111 glutamate metabotropic receptor 1 Rattus norvegicus 249-255 10894022-5 2000 The renal sodium retention in congestive heart failure is a consequence of the activation of the sympathetic nervous system and of the renin-angiotensin-aldosterone system. Sodium 10-16 renin Homo sapiens 135-140 10759607-1 2000 Changes in angiotensin-converting enzyme (ACE) activity appear to be important in mediating the natriuresis which ensues after administration of an oral or gastric sodium load. Sodium 164-170 angiotensin I converting enzyme Rattus norvegicus 42-45 10759607-2 2000 In this study, we sought to determine the time course of the changes in ACE activity in the kidney which occur after sodium ingestion. Sodium 117-123 angiotensin I converting enzyme Rattus norvegicus 72-75 10759607-4 2000 Angiotensin-converting enzyme activity was measured by generation of histidyl-leucine in homogenates of kidneys harvested at varying time-points after gastric sodium administration. Sodium 159-165 angiotensin I converting enzyme Rattus norvegicus 0-29 10759607-6 2000 Intragastric instillation of both the sodium-containing solution and its iso-osmotic urea control solution resulted in significant increases in renal ACE activity (NaCl: P < 0.0005; Urea: P < 0.01). Sodium 38-44 angiotensin I converting enzyme Rattus norvegicus 150-153 10759607-7 2000 The increase in renal ACE activity after gastric sodium loading was more prolonged than after the urea control (P < 0.025, NaCl vs. urea at 90 min). Sodium 49-55 angiotensin I converting enzyme Rattus norvegicus 22-25 10759607-8 2000 This prolonged increase in renal ACE activity appeared to reflect a response to absorbed sodium as intravenous sodium administration caused a significant increase in renal ACE activity at 90 min (P < 0.0005). Sodium 89-95 angiotensin I converting enzyme Rattus norvegicus 33-36 10759607-8 2000 This prolonged increase in renal ACE activity appeared to reflect a response to absorbed sodium as intravenous sodium administration caused a significant increase in renal ACE activity at 90 min (P < 0.0005). Sodium 89-95 angiotensin I converting enzyme Rattus norvegicus 172-175 10759607-8 2000 This prolonged increase in renal ACE activity appeared to reflect a response to absorbed sodium as intravenous sodium administration caused a significant increase in renal ACE activity at 90 min (P < 0.0005). Sodium 111-117 angiotensin I converting enzyme Rattus norvegicus 33-36 10759607-8 2000 This prolonged increase in renal ACE activity appeared to reflect a response to absorbed sodium as intravenous sodium administration caused a significant increase in renal ACE activity at 90 min (P < 0.0005). Sodium 111-117 angiotensin I converting enzyme Rattus norvegicus 172-175 10759607-10 2000 We conclude that gastric sodium loading increases renal ACE activity. Sodium 25-31 angiotensin I converting enzyme Rattus norvegicus 56-59 10907960-1 2000 Active iodide uptake across the basal membrane mediated by human sodium iodide symporter (hNIS) has been shown to be a process coupled with the flow of sodium. Sodium 65-71 solute carrier family 5 member 5 Homo sapiens 90-94 10818067-8 2000 The results suggest that increased angiotensin II, in response to sodium restriction and valsartan infusion, stimulates AT(2)R, which mediates a BK and NO cascade. Sodium 66-72 angiotensinogen Rattus norvegicus 35-49 10773231-4 2000 The arterial changes are chronically modulated by hormonal counterregulatory mechanisms since, when sodium intake is high, bradykinin blockade produces more carotid hypertrophy, and when sodium intake is normal, less aortic collagen accumulates because of AT(1)-receptor blockade. Sodium 100-106 kininogen 1 Homo sapiens 123-133 10928293-6 2000 The relationship between urinary volume and urinary ET-1 was stronger than that of urinary sodium with ET-1 excretion because sodium was excluded from the multivariable model when urinary volume was introduced. Sodium 91-97 endothelin 1 Homo sapiens 103-107 10928293-11 2000 Since urinary ET-1 reflects its renal synthesis, our data support the notion that renal ET-1 plays a role in the regulation of sodium balance in patients with mild hypertension. Sodium 127-133 endothelin 1 Homo sapiens 88-92 11043938-5 2000 This observation could be due to a simple ionic interaction between Asp189 and the sodium ion or a more complicated structural rearrangement of the thrombin S1 pocket. Sodium 83-89 coagulation factor II, thrombin Homo sapiens 148-156 10872180-2 2000 Insulin induces pressor effects by mechanisms of increased sympathetic activity, renal sodium retention and proliferation of vascular smooth muscle cells. Sodium 87-93 insulin Homo sapiens 0-7 10762090-1 2000 Glial (GLT-1 and GLAST) and neuronal (EAAC1) high-affinity transporters mediate the sodium dependent glutamate reuptake in mammalian brain. Sodium 84-90 solute carrier family 1 member 2 Homo sapiens 7-12 10762090-1 2000 Glial (GLT-1 and GLAST) and neuronal (EAAC1) high-affinity transporters mediate the sodium dependent glutamate reuptake in mammalian brain. Sodium 84-90 solute carrier family 1 member 3 Homo sapiens 17-22 10981140-3 2000 Activation of the renin-angiotensin and sympathetic nervous systems and physical compression of the kidneys appear to contribute to obesity-induced increases in sodium reabsorption and hypertension. Sodium 161-167 renin Homo sapiens 18-23 10762090-1 2000 Glial (GLT-1 and GLAST) and neuronal (EAAC1) high-affinity transporters mediate the sodium dependent glutamate reuptake in mammalian brain. Sodium 84-90 solute carrier family 1 member 1 Homo sapiens 38-43 10864003-6 2000 In the presence of calcium reconstituted ICln channels are more permeable to bromide than chloride, and more permeable to potassium than sodium. Sodium 137-143 chloride nucleotide-sensitive channel 1A pseudogene 1 Homo sapiens 41-45 10803735-0 2000 Mechanisms by which intrarenal dopamine and ANP interact to regulate sodium metabolism. Sodium 69-75 natriuretic peptide A Homo sapiens 44-47 10803735-9 2000 This phenomenon may explain how ANP and dopamine act in concert to regulate sodium metabolism. Sodium 76-82 natriuretic peptide A Homo sapiens 32-35 10727937-11 2000 On comparing carnitine transport into rat kidney brush-border membrane vesicles and OCTN2, a sodium-dependent high-affinity human carnitine transporter, cloned recently from human kidney also expressed in muscle, the Km values are similar but driving forces, pattern of inhibition and stereospecificity are different. Sodium 93-99 solute carrier family 22 member 5 Rattus norvegicus 84-89 10760064-8 2000 RESULTS: Treatment of rats in the amygdala with ASDN against the mineralocorticoid receptor inhibited DOCA-induced sodium intake, whereas ASDN against the glucocorticoid receptor or sense/scrambled sequences had no effect. Sodium 115-121 nuclear receptor subfamily 3, group C, member 2 Rattus norvegicus 65-91 10772659-6 2000 Sodium-dependent proton secretion in NHE3(-/-) mice was approximately 50% that of wild-type mice. Sodium 0-6 solute carrier family 9 (sodium/hydrogen exchanger), member 3 Mus musculus 37-41 10772659-8 2000 Luminal sodium-dependent proton secretion was the same in NHE3(-/-)/NHE2(-/-) as in NHE3(-/-) mice. Sodium 8-14 solute carrier family 9 (sodium/hydrogen exchanger), member 3 Mus musculus 58-62 10763854-10 2000 We conclude that LY293 11 sodium is a selective leukotriene B4 receptor antagonist with potent pulmonary anti-inflammatory activity. Sodium 26-32 leukotriene B4 receptor 1 Cavia porcellus 48-71 10692470-0 2000 Inherited defects of sodium-dependent glutamate transport mediated by glutamate/aspartate transporter in canine red cells due to a decreased level of transporter protein expression. Sodium 21-27 solute carrier family 1 member 3 Canis lupus familiaris 70-101 10677382-1 2000 Atrial natriuretic peptide (ANP) plays an important role in the regulation of blood pressure through sodium-water homoeostasis. Sodium 101-107 natriuretic peptide A Homo sapiens 0-26 10744346-13 2000 A final group of animals received AngII (100 ng + 50 ng/h) concomitantly with captopril i.c.v., which increased blood pressure, RBF and urine flow, absolute and fractional sodium excretions by 8 (P < 0.05), 22 (P < 0.001 ) and 52-149% (P < 0.05-0.01), respectively. Sodium 172-178 angiotensinogen Rattus norvegicus 34-39 10677382-1 2000 Atrial natriuretic peptide (ANP) plays an important role in the regulation of blood pressure through sodium-water homoeostasis. Sodium 101-107 natriuretic peptide A Homo sapiens 28-31 10677399-2 2000 OBJECTIVE: To determine whether the response to an ACE inhibitor, assessed by urine sodium excretion, was different in patients with low renin versus those with high renin. Sodium 84-90 angiotensin I converting enzyme Homo sapiens 51-54 10757221-4 2000 Evidence suggests that endothelin-1 within the renal medulla is activated in conditions of salt loading and inhibits reabsorption of sodium in a nitric oxide-dependent manner. Sodium 133-139 endothelin 1 Homo sapiens 23-35 10677399-15 2000 There is thus tentative support for renin profiling in targeting ACE inhibitors to the most deserving, by showing that short term sodium retention does not occur in low renin patients if ACE inhibitors are withdrawn. Sodium 130-136 renin Homo sapiens 36-41 10677399-15 2000 There is thus tentative support for renin profiling in targeting ACE inhibitors to the most deserving, by showing that short term sodium retention does not occur in low renin patients if ACE inhibitors are withdrawn. Sodium 130-136 angiotensin I converting enzyme Homo sapiens 65-68 10770262-7 2000 The results showed that (1) Sodium was positively, and 3MH negatively associated with systolic and diastolic BP (SBP, DBP) in both the total sample and in those who were not administered anti-hypertensive drugs; these associations were all significant (p< 0.05), and remained so after adjustment for age, sex, body mass index [BMI, weight (kg)/height (m2)], alcohol intake and potassium excretion. Sodium 28-34 D-box binding PAR bZIP transcription factor Homo sapiens 118-121 10720587-6 2000 The administration of big ET-1 induced marked diuretic and natriuretic responses (urinary flow rate increased from 8.5+/-1 to 110+/-14 microL/min, and fractional excretion of sodium increased from 0.38+/-0.13% to 7.51+/-1.24%). Sodium 175-181 endothelin 1 Rattus norvegicus 26-30 10770262-9 2000 In general, subjects who had higher sodium and lower 3MH levels had higher mean SBP and DBP. Sodium 36-42 D-box binding PAR bZIP transcription factor Homo sapiens 88-91 10726708-2 2000 Inhibition by xenobiotics such as liquorice or mutations in the HSD11 B2 gene, as occur in the rare monogenic hypertensive syndrome of apparent mineralocorticoid excess (AME), result in a compromised 11 betaHSD2 enzyme activity, which in turn leads to overstimulation of the MR by cortisol, sodium retention, hypokalaemia, low plasma renin and aldosterone concentrations, and hypertension. Sodium 291-297 renin Homo sapiens 334-339 10675242-7 2000 Compared to control monolayers, lipopolysaccharide, prostaglandin E2, IL-1alpha, and TNF-alpha decreased mucosal-to-serosal and net sodium and chloride fluxes and increased serosal-to-mucosal movement of sodium and unmeasured ions. Sodium 132-138 tumor necrosis factor Homo sapiens 85-94 10675242-7 2000 Compared to control monolayers, lipopolysaccharide, prostaglandin E2, IL-1alpha, and TNF-alpha decreased mucosal-to-serosal and net sodium and chloride fluxes and increased serosal-to-mucosal movement of sodium and unmeasured ions. Sodium 204-210 tumor necrosis factor Homo sapiens 85-94 10644053-4 2000 The reduction in GCS activity was further augmented in SHR on a high sodium diet. Sodium 69-75 glutamate-cysteine ligase, catalytic subunit Rattus norvegicus 17-20 10860861-1 2000 The ubiquitous form of the sodium-hydrogen exchanger, NHE1, is devoted to the regulation of intracellular pH and cell volume. Sodium 27-33 solute carrier family 9 member A1 Homo sapiens 54-58 10644053-5 2000 Renal GCS activity in untreated SHR was 234 +/- 14 and 240 +/- 18 nmol/min/mg protein (mean +/- SD) on a low and high sodium diet, respectively. Sodium 118-124 glutamate-cysteine ligase, catalytic subunit Rattus norvegicus 6-9 10660625-5 2000 When expressed in Xenopus oocytes, OAT4 mediated the high affinity transport of estrone sulfate (K(m) = 1.01 microM) and dehydroepiandrosterone sulfate (K(m) = 0.63 microM) in a sodium-independent manner. Sodium 178-184 solute carrier family 22 member 11 Homo sapiens 35-39 10666300-0 2000 Phospholipase A(2) is involved in thapsigargin-induced sodium influx in human lymphocytes. Sodium 55-61 phospholipase A2 group IB Homo sapiens 0-17 10650139-0 2000 Blockade of U50488H on sodium currents in acutely isolated mice hippocampal CA3 pyramidal neurons. Sodium 23-29 carbonic anhydrase 3 Mus musculus 76-79 10711725-6 2000 Dietary sodium did not affect 11beta-HSD2 mRNA expression in collecting tubules of the medulla: 11beta-HSD1 mRNA in proximal tubules of the inner cortex/outer medulla was lower after a high sodium diet. Sodium 190-196 hydroxysteroid 11-beta dehydrogenase 1 Rattus norvegicus 96-107 10656319-17 2000 Sodium addition to a Na-free glass ionomer confirms the role of this cement in enhancing pH change in NaF solution. Sodium 0-6 C-X-C motif chemokine ligand 8 Homo sapiens 102-105 10671945-0 2000 Insulin-like growth factor I administration induces fluid and sodium retention in healthy adults: possible involvement of renin and atrial natriuretic factor. Sodium 62-68 insulin like growth factor 1 Homo sapiens 0-28 10671945-13 2000 Diurnal sodium excretion (mmol) was reduced during IGF-I administration (control, 151 +/- 8; IGF-I, 124 +/- 7; P < 0.05). Sodium 8-14 insulin like growth factor 1 Homo sapiens 51-56 10671945-13 2000 Diurnal sodium excretion (mmol) was reduced during IGF-I administration (control, 151 +/- 8; IGF-I, 124 +/- 7; P < 0.05). Sodium 8-14 insulin like growth factor 1 Homo sapiens 93-98 10671945-14 2000 CONCLUSION: IGF-I treatment causes fluid and sodium retention. Sodium 45-51 insulin like growth factor 1 Homo sapiens 12-17 10671945-16 2000 The present data suggest that the fluid and sodium retaining effect of GH is at least partly mediated through IGF-I. Sodium 44-50 insulin like growth factor 1 Homo sapiens 110-115 10679496-0 2000 Regulation of sodium balance and blood pressure by the AT(1A) receptor for angiotensin II. Sodium 14-20 angiotensin II receptor, type 1a Mus musculus 55-60 10679496-2 2000 On a 0.4% sodium diet, systolic blood pressures were significantly lower in Agtr1a-/- than in +/+ mice. Sodium 10-16 angiotensin II receptor, type 1a Mus musculus 76-82 10679496-6 2000 On the high-salt diet, urinary sodium excretion increased to similar levels in Agtr1a+/+ and -/- mice. Sodium 31-37 angiotensin II receptor, type 1a Mus musculus 79-85 10679496-7 2000 Although urinary sodium excretion was substantially reduced in both groups during the low-salt diet, cumulative sodium balances became negative in Agtr1a-/- mice despite a 6-fold increase in urinary aldosterone. Sodium 112-118 angiotensin II receptor, type 1a Mus musculus 147-153 10679496-8 2000 We infer, therefore, that the reduced blood pressures in Agtr1a-/- mice on a normal diet are caused by depletion of sodium and extracellular volume. Sodium 116-122 angiotensin II receptor, type 1a Mus musculus 57-63 10679496-9 2000 Their "sodium sensitivity" suggests a critical role for renal AT(1A) receptors to modulate sodium handling. Sodium 7-13 angiotensin II receptor, type 1a Mus musculus 62-67 10679496-9 2000 Their "sodium sensitivity" suggests a critical role for renal AT(1A) receptors to modulate sodium handling. Sodium 91-97 angiotensin II receptor, type 1a Mus musculus 62-67 10790760-5 2000 As cardiac diseases progress, the heart dilates, plasma norepinephrine increases, atrial natriuretic factor is released and the renin-angiotensin-aldosterone system is suppressed to maintain water and sodium excretion. Sodium 201-207 renin Homo sapiens 128-133 10790760-7 2000 In more advanced stages, atrial natriuretic factor suppression of the renin-angiotensin-aldosterone system is overridden by overt sympathetic activation and sodium and water retention ensues. Sodium 157-163 renin Homo sapiens 70-75 10707568-2 2000 In this theory, insulin resistance and the resultant hyperinsulinemia are considered to raise blood pressure through 1) sympathetic nervous system activation, 2) renal sodium retention, 3) renin-angiotensin system stimulation, and 4) intracellular calcium accumulation in vascular smooth muscle. Sodium 168-174 insulin Homo sapiens 16-23 10661508-3 2000 In man, hyponatremia is frequently associated with azotemia and hemo-dialysis usually corrects rapidly the serum sodium (SNa) but only few patients apparently develop demyelination. Sodium 113-119 snail family transcriptional repressor 1 Homo sapiens 121-124 10618583-2 2000 Recent treatment strategies have focused on attenuating the effects of angiotensin (Ang) II, which include vasoconstriction, sodium retention, sympathetic activation, and cell growth. Sodium 125-131 angiotensinogen Homo sapiens 71-91 10691781-4 2000 In the kidney, ANG II at the AT2 receptor stimulates a vasodilator cascade of bradykinin (BK), NO and cyclic GMP which is tonically activated only during conditions of increased ANG II, such as sodium depletion. Sodium 194-200 angiotensinogen Homo sapiens 15-21 10691781-4 2000 In the kidney, ANG II at the AT2 receptor stimulates a vasodilator cascade of bradykinin (BK), NO and cyclic GMP which is tonically activated only during conditions of increased ANG II, such as sodium depletion. Sodium 194-200 kininogen 1 Homo sapiens 78-88 10691781-4 2000 In the kidney, ANG II at the AT2 receptor stimulates a vasodilator cascade of bradykinin (BK), NO and cyclic GMP which is tonically activated only during conditions of increased ANG II, such as sodium depletion. Sodium 194-200 kininogen 1 Homo sapiens 90-92 10691781-4 2000 In the kidney, ANG II at the AT2 receptor stimulates a vasodilator cascade of bradykinin (BK), NO and cyclic GMP which is tonically activated only during conditions of increased ANG II, such as sodium depletion. Sodium 194-200 angiotensinogen Homo sapiens 178-184 10691781-7 2000 In the gastrointestinal tract, physiological quantities of ANG II stimulate the AT2 receptor releasing NO and cGMP leading to increased sodium and water absorption. Sodium 136-142 angiotensinogen Homo sapiens 59-65 10678288-2 2000 The kidney is an important site of action of Ang II AT1 receptor blockers because intrarenal Ang II not only vasoconstricts the renal vasculature but also reduces sodium excretion and suppresses the pressure natriuresis relationship. Sodium 163-169 angiotensinogen Rattus norvegicus 45-51 10678288-11 2000 The collective actions of Ang II blockers on tubular transport and renal hemodynamics provide long-term effects to regulate sodium balance, which contributes to the long-term control of hypertension. Sodium 124-130 angiotensinogen Rattus norvegicus 26-32 10818397-5 2000 The renin-angiotensin-aldosterone system is a major determinant of sodium balance in pregnancy. Sodium 67-73 renin Homo sapiens 4-9 10644866-1 2000 BACKGROUND: In surgical patients, hypoalbuminemia may occur as a component of acute-phase response (APR) syndrome, which we hypothesized could decrease serum sodium levels. Sodium 158-164 phorbol-12-myristate-13-acetate-induced protein 1 Homo sapiens 100-103 11193601-4 2000 The link between active sodium transport and glucose is the coupled transport of sodium and glucose across the brush border membrane of enterocytes by the Na+/glucose cotransporter (SGLT1). Sodium 24-30 solute carrier family 5 member 1 Homo sapiens 182-187 11193601-4 2000 The link between active sodium transport and glucose is the coupled transport of sodium and glucose across the brush border membrane of enterocytes by the Na+/glucose cotransporter (SGLT1). Sodium 81-87 solute carrier family 5 member 1 Homo sapiens 182-187 11055473-1 2000 BACKGROUND: In order to explore the hypothesis of an atrial natriuretic factor (ANF) deficiency in prehypertension, we compared the response to sodium loading on ANF and renal function in subjects with positive and negative histories of hypertension. Sodium 144-150 natriuretic peptide A Homo sapiens 162-165 10706418-3 2000 bolus or short-term infusion) of AVP to rats, the relationship between blood concentrations and its effect on both mean arterial pressure (hemodynamic effect) and urinary sodium concentration (anti-diuretic effect) was described on the basis of an integrated pharmacokinetic-pharmacodynamic (PK-PD) model. Sodium 171-177 arginine vasopressin Rattus norvegicus 33-36 10855734-1 2000 Insulin increases renal sodium reabsorption which may contribute to hypertension. Sodium 24-30 insulin Homo sapiens 0-7 11055473-9 2000 Increasing sodium intake caused a similar increase in ANF in OH and ON but cGMP did not change significantly. Sodium 11-17 natriuretic peptide A Homo sapiens 54-57 11055473-10 2000 As expected the activity of the renin-angiotensin-aldosterone system was decreased by enhancing sodium intake but with both low and high sodium intake plasma renin concentration was significantly higher in OH than in ON. Sodium 96-102 renin Homo sapiens 32-37 11055473-17 2000 In particular, in OH and ON an identical increase in plasma ANF concentration in response to sodium loading was found. Sodium 93-99 natriuretic peptide A Homo sapiens 60-63 10600659-1 2000 Changes in the rate of formation of angiotensin II (ANG II) participate in mediating the natriuresis that occurs in direct response to a gastric sodium stimulus (upper-gut sodium monitor). Sodium 145-151 angiotensinogen Rattus norvegicus 36-50 10600659-1 2000 Changes in the rate of formation of angiotensin II (ANG II) participate in mediating the natriuresis that occurs in direct response to a gastric sodium stimulus (upper-gut sodium monitor). Sodium 145-151 angiotensinogen Rattus norvegicus 52-58 10600659-1 2000 Changes in the rate of formation of angiotensin II (ANG II) participate in mediating the natriuresis that occurs in direct response to a gastric sodium stimulus (upper-gut sodium monitor). Sodium 172-178 angiotensinogen Rattus norvegicus 36-50 10600659-1 2000 Changes in the rate of formation of angiotensin II (ANG II) participate in mediating the natriuresis that occurs in direct response to a gastric sodium stimulus (upper-gut sodium monitor). Sodium 172-178 angiotensinogen Rattus norvegicus 52-58 10600659-8 2000 Hepatic ACE activity decreased in response to sodium (P<0.005) from 30 min. Sodium 46-52 angiotensin I converting enzyme Rattus norvegicus 8-11 10601066-1 2000 BACKGROUND: The renin-angiotensin system may be implicated in the subtle sodium handling abnormality in preascitic cirrhosis. Sodium 73-79 renin Homo sapiens 16-21 10893650-7 2000 Rather, we should recognise the importance of adequate drug dosing and modest reductions in dietary sodium intake in augmenting the BP lowering effect of ACE inhibitors in hypertensive African-Americans. Sodium 100-106 angiotensin I converting enzyme Homo sapiens 154-157 10736756-3 2000 In this theory, insulin resistance and the resultant hyperinsulinemia are considered to raise blood pressure through 1) sympathetic nervous system activation, 2) renal sodium retention, 3) renin-angiotensin system stimulation, and 4) intracellular calcium accumulation in vascular smooth muscle. Sodium 168-174 insulin Homo sapiens 16-23 10627583-8 2000 However, over the ensuing 48 hr period, a sharp rise in the proportion of rBII/IIA sodium current occurred, confirming the idea, based on previous mRNA measurements, that two distinct sodium channel types appear sequentially during neuronal differentiation of PC12 cells. Sodium 83-89 calcium voltage-gated channel subunit alpha1 E Rattus norvegicus 74-82 10765111-5 2000 RESULTS: ICV injections of ANG II and ANG III at 5 pmol in rats on a normal sodium diet did not significantly alter the blood pressure, but significantly increased renal plasma flow, glomerular filtration rate, urine flow, and absolute and fractional excretions of sodium and potassium. Sodium 265-271 angiotensinogen Rattus norvegicus 27-33 10765111-11 2000 CONCLUSIONS: Centrally administered ANG III is as potent as ANG II in causing pressor and renal effects in rats on normal and high sodium intake. Sodium 131-137 angiotensinogen Rattus norvegicus 36-42 10647278-4 1999 After introducing the therapy with demeclocycline, a tetracycline type antibiotic that inhibits the renal action of antidiuretic hormone, serum sodium levels began to rise gradually, and the urinary sodium excretion slowly decreased. Sodium 144-150 arginine vasopressin Homo sapiens 116-136 11035430-4 2000 Both non-selective Cox inhibitors and selective Cox-2 inhibitors induce renal side effects, including sodium retention and reduction of the glomerular filtration rate. Sodium 102-108 mitochondrially encoded cytochrome c oxidase II Homo sapiens 48-53 10858623-10 2000 Treatment of sodium-deplete rats, adrenalectomized or intact, with the angiotensin II-type 1 receptor antagonist, ZD7155, decreased sodium intake and Fos expression in the subfornical organ but not in the organum vasculosum of the lamina terminalis or median preoptic nucleus. Sodium 13-19 angiotensin II receptor, type 1b Rattus norvegicus 71-101 10858623-10 2000 Treatment of sodium-deplete rats, adrenalectomized or intact, with the angiotensin II-type 1 receptor antagonist, ZD7155, decreased sodium intake and Fos expression in the subfornical organ but not in the organum vasculosum of the lamina terminalis or median preoptic nucleus. Sodium 132-138 angiotensin II receptor, type 1b Rattus norvegicus 71-101 10858623-12 2000 Furthermore, the results obtained with the administration of the angiotensin receptor antagonist are consistent with the proposal that sodium appetite of the sodium-deplete rat, adrenalectomized or intact, is mediated by circulating angiotensin II acting in the subfornical organ. Sodium 135-141 angiotensinogen Rattus norvegicus 233-247 10858623-12 2000 Furthermore, the results obtained with the administration of the angiotensin receptor antagonist are consistent with the proposal that sodium appetite of the sodium-deplete rat, adrenalectomized or intact, is mediated by circulating angiotensin II acting in the subfornical organ. Sodium 158-164 angiotensinogen Rattus norvegicus 233-247 10619573-4 1999 Angiotensin II also alters renal sodium and water absorption through its ability to stimulate the zona glomerulosa cells of the adrenal cortex to synthesize and secrete aldosterone. Sodium 33-39 angiotensinogen Homo sapiens 0-14 10643229-4 1999 When individuals with a genetic program for retention of sodium and calories (insulin resistance) encounter the stress and unwholesome lifestyle of modern society, cardiovascular disease may soon develop, potential consequences being myocardial infarction or stroke. Sodium 57-63 insulin Homo sapiens 78-85 10619595-2 1999 Because Ang II affects blood pressure control, sodium and water homeostasis, and cardiovascular function and structure, a great deal of research effort has been directed toward blocking the RAS. Sodium 47-53 angiotensinogen Homo sapiens 8-14 10583449-1 1999 BACKGROUND: In essential hypertension an elevated renal vascular resistance (RVR) may be a marker of renin-angiotensin-aldosterone system-mediated impairment of renal sodium excretion. Sodium 167-173 renin Homo sapiens 101-106 10601129-1 1999 The renin-angiotensin system is a major regulator of body sodium, predominantly through the actions of intrarenal angiotensin II of unclear origin. Sodium 58-64 renin Homo sapiens 4-9 10585895-11 1999 Thus the sodium-retaining effect of insulin was more pronounced in subjects with a strong genetic predisposition to essential hypertension than in subjects with normotensive parents. Sodium 9-15 insulin Homo sapiens 36-43 10601129-2 1999 We show that polarized epithelium of the proximal tubule synthesizes and secretes angiotensinogen at its apical side and that the protein can be detected in urine as a function of dietary sodium. Sodium 188-194 angiotensinogen Homo sapiens 82-97 10601129-3 1999 Furthermore, we demonstrate that renin is expressed and secreted in a restricted nephron segment, the connecting tubule, also in a sodium-dependent fashion. Sodium 131-137 renin Homo sapiens 33-38 10601129-4 1999 A paracrine renin-angiotensin system operating along the entire nephron may contribute to long-term arterial pressure regulation by integrating distant tubular sodium-reabsorbing functions. Sodium 160-166 renin Homo sapiens 12-17 10581309-25 1999 The positive inotropic effect of SIN-1 (100 microM) was abolished in sodium-free solutions, a treatment that eliminates the activity of the sodium-calcium exchanger. Sodium 69-75 MAPK associated protein 1 Homo sapiens 33-38 10589704-8 1999 AngII infusion attenuated the absolute and fractional sodium excretion responses to volume expansion (3.4 +/- 1.2 microEq/min x g and 2.5 +/- 0.5%, respectively). Sodium 54-60 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 0-5 10776180-4 1999 Women with mastitis, as indicated by elevated breast milk sodium concentrations, had higher median levels lysozyme (290 vs 221 mg/L, p < 0.04), SLPI (38 vs 19 mg/L, p < 0.0001) and HIV (920 copies/mL vs undetectable, p < 0.0001) compared with women without mastitis. Sodium 58-64 lysozyme Homo sapiens 106-114 10776180-4 1999 Women with mastitis, as indicated by elevated breast milk sodium concentrations, had higher median levels lysozyme (290 vs 221 mg/L, p < 0.04), SLPI (38 vs 19 mg/L, p < 0.0001) and HIV (920 copies/mL vs undetectable, p < 0.0001) compared with women without mastitis. Sodium 58-64 secretory leukocyte peptidase inhibitor Homo sapiens 147-151 10565843-7 1999 Expressed NTCP exhibited high-affinity, sodium-dependent uptake of taurocholate, and as expected, this was markedly inhibited by bile acids and organic anions. Sodium 40-46 solute carrier family 10 member 1 Homo sapiens 10-14 10581309-25 1999 The positive inotropic effect of SIN-1 (100 microM) was abolished in sodium-free solutions, a treatment that eliminates the activity of the sodium-calcium exchanger. Sodium 140-146 MAPK associated protein 1 Homo sapiens 33-38 10594793-11 1999 CONCLUSIONS: Taken together, these results suggest that there is a relationship between the AGT1R A1166-->C polymorphism and the humoral and renal hemodynamic responses to AGT1R blockade and to Ang II infusion in the sodium-replete state, and that the C allele is associated with enhanced intrarenal and peripheral Ang II activity. Sodium 220-226 angiotensinogen Homo sapiens 197-203 10594793-11 1999 CONCLUSIONS: Taken together, these results suggest that there is a relationship between the AGT1R A1166-->C polymorphism and the humoral and renal hemodynamic responses to AGT1R blockade and to Ang II infusion in the sodium-replete state, and that the C allele is associated with enhanced intrarenal and peripheral Ang II activity. Sodium 220-226 angiotensinogen Homo sapiens 318-324 10556530-1 1999 The classical short-term effect (within minutes) of arginine vasopressin (AVP) consists in increasing sodium, chloride and water transport in kidney cells. Sodium 102-108 arginine vasopressin Rattus norvegicus 61-72 10633465-4 1999 The CaR also affects the renal handling of sodium, magnesium and water. Sodium 43-49 calcium sensing receptor Homo sapiens 4-7 10842655-3 1999 The mechanisms responsible for increased sodium reabsorption and altered pressure natriuresis in obesity include activation of the renin-angiotension and sympathetic nervous systems, and physical compression of the kidneys due to accumulation of intrarenal fat and extracellular matrix. Sodium 41-47 renin Homo sapiens 131-136 10539810-1 1999 BACKGROUND: High angiotensin II levels in relation to the corresponding urinary sodium excretion have been found to modulate left ventricular (LV) structure in middle-aged hypertensive patients. Sodium 80-86 angiotensinogen Homo sapiens 17-31 10556530-1 1999 The classical short-term effect (within minutes) of arginine vasopressin (AVP) consists in increasing sodium, chloride and water transport in kidney cells. Sodium 102-108 arginine vasopressin Rattus norvegicus 74-77 10539810-8 1999 The increase of sodium excretion at high salt intake was related to a physiologically expected decrease of angiotensin II and aldosterone levels in normotensive (r = -0.36, P <.01 and r = -0.32; P =.016, respectively) but not in hypertensive patients. Sodium 16-22 angiotensinogen Homo sapiens 107-121 10537144-0 1999 The in vivo effects of adrenocorticotropin and sodium restriction on the formation of the different species of steroidogenic acute regulatory protein in rat adrenal. Sodium 47-53 steroidogenic acute regulatory protein Rattus norvegicus 111-149 10517915-8 1999 In the patient group there was an inverse correlation between: (a) absolute distal sodium reabsorption and active renin (r -0.59, p<0.05); (b) fractional distal sodium reabsorption and sodium excretion (r -0.66, p<0.03). Sodium 83-89 renin Homo sapiens 114-119 10583426-10 1999 In the kidney, insulin spares sodium and uric acid from excretion; in chronic hyperinsulinaemic states, these effects may contribute to high blood pressure and hyperuricaemia. Sodium 30-36 insulin Homo sapiens 15-22 10539974-5 1999 Sodium-dependent inactivation of NCX1.3 was considerably more pronounced than that of NCX1.4 and resulted in nearly complete inhibition of steady state currents. Sodium 0-6 solute carrier family 8 member A1 Canis lupus familiaris 33-37 10516282-0 1999 Vasopressin stimulates sodium transport in A6 cells via a phosphatidylinositide 3-kinase-dependent pathway. Sodium 23-29 arginine vasopressin Homo sapiens 0-11 10523346-18 1999 These experiments indicate that adaptations in NO activity lead to relatively low TGF responsiveness, which will offset the simultaneous sodium-retaining actions of angiotensin II on proximal tubular reabsorption and TGF responsiveness. Sodium 137-143 angiotensinogen Rattus norvegicus 165-179 10523341-0 1999 The role of alpha-adducin polymorphism in blood pressure and sodium handling regulation may not be excluded by a negative association study. Sodium 61-67 adducin 1 Homo sapiens 12-25 10498674-0 1999 Insulin stimulates transepithelial sodium transport by activation of a protein phosphatase that increases Na-K ATPase activity in endometrial epithelial cells. Sodium 35-41 insulin Homo sapiens 0-7 10516741-10 1999 However, hypertensives have a delay in resetting the adrenal responsiveness to angiotensin II suggesting that they have altered sodium perception during rapid changes in salt balance. Sodium 128-134 angiotensinogen Homo sapiens 79-93 10516741-1 1999 We investigated sodium and volume-dependent mechanisms in the modulation of adrenal and renal vascular responsiveness to angiotensin II in hypertensive (n = 9) and normal subjects (n = 5) who demonstrated normal responses during steady-state salt balance (intact modulation). Sodium 16-22 angiotensinogen Homo sapiens 121-135 10528658-4 1999 METHODS: We assessed the relationship between the effects of sequential physiological and supraphysiological insulin dosages (50 and 150 mU/kg/h) on renal sodium handling, and insulin sensitivity and salt sensitivity using the euglycaemic clamp technique and clearances of [131I]hippuran, [125I]iothalamate, sodium, and lithium in 20 normal subjects displaying a wide range of insulin sensitivity. Sodium 155-161 insulin Homo sapiens 109-116 10504466-2 1999 Experimental evidence indicates that ultrafiltered IGF-I, HGF, and TGF-beta may contribute to increased tubular phosphate and sodium absorption, synthesis of extracellular matrix proteins, and secretion of chemokines such as monocyte chemoattractant protein-1 (MCP-1). Sodium 126-132 insulin like growth factor 1 Homo sapiens 51-56 10504466-2 1999 Experimental evidence indicates that ultrafiltered IGF-I, HGF, and TGF-beta may contribute to increased tubular phosphate and sodium absorption, synthesis of extracellular matrix proteins, and secretion of chemokines such as monocyte chemoattractant protein-1 (MCP-1). Sodium 126-132 transforming growth factor beta 1 Homo sapiens 67-75 10528658-0 1999 Insulin"s acute effects on glomerular filtration rate correlate with insulin sensitivity whereas insulin"s acute effects on proximal tubular sodium reabsorption correlation with salt sensitivity in normal subjects. Sodium 141-147 insulin Homo sapiens 97-104 10528658-7 1999 RESULTS: During the successive insulin infusions, GFR increased by 5.9% (P = 0.003) and 10.9% (P<0.001), while fractional sodium excretion decreased by 34 and 50% (both P<0.001). Sodium 125-131 insulin Homo sapiens 31-38 10528658-1 1999 BACKGROUND: Insulin induces sodium retention by increasing distal tubular sodium reabsorption. Sodium 28-34 insulin Homo sapiens 12-19 10528658-1 1999 BACKGROUND: Insulin induces sodium retention by increasing distal tubular sodium reabsorption. Sodium 74-80 insulin Homo sapiens 12-19 10528658-9 1999 Insulin sensitivity correlated with changes in GFR during physiological (r = 0.60, P = 0.005) and supraphysiological (r = 0.58, P = 0.007) hyperinsulinaemia, but not with changes in proximal tubular sodium reabsorption. Sodium 199-205 insulin Homo sapiens 0-7 10528658-2 1999 Opposite effects of insulin to offset insulin-induced sodium retention are supposedly increases in glomerular filtration rate (GFR) and decreases in proximal tubular sodium reabsorption. Sodium 54-60 insulin Homo sapiens 20-27 10528658-2 1999 Opposite effects of insulin to offset insulin-induced sodium retention are supposedly increases in glomerular filtration rate (GFR) and decreases in proximal tubular sodium reabsorption. Sodium 54-60 insulin Homo sapiens 38-45 10528658-12 1999 CONCLUSIONS: Insulin sensitivity and salt sensitivity correlate with changes in different elements of renal sodium handling, but not with overall sodium excretion, during insulin infusion. Sodium 108-114 insulin Homo sapiens 13-20 10528658-2 1999 Opposite effects of insulin to offset insulin-induced sodium retention are supposedly increases in glomerular filtration rate (GFR) and decreases in proximal tubular sodium reabsorption. Sodium 166-172 insulin Homo sapiens 20-27 10528658-2 1999 Opposite effects of insulin to offset insulin-induced sodium retention are supposedly increases in glomerular filtration rate (GFR) and decreases in proximal tubular sodium reabsorption. Sodium 166-172 insulin Homo sapiens 38-45 10526565-2 1999 RELATIVE PROGNOSTIC VALUES: Neuron specific enolase (NSE) would have a pretherapeutic prognostic value better than LDH (lacto-dehydrogenase) and perhaps better than serum sodium, biocarbonates, and uric acid. Sodium 171-177 enolase 2 Homo sapiens 53-56 10489382-12 1999 The factors that mediate enhanced adrenal response to Ang II with sodium restriction may be defective, suggesting the existence of alternative physiological mechanisms for sodium homeostasis in the low-renin state. Sodium 66-72 angiotensinogen Homo sapiens 54-60 10502662-0 1999 Renal interstitial hydrostatic pressure and urinary sodium excretion in rats with angiotensin-converting enzyme inhibitor-induced papillary atrophy. Sodium 52-58 angiotensin I converting enzyme Rattus norvegicus 82-111 10489382-12 1999 The factors that mediate enhanced adrenal response to Ang II with sodium restriction may be defective, suggesting the existence of alternative physiological mechanisms for sodium homeostasis in the low-renin state. Sodium 172-178 angiotensinogen Homo sapiens 54-60 10489382-12 1999 The factors that mediate enhanced adrenal response to Ang II with sodium restriction may be defective, suggesting the existence of alternative physiological mechanisms for sodium homeostasis in the low-renin state. Sodium 172-178 renin Homo sapiens 202-207 10489099-7 1999 Because of the sodium-retaining effects of insulin, it has been postulated that insulin resistance with associated hyperinsulinaemia may be critical for the pathogenesis of salt-sensitivity in essential hypertensive subjects. Sodium 15-21 insulin Homo sapiens 43-50 10489099-7 1999 Because of the sodium-retaining effects of insulin, it has been postulated that insulin resistance with associated hyperinsulinaemia may be critical for the pathogenesis of salt-sensitivity in essential hypertensive subjects. Sodium 15-21 insulin Homo sapiens 80-87 10638177-14 1999 CONCLUSIONS: This hormonal anomaly may be ascribed to a lower excretion of sodium with consequent expansion of extracellular volume due to antinatriuretic action of insulin often found at high plasmatic levels particularly in NIDDM. Sodium 75-81 insulin Homo sapiens 165-172 10489110-11 1999 CONCLUSIONS: In PIH, elevated hANP might be important as a counterbalance to the presence of the active vasopressors and sodium retention. Sodium 121-127 natriuretic peptide A Homo sapiens 30-34 10495090-0 1999 Intraventricular neuropeptide Y decreases need-induced sodium appetite and increases pica in rats. Sodium 55-61 neuropeptide Y Rattus norvegicus 17-31 10569225-4 1999 Gastroesophageal reflux, iron deficiency, calcium and sodium excesses or deficiencies may be influenced by the type and amount of milk fed to the infant. Sodium 54-60 Weaning weight-maternal milk Bos taurus 130-134 10495090-6 1999 Administration of NPY resulted in increased food intake, increased kaolin consumption, and decreased need-induced sodium intake. Sodium 114-120 neuropeptide Y Rattus norvegicus 18-21 10426382-4 1999 Our recent observation that insulin levels are increased in a specific subset of patients with normal/high-renin hypertension, the nonmodulators, provided the background for the current hypothesis: to ascertain whether abnormalities in lipid and carbohydrate metabolism are observed in the same patients in whom alterations in sodium transport, sodium homeostasis, and the renin-aniotensin system response have been identified. Sodium 345-351 insulin Homo sapiens 28-35 10426382-4 1999 Our recent observation that insulin levels are increased in a specific subset of patients with normal/high-renin hypertension, the nonmodulators, provided the background for the current hypothesis: to ascertain whether abnormalities in lipid and carbohydrate metabolism are observed in the same patients in whom alterations in sodium transport, sodium homeostasis, and the renin-aniotensin system response have been identified. Sodium 327-333 insulin Homo sapiens 28-35 10440258-6 1999 The inhibitory effect of thrombin on ouabain-sensitive potassium (86Rb) uptake was suppressed in the presence of hirudin (an antagonist for thrombin receptors) but persisted in the presence of amphotericin B (a pseudo ionophore that effectively clamps plasma membrane sodium permeability at a high value). Sodium 268-274 coagulation factor II, thrombin Homo sapiens 25-33 10440258-13 1999 The functional significance of the thrombin-mediated change of lens active sodium-potassium transport is unclear since appreciable amounts of thrombin may only be presented to the lens during instances of blood-aqueous-barrier breakdown. Sodium 75-81 coagulation factor II, thrombin Homo sapiens 35-43 10440258-0 1999 Thrombin inhibits active sodium-potassium transport in porcine lens. Sodium 25-31 coagulation factor II, thrombin Homo sapiens 0-8 10440258-2 1999 In the present study, experiments were conducted to determine the influence of thrombin on active sodium-potassium transport in porcine lenses. Sodium 98-104 coagulation factor II, thrombin Homo sapiens 79-87 10446934-15 1999 Therefore, submaximal ACE inhibition enhanced sodium excretion mainly by increasing RBF and GFR, whereas submaximal AT1 receptor blockade decreased tubular sodium and water reabsorption. Sodium 46-52 angiotensin I converting enzyme Homo sapiens 22-25 10407194-1 1999 The serotonin transporter (SERT) is a member of a highly homologous family of sodium/chloride dependent neurotransmitter transporters responsible for reuptake of biogenic amines from the extracellular fluid. Sodium 78-84 solute carrier family 6 member 4 Homo sapiens 4-25 10444029-10 1999 These findings indicate that diabetic glomerular sclerosis causes glomerular ultrafiltration of IGF-I, and they suggest that tubular fluid IGF-I may contribute to sodium (and fluid) retention that is commonly observed in patients with severe diabetic nephropathy. Sodium 163-169 insulin like growth factor 1 Homo sapiens 139-144 10437737-2 1999 Angiotensin II is the principal effector hormone in the RAS, causing vasoconstriction and increased sodium and water retention, leading to increased blood pressure. Sodium 100-106 angiotensinogen Homo sapiens 0-14 10407194-1 1999 The serotonin transporter (SERT) is a member of a highly homologous family of sodium/chloride dependent neurotransmitter transporters responsible for reuptake of biogenic amines from the extracellular fluid. Sodium 78-84 solute carrier family 6 member 4 Homo sapiens 27-31 10393883-5 1999 Also, Src has been found to amplify the up-regulation of NMDA receptor function that is produced by raising the intracellular concentration of sodium. Sodium 143-149 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 6-9 10400628-11 1999 These results indicate that shear stress-mediated ERK1/2 activation is regulated by extracellular sodium and demonstrate that ion transport via Na+ channels modulates EC responses to shear stress. Sodium 98-104 mitogen-activated protein kinase 3 Homo sapiens 50-56 10391915-3 1999 The amino acid transport activity induced by the co-expression of 4F2hc and LAT-2 was sodium-independent and showed broad specificity for small and large zwitterionic amino acids, as well as bulky analogs (e.g. BCH (2-aminobicyclo-(2,2,1)-heptane-2-carboxylic acid)). Sodium 86-92 chimerin 2 Homo sapiens 211-214 10393883-6 1999 Sodium concentration increases in neuronal dendrites during high levels of firing activity, which is precisely when Src becomes activated. Sodium 0-6 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 116-119 10430112-8 1999 CONCLUSION: In salt-depleted subjects, selective inhibition of COX-2 causes sodium and potassium retention. Sodium 76-82 prostaglandin-endoperoxide synthase 2 Homo sapiens 63-68 10495475-5 1999 Because glucose transport across these barriers is mediated exclusively by the sodium-independent glucose transporter GLUT1, changes in endothelial glucose transport and GLUT1 abundance in the barriers of the brain and retina may have profound consequences on glucose delivery to these tissues and major implications in the development of two major diabetic complications, namely insulin-induced hypoglycemia and diabetic retinopathy. Sodium 79-85 insulin Homo sapiens 380-387 10778592-12 1999 The study highlights that patients with diabetes mellitus have tendency to retain sodium under the influence of insulin but this needs further evaluation. Sodium 82-88 insulin Homo sapiens 112-119 10369799-22 1999 Decreased synthesis of ET-1, which normally antagonizes the action of [Arg8]vasopressin, may allow increased water (and sodium) reabsorption at the level of the inner medullary collecting duct. Sodium 120-126 endothelin 1 Rattus norvegicus 23-27 10381797-1 1999 The amiloride-sensitive epithelial sodium channel (ENaC) contributes to the regulation of the sodium balance and blood pressure because it mediates a rate-limiting step in sodium transport across the epithelium of the distal nephron. Sodium 35-41 sodium channel epithelial 1 subunit gamma Rattus norvegicus 51-55 10381797-1 1999 The amiloride-sensitive epithelial sodium channel (ENaC) contributes to the regulation of the sodium balance and blood pressure because it mediates a rate-limiting step in sodium transport across the epithelium of the distal nephron. Sodium 94-100 sodium channel epithelial 1 subunit gamma Rattus norvegicus 51-55 10371376-4 1999 Systemic insulin resistance as assessed by the fasting plasma glucose-to-insulin ratio was aggravated by dietary sodium restriction (normal sodium: 1.2 +/- 0.1 mmol/mIU; low sodium 0.6 +/- 0.1, P < .05). Sodium 113-119 insulin Homo sapiens 9-16 10371376-4 1999 Systemic insulin resistance as assessed by the fasting plasma glucose-to-insulin ratio was aggravated by dietary sodium restriction (normal sodium: 1.2 +/- 0.1 mmol/mIU; low sodium 0.6 +/- 0.1, P < .05). Sodium 113-119 insulin Homo sapiens 73-80 10371376-4 1999 Systemic insulin resistance as assessed by the fasting plasma glucose-to-insulin ratio was aggravated by dietary sodium restriction (normal sodium: 1.2 +/- 0.1 mmol/mIU; low sodium 0.6 +/- 0.1, P < .05). Sodium 140-146 insulin Homo sapiens 9-16 10371376-8 1999 This impairment of the vasodilating effect of insulin could be a factor attenuating the blood pressure lowering effect of a low sodium diet. Sodium 128-134 insulin Homo sapiens 46-53 10354286-0 1999 Insulin-dependent diabetic sibling pairs are concordant for sodium-hydrogen antiport activity. Sodium 60-66 insulin Homo sapiens 0-7 10349832-7 1999 Finally, reducing extracellular sodium prevented the glutamatergic activation of SAPK but only partially blocked that of ERK. Sodium 32-38 mitogen-activated protein kinase 9 Homo sapiens 81-85 10349832-7 1999 Finally, reducing extracellular sodium prevented the glutamatergic activation of SAPK but only partially blocked that of ERK. Sodium 32-38 mitogen-activated protein kinase 1 Homo sapiens 121-124 10354286-1 1999 UNLABELLED: Insulin-dependent diabetic sibling pairs are concordant for sodium-hydrogen antiport activity. Sodium 72-78 insulin Homo sapiens 12-19 10390128-3 1999 Further, COX-2 expression may be up-regulated at certain sites: in the kidney during sodium restriction; in the microglia of cognitive centers within the hippocampus and cortex in Alzheimer"s disease; and in intestinal adenomas and colon tumors. Sodium 85-91 prostaglandin-endoperoxide synthase 2 Homo sapiens 9-14 10339618-4 1999 In AT2-null mice, infusion of ANG II (4 pmol/kg/min) for 7 days produced a marked and sustained increase in SBP [from 116 +/- 0.5 to 208 +/- 1 mmHg (P < 0.0001) (1 mmHg = 133 Pa)] and reduction in urinary sodium excretion (UNaV) [from 0.6 +/- 0.01 to 0.05 +/- 0.002 mM/day (P < 0.0001)] whereas neither SBP nor UNaV changed in WT mice. Sodium 208-214 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 30-36 10352121-5 1999 When mounted in modified Ussing chambers, IRPTC generate a transmembrane current, and angiotensin II (10 pM to 10 microM) increases this sodium-dependent current. Sodium 137-143 angiotensinogen Rattus norvegicus 86-100 10330055-12 1999 The inhibition of HCO-3 absorption by ANG II in the MTAL may play a key role in the ability of the kidney to regulate sodium balance and extracellular fluid volume independently of acid-base balance. Sodium 118-124 angiotensinogen Rattus norvegicus 38-44 10234035-4 1999 VIP directly depolarized cells via activation of an inward current; these effects were attenuated and potentiated in low-sodium and low-calcium medium, respectively. Sodium 121-127 vasoactive intestinal peptide Rattus norvegicus 0-3 10234035-8 1999 We conclude that VIP excites mPRF neurons by activation of a sodium current. Sodium 61-67 vasoactive intestinal peptide Rattus norvegicus 17-20 10342788-2 1999 We have recently shown that this endogenously produced and luminally secreted angiotensin II regulates proximal tubule volume reabsorption, which is a reflection of sodium transport within this segment. Sodium 165-171 angiotensinogen Homo sapiens 78-92 10342783-0 1999 Enhanced blood pressure response to mild sodium reduction in subjects with the 235T variant of the angiotensinogen gene. Sodium 41-47 angiotensinogen Homo sapiens 99-114 10342783-8 1999 The angiotensinogen gene accounts for some of the interindividual variation of the blood pressure response to sodium reduction. Sodium 110-116 angiotensinogen Homo sapiens 4-19 10376850-10 1999 These results indicate that the abnormal proton activation of red blood cell sodium-proton exchange in hypertensives reflects an abnormal regulation of PKC translocation to the cell membrane, associated to hyperinsulinaemia and probably insulin resistance. Sodium 77-83 insulin Homo sapiens 211-218 10215647-12 1999 Selective inhibition of Cox-2 by MK-966 caused a clinically insignificant and transient retention of sodium, but no depression of GFR. Sodium 101-107 mitochondrially encoded cytochrome c oxidase II Homo sapiens 24-29 10212290-11 1999 Sodium entry is also hypothesized to compromise clearance of cytosolic Ca2+ by routes other than mitochondrial uptake, probably by enhancing ATP depletion, accounting for the large inhibition of the Ca2+ increase by the combination of CNQX and lidocaine. Sodium 0-6 carbonic anhydrase 2 Rattus norvegicus 71-74 10212290-11 1999 Sodium entry is also hypothesized to compromise clearance of cytosolic Ca2+ by routes other than mitochondrial uptake, probably by enhancing ATP depletion, accounting for the large inhibition of the Ca2+ increase by the combination of CNQX and lidocaine. Sodium 0-6 carbonic anhydrase 2 Rattus norvegicus 199-202 10344351-13 1999 We observed a highly significant inverse correlation between the plasma endothelin-1 concentrations and the ability to excrete a given water and sodium load, suggesting that the endothelin system plays a role in the regulation of water excretion in patients with liver cirrhosis. Sodium 145-151 endothelin 1 Homo sapiens 72-84 10215647-14 1999 Our data suggest that acute sodium retention by nonsteroidal anti-inflammatory drugs in healthy elderly subjects is mediated by the inhibition of Cox-2, whereas depression of GFR is due to inhibition of Cox-1. Sodium 28-34 mitochondrially encoded cytochrome c oxidase II Homo sapiens 146-151 10361429-3 1999 Angiotensin II in the brain increases water and sodium intake, raises blood pressure, attenuates baro-reflex function, and increases vasopressin secretion. Sodium 48-54 angiotensinogen Homo sapiens 0-14 10456229-1 1999 In many mammalian tissue types an integral membrane protein--the sodium/calcium (Na/Ca) exchanger--plays a key role in intracellular Ca homeostasis, and evidence suggests that Na/Ca exchange function can be modulated by cAMP-dependent phosphorylation. Sodium 65-71 nascent polypeptide associated complex subunit alpha Homo sapiens 81-86 10361442-2 1999 In addition, AngII enhances tubular reabsorption of sodium in proximal tubules directly and indirectly as a consequence of glomerulotubular balance. Sodium 52-58 angiotensinogen Homo sapiens 13-18 10375961-10 1999 The intravenous administration of IL-1 beta increased the urinary sodium excretion. Sodium 66-72 interleukin 1 beta Homo sapiens 34-43 10375961-11 1999 The pretreatement of HS142-1, an ANH antagonist, abolished the increase in urinary sodium excretion induced by IL-1 beta. Sodium 83-89 interleukin 1 beta Homo sapiens 111-120 10216225-6 1999 Whole-cell patch-clamp studies demonstrate that TTX-R sodium currents in IB4+ neurons have a more hyperpolarized voltage-dependence of activation and inactivation than do IB4- neurons, suggesting different electrophysiological properties for SNS/PN3 and NaN. Sodium 54-60 sodium channel, voltage-gated, type X, alpha Mus musculus 246-249 10196218-1 1999 Parathyroid hormone (PTH) is a potent inhibitor of mammalian renal proximal tubule sodium absorption via suppression of the apical membrane Na/H exchanger (NHE-3). Sodium 83-89 parathyroid hormone Homo sapiens 0-19 10196218-1 1999 Parathyroid hormone (PTH) is a potent inhibitor of mammalian renal proximal tubule sodium absorption via suppression of the apical membrane Na/H exchanger (NHE-3). Sodium 83-89 parathyroid hormone Homo sapiens 21-24 10323304-10 1999 Following cessation of ICV AII infusion, arterial pressure and sodium excretion returned to values not significantly different from control. Sodium 63-69 angiotensinogen Rattus norvegicus 27-30 10323304-12 1999 These data confirm that low dose ICV AII causes hypertension and sodium retention in rats raised from weaning on moderately elevated sodium intake. Sodium 65-71 angiotensinogen Rattus norvegicus 37-40 10323304-12 1999 These data confirm that low dose ICV AII causes hypertension and sodium retention in rats raised from weaning on moderately elevated sodium intake. Sodium 133-139 angiotensinogen Rattus norvegicus 37-40 10456229-1 1999 In many mammalian tissue types an integral membrane protein--the sodium/calcium (Na/Ca) exchanger--plays a key role in intracellular Ca homeostasis, and evidence suggests that Na/Ca exchange function can be modulated by cAMP-dependent phosphorylation. Sodium 65-71 nascent polypeptide associated complex subunit alpha Homo sapiens 176-181 11715942-3 1999 In the lung, the loss of CFTR activity results in abnormal epithelial ion transport, including defective cyclic AMP-mediated chloride (Cl-) efflux and the hyper absorption of sodium ions. Sodium 175-181 CF transmembrane conductance regulator Homo sapiens 25-29 10981059-6 1999 This action of angiotensin II occurs when the renin-angiotensin system is activated, as in sodium depletion. Sodium 91-97 angiotensinogen Homo sapiens 15-29 10201880-7 1999 However, when AngII levels are inappropriately elevated, this necessitates increased arterial pressure to maintain sodium and water balance. Sodium 115-121 angiotensinogen Homo sapiens 14-19 10207168-9 1999 SDCT2 expressed in Xenopus oocytes mediated sodium-dependent transport of di- and tricarboxylates with substrate preference for succinate rather than citrate, but excluding monocarboxylates. Sodium 44-50 solute carrier family 13 (sodium-dependent dicarboxylate transporter), member 3 L homeolog Xenopus laevis 0-5 10194528-9 1999 Previous studies have found that adrenals from animals on a low sodium diet exhibit increased responsiveness to VIP. Sodium 64-70 vasoactive intestinal peptide Rattus norvegicus 112-115 10205239-8 1999 During high sodium intake, plasma renin activity and aldosterone decreased and plasma atrial natriuretic peptide increased; these changes did not correlate with the change in mean arterial pressure, insulin resistance, or change in urinary nitrate excretion. Sodium 12-18 renin Homo sapiens 34-39 10205239-10 1999 The results also demonstrate that insulin-resistant individuals have an impaired natriuretic response to high sodium intake. Sodium 110-116 insulin Homo sapiens 34-41 10205240-1 1999 We hypothesized that short-term exposure to angiotensin II (Ang II) could result in structural and functional changes in the kidney that would favor sodium retention and the development of sustained hypertension. Sodium 149-155 angiotensinogen Rattus norvegicus 44-58 10205240-1 1999 We hypothesized that short-term exposure to angiotensin II (Ang II) could result in structural and functional changes in the kidney that would favor sodium retention and the development of sustained hypertension. Sodium 149-155 angiotensinogen Rattus norvegicus 60-66 10205241-9 1999 Plasma renin levels, measured in 20 patients, were elevated in most cases and correlated inversely (r=-0.63, P<0.01) with the plasma sodium concentration. Sodium 136-142 renin Homo sapiens 7-12 10194528-10 1999 Specific VIP binding sites were identified, although the concentration or affinity of binding sites in the low sodium group was not significantly different from the controls. Sodium 111-117 vasoactive intestinal peptide Rattus norvegicus 9-12 10194528-11 1999 In the low sodium group VIP was found to increase catecholamine release to the same extent as in the control group, however, in contrast to the control group, the adrenal response to VIP was not altered by adrenergic antagonists in the low sodium group. Sodium 11-17 vasoactive intestinal peptide Rattus norvegicus 24-27 10066920-2 1999 Regulation of the amiloride-sensitive epithelial sodium channel (ENaC) is essential for the control of body sodium homeostasis. Sodium 49-55 sodium channel epithelial 1 subunit gamma Rattus norvegicus 65-69 10333344-0 1999 Role of insulin resistance in the genesis of sodium sensitivity in essential hypertension. Sodium 45-51 insulin Homo sapiens 8-15 10333344-2 1999 It was examined whether sodium sensitivity was associated with insulin resistance, an important atherosclerotic cardiovascular risk factor in essential hypertension. Sodium 24-30 insulin Homo sapiens 63-70 10333344-6 1999 The insulin resistance index was positively correlated with the sodium sensitivity index, while was negatively correlated with fractional excretion of sodium (FE(Na)) obtained during a high sodium diet. Sodium 64-70 insulin Homo sapiens 4-11 10333344-6 1999 The insulin resistance index was positively correlated with the sodium sensitivity index, while was negatively correlated with fractional excretion of sodium (FE(Na)) obtained during a high sodium diet. Sodium 151-157 insulin Homo sapiens 4-11 10333344-6 1999 The insulin resistance index was positively correlated with the sodium sensitivity index, while was negatively correlated with fractional excretion of sodium (FE(Na)) obtained during a high sodium diet. Sodium 151-157 insulin Homo sapiens 4-11 10333344-9 1999 These results showed that insulin resistance might participate in the genesis of sodium sensitivity in essential hypertension by enhancing tubular sodium reabsorption, as reflected in decreased FE(Na) and augmented creatinine clearance. Sodium 81-87 insulin Homo sapiens 26-33 10333344-9 1999 These results showed that insulin resistance might participate in the genesis of sodium sensitivity in essential hypertension by enhancing tubular sodium reabsorption, as reflected in decreased FE(Na) and augmented creatinine clearance. Sodium 147-153 insulin Homo sapiens 26-33 10333344-10 1999 Insulin resistance seemed elevated in sodium sensitive state of essential hypertension, leading to future cardiovascular events. Sodium 38-44 insulin Homo sapiens 0-7 10333377-10 1999 The serotonin transporter is known to play a critical role in the termination of serotonergic neurotransmission by sodium-dependent uptake of 5-HT into the presynaptic neuron. Sodium 115-121 solute carrier family 6 member 4 Homo sapiens 4-25 10225537-6 1999 Besides its induction in cells at inflammatory sites, COX-2 is known to be induced in the kidney in response to sodium depletion or in hyperfiltration states; in postsynaptic excitatory neurons in the brain after electroconvulsive stimulation, in the ovary and uterus during ovulation and implantation; in intestinal epithelium after bacterial infection; as well as in colon adenoma and carcinoma cells. Sodium 112-118 mitochondrially encoded cytochrome c oxidase II Homo sapiens 54-59 10213527-4 1999 This feedback inhibition for renin release and suppression of aldosterone is reduced with normal sodium intake. Sodium 97-103 renin Homo sapiens 29-34 10051289-2 1999 Combined angiotensin II type I (AT1) receptor blockade and ACE inhibition more completely suppresses the activated renin-angiotensin system than either intervention alone in sodium-depleted normal individuals. Sodium 174-180 angiotensin I converting enzyme Homo sapiens 59-62 10051289-2 1999 Combined angiotensin II type I (AT1) receptor blockade and ACE inhibition more completely suppresses the activated renin-angiotensin system than either intervention alone in sodium-depleted normal individuals. Sodium 174-180 renin Homo sapiens 115-120 10070111-3 1999 Acute intervention with the inducible NO synthase (iNOS)-selective inhibitor S-methylisothiourea resulted in an increase of amiloride-sensitive sodium absorption observed as a hyperpolarization of nasal transepithelial potential difference. Sodium 144-150 nitric oxide synthase 2, inducible Mus musculus 28-49 10372513-0 1999 Effects of the alpha antagonists and agonists injected into the lateral hypothalamus on the water and sodium intake induced by angiotensin II injection into the subfornical organ. Sodium 102-108 angiotensinogen Homo sapiens 127-141 10372513-5 1999 Previous administration of clonidine (an alpha2-adrenergic agonist) or noradrenaline into the LH increased, whereas pretreatment with phenylephrine decreased the sodium intake induced by injection of ANG II into the SFO. Sodium 162-168 angiotensinogen Homo sapiens 200-206 10070111-3 1999 Acute intervention with the inducible NO synthase (iNOS)-selective inhibitor S-methylisothiourea resulted in an increase of amiloride-sensitive sodium absorption observed as a hyperpolarization of nasal transepithelial potential difference. Sodium 144-150 nitric oxide synthase 2, inducible Mus musculus 51-55 10028059-3 1999 Though it has been shown that sodium ions and amiloride molecules interact at unique regions of the NHE-1 protein, physiological experiments reveal a competitive relationship between the two under some circumstances. Sodium 30-36 solute carrier family 9 member A1 Homo sapiens 100-105 10204985-7 1999 The extent of fluoride and sodium incorporation in the apatites formed varied depending on the NaF concentration of the solution. Sodium 27-33 C-X-C motif chemokine ligand 8 Homo sapiens 95-98 10091588-3 1999 Under low sodium concentration (5 mM Na+) the BPTI affinity for alpha-thrombin was roughly threefold lower than in the presence of 150 mM sodium (Ki = 320 microM vs. 100 microM). Sodium 10-16 coagulation factor II, thrombin Homo sapiens 70-78 9990089-0 1999 Two serine residues of the glutamate transporter GLT-1 are crucial for coupling the fluxes of sodium and the neurotransmitter. Sodium 94-100 solute carrier family 1 member 2 Homo sapiens 49-54 10022444-8 1999 Urine sodium excretion, increased by NEP inhibition (P < 0.05) and by BNP (P = 0.05), was unchanged during combined treatment. Sodium 6-12 membrane metalloendopeptidase Homo sapiens 37-40 10067792-6 1999 RESULTS: Sodium depletion resulted in activation of the renin-angiotensin and sympathetic nervous systems, as indicated by increased levels of plasma renin, aldosterone and heart rate (P < 0.05). Sodium 9-15 renin Homo sapiens 56-61 10067792-1 1999 OBJECTIVE: Sodium depletion stimulates the renin-angiotensin and sympathetic nervous systems, which may affect the role of each of these systems in the regulation of vascular tone. Sodium 11-17 renin Homo sapiens 43-48 10067792-6 1999 RESULTS: Sodium depletion resulted in activation of the renin-angiotensin and sympathetic nervous systems, as indicated by increased levels of plasma renin, aldosterone and heart rate (P < 0.05). Sodium 9-15 renin Homo sapiens 150-155 10067792-11 1999 CONCLUSIONS: In sodium-depleted subjects, endogenous angiotensin II appears to play a role in the regulation of forearm vascular tone, in contrast to sodium-replete conditions. Sodium 16-22 angiotensinogen Homo sapiens 53-67 9927610-0 1999 Pivotal role of an aspartate residue in sodium sensitivity and coupling to G proteins of neurotensin receptors. Sodium 40-46 neurotensin Homo sapiens 89-100 10048594-11 1999 This study has demonstrated that P2X7 receptor function can be markedly affected by a wide range of ions and that physiological concentrations of sodium and chloride ions, as well as divalent cations, contribute to the low potency of ATP as an agonist at this receptor. Sodium 146-152 purinergic receptor P2X 7 Homo sapiens 33-46 9927610-2 1999 NTR1 couples to Galphaq to stimulate phospholipase C and its binding affinity for neurotensin is decreased by sodium ions and GTP analogs. Sodium 110-116 neurotensin Homo sapiens 82-93 9927610-6 1999 We demonstrate that the presence of the Asp residue determines by itself the occurrence of the sodium effect on neurotensin affinity for both wild-type and mutated NTR1 and -2. Sodium 95-101 neurotensin Homo sapiens 112-123 9887174-7 1999 Intravenous infusion of ANG II induced equal drinking responses despite reduced pressor responses in the BDL rats relative to sham-ligated rats during both ad libitum and sodium-depleted conditions. Sodium 171-177 angiotensinogen Rattus norvegicus 24-30 10676448-5 1999 We have investigated the role of cholecystokinin (CCK) in the control of sodium appetite. Sodium 73-79 cholecystokinin Homo sapiens 33-48 9934750-12 1999 Only interleukin-6 levels had significant correlations with Child score, plasma renin activity, serum and urinary sodium, and mean arterial pressure (r > or = 0.4, p < 0.005). Sodium 114-120 interleukin 6 Homo sapiens 5-18 10676448-5 1999 We have investigated the role of cholecystokinin (CCK) in the control of sodium appetite. Sodium 73-79 cholecystokinin Homo sapiens 50-53 10505665-2 1999 Hence, altered dietary sodium (Na) intake, changes in renal perfusion pressure, and/or renal adrenoreceptor activity would lead to changes in renin release and plasma angiotensin II (Ang II) concentration, which in turn contribute to regulation of blood pressure and sodium balance. Sodium 23-29 renin Homo sapiens 142-147 10505665-2 1999 Hence, altered dietary sodium (Na) intake, changes in renal perfusion pressure, and/or renal adrenoreceptor activity would lead to changes in renin release and plasma angiotensin II (Ang II) concentration, which in turn contribute to regulation of blood pressure and sodium balance. Sodium 23-29 angiotensinogen Homo sapiens 167-181 10505665-2 1999 Hence, altered dietary sodium (Na) intake, changes in renal perfusion pressure, and/or renal adrenoreceptor activity would lead to changes in renin release and plasma angiotensin II (Ang II) concentration, which in turn contribute to regulation of blood pressure and sodium balance. Sodium 23-29 angiotensinogen Homo sapiens 183-189 10505665-2 1999 Hence, altered dietary sodium (Na) intake, changes in renal perfusion pressure, and/or renal adrenoreceptor activity would lead to changes in renin release and plasma angiotensin II (Ang II) concentration, which in turn contribute to regulation of blood pressure and sodium balance. Sodium 267-273 renin Homo sapiens 142-147 10505665-2 1999 Hence, altered dietary sodium (Na) intake, changes in renal perfusion pressure, and/or renal adrenoreceptor activity would lead to changes in renin release and plasma angiotensin II (Ang II) concentration, which in turn contribute to regulation of blood pressure and sodium balance. Sodium 267-273 angiotensinogen Homo sapiens 167-181 10505665-2 1999 Hence, altered dietary sodium (Na) intake, changes in renal perfusion pressure, and/or renal adrenoreceptor activity would lead to changes in renin release and plasma angiotensin II (Ang II) concentration, which in turn contribute to regulation of blood pressure and sodium balance. Sodium 267-273 angiotensinogen Homo sapiens 183-189 9892172-5 1999 Experimental evidence indicates that angiotensin II possibly formed and acting locally may be implicated in the genesis of cardiac hypertrophy; however, angiotensin II by itself causes relatively minor hypertrophy, but this becomes intensified if there is a high sodium intake and a high angiotensin II level. Sodium 263-269 angiotensinogen Rattus norvegicus 37-51 9931123-3 1999 However, only the plasma renin level responds to changes in blood pressure and sodium balance to maintain blood pressure homeostasis. Sodium 79-85 renin Homo sapiens 25-30 9892162-5 1999 Although the mechanisms responsible for the regulation of intratubular AngII concentrations remain to be determined, micropuncture studies have provided direct evidence that activation of intraluminal AT1 receptors by AngII exerts a substantial stimulatory influence on sodium and bicarbonate transport by both proximal and distal tubules. Sodium 270-276 angiotensinogen Homo sapiens 218-223 9892172-5 1999 Experimental evidence indicates that angiotensin II possibly formed and acting locally may be implicated in the genesis of cardiac hypertrophy; however, angiotensin II by itself causes relatively minor hypertrophy, but this becomes intensified if there is a high sodium intake and a high angiotensin II level. Sodium 263-269 angiotensinogen Rattus norvegicus 153-167 9892172-5 1999 Experimental evidence indicates that angiotensin II possibly formed and acting locally may be implicated in the genesis of cardiac hypertrophy; however, angiotensin II by itself causes relatively minor hypertrophy, but this becomes intensified if there is a high sodium intake and a high angiotensin II level. Sodium 263-269 angiotensinogen Rattus norvegicus 153-167 10076924-5 1999 These findings suggest that inhibition of angiotensin II action by candesartan can improve insulin sensitivity and inhibit the sodium-retaining action associated with hyperinsulinaemia in essential hypertension. Sodium 127-133 angiotensinogen Homo sapiens 42-56 9893061-9 1999 Other cellular responses that require PKC activation in these cells, such as sodium-dependent phosphate transport and cAMP-independent secretion of plasminogen activator, were induced by PTH(1-34) but not by hPTH(3-34) or hPTH(7-34). Sodium 77-83 parathyroid hormone Rattus norvegicus 187-190 9916128-4 1999 Both could be blocked by PD or L-NAME, suggesting that the effects of sodium restriction occur via ANG II at the AT2 receptor. Sodium 70-76 angiotensinogen Rattus norvegicus 99-105 10429360-1 1999 Since adducin modulates cellular sodium retention, its follows that ADD1, which encodes the alpha-subunit of adducin, is an attractive candidate gene for blood pressure variation. Sodium 33-39 adducin 1 Homo sapiens 68-72 9893137-13 1999 CONCLUSIONS: The renal microcirculation in sodium-replete women may respond differently to Ang II than that of men, with the female sex predicting a lesser augmentation of FF and possibly a blunted increase in intraglomerular pressure. Sodium 43-49 angiotensinogen Homo sapiens 91-97 9857212-4 1999 Two approaches were used to probe for the three subunits of ENaC in the anterior and posterior tongue of the rats in sodium balance. Sodium 117-123 sodium channel epithelial 1 subunit gamma Rattus norvegicus 60-64 9922372-4 1999 The process of adaptation is associated with various changes in genetic expression, including a general activation that causes hypertrophy, isogenic shifts which result in the appearance of a slow isomyosin, and a new Na+-K+-ATPase with a low affinity for sodium, reactivation of genes encoding for atrial natriuretic factor and the renin-angiotensin system, and a diminished concentration of sarcoplasmic reticulum Ca2+-ATPase, beta-adrenergic receptors, and the potassium channel responsible for transient outward current. Sodium 256-262 renin Homo sapiens 333-338 10207252-8 1999 Second, activation of the tubuloglomerular feedback system enhances intrarenal angiotensin II release, which augments proximal sodium absorption. Sodium 127-133 angiotensinogen Homo sapiens 79-93 10207260-9 1999 GH may also raise preload through its sodium-retaining action and its interference with the hormonal system that regulates water and electrolyte metabolism. Sodium 38-44 growth hormone 1 Homo sapiens 0-2 10063831-4 1999 We have also excluded the MN1 disease locus from the chromosomal regions containing the genes for the muscle sodium (alpha- and beta-subunits) and chloride channels, both of which are involved in other myotonic disorders. Sodium 109-115 MN1 proto-oncogene, transcriptional regulator Homo sapiens 26-29 10573789-6 1999 Multiple agents, including vasopressin, glucagon, calcitonin, parathyroid hormone, beta-adrenergic agonist, insulin, angiotensin II, prostaglandins and calcium and magnesium ions influence sodium transport in the thick ascending limb, indicating that all of these factors may potentially play a role in enuresis. Sodium 189-195 parathyroid hormone Homo sapiens 62-81 10390859-4 1999 For bradykinin and kemptide, a significant mobility difference between protonated and sodiated species (where sodium replaced a proton in singly and doubly charged peptides) was demonstrated. Sodium 110-116 kininogen 1 Homo sapiens 4-14 9860786-2 1998 Because this phenomenon is reversed by ACE inhibition, abnormalities of renal sodium handling may depend on intrarenal changes of angiotensin II (AII)/nitric oxide (NO) levels. Sodium 78-84 angiotensin I converting enzyme Homo sapiens 39-42 9860786-2 1998 Because this phenomenon is reversed by ACE inhibition, abnormalities of renal sodium handling may depend on intrarenal changes of angiotensin II (AII)/nitric oxide (NO) levels. Sodium 78-84 angiotensinogen Homo sapiens 130-144 9860786-2 1998 Because this phenomenon is reversed by ACE inhibition, abnormalities of renal sodium handling may depend on intrarenal changes of angiotensin II (AII)/nitric oxide (NO) levels. Sodium 78-84 angiotensinogen Homo sapiens 146-149 9928060-0 1998 Effect of sodium depletion by frusemide on tissue concentrations and metabolism of VIP. Sodium 10-16 vasoactive intestinal peptide Homo sapiens 83-86 9920685-6 1998 A physiological role for ANG II in water intake induced by sodium depletion has recently been disputed, but the simplest explanation for the data remains that elevated levels of circulating ANG II bind to receptors in the SFO to generate daytime water drinking during sodium depletion. Sodium 59-65 angiotensinogen Rattus norvegicus 25-31 9837945-2 1998 Cells deleted for SOP1 exhibited sensitivity to sodium stress, but showed no sensitivity to general osmotic stress. Sodium 48-54 Rab GTPase-binding protein SRO7 Saccharomyces cerevisiae S288C 18-22 9920685-6 1998 A physiological role for ANG II in water intake induced by sodium depletion has recently been disputed, but the simplest explanation for the data remains that elevated levels of circulating ANG II bind to receptors in the SFO to generate daytime water drinking during sodium depletion. Sodium 268-274 angiotensinogen Rattus norvegicus 190-196 9951557-8 1998 On the other hand, while there was a decrease in water intake (45%, N = 9, P < 0.01), ANG II-induced sodium intake was significantly increased (70%, N = 8, P < 0.01) following injection of the V1-type vasopressin antagonist d(CH2)5-Tyr(Me)-AVP into the SON. Sodium 104-110 angiotensinogen Rattus norvegicus 89-95 9951557-9 1998 These results suggest that both AT1 and V1 receptors within the SON may be involved in water and sodium intake induced by the activation of ANG II receptors within the MSA. Sodium 97-103 angiotensinogen Rattus norvegicus 140-146 9848775-5 1998 In hREN without controlled renal function, urine flow and sodium excretion increased from 13 to 169 microl/min per g kidney wet weight (kwt) and from 1 to 30 micromol/min per g kwt, respectively, as renal perfusion pressure was increased from 67 to 135 mmHg. Sodium 58-64 renin Homo sapiens 3-7 9886874-3 1998 Production of ET-1 is enhanced in several experimental models of hypertension in the rat, such as sodium-sensitive forms, e.g. deoxycorticosterone acetate (DOCA)-salt hypertensive, DOCA-salt-treated spontaneously hypertensive rats (SHR) and Dahl salt-sensitive rats, as well as other models such as stroke-prone SHR, angiotensin II-infused rats and fructose-fed rats, and possibly 1-K 1C Goldblatt hypertensive rats. Sodium 98-104 endothelin 1 Rattus norvegicus 14-18 9869490-2 1998 Because inhibiting the Na-H exchanger (NHE) limits intracellular sodium ([Na]i) and subsequent [Ca]i accumulation, we hypothesized that NHE inhibition would attenuate regional dysfunction in response to 25 cycles of ischemia (I, 2-min) and reperfusion (R, 8-min) of the left circumflex coronary artery (LCx) in conscious swine. Sodium 65-71 solute carrier family 9 member A2 Sus scrofa 23-37 9869490-2 1998 Because inhibiting the Na-H exchanger (NHE) limits intracellular sodium ([Na]i) and subsequent [Ca]i accumulation, we hypothesized that NHE inhibition would attenuate regional dysfunction in response to 25 cycles of ischemia (I, 2-min) and reperfusion (R, 8-min) of the left circumflex coronary artery (LCx) in conscious swine. Sodium 65-71 solute carrier family 9 member A2 Sus scrofa 39-42 9869490-2 1998 Because inhibiting the Na-H exchanger (NHE) limits intracellular sodium ([Na]i) and subsequent [Ca]i accumulation, we hypothesized that NHE inhibition would attenuate regional dysfunction in response to 25 cycles of ischemia (I, 2-min) and reperfusion (R, 8-min) of the left circumflex coronary artery (LCx) in conscious swine. Sodium 65-71 solute carrier family 9 member A2 Sus scrofa 136-139 9886874-3 1998 Production of ET-1 is enhanced in several experimental models of hypertension in the rat, such as sodium-sensitive forms, e.g. deoxycorticosterone acetate (DOCA)-salt hypertensive, DOCA-salt-treated spontaneously hypertensive rats (SHR) and Dahl salt-sensitive rats, as well as other models such as stroke-prone SHR, angiotensin II-infused rats and fructose-fed rats, and possibly 1-K 1C Goldblatt hypertensive rats. Sodium 98-104 angiotensinogen Rattus norvegicus 317-331 9853274-1 1998 BACKGROUND: Non-steroidal anti-inflammatory drugs are known to promote sodium retention and to blunt the blood pressure lowering effects of several classes of antihypertensive agents including beta-blockers, diuretics and angiotensin converting enzyme (ACE) inhibitors. Sodium 71-77 angiotensin I converting enzyme Homo sapiens 222-251 9853270-2 1998 Several lines of evidence have shown that renin gene expression and release are up-regulated by beta-adrenergic stimulation, sodium depletion, and angiotensin converting enzyme inhibition, but down-regulated by cytokines. Sodium 125-131 renin Homo sapiens 42-47 9853274-1 1998 BACKGROUND: Non-steroidal anti-inflammatory drugs are known to promote sodium retention and to blunt the blood pressure lowering effects of several classes of antihypertensive agents including beta-blockers, diuretics and angiotensin converting enzyme (ACE) inhibitors. Sodium 71-77 angiotensin I converting enzyme Homo sapiens 253-256 10098717-0 1998 The family of sodium-dependent glutamate transporters: a focus on the GLT-1/EAAT2 subtype. Sodium 14-20 solute carrier family 1 member 2 Homo sapiens 70-75 10098717-0 1998 The family of sodium-dependent glutamate transporters: a focus on the GLT-1/EAAT2 subtype. Sodium 14-20 solute carrier family 1 member 2 Homo sapiens 76-81 9822114-1 1998 Traditionally, arginine vasopressin modulation of renal water, sodium, and urea excretion has been considered somewhat in isolation from factors that control divalent mineral ion homeostasis. Sodium 63-69 arginine vasopressin Homo sapiens 24-35 9849902-5 1998 In hypertonic medium (400 mosmol/ll), TFF1 and TFF3 were down-regulated, whereas TFF2 was up-regulated by elevated concentrations of sodium or chloride in MKN45. Sodium 133-139 trefoil factor 2 Homo sapiens 81-85 9791080-14 1998 Plasma sodium concentration and osmolality decreased during ANP infusion in SW and FW eels, and they were restored after saline infusion. Sodium 7-13 natriuretic peptide A Homo sapiens 60-63 9832178-8 1998 Our results suggest that renal ET-1 may be responsible for the renal handling of sodium homeostasis, and alteration of renal ET-1 synthesis may be a contributory factor in the pathogenesis of essential hypertension and salt sensitivity. Sodium 81-87 endothelin 1 Homo sapiens 31-35 9791046-6 1998 During atrial natriuretic peptide infusion, urinary endothelin-1 directly correlated with plasma atrial natriuretic peptide, urinary cGMP and sodium excretion.3. Sodium 142-148 endothelin 1 Homo sapiens 52-64 9822438-4 1998 With sodium restriction, plasma renin activity rose from 0.65 to 3.03 ng. Sodium 5-11 renin Homo sapiens 32-37 9887383-3 1998 A cDNA encoding for the beta 2 subunit of the human brain sodium channel, SCN2B, has been recently assigned to the same chromosomal interval by FISH. Sodium 58-64 sodium voltage-gated channel beta subunit 2 Homo sapiens 74-79 9797475-2 1998 A positive correlation between the fractional excretions of calcium and sodium was found in all groups, but the PHPx patients excreted more calcium for the same amount of sodium than control subjects. Sodium 171-177 SRY-box transcription factor 3 Homo sapiens 112-116 9814499-1 1998 Antipeptide antibodies raised against the carboxyl-terminal region of the human sodium/iodide (Na+/I-) symporter (hNIS) were used to investigate by immunohistochemistry the presence and distribution of the hNIS protein in normal thyroid tissues, in some pathological nonneoplastic thyroid tissues, and in different histotypes of thyroid neoplasms. Sodium 80-86 solute carrier family 5 member 5 Homo sapiens 95-112 9855447-7 1998 Significant correlations were observed between plasma ANP and urinary cGMP excretion (r = 0.48, P < .025 and r = 0.43, P < .05 in Htx recipients and control subjects) and between plasma ANP and urinary sodium excretion (r = 0.64, P < .001 in Htx recipients). Sodium 208-214 natriuretic peptide A Homo sapiens 54-57 9814499-1 1998 Antipeptide antibodies raised against the carboxyl-terminal region of the human sodium/iodide (Na+/I-) symporter (hNIS) were used to investigate by immunohistochemistry the presence and distribution of the hNIS protein in normal thyroid tissues, in some pathological nonneoplastic thyroid tissues, and in different histotypes of thyroid neoplasms. Sodium 80-86 solute carrier family 5 member 5 Homo sapiens 114-118 9839820-6 1998 The homologous relationship between rPN3 and hPN3 is defined by (i) a high level of sequence identity (ii) sodium currents that are highly resistant to tetrodotoxin (TTX) (iii) similar tissue distribution profiles and (iv) orthologous chromosomal map positions. Sodium 107-113 sodium voltage-gated channel alpha subunit 10 Rattus norvegicus 36-40 9786924-7 1998 These data indicate that the loss of NCC activity in the mouse causes only subtle perturbations of sodium and fluid volume homeostasis, but renal handling of Mg2+ and Ca2+ are altered, as observed in Gitelman"s syndrome. Sodium 99-105 solute carrier family 12, member 3 Mus musculus 37-40 9828151-7 1998 In the medium containing choline instead of sodium or the medium without potassium, an elevation of [Mg2+]i with addition of insulin/IGF-1 was moderately suppressed. Sodium 44-50 insulin Homo sapiens 125-132 9855309-0 1998 Voltage-activated sodium currents in a cell line expressing a Cu,Zn superoxide dismutase typical of familial ALS. Sodium 18-24 superoxide dismutase 1 Homo sapiens 62-88 9792817-5 1998 The replacement of extracellular sodium with Li reduced CT1-mediated L-carnitine uptake to 19.8%. Sodium 33-39 solute carrier family 22 member 5 Rattus norvegicus 56-59 9757019-1 1998 The neuropeptides angiotensin II (AngII) and oxytocin (OT) play important but opposing roles in the regulation of sodium appetite in the rat, AngII as a stimulatory peptide and OT as an inhibitory peptide. Sodium 114-120 angiotensinogen Rattus norvegicus 18-32 9757019-1 1998 The neuropeptides angiotensin II (AngII) and oxytocin (OT) play important but opposing roles in the regulation of sodium appetite in the rat, AngII as a stimulatory peptide and OT as an inhibitory peptide. Sodium 114-120 angiotensinogen Rattus norvegicus 34-39 9828151-9 1998 Insulin/ IGF-1 translocates Mg2+ from the extracellular space to intracellular space and these effects are affected by external sodium and potassium. Sodium 128-134 insulin Homo sapiens 0-7 9828151-9 1998 Insulin/ IGF-1 translocates Mg2+ from the extracellular space to intracellular space and these effects are affected by external sodium and potassium. Sodium 128-134 insulin like growth factor 1 Homo sapiens 9-14 9828151-7 1998 In the medium containing choline instead of sodium or the medium without potassium, an elevation of [Mg2+]i with addition of insulin/IGF-1 was moderately suppressed. Sodium 44-50 insulin like growth factor 1 Homo sapiens 133-138 9774359-6 1998 min-1 Ang II SC for 12 weeks on high sodium diet (2% NaCl). Sodium 37-43 angiotensinogen Rattus norvegicus 6-12 9774359-28 1998 Ang II induced hypertension and structural vascular changes are dose- and time-dependent and synergistically enhanced by dietary sodium supplementation. Sodium 129-135 angiotensinogen Rattus norvegicus 0-6 9802016-0 1998 The Nha1 antiporter of Saccharomyces cerevisiae mediates sodium and potassium efflux. Sodium 57-63 Nha1p Saccharomyces cerevisiae S288C 4-8 9830275-4 1998 The 24-hour urinary excretion of ET-1 in patients with GN or CRF showed significant correlation with the urinary excretion of sodium (r = 0.27, p < 0.05). Sodium 126-132 endothelin 1 Homo sapiens 33-37 9730777-3 1998 AII increased renal vascular resistance (RVR), glomerular filtration rate (GFR) and urinary volume (UV) and sodium excretion (UNaV) without changing the fractional excretion of water or electrolytes. Sodium 108-114 angiotensinogen Rattus norvegicus 0-3 9814852-0 1998 NHE-1 is the sodium-hydrogen exchanger isoform present in erythroid cells. Sodium 13-19 solute carrier family 9 member A1 Homo sapiens 0-5 9752889-0 1998 Strict dietary sodium reduction worsens insulin sensitivity by increasing sympathetic nervous activity in patients with primary hypertension. Sodium 15-21 insulin Homo sapiens 40-47 9724315-3 1998 Renal ET-1 formation is affected by sodium intake, because 1 wk of high sodium decreased urinary ET-1 excretion (-34%, P < 0.05), whereas a low-sodium diet increased ET-1 excretion (66%, P < 0.05) and mRNA expression for preproendothelin-1 in epithelial cells of medullary collecting ducts and endothelial cells of the peritubular capillary network. Sodium 72-78 endothelin 1 Homo sapiens 227-245 9752889-4 1998 Strict dietary sodium reduction to 30 mmol/day for 1 week resulted in no further decrease in blood pressure, but it increased plasma insulin by 40.6% without changing plasma glucose. Sodium 15-21 insulin Homo sapiens 133-140 9752889-7 1998 These results indicate that dietary sodium restriction leads to a deterioration of insulin sensitivity when plasma norepinephrine levels increase, and suggest that moderate dietary sodium reduction may lower blood pressure without a distinct adverse effect on glucose metabolism in subjects with primary hypertension. Sodium 36-42 insulin Homo sapiens 83-90 9752890-3 1998 The aim of this study is to clarify the influence of aging on insulin sensitivity in glucose metabolism and on renal sodium handling under hyperinsulinemia, which may relate to high blood pressure in insulin-resistant subjects. Sodium 117-123 insulin Homo sapiens 144-151 9752890-16 1998 These results suggested that both the impairments of the insulin sensitivity and insulin-induced vasodilation at the renal artery with aging may partially contribute to age-related elevation of blood pressure through renal sodium retention by compensating hyperinsulinemia. Sodium 223-229 insulin Homo sapiens 57-64 9724315-3 1998 Renal ET-1 formation is affected by sodium intake, because 1 wk of high sodium decreased urinary ET-1 excretion (-34%, P < 0.05), whereas a low-sodium diet increased ET-1 excretion (66%, P < 0.05) and mRNA expression for preproendothelin-1 in epithelial cells of medullary collecting ducts and endothelial cells of the peritubular capillary network. Sodium 72-78 endothelin 1 Homo sapiens 227-245 9736347-1 1998 Atrial natriuretic peptide (ANP) is one of the cardiac peptides implicated in volume and sodium homeostasis. Sodium 89-95 natriuretic peptide A Homo sapiens 0-26 9736347-1 1998 Atrial natriuretic peptide (ANP) is one of the cardiac peptides implicated in volume and sodium homeostasis. Sodium 89-95 natriuretic peptide A Homo sapiens 28-31 9740601-10 1998 We conclude that the angiotensinogen genotype may affect blood pressure response to sodium or weight reduction and the development of hypertension. Sodium 84-90 angiotensinogen Homo sapiens 21-36 10684103-0 1998 [Effects of plasma endothelin-1 and aldosterone on sodium retention in children with nephrotic syndrome]. Sodium 51-57 endothelin 1 Homo sapiens 19-31 10684103-6 1998 Plasma ET-1 was positively correlated with the serum sodium ionic concentration and negatively correlated with the serum Alb(r = 0.486, P < 0.01; r = 0.490, P < 0.01, respectively). Sodium 53-59 endothelin 1 Homo sapiens 7-11 10684103-7 1998 In conclusion, the sodium retention with nephrotic syndrome might be correlated with reduction of secreted sodium in the kidney, suggesting that ET-1 plays an important role in pathogenesis. Sodium 19-25 endothelin 1 Homo sapiens 145-149 10684103-7 1998 In conclusion, the sodium retention with nephrotic syndrome might be correlated with reduction of secreted sodium in the kidney, suggesting that ET-1 plays an important role in pathogenesis. Sodium 107-113 endothelin 1 Homo sapiens 145-149 9855025-2 1998 Because angiotensin II affects blood pressure control, sodium and water homeostasis, and cardiovascular function and structure, a great deal of research effort has been directed toward blocking the renin-angiotensin system. Sodium 55-61 angiotensinogen Homo sapiens 8-22 9736294-7 1998 A low-sodium diet had no significant effect on BP or on cardiac size, but prevented the cardiac hypertrophy produced by Ang II without altering the BP response. Sodium 6-12 angiotensinogen Rattus norvegicus 120-126 9688688-2 1998 In rats on normal sodium intake, ANG II at low dose stimulated net jejunal fluid absorption, whereas at a high dose the peptide inhibited absorption. Sodium 18-24 angiotensinogen Rattus norvegicus 33-39 9739038-0 1998 Epidermal growth factor and human growth hormone induce two sodium-dependent arginine transport systems after massive enterectomy. Sodium 60-66 growth hormone 1 Homo sapiens 34-48 9789303-4 1998 An increase in peripheral AVP results in suppression of amino acid permeability and increases in transport of sodium, potassium ions and water. Sodium 110-116 arginine vasopressin Homo sapiens 26-29 9679185-12 1998 The data demonstrate that plasma vasopressin and angiotensin II concentrations decrease during WI in hydrated humans, concomitantly with initial increases in CH2O and sodium excretion. Sodium 167-173 arginine vasopressin Homo sapiens 33-44 9688688-8 1998 In rats on normal sodium intake, low-dose ANG II increased jejunal interstitial and luminal (loop) fluid concentrations of cGMP. Sodium 18-24 angiotensinogen Rattus norvegicus 42-48 9688688-13 1998 The data demonstrate that ANG II mediates jejunal sodium and water absorption by an action at the AT2 receptor involving cGMP formation. Sodium 50-56 angiotensinogen Rattus norvegicus 26-32 9719044-5 1998 A sodium-deficient diet, angiotensin-converting enzyme inhibition, and beta1-adrenergic stimulation each increased both human and mouse plasma renin concentration significantly, whereas elevated blood pressure and/or increased plasma angiotensin II levels suppressed them. Sodium 2-8 renin Homo sapiens 143-148 9760076-6 1998 Low dose ICV AII infusion (20 ng min(-1) )increased mean arterial pressure by 12+/-2 mm Hg and decreased urinary sodium excretion for three consecutive days. Sodium 113-119 angiotensinogen Rattus norvegicus 13-16 9760076-9 1998 Following cessation of ICV AII infusion, arterial pressure and sodium excretion returned to values not significantly different from control in both groups of rats. Sodium 63-69 angiotensinogen Rattus norvegicus 27-30 9760076-10 1998 These data confirm that low dose ICV AII causes hypertension and sodium retention in rats raised from early age on moderately elevated sodium intakes. Sodium 65-71 angiotensinogen Rattus norvegicus 37-40 9760076-10 1998 These data confirm that low dose ICV AII causes hypertension and sodium retention in rats raised from early age on moderately elevated sodium intakes. Sodium 135-141 angiotensinogen Rattus norvegicus 37-40 9703338-0 1998 Enhanced responsiveness of blood pressure to sodium intake and to angiotensin II is associated with insulin resistance in IDDM patients with microalbuminuria. Sodium 45-51 insulin Homo sapiens 100-107 9703338-3 1998 Moreover, under high-sodium conditions, angiotensin II infusion (3 ng x kg(-1) x min(-1)) caused a greater increase in mean BP (14 +/- 2 vs. 7.4 +/- 1 mmHg; P < 0.05) and a smaller reduction in renal plasma flow (-122 +/- 29 vs. -274 +/- 41 ml x min(-1) x 1.73 m2; P < 0.05) in microalbuminuric than in normoalbuminuric IDDM patients. Sodium 21-27 angiotensinogen Homo sapiens 40-54 9703338-4 1998 Under low sodium conditions, aldosterone increments after angiotensin II infusion were lower (P < 0.05) in microalbuminuric than in normoalbuminuric IDDM patients. Sodium 10-16 angiotensinogen Homo sapiens 58-72 9679045-7 1998 CONCLUSIONS: In preascitic cirrhosis, sodium retention occurs in response to lower body negative pressure, which was associated with increased renal renin-angiotensin activity. Sodium 38-44 renin Homo sapiens 149-154 9679045-8 1998 Stimulation of the intrarenal renin-angiotensin system may be the initial renal pathophysiological change causing sodium retention in cirrhosis. Sodium 114-120 renin Homo sapiens 30-35 9694924-1 1998 Neuropeptide Y (NPY) is a unique modulator of renal function that enhances urine flow and sodium excretion despite marked reductions in renal blood flow. Sodium 90-96 neuropeptide Y Rattus norvegicus 0-14 9694924-1 1998 Neuropeptide Y (NPY) is a unique modulator of renal function that enhances urine flow and sodium excretion despite marked reductions in renal blood flow. Sodium 90-96 neuropeptide Y Rattus norvegicus 16-19 9644212-8 1998 These findings suggest that sodium deficiency stimulates adrenal AT1A and AT1B receptor mRNA levels primarily via an ANGII-AT1-independent mechanism. Sodium 28-34 angiotensin II receptor, type 1b Rattus norvegicus 74-78 9644212-9 1998 The preferential increase of adrenal AT1B mRNA during a low-salt intake could be explained by the elevation of endogenous ANGII levels during sodium deficiency, suggesting that endogenous ANGII acts as an enhancer for adrenal AT1B but not for AT1A receptor gene expression via ANGII-AT1 receptors. Sodium 142-148 angiotensin II receptor, type 1b Rattus norvegicus 37-41 9644212-8 1998 These findings suggest that sodium deficiency stimulates adrenal AT1A and AT1B receptor mRNA levels primarily via an ANGII-AT1-independent mechanism. Sodium 28-34 angiotensinogen Rattus norvegicus 117-122 9644212-9 1998 The preferential increase of adrenal AT1B mRNA during a low-salt intake could be explained by the elevation of endogenous ANGII levels during sodium deficiency, suggesting that endogenous ANGII acts as an enhancer for adrenal AT1B but not for AT1A receptor gene expression via ANGII-AT1 receptors. Sodium 142-148 angiotensinogen Rattus norvegicus 122-127 9644212-9 1998 The preferential increase of adrenal AT1B mRNA during a low-salt intake could be explained by the elevation of endogenous ANGII levels during sodium deficiency, suggesting that endogenous ANGII acts as an enhancer for adrenal AT1B but not for AT1A receptor gene expression via ANGII-AT1 receptors. Sodium 142-148 angiotensinogen Rattus norvegicus 188-193 9644212-9 1998 The preferential increase of adrenal AT1B mRNA during a low-salt intake could be explained by the elevation of endogenous ANGII levels during sodium deficiency, suggesting that endogenous ANGII acts as an enhancer for adrenal AT1B but not for AT1A receptor gene expression via ANGII-AT1 receptors. Sodium 142-148 angiotensinogen Rattus norvegicus 188-193 9651311-4 1998 Our findings indicate that Bcl-xl forms a cation-selective channel that conducts sodium but not calcium and that Bcl-xl channel activity is reversibly inhibited by luminal calcium with a half-dissociation constant of approximately 60 microM. Sodium 81-87 BCL2 like 1 Homo sapiens 27-33 9674650-2 1998 The 460Trp mutation of the human alpha-adducin gene has been associated with hypertension, in particular hypertension sensitive to sodium restriction. Sodium 131-137 adducin 1 Homo sapiens 33-46 9662488-18 1998 The lithium clearance data suggest that an increased proximal tubular reabsorption rate may contribute to the decreased sodium clearance during recombinant interleukin-2 treatment. Sodium 120-126 interleukin 2 Homo sapiens 156-169 9674641-1 1998 Angiotensin II exerts its effects on cardiovascular function and water and sodium homeostasis by interacting with plasma membrane receptors on target organs. Sodium 75-81 angiotensinogen Rattus norvegicus 0-14 9717743-2 1998 In the present studies, we examined the initial aggregation process of lysozyme (initial crystallization process of lysozyme) in D2O/H2O with sodium ions or potassium ions, and investigated the relationship between the surface hydrophobicity and the aggregation rate of lysozyme. Sodium 142-148 lysozyme Homo sapiens 71-79 9661610-7 1998 Our data taken in conjunction with those of previous studies evaluating sodium and calcium excretion in diseases characterized by inactivating or activating mutations in the calcium receptor, are consistent with the hypothesis that PTH-independent, calcium-dependent changes in renal calcium, magnesium, and sodium handling may be mediated at least in part by this receptor, which is known to be located in the loop of Henle. Sodium 72-78 parathyroid hormone Homo sapiens 232-235 9661610-7 1998 Our data taken in conjunction with those of previous studies evaluating sodium and calcium excretion in diseases characterized by inactivating or activating mutations in the calcium receptor, are consistent with the hypothesis that PTH-independent, calcium-dependent changes in renal calcium, magnesium, and sodium handling may be mediated at least in part by this receptor, which is known to be located in the loop of Henle. Sodium 308-314 parathyroid hormone Homo sapiens 232-235 9717743-2 1998 In the present studies, we examined the initial aggregation process of lysozyme (initial crystallization process of lysozyme) in D2O/H2O with sodium ions or potassium ions, and investigated the relationship between the surface hydrophobicity and the aggregation rate of lysozyme. Sodium 142-148 lysozyme Homo sapiens 116-124 9717743-3 1998 The effect of sodium ions or potassium ions on the initial aggregation process of lysozyme in D2O was clearly different from H2O. Sodium 14-20 lysozyme Homo sapiens 82-90 9717743-2 1998 In the present studies, we examined the initial aggregation process of lysozyme (initial crystallization process of lysozyme) in D2O/H2O with sodium ions or potassium ions, and investigated the relationship between the surface hydrophobicity and the aggregation rate of lysozyme. Sodium 142-148 lysozyme Homo sapiens 116-124 9674690-1 1998 Angiotensin (ANG) II is a powerful and phylogenetically widespread stimulus to thirst and sodium appetite. Sodium 90-96 angiotensinogen Homo sapiens 0-20 9674690-17 1998 But it is also certain that other mechanisms of thirst and sodium appetite still operate when the effects of circulating ANG II are blocked or absent, although it is not known whether this is also true for angiotensin peptides formed in the brain. Sodium 59-65 angiotensinogen Homo sapiens 121-127 9674690-18 1998 Whether ANG II should be regarded primarily as a hormone released in hypovolemia helping to defend the blood volume, a neurotransmitter or paracrine agent with a privileged role in the neural pathways for thirst and sodium appetite of all kinds, a neural organizer especially in sodium appetit Sodium 279-285 angiotensinogen Homo sapiens 8-14 10085711-2 1998 The defect of the ANP precursor gene leading to the decrease of ANP synthesis are a cause of the development of sodium-sensitive hypertension in animals. Sodium 112-118 natriuretic peptide A Homo sapiens 18-21 10085711-2 1998 The defect of the ANP precursor gene leading to the decrease of ANP synthesis are a cause of the development of sodium-sensitive hypertension in animals. Sodium 112-118 natriuretic peptide A Homo sapiens 64-67 10085711-3 1998 Recent findings in African-Americans who are a model of sodium-sensitive population, reveal a strong association between Sma I polymorphism at intron 2 (the polymorphic site is identical for Hpa II restriction enzyme) or both Sma I and Sca I polymorphism at exon 3 of ANP precursor gene and essential hypertension. Sodium 56-62 suppressor of cancer cell invasion Homo sapiens 236-241 10085711-6 1998 The frequency of Sca I M allele (allele with mutation) was significantly higher in SS group as compared to sodium-nonsensitive hypertensives. Sodium 107-113 suppressor of cancer cell invasion Homo sapiens 17-22 10085711-7 1998 Our results suggest that, in contrast to Black hypertensives, in Caucasians with essential hypertension the Sma I polymorphism is very rare and the Sca I polymorphism of ANP precursor gene is associated with sodium-sensitivity of blood pressure. Sodium 208-214 suppressor of cancer cell invasion Homo sapiens 148-153 10085711-7 1998 Our results suggest that, in contrast to Black hypertensives, in Caucasians with essential hypertension the Sma I polymorphism is very rare and the Sca I polymorphism of ANP precursor gene is associated with sodium-sensitivity of blood pressure. Sodium 208-214 natriuretic peptide A Homo sapiens 170-173 9636153-2 1998 Previous work has shown that yeast cells deficient in Ppz1 protein phosphatase or overexpressing Hal3p, a novel regulatory protein of unknown function, exhibit increased resistance to sodium and lithium, whereas cells lacking Hal3p display increased sensitivity. Sodium 184-190 salt homeostasis regulator Saccharomyces cerevisiae S288C 54-58 9681711-0 1998 The blunting of the antiproteinuric efficacy of ACE inhibition by high sodium intake can be restored by hydrochlorothiazide. Sodium 71-77 angiotensin I converting enzyme Homo sapiens 48-51 9681711-1 1998 BACKGROUND: Dietary sodium restriction enhances the antiproteinuric and blood pressure lowering effect of ACE inhibition. Sodium 20-26 angiotensin I converting enzyme Homo sapiens 106-109 9681711-3 1998 We therefore investigated whether the blunting of the antiproteinuric and blood pressure lowering efficacy of ACE inhibition by high sodium intake can be restored by the addition of a diuretic. Sodium 133-139 angiotensin I converting enzyme Homo sapiens 110-113 9681711-8 1998 CONCLUSION: Addition of hydrochlorothiazide can overcome the blunting of the therapeutic efficacy of ACE inhibition on proteinuria and blood pressure by a high sodium intake. Sodium 160-166 angiotensin I converting enzyme Homo sapiens 101-104 9631833-3 1998 In the kidney, IGF-I dilates the resistance-regulating microvasculature, increases glomerular filtration rate, and promotes tubular phosphate and possibly sodium absorption. Sodium 155-161 insulin like growth factor 1 Homo sapiens 15-20 9582047-7 1998 DATA SYNTHESIS: In 58 trials of hypertensive persons, the effect of reduced sodium intake as measured by urinary sodium excretion (mean, 118 mmol/24 h) on SBP was 3.9 mm Hg (95% confidence interval [CI], 3.0-4.8 mm Hg) (P<.001) and on DBP was 1.9 mm Hg (95% CI, 1.3-2.5 mm Hg) (P<.001). Sodium 76-82 D-box binding PAR bZIP transcription factor Homo sapiens 238-241 9841553-2 1998 The physiological state associated with water and sodium ingestion was produced by the concurrent subcutaneous administration of the diuretic furosemide (10 mg/kg) and a low dose of the angiotensin-converting enzyme (ACE) inhibitor captopril (5 mg/kg; Furo/Cap treatment). Sodium 50-56 angiotensin I converting enzyme Rattus norvegicus 217-220 9607177-12 1998 The finding of reduced slope after Na depletion or Na load supports the hypothesis that, as MHS rats, humans bearing one W alpha-adducin variant display an increased of renal tubular sodium reabsorption. Sodium 183-189 adducin 1 Homo sapiens 123-136 9603530-1 1998 BACKGROUND: The renin-angiotensin system regulates blood pressure through its effects on vascular tone, renal hemodynamics, and renal sodium and fluid balance. Sodium 134-140 renin Homo sapiens 16-21 9582047-10 1998 In plasma, the renin level increased 3.6-fold (P<.001), and the aldosterone level increased 3.2-fold (P<.001); the increases were proportional to the degree of sodium reduction for both renin (r=0.66; P<.001) and aldosterone (r=0.64; P<.001). Sodium 166-172 renin Homo sapiens 15-20 9644045-6 1998 We conclude that reductions of plasma ANG II associated with incremental increases of daily sodium intake result in a rise of renal cortical flow. Sodium 92-98 angiotensinogen Rattus norvegicus 38-44 9612329-9 1998 The data indicate that increased production of NO is an important part of the adaptation to increased dietary sodium intake in healthy humans, with respect to renal hemodynamics, sodium excretion, and the secretion of renin. Sodium 110-116 renin Homo sapiens 218-223 9589654-7 1998 Dietary sodium restriction may result in a decrease in peripheral insulin sensitivity in normotensive patients with NIDDM, possibly via an elevation in prevailing angiotensin II concentrations. Sodium 8-14 angiotensinogen Homo sapiens 163-177 9630341-0 1998 The receptor subtype mediating the action of angiotensin II on intracellular sodium in rat proximal tubules. Sodium 77-83 angiotensinogen Rattus norvegicus 45-59 9630341-2 1998 An investigation was undertaken to explore the subtype of receptor involved in mediating the actions of angiotensin II on intracellular sodium content in suspensions of isolated proximal tubules of the rat. Sodium 136-142 angiotensinogen Rattus norvegicus 104-118 9630341-10 1998 Angiotensin II 10(-5) M, administered to the tubular suspension in the presence of 10(-4) M PD123319, decreased (P < 0.01, n = 6) intracellular sodium content by 16% in the first 5 min, but in the following 25 min returned to steady state levels. Sodium 147-153 angiotensinogen Rattus norvegicus 0-14 9630341-13 1998 These findings show that at both the high and low concentrations of angiotensin II, its modulation of intracellular sodium levels within the proximal tubule cells is mediated via the activation of AT1 receptors. Sodium 116-122 angiotensinogen Rattus norvegicus 68-82 9591752-3 1998 A negative sodium balance was present throughout the diet and was associated with a moderate reduction in plasma volume, a marked activation of the renin-aldosterone system, and a concomitant reduction in C- and N-terminal ANF prohormone levels. Sodium 11-17 renin Homo sapiens 148-153 9572288-3 1998 The two high-affinity sodium-dependent glial transporters [glutamate transporter 1 (GLT-1) and glutamate aspartate transporter (GLAST)] mediate the bulk of glutamate transport. Sodium 22-28 solute carrier family 1 member 2 Rattus norvegicus 59-82 9572288-3 1998 The two high-affinity sodium-dependent glial transporters [glutamate transporter 1 (GLT-1) and glutamate aspartate transporter (GLAST)] mediate the bulk of glutamate transport. Sodium 22-28 solute carrier family 1 member 2 Rattus norvegicus 84-89 9591752-3 1998 A negative sodium balance was present throughout the diet and was associated with a moderate reduction in plasma volume, a marked activation of the renin-aldosterone system, and a concomitant reduction in C- and N-terminal ANF prohormone levels. Sodium 11-17 natriuretic peptide A Homo sapiens 223-226 9650340-14 1998 Alpha-adducin is a renal tubular protein, regulating the sodium balance. Sodium 57-63 adducin 1 Homo sapiens 0-13 9773124-1 1998 The renin-angiotensin system is involved in the control of sodium and water balance, mitogenesis and the regulation of vascular tone as well as of the activity of the sympathetic nervous system. Sodium 59-65 renin Homo sapiens 4-9 9581306-4 1998 The responses to intranasal arginine-vasopressin were prompt, normalizing the serum levels of sodium and increasing urinary osmolality, allowing a better metabolic balance, avoiding continuing damage to the already compromised CNS. Sodium 94-100 arginine vasopressin Homo sapiens 37-48 9575931-1 1998 Both brain ouabain-like activity ("ouabain") and brain angiotensin II (ANG II) contribute to the sympathoexcitatory and pressor responses to high sodium intake in spontaneously hypertensive (SHR) and Dahl salt-sensitive (Dahl S) rats. Sodium 146-152 angiotensinogen Rattus norvegicus 71-77 9575821-0 1998 Phosphatidylinositol 3-kinase activation is required for insulin-stimulated sodium transport in A6 cells. Sodium 76-82 insulin Homo sapiens 57-64 9575821-1 1998 Insulin stimulates amiloride-sensitive sodium transport in models of the distal nephron. Sodium 39-45 insulin Homo sapiens 0-7 9575821-3 1998 Functionally, a specific inhibitor of PI 3-kinase, LY-294002, blocks basal as well as insulin-stimulated sodium transport in a dose-dependent manner (IC50 approximately 6 microM). Sodium 105-111 insulin Homo sapiens 86-93 9605566-12 1998 Extracellular sodium and proton concentrations also modulated the voltage-dependence of L-serine-O-sulphate EC50 values for EAAT2. Sodium 14-20 solute carrier family 1 member 2 Homo sapiens 124-129 9605385-4 1998 In the normotensive group prekallikrein levels and renin activity correlated negatively with urinary sodium and chloride excretion during basal conditions and partially during the infusion. Sodium 101-107 renin Homo sapiens 51-56 9562936-10 1998 Patients discharged on a recommended ACE inhibitor dose were more likely to be African-American and had lower sodium levels and higher mean arterial pressures than patients discharged on lower ACE inhibitor doses. Sodium 110-116 angiotensin I converting enzyme Homo sapiens 37-40 9749785-0 1998 Modulation of the voltage-gated sodium current in rat striatal neurons by DARPP-32, an inhibitor of protein phosphatase. Sodium 32-38 protein phosphatase 1, regulatory (inhibitor) subunit 1B Rattus norvegicus 74-82 9555654-2 1998 Because cytochrome P-450-dependent arachidonate metabolites participate in the regulation of renal sodium transport and BP, this study tested the hypothesis that these renal responses to acute hypertension would be prevented if cytochrome P-450 metabolism were inhibited by cobalt chloride (CoCl2). Sodium 99-105 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 8-24 9555654-2 1998 Because cytochrome P-450-dependent arachidonate metabolites participate in the regulation of renal sodium transport and BP, this study tested the hypothesis that these renal responses to acute hypertension would be prevented if cytochrome P-450 metabolism were inhibited by cobalt chloride (CoCl2). Sodium 99-105 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 228-244 9749785-5 1998 Injection of phospho-DARPP-32, but not of the unphosphorylated form, reduced the sodium current amplitude. Sodium 81-87 protein phosphatase 1, regulatory (inhibitor) subunit 1B Rattus norvegicus 21-29 9749785-7 1998 Our results indicate that, in striatal neurons, sodium channels are under dynamic control by phosphorylation/dephosphorylation, and that phospho-DARPP-32 reduces sodium current by stabilizing a phosphorylated state of the channel or an associated regulatory protein. Sodium 48-54 protein phosphatase 1, regulatory (inhibitor) subunit 1B Rattus norvegicus 145-153 9547354-1 1998 The sodium-dependent, high affinity serotonin [5-hydroxytryptamine (5-HT)] transporter (5-HTT) provides the primary mechanism for inactivation of 5-HT after its release into the synaptic cleft. Sodium 4-10 solute carrier family 6 (neurotransmitter transporter, serotonin), member 4 Mus musculus 88-93 9797192-0 1998 Regulation of vascular type 1 angiotensin II receptor in hypertension and sodium loading: role of angiotensin II. Sodium 74-80 angiotensinogen Rattus norvegicus 30-44 9530121-0 1998 Insulin sensitivity is associated with blood pressure response to sodium in older hypertensives. Sodium 66-72 insulin Homo sapiens 0-7 9516469-1 1998 The sodium-calcium exchange activity is mediated by proteins encoded in a small gene family, of which the gene NCX1 is ubiquitously expressed in mammalian tissues. Sodium 4-10 solute carrier family 8 member A1 Homo sapiens 111-115 9482802-1 1998 The novel sodium channel PN3/alpha-SNS, which was cloned from a rat dorsal root ganglion (DRG) cDNA library, is expressed predominantly in small sensory neurons and may contribute to the tetrodotoxin-resistant (TTXR) sodium current that is believed to be associated with central sensitization in chronic neuropathic pain states. Sodium 10-16 sodium voltage-gated channel alpha subunit 10 Rattus norvegicus 25-28 9530121-1 1998 The purpose of this study was to determine whether sodium-resistant hypertensives are more insulin resistant and whether dietary sodium restriction improves insulin sensitivity in older hypertensives. Sodium 51-57 insulin Homo sapiens 91-98 9530121-1 1998 The purpose of this study was to determine whether sodium-resistant hypertensives are more insulin resistant and whether dietary sodium restriction improves insulin sensitivity in older hypertensives. Sodium 129-135 insulin Homo sapiens 157-164 10407367-4 1998 Similarly, intravenous saline infusion (2 mmol/kg/60 min) resulted in remarkable elevation of plasma ANF levels in patients and in controls (28.89+/-4.72 pg/ml and 20.18+/-2.48 pg/ml, respectively) and in increased urinary sodium and potassium excretion rates in both groups. Sodium 223-229 natriuretic peptide A Homo sapiens 101-104 9543596-1 1998 BACKGROUND: In a previous study we found that high angiotensin II levels in relation to the corresponding urinary sodium excretion aggravate left ventricular hypertrophy in hypertensive patients. Sodium 114-120 angiotensinogen Homo sapiens 51-65 9543596-9 1998 Subgroup analysis revealed that the increase in sodium excretion at high salt intake was related to the decrease in angiotensin II levels in normotensive (r = -0.43, p < 0.05), but not in hypertensive subjects (r = 0.16, n.s.). Sodium 48-54 angiotensinogen Homo sapiens 116-130 9495259-1 1998 Endothelin-1 (ET-1) is a cardiovascular peptide that binds to two distinct receptors, ET(A) and ET(B), resulting in systemic and regional vasoconstriction, alteration in sodium excretion, mitogenesis, and release of other vasoactive peptides such as atrial natriuretic peptide (ANP). Sodium 170-176 endothelin 1 Canis lupus familiaris 0-12 9495259-1 1998 Endothelin-1 (ET-1) is a cardiovascular peptide that binds to two distinct receptors, ET(A) and ET(B), resulting in systemic and regional vasoconstriction, alteration in sodium excretion, mitogenesis, and release of other vasoactive peptides such as atrial natriuretic peptide (ANP). Sodium 170-176 endothelin 1 Canis lupus familiaris 14-18 9495259-12 1998 The present investigation supports the conclusion that endogenous ET-1 participates in the systemic and pulmonary vasoconstriction, the elevation of ANP, and the sodium retention that characterize this model of experimental CHF, suggesting a potential therapeutic role for ET(A) receptor antagonism in CHF. Sodium 162-168 endothelin 1 Canis lupus familiaris 66-70 9478930-8 1998 As in adrenals cardiac 11beta-hydroxylase and aldosterone-synthase mRNAs were independently regulated by 1 week"s treatment with either low sodium and high potassium diet (which increased aldosterone synthase mRNA level only), angiotensin II (which raised level of both mRNAs), or adrenocorticotropin (which stimulated the 11beta-hydroxylase gene exclusively). Sodium 140-146 angiotensinogen Rattus norvegicus 227-241 9495269-0 1998 Human vascular renin-angiotensin system and its functional changes in relation to different sodium intakes. Sodium 92-98 renin Homo sapiens 15-20 9495269-7 1998 In high sodium diet subjects, plasma renin activity decreased, and de novo Ang I and Ang II formation by forearm vascular tissue increased to 22 and 14 fmol x 100 mL(-1) x min(-1), respectively (P<.01). Sodium 8-14 renin Homo sapiens 37-42 10990445-0 1998 Differential effects of fluoride and insulin-like growth factor I on sodium-dependent alanine and phosphate transport in a human osteoblast-like cell line. Sodium 69-75 insulin like growth factor 1 Homo sapiens 37-65 9493132-0 1998 Tumor necrosis factor-alpha increases sodium and chloride conductance across the tight junction of CACO-2 BBE, a human intestinal epithelial cell line. Sodium 38-44 tumor necrosis factor Homo sapiens 0-27 10026831-2 1998 With the onset of vasopressin escape, water excretion increases despite sustained administration of vasopressin, allowing water balance to be re-established and the serum sodium to be stabilized at a steady, albeit decreased, level. Sodium 171-177 arginine vasopressin Rattus norvegicus 18-29 10026831-2 1998 With the onset of vasopressin escape, water excretion increases despite sustained administration of vasopressin, allowing water balance to be re-established and the serum sodium to be stabilized at a steady, albeit decreased, level. Sodium 171-177 arginine vasopressin Rattus norvegicus 100-111 9458830-4 1998 On all levels of dietary sodium intake, there was a significant (approximately 2-fold) increase in plasma ANP levels after intravenous saline infusion. Sodium 25-31 natriuretic peptide A Homo sapiens 106-109 9830501-3 1998 Mutant BN-Ka rats showed no visible changes, but they were very sensitive to excess sodium ingestion and to the tendency of sodium to accumulate in the body by aldosterone released by angiotensin II, so that sodium was accumulated in erythrocytes and cerebrospinal fluid in BN-Ka rats and hypertension was induced. Sodium 124-130 angiotensinogen Rattus norvegicus 184-198 9458898-5 1998 In the face of a 36% reduction in GFR in response to the highest dose of ET-1, urinary sodium excretion (UNaV) increased threefold from 0.57 +/- 0.11 to 1.6 +/- 0.10 mumol.100 g-1.min-1. Sodium 87-93 endothelin 1 Rattus norvegicus 73-77 9458898-12 1998 In contrast, CYP450 products promoted sodium excretion despite negative effects on renal hemodynamics. Sodium 38-44 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 13-19 9558460-7 1998 According to the model, inhibition of sodium entry through either the Na-Cl cotransporter or the Na+ channel hyperpolarizes the cell, as does parathyroid hormone, thereby activating the calcium entry channel and increasing the driving force for diffusional entry. Sodium 38-44 parathyroid hormone Homo sapiens 142-161 9830516-11 1998 These results demonstrate that bradykinin counteracts ANP-stimulated sodium and water excretion, by acting directly on the kidney. Sodium 69-75 kininogen 1 Homo sapiens 31-41 9830501-3 1998 Mutant BN-Ka rats showed no visible changes, but they were very sensitive to excess sodium ingestion and to the tendency of sodium to accumulate in the body by aldosterone released by angiotensin II, so that sodium was accumulated in erythrocytes and cerebrospinal fluid in BN-Ka rats and hypertension was induced. Sodium 124-130 angiotensinogen Rattus norvegicus 184-198 9458239-5 1998 Following Ad.CMV-cHK injection, a significant increase in urine excretion, urinary sodium output, kinin, and cGMP level was observed. Sodium 83-89 choline kinase alpha Rattus norvegicus 17-20 9701701-0 1998 Water and sodium retention during short-term administration of growth hormone to short normal children. Sodium 10-16 growth hormone 1 Homo sapiens 63-77 9449400-1 1998 Both microalbuminuria (>0.290 nmol/min [20 microg/min]) and high sodium-lithium countertransport (SLC) in diabetic or hypertensive humans are predictive of overt nephropathy and more aggressive cardiovascular complications, perhaps induced by insulin resistance. Sodium 68-74 insulin Homo sapiens 246-253 9638501-3 1998 Oral administration of BP102 (10-100 mg/kg), an NEP inhibitor, increased urine volume and urinary sodium excretion in a dose-dependent manner in anesthetized Sprague-Dawley rats. Sodium 98-104 Blood pressure QTL 102 Rattus norvegicus 23-28 9453352-4 1998 In DS rats, a high-sodium diet increased systolic pressure (190+/-4 versus 152+/-2 mm Hg, P<.05) and aortic ET-1 protein content (4.2-fold, P<.0001) and induced aortic hypertrophy as assessed by tissue weight (P<.0001). Sodium 19-25 endothelin 1 Rattus norvegicus 111-115 9453352-5 1998 Sodium diet markedly reduced NO-mediated endothelium-dependent relaxations to acetylcholine (49+/-4% versus 81+/-4%, P<.0001) and contractions to ET-1 (92+/-7 versus 136+/-8% of KCl, P=.0011). Sodium 0-6 endothelin 1 Rattus norvegicus 149-153 9559415-8 1998 Thus, the renin-angiotensin-aldosterone axis may contribute to cardiorenal hemodynamics and renal sodium handling in patients with mild CHF. Sodium 98-104 renin Homo sapiens 10-15 9930375-4 1998 ANG-II regulates blood pressure by controlling sodium reabsorption in the proximal tubule, altering the glomerular filtration rate and renal blood flow, and by modifying the production and release of aldosterone in the adrenal gland. Sodium 47-53 angiotensinogen Homo sapiens 0-6 9417150-12 1998 CONCLUSION: The data suggest that patients with CF are so successful in compensating for volume depletion by vigorous activation of the renin-angiotensin system that salt depletion/dehydration cannot be recognized easily by routine clinical measurements, eg, capillary refill, serum sodium levels, or tachycardia. Sodium 283-289 renin Homo sapiens 136-141 9861615-6 1998 Circulating hormones like angiotensin II and adrenocorticotropin hormone, which are released in response to sodium deficiency and adrenalectomy, could regulate the activity of Na+ channels through G-protein linked second-messenger systems. Sodium 108-114 angiotensinogen Homo sapiens 26-40 9769930-7 1998 A forward regression analysis showed that the DPG level and the levels of inorganic phosphates and natrium (Na+) played a significant role in determining the position of the ODC according to the following equation: P50 (mmHg) = 34.5 + 0.225 DPG + 0.62 Pi-0.09 Na+, where DPG is in micromol.gHb-1 and Pi and Na+ in mEq.l-1. Sodium 99-106 nuclear factor kappa B subunit 1 Homo sapiens 215-218 9407070-0 1997 Transcriptional regulation of sodium transport by vasopressin in renal cells. Sodium 30-36 arginine vasopressin Rattus norvegicus 50-61 9432652-3 1997 The normal osmoregulation is an accurate operation which ensures the steadiness of serum sodium level by regulating vasopressin (ADH) release and water intake. Sodium 89-95 arginine vasopressin Homo sapiens 116-127 9398143-5 1997 More specifically, there is evidence to support the hypothesis that elevated plasma insulin concentrations may enhance renal sodium retention and decrease urinary uric acid clearance. Sodium 125-131 insulin Homo sapiens 84-91 9435650-2 1997 A 2-h infusion of GLP-2 produced a marked acceleration of sodium-dependent glucose uptake into BBM vesicles with a significant overshoot. Sodium 58-64 mast cell protease 10 Rattus norvegicus 18-23 9443776-5 1997 However, thrombin evoked intracellular Ca2+ was not correlated with systolic blood pressure (r = -0.338, P = .17), and was lowered by sodium loading and ovariectomy (360+/-23 to 285+/-9, 296+/-10 nmol/L, P < .05). Sodium 134-140 coagulation factor II Rattus norvegicus 9-17 9534323-1 1997 Renin-angiotensin system promotes sodium and chloride retention, participates in the defense response to hypovolemia and, in congestive heart failure, contributes to edema formation and progression of the disease. Sodium 34-40 renin Homo sapiens 0-5 9534323-12 1997 The role of these drugs becomes particularly relevant during acute renin-angiotensin system activation due to hypovolemia; in this setting ACE-inhibitors counteract sodium and chloride retention resulting in a potential hazard due to interference with the defence mechanisms toward hypovolemia, and an amplification of extracorporeal ultrafiltration efficacy by preventing edema recovery after its mechanical removal. Sodium 165-171 angiotensin I converting enzyme Homo sapiens 139-142 9389507-0 1997 Influence of dietary sodium restriction on angiotensin II receptors in rat adrenals. Sodium 21-27 angiotensinogen Rattus norvegicus 43-57 9389507-11 1997 Cell suspensions from rats fed a low sodium diet showed a 2.7- and 2.1-fold increase in total AII receptors in adrenal ZG and ZFR + M cells when compared with controls. Sodium 37-43 angiotensinogen Rattus norvegicus 94-97 9389507-12 1997 Based on Losartan displacement, we calculated that [125I]AII bound to AT1 and to AT2 receptors was increased in both ZG and ZFR + M cell preparations under sodium restriction. Sodium 156-162 angiotensinogen Rattus norvegicus 57-60 9532514-2 1997 Blocking this enzymatic cascade has been the focus of considerable research to the extent that the renin-angiotensin system is implicated in the control of blood pressure, sodium and water homeostasis, and cardiovascular function and structure. Sodium 172-178 renin Homo sapiens 99-104 9403588-3 1997 Endothelin-1, a potent vasoconstrictor and regulator of sodium reabsorption in the nephron, has a pathophysiological potential in the development of hypertension. Sodium 56-62 endothelin 1 Rattus norvegicus 0-12 9403588-11 1997 We conclude that high ECE-1 gene expression in the nephron, via increase of endothelin-1 synthesis, may promote sodium retention that contributes to the development and/or maintenance of hypertension in SHR. Sodium 112-118 endothelin converting enzyme 1 Rattus norvegicus 22-27 9403588-11 1997 We conclude that high ECE-1 gene expression in the nephron, via increase of endothelin-1 synthesis, may promote sodium retention that contributes to the development and/or maintenance of hypertension in SHR. Sodium 112-118 endothelin 1 Rattus norvegicus 76-88 9407415-0 1997 Angiotensin converting enzyme insertion/deletion polymorphism and short-term renal response to ACE inhibition: role of sodium status. Sodium 119-125 angiotensin I converting enzyme Homo sapiens 0-29 9407415-4 1997 Short-term responses to ACEi are enhanced by stimulating the renin-angiotensin system, that is, sodium restriction. Sodium 96-102 angiotensin I converting enzyme Homo sapiens 24-28 9407415-5 1997 We hypothesized that the ACE genotype influences sodium dependency of the response to ACEi. Sodium 49-55 angiotensin I converting enzyme Homo sapiens 25-28 9407415-5 1997 We hypothesized that the ACE genotype influences sodium dependency of the response to ACEi. Sodium 49-55 angiotensin I converting enzyme Homo sapiens 86-90 9407415-10 1997 Interestingly, the responses to ACEi of proteinuria (r = 0.42, P < 0.05) and blood pressure (r = 0.41, P < 0.05) correlated with urinary sodium excretion in DD genotype but not in the ID (r = 0.05 and 0.17, resp) or II genotype (r = 0.09 and 0.08, respectively). Sodium 143-149 angiotensin I converting enzyme Homo sapiens 32-36 9407415-11 1997 Thus, in the DD group, individuals with a high sodium excretion had a less effective response to ACEi. Sodium 47-53 angiotensin I converting enzyme Homo sapiens 97-101 9407415-12 1997 We conclude that differences in sodium status could account for disparities between studies on the relationship between ACE genotype and response to ACEi, and that sodium restriction might be a strategy to circumvent treatment resistance in the DD genotype. Sodium 32-38 angiotensin I converting enzyme Homo sapiens 120-123 9407415-12 1997 We conclude that differences in sodium status could account for disparities between studies on the relationship between ACE genotype and response to ACEi, and that sodium restriction might be a strategy to circumvent treatment resistance in the DD genotype. Sodium 32-38 angiotensin I converting enzyme Homo sapiens 149-153 9640078-7 1997 The higher concentration of ANP in plasma has been found in T2238-->C transition patients on normal and high sodium diet as compared with patients without mutation. Sodium 112-118 natriuretic peptide A Homo sapiens 28-31 9640078-0 1997 [Mutation T-->C of nucleotide 2238 in the gene of atrial natriuretic peptide (ANP) precursor and heterogeneity of sodium-sensitive hypertension. Sodium 117-123 natriuretic peptide A Homo sapiens 81-84 9640078-8 1997 These preliminary results suggest that the heterogeneity of sodium-sensitive hypertension is associated with the T2238-->C mutation of the ANP precursor gene. Sodium 60-66 natriuretic peptide A Homo sapiens 142-145 9640078-2 1997 Atrial natriuretic peptide (ANP) is involved in the pathogenesis of sodium-sensitive hypertension. Sodium 68-74 natriuretic peptide A Homo sapiens 0-26 9640078-2 1997 Atrial natriuretic peptide (ANP) is involved in the pathogenesis of sodium-sensitive hypertension. Sodium 68-74 natriuretic peptide A Homo sapiens 28-31 9366557-1 1997 Arginine vasopressin (AVP) and corticosteroid hormones are involved in sodium reabsorption regulation in the renal collecting duct. Sodium 71-77 arginine vasopressin Rattus norvegicus 9-20 9640078-4 1997 The aim of our study was the analysis of the Sca I gene polymorphism in 23 patients with sodium-sensitive hypertension, the molecular characteristic of the mutation and the comparison of the blood pressure values, plasma renin activity, plasma ANP and aldosterone concentration between patients with or without mutation. Sodium 89-95 suppressor of cancer cell invasion Homo sapiens 45-50 9372692-1 1997 This study was undertaken to define the impact of arginine vasopressin (AVP) and atrial natriuretic peptide (ANP) on sodium homeostasis in patients with lung cancer. Sodium 117-123 arginine vasopressin Homo sapiens 59-70 9397239-1 1997 The effect of dietary sodium supplementation on angiotensin II (ANG II)-induced stimulation of vascular glycosaminoglycan (GAG) synthesis of rats was investigated. Sodium 22-28 angiotensinogen Rattus norvegicus 48-62 9397239-1 1997 The effect of dietary sodium supplementation on angiotensin II (ANG II)-induced stimulation of vascular glycosaminoglycan (GAG) synthesis of rats was investigated. Sodium 22-28 angiotensinogen Rattus norvegicus 64-70 9372692-1 1997 This study was undertaken to define the impact of arginine vasopressin (AVP) and atrial natriuretic peptide (ANP) on sodium homeostasis in patients with lung cancer. Sodium 117-123 natriuretic peptide A Homo sapiens 81-107 9372692-1 1997 This study was undertaken to define the impact of arginine vasopressin (AVP) and atrial natriuretic peptide (ANP) on sodium homeostasis in patients with lung cancer. Sodium 117-123 natriuretic peptide A Homo sapiens 109-112 9372692-8 1997 Urinary sodium concentration increased during the saline infusion proportional to the initial plasma level of ANP (p = 0.0045). Sodium 8-14 natriuretic peptide A Homo sapiens 110-113 9372692-10 1997 ANP plasma levels in patients with lung cancer are associated with the ability to excrete a sodium load but do not appear to downregulate renin, angiotensin II, and aldosterone production. Sodium 92-98 natriuretic peptide A Homo sapiens 0-3 9374816-1 1997 Recent studies in rats suggest that vasopressin and the resulting urinary concentrating activity reduce the capacity of the kidney to excrete sodium. Sodium 142-148 arginine vasopressin Rattus norvegicus 36-47 9397239-2 1997 Measurements were performed both ex vivo and in vivo to validate the in vivo measurements and to estimate the relative contribution of intrinsic and extrinsic influences to ANG II-stimulated GAG synthesis in sodium-fed rats. Sodium 208-214 angiotensinogen Rattus norvegicus 173-179 9397239-5 1997 Systolic blood pressure of ANG II-treated rats on normal sodium diet was unchanged, but it increased by 13 mm Hg (P < .05) in the rats on the combined treatment of ANG II and a high sodium diet. Sodium 57-63 angiotensinogen Rattus norvegicus 27-33 9397242-3 1997 Plasma VP was determined in 12 normotensive subjects and 12 patients with mild essential hypertension on a regular sodium diet, and in eight hypertensive patients on a high sodium (250 mmol/day) and a low sodium (25 mmol/day) diet. Sodium 115-121 arginine vasopressin Homo sapiens 7-9 9397242-7 1997 Levels of VP in the plasma was higher in the high sodium than in the low sodium period, but the difference was not significant. Sodium 50-56 arginine vasopressin Homo sapiens 10-12 9397242-7 1997 Levels of VP in the plasma was higher in the high sodium than in the low sodium period, but the difference was not significant. Sodium 73-79 arginine vasopressin Homo sapiens 10-12 9374816-13 1997 The less efficient sodium excretion occurring at low V is probably due to the influence of vasopressin on water, urea, and sodium movements across the collecting ducts. Sodium 123-129 arginine vasopressin Homo sapiens 91-102 9374825-5 1997 In perindopril-treated LH rats, a 4-wk infusion of ANG II (200 ng.kg-1.min-1) but not of NE (1,000 ng.kg-1.min-1) restored hypertension, mimicked the hemodynamic alterations seen in untreated LH rats, and produced a brief sodium retention. Sodium 222-228 angiotensinogen Rattus norvegicus 51-57 9463638-8 1997 Sodium depletion elevated plasma renin activity and angiotensin II concentrations (p < or = 0.002) after which acute local administration of losartan increased forearm blood flow in a dose dependent manner (maximum of 69 +/- 17%; p < 0.001). Sodium 0-6 angiotensinogen Homo sapiens 52-66 9463638-0 1997 Endogenous angiotensin II contributes to basal peripheral vascular tone in sodium deplete but not sodium replete man. Sodium 75-81 angiotensinogen Homo sapiens 11-25 9369279-0 1997 Sensitivity of blood pressure and renin activation during sodium restriction. Sodium 58-64 renin Homo sapiens 34-39 9430825-12 1997 These data suggest a physiologic role of sodium balance (possibly mediated via endogenous AII) in the control of thirst in normal humans. Sodium 41-47 angiotensinogen Homo sapiens 90-93 9369279-1 1997 The objective of the present study was to explore the interrelationships among cumulative sodium loss, renin activation, and blood pressure changes during sodium restriction in essential hypertensive patients. Sodium 155-161 renin Homo sapiens 103-108 9369279-2 1997 Specifically, we wanted to know whether the degree of sodium sensitivity of blood pressure depends on renin activation during steady state or on initial renin activation during the first days of sodium restriction. Sodium 54-60 renin Homo sapiens 102-107 9369279-7 1997 Baseline sodium excretion and the activation of renin during the first 3 days both appeared to be predictors of total sodium loss after 7 days. Sodium 118-124 renin Homo sapiens 48-53 9369279-8 1997 Changes in blood pressure were not related to changes in sodium balance, but they were to baseline blood pressure, baseline norepinephrine, and renin activation during the early phase of sodium restriction. Sodium 187-193 renin Homo sapiens 144-149 9369279-9 1997 In addition, blood pressure appeared to fall more when the normal relationship between sodium loss and early (but not late) activation of renin was disturbed. Sodium 87-93 renin Homo sapiens 138-143 9322186-9 1997 Ingestion of sugars, fats, and sodium have been linked to decreased insulin sensitivity, while caloric restriction, exercise, ingestion of chromium, vanadium, soluble fibers, magnesium, and certain antioxidants are associated with greater insulin sensitivity. Sodium 31-37 insulin Homo sapiens 68-75 9369271-4 1997 Angiotensin-converting enzyme inhibition in the diabetic patients on a high sodium diet decreased daytime diastolic blood pressure and increased femoral artery distensibility. Sodium 76-82 angiotensin I converting enzyme Homo sapiens 0-29 9369271-5 1997 The blood pressure decrease in response to angiotensin-converting enzyme inhibition correlated significantly with the blood pressure increase to sodium (for 24-hour systolic and diastolic blood pressure, r=.72, P<.001 and r=.76, P<.001). Sodium 145-151 angiotensin I converting enzyme Homo sapiens 43-72 9369271-6 1997 In addition, we found that in the diabetic patients on a high sodium diet, the renal blood flow response to exogenous angiotensin II was not bimodally distributed, as is the case in essential hypertension, in which a subgroup of the patients are characterized by sodium sensitivity of the blood pressure and an abnormal renal blood flow response to exogenous angiotensin II ("nonmodulator phenotype"). Sodium 62-68 angiotensinogen Homo sapiens 118-132 9369271-6 1997 In addition, we found that in the diabetic patients on a high sodium diet, the renal blood flow response to exogenous angiotensin II was not bimodally distributed, as is the case in essential hypertension, in which a subgroup of the patients are characterized by sodium sensitivity of the blood pressure and an abnormal renal blood flow response to exogenous angiotensin II ("nonmodulator phenotype"). Sodium 263-269 angiotensinogen Homo sapiens 118-132 9334265-2 1997 In oocyte injection assays, CAT3 cRNA exhibited a saturable, sodium ion-independent transport activity with high affinity for L-arginine and L-lysine (Km = 40-60 and 115-165 microM, respectively). Sodium 61-67 dominant cataract 3 Mus musculus 28-32 9322478-9 1997 IMPLICATIONS: Continuous intravenous infusion of atrial natriuretic peptide, 0.1 microgram.kg-1.min-1, during gastrectomy was associated with higher water and sodium excretion and lower arterial blood pressure. Sodium 159-165 natriuretic peptide A Homo sapiens 49-75 9336660-1 1997 OBJECTIVE: To assess fully the vasodilatory and sodium-retaining effects of insulin. Sodium 48-54 insulin Homo sapiens 76-83 9336660-8 1997 Subsequent higher doses of insulin improved urinary volume and sodium excretion to above baseline levels associated with renal and forearm vasodilatation, although mean arterial pressure remained unaltered. Sodium 63-69 insulin Homo sapiens 27-34 9338654-3 1997 METHODS: Excretion rates of sodium and water were correlated with the excretion of urodilatin and with circulating levels of atrial natriuretic factor, antidiuretic hormone, aldosterone, and plasma renin activity during a period of 16 hours in 12 patients having had coronary artery bypass operations and with approximately a 400% elevation in levels of atrial natriuretic factor. Sodium 28-34 renin Homo sapiens 198-203 9295340-1 1997 Palytoxin is a novel skin tumor promoter that does not activate protein kinase C. Previous studies demonstrated that palytoxin stimulates a sodium-dependent signaling pathway that activates the c-Jun NH2-terminal kinase/stress-activated protein kinase (JNK) in Swiss 3T3 fibroblasts. Sodium 140-146 mitogen-activated protein kinase 8 Homo sapiens 194-251 9323090-7 1997 Adrenomedullin increased urine sodium (threefold, P<.05), creatinine (P<.05) and cAMP excretion (P<.01), creatinine clearance (P<.05), and renal production of cAMP (P<.05), whereas urine output was maintained during infusion and raised after infusion (P<.05). Sodium 31-37 pro-adrenomedullin Ovis aries 0-14 9323090-11 1997 Despite the clear fall in arterial pressure, adrenomedullin increased creatinine clearance and sodium excretion and maintained urine output. Sodium 95-101 pro-adrenomedullin Ovis aries 45-59 9295340-1 1997 Palytoxin is a novel skin tumor promoter that does not activate protein kinase C. Previous studies demonstrated that palytoxin stimulates a sodium-dependent signaling pathway that activates the c-Jun NH2-terminal kinase/stress-activated protein kinase (JNK) in Swiss 3T3 fibroblasts. Sodium 140-146 mitogen-activated protein kinase 8 Homo sapiens 253-256 9295340-6 1997 Sodium appears to play an important role in the regulation of JNK and SEK1 by palytoxin. Sodium 0-6 mitogen-activated protein kinase 8 Homo sapiens 62-65 9295340-6 1997 Sodium appears to play an important role in the regulation of JNK and SEK1 by palytoxin. Sodium 0-6 mitogen-activated protein kinase kinase 4 Homo sapiens 70-74 9295340-7 1997 Activation of JNK and SEK1 by palytoxin, but not anisomycin, requires extracellular sodium. Sodium 84-90 mitogen-activated protein kinase 8 Homo sapiens 14-17 9295340-7 1997 Activation of JNK and SEK1 by palytoxin, but not anisomycin, requires extracellular sodium. Sodium 84-90 mitogen-activated protein kinase kinase 4 Homo sapiens 22-26 9295340-8 1997 Complementary studies showed that the sodium ionophore gramicidin can mimic palytoxin by regulating JNK and SEK1 through a sodium-dependent mechanism. Sodium 38-44 mitogen-activated protein kinase 8 Homo sapiens 100-103 9295340-8 1997 Complementary studies showed that the sodium ionophore gramicidin can mimic palytoxin by regulating JNK and SEK1 through a sodium-dependent mechanism. Sodium 38-44 mitogen-activated protein kinase kinase 4 Homo sapiens 108-112 9295340-9 1997 Collectively, these results demonstrate that palytoxin stimulates a sodium-dependent signaling pathway that activates the SEK1/JNK/c-Jun protein kinase cascade. Sodium 68-74 mitogen-activated protein kinase kinase 4 Homo sapiens 122-126 9295340-9 1997 Collectively, these results demonstrate that palytoxin stimulates a sodium-dependent signaling pathway that activates the SEK1/JNK/c-Jun protein kinase cascade. Sodium 68-74 mitogen-activated protein kinase 8 Homo sapiens 127-130 9334989-4 1997 ANG II (10 pmol) injection into the MnPO of sham-lesioned rats induced water and sodium intake and pressor responses. Sodium 81-87 angiotensinogen Rattus norvegicus 0-6 9334989-8 1997 In lesioned rats ANG II-induced sodium intake was reduced by phenylephrine and noradrenaline, whereas clonidine produced no change. Sodium 32-38 angiotensinogen Rattus norvegicus 17-23 9321816-1 1997 The hypertensinogenic action of dietary sodium supplementation was investigated in angiotensin II (ANG II)-treated rats. Sodium 40-46 angiotensinogen Rattus norvegicus 83-97 9310305-0 1997 Extracellular sodium concentration has diverse effects on the hypoxia-induced increase in intracellular Ca2+ in rat hippocampal slices. Sodium 14-20 carbonic anhydrase 2 Rattus norvegicus 104-107 9321816-2 1997 We hypothesized that high-sodium diet would potentiate ANG II-induced vasoconstriction and hypertension, including the development of structural vascular changes, through synergistic action with ANG II in stimulating sympathetic activity and vascular growth. Sodium 26-32 angiotensinogen Rattus norvegicus 55-61 9321816-8 1997 High-sodium diet increased vasoconstrictor responses to ANG II (P < 0.01) and nerve stimulation (P < 0.02), but not to NE or AVP, and in combination with ANG II treatment further potentiated vasoconstrictor responses to ANG II (synergism). Sodium 5-11 angiotensinogen Rattus norvegicus 56-62 9321816-2 1997 We hypothesized that high-sodium diet would potentiate ANG II-induced vasoconstriction and hypertension, including the development of structural vascular changes, through synergistic action with ANG II in stimulating sympathetic activity and vascular growth. Sodium 26-32 angiotensinogen Rattus norvegicus 195-201 9321816-8 1997 High-sodium diet increased vasoconstrictor responses to ANG II (P < 0.01) and nerve stimulation (P < 0.02), but not to NE or AVP, and in combination with ANG II treatment further potentiated vasoconstrictor responses to ANG II (synergism). Sodium 5-11 angiotensinogen Rattus norvegicus 160-166 9321816-13 1997 Thus short-term administration of high-sodium diet appears to potentiate vasoconstrictor responses to ANG II by facilitating sympathetic neurotransmission, and long-term administration of high-sodium diet raises SBP by potentiating the trophic vascular effects of ANG II. Sodium 39-45 angiotensinogen Rattus norvegicus 102-108 9314413-11 1997 This increase in arterial pressure was associated with significant (P<.05) decreases in sodium excretion, leading to the retention of 5.4+/-0.6 mmol/L total sodium over the 5 days of Ang II infusion. Sodium 160-166 angiotensinogen Rattus norvegicus 186-192 9324100-0 1997 Effect of dietary sodium on insulin sensitivity in older, obese, sedentary hypertensives. Sodium 18-24 insulin Homo sapiens 28-35 9324100-1 1997 Increased dietary sodium intake has been associated with an increase in blood pressure as well as a decrease in insulin-mediated glucose disposal in young healthy adults. Sodium 18-24 insulin Homo sapiens 112-119 9324100-2 1997 The purpose of this study was to determine whether dietary sodium intake is associated with changes in oral glucose tolerance, insulin sensitivity, and blood pressure in older, sedentary, overweight hypertensives. Sodium 59-65 insulin Homo sapiens 127-134 9368669-4 1997 The procoagulant and anticoagulant functions of thrombin can be modulated by sodium binding, site-directed mutagenesis, and a small synthetic molecule. Sodium 77-83 coagulation factor II, thrombin Homo sapiens 48-56 9314415-1 1997 We have previously shown that sodium restriction upregulates the genes encoding angiotensin II receptor (AT1) subtypes, AT1A and AT1B, in the adrenal gland and that this upregulation is mediated by activation of the AT1 receptor. Sodium 30-36 angiotensin II receptor, type 1b Rattus norvegicus 129-133 9314415-2 1997 There are multiple interactions between the renin-angiotensin and the adrenergic nervous systems; thus, we conducted the present experiment to investigate whether low sodium-induced upregulation of adrenal AT1A and AT1B is modulated by the alpha1-adrenoreceptor. Sodium 167-173 angiotensin II receptor, type 1b Rattus norvegicus 215-219 9314415-11 1997 These data suggest that the sympathetic nervous system exerts an inhibitory action, via activation of the alpha1-adrenoreceptor, on AT1A and AT1B gene expression in the adrenal gland during sodium depletion. Sodium 190-196 angiotensin II receptor, type 1b Rattus norvegicus 141-145 9269534-3 1997 Inhibition of nitric oxide synthase (NOS) reduces renal blood flow by approximately 25% and markedly reduces sodium excretion without reductions in filtered load. Sodium 109-115 nitric oxide synthase 2 Homo sapiens 14-35 9306261-8 1997 The ACE inhibition during control diet lowered blood pressure and decreased left ventricular weight in young rats only and these effects were completely blocked by a high-sodium diet. Sodium 171-177 angiotensin I converting enzyme Rattus norvegicus 4-7 9301430-12 1997 Plasma renin activity during a regular sodium diet, an index of renin status, was significantly and inversely correlated with the change in blood pressure during sodium restriction, but not with any change in the parameters of calcium metabolism. Sodium 39-45 renin Homo sapiens 7-12 9301430-12 1997 Plasma renin activity during a regular sodium diet, an index of renin status, was significantly and inversely correlated with the change in blood pressure during sodium restriction, but not with any change in the parameters of calcium metabolism. Sodium 39-45 renin Homo sapiens 64-69 9301430-12 1997 Plasma renin activity during a regular sodium diet, an index of renin status, was significantly and inversely correlated with the change in blood pressure during sodium restriction, but not with any change in the parameters of calcium metabolism. Sodium 162-168 renin Homo sapiens 7-12 9263989-5 1997 ECF volume depletion by dietary sodium restriction enhanced Agtr1a gene expression in the adrenal gland of wild-type mice. Sodium 32-38 angiotensin II receptor, type 1a Mus musculus 60-66 9285146-15 1997 The defective sodium excretion, which dominates the effect of the low sodium diet, results in volume overload, increased ANF and volume-dependent hypertension. Sodium 14-20 natriuretic peptide A Homo sapiens 121-124 9285146-15 1997 The defective sodium excretion, which dominates the effect of the low sodium diet, results in volume overload, increased ANF and volume-dependent hypertension. Sodium 70-76 natriuretic peptide A Homo sapiens 121-124 9228014-4 1997 When expressed in Xenopus laevis oocytes, OAT1 mediated sodium-independent para-aminohippurate (PAH) uptake (Km = 14.3 +/- 2.9 microM). Sodium 56-62 ornithine aminotransferase L homeolog Xenopus laevis 42-46 9218502-10 1997 During normal sodium intake, Ang II caused a twofold increase in RIF cGMP. Sodium 14-20 angiotensinogen Rattus norvegicus 29-35 9269636-7 1997 RESULTS: Insulin infusion alone was accompanied by a significant 50% reduction in urinary sodium excretion. Sodium 90-96 insulin Homo sapiens 9-16 9269636-8 1997 Following amlodipine pretreatment, euglycaemic insulin infusion was associated with an attenuated antinatriuretic response and the cumulative sodium excretion following 135 min of insulin infusion was significantly higher (24 +/- 4 vs 18 +/- 3 mmol; P < 0.05) as compared to insulin infusion alone. Sodium 142-148 insulin Homo sapiens 180-187 9269636-8 1997 Following amlodipine pretreatment, euglycaemic insulin infusion was associated with an attenuated antinatriuretic response and the cumulative sodium excretion following 135 min of insulin infusion was significantly higher (24 +/- 4 vs 18 +/- 3 mmol; P < 0.05) as compared to insulin infusion alone. Sodium 142-148 insulin Homo sapiens 180-187 9269636-12 1997 CONCLUSION: Pretreatment with a calcium-channel blocker, amlodipine, attenuates the antinatriuretic effects of insulin leading to a significantly higher cumulative sodium excretion at the end of insulin infusion, which may be of clinical importance. Sodium 164-170 insulin Homo sapiens 111-118 9218502-15 1997 During normal sodium intake, 7-NI blocked the Ang II-induced increase in RIF cGMP. Sodium 14-20 angiotensinogen Rattus norvegicus 46-52 9218502-18 1997 These data demonstrate that activation of the renin- angiotensin system during sodium depletion increases renal nitric oxide production through stimulation by Ang II at the angiotensin AT2 receptor. Sodium 79-85 angiotensinogen Rattus norvegicus 159-165 9214404-5 1997 We hypothesized that sodium depletion is critical to the increase in TGF-beta1 expression, which, in turn, results in excessive matrix accumulation. Sodium 21-27 transforming growth factor, beta 1 Rattus norvegicus 69-78 9249534-11 1997 Long-term treatment with captopril restores this reflex pathway in SHR, lending support to the concept that angiotensin II is critically linked to heightened sympathetic nerve activity and abnormal sodium metabolism in this strain. Sodium 198-204 angiotensinogen Rattus norvegicus 108-122 9214404-0 1997 Sodium depletion enhances fibrosis and the expression of TGF-beta1 and matrix proteins in experimental chronic cyclosporine nephropathy. Sodium 0-6 transforming growth factor, beta 1 Rattus norvegicus 57-66 9247758-9 1997 In a study looking at the interaction of sodium and angiotensin II high sodium intake caused left ventricular hypertrophy and injections of angiotensin II caused further left ventricular hypertrophy. Sodium 72-78 angiotensinogen Rattus norvegicus 52-66 9247766-0 1997 Pharmacological demonstration of the additive effects of angiotensin-converting enzyme inhibition and angiotensin II antagonism in sodium depleted healthy subjects. Sodium 131-137 angiotensinogen Homo sapiens 102-116 9247766-5 1997 The combination of captopril 50 mg and losartan 50 mg had additive effects on blood pressure fall and renin release in sodium-depleted normotensive subjects. Sodium 119-125 renin Homo sapiens 102-107 9231831-8 1997 After 4 weeks of high sodium, circulating plasma renin activity and angiotensin II fell by 94% and 82%, respectively. Sodium 22-28 angiotensinogen Rattus norvegicus 68-82 9231815-2 1997 We recently reported strong sodium retention and renal vasoconstriction during pathophysiological increments in plasma ET-1. Sodium 28-34 endothelin 1 Homo sapiens 119-123 9231831-10 1997 This study demonstrates that microvascular density is reduced in reduced renal mass hypertensive rats following exposure to high sodium diet and this is associated with a fall in circulating plasma renin activity and angiotensin II levels. Sodium 129-135 angiotensinogen Rattus norvegicus 217-231 9195904-1 1997 The gamma-aminobutyric acid (GABA) transporter GAT-1 is located in nerve terminals and catalyzes the electrogenic reuptake of the neurotransmitter with two sodium ions and one chloride. Sodium 156-162 solute carrier family 6 member 1 Homo sapiens 47-52 9195904-6 1997 The nontransportable analog SKF 100330A potently inhibits the sodium-dependent transient in the wild type GAT-1 but not in the Y140W transporter. Sodium 62-68 solute carrier family 6 member 1 Homo sapiens 106-111 9171961-4 1997 In the present study we sought to determine whether gastric sodium administration also modulates angiotensin-converting enzyme (ACE) activity in the kidney. Sodium 60-66 angiotensin I converting enzyme Rattus norvegicus 97-126 9171961-4 1997 In the present study we sought to determine whether gastric sodium administration also modulates angiotensin-converting enzyme (ACE) activity in the kidney. Sodium 60-66 angiotensin I converting enzyme Rattus norvegicus 128-131 9228552-4 1997 Subcutaneous infusion of angiotensin II (20 mg/day/rat) also enhanced the concentration of sodium in erythrocytes and in cerebrospinal fluid and increased the systemic pressure by releasing aldosterone. Sodium 91-97 angiotensinogen Rattus norvegicus 25-39 9171956-2 1997 The natriuresis engendered by stimulation of the gastric sodium monitor is mediated in part by a decrease in the circulating concentration of angiotensin II (AngII). Sodium 57-63 angiotensinogen Rattus norvegicus 142-156 9171956-2 1997 The natriuresis engendered by stimulation of the gastric sodium monitor is mediated in part by a decrease in the circulating concentration of angiotensin II (AngII). Sodium 57-63 angiotensinogen Rattus norvegicus 158-163 9171956-11 1997 In the liver, ACE activity decreased from control after both sodium (P < 0.005) and urea (P < 0.025) administration. Sodium 61-67 angiotensin I converting enzyme Rattus norvegicus 14-17 9171956-15 1997 We conclude that stimulation of the gastric sodium monitor results in a decrease in ACE activity in the liver. Sodium 44-50 angiotensin I converting enzyme Rattus norvegicus 84-87 9228552-5 1997 A 4-day infusion of 0.3 M sodium solution (6 ml/kg/h) to the abdominal aorta of conscious and un-restrained mutant BN-Ka rats increased the pressor responses of the arterioles to norepinephrine and angiotensin II (i.a.) Sodium 26-32 angiotensinogen Rattus norvegicus 198-212 9185100-3 1997 Similarly, ANP appeared to be mainly involved in the physiological down-regulation of salt excretion (that is, during the shift from a normal to low-sodium diet). Sodium 149-155 natriuretic peptide A Homo sapiens 11-14 9186859-11 1997 It is concluded that, in the perfused rat, OVX results in decreased excretion of calcium and sodium as a result of estrogen effects on the renal proximal tubule, an effect dependent on PTH. Sodium 93-99 parathyroid hormone Rattus norvegicus 185-188 9185100-5 1997 Indeed, low-dose ANP promoted a marked increase of sodium excretion in CRF patients to the same levels observed in normals, likely because the renal patients exhibited a more marked pANP increment secondary to the lower renal catabolism of the infused hormone. Sodium 51-57 natriuretic peptide A Homo sapiens 17-20 9185100-9 1997 Hence, ANP per se not only plays a significant role in the up- and down-regulation of sodium excretion in healthy state and chronic renal disease, but it may also be considered to be a powerful and unique diuretic agent in CRF at nonhypotensive dosages. Sodium 86-92 natriuretic peptide A Homo sapiens 7-10 9185106-3 1997 Among them, the renin-angiotensin-aldosterone axis, the sympathetic nervous system, the non-osmotic release of vasopressin and the endothelins are activated to increase vascular resistance and enhance sodium and water renal retention. Sodium 201-207 arginine vasopressin Homo sapiens 111-122 9170000-1 1997 BACKGROUND: Results from previous studies suggested that a blunted response of renal plasma flow (RPF) to angiotensin II infusion during a high-sodium diet (a phenotype associated with nonmodulation) is an intermediate phenotype for essential hypertension. Sodium 144-150 angiotensinogen Homo sapiens 106-120 9149697-12 1997 INTERPRETATION: Our findings of significant linkage of the alpha-adducin locus to essential hypertension and greater sensitivity to changes in sodium balance among patients with the mutant allele suggest that alpha-adducin is associated with a salt-sensitive form of essential hypertension. Sodium 143-149 adducin 1 Homo sapiens 209-222 9149697-13 1997 We suggest the alpha-adducin polymorphism may identify hypertensive patients who will benefit from diuretic treatment or manoeuvres to reduce total body sodium. Sodium 153-159 adducin 1 Homo sapiens 15-28 9152098-10 1997 Only basal positive psychotic symptoms (P < .09) and plasma sodium (P < .18) were even marginally associated with the peak antidiuretic hormone responses, but neither factor could explain the difference in the response by the 2 groups. Sodium 63-69 arginine vasopressin Homo sapiens 129-149 9159566-9 1997 Sodium clearance (CL(Na)) and CL(Li) were elevated with the four lowest doses but increased further from 7.5 microg kg(-1) min(-1) onwards. Sodium 0-6 CD59 molecule (CD59 blood group) Homo sapiens 123-129 9159566-12 1997 Fractional distal reabsorption of sodium (FDR(Na) = (CL(Li)-CL(Na))/CL(Li)) decreased with all doses, reaching its nadir with 7.5 microg kg(-1) min(-1) [from 95.9 (94.6-97.2) % with placebo to 91.5 (90.0-93.0) % (P<0.01)] whereafter a flat dose-response curve was observed. Sodium 34-40 CD59 molecule (CD59 blood group) Homo sapiens 144-150 9170001-4 1997 RESULTS: There was some evidence that measures of the renal plasma flow and of its response to angiotensin II infusion during the high-sodium diet were statistically significant predictors of measures of blood pressure in women; there was less evidence for this for blood pressures in men. Sodium 135-141 angiotensinogen Homo sapiens 95-109 15511835-10 1997 There was a significant negative correlation between serum sodium level and log (plasma) ANP level in all pregnant subjects (r=- 0.51, P < 0.05). Sodium 59-65 natriuretic peptide A Homo sapiens 89-92 9141514-8 1997 Altogether, our results indicate a differential, tissue-specific expression of hMR mRNA isoforms, hMR beta being down-regulated in situations of positive sodium balance, independently of aldosterone levels. Sodium 154-160 roundabout guidance receptor 4 Homo sapiens 98-106 15511835-12 1997 A relationship between ANP and pre-eclampsia seems unlikely but ANP is probably involved in the regulation of sodium and water balance in normal pregnancy and in pre-eclampsia. Sodium 110-116 natriuretic peptide A Homo sapiens 64-67 9094251-3 1997 Insulin induced increases in transepithelial sodium transport, as measured by the short-circuit current (Isc), and in the initial rate of [3H]ouabain binding determined when the preparation was bathed in K+-containing solutions. Sodium 45-51 insulin Homo sapiens 0-7 9267147-10 1997 These results indicate that 1) reduction in insulin sensitivity plays a role in age-related acceleration of hypertension and of glucose intolerance; 2) in patients with essential hypertension, selective insulin resistance with respect to glucose metabolism can be found even in those who are young; and 3) both sodium retention and pressor system activation via insulin might cause blood pressure to increase in patients with essential hypertension. Sodium 311-317 insulin Homo sapiens 44-51 9145941-4 1997 The IL-1beta-induced decrease in sodium excretion was abolished in renal-denervated rats. Sodium 33-39 interleukin 1 beta Rattus norvegicus 4-12 9267147-10 1997 These results indicate that 1) reduction in insulin sensitivity plays a role in age-related acceleration of hypertension and of glucose intolerance; 2) in patients with essential hypertension, selective insulin resistance with respect to glucose metabolism can be found even in those who are young; and 3) both sodium retention and pressor system activation via insulin might cause blood pressure to increase in patients with essential hypertension. Sodium 311-317 insulin Homo sapiens 203-210 9267147-10 1997 These results indicate that 1) reduction in insulin sensitivity plays a role in age-related acceleration of hypertension and of glucose intolerance; 2) in patients with essential hypertension, selective insulin resistance with respect to glucose metabolism can be found even in those who are young; and 3) both sodium retention and pressor system activation via insulin might cause blood pressure to increase in patients with essential hypertension. Sodium 311-317 insulin Homo sapiens 203-210 9140004-3 1997 We also hypothesized that BNP replacement in AHF would reduce cardiac filling pressures, increase sodium excretion, and inhibit circulating renin. Sodium 98-104 natriuretic peptide B Canis lupus familiaris 26-29 9226397-2 1997 The present work investigates whether (1) vasopressin also inhibits sodium intake when injected i.c.v., and (2) the effect of oxytocin and of vasopressin on sodium intake is affected by i.c.v. Sodium 68-74 arginine vasopressin Rattus norvegicus 42-53 9226397-2 1997 The present work investigates whether (1) vasopressin also inhibits sodium intake when injected i.c.v., and (2) the effect of oxytocin and of vasopressin on sodium intake is affected by i.c.v. Sodium 157-163 arginine vasopressin Rattus norvegicus 142-153 9143495-2 1997 A TTXi VGSC, named SNS, that accounts for the tetrodotoxin-resistant sodium current described in sensory neurons has been cloned from rat dorsal root ganglia. Sodium 69-75 sodium channel, voltage-gated, type X, alpha Mus musculus 7-11 9140049-0 1997 Insulin-like growth factor I stimulates apical sodium/hydrogen exchange in human proximal tubule cells. Sodium 47-53 insulin like growth factor 1 Homo sapiens 0-28 9140004-8 1997 Compared with control, exogenous supplemental BNP in AHF resulted in marked increases in circulating cGMP (65 +/- 6 vs. 18 +/- 5 pg/ml, P < 0.05), with reductions in PCWP (9.1 +/- 0.9 vs. 12.9 +/- 1.1 mmHg, P < 0.05) and increased urinary sodium excretion (120 +/- 36.8 vs. 24 +/- 6.3 microeq/min, P < 0.05) via reductions in distal tubular sodium reabsorption (94.3 +/- 1.8 vs. 98.0 +/- 0.4%, P < 0.05). Sodium 245-251 natriuretic peptide B Canis lupus familiaris 46-49 9140049-1 1997 To determine whether insulin-like growth factor I (IGF-I) stimulated apical sodium/hydrogen exchange (NHE), confluent primary human proximal tubule cells (PTC) were incubated for 48 h in serum-free media in the presence or absence of 100 ng/ml IGF-I. Sodium 76-82 insulin like growth factor 1 Homo sapiens 51-56 9140004-8 1997 Compared with control, exogenous supplemental BNP in AHF resulted in marked increases in circulating cGMP (65 +/- 6 vs. 18 +/- 5 pg/ml, P < 0.05), with reductions in PCWP (9.1 +/- 0.9 vs. 12.9 +/- 1.1 mmHg, P < 0.05) and increased urinary sodium excretion (120 +/- 36.8 vs. 24 +/- 6.3 microeq/min, P < 0.05) via reductions in distal tubular sodium reabsorption (94.3 +/- 1.8 vs. 98.0 +/- 0.4%, P < 0.05). Sodium 350-356 natriuretic peptide B Canis lupus familiaris 46-49 9251765-2 1997 Intraperitoneal (ip) injection of alpha-MSH (3 and 9.6 nmol) induced a significant increase in urinary sodium, potassium and water excretion. Sodium 103-109 proopiomelanocortin Homo sapiens 34-43 10495782-6 1997 The Ang II-infused rats responded to acute doses of losartan (10 mg/kg) with progressive reductions in arterial pressure and significant increases in cortical blood flow (34 +/- 12% increase), renal plasma flow, GFR, and sodium excretion; however, the increases in renal blood flow and GFR were not sustained as systemic arterial pressure decreased. Sodium 221-227 angiotensinogen Rattus norvegicus 4-10 9176040-9 1997 The 20 ng min-1 kg-1 dose increased the urinary sodium excretion and urinary flow rate compared with the effects of placebo. Sodium 48-54 CD59 molecule (CD59 blood group) Homo sapiens 10-20 9093186-9 1997 CONCLUSION: The production of copious cervical secretions at the time of ovulation in part may be because of the transport of sodium and water across endocervical cell membranes as a result of E2-stimulated CFTR mRNA and protein. Sodium 126-132 CF transmembrane conductance regulator Homo sapiens 207-211 9095083-6 1997 The renal cytolocalization of the Ang II/AVP receptor to the outer medullary thick ascending limb tubules and inner medullary collecting ducts is consistent with the well-established AVP stimulation of sodium and water reabsorption in these tubules. Sodium 202-208 arginine vasopressin Homo sapiens 41-44 9095083-6 1997 The renal cytolocalization of the Ang II/AVP receptor to the outer medullary thick ascending limb tubules and inner medullary collecting ducts is consistent with the well-established AVP stimulation of sodium and water reabsorption in these tubules. Sodium 202-208 arginine vasopressin Homo sapiens 183-186 9134051-1 1997 The objective of the present-study was to determine whether acute inhibition of angiotensin converting enzyme (ACE), normalizes intrarenal sodium handling, renal haemodynamics and renal dopamine output in response to an i.v. Sodium 139-145 angiotensin I converting enzyme Homo sapiens 111-114 9099907-12 1997 The sexual-dimorphic expression 11 beta-HSD2 in kidney and colon may reflect male-female differences in sodium homeostasis, and the absent expression of 11 beta-HSD2 in late gestation may facilitate glucocorticoid-dependent maturation of mouse fetal tissues. Sodium 104-110 hydroxysteroid 11-beta dehydrogenase 2 Mus musculus 32-44 9134051-1 1997 The objective of the present-study was to determine whether acute inhibition of angiotensin converting enzyme (ACE), normalizes intrarenal sodium handling, renal haemodynamics and renal dopamine output in response to an i.v. Sodium 139-145 angiotensin I converting enzyme Homo sapiens 80-109 9134051-10 1997 In conclusion, this study demonstrates that patients with type 1 diabetes and early nephropathy display abnormalities in renal haemodynamics, natriuresis and urinary dopamine mobilization in response to a sodium load, which can be reversed by short-term inhibition of ACE. Sodium 205-211 angiotensin I converting enzyme Homo sapiens 268-271 9060995-10 1997 Na-SP, which was prepared by replacement of the calcium with sodium, stimulated the t-PA production similarly to Ca-SP. Sodium 61-67 plasminogen activator, tissue type Homo sapiens 84-88 9127682-10 1997 A sodium content of 50-90 mmol.L-1 may be necessary for optimal rehydration; however commercial sports drinks are formulated with a more moderate sodium content (10-25 mmol.L-1). Sodium 2-8 immunoglobulin kappa variable 1-16 Homo sapiens 31-34 9062366-0 1997 Regulation of angiotensin II receptor AT1 subtypes in renal afferent arterioles during chronic changes in sodium diet. Sodium 106-112 angiotensinogen Rattus norvegicus 14-28 9041252-7 1997 CONCLUSIONS: In cirrhosis, sinusoidal portal hypertension and an activated renin-angiotensin-aldosterone system seem to be important in the pathogenesis of sodium retention. Sodium 156-162 renin Homo sapiens 75-80 9062366-1 1997 Studies determined the effects of chronic changes in sodium diet on the expression, regulation, and function of different angiotensin II (ANG II) receptor subtypes in renal resistance vessels. Sodium 53-59 angiotensinogen Rattus norvegicus 122-136 9062366-1 1997 Studies determined the effects of chronic changes in sodium diet on the expression, regulation, and function of different angiotensin II (ANG II) receptor subtypes in renal resistance vessels. Sodium 53-59 angiotensinogen Rattus norvegicus 138-144 9062366-4 1997 ANG II produced less pronounced renal vasoconstriction in rats fed a low- compared with high-sodium diet (16% vs. 56% decrease in renal blood flow, P < 0.001). Sodium 93-99 angiotensinogen Rattus norvegicus 0-6 9062366-5 1997 After acute blockade of ANG II formation by iv enalaprilat injection in sodium-restricted animals, ANG II produced a 40% decrease in renal blood flow, a level between untreated dietary groups and less than high salt diet. Sodium 72-78 angiotensinogen Rattus norvegicus 99-105 9468457-15 1997 This was observed in patients as well as in healthy subjects, but the effects of Ang II on renal haemodynamics and sodium handling were more pronounced in diabetic patients. Sodium 115-121 angiotensinogen Homo sapiens 81-87 9468457-17 1997 In contrast, the effects of Ang II on renal perfusion and sodium handling are more pronounced in patients with NIDDM than they are in healthy subjects. Sodium 58-64 angiotensinogen Homo sapiens 28-34 9062366-9 1997 In vitro equilibrium-saturation 125I-ANG II binding studies on freshly isolated afferent arterioles indicated that ANG II receptor density was lower in the low- vs. high-sodium animals (157 vs. 298 fmol/mg, P < 0.04); affinity was similar (0.65 nM). Sodium 170-176 angiotensinogen Rattus norvegicus 115-121 9062366-16 1997 Chronic changes in sodium intake caused parallel regulation of expression and amount of receptor protein of the two AT1 receptor genes that modulate receptor function and altered reactivity of renal vessels to ANG II. Sodium 19-25 angiotensinogen Rattus norvegicus 210-216 9296068-12 1997 Angiotensiongen is the substrate of renin, and the renin-angiotensinogen reaction is the first and limiting step in the pathway that leads to production of angiotensin II, a peptide with important effects on blood pressure control and the metabolism of water and sodium. Sodium 263-269 renin Homo sapiens 36-41 9296068-12 1997 Angiotensiongen is the substrate of renin, and the renin-angiotensinogen reaction is the first and limiting step in the pathway that leads to production of angiotensin II, a peptide with important effects on blood pressure control and the metabolism of water and sodium. Sodium 263-269 renin Homo sapiens 51-56 9296068-12 1997 Angiotensiongen is the substrate of renin, and the renin-angiotensinogen reaction is the first and limiting step in the pathway that leads to production of angiotensin II, a peptide with important effects on blood pressure control and the metabolism of water and sodium. Sodium 263-269 angiotensinogen Homo sapiens 57-72 9296068-12 1997 Angiotensiongen is the substrate of renin, and the renin-angiotensinogen reaction is the first and limiting step in the pathway that leads to production of angiotensin II, a peptide with important effects on blood pressure control and the metabolism of water and sodium. Sodium 263-269 angiotensinogen Homo sapiens 156-170 9139340-3 1997 Activation of the renin-angiotensin-aldosterone system contributes to progression to heart failure by at least two mechanisms: (1) increased left ventricular loading conditions due to vasoconstriction and retention of sodium; (2) direct effects on the myocardium resulting in myocyte hypertrophy and interstitial fibrosis. Sodium 218-224 renin Homo sapiens 18-23 9022559-3 1997 With multivariate adjustment for underestimation, the estimated effect of a sodium intake higher by 100 mmol/d was higher SBP/DBP (diastolic blood pressure) by approximately 3-6/0-3 mm Hg. Sodium 76-82 D-box binding PAR bZIP transcription factor Homo sapiens 126-129 9022559-5 1997 In tests of prior cross-population hypotheses (n = 52), significant, independent relations were found between sample 24-h median urinary sodium excretion and sample median SBP and DBP, prevalence rate of hypertension, and slope of SBP and DBP from age 20 to 59 y (median sodium intake greater by 100 mmol/d was associated with a 30-y increase in SBP/DBP, i.e., at the age of 55 y compared with 25 y, of 10-11/6 mm Hg. Sodium 137-143 D-box binding PAR bZIP transcription factor Homo sapiens 180-183 9022559-5 1997 In tests of prior cross-population hypotheses (n = 52), significant, independent relations were found between sample 24-h median urinary sodium excretion and sample median SBP and DBP, prevalence rate of hypertension, and slope of SBP and DBP from age 20 to 59 y (median sodium intake greater by 100 mmol/d was associated with a 30-y increase in SBP/DBP, i.e., at the age of 55 y compared with 25 y, of 10-11/6 mm Hg. Sodium 137-143 D-box binding PAR bZIP transcription factor Homo sapiens 239-242 9022559-5 1997 In tests of prior cross-population hypotheses (n = 52), significant, independent relations were found between sample 24-h median urinary sodium excretion and sample median SBP and DBP, prevalence rate of hypertension, and slope of SBP and DBP from age 20 to 59 y (median sodium intake greater by 100 mmol/d was associated with a 30-y increase in SBP/DBP, i.e., at the age of 55 y compared with 25 y, of 10-11/6 mm Hg. Sodium 137-143 D-box binding PAR bZIP transcription factor Homo sapiens 239-242 9022564-4 1997 Ischemic and nephrotoxic injuries are induced more readily in sodium-depleted animals and patients because of impaired renal hemodynamics and activation of the renin-angiotensin system. Sodium 62-68 renin Homo sapiens 160-165 9022564-10 1997 Finally, there is evidence that activation of the renin-angiotensin system by sodium depletion will enhance the growth of cysts in animal models of cystic renal disease. Sodium 78-84 renin Homo sapiens 50-55 9048354-6 1997 Dysfunctional CFTR in the sweat ducts of CF patients are responsible for excessive chloride and sodium losses, especially in warm weather. Sodium 96-102 CF transmembrane conductance regulator Homo sapiens 14-18 9040450-1 1997 The combination of single oral doses of an angiotensin I-converting enzyme inhibitor (captopril) and a type 1 angiotensin II receptor antagonist (losartan) has additive effects on blood pressure fall and renin release in sodium-depleted normotensive subjects. Sodium 221-227 renin Homo sapiens 204-209 9140798-1 1997 Atrial natriuretic peptide (ANP) which alters sodium balance, blood volume and vascular tone represents an important candidate for investigating the genetic basis of essential hypertension (EH). Sodium 46-52 natriuretic peptide A Homo sapiens 0-26 9140798-1 1997 Atrial natriuretic peptide (ANP) which alters sodium balance, blood volume and vascular tone represents an important candidate for investigating the genetic basis of essential hypertension (EH). Sodium 46-52 natriuretic peptide A Homo sapiens 28-31 9071983-6 1997 Infusion of vasopressin at 160 pg/min produced plasma concentrations of 10.1 +/- 2.1 pmol/l and this led to a significant increase in sodium excretion and a significant decrease in urine flow rate. Sodium 134-140 arginine vasopressin Rattus norvegicus 12-23 9210098-3 1997 ANG II injected into the MnPO of MH-lesioned rats increased sodium intake compared with sham-lesioned rats. Sodium 60-66 angiotensinogen Rattus norvegicus 0-6 9110383-2 1997 The present studies tested the hypothesis that prior to 12 days of age sodium appetite, induced by either central administration of angiotensin II (AngII) or adrenalectomy, is inhibited by endogenous oxytocin (OT). Sodium 71-77 angiotensinogen Rattus norvegicus 132-146 9110383-2 1997 The present studies tested the hypothesis that prior to 12 days of age sodium appetite, induced by either central administration of angiotensin II (AngII) or adrenalectomy, is inhibited by endogenous oxytocin (OT). Sodium 71-77 angiotensinogen Rattus norvegicus 148-153 9110383-6 1997 The OT antagonist also potentiated sodium intake after AngII pretreatment. Sodium 35-41 angiotensinogen Rattus norvegicus 55-60 9030899-5 1997 We suggest that endothelin-1 and the endothelin ETA receptor play an important role in water and sodium retention, and in renal vasoconstriction in this model of hypertension. Sodium 97-103 endothelin 1 Rattus norvegicus 16-28 8988947-6 1997 Regression analyses confirmed direct independent relations of body mass index, alcohol intake, sodium, and ratio of sodium to potassium to SBP and DBP, and an inverse relation of potassium to SBP and DBP. Sodium 116-122 D-box binding PAR bZIP transcription factor Homo sapiens 147-150 8995423-1 1997 A theoretical 12-transmembrane segment model based on the hydrophobic moment has been proposed for the transmembrane topology of the glycine transporter GLYT1 and all other members of the sodium- and chloride-dependent transporter family. Sodium 188-194 solute carrier family 6 member 9 Homo sapiens 153-158 9021647-7 1997 These results suggest that central vasopressin is required for the complete development of DOCA-salt hypertension and the mechanism is, in part, due to enhanced sodium intake through the additive effect of central vasopressin and DOCA-salt. Sodium 161-167 arginine vasopressin Rattus norvegicus 35-46 9021647-7 1997 These results suggest that central vasopressin is required for the complete development of DOCA-salt hypertension and the mechanism is, in part, due to enhanced sodium intake through the additive effect of central vasopressin and DOCA-salt. Sodium 161-167 arginine vasopressin Rattus norvegicus 214-225 9048137-11 1997 Plasma renin activity and aldosterone are generally elevated at landing, consistent with sodium retention, but inflight levels have been variable. Sodium 89-95 renin Homo sapiens 7-12 9002526-3 1997 ET-1 exerts a wide range of biologic effects in the kidney, including constriction of most renal vessels, mesangial cell contraction, inhibition of sodium and water reabsorption by the nephron, enhancement of glomerular cell proliferation, and stimulation of extracellular matrix accumulation. Sodium 148-154 endothelin 1 Homo sapiens 0-4 9116921-6 1997 In the salt-sensitive patients whose mean arterial pressure increased more than 5 mmHg during high sodium intake, sodium loading increased cardiac index and terminal aortic flow, but decreased superior mesenteric and renal flows, while plasma noradrenaline concentrations remained unchanged and plasma arginine vasopressin increased significantly. Sodium 114-120 arginine vasopressin Homo sapiens 311-322 9002526-10 1997 Deranged ET-1 production in the nephron may cause inappropriate sodium and water retention, thereby contributing to the development and/or maintenance of hypertension. Sodium 64-70 endothelin 1 Homo sapiens 9-13 9116921-7 1997 These hemodynamic responses to sodium in the salt-sensitive patients were more effectively inhibited by benidipine than by nifedipine, although neither of them had any influence on sodium-induced changes in plasma noradrenaline or arginine vasopressin concentration. Sodium 31-37 arginine vasopressin Homo sapiens 240-251 9043811-12 1997 Evidence is reviewed that suggests that a lack of the normal suppression in AngII and/or sympathetic activity in response to an increase in sodium intake produces salt-sensitive hypertension. Sodium 140-146 angiotensinogen Homo sapiens 76-81 8994730-1 1997 The renin-angiotensin system regulates blood pressure and sodium homeostasis through a series of coordinated substrate-enzyme interactions. Sodium 58-64 renin Homo sapiens 4-9 8971091-6 1997 Sodium restriction in diabetic rats reduced GFR, restored plasma angiotensin II to control values, and retarded kidney growth when compared with diabetic rats receiving a normal sodium diet. Sodium 0-6 angiotensinogen Rattus norvegicus 65-79 9050972-0 1997 An abnormal sodium metabolism in Japanese patients with essential hypertension, judged by serum sodium distribution, renal function and the renin-aldosterone system. Sodium 12-18 renin Homo sapiens 140-145 9013446-1 1997 The authors recently reported that infusion of endothelin-1 in humans to obtain pathophysiological plasma levels causes profound renal vasoconstriction and sodium retention. Sodium 156-162 endothelin 1 Homo sapiens 47-59 9013446-9 1997 Sodium excretion rate decreased during endothelin-1 infusion, from a baseline value of 182 +/- 33 to 84 +/- 28 mumol/min at the end of the endothelin-1 infusion. Sodium 0-6 endothelin 1 Homo sapiens 39-51 9013446-9 1997 Sodium excretion rate decreased during endothelin-1 infusion, from a baseline value of 182 +/- 33 to 84 +/- 28 mumol/min at the end of the endothelin-1 infusion. Sodium 0-6 endothelin 1 Homo sapiens 139-151 9171309-5 1997 Intravenous administration of the selective nonpeptide vasopressin V2 antagonist OPC-31260 decreased sodium concentration and osmolality in urine to lower values than in plasma. Sodium 101-107 arginine vasopressin Homo sapiens 55-66 9058368-7 1997 While serum osteocalcin was raised with increasing urinary sodium in Oophx rats (p = 0.035), there was no effect on osteocalcin levels in sham-operated rats. Sodium 59-65 bone gamma-carboxyglutamate protein Rattus norvegicus 12-23 9044449-0 1997 Arginine vasopressin increases renal sodium excretion in the anesthetized rat through V1 receptors. Sodium 37-43 arginine vasopressin Rattus norvegicus 9-20 8957033-15 1996 It is concluded that in progressive chronic nephropathy ACE-inhibitor treatment was associated with different adaptive tubular changes in the handling of sodium, water, and protein compared with conventional antihypertensive therapy. Sodium 154-160 angiotensin I converting enzyme Homo sapiens 56-59 9392838-2 1997 The present study investigated the effects of sodium loading on mRNA encoding the angiotensin II precursor, angiotensinogen (AOGEN), and the natriuretic peptides, atrial natriuretic peptide (ANP) and C-type natriuretic peptide (CNP) in rat brain using quantitative in situ hybridization histochemistry of [35S]- and [33P]-labeled oligonucleotide probes. Sodium 46-52 angiotensinogen Rattus norvegicus 82-96 8958582-4 1996 Sodium deprivation enhanced the expression of angiotensinogen, renin, AT1A and AT1B receptor subtypes in the hypothalamus, but suppressed them in the brainstem. Sodium 0-6 angiotensinogen Rattus norvegicus 46-61 8958582-4 1996 Sodium deprivation enhanced the expression of angiotensinogen, renin, AT1A and AT1B receptor subtypes in the hypothalamus, but suppressed them in the brainstem. Sodium 0-6 angiotensin II receptor, type 1b Rattus norvegicus 79-83 8958582-6 1996 Both AT1A and AT1B mRNAs changed in a similar magnitude in each tissue examined upon dietary sodium intake. Sodium 93-99 angiotensin II receptor, type 1b Rattus norvegicus 14-18 9222431-0 1996 Central interaction between atrial natriuretic peptide and angiotensin II in the control of sodium intake and excretion in female rats. Sodium 92-98 angiotensinogen Rattus norvegicus 59-73 8997320-9 1996 In conclusion, endogenous ANG II chronically supports RSNA, LSNA, and HR in conscious, normotensive low and normal sodium intake rats. Sodium 115-121 angiotensinogen Rattus norvegicus 26-32 9222431-4 1996 ANG II (21 microM) injection in intact, ovariectomized, and estrogen-treated ovariectomized rats increased sodium intake (3.8 +/- 0.4, 1.8 +/- 0.3 and 1.2 +/- 0.2 ml/120 min, respectively) (N = 11) and increased sodium excretion (166 +/- 18, 82 +/- 22 and 86 +/- 12 microEq/120 min, respectively) (N = 11). Sodium 107-113 angiotensinogen Rattus norvegicus 0-6 9222431-4 1996 ANG II (21 microM) injection in intact, ovariectomized, and estrogen-treated ovariectomized rats increased sodium intake (3.8 +/- 0.4, 1.8 +/- 0.3 and 1.2 +/- 0.2 ml/120 min, respectively) (N = 11) and increased sodium excretion (166 +/- 18, 82 +/- 22 and 86 +/- 12 microEq/120 min, respectively) (N = 11). Sodium 212-218 angiotensinogen Rattus norvegicus 0-6 9222431-6 1996 Concomitant injection of ANG II and ANP into the MnPO of intact (N = 12), ovariectomized (N = 10) and estrogen-treated ovariectomized (N = 10) rats caused smaller effects than those produced by each peptide given alone: 1.3 +/- 0.2, 0.9 +/- 0.2 and 0.3 +/- 0.1 ml/120 min for sodium intake, respectively, and 86 +/- 9, 58 +/- 7, and 22 +/- 4 microEq/120 min for sodium excretion, respectively. Sodium 276-282 angiotensinogen Rattus norvegicus 25-31 9222431-6 1996 Concomitant injection of ANG II and ANP into the MnPO of intact (N = 12), ovariectomized (N = 10) and estrogen-treated ovariectomized (N = 10) rats caused smaller effects than those produced by each peptide given alone: 1.3 +/- 0.2, 0.9 +/- 0.2 and 0.3 +/- 0.1 ml/120 min for sodium intake, respectively, and 86 +/- 9, 58 +/- 7, and 22 +/- 4 microEq/120 min for sodium excretion, respectively. Sodium 362-368 angiotensinogen Rattus norvegicus 25-31 9222431-7 1996 Taken together, these results demonstrate that there is an antagonistic interaction of ANP and ANG II on sodium intake and excretion, and that reproductive hormones affect this interaction. Sodium 105-111 angiotensinogen Rattus norvegicus 95-101 8976805-13 1996 In the whole population of patients with non-insulin-dependent diabetes mellitus, the increase in intracellular pH after exposure to angiotensin II was positively correlated with intracellular free calcium increase (r = 0.53; P < 0.05), suggesting a possible role of intracellular free calcium levels in the activation of the sodium-hydrogen antiport. Sodium 329-335 angiotensinogen Homo sapiens 133-147 8939808-1 1996 Mutants of Saccharomyces cerevisiae lacking activity of the Ca2+/calmodulin-dependent protein phosphatase calcineurin, show sensitivity to high concentrations of sodium that is partly reversed by the external supply of Ca2+. Sodium 162-168 calmodulin Saccharomyces cerevisiae S288C 65-75 8952589-6 1996 Compared with control SHR on high sodium, SHR on high sodium that were treated with Fab fragments had significantly increased sympathoexcitatory and pressor responses to central Ang II injection, consistent with a decrease in brain Ang II receptor occupancy. Sodium 54-60 angiotensinogen Rattus norvegicus 178-184 8952589-8 1996 Brain Ang II receptor stimulation appears to be downstream of "ouabain" in the pathways mediating sympathoexcitatory and pressor effects of high sodium. Sodium 145-151 angiotensinogen Rattus norvegicus 6-12 8986922-0 1996 Regulation of type 1 angiotensin II receptor and its subtype gene expression in kidney by sodium loading and angiotensin II infusion. Sodium 90-96 angiotensinogen Rattus norvegicus 21-35 8951724-0 1996 The action of angiotensin II on the intracellular sodium content of suspensions of rat proximal tubules. Sodium 50-56 angiotensinogen Rattus norvegicus 14-28 8951724-4 1996 AII at 10(-11) M produced an increase in intracellular sodium content of approximately 20% (P < 0.001) from the steady-state level 5 min after the addition of the drug; intracellular sodium content then gradually returned to baseline levels over the subsequent 25 min. Sodium 55-61 angiotensinogen Rattus norvegicus 0-3 8951724-4 1996 AII at 10(-11) M produced an increase in intracellular sodium content of approximately 20% (P < 0.001) from the steady-state level 5 min after the addition of the drug; intracellular sodium content then gradually returned to baseline levels over the subsequent 25 min. Sodium 186-192 angiotensinogen Rattus norvegicus 0-3 8951724-6 1996 Addition of AII at 10(-5) M resulted in a significant 20% decrease (P < 0.01) in the steady-state intracellular sodium level within 5 min. Sodium 115-121 angiotensinogen Rattus norvegicus 12-15 8951724-14 1996 It is well known that AII at high doses inhibits and at low doses stimulates sodium transport across proximal tubular epithelial cells. Sodium 77-83 angiotensinogen Rattus norvegicus 22-25 8951724-15 1996 From the present data it is proposed that AII has a transient biphasic action on intracellular sodium content which may reflect the stimulation of the Na(+)-H+ exchanger. Sodium 95-101 angiotensinogen Rattus norvegicus 42-45 8945984-0 1996 Dietary sodium effects on renin and angiotensinogen gene expression in preweanling WKY and SHR. Sodium 8-14 angiotensinogen Rattus norvegicus 36-51 8900380-0 1996 Role of urinary arginine vasopressin in the sodium excretion in patients with chronic renal failure. Sodium 44-50 arginine vasopressin Homo sapiens 25-36 8923799-0 1996 The neuronal role of angiotensin II in thirst, sodium appetite, cognition and memory. Sodium 47-53 angiotensinogen Rattus norvegicus 21-35 9196552-4 1996 In the same animals, [Sar1, Ala8]ANG II, DuP753, and PD123319 blocked the sodium intake induced by ANG II (9.2 +/- 1.6 vs 3.3 +/- 0.6, 1.8 +/- 0.3, and 1.4 +/- 0.2 ml/2 h respectively). Sodium 74-80 angiotensinogen Rattus norvegicus 28-39 8922348-8 1996 However, the effect of insulin on sodium handling was not altered by the stress. Sodium 34-40 insulin Homo sapiens 23-30 9196552-4 1996 In the same animals, [Sar1, Ala8]ANG II, DuP753, and PD123319 blocked the sodium intake induced by ANG II (9.2 +/- 1.6 vs 3.3 +/- 0.6, 1.8 +/- 0.3, and 1.4 +/- 0.2 ml/2 h respectively). Sodium 74-80 angiotensinogen Rattus norvegicus 33-39 9196552-5 1996 These results indicate that both DuP753 and PD123329, administered into the PVN, blocked the water and sodium intake induced by administration of ANG II into the same site. Sodium 103-109 angiotensinogen Rattus norvegicus 146-152 8969946-4 1996 Administration of a low sodium diet greatly enhanced the aldosterone response to VIP stimulation. Sodium 24-30 vasoactive intestinal peptide Rattus norvegicus 81-84 8969942-2 1996 11 beta-HSD has been suggested to be important not only in the control of renal sodium retention but also blood pressure. Sodium 80-86 hydroxysteroid 11-beta dehydrogenase 1 Rattus norvegicus 0-7 8969946-5 1996 Receptor binding studies reveal an increase in the number of VIP receptors in zona glomerulosa tissue in the low sodium group. Sodium 113-119 vasoactive intestinal peptide Rattus norvegicus 61-64 8945678-5 1996 In contrast, a nonpressor dose of angiotensin II (3 ng/min) reduced basal sodium excretion and the natriuretic responses to exogenous hANP 99-126 in the presence or absence of BMS-182657. Sodium 74-80 angiotensinogen Homo sapiens 34-48 8901830-8 1996 Six micrograms of the Ang II type 1 receptor inhibitor ZD 7155 blunted the decrease in urine volume and sodium excretion in response to air-jet stress, although the increase in renal sympathetic nerve activity during air-jet stress and the pressor response to exogenous Ang II were not affected. Sodium 104-110 angiotensinogen Rattus norvegicus 22-28 8901845-4 1996 Thus, both AT1 and AT2 work in the direction of sodium retention, suggesting a unique role for angiotensin II in the kidney in terms of blood pressure regulation and sodium metabolism. Sodium 48-54 angiotensin II receptor, type 1a Mus musculus 11-14 8901845-4 1996 Thus, both AT1 and AT2 work in the direction of sodium retention, suggesting a unique role for angiotensin II in the kidney in terms of blood pressure regulation and sodium metabolism. Sodium 166-172 angiotensin II receptor, type 1a Mus musculus 11-14 8983669-8 1996 There is little doubt that an inappropriately high plasma (and tissue) level of renin, related to sodium balance, is associated with increased left ventricular hypertrophy and cardiovascular complications. Sodium 98-104 renin Homo sapiens 80-85 8873664-5 1996 In a normal sodium diet, angiotensin I and II aorta-coronary sinus gradients were tendentially negative (-1.8 +/- 2.5 and -0.9 +/- 1.7 pg/mL, respectively), and the amounts of angiotensin I and II added by cardiac tissues were 6.5 +/- 3.1 and 2.7 +/- 1.3 pg/mL, respectively. Sodium 12-18 angiotensinogen Homo sapiens 25-45 8934356-2 1996 BACKGROUND: Non-modulating hypertensives are a subset of sodium-sensitive hypertensives characterized by a failure to modulate renal, vascular and adrenal glomerulosa responsivenesses to angiotensin II appropriately. Sodium 57-63 angiotensinogen Homo sapiens 187-201 8941579-7 1996 Plasma renin and aldosterone were significantly elevated in the symptomatic children, and strongly correlated with all parameters of tubule sodium reabsorption. Sodium 140-146 renin Homo sapiens 7-12 8873664-6 1996 The low sodium diet caused a significant increase in both plasma renin activity (PRA) and angiotensin I concentration in aortic but not in coronary sinus blood, resulting in a more negative aorta-coronary sinus gradient (-9.7 +/- 3.1 pg/mL, P < .01). Sodium 8-14 angiotensinogen Homo sapiens 90-103 8899893-1 1996 The neuronal mechanism of the sodium appetite initiated in rats by priming with a mineralocorticoid (desoxycorticosterone acetate (DOCA)) treatment and subsequent central angiotensin II (Ang II) was investigated using electrophysiological-iontophoretic techniques and sapid salt stimulation of the tongue in non-anesthetized restrained, DOCA-pretreated (0.5 mg/day s.c. for 3 days) or non-pretreated male Wistar rats. Sodium 30-36 angiotensinogen Rattus norvegicus 171-185 8824289-1 1996 Deletion of the yeast Ser/Thr protein phosphatase PPZ1 results in increased tolerance to sodium and lithium. Sodium 89-95 salt homeostasis regulator Saccharomyces cerevisiae S288C 50-54 8899893-1 1996 The neuronal mechanism of the sodium appetite initiated in rats by priming with a mineralocorticoid (desoxycorticosterone acetate (DOCA)) treatment and subsequent central angiotensin II (Ang II) was investigated using electrophysiological-iontophoretic techniques and sapid salt stimulation of the tongue in non-anesthetized restrained, DOCA-pretreated (0.5 mg/day s.c. for 3 days) or non-pretreated male Wistar rats. Sodium 30-36 angiotensinogen Rattus norvegicus 187-193 8863696-10 1996 A significantly higher release of ANP in the early puerperium after pregnancies complicated by pre-eclampsia may be a mechanism which promotes the renal elimination of excessive body fluids and sodium. Sodium 194-200 natriuretic peptide A Homo sapiens 34-37 8897813-0 1996 Aldosterone and insulin stimulate amiloride-sensitive sodium transport in A6 cells by additive mechanisms. Sodium 54-60 insulin Homo sapiens 16-23 8815755-10 1996 RESULTS: Sodium restriction was associated with a mean decrease (+/- one half of the 95% CI) in plasma sodium levels of 0.9 +/- 0.9 mmol/L from a mean of 139.3 mmol/L during the baseline cycle (P = 0.018), a decrease in urinary sodium excretion of 40.3 +/- 18 mmol/d from a mean of 117 mmol/d during the baseline cycle (P = 0.001), and an increase in plasma renin activity of 0.14 +/- 0.08 ng/(L . Sodium 9-15 renin Homo sapiens 358-363 8904632-4 1996 We conclude that angiotensin II is secreted into proximal tubular fluid and, in the anaesthetized rat, is maintained at a concentration that inhibits sodium and water transport via AT1 receptors. Sodium 150-156 angiotensinogen Rattus norvegicus 17-31 9076343-8 1996 GH causes sodium retention which occurs in part through activation of the renin-angiotensin system. Sodium 10-16 renin Homo sapiens 74-79 8943768-10 1996 In this group, sodium excretion increased significantly during vasopressin infusion, and rapidly returned to baseline values when the vasopressin was discontinued. Sodium 15-21 arginine vasopressin Rattus norvegicus 63-74 8910804-6 1996 The relationship of plasma vasopressin with serum sodium, but not plasma osmolality, during hyperglycemia showed an apparent hypersecretion of vasopressin. Sodium 50-56 arginine vasopressin Homo sapiens 27-38 8910804-6 1996 The relationship of plasma vasopressin with serum sodium, but not plasma osmolality, during hyperglycemia showed an apparent hypersecretion of vasopressin. Sodium 50-56 arginine vasopressin Homo sapiens 143-154 8910804-9 1996 Together, we found that the positive correlation of vasopressin with sodium or osmolality is maintained but significantly altered in patients with untreated diabetes mellitus. Sodium 69-75 arginine vasopressin Homo sapiens 52-63 9004086-6 1996 Renal abnormalities that cause salt-insensitive hypertension are characterized by normal functional kidney mass, and the ability to appropriately modulate the renin-angiotensin system during changes in sodium intake; important causes of salt-insensitive hypertension include widespread increases in preglomerular resistance and increased reabsorption in the proximal tubules and loops of Henle. Sodium 202-208 renin Homo sapiens 159-164 8943768-10 1996 In this group, sodium excretion increased significantly during vasopressin infusion, and rapidly returned to baseline values when the vasopressin was discontinued. Sodium 15-21 arginine vasopressin Rattus norvegicus 134-145 8914428-4 1996 Several mechanisms mediated by hyperinsulinemia can be entertained as follows: 1) sodium and water retention, 2) increased sympathetic nerve activity and reduced catecholamine clearance, 3) increased intracellular calcium concentration and reduced magnesium concentration, 4) increased coagulant activity and impaired fibrinolytic activity, 5) impaired endothelium-dependent NO synthesis and release, 6) increased vascular responsiveness for the vasoactive substrates, 7) increased proliferation of vascular smooth muscle cell by activation of protein kinase C or mediated by insulin and IGF-1 action. Sodium 82-88 insulin Homo sapiens 36-43 8897402-4 1996 AVP is probably important in the related adjustments of renal water excretion whereby changes in plasma sodium concentration induce changes in plasma osmolality and, subsequently, in release of AVP. Sodium 104-110 arginine vasopressin Homo sapiens 0-3 8897402-4 1996 AVP is probably important in the related adjustments of renal water excretion whereby changes in plasma sodium concentration induce changes in plasma osmolality and, subsequently, in release of AVP. Sodium 104-110 arginine vasopressin Homo sapiens 194-197 9387775-2 1996 The effect of microinjection of A II into the AP on renal sodium excretion was studied in the present investigation. Sodium 58-64 angiotensinogen Homo sapiens 32-36 9387775-6 1996 These results strongly suggest that the A II induced changes of renal hemodynamics and urine sodium excretion are mediated through AP. Sodium 93-99 angiotensinogen Homo sapiens 40-44 8822984-0 1996 Angiotensin II related to sodium excretion modulates left ventricular structure in human essential hypertension. Sodium 26-32 angiotensinogen Homo sapiens 0-14 8822984-7 1996 Patients with high Ang II concentrations in relation to sodium excretion had a greater left ventricular mass (318 +/- 77 versus 257 +/- 54 g, P < .02), posterior wall thickness (11.8 +/- 1.9 versus 10.5 +/- 0.8 mm, P < .02), and septal wall thickness (13.6 +/- 1.8 versus 11.9 +/- 1.3 mm, P < .01) than those with "relatively low" Ang II levels in relation to sodium excretion. Sodium 56-62 angiotensinogen Homo sapiens 19-25 8822984-7 1996 Patients with high Ang II concentrations in relation to sodium excretion had a greater left ventricular mass (318 +/- 77 versus 257 +/- 54 g, P < .02), posterior wall thickness (11.8 +/- 1.9 versus 10.5 +/- 0.8 mm, P < .02), and septal wall thickness (13.6 +/- 1.8 versus 11.9 +/- 1.3 mm, P < .01) than those with "relatively low" Ang II levels in relation to sodium excretion. Sodium 369-375 angiotensinogen Homo sapiens 19-25 8822984-2 1996 We conducted a study to investigate the interaction of sodium excretion with Ang II and its potential impact on myocardial hypertrophy. Sodium 55-61 angiotensinogen Homo sapiens 77-83 8879850-20 1996 Given recent experimental data, in patients overly corrected (delta SNa > 15 mEq/1/24 h), the risk of myelinolysis could be greatly reduced by rapidly decreasing the serum sodium through hypotonic fluids administration and dDAVP. Sodium 175-181 snail family transcriptional repressor 1 Homo sapiens 68-71 8703074-2 1996 By means of mutant substrates, it was shown that LY254603 mediates the change in enzymatic substrate specificity through an alteration in thrombin"s S3 substrate recognition site, a mechanism that appeared to be independent of allosteric changes induced by either sodium ions or by thrombomodulin. Sodium 264-270 coagulation factor II, thrombin Homo sapiens 138-146 8876753-15 1996 This illustrated the importance of NPY for the regulation of renal sodium handling. Sodium 67-73 neuropeptide Y Rattus norvegicus 35-38 21143281-9 1996 Centrally administered AngII may act on AT(1) receptors in the median preoptic nucleus and elsewhere to induce drinking, sodium appetite, a sympathetic vasoconstrictor response and vasopressin secretion. Sodium 121-127 angiotensinogen Rattus norvegicus 23-28 21143283-0 1996 Regulation of renal tubular sodium transport by angiotensin II and atrial natriuretic factor. Sodium 28-34 angiotensinogen Homo sapiens 48-62 21143283-0 1996 Regulation of renal tubular sodium transport by angiotensin II and atrial natriuretic factor. Sodium 28-34 natriuretic peptide A Homo sapiens 67-92 21143283-9 1996 Angiotensin II affects transepithelial sodium transport by modulation of Na(+) /H(+) exchange at the luminal membrane and Na(+)/HCO(3) cotransport, Na(+)/K(+)-ATPase activity and K(+) conductance at the basolateral membrane. Sodium 39-45 angiotensinogen Homo sapiens 0-14 21143284-9 1996 The expression of the AT(1) receptor is modulated at the mRNA and protein levels by many factors: conditions that increase levels of AngII (low sodium diet, renovascular hypertension, AngII infusion) up-regulate AT(1) receptor mRNA levels and binding and increase aldosterone secretion. Sodium 144-150 angiotensinogen Homo sapiens 133-138 8877292-5 1996 While acute hyperinsulinaemia resulted in increases in distal tubular fractional and absolute reabsorptions of sodium (p < 0.01) contributing to a fall in CNa (p < 0.01) in control subjects, in diabetic subjects the sodium-retaining effect of insulin was not significant. Sodium 111-117 insulin Homo sapiens 17-24 8879974-10 1996 Systemic and renal haemodynamic effects of ACE inhibition, both beneficial and adverse, are potentiated by sodium depletion. Sodium 107-113 angiotensin I converting enzyme Homo sapiens 43-46 8887762-7 1996 In anaesthetized rats systemic infusion of 1 or 3 micrograms kg-1 min-1 NPY enhanced urine formation and sodium and calcium excretion by a maximum of 110, 110 and 45%, respectively, but did not alter potassium excretion. Sodium 105-111 neuropeptide Y Rattus norvegicus 72-75 8879974-11 1996 Consequently, sodium repletion contributes to the restoration of renal function in patients with ACE inhibitor-induced acute renal failure. Sodium 14-20 angiotensin I converting enzyme Homo sapiens 97-100 8891743-10 1996 In contrast, ACE inhibition with captopril decreased the excretion of sodium dose-dependently in conscious TGR. Sodium 70-76 angiotensin I converting enzyme Rattus norvegicus 13-16 8891743-10 1996 In contrast, ACE inhibition with captopril decreased the excretion of sodium dose-dependently in conscious TGR. Sodium 70-76 thioredoxin reductase 3 Mus musculus 107-110 8887762-12 1996 Intrarenal infusion of 0.3 or 1 microgram kg-1 min-1 NPY reduced RBF to a greater extent than systemic infusion (maximal peak reduction 4 ml min-1) but caused a smaller enhancement or even a reduction of urine formation and sodium excretion. Sodium 224-230 neuropeptide Y Rattus norvegicus 53-56 8887762-15 1996 Systemic NPY infusion enhances urine formation and sodium and calcium excretion. Sodium 51-57 neuropeptide Y Rattus norvegicus 9-12 8790265-2 1996 The renin-angiotensin-aldosterone system, the sympathetic nervous system, and arginine vasopressin are responsible for sodium and water retention in patients with cirrhosis. Sodium 119-125 renin Homo sapiens 4-9 8934386-7 1996 Sodium sensitivity is commonly observed in these patients, so that low doses of diuretics correct the increased pulse pressure, particularly in those with normal or low plasma renin activity. Sodium 0-6 renin Homo sapiens 176-181 8790265-2 1996 The renin-angiotensin-aldosterone system, the sympathetic nervous system, and arginine vasopressin are responsible for sodium and water retention in patients with cirrhosis. Sodium 119-125 arginine vasopressin Homo sapiens 87-98 8888443-6 1996 CONCLUSIONS: These results suggest that increased CGRP may play a role in the systemic vasodilatation in cirrhosis and may contribute to the abnormal distribution of the blood volume, which may lead to abnormal sodium and water handling. Sodium 211-217 calcitonin related polypeptide alpha Homo sapiens 50-54 8770082-9 1996 Blockade of the binding of ANG II to the AT1 receptor by losartan prevents the increases in AT1A and AT1B mRNA expression and the AT1 receptor density induced by sodium depletion, suggesting that these changes in the adrenal gland are mediated by activation of the AT1 receptor. Sodium 162-168 angiotensinogen Rattus norvegicus 27-33 8770133-4 1996 In perindopril-treated LH, ANG II produced a greater reduction in renal blood flow, glomerular filtration rate, and urinary sodium excretion that was not significantly modified by blockade of thromboxane A2-prostaglandin H2 receptors. Sodium 124-130 angiotensinogen Rattus norvegicus 27-33 8770082-1 1996 We have previously demonstrated that two isoforms (AT1A and AT1B) of the angiotensin II (ANG II) type 1 (AT1) receptor exist in the rat kidney and are differentially regulated by a low-sodium diet. Sodium 185-191 angiotensin II receptor, type 1b Rattus norvegicus 60-64 8770082-1 1996 We have previously demonstrated that two isoforms (AT1A and AT1B) of the angiotensin II (ANG II) type 1 (AT1) receptor exist in the rat kidney and are differentially regulated by a low-sodium diet. Sodium 185-191 angiotensinogen Rattus norvegicus 89-95 8770082-2 1996 The present experiment was designed to test the hypothesis that sodium deficiency upregulates AT1A and AT1B gene expression in the adrenal gland by activating the AT1 receptor. Sodium 64-70 angiotensin II receptor, type 1b Rattus norvegicus 103-107 8770082-8 1996 We conclude that sodium deficiency increases both AT1A and AT1B gene expression and elevates the AT1 receptor density in the adrenal gland. Sodium 17-23 angiotensin II receptor, type 1b Rattus norvegicus 59-63 8862220-9 1996 Insulin-induced changes in urate excretion were coupled (r = 0.55, P < .0001) to the respective changes in sodium excretion. Sodium 110-116 insulin Homo sapiens 0-7 8862220-0 1996 Effect of insulin on renal sodium and uric acid handling in essential hypertension. Sodium 27-33 insulin Homo sapiens 10-17 8862220-3 1996 In 37 patients with essential hypertension, we measured the changes in urinary excretion of sodium, potassium, and uric acid in response to physiological euglycemic hyperinsulinemia (by using the insulin clamp technique at an insulin infusion rate of 6 pmol/min/kg). Sodium 92-98 insulin Homo sapiens 170-177 8768839-8 1996 However, urinary excretion of calcium and sodium decreased after PTH-(1-34) infusion in controls, but not in CRR patients. Sodium 42-48 parathyroid hormone Homo sapiens 65-68 8856325-8 1996 These results indicate that the acute glial swelling produced by AP3 results primarily from a fluid shift that accompanies the transport of AP3 and sodium into Muller cells. Sodium 148-154 adaptor-related protein complex 3, beta 1 subunit Mus musculus 65-68 8895036-1 1996 The aims of the present study were to investigate the effects of changes in sodium intake in patients with untreated mild essential hypertension on the hormonal (plasma renin activity and aldosterone) and renal tubular responses to short-term hyperinsulinemia as achieved by an oral glucose tolerance test (OGTT). Sodium 76-82 renin Homo sapiens 169-174 8765216-3 1996 However, complicating the interpretation of the effects of cyclooxygenase inhibition on sodium excretion are the following: (1) products of the other pathways of arachidonic acid metabolism, such as the cytochrome P-450 metabolites, may be attenuated when cyclooxygenase activity is reduced; (2) the proximal tubule has a high biosynthetic capacity for cytochrome P-450 metabolites of arachidonic acid. Sodium 88-94 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 203-219 8768839-9 1996 These results suggest a selective modulation by vitamin D of the renal response to PTH; 1,25-(OH)2D3 facilitates PTH-induced calcium and sodium reabsorption, but does not influence PTH-induced cAMP excretion; phosphorus, potassium, and bicarbonate tubular transport, or 1 alpha-hydroxylation of 25-hydroxyvitamin D3. Sodium 137-143 parathyroid hormone Homo sapiens 83-86 8768839-9 1996 These results suggest a selective modulation by vitamin D of the renal response to PTH; 1,25-(OH)2D3 facilitates PTH-induced calcium and sodium reabsorption, but does not influence PTH-induced cAMP excretion; phosphorus, potassium, and bicarbonate tubular transport, or 1 alpha-hydroxylation of 25-hydroxyvitamin D3. Sodium 137-143 parathyroid hormone Homo sapiens 113-116 8810807-3 1996 complementary DNA was cloned for human Na+/taurocholate cotransporting polypeptide (NTCP) which mediates sodium dependent secondary active hepatic uptake of bile acids. Sodium 105-111 solute carrier family 10 member 1 Homo sapiens 39-82 8865076-9 1996 At rates of 40 and 400 fmol kg-1 min-1, endothelin-1 increased sodium excretion about five- and eightfold, respectively. Sodium 63-69 endothelin 1 Canis lupus familiaris 40-52 8865076-20 1996 It is concluded that endothelin-1 at low plasma concentrations increases sodium excretion while a higher pressor dose of endothelin-1 is antinatriuretic. Sodium 73-79 endothelin 1 Canis lupus familiaris 21-33 8810807-3 1996 complementary DNA was cloned for human Na+/taurocholate cotransporting polypeptide (NTCP) which mediates sodium dependent secondary active hepatic uptake of bile acids. Sodium 105-111 solute carrier family 10 member 1 Homo sapiens 84-88 8869668-4 1996 After prednisolone treatment the most important differences during amino acid infusion were a significantly lower fractional excretion of sodium after 120 min (before prednisolone 26%; after prednisolone-7%; p < 0.05), a more pronounced increase in s-insulin after 120 min (before 118%; after 200%; p < 0.05) and a lower s-potassium. Sodium 138-144 insulin Homo sapiens 254-261 8869668-6 1996 It is suggested that the more pronounced the increases in plasma insulin and the decrease in serum potassium are mediators of the increased distal tubular sodium reabsorption during amino acid infusion during prednisolone treatment. Sodium 155-161 insulin Homo sapiens 65-72 8663355-1 1996 Previous studies have suggested that the enzyme microsomal epoxide hydrolase (mEH) is able to mediate sodium-dependent transport of bile acids such as taurocholate into hepatocytes (von Dippe, P., Amoui, M., Alves, C., and Levy, D.(1993) Am. Sodium 102-108 epoxide hydrolase 1, microsomal Mus musculus 78-81 8765464-0 1996 Arginine vasopressin mediates the chloroquine induced increase in renal sodium excretion. Sodium 72-78 arginine vasopressin Rattus norvegicus 9-20 8663355-8 1996 The transfected MDCK cells also exhibited sodium-dependent transport of cholate at levels 150% of taurocholate in contrast to hepatocytes where cholate transport is only 30% of taurocholate levels, suggesting that total hepatocyte bile acid transport is a function of multiple transport systems with different substrate specificities, where mEH preferentially transports cholate. Sodium 42-48 epoxide hydrolase 1, microsomal Mus musculus 341-344 8663355-11 1996 These results demonstrate that mEH is expressed on the surface of hepatocytes as well as on transfected MDCK cells and is able to mediate sodium-dependent transport of taurocholate and cholate. Sodium 138-144 epoxide hydrolase 1, microsomal Mus musculus 31-34 8663357-16 1996 4F2hc-injected oocytes accumulated substrates to a level higher than CAT1-injected oocytes (i.e. oocytes expressing system y+) and showed exchange of amino acids with the substrate specificity of system y+L and L-leucine-induced outward currents in the absence of extracellular sodium. Sodium 278-284 catalase, gene 1 L homeolog Xenopus laevis 69-73 8864421-4 1996 ANG II alone caused a decrease in glomerular filtration rate (GFR), renal plasma flow, urinary absolute and fractional excretion of sodium, both proximal and distal fractional tubular sodium reabsorption, and urinary flow. Sodium 132-138 angiotensinogen Homo sapiens 0-6 8864421-4 1996 ANG II alone caused a decrease in glomerular filtration rate (GFR), renal plasma flow, urinary absolute and fractional excretion of sodium, both proximal and distal fractional tubular sodium reabsorption, and urinary flow. Sodium 184-190 angiotensinogen Homo sapiens 0-6 8864421-14 1996 Net sodium excretion during the combined infusion with ANG II and ANP seems to reflect the sum of the opposing influences of each peptide. Sodium 4-10 angiotensinogen Homo sapiens 55-61 8864421-8 1996 ANG II + ANP: during a background ANG II infusion, ANP still increased fractional excretion of sodium. Sodium 95-101 angiotensinogen Homo sapiens 0-6 8818931-10 1996 CONCLUSIONS: The independent association between a cluster of risk factors for cardiovascular disease suggestive of insulin resistance and increased proximal sodium reabsorption at the renal tubule indicates a new feature of the metabolic syndrome that, if causal, could be amenable to intervention. Sodium 158-164 insulin Homo sapiens 116-123 8700118-1 1996 It has been proposed that excessive intrarenal conversion of cortisol to 6 beta-hydroxycortisol by CYP3A may mediate increased tubular reabsorption of sodium, leading to a state of mild volume expansion and the clinical phenotype of salt-sensitive hypertension. Sodium 151-157 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-104 8660367-5 1996 Both pH recovery after angiotensin II and alkalinization after aldosterone were blocked in sodium-free medium. Sodium 91-97 angiotensinogen Homo sapiens 23-37 8760660-6 1996 The prevention of the secondary effects of diuretics and ACE inhibitors on renal function, serum sodium, potassium and magnesium concentrations, is based on an initial low dose prescription, the detection and correction of risk factors and strict clinical and biological surveillance. Sodium 97-103 angiotensin I converting enzyme Homo sapiens 57-60 8743487-2 1996 ANF acts on the kidney to increase sodium excretion and GFR, to antagonize renal vasoconstriction, and to inhibit renin secretion. Sodium 35-41 natriuretic peptide A Homo sapiens 0-3 8870314-14 1996 CONCLUSION: This study shows ethnic differences in renin-sodium profile and renal PG synthesis, during changes in dietary sodium. Sodium 57-63 renin Homo sapiens 51-56 8870314-14 1996 CONCLUSION: This study shows ethnic differences in renin-sodium profile and renal PG synthesis, during changes in dietary sodium. Sodium 122-128 renin Homo sapiens 51-56 10968201-6 1996 These data suggest that intracellular sodium accumulation as well as increased blood viscosity may be independently involved in the blood pressure elevation after EPO treatment in patients under maintenance hemodialysis. Sodium 38-44 erythropoietin Homo sapiens 163-166 8776643-8 1996 In ANP, there occurred significant increases in urine flow (p < 0.001), inulin clearance (p < 0.001), filtration fraction (p = 0.007), and fractional clearance of sodium (p < 0.001) and of osmoles (p < 0.001) compared with C. During the study, no differences in mean arterial pressure, heart rate, and right atrial or pulmonary capillary wedge pressure were detected between the groups. Sodium 169-175 natriuretic peptide A Homo sapiens 3-6 8640238-4 1996 These two chromosomal regions harbour the genes encoding the three subunits of the human amiloride sensitive epithelial sodium channel (hENaC): SCNN1B and SCNN1G on 16p and SCNN1A on 12p. Sodium 120-126 sodium channel epithelial 1 subunit alpha Homo sapiens 173-179 8928911-7 1996 Sodium and water balances tended to be more positive during ANG II than during phenylephrine infusions. Sodium 0-6 angiotensinogen Rattus norvegicus 60-66 8671965-10 1996 In patients with nephrotic syndrome (group II), baseline sodium excretion of 10.5+/-6.0 mmol/h was increased to 19.6+/-14.8 mmol/h with ANP infusion (P<0.01). Sodium 57-63 natriuretic peptide A Homo sapiens 136-139 8654575-3 1996 Overexpression of the NHA1 gene results in higher and partially pH-dependent tolerance to sodium and lithium; its disruption leads to an increased sensitivity towards these ions. Sodium 90-96 Nha1p Saccharomyces cerevisiae S288C 22-26 8665776-7 1996 In seven dogs on a "normal" sodium diet (3.5 mmol of NaCl day-1 kg-1) endothelin-1 resulted in decreases in renal blood flow and glomerular filtration rate with a rise in filtration fraction from 0.24 +/- 0.01 to 0.35 +/- 0.01. Sodium 28-34 endothelin 1 Canis lupus familiaris 70-82 8665777-14 1996 All the effects of angiotensin-converting enzyme inhibitors were enhanced by sodium depletion, but sodium depletion in itself did not affect blood pressure (124 +/- 4 mmHg), proteinuria (664 +/- 68 mg/day) or glomerulosclerosis score (30 +/- 5%). Sodium 77-83 angiotensin I converting enzyme Rattus norvegicus 19-48 8621146-6 1996 Sodium restriction resulted in less weight loss in the cirrhotic patients (P = .03), with significantly lower plasma renin activity (P = .001). Sodium 0-6 renin Homo sapiens 117-122 8836955-0 1996 Release of vasopressin in response to altered plasma volume and sodium concentrations following pinealectomy in the rat. Sodium 64-70 arginine vasopressin Rattus norvegicus 11-22 8671370-0 1996 The influence of dietary sodium restriction on renal and ovarian renin and prorenin production during ovarian stimulation. Sodium 25-31 renin Homo sapiens 65-70 8671370-1 1996 In a prospective study, the effect of dietary sodium restriction on plasma and follicular fluid renin and prorenin concentrations and on fertilization measures was investigated during ovarian stimulation. Sodium 46-52 renin Homo sapiens 96-101 8671370-3 1996 Plasma renin and prorenin concentrations were higher in the low sodium than in the normal sodium group. Sodium 64-70 renin Homo sapiens 7-12 8671370-3 1996 Plasma renin and prorenin concentrations were higher in the low sodium than in the normal sodium group. Sodium 90-96 renin Homo sapiens 7-12 8836955-6 1996 Similarly, following infusion of hypertonic saline, the increase in plasma vasopressin per unit increase in plasma sodium was lower in pinealectomized animals than the pineal intact controls. Sodium 115-121 arginine vasopressin Rattus norvegicus 75-86 8671897-6 1996 RESULTS: Insulin induced similar decrements in fractional sodium excretion (N-NIDDM: 43+/-5.9 and 57+/-9.1%,H-N IDDM: 48+/-16.4 and 62+/-12.5%, low and high insulin dose respectively). Sodium 58-64 insulin Homo sapiens 9-16 8671897-11 1996 CONCLUSIONS: The findings suggest that insulin-induced sodium retention may contribute to hypertension in NIDDM if the homeostatic response to offset this effect fails. Sodium 55-61 insulin Homo sapiens 39-46 8671897-2 1996 It has recently been shown that insulin exerts a sodium-retaining effect, which is preserved in NIDDM: We sought to determine whether insulin affected renal sodium handling differently in hypertensive and normotensive NIDDM patients. Sodium 49-55 insulin Homo sapiens 32-39 8613987-0 1996 Effect of sodium on the energetics of thrombin-thrombomodulin interaction and its relevance for protein C hydrolysis. Sodium 10-16 coagulation factor II, thrombin Homo sapiens 38-46 8613987-4 1996 The enthalpic contribution to the free energy of sodium binding is equal to -27 kcal/mol and -21 kcal/mol in the TM-free and TM-bound thrombin forms, respectively. Sodium 49-55 coagulation factor II, thrombin Homo sapiens 134-142 8613987-3 1996 Namely, at 25 degrees C, the value of delta G of sodium binding was found equal to -2.4 kcal/mol in the absence of TM and -3.6 kcal/mol for the thrombin-TM complex. Sodium 49-55 coagulation factor II, thrombin Homo sapiens 144-152 8613987-5 1996 Finally, the entropy change for sodium binding was also affected by TM, being equal to -83 cal/(mol deg) and -58 cal/(mol deg) in TM-free and TM-bound thrombin species, respectively. Sodium 32-38 coagulation factor II, thrombin Homo sapiens 151-159 8743025-5 1996 Physiological mechanisms by which insulin might increase blood pressure include sympathetic nervous system stimulation and enhancement or renal sodium reabsorption. Sodium 144-150 insulin Homo sapiens 34-41 8613987-10 1996 Therefore, the effect of sodium binding to thrombin on the hydrolysis of human Protein C was extensively investigated. Sodium 25-31 coagulation factor II, thrombin Homo sapiens 43-51 8708176-9 1996 In all three TNF groups there were significant increases in sodium and potassium ion concentrations compared to control, but the changes were significantly fewer in the magnesium-substituted calcium-free group than the two other TNF groups. Sodium 60-66 tumor necrosis factor Homo sapiens 13-16 8717063-14 1996 Therefore, if compensatory endogenous hyperinsulinaemia was raised by insulin resistance, these two factors may lead to chronic sodium retention and pressor system stimulation and, in turn, to hypertension in obesity. Sodium 128-134 insulin Homo sapiens 43-50 8732994-4 1996 However, the increase in AII is sufficient for a slight reduction in renal blood flow and a slight increase in exchangeable sodium and blood pressure; in susceptible women, blood pressure may rise considerably. Sodium 124-130 angiotensinogen Homo sapiens 25-28 8691747-3 1996 The plasma membrane of osteogenic cells is endowed with a sodium-dependent Pi transport system that is regulated by osteotropic factors such as parathyroid hormone (PTH), parathyroid hormone-related protein (PTHrP), insulin-like growth factor-1 (IGF-1), platelet-derived growth factor (PDGF) and fluoride. Sodium 58-64 parathyroid hormone Homo sapiens 144-163 8691747-3 1996 The plasma membrane of osteogenic cells is endowed with a sodium-dependent Pi transport system that is regulated by osteotropic factors such as parathyroid hormone (PTH), parathyroid hormone-related protein (PTHrP), insulin-like growth factor-1 (IGF-1), platelet-derived growth factor (PDGF) and fluoride. Sodium 58-64 parathyroid hormone Homo sapiens 165-168 8691747-3 1996 The plasma membrane of osteogenic cells is endowed with a sodium-dependent Pi transport system that is regulated by osteotropic factors such as parathyroid hormone (PTH), parathyroid hormone-related protein (PTHrP), insulin-like growth factor-1 (IGF-1), platelet-derived growth factor (PDGF) and fluoride. Sodium 58-64 insulin like growth factor 1 Homo sapiens 216-244 8691747-3 1996 The plasma membrane of osteogenic cells is endowed with a sodium-dependent Pi transport system that is regulated by osteotropic factors such as parathyroid hormone (PTH), parathyroid hormone-related protein (PTHrP), insulin-like growth factor-1 (IGF-1), platelet-derived growth factor (PDGF) and fluoride. Sodium 58-64 insulin like growth factor 1 Homo sapiens 246-251 9238683-4 1996 In sodium (NaM) and potassium (KM) media, a linear relationship between the internal and external pH was observed. Sodium 3-9 SH3 and cysteine rich domain 3 Homo sapiens 11-14 8931343-1 1996 Renin-angiotensin system plays a prominent role in the sodium and water homeostasis. Sodium 55-61 renin Homo sapiens 0-5 8931343-3 1996 Theoretically, administering of angiotensin converting enzyme inhibitors can enhance sodium and water retention in cirrhotic patients with ascites. Sodium 85-91 angiotensin I converting enzyme Homo sapiens 32-61 8775403-7 1996 METHODS AND RESULTS: In six healthy, sodium-replete men, infusion of synthetic ANF (0.01 microgram.kg.min, Anaritide, Wyeth Laboratories) significantly increased urine flow from 7.1 +/- 0.7 to 11.7 +/- 1.8 ml.min-1 (p < 0.05) and decreased aldosterone from 74.7 +/- 9.0 to 55.8 +/- 6.5 pg.ml-1 (p = N.S.). Sodium 37-43 natriuretic peptide A Homo sapiens 79-82 18406731-4 1996 IGF-I raises proximal tubular phosphate reabsorption and may increase sodium absorption in distal tubules. Sodium 70-76 insulin like growth factor 1 Homo sapiens 0-5 8860099-0 1996 Low dose of ACE-inhibitor enhances sodium excretion in volume expanded patients with borderline hypertension. Sodium 35-41 angiotensin I converting enzyme Homo sapiens 12-15 8613210-2 1996 We have reported that the angiotensin II (Ang II) AT1 receptor antagonist losartan markedly lowers arterial pressure in sodium-replete, normotensive rats. Sodium 120-126 angiotensinogen Rattus norvegicus 26-40 8613210-2 1996 We have reported that the angiotensin II (Ang II) AT1 receptor antagonist losartan markedly lowers arterial pressure in sodium-replete, normotensive rats. Sodium 120-126 angiotensinogen Rattus norvegicus 42-48 8778224-2 1996 Vasopressin caused a dose-dependent increase in sodium excretion when administered at 40-160 pmol/min. Sodium 48-54 arginine vasopressin Rattus norvegicus 0-11 8772622-1 1996 OBJECTIVES: To study the relationship between insulin sensitivity and sodium-lithium countertransport (Na(+)-Li+ CT) in mild, essential hypertension, and to investigate the effect of metformin and metoprolol, respectively. Sodium 70-76 insulin Homo sapiens 46-53 8567042-0 1996 Does the renin-angiotensin system determine the renal and systemic hemodynamic response to sodium in patients with essential hypertension? Sodium 91-97 renin Homo sapiens 9-14 8772586-0 1996 Short-term growth hormone (GH) treatment of GH-deficient adults increases body sodium and extracellular water, but not blood pressure. Sodium 79-85 growth hormone 1 Homo sapiens 11-25 8772586-0 1996 Short-term growth hormone (GH) treatment of GH-deficient adults increases body sodium and extracellular water, but not blood pressure. Sodium 79-85 growth hormone 1 Homo sapiens 27-29 8772586-5 1996 High dose GH caused a 1.2 +/- 0.3 kg increase in body weight (P = 0.01) and a 193 +/- 65 mmol increase in exchangeable sodium (P = 0.008). Sodium 119-125 growth hormone 1 Homo sapiens 10-12 8772586-6 1996 Low dose GH had a lesser effect, with no significant increase in body weight, but an increase in exchangeable sodium of 113 +/- 37 mmol (P = 0.02). Sodium 110-116 growth hormone 1 Homo sapiens 9-11 8772586-14 1996 We conclude that 1) sodium retention is a physiological effect of GH, but does not cause an acute rise in blood pressure; and 2) the mechanism of sodium and fluid retention is not primarily due to enhanced aldosterone secretion or inhibition of ANP release, but more likely to a direct renal tubular effect. Sodium 20-26 growth hormone 1 Homo sapiens 66-68 8815525-5 1996 Insulin therapy is associated with precocious sodium and potassium replacement, and with gradual rehydration coupled to intensive monitoring. Sodium 46-52 insulin Homo sapiens 0-7 8629540-1 1996 Pharmacologic agents that attenuate the influence of the renin-angiotensin-aldosterone system are known to reduce systemic arterial blood pressure through vasodilatory action and enhanced renal clearance of sodium and water. Sodium 207-213 renin Homo sapiens 57-62 8567042-3 1996 Our aim was to clarify the role of the renin-angiotensin system in the renal and systemic adaptation to a change in dietary sodium. Sodium 124-130 renin Homo sapiens 39-44 8567042-15 1996 renin-angiotensin system response to increased sodium intake. Sodium 47-53 renin Homo sapiens 0-5 8867564-4 1996 Assessment of plasma renin activity (PRA) related to concurrent 24 h sodium excretion was used to define patients with high (n = 12), medium (n = 16) and low renin profile (n = 8). Sodium 69-75 renin Homo sapiens 21-26 8635674-9 1996 Combining all patients, there were relevant associations between changes of urinary sodium excretion and blood volume (Spearman correlation coefficient r = 0.57), blood pressure and angiotensin II (diastolic: r = -0.7; systolic: r = -0.48), and exchangeable body sodium and renin activity (r = -0.5). Sodium 84-90 renin Homo sapiens 274-279 8866749-5 1996 Mutant kininogen-deficient Brown Norway-Katholiek rats, which cannot generate kinin in the urine, are very sensitive to salt loading and to sodium retention by aldosterone released by a non-pressor dose of angiotensin II, which results in hypertension. Sodium 140-146 angiotensinogen Rattus norvegicus 206-220 8907569-8 1996 In patients with ascites, endothelin-1 was inversely correlated with both glomerular filtration rate (upright: r = -0.62; p = 0.06; supine: r = -0.71, p < 0.05) and renal sodium excretion (upright: r = -0.82; p < 0.01; supine: r = -0.88; p < 0.001). Sodium 174-180 endothelin 1 Homo sapiens 26-38 8683468-0 1996 Sodium-dependent GABA-induced currents in GAT1-transfected HeLa cells. Sodium 0-6 solute carrier family 6 member 1 Homo sapiens 42-46 8739882-3 1996 Insulin could also promote high blood pressure via its effect in increasing sodium reabsorption and sympathetic nervous system activity. Sodium 76-82 insulin Homo sapiens 0-7 9037790-7 1996 In RLS group total fluid volume infused was higher while sodium requirements was lower than in HLS patients, with statistically significative difference (p < 0.01). Sodium 57-63 RLS1 Homo sapiens 3-6 8955756-4 1996 Sodium correlated negatively with LANP (p = 0.021) and ANF (p = 0.007), while Cl correlated positively with LANP (p = 0.003) and VSDL (p = 0.001). Sodium 0-6 natriuretic peptide A Homo sapiens 55-58 8769841-2 1996 We hypothesized that NO inhibits antidiuretic hormone (ADH)-stimulated fluid reabsorption (J(r)) by the isolated rat cortical collecting duct (CCD) by decreasing water permeability (Pf) and sodium reabsorption (Jna). Sodium 190-196 arginine vasopressin Homo sapiens 55-58 8769841-16 1996 We concluded that 1) NO decreases ADH-stimulated water and sodium transport in the isolate CCD, and 2) water reabsorption is inhibited by a primary effect on Pf. Sodium 59-65 arginine vasopressin Homo sapiens 34-37 8772437-1 1996 The effect of human growth hormone-releasing hormone (hGHRH), a potent stimulator of adenylate cyclase in somatotrophs on the voltage-gated sodium current was determined by perforated patch clamp of cultured rat somatotrophs The amplitude of the voltage-gated sodium current was augmented by 65.3 +/- 20.6% (mean +/- SE, n = 7) by 10 nM hGHRH. Sodium 140-146 growth hormone releasing hormone Homo sapiens 20-52 9162439-1 1996 In the red blood cell membrane, sodium-proton exchange (NHE-1) exchanges intracellular H(+), Li(+), and Na(+) with extracellular Na(+). Sodium 32-38 solute carrier family 9 member A1 Homo sapiens 56-61 8772437-1 1996 The effect of human growth hormone-releasing hormone (hGHRH), a potent stimulator of adenylate cyclase in somatotrophs on the voltage-gated sodium current was determined by perforated patch clamp of cultured rat somatotrophs The amplitude of the voltage-gated sodium current was augmented by 65.3 +/- 20.6% (mean +/- SE, n = 7) by 10 nM hGHRH. Sodium 140-146 growth hormone releasing hormone Homo sapiens 54-59 8772437-1 1996 The effect of human growth hormone-releasing hormone (hGHRH), a potent stimulator of adenylate cyclase in somatotrophs on the voltage-gated sodium current was determined by perforated patch clamp of cultured rat somatotrophs The amplitude of the voltage-gated sodium current was augmented by 65.3 +/- 20.6% (mean +/- SE, n = 7) by 10 nM hGHRH. Sodium 140-146 growth hormone releasing hormone Homo sapiens 337-342 8772437-1 1996 The effect of human growth hormone-releasing hormone (hGHRH), a potent stimulator of adenylate cyclase in somatotrophs on the voltage-gated sodium current was determined by perforated patch clamp of cultured rat somatotrophs The amplitude of the voltage-gated sodium current was augmented by 65.3 +/- 20.6% (mean +/- SE, n = 7) by 10 nM hGHRH. Sodium 260-266 growth hormone releasing hormone Homo sapiens 20-52 8772437-1 1996 The effect of human growth hormone-releasing hormone (hGHRH), a potent stimulator of adenylate cyclase in somatotrophs on the voltage-gated sodium current was determined by perforated patch clamp of cultured rat somatotrophs The amplitude of the voltage-gated sodium current was augmented by 65.3 +/- 20.6% (mean +/- SE, n = 7) by 10 nM hGHRH. Sodium 260-266 growth hormone releasing hormone Homo sapiens 54-59 8772437-6 1996 These results suggest that hGHRH augments the peak amplitude of the voltage-gated sodium current in rat somatotrophs via phosphorylation by cAMP-dependent protein kinase. Sodium 82-88 growth hormone releasing hormone Homo sapiens 27-32 8631044-7 1996 The lack of an effect on renal hemodynamics suggests that this natriuresis results from ANF-mediated inhibition of tubular sodium reabsorption. Sodium 123-129 natriuretic peptide A Homo sapiens 88-91 8993847-9 1996 Centrally administered AngII may act on AT1 receptors in the median preoptic nucleus and elsewhere to induce drinking, sodium appetite, a sympathetic vasoconstrictor response and vasopressin secretion. Sodium 119-125 angiotensinogen Rattus norvegicus 23-28 8993849-0 1996 Regulation of renal tubular sodium transport by angiotensin II and atrial natriuretic factor. Sodium 28-34 angiotensinogen Homo sapiens 48-62 8993849-0 1996 Regulation of renal tubular sodium transport by angiotensin II and atrial natriuretic factor. Sodium 28-34 natriuretic peptide A Homo sapiens 67-92 8697700-0 1996 Characteristics of the sodium/hydrogen exchange in non-insulin-dependent diabetic patients with microalbuminuria and hypertension. Sodium 23-29 insulin Homo sapiens 55-62 8993849-9 1996 Angiotensin II affects transepithelial sodium transport by modulation of Na+/H+ exchange at the luminal membrane and Na+/HCO3 cotransport, Na+/K(+)-ATPase activity and K+ conductance at the basolateral membrane. Sodium 39-45 angiotensinogen Homo sapiens 0-14 8993850-9 1996 The expression of the AT1 receptor is modulated at the mRNA and protein levels by many factors: conditions that increase levels of AngII (low sodium diet, renovascular hypertension, AngII infusion) up-regulate AT1 receptor mRNA levels and binding and increase aldosterone secretion. Sodium 142-148 angiotensinogen Homo sapiens 131-136 8894667-6 1996 Thus we studied the response of the renin-angiotensin-aldosterone system to sodium depletion using a single dose of furosemide. Sodium 76-82 renin Homo sapiens 36-41 8894667-13 1996 During sodium depletion with furosemide, renin as well as aldosterone levels rose significantly in 1 parent and a sibling, respectively. Sodium 7-13 renin Homo sapiens 41-46 8551200-3 1996 Assessment of plasma renin activity (PRA) related to urinary sodium excretion was used to define subgroups with high (n = 12), medium (n = 16) and low renin profiles (n = 8). Sodium 61-67 renin Homo sapiens 21-26 8935572-2 1996 Insulin resistance generated by central obesity, and complex relations with sympathetic activity, dyslipemia, atherosclerosis, sodium retention, altered vascular reactivity and hypertension, lead to pathophysiological connections, that are still to be understood. Sodium 127-133 insulin Homo sapiens 0-7 9239888-2 1996 Insulin produces sympathetic nervous system stimulation, enhances renal sodium retention and it directly modifies vascular mechanisms involved in both contraction and relaxation of the vascular smooth muscle. Sodium 72-78 insulin Homo sapiens 0-7 8649652-11 1996 Angiotensin II elicited a further increase in distal fractional tubular sodium reabsorption in both groups (P < 0.05). Sodium 72-78 angiotensinogen Homo sapiens 0-14 8649652-0 1996 Stimulatory effect of insulin on tubular sodium reabsorption in normotensive subjects with a positive family history of hypertension. Sodium 41-47 insulin Homo sapiens 22-29 8649652-12 1996 CONCLUSION: In normotensive subjects with a positive family history of hypertension, in contrast to control subjects without such history, hyperinsulinaemia caused a marked decrease in urinary sodium excretion in presence of unchanged RPF and GFR indicating a renal tubular effect of insulin located at distal site of the renal tubules. Sodium 193-199 insulin Homo sapiens 144-151 8649652-13 1996 Angiotensin II caused further sodium retention, probably due to an effect on renal haemodynamics. Sodium 30-36 angiotensinogen Homo sapiens 0-14 8832609-1 1996 Neuropeptide Y (NPY) is a vasoconstrictor peptide possibly involved in the regulation of renal sodium handling and renin release. Sodium 95-101 neuropeptide Y Rattus norvegicus 0-14 8832609-1 1996 Neuropeptide Y (NPY) is a vasoconstrictor peptide possibly involved in the regulation of renal sodium handling and renin release. Sodium 95-101 neuropeptide Y Rattus norvegicus 16-19 8878363-3 1996 The chemical analysis of fog during 32 episodes of local fog (pH, chloride, nitrate, sulphate, sodium, ammonia, potassium, magnesium, calcium) has shown a greater concentration of pollutants and greater acidity in the smaller particles (2-6 microns) which are able to penetrate the bronchial tree. Sodium 95-101 zinc finger protein, FOG family member 1 Homo sapiens 25-28 8750761-0 1995 Effect of insulin on renal sodium handling and renal haemodynamics in insulin-dependent (type 1) diabetes mellitus patients. Sodium 27-33 insulin Homo sapiens 10-17 8750761-4 1995 However, type 1 diabetic patients were still sensitive to the distal tubular antinatriuretic effect of insulin, as indicated by an increase in distal sodium reabsorption (95.5 +/- 0.5% to 96.9% +/- 0.4%; P < 0.05) during insulin infusion compared with controls (95.5% +/- 0.6% to 97.4% +/- 0.3%; P < 0.05). Sodium 150-156 insulin Homo sapiens 103-110 7498974-0 1995 Insulin effect on renal sodium reabsorption in adolescent offspring of essential hypertensive parents. Sodium 24-30 insulin Homo sapiens 0-7 8750761-7 1995 In conclusion, the present result demonstrates an intact distal tubular sodium retaining effect in conjunction with a blunted decrease in proximal tubular sodium reabsorption following insulin infusion, which could be the result of an impaired renal vasodilation in type 1 diabetes mellitus. Sodium 155-161 insulin Homo sapiens 185-192 8845091-4 1995 Increased renal tubule absorption of sodium and increased sympathetic nervous system stimulation from insulin have been said to be the mechanisms by which elevated levels of insulin cause hypertension. Sodium 37-43 insulin Homo sapiens 174-181 8594942-9 1995 When ANP was coinfused, significant differences were also observed in urine volume (P = 0.001) and sodium excretion (P = 0.043) between the infusion period (when urine volume and sodium excretion were enhanced) and postinfusion period (when values decreased). Sodium 99-105 natriuretic peptide A Homo sapiens 5-8 8594942-9 1995 When ANP was coinfused, significant differences were also observed in urine volume (P = 0.001) and sodium excretion (P = 0.043) between the infusion period (when urine volume and sodium excretion were enhanced) and postinfusion period (when values decreased). Sodium 179-185 natriuretic peptide A Homo sapiens 5-8 7498974-3 1995 The aim of this study was to evaluate the role of insulin on the increased proximal renal sodium reabsorption previously reported. Sodium 90-96 insulin Homo sapiens 50-57 7498983-1 1995 We previously demonstrated that type 1A angiotensin II (Ang II) receptor (AT1A) is the predominant renal subtype and is upregulated by a low sodium diet. Sodium 141-147 angiotensinogen Rattus norvegicus 56-62 7498983-2 1995 We have now tested the hypothesis that upregulation of AT1A mRNA induced by sodium deficiency is renal specific and is mediated by activation of type 1 Ang II receptor (AT1). Sodium 76-82 angiotensinogen Rattus norvegicus 152-158 7498983-8 1995 Thus, sodium deficiency increases AT1A mRNA in both kidney and adrenal gland, while Ang II receptor blockade by losartan prevents low sodium-induced AT1A mRNA only in adrenal gland. Sodium 134-140 angiotensinogen Rattus norvegicus 84-90 7490619-11 1995 Thrombin-induced brain edema was accompanied by increases in brain sodium and chloride contents and a decrease in brain potassium content. Sodium 67-73 coagulation factor II Rattus norvegicus 0-8 7485139-0 1995 Effects of recombinant human insulin-like growth factor 1 on renal handling of phosphorus, calcium, and sodium in normal humans. Sodium 104-110 insulin like growth factor 1 Homo sapiens 29-57 8866903-0 1995 Threshold sodium excretory and renal blood flow effects of angiotensin converting enzyme inhibition. Sodium 10-16 angiotensin I converting enzyme Rattus norvegicus 59-88 8866903-1 1995 OBJECTIVE: To probe the potential influence of a high renal tubular level of angiotensin II on sodium reabsorption using angiotensin converting enzyme inhibitors and a non-peptide angiotensin antagonist. Sodium 95-101 angiotensinogen Rattus norvegicus 77-91 15299771-4 1995 In addition to this hydrated DNA helix, the monoclinic unit cell (space group P2(1)) accommodates about 20 sodium ions and 12 water molecules in the vicinity of phosphate groups. Sodium 107-113 cyclin dependent kinase inhibitor 1A Homo sapiens 78-83 8554738-0 1995 Sodium ions attenuate the inhibitory effects of neuropeptide Y on norepinephrine release in rat hypothalamus. Sodium 0-6 neuropeptide Y Rattus norvegicus 48-62 8554738-8 1995 When the sodium concentration of the perfusion medium was increased, the inhibitory effects of NPY and UK 14,304 on norepinephrine release were significantly reduced. Sodium 9-15 neuropeptide Y Rattus norvegicus 95-98 8554732-1 1995 Plasma active renin consists of multiple glycoforms, which are differentially stored and secreted by the kidney, have varying plasma half-lives, and appear to have differing effects on renal sodium and water metabolism. Sodium 191-197 renin Homo sapiens 14-19 8554738-10 1995 Moreover, less suppressive effects of NPY and UK 14,304 on norepinephrine release in the presence of excess sodium ions suggest that sodium ions might actively participate in regulating the NPY and alpha 2-adrenergic receptor mediated functions in the central nervous system. Sodium 108-114 neuropeptide Y Rattus norvegicus 190-193 8554738-10 1995 Moreover, less suppressive effects of NPY and UK 14,304 on norepinephrine release in the presence of excess sodium ions suggest that sodium ions might actively participate in regulating the NPY and alpha 2-adrenergic receptor mediated functions in the central nervous system. Sodium 133-139 neuropeptide Y Rattus norvegicus 38-41 8554738-10 1995 Moreover, less suppressive effects of NPY and UK 14,304 on norepinephrine release in the presence of excess sodium ions suggest that sodium ions might actively participate in regulating the NPY and alpha 2-adrenergic receptor mediated functions in the central nervous system. Sodium 133-139 neuropeptide Y Rattus norvegicus 190-193 8583471-11 1995 Accordingly, we found that relatively too high levels of angiotensin II in relation to urinary sodium excretion were associated with left ventricular hypertrophy in these individuals on high salt intake. Sodium 95-101 angiotensinogen Homo sapiens 57-71 7592714-6 1995 Human recombinant IGF-I (10-100 ng/ml) stimulated both sodium-dependent phosphate uptake and 1,25-(OH)2D3 synthesis by these cells, in a time- and dose-dependent manner. Sodium 55-61 insulin like growth factor 1 Homo sapiens 18-23 8731845-0 1995 [Association of plasma insulin with blood pressure and sodium sensitivity in children]. Sodium 55-61 insulin Homo sapiens 23-30 16296241-3 1995 Atrial natriuretic peptide (ANP), realized from the heart during hypervolaemia, increases glomerular filtration rate, renal sodium and water elimination in both experimental animals and healthy men. Sodium 124-130 natriuretic peptide A Homo sapiens 0-26 16296241-3 1995 Atrial natriuretic peptide (ANP), realized from the heart during hypervolaemia, increases glomerular filtration rate, renal sodium and water elimination in both experimental animals and healthy men. Sodium 124-130 natriuretic peptide A Homo sapiens 28-31 16296241-4 1995 In attempt to clarify the possible role of ANP in the mechanism of sodium retention in nephrotic syndrome we carried out this study. Sodium 67-73 natriuretic peptide A Homo sapiens 43-46 8731845-3 1995 It is suggested that insulin resistance was associated with sodium sensitivity, and they might play a role in the development of hypertension in childhood. Sodium 60-66 insulin Homo sapiens 21-28 8547550-11 1995 Venous ET-1 levels were significantly correlated with venous oxygen content, pH, PO2, oxygen saturation, base excess, blood sodium concentration, and potassium concentration. Sodium 124-130 endothelin 1 Homo sapiens 7-11 8568012-6 1995 In addition, insulin can increase production of tissue growth factors and help retain sodium and calcium in cells. Sodium 86-92 insulin Homo sapiens 13-20 8573730-8 1995 Suppression of augmented renal sodium reabsorption and pressor system activities of insulin may be connected with the hypotensive mechanisms and the natriuresis caused by calcium channel blockers. Sodium 31-37 insulin Homo sapiens 84-91 7562563-1 1995 Infusion of endothelin-1 in humans to obtain pathophysiological plasma levels causes mild hypertension, strong sodium retention and renal vasoconstriction. Sodium 111-117 endothelin 1 Homo sapiens 12-24 8580890-8 1995 These results indicate that ANG II induces a greater increase in sodium intake in intact female rats than in ovariectomized rats and that estrogen and progesterone impair water and sodium intake in ovariectomized rats. Sodium 65-71 angiotensinogen Rattus norvegicus 28-34 8569052-7 1995 These results suggest that the sodium accumulation attributable to a lack of kinin generation may be related to increased vascular reactivity to angiotensin II and norepinephrine. Sodium 31-37 angiotensinogen Rattus norvegicus 145-159 7573486-0 1995 Biphasic effect of angiotensin II on intracellular sodium concentration in rat proximal tubules. Sodium 51-57 angiotensinogen Rattus norvegicus 19-33 7584929-0 1995 Recombinant human erythropoietin stimulates tubular reabsorption of sodium in anesthetized rabbits. Sodium 68-74 erythropoietin Homo sapiens 18-32 7657277-4 1995 However, in responders, the mannitol-induced increase in distal tubular sodium delivery resulted in a fivefold increase in urinary sodium excretion during ANP infusion (29 +/- 6 to 154 +/- 40 mumol/min, P < .01). Sodium 72-78 natriuretic peptide A Homo sapiens 155-158 7657277-0 1995 Reversal of atrial natriuretic peptide resistance by increasing distal tubular sodium delivery in patients with decompensated cirrhosis. Sodium 79-85 natriuretic peptide A Homo sapiens 12-38 7657277-1 1995 To test the hypothesis that diminished sodium delivery to the distal tubular site of atrial natriuretic peptide (ANP) action accounts for renal ANP resistance in cirrhosis, 12 cirrhotic patients with ascites were studied at baseline and during the infusion of ANP alone (0.15 micrograms/kg/min), mannitol alone (4 g/hr), and ANP plus mannitol for 3 hours each. Sodium 39-45 natriuretic peptide A Homo sapiens 85-111 7657277-1 1995 To test the hypothesis that diminished sodium delivery to the distal tubular site of atrial natriuretic peptide (ANP) action accounts for renal ANP resistance in cirrhosis, 12 cirrhotic patients with ascites were studied at baseline and during the infusion of ANP alone (0.15 micrograms/kg/min), mannitol alone (4 g/hr), and ANP plus mannitol for 3 hours each. Sodium 39-45 natriuretic peptide A Homo sapiens 113-116 7657277-4 1995 However, in responders, the mannitol-induced increase in distal tubular sodium delivery resulted in a fivefold increase in urinary sodium excretion during ANP infusion (29 +/- 6 to 154 +/- 40 mumol/min, P < .01). Sodium 131-137 natriuretic peptide A Homo sapiens 155-158 7657277-7 1995 Thus, the present results support the hypothesis that diminished distal tubular sodium delivery is a major factor contributing to ANP resistance in cirrhosis. Sodium 80-86 natriuretic peptide A Homo sapiens 130-133 7646525-0 1995 Parathyroid hormone stimulates electrogenic sodium transport in A6 cells. Sodium 44-50 parathyroid hormone Homo sapiens 0-19 9420665-6 1995 The altered degradation and distribution of ANP in patients with heart failure were demonstrated by a great increase in metabolic clearance (on average, 2.5-fold), production (on average, 6-fold), or both, and by a progressive reduction in the distribution spaces of the hormone when compared with normal subjects at the same sodium intake. Sodium 326-332 natriuretic peptide A Homo sapiens 44-47 9420665-7 1995 The ratio between ANP disposal and the daily excretion of sodium (equal to the sodium intake in subjects at a strictly controlled sodium balance) may give a good index of the biologic activity (natriuresis) of the ANP system. Sodium 58-64 natriuretic peptide A Homo sapiens 214-217 9420665-7 1995 The ratio between ANP disposal and the daily excretion of sodium (equal to the sodium intake in subjects at a strictly controlled sodium balance) may give a good index of the biologic activity (natriuresis) of the ANP system. Sodium 79-85 natriuretic peptide A Homo sapiens 214-217 9420665-7 1995 The ratio between ANP disposal and the daily excretion of sodium (equal to the sodium intake in subjects at a strictly controlled sodium balance) may give a good index of the biologic activity (natriuresis) of the ANP system. Sodium 79-85 natriuretic peptide A Homo sapiens 214-217 7478938-1 1995 Renal brush border membrane sodium/phosphate (Na/Pi)-cotransport activity is inhibited by hormonal mechanisms involving activation of protein kinases A and C. The recently cloned rat renal Na/Pi-cotransporter (NaPi-2) contains several protein kinase C but no protein kinase A consensus sites [17, 20]. Sodium 28-34 solute carrier family 34 member 1 Rattus norvegicus 210-216 7641363-0 1995 Additive effects of combined angiotensin-converting enzyme inhibition and angiotensin II antagonism on blood pressure and renin release in sodium-depleted normotensives. Sodium 139-145 angiotensinogen Homo sapiens 74-88 7641363-12 1995 CONCLUSIONS: The combined administration of a standard single oral dose of an ACE inhibitor and an Ang II antagonist to mildly sodium-depleted normal subjects (1) had a major additive effect on plasma renin rise, (2) induced an additional mean blood pressure reduction, and (3) had no additive effect on plasma aldosterone fall. Sodium 127-133 angiotensin I converting enzyme Homo sapiens 78-81 7641363-12 1995 CONCLUSIONS: The combined administration of a standard single oral dose of an ACE inhibitor and an Ang II antagonist to mildly sodium-depleted normal subjects (1) had a major additive effect on plasma renin rise, (2) induced an additional mean blood pressure reduction, and (3) had no additive effect on plasma aldosterone fall. Sodium 127-133 renin Homo sapiens 201-206 7646525-1 1995 The effects of parathyroid hormone (PTH) on sodium homeostasis in the distal tubule are not well defined. Sodium 44-50 parathyroid hormone Homo sapiens 15-34 7543698-1 1995 Cystic fibrosis transmembrane regulator (CFTR), the gene product that is mutated in cystic fibrosis (CF) patients, has a well-recognized function as a cyclic adenosine 3",5"-monophosphate (cAMP)-regulated chloride channel, but this property does not account for the abnormally high basal rate and cAMP sensitivity of sodium ion absorption in CF airway epithelia. Sodium 317-323 CF transmembrane conductance regulator Homo sapiens 0-39 7586717-0 1995 Effects of sodium depletion on tissue concentrations of the natriuretic hormone vasoactive intestinal peptide. Sodium 11-17 vasoactive intestinal peptide Rattus norvegicus 80-109 7543698-1 1995 Cystic fibrosis transmembrane regulator (CFTR), the gene product that is mutated in cystic fibrosis (CF) patients, has a well-recognized function as a cyclic adenosine 3",5"-monophosphate (cAMP)-regulated chloride channel, but this property does not account for the abnormally high basal rate and cAMP sensitivity of sodium ion absorption in CF airway epithelia. Sodium 317-323 CF transmembrane conductance regulator Homo sapiens 41-45 7634895-0 1995 The effect of dietary sodium on the concentrations of vasoactive intestinal peptide in plasma and lung. Sodium 22-28 vasoactive intestinal peptide Rattus norvegicus 54-83 7634895-1 1995 STUDY OBJECTIVES: In this study, we sought to determine whether changes in the concentration of vasoactive intestinal peptide (VIP) in the lung might explain the increase in bronchial reactivity associated with high sodium diets. Sodium 216-222 vasoactive intestinal peptide Rattus norvegicus 96-125 7634895-1 1995 STUDY OBJECTIVES: In this study, we sought to determine whether changes in the concentration of vasoactive intestinal peptide (VIP) in the lung might explain the increase in bronchial reactivity associated with high sodium diets. Sodium 216-222 vasoactive intestinal peptide Rattus norvegicus 127-130 7634895-5 1995 RESULTS: The VIP concentrations in both lung and plasma varied with dietary sodium. Sodium 76-82 vasoactive intestinal peptide Rattus norvegicus 13-16 7634895-6 1995 Plasma VIP level was significantly higher in the rats that had received the low-sodium diet (51.45 +/- 7.35 pmol L-1) than in the rats that had received the high-sodium diet (29.84 +/- 6.83; p < 0.05). Sodium 80-86 vasoactive intestinal peptide Rattus norvegicus 7-10 7634895-6 1995 Plasma VIP level was significantly higher in the rats that had received the low-sodium diet (51.45 +/- 7.35 pmol L-1) than in the rats that had received the high-sodium diet (29.84 +/- 6.83; p < 0.05). Sodium 162-168 vasoactive intestinal peptide Rattus norvegicus 7-10 7634895-7 1995 In the lung, VIP level was greater in the rats that had received the normal-sodium diet (378.13 +/- 41.68 fmol/g) than in rats that had received either the low-sodium diet (137.30 +/- 26.11 fmol/g; p < 0.0005) or the high-sodium diet (182.64 +/- 28.63 fmol/g; p < 0.005). Sodium 76-82 vasoactive intestinal peptide Rattus norvegicus 13-16 7634895-7 1995 In the lung, VIP level was greater in the rats that had received the normal-sodium diet (378.13 +/- 41.68 fmol/g) than in rats that had received either the low-sodium diet (137.30 +/- 26.11 fmol/g; p < 0.0005) or the high-sodium diet (182.64 +/- 28.63 fmol/g; p < 0.005). Sodium 160-166 vasoactive intestinal peptide Rattus norvegicus 13-16 7634895-7 1995 In the lung, VIP level was greater in the rats that had received the normal-sodium diet (378.13 +/- 41.68 fmol/g) than in rats that had received either the low-sodium diet (137.30 +/- 26.11 fmol/g; p < 0.0005) or the high-sodium diet (182.64 +/- 28.63 fmol/g; p < 0.005). Sodium 160-166 vasoactive intestinal peptide Rattus norvegicus 13-16 7634895-8 1995 CONCLUSIONS: The lower plasma and pulmonary concentrations of VIP observed in rats that had received a high-sodium diet suggest that VIP may play a role in the increased bronchial reactivity reported with this diet. Sodium 108-114 vasoactive intestinal peptide Rattus norvegicus 62-65 7634895-8 1995 CONCLUSIONS: The lower plasma and pulmonary concentrations of VIP observed in rats that had received a high-sodium diet suggest that VIP may play a role in the increased bronchial reactivity reported with this diet. Sodium 108-114 vasoactive intestinal peptide Rattus norvegicus 133-136 7586717-2 1995 Variations in dietary sodium intake have been shown to affect the plasma concentration, the metabolic clearance rate and secretion rate of vasoactive intestinal peptide (VIP). Sodium 22-28 vasoactive intestinal peptide Rattus norvegicus 139-168 7586717-2 1995 Variations in dietary sodium intake have been shown to affect the plasma concentration, the metabolic clearance rate and secretion rate of vasoactive intestinal peptide (VIP). Sodium 22-28 vasoactive intestinal peptide Rattus norvegicus 170-173 7586717-3 1995 In this study we sought to determine the effect of sodium depletion on the concentration of VIP in plasma and in three tissues, namely heart, lung and kidney. Sodium 51-57 vasoactive intestinal peptide Rattus norvegicus 92-95 7586717-11 1995 In the group that received frusemide and the low sodium diet, VIP in the lung was significantly lower than the low sodium (P < 0.005) and normal sodium (P < 0.0001) groups. Sodium 49-55 vasoactive intestinal peptide Rattus norvegicus 62-65 7586717-14 1995 We conclude that sodium depletion decreases the concentration of VIP in plasma and in its metabolizing tissues. Sodium 17-23 vasoactive intestinal peptide Rattus norvegicus 65-68 7561631-5 1995 Vasoactive intestinal peptide (VIP), on the other hand, had little effect on aldosterone secretion by cells from normal animals, but was a potent stimulus to aldosterone secretion in cells obtained from sodium-depleted animals. Sodium 203-209 vasoactive intestinal peptide Rattus norvegicus 31-34 7561631-7 1995 Experiments using the angiotensin II receptor blocker, saralasin, were carried out to determine whether the enhanced actions of DALA and VIP seen in sodium depletion may be a result of activation of angiotensin II receptors, known to be increased in sodium depletion. Sodium 149-155 vasoactive intestinal peptide Rattus norvegicus 137-140 7635961-1 1995 The renin-angiotensin system regulates blood pressure and sodium balance. Sodium 58-64 renin Homo sapiens 4-9 7563621-2 1995 Insulin is thought to contribute to hypertension by sodium retention in the kidney. Sodium 52-58 insulin Homo sapiens 0-7 7662589-4 1995 Prolonged sodium restriction increased plasma ALDO level in both SDR and TGR, and significantly raised the volume of ZG. Sodium 10-16 thioredoxin reductase 3 Mus musculus 73-76 7662589-10 1995 In conclusion, our present findings confirm that TGR possess a hypertrophic ZG and an elevated secretory capacity o 18OH-steroids, but show only slight differences in ZG and ZG-cell responses to prolonged sodium deprivation. Sodium 205-211 thioredoxin reductase 3 Mus musculus 49-52 7611241-4 1995 Both angiotensin II antagonists induced a significant increase in urinary sodium excretion. Sodium 74-80 angiotensinogen Homo sapiens 5-19 7478230-2 1995 The injection of ANGII into LV in rats with volume expansion reduced the sodium, potassium and urine excretion in comparison to the control injections of isotonic saline, whereas prazosin (alpha 1 antagonist) potentiated these effects. Sodium 73-79 angiotensinogen Rattus norvegicus 17-22 7618108-5 1995 In contrast, Kv1.5 displayed a negligible sodium conductance on removal of potassium. Sodium 42-48 potassium voltage-gated channel subfamily A member 5 Homo sapiens 13-18 7631830-0 1995 Comparison of systemic and direct intrarenal angiotensin II blockade on sodium excretion in rats. Sodium 72-78 angiotensinogen Rattus norvegicus 45-59 7611241-10 1995 The results of the present analysis show that acute water loading per se may enhance renal sodium excretion and hence modify the level of activity of the renin-angiotensin system expected from a given sodium diet. Sodium 201-207 renin Homo sapiens 154-159 7614037-0 1995 Angiotensin II binding sites in the rat pancreas and their modulation after sodium loading and depletion. Sodium 76-82 angiotensinogen Rattus norvegicus 0-14 7671566-7 1995 Salt restriction increased the antidiuretic effect of arginine vasopressin (2 fmol min-1 kg-1 arginine vasopressin increased urine osmolality from 67.8 +/- 2.6 to 196.3 +/- 35.7 mosmol/l in the high-salt study and from 268.3 +/- 49 mosmol/l in the low-salt study; P < 0.05 between sodium intakes). Sodium 284-290 arginine vasopressin Homo sapiens 63-74 7671566-7 1995 Salt restriction increased the antidiuretic effect of arginine vasopressin (2 fmol min-1 kg-1 arginine vasopressin increased urine osmolality from 67.8 +/- 2.6 to 196.3 +/- 35.7 mosmol/l in the high-salt study and from 268.3 +/- 49 mosmol/l in the low-salt study; P < 0.05 between sodium intakes). Sodium 284-290 CD59 molecule (CD59 blood group) Homo sapiens 83-93 7671566-7 1995 Salt restriction increased the antidiuretic effect of arginine vasopressin (2 fmol min-1 kg-1 arginine vasopressin increased urine osmolality from 67.8 +/- 2.6 to 196.3 +/- 35.7 mosmol/l in the high-salt study and from 268.3 +/- 49 mosmol/l in the low-salt study; P < 0.05 between sodium intakes). Sodium 284-290 arginine vasopressin Homo sapiens 103-114 7594440-2 1995 METHODS: Endogenous levels of angiotensin II in the rats were increased either by unilateral 0.2-mm renal artery clips or by subcutaneous infusions of frusemide (12 mg/day) and by low-sodium diet. Sodium 184-190 angiotensinogen Rattus norvegicus 30-44 7609571-9 1995 The mean plasma arginine vasopressin levels were significantly increased by sodium loading both before and after operation in all groups. Sodium 76-82 arginine vasopressin Homo sapiens 25-36 7560756-4 1995 ANGII injection into the MnPO induced water and sodium intake, and natriuretic, diuretic, pressor and tachycardic responses. Sodium 48-54 angiotensinogen Rattus norvegicus 0-5 7560756-7 1995 LH lesion also reduced the sodium ingestion induced by ANGII (12 ng) into the MnPO. Sodium 27-33 angiotensinogen Rattus norvegicus 55-60 7560756-9 1995 The same occurred with sodium excretion when carbachol (2 nmol) and noradrenaline (20 nmol) were injected into the MnPO of LH-lesioned rats, whereas ANGII (12 ng) induced an increase in sodium excretion. Sodium 186-192 angiotensinogen Rattus norvegicus 149-154 7778532-6 1995 There are some contraindications or cautions for the use of ACE inhibitors in CHF, such as preexisting hypotension, high-renin states such as bilateral renal artery stenosis with hypertensive heart failure, aortic stenosis combined with CHF, overdiuresis with excess sodium depletion, and significant preexisting renal failure. Sodium 267-273 angiotensin I converting enzyme Homo sapiens 60-63 7569729-6 1995 Urinary sodium excretion rate increased in controls (0.23 to 0.52 mmol min-1, p < 0.01), while GFR increased (108 to 117 ml min-1, p < 0.05), and DFRNa decreased (93 to 89%, p < 0.01). Sodium 8-14 CD59 molecule (CD59 blood group) Homo sapiens 71-76 7569729-9 1995 Sodium excretion increased in four of five patients without ascites (0.23 to 0.27 mmol min-1, medians). Sodium 0-6 CD59 molecule (CD59 blood group) Homo sapiens 87-92 7662248-1 1995 Both a high renin-sodium profile and abnormal levels of sex hormones have been linked to myocardial infarction (MI) in men. Sodium 18-24 renin Homo sapiens 12-17 7473515-1 1995 The renin-angiotensin-aldosterone hormonal servo-control system plays a major role in defending normotension and sodium and potassium balance. Sodium 113-119 renin Homo sapiens 4-9 7473515-2 1995 Derangements of the system involving either excess renin-angiotensin vasoconstriction or too much sodium-volume retention for the plasma-renin level can be implicated in sustaining the hypertension of most human hypertensive disorders. Sodium 98-104 renin Homo sapiens 137-142 7736387-8 1995 One of the ANP-producing cell lines was derived from a hyponatremic patient with no other apparent explanation for a low sodium level. Sodium 121-127 natriuretic peptide A Homo sapiens 11-14 7768567-1 1995 It has been suggested that the increased levels of angiotensin II (Ang II) in the contralateral kidney of two-kidney, one clip (2K1C) Goldblatt hypertensive rats act to enhance tubuloglomerular feedback responsiveness and proximal tubular reabsorption and thereby exert a substantial sodium-retaining influence on the nonclipped kidney. Sodium 284-290 angiotensinogen Rattus norvegicus 51-65 7768567-1 1995 It has been suggested that the increased levels of angiotensin II (Ang II) in the contralateral kidney of two-kidney, one clip (2K1C) Goldblatt hypertensive rats act to enhance tubuloglomerular feedback responsiveness and proximal tubular reabsorption and thereby exert a substantial sodium-retaining influence on the nonclipped kidney. Sodium 284-290 angiotensinogen Rattus norvegicus 67-73 7752314-5 1995 Five years postoperatively, ambulation and furosemide administration under low sodium diet stimuli remarkably enhanced plasma renin activity and plasma aldosterone concentration in the aldosterone-producing adenoma enucleation group (p < 0.001), almost similar to that of normal subjects but increment magnitudes were slight (p < 0.05 to < 0.01) in the adrenalectomy group. Sodium 79-85 renin Homo sapiens 126-131 7644128-0 1995 Endothelins stimulate sodium uptake into rat brain capillary endothelial cells through endothelin A-like receptors. Sodium 22-28 endothelin 1 Rattus norvegicus 0-11 7644128-1 1995 The effect of endothelins (ETs) on sodium/hydrogen (Na+/H+) antiport system was examined in cultured rat brain capillary endothelium (RBEC). Sodium 35-41 endothelin 1 Rattus norvegicus 14-25 7752079-5 1995 At this dose, Ang II produced significant decreases in glomerular filtration rate (GFR), filtration fraction (FF), urine volume (UV) and urinary excretion of sodium (UNaV) and potassium (UkV) in SHR without altering any of these parameters in WKY rats. Sodium 158-164 angiotensinogen Rattus norvegicus 14-20 7737737-7 1995 In contrast with microalbuminuria, sodium-hydrogen exchange covaried only with high-density lipoprotein cholesterol and insulin levels. Sodium 35-41 insulin Homo sapiens 120-127 7752079-9 1995 However, the higher dose of Ang II produced significant decrements in GFR, FF, UV, UNaV and fractional excretion of sodium in SHR but not in WKY rats. Sodium 116-122 angiotensinogen Rattus norvegicus 28-34 7733330-6 1995 In conclusion, the components of the normal S1 PCT chloride reabsorption (approximately 300 peq.mm-1.min-1) from the glomerular ultrafiltrate consist of the following: active transport (40-50%), which can be regulated by angiotensin II; sodium-coupled organic solute transport (30%); and passive, chloride concentration gradient-driven transport (20-25%). Sodium 237-243 angiotensinogen Rattus norvegicus 221-235 7784414-5 1995 Renin and aldosterone levels were found increased in group C. Systemic vascular resistance differed significantly in the three groups, being lower in group C. Significant higher values in the Doppler reverse/forward ratio were observed in patients with markedly increased sodium retention and less systemic vascular resistance (group C). Sodium 272-278 renin Homo sapiens 0-5 7733333-4 1995 Infusion of PYY at the lower dose reproduced normal postprandial plasma concentrations and caused significant decreases in glomerular filtration rate (10% reduction), plasma renin activity (30% reduction), and aldosterone levels while increasing sodium excretion by approximately 30% (all P < 0.01). Sodium 246-252 peptide YY Homo sapiens 12-15 7733333-6 1995 Therefore, PYY may be an important mediator of the normal postprandial natriuretic response, and PYY agonists could provide a novel approach to the treatment of patients with sodium overload. Sodium 175-181 peptide YY Homo sapiens 97-100 7721445-3 1995 Our objective was to determine the roles of vasopressin V1 and V2 receptors in mediating the effects of renal perfusion pressure (RPP) on RIHP and sodium excretion (UNaV). Sodium 147-153 arginine vasopressin receptor 2 Rattus norvegicus 44-75 7721403-0 1995 Angiotensin II and sympathetic activity in sodium-restricted essential hypertension. Sodium 43-49 angiotensinogen Homo sapiens 0-14 7721406-1 1995 Endothelin-1 infusion into humans to obtain pathophysiological plasma levels causes mild hypertension, strong renal vasoconstriction, and sodium retention. Sodium 138-144 endothelin 1 Homo sapiens 0-12 7721446-1 1995 This study was designed to determine whether expression of renal messenger RNA (mRNA) encoding the two known angiotensin II type 1 (AT1) receptor subtypes (AT1A and AT1B) can be regulated by dietary sodium. Sodium 199-205 angiotensin II receptor, type 1b Rattus norvegicus 109-145 7721446-1 1995 This study was designed to determine whether expression of renal messenger RNA (mRNA) encoding the two known angiotensin II type 1 (AT1) receptor subtypes (AT1A and AT1B) can be regulated by dietary sodium. Sodium 199-205 angiotensin II receptor, type 1b Rattus norvegicus 165-169 7721446-6 1995 In situ hybridization analysis indicated that AT1B mRNA was expressed in the proximal and collecting tubules of the kidney in rats fed a normal-sodium diet. Sodium 144-150 angiotensin II receptor, type 1b Rattus norvegicus 46-50 7721446-7 1995 The low-sodium diet significantly decreased the percent positive staining area of AT1B mRNA in the renal cortex (5.51 +/- 0.77% versus 2.73 +/- 0.35%, P < .05) and medulla (4.76 +/- 0.70% versus 2.01 +/- 0.43%, P < .05) compared with the control diet. Sodium 8-14 angiotensin II receptor, type 1b Rattus norvegicus 82-86 7787142-8 1995 Insulin infusion caused a significant 13% increase in RPF and lithium clearance in control subjects, and a positive Spearman rank correlation (Rs = 0.41; P < 0.05) was observed between the changes in p-aminohippurate and lithium clearances during insulin infusion in the combined patient group, suggesting that impaired renal vasodilation may contribute to abnormal proximal tubular sodium handling and sodium retention. Sodium 386-392 insulin Homo sapiens 0-7 7787142-1 1995 Insulin infusion during euglycemia causes antinatriuresis and renal vasodilation in healthy humans, whereas the effects of acute insulin infusion on tubular sodium handling and renal hemodynamics in chronic renal disease are unknown. Sodium 157-163 insulin Homo sapiens 129-136 7787142-8 1995 Insulin infusion caused a significant 13% increase in RPF and lithium clearance in control subjects, and a positive Spearman rank correlation (Rs = 0.41; P < 0.05) was observed between the changes in p-aminohippurate and lithium clearances during insulin infusion in the combined patient group, suggesting that impaired renal vasodilation may contribute to abnormal proximal tubular sodium handling and sodium retention. Sodium 406-412 insulin Homo sapiens 0-7 7793338-0 1995 Age-associated alterations in thirst and arginine vasopressin in response to a water or sodium load. Sodium 88-94 arginine vasopressin Homo sapiens 50-61 7603840-0 1995 Expression of the human sodium/proton exchanger NHE-1 in Xenopus laevis oocytes enhances sodium/proton exchange activity and establishes sodium/lithium countertransport. Sodium 24-30 solute carrier family 9 member A1 Homo sapiens 48-53 7603840-1 1995 We investigated whether the human sodium/proton (Na+/H+) exchanger isoform 1 (NHE-1) can mediate sodium/lithium (Na+/Li+) countertransport. Sodium 34-40 solute carrier family 9 member A1 Homo sapiens 78-83 24394272-11 1995 The anabolic action of GH is accompanied by sodium and fluid retention, due to increased sodium pump activity. Sodium 44-50 growth hormone 1 Homo sapiens 23-25 7795831-6 1995 The trial has 80% power to detect an overall treatment effect on DBP of 1.2 mm Hg for weight loss or sodium reduction and a difference of 1.6 mm Hg between the combined intervention and placebo groups. Sodium 101-107 D-box binding PAR bZIP transcription factor Homo sapiens 65-68 7758259-6 1995 The increase in fractional excretion of sodium during a 1 h low-dose dopamine (3 micrograms kg-1 min-1) infusion in Type 1 diabetic patients was negatively correlated with diabetes duration. Sodium 40-46 CD59 molecule (CD59 blood group) Homo sapiens 97-102 7781662-2 1995 After candoxatril treatment, plasma ANP increased to a maximum at 2-4 h and declined to baseline within 24 h. The increases were relatively greater on the high sodium diet, which was also associated with increases in urinary sodium, with highest values at 4h. Sodium 160-166 natriuretic peptide A Homo sapiens 36-39 7738468-9 1995 Only the higher rates of infusion of vasopressin and oxytocin significantly increased the clearance of sodium, by 53 +/- 23 and 62 +/- 18% and glomerular filtration rate (GFR) by 23 +/- 4 and 23 +/- 4% respectively. Sodium 103-109 arginine vasopressin Rattus norvegicus 37-48 7600052-1 1995 Both a retrospective and a prospective study of hypertensive patients have detected a significant positive relationship between pretreatment renin and sodium profiles, and the occurrence of coronary artery disease events during treatment. Sodium 151-157 renin Homo sapiens 141-146 7533790-0 1995 Normalization of raised sodium absorption and raised calcium-mediated chloride secretion by adenovirus-mediated expression of cystic fibrosis transmembrane conductance regulator in primary human cystic fibrosis airway epithelial cells. Sodium 24-30 CF transmembrane conductance regulator Homo sapiens 126-177 7608483-1 1995 BACKGROUND/AIMS: The effects of C-type and brain natriuretic peptides (CNP and BNP, respectively) on renal excretion of sodium and hemodynamics have not yet been studied in cirrhosis. Sodium 120-126 natriuretic peptide B Rattus norvegicus 79-82 7891313-1 1995 Prior studies indicate that the natriuretic effects of atrial natriuretic peptide (ANP) are due, in part, to an inhibition of the passive movement of sodium ions from tubular lumen through apical cation channels into renal tubular epithelium. Sodium 150-156 natriuretic peptide A Homo sapiens 55-81 7891313-1 1995 Prior studies indicate that the natriuretic effects of atrial natriuretic peptide (ANP) are due, in part, to an inhibition of the passive movement of sodium ions from tubular lumen through apical cation channels into renal tubular epithelium. Sodium 150-156 natriuretic peptide A Homo sapiens 83-86 7891313-2 1995 The present work demonstrates that ANP also exerts a potent inhibitory effect on the active pumping of sodium ions by renal tubular sodium and potassium-activated adenosine triphosphatase (Na, K-ATPase). Sodium 103-109 natriuretic peptide A Homo sapiens 35-38 7621605-6 1995 Results show that pro ANF 31-67 and ANF 99-126 are diuretic and natriuretic and that when the two peptides are given in combination sodium excretion increases in an additive fashion. Sodium 132-138 natriuretic peptide A Homo sapiens 36-39 7616606-1 1995 In the choroid plexus carbonic anhydrase II (CAII) supports the transport of bicarbonate ions, sodium ions, and water from blood to the CSF, and in the myelin sheath CAII supports compaction of myelin by stimulating cotransport of ions and water out from between the myelin membranes. Sodium 95-101 carbonic anhydrase 2 Mus musculus 22-43 7616606-1 1995 In the choroid plexus carbonic anhydrase II (CAII) supports the transport of bicarbonate ions, sodium ions, and water from blood to the CSF, and in the myelin sheath CAII supports compaction of myelin by stimulating cotransport of ions and water out from between the myelin membranes. Sodium 95-101 carbonic anhydrase 2 Mus musculus 45-49 7864228-5 1995 However, the lines describing the relationship of log plasma vasopressin to plasma volume and plasma sodium in the rats treated with furosemide for 32 h lay to the left of the same relationships in the rats treated for 8 h or the sham-treated controls. Sodium 101-107 arginine vasopressin Rattus norvegicus 61-72 7642026-8 1995 Although insulin has complex actions on the circulation (including a vasodilator effect), plausible mechanisms by which insulin might raise blood pressure include stimulation of the sympathetic nervous system, alteration of ion transport kinetics, increase of renal sodium retention and stimulation of vascular smooth cells growth. Sodium 266-272 insulin Homo sapiens 120-127 7706990-9 1995 TGF-beta 1 mRNA was very weak or undetectable in the adrenals from rats treated with ACTH for three and five days or from sodium-restricted rats. Sodium 122-128 transforming growth factor, beta 1 Rattus norvegicus 0-10 16031800-3 1995 A severe cyclonic disturbance in early 1988, Cyclone Bola, was associated with changes in pasture sodium, potassium and magnesium, urinary sodium, and serum magnesium concentrations. Sodium 98-104 MHC class I antigen clone 2 Bos taurus 53-57 7617435-1 1995 Human recombinant interleukin-2 (rIL-2) was bath-applied to isolated human cardiocytes while sodium currents were triggered and registered using the whole-cell recording technique. Sodium 93-99 interleukin 2 Homo sapiens 18-31 7792315-1 1995 The renin-angiotensin system is intimately involved in the control of sodium and water balance, the activity of the sympathetic nervous system, mitogenesis and the regulation of vascular tone. Sodium 70-76 renin Homo sapiens 4-9 16031800-3 1995 A severe cyclonic disturbance in early 1988, Cyclone Bola, was associated with changes in pasture sodium, potassium and magnesium, urinary sodium, and serum magnesium concentrations. Sodium 139-145 MHC class I antigen clone 2 Bos taurus 53-57 7768036-3 1995 The selective NEP inhibitor SQ 28603 enhanced the increases in plasma ANP and urinary excretion of ANP, cyclic GMP and sodium stimulated by infusion of human ANP in conscious monkeys. Sodium 119-125 membrane metalloendopeptidase Homo sapiens 14-17 7725634-1 1995 The hypothesis of insulin resistance in the pathogenesis of arterial hypertension as part of the hormonal metabolic X syndrome and our 5H syndrome resp. (association of hyperinzulinism with hyperglycaemia-NIDDM-hyperlipoproteinaemia, hypertension and a hyperandrogenic state in women) is based on sympathomimetic, sodium retention and trophic effects of insulin. Sodium 314-320 insulin Homo sapiens 18-25 7896942-1 1995 A putative choline transporter (CHOT1) has been cloned from rat brain and is reported to express a high-affinity, sodium-dependent, hemicholinium-3-insensitive choline transporter in oocytes. Sodium 114-120 solute carrier family 6 member 8 Rattus norvegicus 11-30 7896942-1 1995 A putative choline transporter (CHOT1) has been cloned from rat brain and is reported to express a high-affinity, sodium-dependent, hemicholinium-3-insensitive choline transporter in oocytes. Sodium 114-120 solute carrier family 6 member 8 Rattus norvegicus 32-37 7896942-1 1995 A putative choline transporter (CHOT1) has been cloned from rat brain and is reported to express a high-affinity, sodium-dependent, hemicholinium-3-insensitive choline transporter in oocytes. Sodium 114-120 solute carrier family 6 member 8 Rattus norvegicus 160-179 7810534-8 1995 In PNS rats, plasma AVP was significantly higher than in control rats (control 0.77 +/- 0.10 pg/mL v PNS 2.13 +/- 0.42 pg/mL; P < 0.005, n = 12), even though there were no differences in plasma osmolality (control 292.0 +/- 2.0 mOsm/kg H2O v PNS 290.3 +/- 2.5 mOsm/kg H2O; P = NS, n = 12) or serum sodium concentration (control 142.7 +/- 0.7 v PNS 142.1 +/- 1.1; PNS, n = 12). Sodium 301-307 arginine vasopressin Rattus norvegicus 20-23 9021256-4 1995 Three sodium-dependent glutamate transporters have now been identified: a neuronal transporter EAAC1, and two astroglial transporters GLT-1 and GLAST. Sodium 6-12 solute carrier family 1 member 1 Homo sapiens 95-100 9021256-4 1995 Three sodium-dependent glutamate transporters have now been identified: a neuronal transporter EAAC1, and two astroglial transporters GLT-1 and GLAST. Sodium 6-12 solute carrier family 1 member 3 Homo sapiens 144-149 7528711-0 1995 Plasma levels of substance P in liver cirrhosis: relationship to the activation of vasopressor systems and urinary sodium excretion. Sodium 115-121 tachykinin precursor 1 Homo sapiens 17-28 8537861-5 1995 Urine sodium concentration, urine osmolality and osmolality and osmolar clearance were elevated significantly as well on day 3, p < .05, and correlated to hANP levels. Sodium 6-12 natriuretic peptide A Homo sapiens 158-162 7529828-4 1995 Using whole-cell, perforated-patch, and single-channel recording, we found that treatment with NGF increased levels of voltage-gated sodium, calcium, and potassium currents. Sodium 133-139 nerve growth factor Homo sapiens 95-98 7815350-11 1995 In conclusion, RB 105 is a new dual inhibitor of ACE and NEP able to target both blood pressure and renal sodium handling in different experimental renin-dependent and -independent models of hypertension. Sodium 106-112 angiotensin I converting enzyme Rattus norvegicus 49-52 7565483-5 1995 Lastly, ET-1 is also an autocrine inhibitor of collecting duct sodium and water reabsorption; reduced nephron ET-1 production may result in fluid retention in essential hypertension. Sodium 63-69 endothelin 1 Homo sapiens 8-12 7854155-9 1995 In contrast, infusion of equipressor doses of Ang II decreased urinary sodium excretion and did not significantly alter the excretion of ET. Sodium 71-77 angiotensinogen Homo sapiens 46-52 8538922-8 1995 Likewise the changes in renal handling of sodium and water in response to ET-1 infusion were unaffected by pretreatment with placebo or isradipine, e.g. sodium excretion (-44.6% versus -40.8%), urine flow rate (-49.8% versus -38.9%) and clearance of lithium (-32.0% versus -29.1%). Sodium 42-48 endothelin 1 Homo sapiens 74-78 8538827-5 1995 A significant decrease in the fractional excretion of sodium, potassium, and phosphate was observed during the last 90 min of the IGF-I infusion period. Sodium 54-60 insulin like growth factor 1 Homo sapiens 130-135 8538922-9 1995 CONCLUSIONS: Intravenous infusion of ET-1 in healthy humans discretely increases diastolic blood pressure and profoundly decreases renal haemodynamics and excretion of sodium and water. Sodium 168-174 endothelin 1 Homo sapiens 37-41 8538913-0 1995 Sodium and insulin--is there a relationship? Sodium 0-6 insulin Homo sapiens 11-18 7716276-4 1994 Results showed that ANG II decreased bile flow and the excretion of sodium, potassium, chloride and bile acids whereas it increased pH, bile osmolality and the excretion rate of bicarbonate and calcium. Sodium 68-74 angiotensinogen Rattus norvegicus 20-26 7792804-7 1995 To further elucidate the pattern of inheritance we studied the response of the renin-angiotensin-aldosterone system to the stimulation by sodium depletion in the familial autosomal dominant form and in two families with sporadic cases. Sodium 138-144 renin Homo sapiens 79-84 7702805-11 1994 Only an insulin dose of 0.8 mU/min on a low sodium diet was able to significantly dilate the norepinephrine preconstricted vein (77 +/- 9% of baseline diameter versus ED50) (P = .002). Sodium 44-50 insulin Homo sapiens 8-15 7702805-7 1994 High sodium diet, however, resulted in a higher calculated insulin/glucose ratio (P = .029) implying reduced tissue sensitivity to insulin. Sodium 5-11 insulin Homo sapiens 59-66 7702805-7 1994 High sodium diet, however, resulted in a higher calculated insulin/glucose ratio (P = .029) implying reduced tissue sensitivity to insulin. Sodium 5-11 insulin Homo sapiens 131-138 7810690-1 1994 Angiotensin II (ANG II) plays an important role in the regulation of solute transport in the kidney, and its effect on proximal tubule sodium and fluid transport has been studied extensively. Sodium 135-141 angiotensinogen Rattus norvegicus 0-14 7810656-11 1994 The inhibition of Na(+)-K(+)-ATPase activity induced by IL-6 provides a putative mechanism for the observed inhibition of sodium-dependent taurocholate uptake. Sodium 122-128 interleukin 6 Homo sapiens 56-60 7810690-1 1994 Angiotensin II (ANG II) plays an important role in the regulation of solute transport in the kidney, and its effect on proximal tubule sodium and fluid transport has been studied extensively. Sodium 135-141 angiotensinogen Rattus norvegicus 16-22 7888547-4 1994 Levels of TNF-alpha correlated significantly with serum levels of C-reactive protein and triglycerides and inversely with serum levels of sodium. Sodium 138-144 tumor necrosis factor Homo sapiens 10-19 7711433-7 1994 By increasing cellular sodium concentration the blockade of Na-K-ATPase would in turn activate cellular calcium uptake bx the Na-Ca exchanger. Sodium 23-29 solute carrier family 8 member A1 Homo sapiens 126-141 7804449-0 1994 Involvement of protein kinase C in the stimulation of sodium-dependent phosphate transport by parathyroid hormone in osteoblast-like cells. Sodium 54-60 parathyroid hormone Rattus norvegicus 94-113 7534728-2 1994 Nitric oxide has also been implicated in the control of the secretion of hormones by the pancreas, hypothalamus, and anterior pituitary gland, and evidence is accumulating that it contributes to the regulation of the secretion of renin and vasopressin, hormones that play key roles in the control of sodium and water balance. Sodium 300-306 renin Homo sapiens 230-235 7994831-11 1994 The impaired ANP response to saline infusion could be due to a different distribution of volume load and contribute to determining the reduced ability to excrete sodium that is commonly described in nonmodulators. Sodium 162-168 natriuretic peptide A Homo sapiens 13-16 7989585-9 1994 Furthermore, sodium intake modifies insulin sensitivity in NTs but not HTs. Sodium 13-19 insulin Homo sapiens 36-43 7977526-7 1994 Urinary osmolality and sodium increased in both indomethacin and indomethacin+arginine vasopressin V2-receptor antagonist groups compared with vehicle (p < 0.05). Sodium 23-29 arginine vasopressin receptor 2 Homo sapiens 87-110 7806569-1 1994 A highly selective, amiloride-sensitive, epithelial sodium channel from rat colon (rENaC), composed of three homologous subunits termed alpha, beta, and gamma rENaC, has been cloned by functional expression and was proposed to mediate electrogenic sodium reabsorption in aldosterone-responsive epithelia. Sodium 52-58 sodium channel epithelial 1 subunit gamma Rattus norvegicus 83-88 7806569-1 1994 A highly selective, amiloride-sensitive, epithelial sodium channel from rat colon (rENaC), composed of three homologous subunits termed alpha, beta, and gamma rENaC, has been cloned by functional expression and was proposed to mediate electrogenic sodium reabsorption in aldosterone-responsive epithelia. Sodium 52-58 sodium channel epithelial 1 subunit gamma Rattus norvegicus 159-164 7882021-9 1994 Replacement of sodium ions with TRIS completely abolished the stimulatory effect of bradykinin on the sensory neurons. Sodium 15-21 kininogen 1 Homo sapiens 84-94 7977842-1 1994 Simultaneous administration of the diuretic furosemide (10 mg/kg) and a low dose of the angiotensin-converting enzyme (ACE) inhibitor captopril (5 mg/kg) results in short-latency thirst and sodium appetite (i.e., the rapid ingestion of water and NaCl solution). Sodium 190-196 angiotensin I converting enzyme Rattus norvegicus 88-117 7977814-4 1994 Sodium excretion rates increased markedly during the infusions of vasopressin in both SHR and DOCA-salt-hypertensive rats but also in their appropriate normotensive controls. Sodium 0-6 arginine vasopressin Rattus norvegicus 66-77 7977814-7 1994 Replacement of the sodium losses that occurred during the vasopressin infusion failed to return pressure toward control levels in SHR but did increase pressure in the DOCA-salt-hypertensive group. Sodium 19-25 arginine vasopressin Rattus norvegicus 58-69 7977842-1 1994 Simultaneous administration of the diuretic furosemide (10 mg/kg) and a low dose of the angiotensin-converting enzyme (ACE) inhibitor captopril (5 mg/kg) results in short-latency thirst and sodium appetite (i.e., the rapid ingestion of water and NaCl solution). Sodium 190-196 angiotensin I converting enzyme Rattus norvegicus 119-122 7977862-1 1994 The present investigations determined the effects of dietary sodium deprivation on the neurohypophysial secretion of arginine vasopressin (AVP) and oxytocin (OT) by rats in response to nonhypotensive hypovolemia induced by subcutaneous injection of 30% polyethylene glycol solution. Sodium 61-67 arginine vasopressin Rattus norvegicus 126-137 7977687-0 1994 Angiotensin II-dependent proximal tubule sodium transport is mediated by cAMP modulation of phospholipase C. Angiotensin II (ANG II) stimulates proximal tubule sodium transport by decreasing adenylyl cyclase activity. Sodium 41-47 angiotensinogen Rattus norvegicus 0-14 7977687-0 1994 Angiotensin II-dependent proximal tubule sodium transport is mediated by cAMP modulation of phospholipase C. Angiotensin II (ANG II) stimulates proximal tubule sodium transport by decreasing adenylyl cyclase activity. Sodium 41-47 angiotensinogen Rattus norvegicus 109-123 7977687-0 1994 Angiotensin II-dependent proximal tubule sodium transport is mediated by cAMP modulation of phospholipase C. Angiotensin II (ANG II) stimulates proximal tubule sodium transport by decreasing adenylyl cyclase activity. Sodium 41-47 angiotensinogen Rattus norvegicus 125-131 7977687-0 1994 Angiotensin II-dependent proximal tubule sodium transport is mediated by cAMP modulation of phospholipase C. Angiotensin II (ANG II) stimulates proximal tubule sodium transport by decreasing adenylyl cyclase activity. Sodium 160-166 angiotensinogen Rattus norvegicus 0-14 7977687-0 1994 Angiotensin II-dependent proximal tubule sodium transport is mediated by cAMP modulation of phospholipase C. Angiotensin II (ANG II) stimulates proximal tubule sodium transport by decreasing adenylyl cyclase activity. Sodium 160-166 angiotensinogen Rattus norvegicus 109-123 7977687-0 1994 Angiotensin II-dependent proximal tubule sodium transport is mediated by cAMP modulation of phospholipase C. Angiotensin II (ANG II) stimulates proximal tubule sodium transport by decreasing adenylyl cyclase activity. Sodium 160-166 angiotensinogen Rattus norvegicus 125-131 7977687-2 1994 To determine the contribution of phospholipase C and adenylyl cyclase to apical (AP) ANG II-dependent sodium transport, unidirectional (AP to basolateral) 22Na flux was measured in rat proximal tubule cells cultured on permeable supports. Sodium 102-108 angiotensinogen Rattus norvegicus 85-91 7977687-3 1994 AP ANG II (100 nM)-dependent sodium flux was prevented by preincubation with concentrations of the phospholipase C inhibitor U-73122 (1 microM) that blocked ANG II-dependent inositol phosphate formation. Sodium 29-35 angiotensinogen Rattus norvegicus 3-9 7977687-3 1994 AP ANG II (100 nM)-dependent sodium flux was prevented by preincubation with concentrations of the phospholipase C inhibitor U-73122 (1 microM) that blocked ANG II-dependent inositol phosphate formation. Sodium 29-35 angiotensinogen Rattus norvegicus 157-163 7977687-4 1994 AP ANG II-dependent sodium flux was also abolished by preincubation with the intracellular calcium mobilization inhibitor 3,4,5-trimethoxybenzoic acid 8-(diethylamino)octyl ester (TMB-8), further suggesting that ANG II-dependent sodium transport was mediated by inositol phosphates. Sodium 20-26 angiotensinogen Rattus norvegicus 3-9 15374267-1 1994 Atrial natriuretic peptide (ANP) is a hormone of relatively recent discovery concerned with sodium homeostasis. Sodium 92-98 natriuretic peptide A Homo sapiens 0-26 15374267-1 1994 Atrial natriuretic peptide (ANP) is a hormone of relatively recent discovery concerned with sodium homeostasis. Sodium 92-98 natriuretic peptide A Homo sapiens 28-31 7977687-4 1994 AP ANG II-dependent sodium flux was also abolished by preincubation with the intracellular calcium mobilization inhibitor 3,4,5-trimethoxybenzoic acid 8-(diethylamino)octyl ester (TMB-8), further suggesting that ANG II-dependent sodium transport was mediated by inositol phosphates. Sodium 20-26 angiotensinogen Rattus norvegicus 212-218 7977687-6 1994 Incubation with dibutyryl cAMP (10 microM) or forskolin (10 microM) prevented ANG II-dependent sodium flux as well as ANG II-dependent inositol phosphate formation. Sodium 95-101 angiotensinogen Rattus norvegicus 78-84 7977687-7 1994 In conclusion, ANG II-dependent proximal tubule sodium transport in cultured cells was transduced by phospholipase C and adenylyl cyclase. Sodium 48-54 angiotensinogen Rattus norvegicus 15-21 7767869-2 1994 The injection of endothelin-1 (1 nmol/kg body weight) induced a sharp and transient decrease in urine flow, sodium and potassium excretion, glomerular filtration rate, renal plasma flow, and renal blood flow, a significant increase in renal vascular resistance, and a small but significant increase in arterial pressure. Sodium 108-114 endothelin 1 Rattus norvegicus 17-29 7828353-1 1994 OBJECTIVE: Growth hormone (GH) replacement therapy in hypopituitary adults is associated with sodium and water retention. Sodium 94-100 growth hormone 1 Homo sapiens 11-25 7828353-1 1994 OBJECTIVE: Growth hormone (GH) replacement therapy in hypopituitary adults is associated with sodium and water retention. Sodium 94-100 growth hormone 1 Homo sapiens 27-29 7882575-4 1994 When the monkeys" diet was changed from 0.55% sodium to 1.1% sodium, the natriuretic response to 100 mumol/kg intravenous of SQ 28,603 increased from 665 +/- 64 to 1015 +/- 224 mu Eq/3 h. An acute oral load of 25 mEq sodium significantly increased the natriuresis stimulated by 300 mumol/kg, p.o., of SQ 28,603 from 700 +/- 332 mu Eq/3 h in normal monkey to 2437 +/- 841 mu Eq/3 h. Therefore, the non-human primate model was appropriate for investigating the effects of sodium loads on the urinary ANP and cGMP responses to exogenous ANP in the presence and absence of NEP inhibitors. Sodium 61-67 membrane metalloendopeptidase Homo sapiens 569-572 7882575-4 1994 When the monkeys" diet was changed from 0.55% sodium to 1.1% sodium, the natriuretic response to 100 mumol/kg intravenous of SQ 28,603 increased from 665 +/- 64 to 1015 +/- 224 mu Eq/3 h. An acute oral load of 25 mEq sodium significantly increased the natriuresis stimulated by 300 mumol/kg, p.o., of SQ 28,603 from 700 +/- 332 mu Eq/3 h in normal monkey to 2437 +/- 841 mu Eq/3 h. Therefore, the non-human primate model was appropriate for investigating the effects of sodium loads on the urinary ANP and cGMP responses to exogenous ANP in the presence and absence of NEP inhibitors. Sodium 61-67 membrane metalloendopeptidase Homo sapiens 569-572 7882575-4 1994 When the monkeys" diet was changed from 0.55% sodium to 1.1% sodium, the natriuretic response to 100 mumol/kg intravenous of SQ 28,603 increased from 665 +/- 64 to 1015 +/- 224 mu Eq/3 h. An acute oral load of 25 mEq sodium significantly increased the natriuresis stimulated by 300 mumol/kg, p.o., of SQ 28,603 from 700 +/- 332 mu Eq/3 h in normal monkey to 2437 +/- 841 mu Eq/3 h. Therefore, the non-human primate model was appropriate for investigating the effects of sodium loads on the urinary ANP and cGMP responses to exogenous ANP in the presence and absence of NEP inhibitors. Sodium 61-67 membrane metalloendopeptidase Homo sapiens 569-572 7833591-1 1994 The renin-angiotensin-aldosterone system (RAAS) is one of the main systems involved in the regulation of blood pressure and sodium homeostasis. Sodium 124-130 renin Homo sapiens 4-9 7833591-7 1994 Furthermore, aging is associated with a reduced adrenal responsiveness to angiotensin II, contributing to lower production of aldosterone and alterations of sodium homeostasis. Sodium 157-163 angiotensinogen Homo sapiens 74-88 7525476-9 1994 After sodium depletion, known to induce hyperactivity of the renin-angiotensin system, adrenal AT1A and AT1B receptor mRNA levels were increased by 60% and 110%, respectively. Sodium 6-12 angiotensin II receptor, type 1b Rattus norvegicus 104-108 7884582-4 1994 Like ACE inhibitors, the angiotensin II inhibitors TCV 116 and losartan cause a marked impairment in the renal adaptation to dietary sodium restriction, suggesting that blockade of the renin-angiotensin system is primarily involved in this process. Sodium 133-139 angiotensinogen Homo sapiens 25-39 7896285-1 1994 Screening for cDNAs encoding proteins similar to the sodium-coupled glutamate transporter GLAST1 led to the isolation of a cDNA clone coding for a protein that turned out to be identical to the recently described neutral amino acid transporter ASCT1. Sodium 53-59 solute carrier family 1 member 3 Homo sapiens 90-96 7929070-1 1994 Our laboratory recently identified a sodium-dependent transport system for phosphate from rat kidney cortex (NaPi-2; Magagnin, S., Werner, A., Markovich, D., Sorribas, V., Stange, G., Biber, J., and Murer, H. (1993) Proc. Sodium 37-43 solute carrier family 34 member 1 Rattus norvegicus 109-115 7965436-1 1994 We investigated the role of endothelin-1 in the renal adaptation to alterations in sodium balance in premature infants. Sodium 83-89 endothelin 1 Homo sapiens 28-40 7965436-6 1994 We conclude that in sodium-depleted premature infants with high urinary sodium excretion, an angiotensin II-mediated increase in renal endothelin-1 production occurs, which acts in concert with angiotensin II to restore sodium balance. Sodium 20-26 angiotensinogen Homo sapiens 93-107 7965436-6 1994 We conclude that in sodium-depleted premature infants with high urinary sodium excretion, an angiotensin II-mediated increase in renal endothelin-1 production occurs, which acts in concert with angiotensin II to restore sodium balance. Sodium 20-26 endothelin 1 Homo sapiens 135-147 7965436-6 1994 We conclude that in sodium-depleted premature infants with high urinary sodium excretion, an angiotensin II-mediated increase in renal endothelin-1 production occurs, which acts in concert with angiotensin II to restore sodium balance. Sodium 20-26 angiotensinogen Homo sapiens 194-208 7965436-6 1994 We conclude that in sodium-depleted premature infants with high urinary sodium excretion, an angiotensin II-mediated increase in renal endothelin-1 production occurs, which acts in concert with angiotensin II to restore sodium balance. Sodium 72-78 angiotensinogen Homo sapiens 93-107 7965436-6 1994 We conclude that in sodium-depleted premature infants with high urinary sodium excretion, an angiotensin II-mediated increase in renal endothelin-1 production occurs, which acts in concert with angiotensin II to restore sodium balance. Sodium 72-78 endothelin 1 Homo sapiens 135-147 7965436-6 1994 We conclude that in sodium-depleted premature infants with high urinary sodium excretion, an angiotensin II-mediated increase in renal endothelin-1 production occurs, which acts in concert with angiotensin II to restore sodium balance. Sodium 72-78 angiotensinogen Homo sapiens 93-107 7965436-6 1994 We conclude that in sodium-depleted premature infants with high urinary sodium excretion, an angiotensin II-mediated increase in renal endothelin-1 production occurs, which acts in concert with angiotensin II to restore sodium balance. Sodium 72-78 endothelin 1 Homo sapiens 135-147 7839775-11 1994 We conclude that infusion of ANP also in the postoperative situation increases GFR, diuresis and sodium excretion. Sodium 97-103 natriuretic peptide A Homo sapiens 29-32 7942823-7 1994 In contrast, angiotensin-converting enzyme inhibition reduced renal blood flow by 30% without evident disruption in tubular function, reflected by low fractional excretion of sodium levels and normal excretion of N-acetyl-glucosaminidase. Sodium 175-181 angiotensin I converting enzyme Homo sapiens 13-42 7943783-4 1994 Our results suggest that short (< 5.0 min) exposure to hypocalcia prompts subsequent, potentially lethal, sodium-dependent calcium entry via the reverse phase of the Na+/Ca2+ exchanger. Sodium 109-115 solute carrier family 8 member A1 Homo sapiens 169-187 7861706-8 1994 During chronically higher sodium intake, serum ANP was significantly higher (median 130 vs. 81 ng/liter, P = 0.0006) and plasma renin tended to be higher (median 20.5 vs. 13.5, P = 0.08) in ADPKD than in control subjects. Sodium 26-32 natriuretic peptide A Homo sapiens 47-50 7861706-8 1994 During chronically higher sodium intake, serum ANP was significantly higher (median 130 vs. 81 ng/liter, P = 0.0006) and plasma renin tended to be higher (median 20.5 vs. 13.5, P = 0.08) in ADPKD than in control subjects. Sodium 26-32 renin Homo sapiens 128-133 7861724-4 1994 At eight weeks following ablation, Ang II blockade (Ang IIX) increased sodium excretion [UNa V, Ang IIX 2.2 +/- 0.4 microEq/min; time control (TC) 1.0 +/- 0.3 microEq/min; P < 0.05] but did not reduce mean arterial pressure (AP, Ang IIX 142 +/- 6 mm Hg; TC 151 +/- 6 mmHg), glomerular transcapillary pressure (delta P, Ang IIX 50 +/- 1 mm Hg; TC 50 +/- 1 mm Hg), or urine albumin excretion (UAlb V: Ang IIX 149 +/- 18 micrograms/min; TC 168 +/- 20 micrograms/min). Sodium 71-77 angiotensinogen Rattus norvegicus 35-41 7861724-6 1994 These findings indicate that within the remant kidney, Ang II promotes sodium retention but does not have an acutely reversible effect on glomerular pressure or permselectivity. Sodium 71-77 angiotensinogen Rattus norvegicus 55-61 7974317-0 1994 Effects of angiotensin converting enzyme inhibition on sodium excretion in patients with hypoxaemic chronic obstructive pulmonary disease. Sodium 55-61 angiotensin I converting enzyme Homo sapiens 11-40 7974317-3 1994 If this was true angiotensin converting enzyme (ACE) inhibition would be expected to lower plasma levels of aldosterone and improve the renal excretion of sodium. Sodium 155-161 angiotensin I converting enzyme Homo sapiens 17-46 7974317-3 1994 If this was true angiotensin converting enzyme (ACE) inhibition would be expected to lower plasma levels of aldosterone and improve the renal excretion of sodium. Sodium 155-161 angiotensin I converting enzyme Homo sapiens 48-51 8087923-7 1994 Sodium excretion increased 3- to 8-fold, 3- to 6-fold, 0- to 2-fold (NS), and 3- to 11-fold, respectively, with proANFs 1-30, 31-67, 79-98, and ANF. Sodium 0-6 natriuretic peptide A Homo sapiens 115-118 7811436-5 1994 This patient consistently demonstrated an abnormally low plasma aldosterone response to AII (3 ng/kg/min) on a low salt (10 mEq sodium) diet while both normotensive and hypertensive. Sodium 128-134 angiotensinogen Homo sapiens 88-91 8082933-1 1994 The angiotensin I-converting enzyme (ACE) gene is found on the locus that has been linked to high blood pressure after sodium loading in rats, so in the present study we investigated the role of vascular ACE for the pathophysiology of hypertension in the corresponding parental strains, Wistar-Kyoto (WKY) rats and stroke-prone spontaneously hypertensive rats (SHRSP), in basal conditions at different ages and after sodium loading. Sodium 119-125 angiotensin I converting enzyme Rattus norvegicus 4-35 8082933-1 1994 The angiotensin I-converting enzyme (ACE) gene is found on the locus that has been linked to high blood pressure after sodium loading in rats, so in the present study we investigated the role of vascular ACE for the pathophysiology of hypertension in the corresponding parental strains, Wistar-Kyoto (WKY) rats and stroke-prone spontaneously hypertensive rats (SHRSP), in basal conditions at different ages and after sodium loading. Sodium 119-125 angiotensin I converting enzyme Rattus norvegicus 37-40 8082933-1 1994 The angiotensin I-converting enzyme (ACE) gene is found on the locus that has been linked to high blood pressure after sodium loading in rats, so in the present study we investigated the role of vascular ACE for the pathophysiology of hypertension in the corresponding parental strains, Wistar-Kyoto (WKY) rats and stroke-prone spontaneously hypertensive rats (SHRSP), in basal conditions at different ages and after sodium loading. Sodium 417-423 angiotensin I converting enzyme Rattus norvegicus 4-35 8082933-1 1994 The angiotensin I-converting enzyme (ACE) gene is found on the locus that has been linked to high blood pressure after sodium loading in rats, so in the present study we investigated the role of vascular ACE for the pathophysiology of hypertension in the corresponding parental strains, Wistar-Kyoto (WKY) rats and stroke-prone spontaneously hypertensive rats (SHRSP), in basal conditions at different ages and after sodium loading. Sodium 417-423 angiotensin I converting enzyme Rattus norvegicus 37-40 7836703-1 1994 Prolactin is known to have renal sodium retention properties in animals. Sodium 33-39 prolactin Homo sapiens 0-9 7852745-5 1994 In TGR (n = 10), urine flow and sodium excretion increased from 30.0 +/- 6.1 to 59.7 +/- 7.2 microliters/min per g kidney weight and from 3.8 +/- 0.9 to 8.5 +/- 1.3 mumol/min per g kidney weight in response to an elevation in RPP from 170 to 212 mmHg. Sodium 32-38 thioredoxin reductase 3 Mus musculus 3-6 7836703-5 1994 The effect of serum prolactin elevation on renal sodium and potassium excretion was studied in all patients after thyrotropin-releasing hormone stimulation (200 micrograms), with seven consecutive hourly urinary samples. Sodium 49-55 prolactin Homo sapiens 20-29 7836703-8 1994 In contrast, in group II with a "high PRL release" (delta prolactin > 1000 mu u/ml, n = 11), significant reductions in urinary sodium (p < 0.01) and potassium (p < 0.02) excretion were observed, which lasted until the third hour after thyrotropin-releasing hormone injection. Sodium 130-136 prolactin Homo sapiens 58-67 7836703-10 1994 The pattern of urinary electrolyte changes and the stability of the ratio UK/UK+Na suggest a possible sodium-retaining effect of prolactin localized proximally to the distal tubule. Sodium 102-108 prolactin Homo sapiens 129-138 8076150-4 1994 This short review focuses on relevant experimental and clinical information of the direct and indirect effects of CGRP on renal function with an emphasis on hemodynamics, sodium excretion, and the renin-angiotensin system. Sodium 171-177 calcitonin related polypeptide alpha Homo sapiens 114-118 7996787-1 1994 Studies were performed to determine the signal transduction mechanism involved in the onset of insulin stimulated electrogenic sodium transport (Ieq) in cultured A6 cells. Sodium 127-133 insulin Homo sapiens 95-102 7967348-0 1994 Insulin activation of red blood cell Na+/H+ exchange decreases the affinity of sodium sites. Sodium 79-85 insulin Homo sapiens 0-7 7967349-1 1994 Elevated levels of the vasocontrictor peptide endothelin-1 have been demonstrated in various pathological conditions that are characterized by sodium retention and/or renal vasoconstriction, such as heart failure, hepatorenal syndrome, renal failure and during administration of cyclosporin and radiocontrast. Sodium 143-149 endothelin 1 Homo sapiens 46-58 7967349-4 1994 Infusion of low dosages of endothelin-1, that result in a twofold increase in plasma levels, decreased sodium excretion by 36%, without a significant effect on systemic and renal hemodynamics. Sodium 103-109 endothelin 1 Homo sapiens 27-39 7967349-5 1994 Infusion of 2.5 ng/kg/min of endothelin-1 further enhanced sodium retention and, in addition, increased renal vascular resistance by 37%. Sodium 59-65 endothelin 1 Homo sapiens 29-41 7825084-3 1994 Renin profiles, obtained by the plotting of PRA against the urinary excretion of sodium, showed a 62% prevalence of low-renin hypertension, the remaining 38% of the patients having normal-renin hypertension. Sodium 81-87 renin Homo sapiens 0-5 7531080-1 1994 Secretion and synthesis of renin are stimulated by the lack of angiotensin II and by a low sodium intake. Sodium 91-97 renin Homo sapiens 27-32 7531080-3 1994 A high sodium intake can overcome the effect of the lack of angiotensin II. Sodium 7-13 angiotensinogen Homo sapiens 60-74 7531084-2 1994 They appear to be linked particularly by the renin angiotensin system and the control of sodium balance. Sodium 89-95 renin Homo sapiens 45-50 8020999-8 1994 By contrast, subcutaneous infusion of the bradykinin antagonist Hoe 140 in Ang II-treated normal rats induced a hypertensive response in parallel with significant increases in heart rate and erythrocyte sodium level. Sodium 203-209 angiotensinogen Rattus norvegicus 75-81 7963509-8 1994 In this metabolic interaction, ANF might counteract the renal sodium-retaining effect of acute hyperglycaemia and hyperinsulinaemia. Sodium 62-68 natriuretic peptide A Homo sapiens 31-34 7963510-4 1994 RESULTS: Plasma levels of BNP and ANP increased significantly on the high sodium intake compared with when the patients were on their normal diet. Sodium 74-80 natriuretic peptide A Homo sapiens 34-37 7963510-8 1994 Compared with the normal diet, BNP and ANP plasma levels showed similar percentage decreases on the low sodium intake and similar percentage increases on the high sodium intake. Sodium 104-110 natriuretic peptide A Homo sapiens 39-42 7963510-9 1994 CONCLUSIONS: These findings suggest that BNP and ANP are released in response to a common stimulus during changes in dietary sodium intake. Sodium 125-131 natriuretic peptide A Homo sapiens 49-52 7963510-10 1994 The changes in plasma BNP and ANP observed with sodium restriction and sodium loading indicate the potential importance of BNP and ANP as a dual peptide system contributing to the maintenance of sodium balance and blood pressure regulation in patients with essential hypertension, during changes in dietary sodium intake. Sodium 48-54 natriuretic peptide A Homo sapiens 30-33 7957590-5 1994 Angiotensin II did not induce significant change in urinary potassium excretion or free water formation but significantly increased both urine volume and urinary sodium excretion. Sodium 162-168 angiotensinogen Rattus norvegicus 0-14 8027224-0 1994 The role of atrial natriuretic factor [alpha-human ANF-(99-126)] in the hormonal and renal adaptation to sodium deficiency. Sodium 105-111 natriuretic peptide A Homo sapiens 12-37 8027224-0 1994 The role of atrial natriuretic factor [alpha-human ANF-(99-126)] in the hormonal and renal adaptation to sodium deficiency. Sodium 105-111 natriuretic peptide A Homo sapiens 51-54 7964866-8 1994 The depolarization was Na+ dependent and amiloride sensitive (250 microM), both indicating an activation of an electrogenic sodium dependent transport system like the Na+/Ca2+ exchanger as a source of the depolarization. Sodium 124-130 solute carrier family 8 member A1 Homo sapiens 167-185 7958155-7 1994 Furthermore, there was a significant positive relationship between ET-1 excretion and urine flow rate (r = 0.67, P < 0.0001), CCR (r = 0.40, P < 0.0025), Cosm (r = 0.58, P < 0.001), sodium (r = 0.56, P < 0.001) and potassium excretion (r = 0.42, P < 0.001). Sodium 191-197 endothelin 1 Homo sapiens 67-71 8206593-5 1994 Atrial natriuretic peptide was able to oppose the antinatriuretic action of insulin in normotensive subjects, increasing urinary sodium excretion significantly to a mean level of 352 +/- 31 mumol/min (P < .05), which did not differ significantly from baseline. Sodium 129-135 insulin Homo sapiens 76-83 7933806-9 1994 The increase in renal tubular ACE activity could result in higher angiotensin II levels, and could consequently play a role in the modification of sodium reabsorption and cellular growth which occurs in the proximal tubule in these experimental models. Sodium 147-153 angiotensin I converting enzyme Rattus norvegicus 30-33 8060573-1 1994 The effect of insulin on sodium reabsorption was studied with the hyperinsulinemic euglycemic clamp technique, using lithium clearance as a marker of sodium reabsorption in the proximal tubule. Sodium 25-31 insulin Homo sapiens 14-21 8060573-3 1994 In the first group, the effect of insulin on sodium and lithium reabsorption was examined. Sodium 45-51 insulin Homo sapiens 34-41 8060573-12 1994 As shown by the increase of CLi and (CLi-CNa/CLi, and the decrease of UNaV and CNa/CLi in the glucose clamp group, insulin decreases urinary sodium excretion by increasing distal sodium reabsorption, whereas it inhibits sodium reabsorption in the proximal tubule. Sodium 141-147 insulin Homo sapiens 115-122 8060573-12 1994 As shown by the increase of CLi and (CLi-CNa/CLi, and the decrease of UNaV and CNa/CLi in the glucose clamp group, insulin decreases urinary sodium excretion by increasing distal sodium reabsorption, whereas it inhibits sodium reabsorption in the proximal tubule. Sodium 179-185 insulin Homo sapiens 115-122 8060573-12 1994 As shown by the increase of CLi and (CLi-CNa/CLi, and the decrease of UNaV and CNa/CLi in the glucose clamp group, insulin decreases urinary sodium excretion by increasing distal sodium reabsorption, whereas it inhibits sodium reabsorption in the proximal tubule. Sodium 179-185 insulin Homo sapiens 115-122 8184959-0 1994 Vasopressin inhibits calcium-coupled sodium efflux system in rat brain. Sodium 37-43 arginine vasopressin Rattus norvegicus 0-11 8181200-0 1994 Effect of erythropoietin on renal excretion of a sodium load. Sodium 49-55 erythropoietin Homo sapiens 10-24 8181200-6 1994 Erythropoietin significantly decreased total sodium excretion during the 4 days after drug administration (erythropoietin = 784 +/- 46 mEq/4 days versus control = 840 +/- 41 mEq/4 days; p < 0.001). Sodium 45-51 erythropoietin Homo sapiens 0-14 8181200-8 1994 We conclude that erythropoietin decreases urine sodium excretion after a sodium load in normal human subjects without altering glomerular filtration rate, blood pressure, or plasma renin activity. Sodium 48-54 erythropoietin Homo sapiens 17-31 8181200-8 1994 We conclude that erythropoietin decreases urine sodium excretion after a sodium load in normal human subjects without altering glomerular filtration rate, blood pressure, or plasma renin activity. Sodium 73-79 erythropoietin Homo sapiens 17-31 7923896-2 1994 This study sought to determine if neutral endopeptidase metabolizes vaso-active intestinal peptide (VIP) and whether changes in the activity of this enzyme might explain the change in VIP metabolism which follows gastric sodium loading. Sodium 221-227 vasoactive intestinal peptide Rattus norvegicus 184-187 8018457-2 1994 As compared with placebo, angiotensin II infusion alone caused significant reductions in absolute rate of sodium excretion, fractional sodium excretion, urine flow rate and effective renal plasma flow (all P < 0.001 vs placebo) but had no effect on glomerular filtration rate. Sodium 106-112 angiotensinogen Homo sapiens 26-40 8018457-2 1994 As compared with placebo, angiotensin II infusion alone caused significant reductions in absolute rate of sodium excretion, fractional sodium excretion, urine flow rate and effective renal plasma flow (all P < 0.001 vs placebo) but had no effect on glomerular filtration rate. Sodium 135-141 angiotensinogen Homo sapiens 26-40 8018457-4 1994 As compared with the effects of angiotensin II alone, indomethacin pre-treatment followed by angiotensin II infusion led to much greater falls in absolute rate of sodium excretion, fractional sodium excretion, urine flow rate and effective renal plasma flow (all P < 0.0001 vs placebo) associated with a significant reduction in glomerular filtration rate (P < 0.0001) not observed with angiotensin II alone. Sodium 163-169 angiotensinogen Homo sapiens 93-107 8018457-4 1994 As compared with the effects of angiotensin II alone, indomethacin pre-treatment followed by angiotensin II infusion led to much greater falls in absolute rate of sodium excretion, fractional sodium excretion, urine flow rate and effective renal plasma flow (all P < 0.0001 vs placebo) associated with a significant reduction in glomerular filtration rate (P < 0.0001) not observed with angiotensin II alone. Sodium 163-169 angiotensinogen Homo sapiens 93-107 8018457-4 1994 As compared with the effects of angiotensin II alone, indomethacin pre-treatment followed by angiotensin II infusion led to much greater falls in absolute rate of sodium excretion, fractional sodium excretion, urine flow rate and effective renal plasma flow (all P < 0.0001 vs placebo) associated with a significant reduction in glomerular filtration rate (P < 0.0001) not observed with angiotensin II alone. Sodium 192-198 angiotensinogen Homo sapiens 93-107 8018457-4 1994 As compared with the effects of angiotensin II alone, indomethacin pre-treatment followed by angiotensin II infusion led to much greater falls in absolute rate of sodium excretion, fractional sodium excretion, urine flow rate and effective renal plasma flow (all P < 0.0001 vs placebo) associated with a significant reduction in glomerular filtration rate (P < 0.0001) not observed with angiotensin II alone. Sodium 192-198 angiotensinogen Homo sapiens 93-107 8168694-5 1994 Here we summarize both old and new evidence that several major substances believed to be involved in the regulation of sodium metabolism and blood pressure, i.e., the antidiuretic agents angiotensin II and norepinephrine, and the diuretic agents dopamine and atrial natriuretic peptide (ANP), may achieve their effects through a common pathway that involves reversible activation/deactivation of renal tubular Na+,K(+)-ATPase. Sodium 119-125 angiotensinogen Rattus norvegicus 187-201 8168694-10 1994 These results indicate that regulation of sodium excretion by norepinephrine, angiotensin II, dopamine, and ANP can be accounted for by a bidirectionally regulated intracellular protein phosphorylation cascade that modulates the activity of renal tubular Na+,K(+)-ATPase. Sodium 42-48 angiotensinogen Rattus norvegicus 78-92 8064168-7 1994 RESULTS: The plasma ANF concentration rose five- to eightfold during the infusion of ANF, which induced an increase in urinary sodium excretion, a small increase in GFR and a decrease in the effective renal plasma flow. Sodium 127-133 natriuretic peptide A Homo sapiens 20-23 8064168-7 1994 RESULTS: The plasma ANF concentration rose five- to eightfold during the infusion of ANF, which induced an increase in urinary sodium excretion, a small increase in GFR and a decrease in the effective renal plasma flow. Sodium 127-133 natriuretic peptide A Homo sapiens 85-88 8169834-2 1994 Intrarenal bradykinin injections of 0.1, 1 and 10 ng/kg, respectively, increased the area over the curve of the renal blood flow response (RBF) by 6 +/- 2, 15 +/- 2 and 101 +/- 8 ml, respectively, sodium excretion by 0.6 +/- 0.4, 2.9 +/- 0.5 and 21.8 +/- 1.3 microEq/min, respectively and urinary cyclic GMP excretion by 23 +/- 12, 56 +/- 22 and 210 +/- 35 pmol/min, respectively. Sodium 197-203 kininogen 1 Canis lupus familiaris 11-21 8072428-2 1994 The common presumption that hyperinsulinemia mediates this connection is based on studies demonstrating various pressor effects of insulin, such as sodium retention, activation of the sympathetic nervous system, and stimulation of renin output. Sodium 148-154 insulin Homo sapiens 33-40 8169834-5 1994 Captopril also significantly prolonged the sodium response to 10 ng/kg of bradykinin although the peak natriuretic activity (32 +/- 5 microEq/min) was not significantly different from the natriuresis obtained under control conditions (22 +/- 1 microEq/min). Sodium 43-49 kininogen 1 Canis lupus familiaris 74-84 8147862-0 1994 Protein kinase C is crucial for the stimulation of sodium-dependent phosphate transport by parathyroid hormone-related peptide in osteoblast-like cells. Sodium 51-57 proline rich transmembrane protein 2 Homo sapiens 0-16 8147862-7 1994 These results indicate that the messenger system mediated by PKC, rather than adenylate cyclase or cytosolic calcium, plays a crucial role in the regulation of sodium-dependent Pi transport by PTHrP in the osteoblast-like cells. Sodium 160-166 proline rich transmembrane protein 2 Homo sapiens 61-64 8160866-5 1994 Compared with values in control rats, ANG II-infused rats had significantly (P < 0.05) lower urine flow and absolute and fractional sodium excretion at renal artery pressures of 115-150 mmHg. Sodium 135-141 angiotensinogen Rattus norvegicus 38-44 8160789-8 1994 It is suggested that ET-1 at plasma concentrations found in certain pathophysiological conditions in humans may influence renal perfusion and renal sodium and water excretion. Sodium 148-154 endothelin 1 Homo sapiens 21-25 8160866-9 1994 The data indicate that rats with ANG II-induced hypertension have a rightward shift of the pressure-natriuresis curve caused primarily by a decrease in fractional excretion of sodium. Sodium 176-182 angiotensinogen Rattus norvegicus 33-39 8166243-4 1994 Inhibition of Na(+)-Ca2+ exchange by removal of external sodium, which was replaced by choline, augmented the ANG II-induced [Ca2+]i increase to 174 +/- 26 nM (n = 11; P < 0.05 compared with control). Sodium 57-63 angiotensinogen Rattus norvegicus 110-116 8124802-7 1994 Suppression of plasma renin activity and aldosterone by high-sodium diet was blunted in cardiac transplant recipients compared with healthy subjects (respectively, plasma renin activity: 1.41 +/- 0.30 versus 0.68 +/- 0.21 ng.mL-1 x h-1, P < .05; aldosterone: 391 +/- 35 versus 166 +/- 21 pmol/L, P < .05). Sodium 61-67 renin Homo sapiens 22-27 8019752-10 1994 Big ET-1 but not ET-1, produced a significant increase in water and sodium excretion. Sodium 68-74 endothelin 1 Rattus norvegicus 4-8 8124802-7 1994 Suppression of plasma renin activity and aldosterone by high-sodium diet was blunted in cardiac transplant recipients compared with healthy subjects (respectively, plasma renin activity: 1.41 +/- 0.30 versus 0.68 +/- 0.21 ng.mL-1 x h-1, P < .05; aldosterone: 391 +/- 35 versus 166 +/- 21 pmol/L, P < .05). Sodium 61-67 renin Homo sapiens 171-176 8156731-14 1994 The enhanced erythrocyte sodium transport, if this reflects what happens in the renal tubular cell, combined with a decrease in urinary sodium excretion, during treatment with recombinant human growth hormone could indicate an increase in tubular sodium reabsorption induced by the hormone. Sodium 136-142 growth hormone 1 Homo sapiens 194-208 8076424-10 1994 This might be explained by progressive sodium retention as GFR falls leading to volume expansion and increased ANP secretion. Sodium 39-45 natriuretic peptide A Homo sapiens 111-114 8156731-15 1994 An increased plasma renin activity associated with the lack of blood pressure rise would reinforce sodium and water retention. Sodium 99-105 renin Homo sapiens 20-25 8156731-0 1994 Effect of recombinant human growth hormone on cellular sodium metabolism. Sodium 55-61 growth hormone 1 Homo sapiens 28-42 8125556-6 1994 Fractional excretion of sodium was reduced, and fractional proximal and distal tubular reabsorption of sodium were increased to the same extent in both groups during insulin infusion. Sodium 103-109 insulin Homo sapiens 166-173 8156731-2 1994 The effect of treatment with recombinant human growth hormone on urinary sodium excretion, total body water, the renin-angiotensin system and erythrocyte sodium metabolism was investigated in 16 adults with growth hormone deficiency. Sodium 73-79 growth hormone 1 Homo sapiens 47-61 8156731-7 1994 One week of treatment with recombinant human growth hormone caused a decrease in urinary sodium excretion in 9/10 patients and an increase in erythrocyte sodium content. Sodium 89-95 growth hormone 1 Homo sapiens 45-59 8156731-7 1994 One week of treatment with recombinant human growth hormone caused a decrease in urinary sodium excretion in 9/10 patients and an increase in erythrocyte sodium content. Sodium 154-160 growth hormone 1 Homo sapiens 45-59 8156731-10 1994 Six months of treatment with recombinant human growth hormone caused significant increases in total body water, erythrocyte sodium content and sodium transmembrane influx. Sodium 124-130 growth hormone 1 Homo sapiens 47-61 8156731-10 1994 Six months of treatment with recombinant human growth hormone caused significant increases in total body water, erythrocyte sodium content and sodium transmembrane influx. Sodium 143-149 growth hormone 1 Homo sapiens 47-61 8156731-14 1994 The enhanced erythrocyte sodium transport, if this reflects what happens in the renal tubular cell, combined with a decrease in urinary sodium excretion, during treatment with recombinant human growth hormone could indicate an increase in tubular sodium reabsorption induced by the hormone. Sodium 25-31 growth hormone 1 Homo sapiens 194-208 8156731-14 1994 The enhanced erythrocyte sodium transport, if this reflects what happens in the renal tubular cell, combined with a decrease in urinary sodium excretion, during treatment with recombinant human growth hormone could indicate an increase in tubular sodium reabsorption induced by the hormone. Sodium 136-142 growth hormone 1 Homo sapiens 194-208 7514971-6 1994 Insulin is thought to raise blood pressure by a few possible mechanisms (e.g. stimulating sympathetic nervous system activity, enhancing renal tubular sodium reabsorption). Sodium 151-157 insulin Homo sapiens 0-7 8021478-6 1994 A high perfusate concentration of endothelin-1 markedly reduced urinary sodium excretion, resulting in a significant rightwards shift of the pressure-natriuresis curve. Sodium 72-78 endothelin 1 Rattus norvegicus 34-46 8190756-0 1994 Synergist interaction between angiotensin II and DOCA on sodium and water balance in rats. Sodium 57-63 angiotensinogen Rattus norvegicus 30-44 8006915-3 1994 Compared with whites plasma renin is low in blacks independently of age, the level of BP and dietary sodium consumption. Sodium 101-107 renin Homo sapiens 28-33 8190756-1 1994 Blockade of central angiotensin receptors with the specific antagonist [Leu8]-ANG II abolished water ingestion and water and sodium excretion induced by infusion of angiotensin II (ANGII) into the lateral ventricle (LV) of rats. Sodium 125-131 angiotensinogen Rattus norvegicus 165-179 8190756-1 1994 Blockade of central angiotensin receptors with the specific antagonist [Leu8]-ANG II abolished water ingestion and water and sodium excretion induced by infusion of angiotensin II (ANGII) into the lateral ventricle (LV) of rats. Sodium 125-131 angiotensinogen Rattus norvegicus 181-186 8190756-4 1994 When central ANGII infusion was combined with peripheral DOCA, the water intake was similar to that induced by ANGII alone and the ingestion of 3% NaCl was increased, whereas sodium excretion was inhibited. Sodium 175-181 angiotensinogen Rattus norvegicus 13-18 8190756-5 1994 When ANGII was infused alone, a detailed temporal analysis of fluid and sodium balance showed a negative balance similar those saline controls that persisted throughout the experiment. Sodium 72-78 angiotensinogen Rattus norvegicus 5-10 8190756-6 1994 Combined administration of ANGII and DOCA induce significant changes in water and sodium balance. Sodium 82-88 angiotensinogen Rattus norvegicus 27-32 8190756-8 1994 The data support an interaction of central ANGII and DOCA on sodium intake and water and sodium balance. Sodium 61-67 angiotensinogen Rattus norvegicus 43-48 8190756-8 1994 The data support an interaction of central ANGII and DOCA on sodium intake and water and sodium balance. Sodium 89-95 angiotensinogen Rattus norvegicus 43-48 8106444-11 1994 These results suggest that each of the three PKC isotypes contribute to the regulation of sodium-dependent phosphate uptake, but through distinct mechanisms. Sodium 90-96 protein kinase C, alpha Mus musculus 45-48 17972817-1 1994 Atrial natriuretic paptide (ANP) a potent hormone with important role in sodium homeostasis has been widely investigated in experimental and clinical hepatology during last years. Sodium 73-79 natriuretic peptide A Homo sapiens 28-31 8141158-2 1994 To elucidate the role of a mechanism responsible for renal sodium reabsorption on the time-course of renin suppression, 16 young borderline hypertensive patients were studied by analyzing the relationship between the level of baseline activation of lymphocyte Na+:H+ exchange and the degree of plasma renin activity (PRA) suppression in response to saline loading. Sodium 59-65 renin Homo sapiens 101-106 8137388-2 1994 The fact that one of the breakdown products of the common precursor (proopiomelanocortin, POMC) ACTH and opioid peptides, i.e. ACTH 1-24 has a saluretic effect (balancing perhaps sodium retention after activation of the adrenal cortex) was not generally accepted yet although MSH as well as some fragments of the ACTH molecule have a natriuretic effect. Sodium 179-185 proopiomelanocortin Homo sapiens 90-94 8137388-2 1994 The fact that one of the breakdown products of the common precursor (proopiomelanocortin, POMC) ACTH and opioid peptides, i.e. ACTH 1-24 has a saluretic effect (balancing perhaps sodium retention after activation of the adrenal cortex) was not generally accepted yet although MSH as well as some fragments of the ACTH molecule have a natriuretic effect. Sodium 179-185 proopiomelanocortin Homo sapiens 96-100 8137388-2 1994 The fact that one of the breakdown products of the common precursor (proopiomelanocortin, POMC) ACTH and opioid peptides, i.e. ACTH 1-24 has a saluretic effect (balancing perhaps sodium retention after activation of the adrenal cortex) was not generally accepted yet although MSH as well as some fragments of the ACTH molecule have a natriuretic effect. Sodium 179-185 proopiomelanocortin Homo sapiens 127-131 8137388-2 1994 The fact that one of the breakdown products of the common precursor (proopiomelanocortin, POMC) ACTH and opioid peptides, i.e. ACTH 1-24 has a saluretic effect (balancing perhaps sodium retention after activation of the adrenal cortex) was not generally accepted yet although MSH as well as some fragments of the ACTH molecule have a natriuretic effect. Sodium 179-185 proopiomelanocortin Homo sapiens 276-279 8137388-2 1994 The fact that one of the breakdown products of the common precursor (proopiomelanocortin, POMC) ACTH and opioid peptides, i.e. ACTH 1-24 has a saluretic effect (balancing perhaps sodium retention after activation of the adrenal cortex) was not generally accepted yet although MSH as well as some fragments of the ACTH molecule have a natriuretic effect. Sodium 179-185 proopiomelanocortin Homo sapiens 127-131 8141170-4 1994 Insulin-resistance has been postulated to be responsible for enhanced sodium retention in obese individuals; therefore, insulin-resistance may be critical to the pathogenesis of sodium-sensitivity in individuals with essential hypertension. Sodium 178-184 insulin Homo sapiens 120-127 8141170-5 1994 This article summarizes the data relating insulin and or insulin-resistance to sodium sensitivity in obesity, diabetes, and in non-obese subjects with essential hypertension. Sodium 79-85 insulin Homo sapiens 42-49 8141170-5 1994 This article summarizes the data relating insulin and or insulin-resistance to sodium sensitivity in obesity, diabetes, and in non-obese subjects with essential hypertension. Sodium 79-85 insulin Homo sapiens 57-64 8141158-5 1994 These findings suggest that a mechanism influencing renal sodium reabsorption as Na+:H+ exchange could also affect the control of plasma renin activity, and concur with the development of salt-sensitive high blood pressure. Sodium 58-64 renin Homo sapiens 137-142 8141330-1 1994 Nitric oxide (NO), guanosine 3",5"-cyclic monophosphate (cGMP), and endothelin-1 (ET-1) inhibit collecting duct sodium reabsorption. Sodium 112-118 endothelin 1 Rattus norvegicus 68-80 8141330-1 1994 Nitric oxide (NO), guanosine 3",5"-cyclic monophosphate (cGMP), and endothelin-1 (ET-1) inhibit collecting duct sodium reabsorption. Sodium 112-118 endothelin 1 Rattus norvegicus 82-86 8141164-2 1994 In insulin-resistant hypertensive subjects, insulin infusion during euglycemic clamp promotes a transient sodium retention by stimulating proximal tubular Na+ reabsorption, but chronic hypertension usually is not associated with extracellular fluid and plasma volume expansion. Sodium 106-112 insulin Homo sapiens 44-51 8141164-3 1994 In essential hypertensive subjects, intracellular potassium is decreased and intracellular sodium increased, which is consistent with insulin resistance. Sodium 91-97 insulin Homo sapiens 134-141 8141164-10 1994 These data indicate that insulin may play a role in the pathogenesis of hypertension and its major complications by amplifying the effects of sodium, vasoconstrictors, and growth factors. Sodium 142-148 insulin Homo sapiens 25-32 8141170-0 1994 The relationship of sodium sensitivity to insulin resistance. Sodium 20-26 insulin Homo sapiens 42-49 8141170-4 1994 Insulin-resistance has been postulated to be responsible for enhanced sodium retention in obese individuals; therefore, insulin-resistance may be critical to the pathogenesis of sodium-sensitivity in individuals with essential hypertension. Sodium 70-76 insulin Homo sapiens 0-7 8141170-4 1994 Insulin-resistance has been postulated to be responsible for enhanced sodium retention in obese individuals; therefore, insulin-resistance may be critical to the pathogenesis of sodium-sensitivity in individuals with essential hypertension. Sodium 178-184 insulin Homo sapiens 0-7 8021469-8 1994 Among the subjects with a low or normal renin-sodium profile, 1% (one of 82) had a false-positive result. Sodium 46-52 renin Homo sapiens 40-45 8141416-1 1994 The central site of action and the neuronal mechanism of the robust sodium appetite initiated in rats by the synergistic action of a peripheral priming with mineralocorticoid [deoxycorticosterone acetate (DOCA)] and subsequent central angiotensin II (ANG II) were investigated using iontophoretic and electrophysiological techniques in urethan-anesthetized, DOCA-pretreated (0.5 mg/day sc for 3 days) or nonpretreated male Wistar rats. Sodium 68-74 angiotensinogen Rattus norvegicus 235-249 8141416-1 1994 The central site of action and the neuronal mechanism of the robust sodium appetite initiated in rats by the synergistic action of a peripheral priming with mineralocorticoid [deoxycorticosterone acetate (DOCA)] and subsequent central angiotensin II (ANG II) were investigated using iontophoretic and electrophysiological techniques in urethan-anesthetized, DOCA-pretreated (0.5 mg/day sc for 3 days) or nonpretreated male Wistar rats. Sodium 68-74 angiotensinogen Rattus norvegicus 251-257 8141416-7 1994 This forebrain region, therefore, contains neurons that undergo a mineralocorticoid pretreatment-induced and/or a rapid aldosterone-induced sensitization to ANG II, which may be the neuronal mechanism whereby a persistent sodium appetite, induced by the synergistic action of these two hormones, is stimulated. Sodium 222-228 angiotensinogen Rattus norvegicus 157-163 7507836-0 1994 Both low sodium and high potassium intake increase the level of adrenal angiotensin-II receptor type 1, but not that of adrenocorticotropin receptor. Sodium 9-15 angiotensinogen Rattus norvegicus 72-86 8021469-6 1994 Renin responses were analyzed according to baseline renin-sodium profile. Sodium 58-64 renin Homo sapiens 52-57 8310408-7 1994 Anti-ET-1 antibody administration (5 nmol/kg body, four times intravenously) decreased plasma creatinine concentration and BUN level and increased urine volume and urinary sodium excretion 3 hours after endotoxin injection (creatinine, p = 0.07; BUN, p < 0.05; urine volume, p < 0.01; urinary sodium excretion, p < 0.01; anti-ET-1 vs shams). Sodium 172-178 endothelin 1 Rattus norvegicus 5-9 8021469-6 1994 Renin responses were analyzed according to baseline renin-sodium profile. Sodium 58-64 renin Homo sapiens 0-5 8189427-5 1994 SGLT1 alone is able to translocate glucose together with sodium; however, RS1 increases the Vmax of transport expressed by SGLT1. Sodium 57-63 solute carrier family 5 member 1 Homo sapiens 0-5 8183630-1 1994 The sodium/calcium (Na+/Ca2+) exchanger is often considered to be a key regulator of the cytoplasmic calcium concentration ([Ca2+]) in smooth muscle but neither its precise role in Ca2+ homeostasis nor even its existence in smooth muscle are generally agreed upon. Sodium 4-10 solute carrier family 8 member A1 Homo sapiens 20-39 8153287-9 1994 Reversed sodium rhythm was associated with reversed circadian rhythms for GFR, effective renal plasma flow and urine flow, and blunting or reversal of the day-night differences in blood pressure and plasma renin activity. Sodium 9-15 renin Homo sapiens 206-211 8310408-7 1994 Anti-ET-1 antibody administration (5 nmol/kg body, four times intravenously) decreased plasma creatinine concentration and BUN level and increased urine volume and urinary sodium excretion 3 hours after endotoxin injection (creatinine, p = 0.07; BUN, p < 0.05; urine volume, p < 0.01; urinary sodium excretion, p < 0.01; anti-ET-1 vs shams). Sodium 299-305 endothelin 1 Rattus norvegicus 5-9 7638038-7 1994 The exaggerated responsiveness in sodium excretion in patients with hypothyroidism was associated with significantly decreased pre-infusion ANP plasma levels (16.1 +/- 11.1 pg/ml vs. 44.4 +/- 14.4 pg/ml; P < 0.001) and also with sluggish response to the volume expansion (+24% vs. +48%). Sodium 34-40 natriuretic peptide A Homo sapiens 140-143 7638038-10 1994 This exaggerated responsiveness of sodium excretion can be demonstrated in spite of a sluggish response in ANP. Sodium 35-41 natriuretic peptide A Homo sapiens 107-110 7889207-2 1994 Endothelium-derived nitric oxide (EDNO) and angiotensin II play a role in the regulation of vascular tone and sodium handling. Sodium 110-116 angiotensinogen Rattus norvegicus 44-58 8304017-12 1994 CONCLUSION: The results suggest that the competitive relationship between ANP and the renin-aldosterone system in regulating sodium balance and fluid volume is preserved during pregnancy. Sodium 125-131 renin Homo sapiens 86-91 8304488-0 1994 Angiotensin II suppression is a major factor permitting excretion of an acute sodium load in humans. Sodium 78-84 angiotensinogen Homo sapiens 0-14 7889207-3 1994 The objective of this study was to determine the role played by angiotensin II in mediating the arterial pressure and renal response to increments in sodium intake during chronic EDNO inhibition. Sodium 150-156 angiotensinogen Rattus norvegicus 64-78 7795547-5 1994 ANF may also be a long-term regulator of salt and water homeostasis by modulating the renal excretion of sodium. Sodium 105-111 natriuretic peptide A Homo sapiens 0-3 7954533-6 1994 Activation of the renin-angiotensin system favours the proximal tubular reabsorption of sodium and water, which may result in dilutional hyponatraemia. Sodium 88-94 renin Homo sapiens 18-23 8306484-10 1994 Plasma ANF (supine and erect) was significantly lower (2.8 +/- 0.6, 1.6 +/- 0.2 pmol/l) on the low sodium diet when compared to the high sodium diet (8.6 +/- 2.4, 5.0 +/- 1.6 pmol/l (P < 0.05)). Sodium 99-105 natriuretic peptide A Homo sapiens 7-10 8306484-10 1994 Plasma ANF (supine and erect) was significantly lower (2.8 +/- 0.6, 1.6 +/- 0.2 pmol/l) on the low sodium diet when compared to the high sodium diet (8.6 +/- 2.4, 5.0 +/- 1.6 pmol/l (P < 0.05)). Sodium 137-143 natriuretic peptide A Homo sapiens 7-10 7522207-1 1994 Human growth hormone (GH) mediates longitudinal bone growth and also exerts a variety of other biological effects, e.g. lactogenic, insulin-like, diabetogenic, lipolytic, protein-anabolic and sodium/water-retaining effects. Sodium 192-198 growth hormone 1 Homo sapiens 6-20 7713395-6 1994 One of the 8 variants is recessive, has homozygous genotype frequency estimated as 8.8% of the population, and increases sodium-lithium countertransport, the passive sodium leak, body mass index, and triglyceride; the genetic variant may coincide with an insulin resistance gene. Sodium 121-127 insulin Homo sapiens 255-262 7506698-0 1994 Regulation of angiotensin II receptors in rat brain during dietary sodium changes. Sodium 67-73 angiotensinogen Rattus norvegicus 14-28 7506698-1 1994 Activation of the renin-angiotensin system by sodium deficiency is associated with reciprocal changes in the expression of angiotensin II receptors in adrenal glomerulosa and vascular smooth muscle cells. Sodium 46-52 angiotensinogen Rattus norvegicus 123-137 7506698-5 1994 The expression of AT1A and AT1B receptor subtype mRNAs was determined by quantitative reverse transcriptase-polymerase chain reaction during changes in sodium intake. Sodium 152-158 angiotensin II receptor, type 1b Rattus norvegicus 27-31 7506698-6 1994 The results revealed that sodium deprivation enhanced the expression of AT1B receptors in decorticated brains by 164% compared with high sodium intake. Sodium 26-32 angiotensin II receptor, type 1b Rattus norvegicus 72-76 7522207-1 1994 Human growth hormone (GH) mediates longitudinal bone growth and also exerts a variety of other biological effects, e.g. lactogenic, insulin-like, diabetogenic, lipolytic, protein-anabolic and sodium/water-retaining effects. Sodium 192-198 growth hormone 1 Homo sapiens 22-24 7759206-2 1994 In the present study we aimed to investigate plasma and urinary Epo levels and their renal handling in relation to beta 2-microglobulin (beta 2m), sodium metabolism and the renin-angiotensin-aldosterone system (RAAS), respectively, in patients with sub-nephrotic range proteinuria (SNP), microalbuminuric diabetics and hypertensives, and in healthy subjects studied on a standardized diet containing 120 mmol sodium and 70 g protein per day. Sodium 147-153 erythropoietin Homo sapiens 64-67 7759206-2 1994 In the present study we aimed to investigate plasma and urinary Epo levels and their renal handling in relation to beta 2-microglobulin (beta 2m), sodium metabolism and the renin-angiotensin-aldosterone system (RAAS), respectively, in patients with sub-nephrotic range proteinuria (SNP), microalbuminuric diabetics and hypertensives, and in healthy subjects studied on a standardized diet containing 120 mmol sodium and 70 g protein per day. Sodium 409-415 erythropoietin Homo sapiens 64-67 7700069-4 1994 Some key findings on the interrelationships of insulin and the RAAS with regard to sodium metabolism are also brought into focus. Sodium 83-89 insulin Homo sapiens 47-54 8282372-8 1994 These results indicate that selective insulin resistance with respect to glucose metabolism exists in essential hypertensive patients and that insulin action on renal sodium handling and pressor systems was maintained in these patients. Sodium 167-173 insulin Homo sapiens 143-150 8151603-0 1994 Nephropathy and changes in sodium-lithium countertransport kinetics in type 2 (non-insulin-dependent) diabetes mellitus. Sodium 27-33 insulin Homo sapiens 83-90 8151606-7 1994 Thus the antihypertensive effect of ACE inhibitors can be augmented by sodium restriction alone but supplementing the diet with fish oil may yield additional cardiovascular benefits. Sodium 71-77 angiotensin I converting enzyme Homo sapiens 36-39 8058982-1 1994 It has been postulated that insulin resistance and the concomitant compensatory hyperinsulinemia contribute to the pathogenesis of hypertension; possible by stimulating the sympathetic nervous system, promoting renal sodium reabsorption, modulating cation transport, and/or stimulating vascular smooth muscle hypertrophy. Sodium 217-223 insulin Homo sapiens 28-35 8301562-11 1994 These results demonstrate the pivotal role of angiotensin II in the development of sodium retention and of the blunted renal response to ANF in CHF, and indicate why losartan is useful therapy for cardiac edema. Sodium 83-89 angiotensinogen Rattus norvegicus 46-60 7816287-4 1994 Absolute proximal reabsorption of sodium was increased at baseline in the diabetic group, and fell during ANGII. Sodium 34-40 angiotensinogen Homo sapiens 106-111 7816287-9 1994 Reduced fractional proximal tubular responsiveness to exogenous angiotensin II is consistent with a role for endogenous angiotensin II as one mediator of increased tubular reabsorption of sodium in type 1 diabetes, but the data does not exclude alternative mechanisms. Sodium 188-194 angiotensinogen Homo sapiens 64-78 7816287-9 1994 Reduced fractional proximal tubular responsiveness to exogenous angiotensin II is consistent with a role for endogenous angiotensin II as one mediator of increased tubular reabsorption of sodium in type 1 diabetes, but the data does not exclude alternative mechanisms. Sodium 188-194 angiotensinogen Homo sapiens 120-134 8285286-10 1993 These studies also demonstrate that in TIVCC, a model of low cardiac output and congestive failure that results in marked sodium retention with edema in which there is activation of the RAAS, the renal actions of BNP are attenuated while the vasoactive actions are enhanced. Sodium 122-128 natriuretic peptide B Canis lupus familiaris 213-216 7809956-2 1994 Adenylate cyclase sensitivity to sodium inhibition was different upon cyclase stimulation with 1-isoproterenol, Gpp(NH)p and NaF. Sodium 33-39 C-X-C motif chemokine ligand 8 Homo sapiens 125-128 8285286-4 1993 In normal dogs BNP increased glomerular filtration rate, renal blood flow, and urinary sodium excretion and decreased proximal and distal fractional reabsorption of sodium with activation of urinary guanosine 3",5"-cyclic monophosphate (cGMP). Sodium 87-93 natriuretic peptide B Canis lupus familiaris 15-18 8285286-4 1993 In normal dogs BNP increased glomerular filtration rate, renal blood flow, and urinary sodium excretion and decreased proximal and distal fractional reabsorption of sodium with activation of urinary guanosine 3",5"-cyclic monophosphate (cGMP). Sodium 165-171 natriuretic peptide B Canis lupus familiaris 15-18 8285286-6 1993 In TIVCC, a state characterized by chronic reductions of cardiac output, avid sodium retention, edema, and activation of the renin-angiotensin-aldosterone system (RAAS), the renal actions of BNP were absent in association with marked attenuation of the urinary cGMP response. Sodium 78-84 natriuretic peptide B Canis lupus familiaris 191-194 8148670-7 1993 By demonstrating an absence of PRL action on jejunal calcium fluxes when sodium-free test solution was used, we reconfirmed the sodium-dependent PRL action on passive calcium absorption. Sodium 128-134 prolactin Rattus norvegicus 145-148 8299475-3 1993 The main concerns of insulin therapy are weight gain, hyperinsulinemia, hypoglycemia, and possibly sodium and fluid retention. Sodium 99-105 insulin Homo sapiens 21-28 8263145-7 1993 This abnormality in AVP secretion and thirst was corrected after glucocorticoid replacement with normalization of plasma sodium concentrations and osmolality. Sodium 121-127 arginine vasopressin Homo sapiens 20-23 8179835-3 1993 Also, the renin-aldosterone stimulation testing on this patient performed by sodium restricted diet and furosemide, upright position and by angiotensin converting enzyme inhibition (captopril, 50 mg) showed the blunted renin and aldosterone responses to each of these stimuli, almost no changes from baseline renin and aldosterone levels, it was concluded that the underlying defect responsible for hyperkalemia in this case was hyporeninemic hypoaldosteronism and this was aggravated by other factors or drugs affecting potassium homeostasis. Sodium 77-83 renin Homo sapiens 10-15 8179835-3 1993 Also, the renin-aldosterone stimulation testing on this patient performed by sodium restricted diet and furosemide, upright position and by angiotensin converting enzyme inhibition (captopril, 50 mg) showed the blunted renin and aldosterone responses to each of these stimuli, almost no changes from baseline renin and aldosterone levels, it was concluded that the underlying defect responsible for hyperkalemia in this case was hyporeninemic hypoaldosteronism and this was aggravated by other factors or drugs affecting potassium homeostasis. Sodium 77-83 renin Homo sapiens 219-224 8179835-3 1993 Also, the renin-aldosterone stimulation testing on this patient performed by sodium restricted diet and furosemide, upright position and by angiotensin converting enzyme inhibition (captopril, 50 mg) showed the blunted renin and aldosterone responses to each of these stimuli, almost no changes from baseline renin and aldosterone levels, it was concluded that the underlying defect responsible for hyperkalemia in this case was hyporeninemic hypoaldosteronism and this was aggravated by other factors or drugs affecting potassium homeostasis. Sodium 77-83 renin Homo sapiens 219-224 8134255-6 1993 Serum aldosterone levels (P < 0.01) as well as serum renin levels (P < 0.05) significantly decreased with increasing sodium intake. Sodium 123-129 renin Homo sapiens 56-61 8116019-1 1993 It has been postulated that insulin resistance and the concomitant compensatory hyperinsulinemia contribute to the pathogenesis of hypertension, possibly by stimulating the sympathetic nervous system, promoting renal sodium reabsorption, modulating cation transport, and/or stimulating vascular smooth muscle hypertrophy. Sodium 217-223 insulin Homo sapiens 28-35 8218295-0 1993 Sodium- and chloride-dependent, cocaine-sensitive, high-affinity binding of nisoxetine to the human placental norepinephrine transporter. Sodium 0-6 solute carrier family 6 member 2 Homo sapiens 110-136 8231568-1 1993 ACE blockade is hazardous in acute sodium loss]. Sodium 35-41 angiotensin I converting enzyme Homo sapiens 0-3 8238092-2 1993 The insulin resistance and hyperinsulinemia associated with hypertension is the result of increased renal tubular sodium reabsorption, increased sympathetic nervous system activity, and increased arterial wall smooth muscle reactivity. Sodium 114-120 insulin Homo sapiens 4-11 8238092-3 1993 In insulin resistant states, intracellular calcium and sodium accumulation is thought to be the fundamental underlying abnormality. Sodium 55-61 insulin Homo sapiens 3-10 8241425-10 1993 The result shows that the association of insulin as a function of pH and ionic strength can be described by an effective charge equal to the charge derived from proton titration reduced by the number of sodium ions binding to insulin. Sodium 203-209 insulin Homo sapiens 41-48 8241425-10 1993 The result shows that the association of insulin as a function of pH and ionic strength can be described by an effective charge equal to the charge derived from proton titration reduced by the number of sodium ions binding to insulin. Sodium 203-209 insulin Homo sapiens 226-233 8287649-0 1993 Control of sodium excretion in patients with cranial diabetes insipidus maintained on desamino-[8-D-arginine]vasopressin. Sodium 11-17 arginine vasopressin Homo sapiens 109-120 8281727-9 1993 The interaction between insulin and hormonal control of sodium and water balance may be modified by circulating free insulin concentrations. Sodium 56-62 insulin Homo sapiens 24-31 8281727-9 1993 The interaction between insulin and hormonal control of sodium and water balance may be modified by circulating free insulin concentrations. Sodium 56-62 insulin Homo sapiens 117-124 8112708-1 1993 The renin-angiotensin system (RAS) is known as a system which constricts vessels and enhances renal retention of sodium and water to raise the blood pressure. Sodium 113-119 renin Homo sapiens 4-9 8263040-7 1993 The 1 alpha,25-dihydroxyvitamin D3-induced increments in osteocalcin and osteopontin mRNA levels were abolished in sodium-free medium. Sodium 115-121 bone gamma-carboxyglutamate protein Rattus norvegicus 57-68 7910063-0 1993 Blood pressure response to angiotensin converting enzyme inhibitor in essential hypertension: its relation to the renin status and natriuresis during acute sodium loading. Sodium 156-162 angiotensin I converting enzyme Homo sapiens 27-56 8252410-1 1993 Vasopressin generates a voltage-gated, sodium-dependent current in facial motoneurons in brainstem slices. Sodium 39-45 arginine vasopressin Homo sapiens 0-11 8238340-8 1993 Intrarenal administration of BK at 0.25 ng.kg-1 x min-1 during low sodium balance caused an increase in urine flow rate and urinary sodium excretion. Sodium 67-73 kininogen 1 Canis lupus familiaris 29-31 8238340-8 1993 Intrarenal administration of BK at 0.25 ng.kg-1 x min-1 during low sodium balance caused an increase in urine flow rate and urinary sodium excretion. Sodium 132-138 kininogen 1 Canis lupus familiaris 29-31 8267942-0 1993 Stimulation of renal interstitial bradykinin by sodium depletion. Sodium 48-54 kininogen 1 Canis lupus familiaris 34-44 8242257-12 1993 When 6 micrograms kg-1 h-1 of angiotensin II was infused directly into the fetus RBF fell from 69 +/- 10.1 ml min-1 to 31 +/- 13.9 ml min-1, GFR rose (P < 0.05) and urine flow (P < 0.01) and sodium excretion increased in all fetuses. Sodium 197-203 angiotensinogen Homo sapiens 30-44 8214924-0 1993 Role of atrial natriuretic factor in impaired sodium excretion of normocapnic and hypercapnic patients with chronic obstructive lung disease. Sodium 46-52 natriuretic peptide A Homo sapiens 8-33 8214924-9 1993 An increased secretory response of ANF to volume expansion may help to maintain volume homeostasis in normocapnic patients, while a blunted secretory response of ANF may contribute to sodium retention in hypercapnic patients. Sodium 184-190 natriuretic peptide A Homo sapiens 162-165 8275517-9 1993 Interestingly the modulation of the Na/Ca exchanger (for example, by protons, sodium, calcium, ATP, calmodulin) seems to arise from interactions with the intracellular loop. Sodium 78-84 solute carrier family 8 member A1 Homo sapiens 36-51 8261688-0 1993 Relationship of the antihypertensive effect of vasopressin withdrawal to sodium excretion in the Doca-salt hypertensive rat. Sodium 73-79 arginine vasopressin Rattus norvegicus 47-58 8222513-13 1993 We conclude that the fall in plasma arginine vasopressin concentration during dietary salt restriction, whilst not affecting renal sodium excretion, may be important in the regulation of plasma sodium concentration, plasma renin activity and glomerular filtration. Sodium 194-200 arginine vasopressin Homo sapiens 45-56 8261688-6 1993 Sodium excretion rates were higher during infusions of vasopressin than during phenylephrine infusions. Sodium 0-6 arginine vasopressin Rattus norvegicus 55-66 8263883-7 1993 Among the US whites and Nigerians, sodium explained 4.9% and 6.8%, respectively, of the DBP variance. Sodium 35-41 D-box binding PAR bZIP transcription factor Homo sapiens 88-91 8258953-0 1993 Enhancement of vascular action of arginine vasopressin by diminished extracellular sodium concentration. Sodium 83-89 arginine vasopressin Rattus norvegicus 43-54 8258953-1 1993 The present study was undertaken to examine the effects of diminished extracellular sodium concentration on the vascular action of arginine vasopressin (AVP) in cultured rat vascular smooth muscle cells (VSMC). Sodium 84-90 arginine vasopressin Rattus norvegicus 140-151 8239277-3 1993 When incorporated into this bilayer, the A beta P forms cation selective channels capable of transporting calcium and some monovalent cations including cesium, lithium, potassium, and sodium. Sodium 184-190 amyloid beta precursor protein Homo sapiens 41-47 8212212-8 1993 Urinary sodium excretion tended to be lower in transplant recipients (59 +/- 42 mmol/L) for CTR and 44 +/- 36.7 in LTR than in healthy controls (117 +/- 24.7 mmol/L). Sodium 8-14 calcitonin receptor Homo sapiens 92-95 8372830-7 1993 Atrial natriuretic peptide (ANP), which increases sodium and water excretion, has been suspected to participate in fluid retention. Sodium 50-56 natriuretic peptide A Homo sapiens 0-26 8218608-2 1993 Short-term dietary sodium intake is a known modulator of blood pressure response to infused angiotensin II (A II) in normal subjects. Sodium 19-25 angiotensinogen Homo sapiens 92-106 8218608-2 1993 Short-term dietary sodium intake is a known modulator of blood pressure response to infused angiotensin II (A II) in normal subjects. Sodium 19-25 angiotensinogen Homo sapiens 108-112 8218608-7 1993 Our results indicate that it requires long time before decreased A II responsiveness caused by chronic sodium depletion normalizes in AN patients. Sodium 103-109 angiotensinogen Homo sapiens 65-69 8214150-0 1993 Atrial natriuretic factor counteracts sodium-retaining actions of insulin in normal men. Sodium 38-44 insulin Homo sapiens 66-73 8214150-2 1993 To examine the relationship between the sodium-retaining actions of insulin and atrial natriuretic factor (ANF), 16 healthy subjects were studied on three occasions, approximately 1 wk apart, using standard clearance techniques to evaluate responses during the acute administration of insulin, low-dose ANF, or both. Sodium 40-46 insulin Homo sapiens 68-75 8214150-8 1993 This maneuver abolished insulin-mediated sodium reabsorption. Sodium 41-47 insulin Homo sapiens 24-31 8214150-10 1993 Our findings indicate that insulin at levels found in hyperinsulinemic states caused sodium retention and that physiological increases in plasma ANF concentration abolished the sodium-retaining action of insulin. Sodium 85-91 insulin Homo sapiens 27-34 8214150-10 1993 Our findings indicate that insulin at levels found in hyperinsulinemic states caused sodium retention and that physiological increases in plasma ANF concentration abolished the sodium-retaining action of insulin. Sodium 177-183 natriuretic peptide A Homo sapiens 145-148 8372830-7 1993 Atrial natriuretic peptide (ANP), which increases sodium and water excretion, has been suspected to participate in fluid retention. Sodium 50-56 natriuretic peptide A Homo sapiens 28-31 8223740-5 1993 Compared to placebo, prazosin caused a significant increase in urinary sodium excretion (from 56 +/- 7 to 92 +/- 7 mumol.min-1, P < 0.01), paralleled by significant increases in fractional excretion of sodium and lithium. Sodium 71-77 CD59 molecule (CD59 blood group) Homo sapiens 121-126 8117994-5 1993 When sodium ions were replaced by NMDG in the medium, a response to ET-1 showed a 50% reduction. Sodium 5-11 endothelin 1 Rattus norvegicus 68-72 8349322-0 1993 Enhancement of intracellular sodium by vasopressin in spontaneously hypertensive rats. Sodium 29-35 arginine vasopressin Rattus norvegicus 39-50 8349322-1 1993 The arginine vasopressin-induced increase in intracellular sodium concentration was augmented in cultured rat vascular smooth muscle cells derived from 12-week-old spontaneously hypertensive rats (SHR) compared with those from 12-week-old normotensive Wistar-Kyoto (WKY) rats. Sodium 59-65 arginine vasopressin Rattus norvegicus 13-24 8349322-3 1993 The calcium-free state did not affect the basal intracellular sodium concentration but completely blocked the arginine vasopressin-induced increase in intracellular sodium concentration in both cell groups. Sodium 165-171 arginine vasopressin Rattus norvegicus 119-130 8349322-7 1993 Pretreatment of both cell groups with a calmodulin antagonist, N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide, completely blocked arginine vasopressin-induced intracellular alkalinization and increased intracellular sodium concentration. Sodium 220-226 arginine vasopressin Rattus norvegicus 143-154 8349322-9 1993 These findings therefore indicate that the arginine vasopressin-induced increase in intracellular sodium concentration is augmented in vascular smooth muscle cells of SHR mediated through the enhancement of the mobilization of cytosolic free calcium and the activity of sodium-hydrogen exchange, which depends on an increase in V1 receptor number. Sodium 98-104 arginine vasopressin Rattus norvegicus 52-63 8349322-9 1993 These findings therefore indicate that the arginine vasopressin-induced increase in intracellular sodium concentration is augmented in vascular smooth muscle cells of SHR mediated through the enhancement of the mobilization of cytosolic free calcium and the activity of sodium-hydrogen exchange, which depends on an increase in V1 receptor number. Sodium 270-276 arginine vasopressin Rattus norvegicus 52-63 7904859-0 1993 Atrial natriuretic peptide and blood pressure responses during acute sodium loading in patients with essential hypertension. Sodium 69-75 natriuretic peptide A Homo sapiens 0-26 7904859-1 1993 Atrial natriuretic peptide (ANP) response during acute saline loading and its relationship to changes in blood pressure (BP) and sodium excretion were studied in 21 patients with essential hypertension (EH) and nine normotensive volunteers. Sodium 129-135 natriuretic peptide A Homo sapiens 0-26 8277228-0 1993 Increased cytosolic free sodium concentrations in platelets from type 2 (non-insulin-dependent) diabetic patients is associated with hypertension. Sodium 25-31 insulin Homo sapiens 77-84 8301063-3 1993 In patients with cirrhosis ET-1 was directly correlated to serum creatinine (r = 0.70, P < 0.0001) and aspartate aminotransferase (r = 0.44, P < 0.03) and negatively correlated to serum sodium (r = -0.58, P < 0.003). Sodium 192-198 endothelin 1 Homo sapiens 27-31 8231021-2 1993 Dopamine and DARPP-32 regulate sodium reabsorption in renal tubules by inhibiting the activity of Na+,K(+)-ATPase. Sodium 31-37 protein phosphatase 1, regulatory (inhibitor) subunit 1B Rattus norvegicus 13-21 8112147-4 1993 There was no significant difference between the levels in chronic schistosomiasis and normal control (P > 0.05), the results suggested that ANP played a role in maintaining homeostasis of sodium and fluid in advanced schistosomiasis. Sodium 191-197 natriuretic peptide A Homo sapiens 143-146 8129536-7 1993 In the plasma, ACE activity in sodium-depleted rats was slightly decreased whereas no change occurred in the other models. Sodium 31-37 angiotensin I converting enzyme Rattus norvegicus 15-18 8403783-11 1993 In contrast, the effect of angiotensin II on sodium excretion showed a flat dose-response curve beyond 5 ng min-1 kg-1. Sodium 45-51 angiotensinogen Homo sapiens 27-41 8403783-11 1993 In contrast, the effect of angiotensin II on sodium excretion showed a flat dose-response curve beyond 5 ng min-1 kg-1. Sodium 45-51 CD59 molecule (CD59 blood group) Homo sapiens 108-118 8403783-14 1993 The fractional distal reabsorption of sodium, determined by using the lithium clearance technique, showed a rise with all doses of angiotensin II used and reached statistical significance with the top two doses. Sodium 38-44 angiotensinogen Homo sapiens 131-145 8403783-17 1993 Pressor doses of angiotensin II also have a significant effect on the distal tubule in promoting sodium reabsorption. Sodium 97-103 angiotensinogen Homo sapiens 17-31 8230088-7 1993 Intravascular angiotensin II receptors are implicated in the central release of vasopressin and other hypophyseal hormones, in increasing sympathetic outflow, in the thirst response and, possibly, in cognitive function; in the inotropic and chronotropic effects of angiotensin II on the heart as well as in growth/hypertrophy; in the control of aldosterone release and in the balance between cortisol and aldosterone secretion; and in modulating sodium, chloride and bicarbonate transport within the kidney. Sodium 446-452 angiotensinogen Homo sapiens 14-28 8393428-0 1993 Red blood cell sodium-proton exchange in hypertensive blacks with insulin-resistant glucose disposal. Sodium 15-21 insulin Homo sapiens 66-73 8393428-1 1993 To define the potential pathogenic role of hyperinsulinemia as a mediator of alterations in sodium transport, we have examined red blood cell Na(+)-H+ and Na(+)-Li+ exchanges in a young adult black population characterized for blood pressure and insulin-mediated glucose disposal. Sodium 92-98 insulin Homo sapiens 48-55 7504728-0 1993 Sodium-evoked, calcium-independent vasopressin release from rat isolated neurohypophysial nerve endings. Sodium 0-6 arginine vasopressin Rattus norvegicus 35-46 8230088-7 1993 Intravascular angiotensin II receptors are implicated in the central release of vasopressin and other hypophyseal hormones, in increasing sympathetic outflow, in the thirst response and, possibly, in cognitive function; in the inotropic and chronotropic effects of angiotensin II on the heart as well as in growth/hypertrophy; in the control of aldosterone release and in the balance between cortisol and aldosterone secretion; and in modulating sodium, chloride and bicarbonate transport within the kidney. Sodium 446-452 arginine vasopressin Homo sapiens 80-91 7686902-0 1993 Vasopressin increases cytosolic sodium concentration in hepatocytes and activates calcium influx through cation-selective channels. Sodium 32-38 arginine vasopressin Homo sapiens 0-11 8346382-2 1993 By its natriuretic, diuretic and blood pressure lowering activities ANP is possibly an endogenic antagonist for the sodium-retaining, vasopressor renin-angiotensin-aldosterone system (RAAS). Sodium 116-122 natriuretic peptide A Homo sapiens 68-71 8315780-10 1993 This relationship suggests an altered tubular sodium handling and uric acid metabolism consistent with hyperinsulinemia, insulin resistance being the possible pathophysiological link. Sodium 46-52 insulin Homo sapiens 108-115 8514035-1 1993 BACKGROUND: Sodium retention in cirrhosis has been attributed to an imbalance between vasoconstrictive, antinatriuretic forces such as the renin aldosterone angiotensin system and the sympathetic nervous system, and vasodilatory, natriuretic agents such as atrial natriuretic factor (ANF). Sodium 12-18 renin Homo sapiens 139-144 8514035-1 1993 BACKGROUND: Sodium retention in cirrhosis has been attributed to an imbalance between vasoconstrictive, antinatriuretic forces such as the renin aldosterone angiotensin system and the sympathetic nervous system, and vasodilatory, natriuretic agents such as atrial natriuretic factor (ANF). Sodium 12-18 natriuretic peptide A Homo sapiens 257-282 8514035-1 1993 BACKGROUND: Sodium retention in cirrhosis has been attributed to an imbalance between vasoconstrictive, antinatriuretic forces such as the renin aldosterone angiotensin system and the sympathetic nervous system, and vasodilatory, natriuretic agents such as atrial natriuretic factor (ANF). Sodium 12-18 natriuretic peptide A Homo sapiens 284-287 8514035-4 1993 RESULTS: Before PVS, sodium excretion at baseline and in response to ANF infusion was blunted but became more normal post-PVS. Sodium 21-27 natriuretic peptide A Homo sapiens 69-72 8514035-5 1993 ANF infusion post-PVS induced a significant increase in the glomerular filtration rate and filtration fraction and also in distal delivery of sodium. Sodium 142-148 natriuretic peptide A Homo sapiens 0-3 8514035-6 1993 ANF"s distal effect of increasing the fractional excretion of distally delivered sodium was present pre-PVS and was not significantly increased post-PVS. Sodium 81-87 natriuretic peptide A Homo sapiens 0-3 8376285-7 1993 We suggest that the combined effect of the sustained suppressions of plasma renin activity and plasma aldosterone and norepinephrine concentrations constitutes a mechanism of the increase in renal sodium excretion. Sodium 197-203 renin Homo sapiens 76-81 8355455-0 1993 Role of hyperglycemia and insulin resistance in determining sodium retention in non-insulin-dependent diabetes. Sodium 60-66 insulin Homo sapiens 26-33 8228194-5 1993 Severe sodium restriction increased plasma renin activity and noradrenaline concentration, as well as serum total and low-density lipoprotein-cholesterol and triglycerides. Sodium 7-13 renin Homo sapiens 43-48 8411837-5 1993 The aim of this study was to determine whether patients with essential hypertension (EH) and healthy subjects differ in EPO secretion and whether EPO serum level is related to renin response to dietary sodium restriction and upright position of the body. Sodium 202-208 erythropoietin Homo sapiens 146-149 7812749-0 1993 Characterization of sodium cations in dehydrated faujasites and zeolite EMT by 23Na DOR, 2D nutation, and MAS NMR. Sodium 20-26 tumor protein p53 inducible nuclear protein 2 Homo sapiens 84-87 8327470-1 1993 We have isolated two cDNA clones, NaPi-2 and NaPi-3, by screening rat kidney cortex and human kidney cortex cDNA libraries, respectively, for expression of sodium-dependent phosphate transport in Xenopus laevis oocytes. Sodium 156-162 solute carrier family 34 member 1 Rattus norvegicus 34-40 8503435-5 1993 Fluid and sodium retention with normal concentrations of active renin, angiotensin I and II, and aldosterone has been demonstrated in diabetic renal disease. Sodium 10-16 renin Homo sapiens 64-69 8503435-5 1993 Fluid and sodium retention with normal concentrations of active renin, angiotensin I and II, and aldosterone has been demonstrated in diabetic renal disease. Sodium 10-16 angiotensinogen Homo sapiens 71-91 8392808-7 1993 The localization of MR mRNA to nonepithelial cells in the lamina propria, possibly neuroendocrine cells, suggests that mineralocorticoid-regulated sodium transport across colonic epithelial cells may also involve a paracrine mechanism. Sodium 147-153 nuclear receptor subfamily 3, group C, member 2 Rattus norvegicus 20-22 8500861-6 1993 When the Ang II infusion was repeated with a high sodium intake, plasma atrial natriuretic peptide increased again in low renin and modulating patients, whereas it did not change in non-modulators. Sodium 50-56 angiotensinogen Homo sapiens 9-15 7691497-5 1993 ACE inhibitors must also be administered with caution to sodium-depleted patients. Sodium 57-63 angiotensin I converting enzyme Homo sapiens 0-3 8500861-6 1993 When the Ang II infusion was repeated with a high sodium intake, plasma atrial natriuretic peptide increased again in low renin and modulating patients, whereas it did not change in non-modulators. Sodium 50-56 renin Homo sapiens 122-127 8510517-1 1993 In adults patients, administration of human growth hormone and growth hormone synthesized by recombinant DNA technology (rGH) results in sodium and fluid retention and weight gain. Sodium 137-143 growth hormone 1 Homo sapiens 44-58 8397245-11 1993 At the end of the low-sodium phase there was a significant increase in plasma renin activity and aldosterone levels, but no change in plasma electrolytes. Sodium 22-28 renin Homo sapiens 78-83 8510517-1 1993 In adults patients, administration of human growth hormone and growth hormone synthesized by recombinant DNA technology (rGH) results in sodium and fluid retention and weight gain. Sodium 137-143 growth hormone 1 Homo sapiens 63-77 8494017-0 1993 Insulin resistance and hypertension: connections with sodium metabolism. Sodium 54-60 insulin Homo sapiens 0-7 8498495-0 1993 Effect of sodium intake on insulin sensitivity. Sodium 10-16 insulin Homo sapiens 27-34 8498495-4 1993 This impairment in insulin sensitivity was not related to changes in serum potassium, epinephrine, norepinephrine, cortisol, or growth hormone but was highly correlated with an increment in circulating free fatty acid levels during high sodium intake (r = 0.82, P < 0.05). Sodium 237-243 insulin Homo sapiens 19-26 8498495-5 1993 These data suggest that 1) high sodium intake may exacerbate insulin resistance by increasing circulating free fatty acids, and 2) differences in sodium intake may influence measures of insulin sensitivity in other disease states. Sodium 32-38 insulin Homo sapiens 61-68 8498495-5 1993 These data suggest that 1) high sodium intake may exacerbate insulin resistance by increasing circulating free fatty acids, and 2) differences in sodium intake may influence measures of insulin sensitivity in other disease states. Sodium 146-152 insulin Homo sapiens 186-193 8324299-6 1993 The activation of the renin-aldosterone system in newborns and infants probably represents an important physiological mechanism designed to maintain positive sodium balance. Sodium 158-164 renin Homo sapiens 22-27 8324299-8 1993 The superimposition of a disease process, or the injudicious prescription of a drug, inhibiting renin release or angiotensin II production, could theoretically facilitate sodium wasting in newborns or infants, or precipitate hyporeninaemic hypoaldosteronism in older adults. Sodium 171-177 renin Homo sapiens 96-101 8324299-8 1993 The superimposition of a disease process, or the injudicious prescription of a drug, inhibiting renin release or angiotensin II production, could theoretically facilitate sodium wasting in newborns or infants, or precipitate hyporeninaemic hypoaldosteronism in older adults. Sodium 171-177 angiotensinogen Homo sapiens 113-127 8482447-8 1993 Endothelin 1 significantly decreased net sodium and net chloride absorption and induced a marked increase in prostacyclin release from the serosal surface of stripped colonic mucosa. Sodium 41-47 endothelin 1 Rattus norvegicus 0-12 7685442-3 1993 On the study day, 24-h urinary sodium excretion was approximately 10-20 mmol Na, with an increase in renin and aldosterone levels at baseline. Sodium 31-37 renin Homo sapiens 101-106 8326257-5 1993 Plasma vasopressin and oxytocin concentrations were significantly elevated throughout dehydration to levels which could be reproduced by acutely increasing plasma sodium and decreasing blood volume to the same extent. Sodium 163-169 arginine vasopressin Rattus norvegicus 7-18 8326257-9 1993 Plasma angiotensin II concentrations rose significantly during the later period of sodium retention. Sodium 83-89 angiotensinogen Rattus norvegicus 7-21 8390529-1 1993 OBJECTIVE: The present study examines the effect of angiotensin converting enzyme inhibition on the renal haemodynamic and sodium excretory responses to noradrenaline in man. Sodium 123-129 angiotensin I converting enzyme Homo sapiens 52-81 8350592-8 1993 In one sibling negative values may have been caused by suppression of the renin-angiotensin-system due to high sodium replacement therapy. Sodium 111-117 renin Homo sapiens 74-79 8316748-10 1993 In congestive heart failure and supraventricular tachycardia, the increase in plasma ANF concentration may augment sodium excretion, but anti-natriuretic factors, such as reduction in renal perfusion pressure, may override the natriuretic effect of ANF. Sodium 115-121 natriuretic peptide A Homo sapiens 85-88 8316748-11 1993 Reduced sodium excretion during mechanical ventilation with positive end-expiratory pressure (PEEP) is partly due to a decrease in ANF secretion. Sodium 8-14 natriuretic peptide A Homo sapiens 131-134 8507444-7 1993 Altogether, we suggest that these insulin- and glucose-mediated effects on cellular sodium, if present in other tissues as well, may underlie the increased total body sodium and the salt-dependent hypertension characteristic of chronic diabetic or hyperinsulinemic syndromes. Sodium 84-90 insulin Homo sapiens 34-41 8507444-7 1993 Altogether, we suggest that these insulin- and glucose-mediated effects on cellular sodium, if present in other tissues as well, may underlie the increased total body sodium and the salt-dependent hypertension characteristic of chronic diabetic or hyperinsulinemic syndromes. Sodium 167-173 insulin Homo sapiens 34-41 8484898-1 1993 Sodium depletion in rats elicits a sodium appetite that results from a cerebral action of angiotensin II (ANG II) and aldosterone. Sodium 0-6 angiotensinogen Rattus norvegicus 90-104 8484898-1 1993 Sodium depletion in rats elicits a sodium appetite that results from a cerebral action of angiotensin II (ANG II) and aldosterone. Sodium 0-6 angiotensinogen Rattus norvegicus 106-112 8484898-1 1993 Sodium depletion in rats elicits a sodium appetite that results from a cerebral action of angiotensin II (ANG II) and aldosterone. Sodium 35-41 angiotensinogen Rattus norvegicus 90-104 8484898-1 1993 Sodium depletion in rats elicits a sodium appetite that results from a cerebral action of angiotensin II (ANG II) and aldosterone. Sodium 35-41 angiotensinogen Rattus norvegicus 106-112 8104577-0 1993 Renin suppressibility and blood pressure response during acute sodium loading in patients with essential hypertension. Sodium 63-69 renin Homo sapiens 0-5 8386932-2 1993 In short term infusion studies (2 or 8 h duration), ANF plasma levels as observed after sodium loading (50-70 pg/ml) lowered basal renin (PRA) and aldosterone, but had only a marginal effect on angiotensin II-stimulated aldosterone secretion. Sodium 88-94 natriuretic peptide A Homo sapiens 52-55 8386932-2 1993 In short term infusion studies (2 or 8 h duration), ANF plasma levels as observed after sodium loading (50-70 pg/ml) lowered basal renin (PRA) and aldosterone, but had only a marginal effect on angiotensin II-stimulated aldosterone secretion. Sodium 88-94 renin Homo sapiens 131-136 8481339-2 1993 Sodium restriction increases plasma aldosterone, adrenal glomerulosa AII receptors and the activity of enzymes of the early and late aldosterone biosynthetic pathway. Sodium 0-6 angiotensinogen Rattus norvegicus 69-72 8481339-3 1993 The effects of sodium restriction are mimicked by prolonged administration of low doses of AII, and prevented by blockade of AII formation using converting enzyme inhibitors, indicating that the effects of sodium restriction are mediated by AII. Sodium 15-21 angiotensinogen Rattus norvegicus 91-94 8481339-3 1993 The effects of sodium restriction are mimicked by prolonged administration of low doses of AII, and prevented by blockade of AII formation using converting enzyme inhibitors, indicating that the effects of sodium restriction are mediated by AII. Sodium 15-21 angiotensinogen Rattus norvegicus 125-128 8481339-3 1993 The effects of sodium restriction are mimicked by prolonged administration of low doses of AII, and prevented by blockade of AII formation using converting enzyme inhibitors, indicating that the effects of sodium restriction are mediated by AII. Sodium 15-21 angiotensinogen Rattus norvegicus 125-128 8481339-3 1993 The effects of sodium restriction are mimicked by prolonged administration of low doses of AII, and prevented by blockade of AII formation using converting enzyme inhibitors, indicating that the effects of sodium restriction are mediated by AII. Sodium 206-212 angiotensinogen Rattus norvegicus 125-128 8481339-3 1993 The effects of sodium restriction are mimicked by prolonged administration of low doses of AII, and prevented by blockade of AII formation using converting enzyme inhibitors, indicating that the effects of sodium restriction are mediated by AII. Sodium 206-212 angiotensinogen Rattus norvegicus 125-128 8481339-4 1993 However, the adrenal glomerulotrophic actions of AII are impaired in rats on high sodium diet indicating that other factors are modulating the effects of AII in these conditions. Sodium 82-88 angiotensinogen Rattus norvegicus 49-52 8456103-6 1993 Our results strongly suggest that the brain AT1 receptor subtype mediates the physiologic actions of angiotensin II, such as drinking behavior, the increase in sodium excretion, and vasopressin release. Sodium 160-166 angiotensinogen Rattus norvegicus 101-115 8472740-5 1993 There was a significant positive correlation between the maximal change in ANP level and urinary sodium after nifedipine and felodipine. Sodium 97-103 natriuretic peptide A Homo sapiens 75-78 8489125-2 1993 In patients with low renin essential hypertension, plasma and urinary norepinephrine levels, plasma renin activity and fractional excretion of sodium were significantly lower, while plasma volume, extracellular fluid volume and exchangeable sodium were higher than in normal renin essential hypertension. Sodium 143-149 renin Homo sapiens 21-26 8489125-2 1993 In patients with low renin essential hypertension, plasma and urinary norepinephrine levels, plasma renin activity and fractional excretion of sodium were significantly lower, while plasma volume, extracellular fluid volume and exchangeable sodium were higher than in normal renin essential hypertension. Sodium 241-247 renin Homo sapiens 21-26 8489125-3 1993 The suppression of some renal depressor-natriuretic systems, the dopaminergic, kallikrein-kinin and prostaglandin E2 systems may contribute to the retention of sodium-water in these patients, because these depressor systems were observed to be greatly suppressed in essential hypertension, especially in the low renin group. Sodium 160-166 renin Homo sapiens 312-317 8456961-0 1993 ANP kinetics in normal men: in vivo measurement by a tracer method and correlation with sodium intake. Sodium 88-94 natriuretic peptide A Homo sapiens 0-3 8456961-7 1993 These results indicate that: 1) newly produced ANP is rapidly distributed and degraded, 2) the body pool of the hormone can be considered as a combination of two exchanging spaces, 3) circulating ANP is < or = 1/15 of the body pool, and 4) MCR of ANP is closely related to sodium intake, at least in normal subjects on a free sodium intake diet. Sodium 276-282 natriuretic peptide A Homo sapiens 47-50 8456961-7 1993 These results indicate that: 1) newly produced ANP is rapidly distributed and degraded, 2) the body pool of the hormone can be considered as a combination of two exchanging spaces, 3) circulating ANP is < or = 1/15 of the body pool, and 4) MCR of ANP is closely related to sodium intake, at least in normal subjects on a free sodium intake diet. Sodium 329-335 natriuretic peptide A Homo sapiens 47-50 8460705-14 1993 The results of these studies indicate that a protein that is involved in mediating sodium-dependent bile acid transport is closely related to mEH. Sodium 83-89 epoxide hydrolase 1, microsomal Mus musculus 142-145 8466703-8 1993 The renin response to sodium and volume depletion induced by the low sodium diet and furosemide correlated significantly (P < .001) with the subsequent blood pressure response to the low sodium diet. Sodium 22-28 renin Homo sapiens 4-9 8466703-8 1993 The renin response to sodium and volume depletion induced by the low sodium diet and furosemide correlated significantly (P < .001) with the subsequent blood pressure response to the low sodium diet. Sodium 69-75 renin Homo sapiens 4-9 8466703-8 1993 The renin response to sodium and volume depletion induced by the low sodium diet and furosemide correlated significantly (P < .001) with the subsequent blood pressure response to the low sodium diet. Sodium 69-75 renin Homo sapiens 4-9 8471406-1 1993 A combination of dietary sodium restriction (40 mmol day-1) and frusemide pretreatment has been used to activate the renin angiotensin system (RAS) in order to characterise the haemodynamic and hormonal responses to enalapril in young normotensives. Sodium 25-31 renin Homo sapiens 117-122 8444424-1 1993 A working formulation for the role of ANF in the sodium retention of cirrhosis is summarized in Figure 4. Sodium 49-55 natriuretic peptide A Homo sapiens 38-41 8444424-11 1993 First, ANF may exacerbate arterial vasodilation, leading to further sodium retention. Sodium 68-74 natriuretic peptide A Homo sapiens 7-10 8444424-18 1993 In early compensated cirrhosis, ANF may maintain sodium homeostasis despite the presence of mild antinatriuretic factors. Sodium 49-55 natriuretic peptide A Homo sapiens 32-35 8478039-7 1993 The blood pressure response to Ang II, on the other hand, was greater in salt-sensitive than salt-resistant patients during low but not during high sodium intake. Sodium 148-154 angiotensinogen Homo sapiens 31-37 8478036-1 1993 Insulin resistance has been demonstrated in patients with essential hypertension, and insulin-mediated sodium retention is believed to contribute to hypertension in these individuals. Sodium 103-109 insulin Homo sapiens 86-93 8507814-11 1993 It was concluded that EPO acts within the kidney to cause the production of angiotensin II, which mediates the increased reabsorption of sodium. Sodium 137-143 angiotensinogen Rattus norvegicus 76-90 8478039-11 1993 In fact, we observed increased reactivity to Ang II during low but not during high sodium intake. Sodium 83-89 angiotensinogen Homo sapiens 45-51 8231616-6 1993 Insulin increases the reabsorption of sodium by means of an immediate effect on the kidney tubules. Sodium 38-44 insulin Homo sapiens 0-7 8450052-1 1993 Recent evidence has implicated endothelin-1 (ET-1) as an autocrine inhibitor of inner medullary collecting duct (IMCD) sodium and water transport. Sodium 119-125 endothelin 1 Rattus norvegicus 31-43 8450052-1 1993 Recent evidence has implicated endothelin-1 (ET-1) as an autocrine inhibitor of inner medullary collecting duct (IMCD) sodium and water transport. Sodium 119-125 endothelin 1 Rattus norvegicus 45-49 8450052-8 1993 These results indicate that extracellular sodium concentration inhibits ET-1 production specifically in IMCD cells. Sodium 42-48 endothelin 1 Rattus norvegicus 72-76 8450052-9 1993 We speculate that extracellular sodium concentration, via regulation of ET-1 production, provides a link between volume status and IMCD sodium and water reabsorption. Sodium 32-38 endothelin 1 Rattus norvegicus 72-76 8450052-9 1993 We speculate that extracellular sodium concentration, via regulation of ET-1 production, provides a link between volume status and IMCD sodium and water reabsorption. Sodium 136-142 endothelin 1 Rattus norvegicus 72-76 8383404-2 1993 Atrial natriuretic peptide (ANP) is intimately involved in fluid and sodium homeostasis and exerts marked relaxant activity on vascular smooth muscle pre-contracted with angiotensin. Sodium 69-75 natriuretic peptide A Homo sapiens 0-26 8381523-2 1993 Reabsorbtion of sodium through this channel, which is regulated by hormones such as aldosterone and vasopressin, is one of the essential mechanisms involved in the regulation of sodium balance, blood volume and blood pressure. Sodium 16-22 arginine vasopressin Rattus norvegicus 100-111 8383404-2 1993 Atrial natriuretic peptide (ANP) is intimately involved in fluid and sodium homeostasis and exerts marked relaxant activity on vascular smooth muscle pre-contracted with angiotensin. Sodium 69-75 natriuretic peptide A Homo sapiens 28-31 8383404-11 1993 There was a positive correlation between changes in P-ANP and changes in: a) fractional excretion of sodium, R = 0.54, p < 0.0001, and b) total peripheral resistance. Sodium 101-107 natriuretic peptide A Homo sapiens 54-57 8435072-0 1993 Sodium-dependent co-transported analogues of glucose stimulate ornithine decarboxylase mRNA expression in LLC-PK1 cells. Sodium 0-6 ornithine decarboxylase 1 Sus scrofa 63-86 8498970-6 1993 These prostaglandins may attenuate any direct Ang II-induced vasoconstriction, lower systemic vascular resistance and stimulate renal sodium excretion. Sodium 134-140 angiotensinogen Homo sapiens 46-52 8498972-3 1993 Normally, in the presence of hypertension or sodium-volume excess, plasma renin activity promptly falls to zero. Sodium 45-51 renin Homo sapiens 74-79 8498972-8 1993 These varying, but abnormal renin-sodium products are caused by a renal lesion in which a subpopulation of ischemic nephrons hypersecretes renin and retains sodium despite systemic hypertension and sodium excess. Sodium 34-40 renin Homo sapiens 28-33 8498972-8 1993 These varying, but abnormal renin-sodium products are caused by a renal lesion in which a subpopulation of ischemic nephrons hypersecretes renin and retains sodium despite systemic hypertension and sodium excess. Sodium 157-163 renin Homo sapiens 28-33 8498973-0 1993 Acute effects of a pseudo-tetrapeptide as renin inhibitor on blood pressure and renin-angiotensin system of sodium-repleted and sodium-depleted hypertensive patients. Sodium 108-114 renin Homo sapiens 42-47 8498973-0 1993 Acute effects of a pseudo-tetrapeptide as renin inhibitor on blood pressure and renin-angiotensin system of sodium-repleted and sodium-depleted hypertensive patients. Sodium 108-114 renin Homo sapiens 80-85 8430832-6 1993 Because of the high specificity of losartan, this suggests that, in the normal conscious rat, endogenous ANG II does not control renal vascular tone but does enhance renal sodium reabsorption. Sodium 172-178 angiotensinogen Rattus norvegicus 105-111 8098306-1 1993 Heart failure is a syndrome characterized by the activation of neurohumoral mechanisms (sympathoadrenergic, renin-angiotensin, vasopressin) which cause peripheral vasoconstriction, sodium retention and myocardial hypertrophy. Sodium 181-187 renin Homo sapiens 108-113 8098306-1 1993 Heart failure is a syndrome characterized by the activation of neurohumoral mechanisms (sympathoadrenergic, renin-angiotensin, vasopressin) which cause peripheral vasoconstriction, sodium retention and myocardial hypertrophy. Sodium 181-187 arginine vasopressin Homo sapiens 127-138 8098306-8 1993 Neurohumoral activation can be roughly assessed using some simple laboratory measurements: plasma sodium concentration, for example, is inversely related to the degree of activation of many neurohormones such as norepinephrine, angiotensin II, vasopressin and atrial natriuretic factor. Sodium 98-104 angiotensinogen Homo sapiens 228-242 8098306-8 1993 Neurohumoral activation can be roughly assessed using some simple laboratory measurements: plasma sodium concentration, for example, is inversely related to the degree of activation of many neurohormones such as norepinephrine, angiotensin II, vasopressin and atrial natriuretic factor. Sodium 98-104 arginine vasopressin Homo sapiens 244-255 8098306-11 1993 For example, 3-4 days on a low sodium diet or standing for at least 2 hours can increase plasma renin activity in a normal subject from 1.5 to 5-10 pg/ml/hr. Sodium 31-37 renin Homo sapiens 96-101 8458606-4 1993 Urinary sodium excretion after glucose ingestion was lower in CGN than in C. These data demonstrated that the glucose-induced renin-angiotensin-aldosterone system in patients with chronic renal disease differed from that in healthy subjects. Sodium 8-14 renin Homo sapiens 126-131 8443481-11 1993 The aldosterone to active renin ratio was decreased by angiotensin I converting enzyme inhibition and increased by sodium depletion, showing treatment efficacy. Sodium 115-121 renin Homo sapiens 26-31 8281528-5 1993 ), sodium excretion was significantly increased during therapy with lisinopril but only slightly during nitrendipine, indicating that angiotensin-converting enzyme inhibition may improve the sodium-retaining state of heart transplant recipients associated with ciclosporin A. Sodium 191-197 angiotensin I converting enzyme Homo sapiens 134-163 8380126-0 1993 Atrial natriuretic factor and arginine vasopressin production in tumor cell lines from patients with lung cancer and their relationship to serum sodium. Sodium 145-151 arginine vasopressin Homo sapiens 39-50 8419057-1 1993 The ionic activities and total molalities of sodium, potassium, calcium, lithium, and chloride in a solution of human serum albumin were measured at different values of pH between 4 and 9. Sodium 45-51 albumin Homo sapiens 118-131 8382130-12 1993 Low sodium treatment of the hRN8-12 mice for 2 weeks increased plasma human active renin, renal human renin and renal human renin mRNA levels by 2.6-, 3.8- and 2.8-fold, respectively. Sodium 4-10 renin Homo sapiens 102-107 8382130-13 1993 Thus, the biosynthesis and secretion of renal human renin in these transgenic mice are obviously stimulated by sodium depletion. Sodium 111-117 renin Homo sapiens 52-57 8382130-12 1993 Low sodium treatment of the hRN8-12 mice for 2 weeks increased plasma human active renin, renal human renin and renal human renin mRNA levels by 2.6-, 3.8- and 2.8-fold, respectively. Sodium 4-10 renin Homo sapiens 83-88 8513316-5 1993 The crucial points are the inborn alteration of cellular sodium transport systems and the modulating action of environmental factors, first of all insulin. Sodium 57-63 insulin Homo sapiens 147-154 8382130-12 1993 Low sodium treatment of the hRN8-12 mice for 2 weeks increased plasma human active renin, renal human renin and renal human renin mRNA levels by 2.6-, 3.8- and 2.8-fold, respectively. Sodium 4-10 renin Homo sapiens 102-107 7512468-3 1993 Insulin can increase blood pressure via several mechanisms: increased renal sodium reabsorption, activation of the sympathetic nervous system, alteration of transmembrane ion transport, and hypertrophy of resistance vessels. Sodium 76-82 insulin Homo sapiens 0-7 7922165-7 1993 Local angiotensin II production can have profound influences on renal function, ie, alter glomerular hemodynamics, reduce sodium excretion, and constrict small arterioles. Sodium 122-128 angiotensinogen Homo sapiens 6-20 8436253-1 1993 Insulin resistance in Type 1 (insulin-dependent) diabetes mellitus may be associated with raised erythrocyte sodium-lithium countertransport activity in patients with hypertension, or nephropathy, or both. Sodium 109-115 insulin Homo sapiens 0-7 8200182-0 1993 Effects of short-time insulin suppression on renal sodium excretion in type II diabetic hypertensives. Sodium 51-57 insulin Homo sapiens 22-29 8436253-3 1993 We have therefore examined the relationship between insulin-mediated glucose disposal and erythrocyte sodium-lithium countertransport in 41 normotensive (mean blood pressure 120/74 mmHg), normoalbuminuric (mean albumin excretion 6.2 micrograms/min), normolipidaemic (mean serum cholesterol 4.3 mmol/l and mean serum triglycerides 1.0 mmol/l) Type 1 diabetic patients. Sodium 102-108 insulin Homo sapiens 52-59 8518023-1 1993 Recombinant interleukin-2 (rIL-2) can produce impairment of renal function with hypotension, fluid retention, elevated blood urea nitrogen, oliguria and low fractional sodium excretion; these side-effects are a common cause of reduction or interruption of rIL-2 infusion. Sodium 168-174 interleukin 2 Homo sapiens 12-25 8428706-11 1993 The lowering of plasma ANP levels may represent a decreased ANP secretion due to calcium channel blockade or might also be due to the natriuretic effects of nitrendipine, thus allowing ANP levels to decline as a function of lessened sodium retention. Sodium 233-239 natriuretic peptide A Homo sapiens 23-26 7508068-4 1993 Elevated plasma insulin levels may contribute to the development of hypertension through renal sodium reabsorption, the sympathetic nervous system, the transmembranous cation transport, the renin-angiotensin system, the cardiovascular reactivity, and the atrial natriuretic peptide. Sodium 95-101 insulin Homo sapiens 16-23 8175282-0 1993 Effects of recombinant human erythropoietin on sodium balance in nondialysed children with chronic renal failure. Sodium 47-53 erythropoietin Homo sapiens 29-43 7508015-7 1993 In rats, gamma-MSH-related peptides are involved in the reflex control of sodium excretion in situations such as the natriuresis that occurs (a) from the remaining kidney after acute unilateral nephrectomy, (b) from the contralateral kidney shortly after unilateral ureteral pressure elevation, and (c) after unilateral carotid artery traction. Sodium 74-80 proopiomelanocortin Homo sapiens 9-18 7508039-2 1993 A number of lines of evidence imply that atriopeptin is only of trivial importance in the regulation of sodium excretion during normal living conditions. Sodium 104-110 natriuretic peptide A Homo sapiens 41-52 8381931-4 1993 Insulin infusion reduced both the absolute and fractional urinary excretion rates of sodium (P < 0.001) and potassium (P < 0.001); these effects of insulin were not altered after converting enzyme inhibition. Sodium 85-91 insulin Homo sapiens 0-7 8345832-2 1993 In the present study, in 12 consecutive hospitalized elderly patients (mean age 82.2 years) with moderate to severe hypernatremia (mean serum sodium 166.9 mEq/l), inappropriately low plasma levels of vasopressin were found in relation to serum osmolality (mean 1.8 pg/ml and 343 mosmol/l, respectively). Sodium 142-148 arginine vasopressin Homo sapiens 200-211 8381931-4 1993 Insulin infusion reduced both the absolute and fractional urinary excretion rates of sodium (P < 0.001) and potassium (P < 0.001); these effects of insulin were not altered after converting enzyme inhibition. Sodium 85-91 insulin Homo sapiens 154-161 8289999-7 1993 Remarkable resistance to some hemodynamic and renal effects, while prompt proteinuric effects of BNP, may contribute to the sodium and water retention and urinary protein characteristic of this disorder. Sodium 124-130 natriuretic peptide B Rattus norvegicus 97-100 8302404-4 1993 In essential hypertension a negative correlation found between changes in EPO and PRA levels in response to sodium restriction and upright body position may also reflect an altered regulation of both EPO and renin production. Sodium 108-114 erythropoietin Homo sapiens 74-77 1299941-8 1992 A previous diuretic treatment with sodium depletion may increase the risks of first dose effect and renal intolerance due to the introduction of the ACE inhibitors. Sodium 35-41 angiotensin I converting enzyme Homo sapiens 149-152 8302404-4 1993 In essential hypertension a negative correlation found between changes in EPO and PRA levels in response to sodium restriction and upright body position may also reflect an altered regulation of both EPO and renin production. Sodium 108-114 erythropoietin Homo sapiens 200-203 8302404-4 1993 In essential hypertension a negative correlation found between changes in EPO and PRA levels in response to sodium restriction and upright body position may also reflect an altered regulation of both EPO and renin production. Sodium 108-114 renin Homo sapiens 208-213 1492537-3 1992 The mean basal plasma vasopressin value in the patients (0.6 +/- 0.1 pmol/l) was significantly lower than that in the normal subjects (2.9 +/- 0.3 pmol/l; p < 0.01), whereas the mean serum sodium, plasma osmolality, plasma renin activity and serum aldosterone values were similar in the two groups. Sodium 192-198 arginine vasopressin Homo sapiens 22-33 8322536-5 1993 Animal experiments have shown that rapid increases of the sodium concentration in the renal artery will cause a reduction of renal blood flow (RBF), glomerular filtration rate (GFR) and inhibition of renin secretion, particularly during states of sodium chloride or volume depletion (i.e. with high plasma renin activity). Sodium 58-64 renin Homo sapiens 200-205 8322536-5 1993 Animal experiments have shown that rapid increases of the sodium concentration in the renal artery will cause a reduction of renal blood flow (RBF), glomerular filtration rate (GFR) and inhibition of renin secretion, particularly during states of sodium chloride or volume depletion (i.e. with high plasma renin activity). Sodium 58-64 renin Homo sapiens 306-311 1336310-2 1992 These include both the biochemical effect of VP-stimulated adenosine 3",5"-cyclic monophosphate (cAMP) formation in the CCT and physiological effects of VP-mediated sodium and water retention. Sodium 165-171 arginine vasopressin Rattus norvegicus 153-155 1471538-6 1992 In conclusion, increased A II sensitivity caused by chronic sodium deficiency in AN patients normalized over time as the patients recovered. Sodium 60-66 angiotensinogen Homo sapiens 25-29 1477846-6 1992 Most sodium abnormalities in patients with CNS disease result from altered water excretion secondary to disturbed release of antidiuretic hormone (ADH). Sodium 5-11 arginine vasopressin Homo sapiens 125-145 1483400-2 1992 Elevated levels of insulin play an important role in sodium retention in renal tubules. Sodium 53-59 insulin Homo sapiens 19-26 1294423-3 1992 Venous plasma concentrations of ANP were also studied in relation to urinary sodium and potassium excretion, as well as the renin-angiotensin-aldosterone system. Sodium 77-83 natriuretic peptide A Homo sapiens 32-35 1477846-6 1992 Most sodium abnormalities in patients with CNS disease result from altered water excretion secondary to disturbed release of antidiuretic hormone (ADH). Sodium 5-11 arginine vasopressin Homo sapiens 147-150 1363310-0 1992 Potentiation by m-cresol on transepithelial sodium transport across frog skin induced by insulin. Sodium 44-50 insulin Homo sapiens 89-96 1334976-1 1992 Renal proximal tubule sodium reabsorption is enhanced by apical or basolateral angiotensin II (AII). Sodium 22-28 angiotensinogen Rattus norvegicus 79-93 1334976-1 1992 Renal proximal tubule sodium reabsorption is enhanced by apical or basolateral angiotensin II (AII). Sodium 22-28 angiotensinogen Rattus norvegicus 95-98 22217827-7 1992 Captopril, an inhibitor of angiotensin-I converting enzyme, abolished the enhancing effects of the low sodium regimen on P450scc and P450c18 mRNA levels. Sodium 103-109 angiotensin I converting enzyme Rattus norvegicus 27-58 22217827-15 1992 A-II appears to participate in the mechanism of action of the low sodium intake at this level. Sodium 66-72 angiotensinogen Rattus norvegicus 0-4 1300562-3 1992 The aim of the study was to determine whether and in what extent patients with HA and healthy subjects differ in EPO secretion and whether EPO serum level is related in this patients to renin response to dietary sodium restriction and upright position of the body. Sodium 212-218 erythropoietin Homo sapiens 139-142 1300562-3 1992 The aim of the study was to determine whether and in what extent patients with HA and healthy subjects differ in EPO secretion and whether EPO serum level is related in this patients to renin response to dietary sodium restriction and upright position of the body. Sodium 212-218 renin Homo sapiens 186-191 1448828-7 1992 RESULTS: The arginine vasopressin V1 receptor antagonist and atrial natriuretic peptide significantly (p < 0.05) reduced water and sodium contents in the posterior edematous regions. Sodium 134-140 arginine vasopressin Rattus norvegicus 22-33 1442767-1 1992 Atrial natriuretic factor (ANF) is released from the cardiac atrium in response to stretch and acts through receptors to cause an increase in urinary flow and sodium excretion, vasodilatation, and a reduction in blood volume. Sodium 159-165 natriuretic peptide A Homo sapiens 0-25 1442767-1 1992 Atrial natriuretic factor (ANF) is released from the cardiac atrium in response to stretch and acts through receptors to cause an increase in urinary flow and sodium excretion, vasodilatation, and a reduction in blood volume. Sodium 159-165 natriuretic peptide A Homo sapiens 27-30 1457079-0 1992 Relationship of the renin-angiotensin system and systemic arterial pressure to sodium excretion during atrial natriuretic peptide infusion in men. Sodium 79-85 renin Homo sapiens 20-25 1451221-6 1992 Fractional distal reabsorption of sodium was suppressed from 89.7 +/- 2.8% to 82.1 +/- 5.0% by the hANP, but not by the nicardipine infusion. Sodium 34-40 natriuretic peptide A Homo sapiens 99-103 1363310-2 1992 In this study we found that insulin mixed with m-cresol, normally used as pharmaceutical preparation, shows an earlier and larger stimulating effect on transepithelial sodium transport than insulin alone. Sodium 168-174 insulin Homo sapiens 28-35 1473613-4 1992 Low- and high-dose insulin infusions were followed by a fall in sodium clearance from 1.6 +/- 0.1 ml/min to 1.2 +/- 0.1 and 1.0 +/- 0.1 ml/min, respectively. Sodium 64-70 insulin Homo sapiens 19-26 1473613-6 1992 The distal antinatriuretic effect of insulin was associated with dose- and time-dependent decline in proximal tubular sodium reabsorption. Sodium 118-124 insulin Homo sapiens 37-44 1473613-9 1992 The results also suggest that decreased proximal sodium reabsorption may be a compensatory mechanism counteracting the insulin-induced sodium retention. Sodium 49-55 insulin Homo sapiens 119-126 1473613-9 1992 The results also suggest that decreased proximal sodium reabsorption may be a compensatory mechanism counteracting the insulin-induced sodium retention. Sodium 135-141 insulin Homo sapiens 119-126 1428116-7 1992 The efficacy of angiotensin converting enzyme inhibitors in attenuating proteinuria and experimental glomerular disease may be dependent on sodium intake. Sodium 140-146 angiotensin I converting enzyme Rattus norvegicus 16-45 1428117-1 1992 Endothelin-1 inhibits sodium and water transport systems in the inner medullary collecting duct. Sodium 22-28 endothelin 1 Rattus norvegicus 0-12 1428117-2 1992 Endothelin-1 levels are reduced in the medulla of spontaneously hypertensive rats (SHR), raising the possibility that decreased inner medullary collecting duct production of endothelin-1 could contribute to inappropriate sodium and water retention. Sodium 221-227 endothelin 1 Rattus norvegicus 174-186 1402927-1 1992 The sodium dependence of binding of [3H]-paroxetine, a selective serotonin uptake inhibitor, to the serotonin transporter in rat diencephalon was studied in both brain membranes and tissue sections and compared with that of 5-[3H]hydroxytryptamine ([3H]5-HT) uptake by synaptosomes from the same region. Sodium 4-10 solute carrier family 6 member 4 Rattus norvegicus 100-121 1450929-1 1992 Facial motoneurones of the rat respond to arginine vasopressin by generating a voltage-dependent inward current which is sodium-dependent and is resistant to tetrodotoxin. Sodium 121-127 arginine vasopressin Rattus norvegicus 51-62 1336524-1 1992 OBJECTIVE: The present study examines the role of alpha 1-adrenoceptors in determining the renal haemodynamic and sodium excretory responses to a physiological dose of angiotensin II in man. Sodium 114-120 angiotensinogen Homo sapiens 168-182 1336524-8 1992 Angiotensin II alone also increased fractional reabsorption of sodium delivered to the distal nephron, as evaluated by both the CLi method and by estimation of solute-free water clearance. Sodium 63-69 angiotensinogen Homo sapiens 0-14 1336524-10 1992 CONCLUSIONS: These findings suggest that low doses of circulating angiotensin II are able to modulate UNaV by increasing sodium reabsorption in the proximal and, to some extent, the distal nephron segment in man. Sodium 121-127 angiotensinogen Homo sapiens 66-80 1460897-0 1992 [Influence of arterial pressure and plasma renin activity on tubular reabsorption of sodium]. Sodium 85-91 renin Homo sapiens 43-48 1414888-6 1992 Several experimental and clinical findings suggest that reversal of cardiovascular structural changes secondary to cardiovascular disease and enhancement of renal sodium excretion by ACE inhibitors are important long-term antihypertensive actions possibly mediated by inhibition of the tissue RAS. Sodium 163-169 angiotensin I converting enzyme Homo sapiens 183-186 1327601-6 1992 By inhibiting this potent vasoconstrictor and suppressing its degradation of the powerful vasodilator bradykinin, and by promoting sodium and water excretion, ACE inhibitors contribute to the restoration of normal ventricular function. Sodium 131-137 angiotensin I converting enzyme Homo sapiens 159-162 1490249-0 1992 Role of sodium and water excretion in the antihypertensive effect of vasopressin in the spontaneously hypertensive rat. Sodium 8-14 arginine vasopressin Rattus norvegicus 69-80 1490249-8 1992 Sodium excretion rates increased during the infusions of vasopressin to a greater extent in SHR than in WKY. Sodium 0-6 arginine vasopressin Rattus norvegicus 57-68 1450370-1 1992 The relationship of blood pressure sensitivity to sodium with plasma insulin concentration was examined in young adult (22 to 28 yr) blacks (N = 45). Sodium 50-56 insulin Homo sapiens 69-76 1450370-5 1992 The correlation of fasting plasma insulin concentration with blood pressure or blood pressure sensitivity to sodium was not statistically significant. Sodium 109-115 insulin Homo sapiens 34-41 1457758-8 1992 It is suggested that the cardiorenal complications of diabetes mellitus may be linked to reduced insulin sensitivity, which itself is associated with hypertension, raised sodium-lithium countertransport rates, and cardiovascular disease. Sodium 171-177 insulin Homo sapiens 97-104 1450370-6 1992 There was a significant correlation (after adjustment for adiposity) of blood pressure sensitivity to sodium with both the sum of insulin (r = 0.41; P < 0.01) and the 60-min plasma insulin concentration during the OGTT. Sodium 102-108 insulin Homo sapiens 130-137 1450370-6 1992 There was a significant correlation (after adjustment for adiposity) of blood pressure sensitivity to sodium with both the sum of insulin (r = 0.41; P < 0.01) and the 60-min plasma insulin concentration during the OGTT. Sodium 102-108 insulin Homo sapiens 184-191 1284077-4 1992 Increasing [Ca2+]o from 2.5 to 5 mM or above and substituting external sodium with either sucrose, choline or Li+ induced an oscillatory transient inward current (TI) which peaked 200-300 ms after repolarization from a previous depolarizing pulse. Sodium 71-77 carbonic anhydrase 2 Oryctolagus cuniculus 12-15 1401084-2 1992 Angiotensin II may directly influence renal hemodynamics, glomerular contractility, and tubular sodium reabsorption, thereby promoting sodium and fluid retention in this syndrome. Sodium 96-102 angiotensinogen Rattus norvegicus 0-14 1401084-2 1992 Angiotensin II may directly influence renal hemodynamics, glomerular contractility, and tubular sodium reabsorption, thereby promoting sodium and fluid retention in this syndrome. Sodium 135-141 angiotensinogen Rattus norvegicus 0-14 1289611-4 1992 According to Taugner et al., sodium depletion induces the extension of renin positive part of afferent arterioles from vascular pole toward interlobular artery. Sodium 29-35 LOW QUALITY PROTEIN: renin Oryctolagus cuniculus 71-76 1472949-8 1992 IGF-I binding was inhibited by a variety of salts in a dose-dependent manner, calcium and magnesium salts being more effective than sodium or potassium salts. Sodium 132-138 insulin like growth factor 1 Homo sapiens 0-5 1289611-8 1992 2. whether sodium depletion affects the gradient of tissue renin content within the cortex. Sodium 11-17 LOW QUALITY PROTEIN: renin Oryctolagus cuniculus 59-64 1289611-12 1992 The absolute difference in renin content among the three types of afferent arterioles becomes greater during sodium depletion. Sodium 109-115 LOW QUALITY PROTEIN: renin Oryctolagus cuniculus 27-32 1289612-5 1992 Basal renin release per afferent arteriole decreases steeply from superficial to midcortical to juxtamedullary afferent arterioles during both normal and low sodium intake. Sodium 158-164 LOW QUALITY PROTEIN: renin Oryctolagus cuniculus 6-11 1289612-7 1992 Isoproterenol (1.6 x 10(-4)M) significantly stimulates renin release from all three types of arterioles on either diet; however, only in the superficial arterioles is the increase (delta) greater with dietary sodium restriction. Sodium 209-215 LOW QUALITY PROTEIN: renin Oryctolagus cuniculus 55-60 1438100-8 1992 Insulin induces sodium retention and increases the aldosterone-secreting effect of angiotensin II. Sodium 16-22 insulin Homo sapiens 0-7 1418958-0 1992 Intracerebroventricular angiotensin II-induced thirst and sodium appetite in rat are blocked by the AT1 receptor antagonist, Losartan (DuP 753), but not by the AT2 antagonist, CGP 42112B. Sodium 58-64 angiotensinogen Rattus norvegicus 24-38 1327650-9 1992 The leucocyte ouabain-sensitive sodium efflux rate constant was decreased in both patients with acromegaly and patients with growth hormone deficiency, and there was no correlation with basal energy expenditure, fasting plasma insulin level or serum growth hormone level. Sodium 32-38 growth hormone 1 Homo sapiens 125-139 1505472-0 1992 Increases in cellular sodium concentration by arginine vasopressin and endothelin in cultured rat glomerular mesangial cells. Sodium 22-28 arginine vasopressin Rattus norvegicus 55-66 1505472-1 1992 The present study was undertaken to determine whether arginine vasopressin (AVP), angiotensin-II, and endothelin (ET) increase the cellular sodium concentration ([Na+]i) in cultured rat glomerular mesangial cells. Sodium 140-146 arginine vasopressin Rattus norvegicus 63-74 1505472-1 1992 The present study was undertaken to determine whether arginine vasopressin (AVP), angiotensin-II, and endothelin (ET) increase the cellular sodium concentration ([Na+]i) in cultured rat glomerular mesangial cells. Sodium 140-146 angiotensinogen Rattus norvegicus 82-96 1516945-3 1992 As the major regulator of arterial blood pressure and sodium balance, the renin axis supports normotension or hypertension via angiotensin-mediated vasoconstriction and angiotensin plus aldosterone-induced renal sodium retention. Sodium 54-60 renin Homo sapiens 74-79 1516945-7 1992 Excess plasma renin activity for the sodium balance is created by nephron heterogeneity in which a subpopulation of ischemic nephrons hypersecretes renin and retains sodium. Sodium 37-43 renin Homo sapiens 14-19 1516945-7 1992 Excess plasma renin activity for the sodium balance is created by nephron heterogeneity in which a subpopulation of ischemic nephrons hypersecretes renin and retains sodium. Sodium 37-43 renin Homo sapiens 148-153 1516945-7 1992 Excess plasma renin activity for the sodium balance is created by nephron heterogeneity in which a subpopulation of ischemic nephrons hypersecretes renin and retains sodium. Sodium 166-172 renin Homo sapiens 14-19 1518704-1 1992 To determine if physiologic changes of insulin are capable of inducing sodium retention in insulin-resistant patients, we evaluated the ability of an oral glucose tolerance test to alter urine sodium excretion in 32 obese subjects (13.3 +/- 1 years, weight 82 +/- 5 kg, mean arterial pressure 89.3 +/- 1.5 mm Hg) and 13 nonobese subjects (13.8 +/- 2 years, weight 46 +/- 4 kg, mean arterial pressure 74.5 +/- 2.6 mm Hg). Sodium 71-77 insulin Homo sapiens 39-46 1395105-0 1992 Atrial natriuretic peptide in pregnancy: response to oral sodium supplementation. Sodium 58-64 natriuretic peptide A Homo sapiens 0-26 1395105-3 1992 Previous studies in non-pregnant subjects have suggested that plasma atrial natriuretic peptide (ANP) increases in response to dietary sodium supplementation because of an increase in plasma volume, although this has not been measured directly. Sodium 135-141 natriuretic peptide A Homo sapiens 69-95 1395105-3 1992 Previous studies in non-pregnant subjects have suggested that plasma atrial natriuretic peptide (ANP) increases in response to dietary sodium supplementation because of an increase in plasma volume, although this has not been measured directly. Sodium 135-141 natriuretic peptide A Homo sapiens 97-100 1395105-13 1992 Pregnant women respond to increased dietary sodium with an increase in plasma ANP in the absence of a significant increase in plasma volume. Sodium 44-50 natriuretic peptide A Homo sapiens 78-81 1395105-14 1992 The acute regulation of plasma ANP in response to increases in dietary sodium in pregnant women does not appear to be mediated by changes in intravascular fluid volume. Sodium 71-77 natriuretic peptide A Homo sapiens 31-34 1328362-1 1992 OBJECTIVE: The aim was to study the physiological effects of angiotensin II upon the glomerular and tubular handling of sodium. Sodium 120-126 angiotensinogen Homo sapiens 61-75 1328362-6 1992 Angiotensin II caused an extensive and instantaneous fall in both urinary flow and urinary sodium excretion. Sodium 91-97 angiotensinogen Homo sapiens 0-14 1328362-9 1992 However, when the distal reabsorption was related to the delivery of sodium from the proximal tubules, distal fractional reabsorption in fact increased after 30 min angiotensin II infusion. Sodium 69-75 angiotensinogen Homo sapiens 165-179 1328362-14 1992 The antinatriuretic effect of angiotensin II is caused initially by a combination of a decrease in the GFR and an increase in proximal fractional sodium reabsorption, and later by the enhanced distal fractional reabsorption of sodium. Sodium 146-152 angiotensinogen Homo sapiens 30-44 1328362-14 1992 The antinatriuretic effect of angiotensin II is caused initially by a combination of a decrease in the GFR and an increase in proximal fractional sodium reabsorption, and later by the enhanced distal fractional reabsorption of sodium. Sodium 227-233 angiotensinogen Homo sapiens 30-44 1457334-4 1992 This review concentrates on the effects of GH (derived from either pituitary or recombinant technology) and IGF-1 in three main areas: (1) sodium and water homeostasis; (2) calcium and phosphate balance, bone density and interactions with mineral regulating hormones; (3) fat and lean body mass. Sodium 139-145 growth hormone 1 Homo sapiens 43-45 1280836-7 1992 The permeabilities for sodium, potassium and caesium are similar, consistent with the channel being a fairly non-selective cation channel. Sodium 23-29 transient receptor potential cation channel, subfamily V, member 1 Mus musculus 123-137 1388959-7 1992 In conclusion, our study shows that hyperinsulinemia, decreased sensitivity to insulin, and low levels of HDL cholesterol were most commonly seen in hypertensive subjects with a low sodium sensitivity. Sodium 182-188 insulin Homo sapiens 41-48 1388962-0 1992 The influence of age on renal function and renin and aldosterone responses to sodium-volume expansion and contraction in normotensive and mildly hypertensive humans. Sodium 78-84 renin Homo sapiens 43-48 1529664-6 1992 These results indicate that cerebrospinal fluid is subject to modest chronic and acute changes in osmolality and sodium concentration which may contribute to the osmotic control of AVP secretion. Sodium 113-119 arginine vasopressin Rattus norvegicus 181-184 1325505-1 1992 OBJECTIVE AND DESIGN: The present study was designed to determine whether increases in sodium concentration in the cerebrospinal fluid (CSF) play a role in the augmented hypertension induced by long-term salt loading in spontaneously hypertensive rats (SHR), and whether the enhanced arginine vasopressin (AVP) activity and/or the sympathetic nervous system contribute to the increased hypertension. Sodium 87-93 arginine vasopressin Rattus norvegicus 293-304 1387296-2 1992 This ANP-like material increases sodium output from the gill and kidney while inhibiting sodium uptake in the gut. Sodium 33-39 atrial natriuretic peptide Oncorhynchus mykiss 5-8 1387296-2 1992 This ANP-like material increases sodium output from the gill and kidney while inhibiting sodium uptake in the gut. Sodium 89-95 atrial natriuretic peptide Oncorhynchus mykiss 5-8 1366263-12 1992 Thus, elevations in circulating aldosterone and angiotensin II, relative to sodium intake, have the potential to not only alter sodium homeostasis and vascular tonicity, but also the structure of cardiovascular tissue. Sodium 128-134 angiotensinogen Homo sapiens 48-62 11193277-18 2000 CONCLUSION: During norepinephrine infusion, increasing doses of dopamine from 2 to 6 microg x kg(-1) x min(-1) augments CO, diuresis and sodium excretion in patients treated for septic shock, without changes in creatinine clearance. Sodium 137-143 CD59 molecule (CD59 blood group) Homo sapiens 103-109 1325519-8 1992 When the SSC patients became SST with sodium loading, serum sodium and plasma arginine vasopressin decreased and haematocrit increased, suggesting that the excretion of sodium and water accompanied with a decrease in circulating plasma volume may be responsible for the hemodynamic alteration from SSC to SST. Sodium 38-44 arginine vasopressin Homo sapiens 87-98 1516724-3 1992 The present study, therefore, was undertaken to clarify the role of insulin on renal sodium handling and sympatho-adrenal function in overweight NT. Sodium 85-91 insulin Homo sapiens 68-75 1519421-0 1992 Relationship between plasma growth hormone concentration and cellular sodium transport in acromegaly. Sodium 70-76 growth hormone 1 Homo sapiens 28-42 1519421-1 1992 We investigated the relationship between mean plasma growth hormone (GH) concentration and cellular sodium transport in untreated and treated acromegaly. Sodium 100-106 growth hormone 1 Homo sapiens 53-67 1519421-1 1992 We investigated the relationship between mean plasma growth hormone (GH) concentration and cellular sodium transport in untreated and treated acromegaly. Sodium 100-106 growth hormone 1 Homo sapiens 69-71 1519421-5 1992 In patients with active acromegaly there was a significant positive correlation between IGF-1 and cellular sodium transport, while GH tended to show a negative relationship to the same parameter. Sodium 107-113 insulin like growth factor 1 Homo sapiens 88-93 1519421-6 1992 After successful treatment, both IGF-1 and GH disclosed a positive relationship to cellular sodium transport. Sodium 92-98 insulin like growth factor 1 Homo sapiens 33-38 1519421-6 1992 After successful treatment, both IGF-1 and GH disclosed a positive relationship to cellular sodium transport. Sodium 92-98 growth hormone 1 Homo sapiens 43-45 1519421-8 1992 In conclusion, if this is a generalized phenomenon the results are compatible with a sodium-retaining effect of GH via stimulation of transmembrane sodium transport. Sodium 85-91 growth hormone 1 Homo sapiens 112-114 1519421-8 1992 In conclusion, if this is a generalized phenomenon the results are compatible with a sodium-retaining effect of GH via stimulation of transmembrane sodium transport. Sodium 148-154 growth hormone 1 Homo sapiens 112-114 1519421-9 1992 In active acromegaly this may be counteracted by a sodium transport inhibitor giving the reverse relationship between GH and cellular sodium transport. Sodium 51-57 growth hormone 1 Homo sapiens 118-120 1391635-8 1992 Optical melting curves of the molecules of set 1 were collected as a function of sodium ion concentration from 30 to 120 mM. Sodium 81-87 SET domain containing 1A, histone lysine methyltransferase Homo sapiens 43-48 1322161-0 1992 Low sodium intake enhances sensitivity of 11-deoxycortisol and deoxycorticosterone to ACTH in ACTH-suppressed normal subjects. Sodium 4-10 proopiomelanocortin Homo sapiens 86-90 1322161-0 1992 Low sodium intake enhances sensitivity of 11-deoxycortisol and deoxycorticosterone to ACTH in ACTH-suppressed normal subjects. Sodium 4-10 proopiomelanocortin Homo sapiens 94-98 1507727-3 1992 Only in the AH group, urinary excretion of calcium (u-Ca) was strongly correlated to that of sodium (u-Na) in pre-load of h-PTH, and both increments were also correlated in post-load of h-PTH. Sodium 93-99 parathyroid hormone Homo sapiens 124-127 1437998-4 1992 When zinc insulin (hexamers) and sodium insulin (dimers) were subjected to alpha-chymotryptic degradation, a 3.2-fold difference in the apparent first-order rate constants was observed (zinc insulin being slower than sodium insulin), representing the intrinsic difference in the concentration of total associated species in solution (three times). Sodium 33-39 insulin Homo sapiens 40-47 1437998-4 1992 When zinc insulin (hexamers) and sodium insulin (dimers) were subjected to alpha-chymotryptic degradation, a 3.2-fold difference in the apparent first-order rate constants was observed (zinc insulin being slower than sodium insulin), representing the intrinsic difference in the concentration of total associated species in solution (three times). Sodium 33-39 insulin Homo sapiens 40-47 1437998-4 1992 When zinc insulin (hexamers) and sodium insulin (dimers) were subjected to alpha-chymotryptic degradation, a 3.2-fold difference in the apparent first-order rate constants was observed (zinc insulin being slower than sodium insulin), representing the intrinsic difference in the concentration of total associated species in solution (three times). Sodium 33-39 insulin Homo sapiens 40-47 1437998-6 1992 A maximum increase of 5.4-fold was observed for zinc insulin at a 30 mM NaGC concentration and a 2.1-fold increase was noted for sodium insulin at 10 mM NaGC, both values being close to the theoretical numbers of 6- and 2-fold as predicted by the complete dissociation of hexamers and dimers to monomers. Sodium 129-135 insulin Homo sapiens 136-143 1507492-7 1992 The excretion of ADH in a day was in the urine of diabetic patients positively correlated with HbA1, urinary osmolarity and concentration of sodium in urine, although the pathological meaning of the observed ADH hypersecretion in the development of diabetic complications is currently unknown. Sodium 141-147 arginine vasopressin Homo sapiens 17-20 1499138-0 1992 Serum triglyceride and insulin levels are associated with erythrocyte sodium-lithium counter-transport activity in normoglycaemic individuals. Sodium 70-76 insulin Homo sapiens 23-30 1499138-3 1992 The relationship between erythrocyte sodium-lithium counter-transport activity and concentrations of serum triglycerides, HDL components, insulin and additionally alcohol consumption, could reflect the influence of those variables on erythrocyte structure and function. Sodium 37-43 insulin Homo sapiens 138-145 1597135-0 1992 Dietary potassium supplementation and sodium restriction stimulate aldosterone synthase but not 11 beta-hydroxylase P-450 messenger ribonucleic acid accumulation in rat adrenals and require angiotensin II production. Sodium 38-44 angiotensinogen Rattus norvegicus 190-204 1592449-5 1992 In high-sodium rats, endothelin-1 produced a significant increase in mean arterial pressure and total peripheral resistance; a significant bradycardia was observed only on the first day after the start of the endothelin-1 infusion. Sodium 8-14 endothelin 1 Rattus norvegicus 21-33 1592449-9 1992 The hypertension produced by endothelin-1 infusion cannot be explained by alterations in salt or water balance since endothelin-1 infusion in high sodium animals produced significant increases in mean arterial pressure with no observable changes in water or electrolyte balance. Sodium 147-153 endothelin 1 Rattus norvegicus 117-129 1376811-4 1992 Intrarenal arterial infusion of ET-1 (1.0 ng/kg/min) decreased the baseline level of renal blood flow by 25% and that of urinary excretion of sodium by 54-69% but did not alter basal levels of NE secretion rate. Sodium 142-148 endothelin 1 Canis lupus familiaris 32-36 1376357-0 1992 Substance P produces sodium and bicarbonate secretion in porcine jejunal mucosa through an action on enteric neurons. Sodium 21-27 tachykinin precursor 1 Homo sapiens 0-11 1321309-2 1992 Our experimental studies in normal subjects show that ACTH reproducibly increases blood pressure in association with a rise in cardiac output, plasma and extracellular fluid volumes and exchangeable sodium. Sodium 199-205 proopiomelanocortin Homo sapiens 54-58 1509119-4 1992 Recent research indicates that the urothelium in male rats is damaged under conditions of high urinary pH and sodium levels by a mechanism that involves alpha 2u-globulin and possibly silicate crystalluria. Sodium 110-116 alpha2u globulin Rattus norvegicus 153-170 1319542-4 1992 In response to hANP, patients with HbA1 greater than 8.5% had decreased responses of urinary volume and sodium excretion in comparison to patients with HbA1 less than 8.5% (p less than 0.05) in whom renal responses to hANP did not differ from controls. Sodium 104-110 natriuretic peptide A Homo sapiens 15-19 1319542-6 1992 Impaired renal responses to hANP in diabetes patients with insufficient glycemic control apparently contribute to the mechanisms of diabetic sodium retention. Sodium 141-147 natriuretic peptide A Homo sapiens 28-32 1374402-9 1992 The structural features of the AT3 receptor, including two additional potential phosphorylation sites for protein kinase C, could be related to the distinctive binding properties of the adrenal and vascular receptors and to their differential regulation during altered sodium intake. Sodium 269-275 angiotensin II receptor, type 1b Rattus norvegicus 31-34 1317125-5 1992 Dietary sodium deprivation (0.003 meq/g) and excess (1.34 meq/g) for 7 days significantly (P less than 0.01) increased and decreased renal ANG I (296 +/- 30 and 82.6 +/- 15.8 vs. 161 +/- 18 fmol/g) and ANG II (216 +/- 16 and 45.6 +/- 11.8 vs. 98 +/- 16 fmol/g) contents, respectively. Sodium 8-14 angiotensinogen Rattus norvegicus 202-208 1317125-7 1992 ACE activity was significantly upregulated by sodium deprivation in both kidney (44% increase) and plasma (30% increase). Sodium 46-52 angiotensin I converting enzyme Rattus norvegicus 0-3 1590489-8 1992 At the level of the proximal tubules of the reptilian-type nephrons, prolactin infusion caused a slight reduction in the net reabsorption of sodium and chloride. Sodium 141-147 prolactin Homo sapiens 69-78 1317764-7 1992 The fall in fractional sodium excretion during angiotensin II infusion was reduced after pretreatment with 750 mg of lithium [750 mg of lithium, 2.73 (0.24) to 1.34 (0.08)%; placebo, 2.69 (0.26) to 1.01 (0.11)%; P = 0.02]. Sodium 23-29 angiotensinogen Homo sapiens 47-61 1533193-1 1992 In insulin-dependent diabetes (IDDM), an overactivity of sodium-lithium countertransport (Na+/Li+ CT) has been associated with the risk of nephropathy and hypertension, two conditions of insulin resistance. Sodium 57-63 insulin Homo sapiens 3-10 1381766-7 1992 Baseline urinary sodium excretion was less in the heart failure group (13.3 +/- 14.0 vs. 53.7 +/- 37.3 mumol/min, p less than 0.01) and ANF induced a smaller increase in urinary sodium excretion (22.1 +/- 32.3 mumol/min, p less than 0.05 vs. 305.7 +/- 242.9 mumol/min, p less than 0.001). Sodium 17-23 natriuretic peptide A Homo sapiens 136-139 1381766-7 1992 Baseline urinary sodium excretion was less in the heart failure group (13.3 +/- 14.0 vs. 53.7 +/- 37.3 mumol/min, p less than 0.01) and ANF induced a smaller increase in urinary sodium excretion (22.1 +/- 32.3 mumol/min, p less than 0.05 vs. 305.7 +/- 242.9 mumol/min, p less than 0.001). Sodium 178-184 natriuretic peptide A Homo sapiens 136-139 1534832-0 1992 Responses of atrial natriuretic factor to long-term sodium restriction in mild to moderate hypertension. Sodium 52-58 natriuretic peptide A Homo sapiens 13-38 1534832-7 1992 These results suggest that in mildly to moderately hypertensive subjects long-term sodium restriction decreases high plasma ANF concentrations concomitantly with regression of concentric left ventricular hypertrophy, probably as a result of changes in haemodynamics. Sodium 83-89 natriuretic peptide A Homo sapiens 124-127 1319517-14 1992 Although the data that have been gathered to date allowed us to draw some careful conclusions as to the (patho)physiological role of ANF, the exact place of ANF in sodium homeostatic control must still be better defined. Sodium 164-170 natriuretic peptide A Homo sapiens 157-160 1535400-2 1992 Theoretically, reversal of the sodium-retaining effect of angiotensin II (Ang II) could be involved. Sodium 31-37 angiotensinogen Homo sapiens 58-72 1535400-2 1992 Theoretically, reversal of the sodium-retaining effect of angiotensin II (Ang II) could be involved. Sodium 31-37 angiotensinogen Homo sapiens 74-80 1535400-11 1992 The fact that felodipine reverses sodium retention on exogenous Ang II may be explained by interference with systemic and renal hemodynamic effects of exogenous Ang II. Sodium 34-40 angiotensinogen Homo sapiens 64-70 1411248-4 1992 Treated patients were divided on the basis of their mean overall out-patient clinic (OC) DBP decrease in the sitting position during the 6 months (monthly measurements) into sodium-sensitive (DBP decrease greater than 10 mmHg, n = 17), indeterminate (DBP decrease 5-10 mmHg, n = 18) and sodium-resistant (DBP decrease less than 5 mmHg, n = 8) subgroups. Sodium 174-180 D-box binding PAR bZIP transcription factor Homo sapiens 192-195 1411248-4 1992 Treated patients were divided on the basis of their mean overall out-patient clinic (OC) DBP decrease in the sitting position during the 6 months (monthly measurements) into sodium-sensitive (DBP decrease greater than 10 mmHg, n = 17), indeterminate (DBP decrease 5-10 mmHg, n = 18) and sodium-resistant (DBP decrease less than 5 mmHg, n = 8) subgroups. Sodium 174-180 D-box binding PAR bZIP transcription factor Homo sapiens 192-195 1411248-4 1992 Treated patients were divided on the basis of their mean overall out-patient clinic (OC) DBP decrease in the sitting position during the 6 months (monthly measurements) into sodium-sensitive (DBP decrease greater than 10 mmHg, n = 17), indeterminate (DBP decrease 5-10 mmHg, n = 18) and sodium-resistant (DBP decrease less than 5 mmHg, n = 8) subgroups. Sodium 174-180 D-box binding PAR bZIP transcription factor Homo sapiens 192-195 1411248-5 1992 At 6 months the level of DBP in the supine position was lower than at baseline in both sensitive and resistant subgroups, whereas in the standing position a lower DBP than at baseline was seen only in the sodium-sensitive subgroup. Sodium 205-211 D-box binding PAR bZIP transcription factor Homo sapiens 163-166 1411248-7 1992 Our data suggest that posture should be included in the concept of sodium sensitivity and that an orthostatic test is useful in the prediction of seated and standing DBP decrease produced by moderate, long-term sodium restriction. Sodium 211-217 D-box binding PAR bZIP transcription factor Homo sapiens 166-169 1580276-1 1992 Angiotensin II plays an important role in the kidney by regulating renal flow, glomerular filtration rate, mesangial cell function, and sodium reabsorption. Sodium 136-142 angiotensinogen Homo sapiens 0-14 1582493-2 1992 During the first month of life, increased retention of sodium is present in the SHR which appears to be mediated by the renin-angiotensin system. Sodium 55-61 renin Homo sapiens 120-125 1516268-15 1992 It is concluded that intrarenal AII acts to maintain optimal matching of fluid reabsorption and filtered load in response to changes in sodium balance, as well as to promote acidification of the urine during acidosis and perhaps to potentiate tubular growth following renal injury. Sodium 136-142 angiotensinogen Homo sapiens 32-35 1532566-2 1992 Recumbent plasma renin activity was low during normal sodium intake (135 mmol daily), and the response to upright posture or to low sodium diet (10 mmol daily) was blunted. Sodium 54-60 renin Homo sapiens 17-22 1380591-0 1992 Effects of isradipine on plasma renin activity in sodium-loaded and -depleted conscious rabbits. Sodium 50-56 LOW QUALITY PROTEIN: renin Oryctolagus cuniculus 32-37 1316400-7 1992 Plasma ANP increased significantly on the high- compared with low-sodium diet. Sodium 66-72 natriuretic peptide A Homo sapiens 7-10 1387432-1 1992 Insulin-dependent diabetic patients have a large exchangeable body sodium pool, secondary to sodium retention. Sodium 67-73 insulin Homo sapiens 0-7 1387432-1 1992 Insulin-dependent diabetic patients have a large exchangeable body sodium pool, secondary to sodium retention. Sodium 93-99 insulin Homo sapiens 0-7 1387432-4 1992 Eight insulin-dependent diabetic patients had significantly higher daily sodium excretion rate (147 +/- 16 mmol/day; mean +/- SE) during conventional insulin treatment (daily plasma glucose: 11.6 +/- 1.2 mmol/liter; daily plasma insulin: 27 +/- 3 microU/ml) than during intensified insulin treatment (daily sodium excretion rate: 91 +/- 12, P less than 0.01; daily plasma glucose: 6.8 +/- 0.7, P less than 0.01; daily plasma insulin: 44 +/- 4, P less than 0.01). Sodium 73-79 insulin Homo sapiens 6-13 1387432-4 1992 Eight insulin-dependent diabetic patients had significantly higher daily sodium excretion rate (147 +/- 16 mmol/day; mean +/- SE) during conventional insulin treatment (daily plasma glucose: 11.6 +/- 1.2 mmol/liter; daily plasma insulin: 27 +/- 3 microU/ml) than during intensified insulin treatment (daily sodium excretion rate: 91 +/- 12, P less than 0.01; daily plasma glucose: 6.8 +/- 0.7, P less than 0.01; daily plasma insulin: 44 +/- 4, P less than 0.01). Sodium 73-79 insulin Homo sapiens 150-157 1387432-4 1992 Eight insulin-dependent diabetic patients had significantly higher daily sodium excretion rate (147 +/- 16 mmol/day; mean +/- SE) during conventional insulin treatment (daily plasma glucose: 11.6 +/- 1.2 mmol/liter; daily plasma insulin: 27 +/- 3 microU/ml) than during intensified insulin treatment (daily sodium excretion rate: 91 +/- 12, P less than 0.01; daily plasma glucose: 6.8 +/- 0.7, P less than 0.01; daily plasma insulin: 44 +/- 4, P less than 0.01). Sodium 73-79 insulin Homo sapiens 150-157 1387432-4 1992 Eight insulin-dependent diabetic patients had significantly higher daily sodium excretion rate (147 +/- 16 mmol/day; mean +/- SE) during conventional insulin treatment (daily plasma glucose: 11.6 +/- 1.2 mmol/liter; daily plasma insulin: 27 +/- 3 microU/ml) than during intensified insulin treatment (daily sodium excretion rate: 91 +/- 12, P less than 0.01; daily plasma glucose: 6.8 +/- 0.7, P less than 0.01; daily plasma insulin: 44 +/- 4, P less than 0.01). Sodium 73-79 insulin Homo sapiens 150-157 1387432-4 1992 Eight insulin-dependent diabetic patients had significantly higher daily sodium excretion rate (147 +/- 16 mmol/day; mean +/- SE) during conventional insulin treatment (daily plasma glucose: 11.6 +/- 1.2 mmol/liter; daily plasma insulin: 27 +/- 3 microU/ml) than during intensified insulin treatment (daily sodium excretion rate: 91 +/- 12, P less than 0.01; daily plasma glucose: 6.8 +/- 0.7, P less than 0.01; daily plasma insulin: 44 +/- 4, P less than 0.01). Sodium 73-79 insulin Homo sapiens 150-157 1387432-4 1992 Eight insulin-dependent diabetic patients had significantly higher daily sodium excretion rate (147 +/- 16 mmol/day; mean +/- SE) during conventional insulin treatment (daily plasma glucose: 11.6 +/- 1.2 mmol/liter; daily plasma insulin: 27 +/- 3 microU/ml) than during intensified insulin treatment (daily sodium excretion rate: 91 +/- 12, P less than 0.01; daily plasma glucose: 6.8 +/- 0.7, P less than 0.01; daily plasma insulin: 44 +/- 4, P less than 0.01). Sodium 307-313 insulin Homo sapiens 6-13 1387432-5 1992 Daily sodium excretion rate was also significantly lower (107 +/- 13, P less than 0.01) in the same diabetic patients during intensified insulin treatment along with hyperglycemic clamp (daily plasma glucose: 12.8 +/- 0.3, NS; plasma insulin 48 +/- 4, P less than 0.01). Sodium 6-12 insulin Homo sapiens 137-144 1387432-5 1992 Daily sodium excretion rate was also significantly lower (107 +/- 13, P less than 0.01) in the same diabetic patients during intensified insulin treatment along with hyperglycemic clamp (daily plasma glucose: 12.8 +/- 0.3, NS; plasma insulin 48 +/- 4, P less than 0.01). Sodium 6-12 insulin Homo sapiens 234-241 1385969-6 1992 The second group shows the elevated ANP levels with a positive sodium balance. Sodium 63-69 natriuretic peptide A Homo sapiens 36-39 1385969-10 1992 There is a statistically significant negative correlation between sodium balance and the ANP level. Sodium 66-72 natriuretic peptide A Homo sapiens 89-92 1315019-3 1992 Although it has been presumed that the response to AVP results from augmented sodium transport, there is controversy whether AVP actually does affect sodium transport in mammalian lung epithelium. Sodium 78-84 arginine vasopressin Homo sapiens 51-54 1315019-4 1992 To determine if AVP or aldosterone could alone or together augment sodium transport in the perinatal lung, we studied primary cultures of fetal rat distal lung epithelium in Ussing chambers. Sodium 67-73 arginine vasopressin Rattus norvegicus 16-19 1319570-0 1992 Interleukin-2 inhibits sodium currents in human muscle cells. Sodium 23-29 interleukin 2 Homo sapiens 0-13 1371890-6 1992 Furthermore, TNF formed pH-dependent, voltage-dependent, ion-permeable channels in planar lipid bilayer membranes and increased the sodium permeability of human U937 histiocytic lymphoma cells. Sodium 132-138 tumor necrosis factor Homo sapiens 13-16 1538559-4 1992 MAIN OUTCOME MEASURES: Renin was analyzed as plasma renin activity and as a renin index (logarithm of 24-hour urinary sodium excretion times logarithm of plasma renin activity) (593 patients at baseline and 6 months) to correct for varied sodium intakes. Sodium 118-124 renin Homo sapiens 23-28 1538559-4 1992 MAIN OUTCOME MEASURES: Renin was analyzed as plasma renin activity and as a renin index (logarithm of 24-hour urinary sodium excretion times logarithm of plasma renin activity) (593 patients at baseline and 6 months) to correct for varied sodium intakes. Sodium 118-124 renin Homo sapiens 76-81 1538559-4 1992 MAIN OUTCOME MEASURES: Renin was analyzed as plasma renin activity and as a renin index (logarithm of 24-hour urinary sodium excretion times logarithm of plasma renin activity) (593 patients at baseline and 6 months) to correct for varied sodium intakes. Sodium 118-124 renin Homo sapiens 76-81 1538559-4 1992 MAIN OUTCOME MEASURES: Renin was analyzed as plasma renin activity and as a renin index (logarithm of 24-hour urinary sodium excretion times logarithm of plasma renin activity) (593 patients at baseline and 6 months) to correct for varied sodium intakes. Sodium 239-245 renin Homo sapiens 23-28 1538559-12 1992 As with the weight loss diet, patients on a low sodium/high potassium diet in the highest baseline renin index quartile had a greater reduction in DBP than patients in the lowest baseline renin index quartile. Sodium 48-54 renin Homo sapiens 99-104 1538559-12 1992 As with the weight loss diet, patients on a low sodium/high potassium diet in the highest baseline renin index quartile had a greater reduction in DBP than patients in the lowest baseline renin index quartile. Sodium 48-54 renin Homo sapiens 188-193 1387480-2 1992 It has been assumed that restricted sodium excretion with the kidneys during fasting is mainly caused by activation of the renin-angiotensin-aldosterone system, with ANP contributing to it, insulin not playing the major role in this process. Sodium 36-42 renin Homo sapiens 123-128 1513778-4 1992 Sodium excretion was detected only if ACE had been blocked. Sodium 0-6 angiotensin I converting enzyme Rattus norvegicus 38-41 1310991-6 1992 In order to test the hypothesis regarding the association of B creatine kinase with sodium transport, we examined the creatine kinase enzymes in the rectal (salt-secreting) gland of the dogfish shark which contains high levels of the Na+/K(+)-ATPase. Sodium 84-90 creatine kinase B Homo sapiens 61-78 1310991-14 1992 The conservation of creatine kinase isoform expression in excretory tissue, and the localization of creatine kinase immunoreactivity in the basal region of the tubule cells, demonstrate that subcellular compartmentation of B creatine kinase may underly the functional coupling of creatine kinase activity with sodium transport. Sodium 310-316 creatine kinase B Homo sapiens 223-240 1531869-6 1992 The results suggest that ANP may play a role in the regulation of impaired water and sodium homeostasis in toxemic pregnancy. Sodium 85-91 natriuretic peptide A Homo sapiens 25-28 1316834-3 1992 The aim of this study was to determine the relationship between plasma ANP, cGMP excretion (cGMPex) and sodium excretion (Naex) in preterm infants in the first days after birth. Sodium 104-110 natriuretic peptide A Homo sapiens 71-74 1733729-13 1992 Furthermore, these data underline the importance of an interaction between regulation of PRL secretion and water and sodium homeostasis. Sodium 117-123 prolactin Rattus norvegicus 89-92 1735594-5 1992 The low sodium diet and enalapril increased renin in the d-AF (53.1 +/- 6.9 and 68.4 +/- 8.1, respectively) but not in the GL (3.3 +/- 1.0 and 3.6 +/- 0.7). Sodium 8-14 LOW QUALITY PROTEIN: renin Oryctolagus cuniculus 44-49 1735598-5 1992 The renin-angiotensin-aldosterone system was significantly less activated with women in the supine position in pregnancy-induced hypertensive and chronic hypertensive women; however, as opposed to pregnancy-induced hypertensive women, those with chronic hypertension reassumed their humoral response to upright posture, which was accompanied by a significant reduction in sodium excretion. Sodium 372-378 renin Homo sapiens 4-9 1543532-9 1992 While sodium depletion of sheep caused a rise in renin mRNA in the kidney, adrenalectomy also led to a large increase in renal renin mRNA. Sodium 6-12 renin Ovis aries 49-54 1639459-12 1992 In the urine, the ratio of the fractional excretion of potassium to that of sodium was decreased by both oral glucose (-22%, p less than 0.01) and ACE inhibition (-21%, p less than 0.001). Sodium 76-82 angiotensin I converting enzyme Homo sapiens 147-150 1639461-7 1992 Exogenous insulin induced a similar reduction in fractional sodium excretion in normotensive and hypertensive diabetics (43 +/- 5.9% and 48 +/- 16.4% during the low insulin dose and 57 +/- 9.1% and 62 +/- 12.5% during the high insulin dose, respectively). Sodium 60-66 insulin Homo sapiens 10-17 1556167-9 1992 We discuss these results in terms of a model where sodium ions entering the compartment between the tubular membrane and the SR junctional membrane carry counter charges through the SR K+ channels and help to maintain the SR Ca2+ release. Sodium 51-57 ribosomal protein S6 kinase B2 Homo sapiens 182-186 1620579-3 1992 In cells expressing the oncogene, but not in NIH fibroblasts not expressing the oncogene, bradykinin elicits calcium oscillations, which are detected by fura-2 fluorescence and amplified by a decrease of extracellular sodium activity. Sodium 218-224 kininogen 1 Homo sapiens 90-100 1531798-8 1992 Although blood pressure was not changed significantly, the enhanced response of ADH to a sodium and volume load may play a role in part in the pathophysiology of EHT. Sodium 89-95 arginine vasopressin Homo sapiens 80-83 1635890-4 1992 And prior episodes of sodium depletion produce enhancements of subsequent salt appetites, but only if the prior depletions were accompanied by angiotensin II and aldosterone action. Sodium 22-28 angiotensinogen Rattus norvegicus 143-157 1315588-1 1992 Hypertensive obese subjects with glucose intolerance have hyperinsulinaemia, insulin resistance and intracellular cation imbalance resulting in increased sodium content. Sodium 154-160 insulin Homo sapiens 63-70 1317974-0 1992 [Effect of intracerebroventricular injections of ANG II and ANG II antibody on renal sodium excretion and Na+.K(+)-ATPase in rat]. Sodium 85-91 angiotensinogen Rattus norvegicus 49-55 1317974-0 1992 [Effect of intracerebroventricular injections of ANG II and ANG II antibody on renal sodium excretion and Na+.K(+)-ATPase in rat]. Sodium 85-91 angiotensinogen Rattus norvegicus 60-66 1317974-2 1992 microinjection of angiotensin II (ANG II) in a dose of 16 pg evoked a significant increase in renal sodium excretion which began within 15 min and lasted for 90 min. Sodium 100-106 angiotensinogen Rattus norvegicus 18-32 1317974-2 1992 microinjection of angiotensin II (ANG II) in a dose of 16 pg evoked a significant increase in renal sodium excretion which began within 15 min and lasted for 90 min. Sodium 100-106 angiotensinogen Rattus norvegicus 34-40 1352037-1 1992 The 98 amino acid (a.a.) N-terminus of the 126 a.a. atrial natriuretic factor (ANF) prohormone contains three peptides consisting of a.a. 1-30 (proANF 1-30), a.a. 31-67 (proANF 31-67) and a.a. 79-98 (proANF 79-98) with blood pressure lowering, sodium and/or potassium excreting properties similar to atrial natriuretic factor (a.a. 99-126, C-terminus of prohormone). Sodium 244-250 natriuretic peptide A Homo sapiens 52-77 1352037-1 1992 The 98 amino acid (a.a.) N-terminus of the 126 a.a. atrial natriuretic factor (ANF) prohormone contains three peptides consisting of a.a. 1-30 (proANF 1-30), a.a. 31-67 (proANF 31-67) and a.a. 79-98 (proANF 79-98) with blood pressure lowering, sodium and/or potassium excreting properties similar to atrial natriuretic factor (a.a. 99-126, C-terminus of prohormone). Sodium 244-250 natriuretic peptide A Homo sapiens 79-82 1370468-5 1992 With sodium as the current vehicle, conductance is increased by voltage, insulin (Km = 5 +/- 0.6 x 10(-9) M), and hydrolyzable guanine nucleotides. Sodium 5-11 insulin Homo sapiens 73-80 1370468-8 1992 These findings in the reconstituted system were verified in patch-clamped whole muscle cells where an insulin and cGMP-dependent sodium current inhibited by mu-conotoxin could be demonstrated. Sodium 129-135 insulin Homo sapiens 102-109 1633072-7 1992 Activity of the renin-angiotensin system is associated with sodium and water retention and plasma volume expansion. Sodium 60-66 renin Homo sapiens 16-21 1581516-1 1992 Sodium-23 Nuclear Magnetic Resonance relaxation spectroscopy has been used to investigate the state of intracellular Na+ in control and CCl4-treated rat livers. Sodium 0-6 C-C motif chemokine ligand 4 Rattus norvegicus 136-140 1540848-5 1992 But ANG II action within the AV3V might be important for the rapid burst of sodium intake that immediately follows a period of depletion. Sodium 76-82 angiotensinogen Rattus norvegicus 4-10 1330385-1 1992 19-hydroxy-androstenedione (19-OH-A), a C19 steroid, is an amplifier of the sodium retaining action of aldosterone under the control of ACTH and renin-angiotensin system. Sodium 76-82 proopiomelanocortin Homo sapiens 136-140 1330385-1 1992 19-hydroxy-androstenedione (19-OH-A), a C19 steroid, is an amplifier of the sodium retaining action of aldosterone under the control of ACTH and renin-angiotensin system. Sodium 76-82 renin Homo sapiens 145-150 1728438-2 1992 BACKGROUND: The participation of the renin-angiotensin system in the control of blood pressure in normal, sodium-replete subjects is not clear. Sodium 106-112 renin Homo sapiens 37-42 1426693-2 1992 Using aspirated gastric juice, we measured sodium ion concentration, bile acid levels and phospholipase A2 activity and found that sodium ion levels increase along with these other standard markers during DGR. Sodium 131-137 phospholipase A2 group IB Homo sapiens 90-106 1284147-2 1992 Several mechanisms have been proposed to explain hyperinsulinemia, insulin resistance and its relationship to hypertension; reduced sodium excretion, activation of the sympathetic nervous system, increased activity of the sodium/hydrogen pump, and stimulation of cellular growth. Sodium 222-228 insulin Homo sapiens 54-61 1733582-1 1992 With electrolyte reference fluid (ERF)00, results from Kodak Ektachem slides for the direct potentiometric assay of sodium in plasma were significantly correlated with results from flame photometry, but also appeared to be systematically higher, especially in hypernatremic patients. Sodium 116-122 ETS2 repressor factor Homo sapiens 34-37 1309326-0 1992 pH dependence of inhibition of arginine vasopressin-induced adenosine 3",5"-monophosphate production by cellular sodium depletion in rat renal inner medullary collecting duct cells in culture. Sodium 113-119 arginine vasopressin Rattus norvegicus 40-51 1730458-0 1992 Effects of insulin on renal sodium excretion. Sodium 28-34 insulin Homo sapiens 11-18 1730458-1 1992 The ability of insulin to decrease urinary sodium excretion has been recognized for more than 30 years. Sodium 43-49 insulin Homo sapiens 15-22 1730458-4 1992 Data from amphibian transporting epithelia suggest a potential for interactions between insulin and several other peptide hormones in the regulation of sodium transport. Sodium 152-158 insulin Homo sapiens 88-95 1730458-5 1992 The following discussion attempts to review our knowledge of the effects of insulin on renal sodium reabsorption and describes new data suggesting that insulin"s antinatriuretic response is dependent on antidiuretic hormone but independent of the angiotensin and prostaglandin systems. Sodium 93-99 insulin Homo sapiens 152-159 1739390-1 1992 Plasma sodium concentration depends on water balance, and is normally maintained in a narrow range by an integrated system involving the precise regulation of water intake via thirst mechanism and control of water output via vasopressin secretion. Sodium 7-13 arginine vasopressin Homo sapiens 225-236 1493845-3 1992 Plasma renin activity and aldosterone concentration both fell significantly when sodium intake was increased; plasma angiotensin II concentration also fell, but not significantly. Sodium 81-87 renin Homo sapiens 7-12 1493845-8 1992 The 5-HT2 receptor antagonist ketanserin (1 mumol.l-1 in vitro) reduced the extent of aggregation induced by 5 mumol.l-1 ADP after the volunteers had taken a high sodium diet, whereas the angiotensin II receptor antagonist saralasin (1 nmol.l-1) increased the rate of aggregation after the low sodium diet. Sodium 163-169 5-hydroxytryptamine receptor 2A Homo sapiens 4-18 1493845-8 1992 The 5-HT2 receptor antagonist ketanserin (1 mumol.l-1 in vitro) reduced the extent of aggregation induced by 5 mumol.l-1 ADP after the volunteers had taken a high sodium diet, whereas the angiotensin II receptor antagonist saralasin (1 nmol.l-1) increased the rate of aggregation after the low sodium diet. Sodium 294-300 5-hydroxytryptamine receptor 2A Homo sapiens 4-18 1309874-0 1992 The acute renal actions of angiotensin converting enzyme inhibitors in the sodium-depleted conscious primate are mediated by inhibition of the renin-angiotensin system. Sodium 75-81 angiotensin-converting enzyme Callithrix jacchus 27-56 1312549-5 1992 METHODS: The renal sites of ANF action were established by simultaneous measurements of 51Cr-ethylenediaminetetraacetate lithium and sodium clearances. Sodium 133-139 natriuretic peptide A Homo sapiens 28-31 1312549-11 1992 The renal effects of ANF administration were characterized by an unaltered GFR and significant increases in the renal clearances of lithium (a marker of end-proximal fluid delivery) and sodium when compared with vehicle infusions, whereas urine flow did not change. Sodium 186-192 natriuretic peptide A Homo sapiens 21-24 1312549-15 1992 CONCLUSIONS: These results indicate that even small increases in plasma ANF, as can be found during physiological conditions, induce natriuresis in patients with essential hypertension by enhancing fluid delivery from the proximal tubules, in addition to impairing distal fractional sodium reabsorption. Sodium 283-289 natriuretic peptide A Homo sapiens 72-75 1309874-1 1992 The purpose of this study was to determine if the changes in renal function acutely produced by an inhibitor of angiotensin converting enzyme (ACE) in the sodium-depleted conscious marmoset can be explained primarily by blockade of the renin-angiotensin system. Sodium 155-161 angiotensin-converting enzyme Callithrix jacchus 112-141 1309874-1 1992 The purpose of this study was to determine if the changes in renal function acutely produced by an inhibitor of angiotensin converting enzyme (ACE) in the sodium-depleted conscious marmoset can be explained primarily by blockade of the renin-angiotensin system. Sodium 155-161 angiotensin-converting enzyme Callithrix jacchus 143-146 1331894-1 1992 The antinatriuretic effect of angiotensin II (Ang II) is generally attributed to a decreased glomerular filtration rate (GFR) and an increased proximal tubular sodium reabsorption. Sodium 160-166 angiotensinogen Homo sapiens 30-44 1331894-1 1992 The antinatriuretic effect of angiotensin II (Ang II) is generally attributed to a decreased glomerular filtration rate (GFR) and an increased proximal tubular sodium reabsorption. Sodium 160-166 angiotensinogen Homo sapiens 46-52 1331894-9 1992 These data suggest that the antinatriuretic effect of modestly hypertensive dosages of Ang II is not only due to a decrease in GFR and an increase in proximal sodium reabsorption, but also involves a rise in fractional reabsorption in a distal nephron segment. Sodium 159-165 angiotensinogen Homo sapiens 87-93 1412440-10 1992 Pre-treatment with the calcium entry blocker nitrendipine enhanced the natriuretic effect of atrial natriuretic factor (ANF) in sodium replete normal volunteers. Sodium 128-134 natriuretic peptide A Homo sapiens 93-118 1553017-0 1992 Sodium depletion enhances the antiproteinuric effect of ACE inhibition in established experimental nephrosis. Sodium 0-6 angiotensin I converting enzyme Homo sapiens 56-59 1412440-10 1992 Pre-treatment with the calcium entry blocker nitrendipine enhanced the natriuretic effect of atrial natriuretic factor (ANF) in sodium replete normal volunteers. Sodium 128-134 natriuretic peptide A Homo sapiens 120-123 1412440-11 1992 Facilitation of sodium excretion by human ANF may be an additional diuretic mechanism of calcium entry blockers. Sodium 16-22 natriuretic peptide A Homo sapiens 42-45 1412446-5 1992 Both Ang II and ANP receptors are modulated by alterations in sodium and fluid intake, and the peptides themselves. Sodium 62-68 angiotensinogen Homo sapiens 5-11 1412446-5 1992 Both Ang II and ANP receptors are modulated by alterations in sodium and fluid intake, and the peptides themselves. Sodium 62-68 natriuretic peptide A Homo sapiens 16-19 1767828-0 1991 Insulin resistance is associated with high sodium-lithium countertransport in essential hypertension. Sodium 43-49 insulin Homo sapiens 0-7 1410425-4 1992 It is likely that in response to hypertonicity they signal the SON and PVN to release vasopressin and elsewhere to elicit other osmoregulatory responses such as thirst and the excretion of sodium. Sodium 189-195 arginine vasopressin Rattus norvegicus 86-97 1836728-2 1991 The ANG II-induced decrease glomerular size (36%) and (18%) in low and normal-sodium rats, respectively. Sodium 78-84 angiotensinogen Rattus norvegicus 4-10 1686388-6 1991 The DNA polymorphisms detected in the growth hormone skeletal muscle sodium channel complex (GH1-SCN4A) and by flanking polymorphic markers (D17S74 and D17S40) demonstrated no recombinants between the disease phenotypes and this complex. Sodium 69-75 growth hormone 1 Homo sapiens 93-96 1836308-6 1991 Evidence that the kidneys produce their own natriuretic peptide may partly explain why investigations of the effects of endogenous atriopeptin on renal sodium excretion often have yielded inconsistent results. Sodium 152-158 natriuretic peptide A Homo sapiens 131-142 1659502-15 1991 3) In this preparation the major part of excitation-induced sodium fluxes are mediated by the Na-Ca exchanger, with only a relatively small direct participation of sodium channels. Sodium 60-66 solute carrier family 8 member A1 Rattus norvegicus 94-109 1954673-10 1991 We conclude 1) that intracellular calcium induces Na-Na exchange through the Na-Ca exchanger in sodium-loaded cells exposed to calcium; and 2) that Na-Na exchange can be activated by calcium that enters the cell through calcium channels. Sodium 96-102 solute carrier family 8 member A1 Rattus norvegicus 77-92 1284137-6 1992 The reasons for the association of insulin resistance and essential hypertension can be sought in at least four general types of mechanisms: sodium retention, sympathetic nervous system overactivity, disturbed membrane ion transport, and proliferation of vascular smooth-muscle cells. Sodium 141-147 insulin Homo sapiens 35-42 1284139-8 1992 Other actions of insulin, such as the transport of ions, (e.g., sodium and potassium), synthesis of insulin-like growth factor-binding proteins, translocation of transporter proteins, and regulation of enzyme activities, are much more difficult to quantify. Sodium 64-70 insulin Homo sapiens 17-24 1797446-6 1991 During infusion of low doses of VIP (0.1 and 0.4 nmol/h per 200 g), a small increase in fractional and absolute excretion of sodium occurred but this did not differ from that occurring in the time control group. Sodium 125-131 vasoactive intestinal peptide Rattus norvegicus 32-35 1797446-7 1991 In the high dose VIP group (1.2 nmol/h per 200 g), significant falls occurred in MAP and GFR, and absolute sodium excretion fell (though not significantly) from its baseline level. Sodium 107-113 vasoactive intestinal peptide Rattus norvegicus 17-20 1797446-9 1991 These findings suggest that systemic VIP has no net natriuretic effect in the rat, but produces haemodynamic changes associated with reduced sodium excretion at high doses. Sodium 141-147 vasoactive intestinal peptide Rattus norvegicus 37-40 1659502-18 1991 An undetermined part of the calcium-dependent sodium fluxes, however, could be a direct Na-Na exchange through the activated Na-Ca exchanger. Sodium 46-52 solute carrier family 8 member A1 Rattus norvegicus 125-140 1778597-5 1991 These results suggest a profound effect of dietary sodium intake on the pulsatile pattern of aldosterone secretion, particularly in normal PRA essential hypertension. Sodium 51-57 S100 calcium binding protein A6 Homo sapiens 139-142 1813374-6 1991 Last, we show that this excess sodium intake is abolished by intracerebroventricular captopril thereby suggesting that it is caused by activation of cerebral angiotensin II and harmonizing its mechanism with current concepts. Sodium 31-37 angiotensinogen Rattus norvegicus 158-172 1761331-8 1991 However, in the erect position, which is associated with even further increases in activity of the renin angiotensin aldosterone system, the reduction in diuresis and natriuresis that a fall in glomerular filtration rate would cause is offset by abolition of the rise in sodium retaining hormones, angiotensin II and aldosterone that mediate the antinatriuretic effect of the erect position. Sodium 271-277 renin Homo sapiens 99-104 1835959-7 1991 Plasma renin activity was suppressed by treatment on the low but not on the high sodium diet (p less than 0.05). Sodium 81-87 renin Homo sapiens 7-12 1791616-5 1991 Insulin may be a vascular growth factor as well as a local hormone facilitating a rise in intracellular sodium concentration. Sodium 104-110 insulin Homo sapiens 0-7 1836003-0 1991 ANF and the renin-angiotensin system in the regulation of sodium balance: longitudinal studies in experimental heart failure. Sodium 58-64 natriuretic peptide A Homo sapiens 0-3 1836003-0 1991 ANF and the renin-angiotensin system in the regulation of sodium balance: longitudinal studies in experimental heart failure. Sodium 58-64 renin Homo sapiens 12-17 1836003-1 1991 Over the last three decades the role of the renin-aldosterone axis for the renal conservation of sodium has become well established. Sodium 97-103 renin Homo sapiens 44-49 1836003-2 1991 In the last several years information has accumulated to indicate that ANF is an important complementary hormonal system involved in the elimination of sodium surfeit. Sodium 152-158 natriuretic peptide A Homo sapiens 71-74 1836003-3 1991 Evidence has been presented to suggest that ANF and the renin-aldosterone axis function in an integrated manner for the regulation of sodium balance, with their primary actions exerted in the postprandial and postabsorptive phases, respectively. Sodium 134-140 natriuretic peptide A Homo sapiens 44-47 1836003-3 1991 Evidence has been presented to suggest that ANF and the renin-aldosterone axis function in an integrated manner for the regulation of sodium balance, with their primary actions exerted in the postprandial and postabsorptive phases, respectively. Sodium 134-140 renin Homo sapiens 56-61 1836003-5 1991 The significance of ANF as a compensatory mechanism in chronic heart failure remains to be fully elucidated, although the available longitudinal data in experimental animal models suggest that the role of ANF in the maintenance of sodium balance should be most apparent during the early and mild stages of heart failure, before a marked reduction in cardiac performance leads to an excessive activation of the renin-aldosterone axis that in turn can effectively override the natriuretic actions of ANF. Sodium 231-237 natriuretic peptide A Homo sapiens 205-208 1836003-5 1991 The significance of ANF as a compensatory mechanism in chronic heart failure remains to be fully elucidated, although the available longitudinal data in experimental animal models suggest that the role of ANF in the maintenance of sodium balance should be most apparent during the early and mild stages of heart failure, before a marked reduction in cardiac performance leads to an excessive activation of the renin-aldosterone axis that in turn can effectively override the natriuretic actions of ANF. Sodium 231-237 natriuretic peptide A Homo sapiens 205-208 1661645-10 1991 Clinical signs of sodium retention were evident during the first 3 months of treatment with recombinant human growth hormone. Sodium 18-24 growth hormone 1 Homo sapiens 110-124 1834440-13 1991 The infusion of ANF did not affect MAP, but it increased urine output (16.1 +/- 5.0 ml/min, when the data obtained during the 30-min infusion and a 30-min period after the infusion were combined) and urinary sodium excretion (1,651 +/- 514 microEq/min) significantly (p less than 0.05 and p less than 0.01, respectively) as compared with the corresponding values of 3.3 +/- 1.1 ml/min and 386 +/- 141 microEq/min after placebo. Sodium 208-214 natriuretic peptide A Homo sapiens 16-19 1824254-6 1991 The direct interaction of the IFN with GM-CFC was confirmed by showing its ability to rapidly activate the sodium/hydrogen antiport in GM-CFC, as do the mitogens GM-CSF, M-CSF, and IL-3. Sodium 107-113 interferon alpha 1 Homo sapiens 30-33 1824254-7 1991 However, the effect of IFN-gamma on intracellular pH and DNA synthesis was transient and pretreatment with IFN markedly inhibited the ability of GM-CSF, M-CSF, and IL-3 to activate the sodium/hydrogen antiport. Sodium 185-191 interferon gamma Homo sapiens 23-32 1824254-7 1991 However, the effect of IFN-gamma on intracellular pH and DNA synthesis was transient and pretreatment with IFN markedly inhibited the ability of GM-CSF, M-CSF, and IL-3 to activate the sodium/hydrogen antiport. Sodium 185-191 interferon alpha 1 Homo sapiens 23-26 1959623-3 1991 This study shows, based on parallel experiments studying [Na+]i, [Ca2+]i and vasopressin secretion, that sodium acts directly to regulate secretion in isolated nerve endings from the rat neurohypophysis. Sodium 105-111 arginine vasopressin Rattus norvegicus 77-88 1661645-12 1991 We conclude that treatment with recombinant human growth hormone in adults with growth hormone deficiency resulted in small increases in left ventricular pre-load, due to the sodium-retaining action of growth hormone. Sodium 175-181 growth hormone 1 Homo sapiens 50-64 1661645-12 1991 We conclude that treatment with recombinant human growth hormone in adults with growth hormone deficiency resulted in small increases in left ventricular pre-load, due to the sodium-retaining action of growth hormone. Sodium 175-181 growth hormone 1 Homo sapiens 80-94 1937665-1 1991 The present study investigated the effect of the anion accompanying sodium on the development of angiotensin II-induced hypertension in rats and the role of the sympathetic nervous system and extracellular fluid volume in its mechanism. Sodium 68-74 angiotensinogen Rattus norvegicus 97-111 1937678-8 1991 Thus, these individuals have an enhanced adrenal response to Ang II under circumstances in which it should be reduced, thereby leading to lower renin levels and a tendency toward sodium retention. Sodium 179-185 angiotensinogen Homo sapiens 61-67 1937665-3 1991 High dietary intake of sodium chloride significantly augmented the angiotensin II-induced hypertension (mean blood pressure on day 13, 165 +/- 6 versus 142 +/- 6 mm Hg, p less than 0.05), but equimolar sodium loading provided as sodium citrate failed to enhance angiotensin II hypertension (140 +/- 6 mm Hg). Sodium 23-29 angiotensinogen Rattus norvegicus 67-81 1937678-9 1991 The second group has the opposite defect; that is, on a low sodium diet, they have a reduced adrenal response to Ang II. Sodium 60-66 angiotensinogen Homo sapiens 113-119 1937665-3 1991 High dietary intake of sodium chloride significantly augmented the angiotensin II-induced hypertension (mean blood pressure on day 13, 165 +/- 6 versus 142 +/- 6 mm Hg, p less than 0.05), but equimolar sodium loading provided as sodium citrate failed to enhance angiotensin II hypertension (140 +/- 6 mm Hg). Sodium 23-29 angiotensinogen Rattus norvegicus 262-276 1937678-11 1991 The sodium sensitivity of their blood pressure arises not from the adrenal abnormality but from the associated defect in sodium-dependent, Ang II-mediated changes in renal blood flow. Sodium 4-10 angiotensinogen Homo sapiens 139-145 1937678-11 1991 The sodium sensitivity of their blood pressure arises not from the adrenal abnormality but from the associated defect in sodium-dependent, Ang II-mediated changes in renal blood flow. Sodium 121-127 angiotensinogen Homo sapiens 139-145 1937678-6 1991 In normal subjects, the response of the adrenal glomerulosa cell to Ang II varies with the level of sodium intake, with sodium restriction enhancing the response. Sodium 100-106 angiotensinogen Homo sapiens 68-74 1937681-10 1991 The resultant renal vasoconstriction limits the distal tubular delivery of sodium and water, thus maximizing the water-retaining effect of vasopressin and impairing the normal escape from the sodium-retaining effects of aldosterone. Sodium 75-81 arginine vasopressin Homo sapiens 139-150 1937678-6 1991 In normal subjects, the response of the adrenal glomerulosa cell to Ang II varies with the level of sodium intake, with sodium restriction enhancing the response. Sodium 120-126 angiotensinogen Homo sapiens 68-74 1666809-1 1991 Parathyroid hormone (1-34) [PTH-(1-34)] has been shown to stimulate sodium-dependent phosphate transport (NaPiT) in UMR-106 osteoblast-like cells through a cAMP-dependent mechanism. Sodium 68-74 parathyroid hormone Rattus norvegicus 28-31 1741989-4 1991 However, if adequate volume is unavailable because of sodium restriction, sustained activation of the renin-angiotensin system increases blood pressure sufficiently to restore nephron perfusion. Sodium 54-60 renin Homo sapiens 102-107 1805062-2 1991 The results obtained showed that not only the increased function of the renin-angiotensin-aldosterone system, but the higher activity of the sympathoadrenal system in the presence of weakened adrenocortical glucocorticoid and epiphyseal functions late in CCI played a role in the mechanisms responsible for sodium retention in the patients with the disease. Sodium 307-313 renin Homo sapiens 72-77 1808355-3 1991 Angiotensin II was recognized as the key regulator of renal sodium excretion, because it reduced the urinary Na/K ratio. Sodium 60-66 angiotensinogen Homo sapiens 0-14 1835288-1 1991 PURPOSE: Sodium retention in cirrhosis has been attributed to an imbalance between vasoconstrictive antinatriuretic forces such as the sympathetic nervous system and vasodilatory natriuretic agents such as atrial natriuretic factor (ANF). Sodium 9-15 natriuretic peptide A Homo sapiens 206-231 1764632-6 1991 On the other hand, prolactin significantly increased the plasma 45Ca content by 57, 42 and 28% at 5, 15 and 30 min respectively, when the electrolyte solution contained sodium. Sodium 169-175 prolactin Rattus norvegicus 19-28 1764632-8 1991 Compared with the saline control, the plasma 45Ca content in prolactin treated animals was significantly elevated by 63% at 5 min when the test solution was a sodium-free electrolyte solution. Sodium 159-165 prolactin Rattus norvegicus 61-70 1741989-5 1991 Thus, depending upon the availability of volume, renal perfusion and sodium balance can be restored either by volume retention or by increased angiotensin II (ANGII) formation and peripheral vasoconstriction. Sodium 69-75 angiotensinogen Homo sapiens 143-157 1741989-5 1991 Thus, depending upon the availability of volume, renal perfusion and sodium balance can be restored either by volume retention or by increased angiotensin II (ANGII) formation and peripheral vasoconstriction. Sodium 69-75 angiotensinogen Homo sapiens 159-164 1914196-3 1991 The plasma renin value directly reflects the presence and degree of renin-mediated vasoconstriction, and, inversely, defines the predominance of sodium-related vasoconstriction. Sodium 145-151 renin Homo sapiens 11-16 1928340-0 1991 Dissociation in plasma renin and adrenal ANG II and aldosterone responses to sodium restriction in rats. Sodium 77-83 angiotensinogen Rattus norvegicus 41-47 1838024-2 1991 A number of nephron segments may contribute to the ANP-induced natriuresis; however, this review will focus on the cellular mechanisms of ANP inhibition of electrogenic sodium reabsorption by the inner medullary collecting duct. Sodium 169-175 natriuretic peptide A Homo sapiens 138-141 1838024-7 1991 These cGMP-dependent mechanisms inhibiting sodium reabsorption across the inner medullary collecting duct account for a substantial component of the natriuresis following a rise in ANP levels. Sodium 43-49 natriuretic peptide A Homo sapiens 181-184 1838025-1 1991 Endogenous atrial natriuretic factor (ANF) serves a functional role to maintain sodium homeostasis and inhibit activation of the renin-angiotensin-aldosterone system in acute congestive heart failure despite arterial hypotension. Sodium 80-86 natriuretic peptide A Homo sapiens 11-36 1838025-1 1991 Endogenous atrial natriuretic factor (ANF) serves a functional role to maintain sodium homeostasis and inhibit activation of the renin-angiotensin-aldosterone system in acute congestive heart failure despite arterial hypotension. Sodium 80-86 natriuretic peptide A Homo sapiens 38-41 1838025-3 1991 This relative deficiency of ANF results in a progressive inability to excrete sodium and antagonize the renin-angiotensin-aldosterone system. Sodium 78-84 natriuretic peptide A Homo sapiens 28-31 1838025-7 1991 In addition, agents that selectively bind to biologically inactive ANF clearance receptors increase endogenous plasma ANF and promote increases in renal sodium excretion. Sodium 153-159 natriuretic peptide A Homo sapiens 67-70 1838027-1 1991 The identification of the atrial natriuretic peptides (ANP) as a new hormonal system has provided a new perspective on the mechanisms controlling renal sodium excretion and abnormalities in sodium homeostasis. Sodium 152-158 natriuretic peptide A Homo sapiens 55-58 1838027-1 1991 The identification of the atrial natriuretic peptides (ANP) as a new hormonal system has provided a new perspective on the mechanisms controlling renal sodium excretion and abnormalities in sodium homeostasis. Sodium 190-196 natriuretic peptide A Homo sapiens 55-58 1838027-2 1991 The present article focuses on the potential importance of ANP (ANF 99-126) in essential hypertension with particular reference to circulating ANP levels and the relationship between the ANP and the renin-angiotensin system in the control of sodium balance and blood pressure. Sodium 242-248 natriuretic peptide A Homo sapiens 59-62 1838027-2 1991 The present article focuses on the potential importance of ANP (ANF 99-126) in essential hypertension with particular reference to circulating ANP levels and the relationship between the ANP and the renin-angiotensin system in the control of sodium balance and blood pressure. Sodium 242-248 renin Homo sapiens 199-204 1838027-5 1991 This is further supported by studies during alterations in dietary sodium intake, as sodium restriction high-lighted important relationships between ANP and the renin angiotensin system. Sodium 67-73 natriuretic peptide A Homo sapiens 149-152 1838027-5 1991 This is further supported by studies during alterations in dietary sodium intake, as sodium restriction high-lighted important relationships between ANP and the renin angiotensin system. Sodium 85-91 natriuretic peptide A Homo sapiens 149-152 1838027-5 1991 This is further supported by studies during alterations in dietary sodium intake, as sodium restriction high-lighted important relationships between ANP and the renin angiotensin system. Sodium 85-91 renin Homo sapiens 161-166 1914196-8 1991 Conversely, low-renin equally hypertensive patients have relatively more sodium volume and are less vasoconstricted; they are generally responsive to natriuretic drugs (e.g., diuretics or calcium antagonists) and appear relatively protected from vascular sequelae such as stroke and heart attack. Sodium 73-79 renin Homo sapiens 16-21 1914197-4 1991 Patients with severe hypertension, especially that associated with end-stage renal disease, tended to respond with moderate increases in blood pressure and plasma AVP after sodium overload and had a modest blood pressure fall (10-20 mmHg) in response to a single intravenous bolus of the AVP antagonist. Sodium 173-179 arginine vasopressin Homo sapiens 163-166 1914203-5 1991 The chief instruments of this strategy are the renin-sodium profile and the response of plasma renin activity and blood pressure to specific antirenin system drugs. Sodium 53-59 renin Homo sapiens 47-52 1914203-10 1991 In our present state of knowledge, the basic diagnostic biochemical workup includes the renin-sodium profile and the 24-h urinary sodium, potassium, and microalbumin excretion rates. Sodium 94-100 renin Homo sapiens 88-93 1959244-10 1991 However, high-renin patients generally respond more vigorously, and the hypotensive response is enhanced by sodium depletion. Sodium 108-114 renin Homo sapiens 14-19 1770468-1 1991 The objectives of this study were to assess the possible role of insulin as a regulator of red blood cell sodium-lithium countertransport and to examine the relationship of countertransport activity to change over time in insulin, blood pressure, and other variables. Sodium 106-112 insulin Homo sapiens 65-72 1745008-0 1991 Changes in intracellular sodium during the hydroosmotic response to vasopressin. Sodium 25-31 arginine vasopressin Homo sapiens 68-79 1752291-1 1991 Acute hyperinsulinaemia, achieving insulin levels within the physiological range, induces sodium retention. Sodium 90-96 insulin Homo sapiens 11-18 1837565-6 1991 The change in urinary sodium excretion was significantly correlated with the change in plasma ANF (r = 0.75, P less than 0.01) in ISH. Sodium 22-28 natriuretic peptide A Homo sapiens 94-97 1745008-3 1991 We hypothesized that the hydroosmotic response to VP may be associated with a net increase in sodium either as an aid in maintaining the intracellular osmolality or as part of a Na-Ca exchange process. Sodium 94-100 arginine vasopressin Homo sapiens 50-52 1921483-7 1991 These results suggest that the renal renin-angiotensin system plays a central role in the alterations in renal hemodynamics and sodium management associated with the development of hypertension in ADPKD. Sodium 128-134 renin Homo sapiens 37-42 1959025-4 1991 And prior episodes of sodium depletion produce enhancements of subsequent salt appetites, but only if the prior depletions were accompanied by angiotensin II and aldosterone action. Sodium 22-28 angiotensinogen Rattus norvegicus 143-157 1959025-5 1991 Need-free salt intake, which occurs daily when the rat is in positive sodium balance is also enhanced by prior activations of angiotensin II and aldosterone. Sodium 70-76 angiotensinogen Rattus norvegicus 126-140 1649225-8 1991 In addition to culture density, removal of extracellular calcium or sodium during irradiation, treatment with amiloride, or inhibition of new mRNA synthesis with cordycepin was shown to influence the UVR-induced alteration in release of IL-3 or GM-CSF bioactivity from both confluent and subconfluent PAM 212 cells. Sodium 68-74 interleukin 3 Mus musculus 237-241 1659794-3 1991 Plasma renin activity (PRA) plasma concentration of active renin, atrial natriuretic hormone and urinary cyclic GMP were higher in patients in NYHA Class IV than in those in Classes II-III, whilst plasma sodium, angiotensinogen, prealbumin and retinol-binding protein concentrations were lower in Class IV patients than in patients in Classes II-III. Sodium 204-210 renin Homo sapiens 7-12 1659794-7 1991 The serum sodium was negatively correlated with active renin (r = -0.66, p less than 0.0001) in these patients not receiving converting enzyme inhibitors. Sodium 10-16 renin Homo sapiens 55-60 1800798-0 1991 Angiotensinogen excretion in rat urine: effects of lipopolysaccharide treatment and sodium balance. Sodium 84-90 angiotensinogen Rattus norvegicus 0-15 1831329-3 1991 Hypertonic saline alone produced a progressive rise in plasma vasopressin with increasing serum sodium. Sodium 96-102 arginine vasopressin Homo sapiens 62-73 1831329-4 1991 During hypertonic saline alone, vasopressin levels began to rise at an increment in serum sodium of 1.67 +/- 0.35 mM in the young and 1.43 +/- 0.32 mM in the elderly and rose linearly with increasing serum sodium. Sodium 90-96 arginine vasopressin Homo sapiens 32-43 1831329-4 1991 During hypertonic saline alone, vasopressin levels began to rise at an increment in serum sodium of 1.67 +/- 0.35 mM in the young and 1.43 +/- 0.32 mM in the elderly and rose linearly with increasing serum sodium. Sodium 206-212 arginine vasopressin Homo sapiens 32-43 1831329-5 1991 When ANP was infused with hypertonic saline (with peak ANP levels of approximately 1,000 pM), vasopressin levels began to rise at an increment in serum sodium of 4.43 +/- 0.67 mM in the young and 4.57 +/- 0.43 mM in the elderly (P less than 0.01 vs. saline alone). Sodium 152-158 natriuretic peptide A Homo sapiens 5-8 1831329-5 1991 When ANP was infused with hypertonic saline (with peak ANP levels of approximately 1,000 pM), vasopressin levels began to rise at an increment in serum sodium of 4.43 +/- 0.67 mM in the young and 4.57 +/- 0.43 mM in the elderly (P less than 0.01 vs. saline alone). Sodium 152-158 arginine vasopressin Homo sapiens 94-105 1831329-6 1991 Furthermore, the vasopressin response for any given serum sodium was significantly reduced in both young and elderly subjects, resulting in a rightward displacement of the curve relating vasopressin response to sodium concentration (P less than 0.001). Sodium 58-64 arginine vasopressin Homo sapiens 17-28 1831329-6 1991 Furthermore, the vasopressin response for any given serum sodium was significantly reduced in both young and elderly subjects, resulting in a rightward displacement of the curve relating vasopressin response to sodium concentration (P less than 0.001). Sodium 58-64 arginine vasopressin Homo sapiens 187-198 1831329-6 1991 Furthermore, the vasopressin response for any given serum sodium was significantly reduced in both young and elderly subjects, resulting in a rightward displacement of the curve relating vasopressin response to sodium concentration (P less than 0.001). Sodium 211-217 arginine vasopressin Homo sapiens 17-28 1831329-6 1991 Furthermore, the vasopressin response for any given serum sodium was significantly reduced in both young and elderly subjects, resulting in a rightward displacement of the curve relating vasopressin response to sodium concentration (P less than 0.001). Sodium 211-217 arginine vasopressin Homo sapiens 187-198 1833019-0 1991 The interaction between atrial natriuretic peptides and angiotensin II in controlling sodium and water excretion in the rat. Sodium 86-92 angiotensinogen Rattus norvegicus 56-70 1833019-9 1991 In another group of rats given captopril, angiotensin II at ongkg-1 min1 was also infused; this had no effect on blood pressure or renal haemodynamics, but partially restored basal levels of sodium and water excretion to those obtained before captopril. Sodium 191-197 angiotensinogen Rattus norvegicus 42-56 1833019-11 1991 In rats infused with angiotensin II at 15ngkg-1min1" together with the captopril the basal levels of fluid output were unchanged, while the magnitudes of the urine flow and sodium excretory responses to atriopeptin III were identical to those obtained before captopril and angiotensin II.5. Sodium 173-179 angiotensinogen Rattus norvegicus 21-35 1833197-2 1991 The important vasoconstrictor, fluid and sodium retaining factors are the renin-angiotensin-aldosterone system, sympathetic nerve activity and vasopressin; the vasodilator, volume and sodium eliminating factors are atrial natriuretic peptide, vasodilator prostaglandins, such as prostacyclin and prostaglandin E2, dopamine, bradykinin and, possibly, endothelium-derived relaxing factor and vasoactive intestinal peptide. Sodium 41-47 renin Homo sapiens 74-79 1833197-5 1991 In more severe heart failure, the renin-angiotensin-aldosterone system is activated, leading to an increase of peripheral and renal vascular resistance and fluid and sodium retention. Sodium 166-172 renin Homo sapiens 34-39 1885227-4 1991 Hypertensive patients with elevated sodium-lithium countertransport activity showed elevated glomerular filtration rate (118 +/- 2 versus 109 +/- 2 ml/min.1.73 m2; p less than 0.001), albumin excretion rate (23 +/- 3 versus 14 +/- 2 micrograms/min; p less than 0.001), larger kidney volume (250 +/- 15 versus 203 +/- 13 ml.1.73 m2; p less than 0.01), lower lithium clearance rate (26.7 +/- 0.3 versus 28.9 +/- 0.3 ml/min.1.73 m2; p less than 0.01), and higher total body exchangeable sodium (2,716 +/- 33 versus 2,485 +/- 41 mmol.1.73 m2; p less than 0.01). Sodium 36-42 CD59 molecule (CD59 blood group) Homo sapiens 151-156 1885227-4 1991 Hypertensive patients with elevated sodium-lithium countertransport activity showed elevated glomerular filtration rate (118 +/- 2 versus 109 +/- 2 ml/min.1.73 m2; p less than 0.001), albumin excretion rate (23 +/- 3 versus 14 +/- 2 micrograms/min; p less than 0.001), larger kidney volume (250 +/- 15 versus 203 +/- 13 ml.1.73 m2; p less than 0.01), lower lithium clearance rate (26.7 +/- 0.3 versus 28.9 +/- 0.3 ml/min.1.73 m2; p less than 0.01), and higher total body exchangeable sodium (2,716 +/- 33 versus 2,485 +/- 41 mmol.1.73 m2; p less than 0.01). Sodium 36-42 CD59 molecule (CD59 blood group) Homo sapiens 417-422 1831860-0 1991 Role of atrial natriuretic factor in sodium and water retention in patients with schistosomal hepatic fibrosis. Sodium 37-43 natriuretic peptide A Homo sapiens 8-33 1942773-0 1991 Insulin increases sodium reabsorption in diluting segment in humans: evidence for indirect mediation through hypokalemia. Sodium 18-24 insulin Homo sapiens 0-7 1837568-9 1991 These results therefore indicated that hypotension caused by hemodynamic alteration and extremely stimulated renin release might effect on proximal tubular sodium reabsorption and GFR, leading to sodium retention and diuretic resistance in cirrhosis. Sodium 156-162 renin Homo sapiens 109-114 1837568-9 1991 These results therefore indicated that hypotension caused by hemodynamic alteration and extremely stimulated renin release might effect on proximal tubular sodium reabsorption and GFR, leading to sodium retention and diuretic resistance in cirrhosis. Sodium 196-202 renin Homo sapiens 109-114 1653713-7 1991 Sodium clearance/lithium clearance was slightly increased after infusion of 0.03 microgram/kg/min of alpha hANP in hypertensive subjects. Sodium 0-6 natriuretic peptide A Homo sapiens 107-111 1653713-14 1991 Moreover, it is considered that ANP increases sodium and water excretion through its effect on both renal glomeruli and distal tubules in EH. Sodium 46-52 natriuretic peptide A Homo sapiens 32-35 1651740-4 1991 The time-course of ANF response to sodium loading was significantly delayed in BHT characterized by normal venous distensibility. Sodium 35-41 natriuretic peptide A Homo sapiens 19-22 1956022-12 1991 Insulin resistance and compensatory hyperinsulinaemia might lead to an increase in BP by a number of putative mechanisms, such as enhancing renal sodium retention, by an effect on cell membrane ion exchange mechanisms or by enhancing activity of the sympathetic nervous system. Sodium 146-152 insulin Homo sapiens 0-7 1873017-1 1991 This study attempted to evaluate the effect of anion associated with sodium loading on the development of angiotensin II (AII)-induced hypertension in rats. Sodium 69-75 angiotensinogen Rattus norvegicus 106-120 1873017-1 1991 This study attempted to evaluate the effect of anion associated with sodium loading on the development of angiotensin II (AII)-induced hypertension in rats. Sodium 69-75 angiotensinogen Rattus norvegicus 122-125 1873017-3 1991 High dietary intake of sodium chloride significantly augmented the AII-induced hypertension (systolic blood pressure on day 12, 166 +/- 4 mm Hg), but equimolar sodium loading provided as sodium citrate failed to enhance AII hypertension (systolic blood pressure on day 12, 136 +/- 8 mm Hg). Sodium 23-29 angiotensinogen Rattus norvegicus 67-70 1873017-4 1991 Thus, the data suggest that the full expression of salt (NaCl) sensitivity in AII hypertension depends on high dietary intake of both sodium and chloride. Sodium 134-140 angiotensinogen Rattus norvegicus 78-81 1647996-5 1991 Yet for each picomolar increment in plasma ANP during immersion, the corresponding increases in urinary excretion of cyclic guanosine monophosphate (26 vs. 279 pmol/min) and sodium (9 vs. 47 mumol/min) and the reciprocal lowering of RVR (0.7 vs. 1.9 U) were blunted in the diabetic versus control group. Sodium 174-180 natriuretic peptide A Homo sapiens 43-46 1830563-9 1991 The blood pressure lowering was due to specific renin inhibition as exemplified by the influence of the kidney, sodium status, species, or stereoselectivity. Sodium 112-118 renin Homo sapiens 48-53 1836782-4 1991 On the other hand a decrease of plasma ANF in normal man similar to that reported in Bartter"s subjects may explain the sodium retention caused by the drug in normals. Sodium 120-126 natriuretic peptide A Homo sapiens 39-42 1831369-3 1991 Plasma levels of BNP increased time-dependently during the development of CHF, and were more than four-fold higher in sodium retaining rats than in control rats. Sodium 118-124 natriuretic peptide B Rattus norvegicus 17-20 1831369-4 1991 The data suggest that BNP secretion from the atria is increased in CHF, and that resistance to BNP, in addition to the relative resistance to atrial natriuretic factor, may contribute to sodium retention in CHF. Sodium 187-193 natriuretic peptide B Rattus norvegicus 95-98 1918810-8 1991 Since activation of the renal nerve is known to induce sodium reabsorption from the renal tubule and renin release, the relevance of the present finding is discussed in relation to the effect of AII on sodium excretion. Sodium 202-208 angiotensinogen Rattus norvegicus 195-198 1708901-12 1991 Furthermore, our data indicated that the sodium cation, irrespective of the anion, was primarily important in regulating renal angiotensinogen mRNA levels. Sodium 41-47 angiotensinogen Rattus norvegicus 127-142 1873917-7 1991 Sodium restriction increased PAI, PAII, and PRA, but did not alter UV-AI and UV-AII. Sodium 0-6 NLR family pyrin domain containing 3 Homo sapiens 35-38 1864303-2 1991 In the normal kidney (N = 5), intrarenal infusion of porcine BNP-(1-26) (pBNP) at a dose of 50 ng/kg per min attenuated the renin secretion rate significantly to 9 +/- 27% of control without exerting a significant effect on mean arterial pressure (MAP), renal blood flow (RBF) or glomerular filtration rate (GFR); urine flow (V) was significantly increased to 260 +/- 33% of control and urinary excretion of sodium (UNaV) to 480 +/- 140% of control. Sodium 408-414 natriuretic peptide B Canis lupus familiaris 61-64 1864303-6 1991 Our results indicate that BNP inhibits renin secretion through sodium delivery to the macula densa and effectively inhibits the tubuloglomerular feedback response that is activated by intrarenal hypertonic saline infusion. Sodium 63-69 natriuretic peptide B Canis lupus familiaris 26-29 1647690-0 1991 Mechanisms of sodium retention in heart failure: relation to the renin-angiotensin-aldosterone system. Sodium 14-20 renin Homo sapiens 65-70 1873002-5 1991 The decrease in MBP appeared to be significantly higher in sodium-sensitive (11.2 mm Hg, P less than .001) than in sodium-insensitive (5.7 mm Hg, P less than .05) patients and was in salt-sensitive patients significantly correlated to the increase in plasma renin activity (PRA). Sodium 59-65 renin Homo sapiens 258-263 2058747-10 1991 These results indicate that the shift of the PN relationship during infusion of ANG II is due to a decrease in filtered load and enhanced tubular reabsorption of sodium. Sodium 162-168 angiotensinogen Rattus norvegicus 80-86 1868507-4 1991 Upon removal of sodium from the perfusing medium, basal release of VP and OT increased by 3.95 +/- 0.23- and 3.71 +/- 0.22-fold, respectively, followed by a decline to about double the levels in normal (150 mM) sodium (P less than or equal to 0.1). Sodium 16-22 arginine vasopressin Rattus norvegicus 67-69 1868507-4 1991 Upon removal of sodium from the perfusing medium, basal release of VP and OT increased by 3.95 +/- 0.23- and 3.71 +/- 0.22-fold, respectively, followed by a decline to about double the levels in normal (150 mM) sodium (P less than or equal to 0.1). Sodium 211-217 arginine vasopressin Rattus norvegicus 67-69 1868507-6 1991 Compared to neurosecretosomes perfused in normal (150 mM) sodium, omission of sodium from the medium augmented ionomycin-induced VP and OT secretion by 66 +/- 5- and 20 +/- 3-fold, respectively, and A23187-induced secretion was increased 1.3 +/- 0.4- and 1.3 +/- 0.1-fold (P less than or equal to 0.01 for both ionophores). Sodium 78-84 arginine vasopressin Rattus norvegicus 129-131 1879402-1 1991 The level of sodium intake has a reciprocal influence on the vascular and adrenal responses to angiotensin II, with sodium restriction enhancing the adrenal responses and reducing vascular, and particularly renal vascular, responses. Sodium 13-19 angiotensinogen Homo sapiens 95-109 1879402-6 1991 In these patients, sodium intake modifies either adrenal or vascular responses, including renal vascular responses, to angiotensin II--resulting in a reduced aldosterone response to angiotensin II with sodium restriction. Sodium 19-25 angiotensinogen Homo sapiens 119-133 1879402-6 1991 In these patients, sodium intake modifies either adrenal or vascular responses, including renal vascular responses, to angiotensin II--resulting in a reduced aldosterone response to angiotensin II with sodium restriction. Sodium 19-25 angiotensinogen Homo sapiens 182-196 1879402-6 1991 In these patients, sodium intake modifies either adrenal or vascular responses, including renal vascular responses, to angiotensin II--resulting in a reduced aldosterone response to angiotensin II with sodium restriction. Sodium 202-208 angiotensinogen Homo sapiens 119-133 1879402-6 1991 In these patients, sodium intake modifies either adrenal or vascular responses, including renal vascular responses, to angiotensin II--resulting in a reduced aldosterone response to angiotensin II with sodium restriction. Sodium 202-208 angiotensinogen Homo sapiens 182-196 2060872-4 1991 We have examined the effect of the non-pressor (V2) synthetic vasopressin analogue 1-deamino-8-D-arginine (desmopressin) on renal and ileal sodium and water excretion in ileostomy patients during acute adaptation to a low sodium diet. Sodium 140-146 arginine vasopressin Homo sapiens 62-73 1675203-10 1991 During angiotensin II infusion, sham-lesion rats exhibited a progressive increase in arterial pressure and the depressor response to ganglion blockade and a decrease in urinary sodium excretion. Sodium 177-183 angiotensinogen Rattus norvegicus 7-21 2045142-1 1991 When the function of the renin system is inhibited, blood pressure becomes more dependent on changes in sodium and water balance. Sodium 104-110 renin Homo sapiens 25-30 2045176-11 1991 A rise in plasma fatty acids and fall in insulin in response to salt loads could act in concert to increase sodium excretion, constituting a physiological mechanism contributing to salt and water balance. Sodium 108-114 insulin Homo sapiens 41-48 1827451-4 1991 ANF significantly enhanced urinary sodium excretion above preinfusion values in both study phases in both groups. Sodium 35-41 natriuretic peptide A Homo sapiens 0-3 1851181-6 1991 In the diabetic subjects, however, the responses of plasma 18-OHB and PA to both ACTH injection and graded AII infusions on a 100-mmol, but not on a 170-mmol, sodium intake were subnormal (P less than 0.05 or P less than 0.01) and were similar to those on a 170-mmol sodium intake. Sodium 159-165 angiotensinogen Homo sapiens 107-110 1646297-0 1991 Vasopressin generates a persistent voltage-dependent sodium current in a mammalian motoneuron. Sodium 53-59 arginine vasopressin Homo sapiens 0-11 1646297-10 1991 Our results suggest that vasopressin increases the excitability of facial motoneurons by generating a persistent sodium-dependent membrane current that is voltage gated and TTX resistant. Sodium 113-119 arginine vasopressin Homo sapiens 25-36 1876234-2 1991 Both chronic sodium or chloride depletion produced significant extracellular fluid volume contraction, stimulation of the circulating renin-angiotensin system and increased the number of angiotensin II receptors in the anterior pituitary gland. Sodium 13-19 angiotensinogen Rattus norvegicus 187-201 1876234-0 1991 Chronic sodium or chloride depletion upregulates angiotensin II receptors in the anterior pituitary lobe of young rats. Sodium 8-14 angiotensinogen Rattus norvegicus 49-63 1876234-1 1991 The effect of chronic (35 days) and selective sodium or chloride depletion on the regulation of angiotensin II receptors in the anterior pituitary gland of young male rats was studied by quantitative autoradiography. Sodium 46-52 angiotensinogen Rattus norvegicus 96-110 1876234-3 1991 Changes in angiotensin II receptors in both sodium- and chloride-depleted animals were associated with increased plasma prolactin levels. Sodium 44-50 angiotensinogen Rattus norvegicus 11-25 1876234-3 1991 Changes in angiotensin II receptors in both sodium- and chloride-depleted animals were associated with increased plasma prolactin levels. Sodium 44-50 prolactin Rattus norvegicus 120-129 1947721-1 1991 Diabetic patients treated with insulin injected subcutaneously are characterized by peripheral hyperinsulinaemia and an increased mass of total body exchangeable sodium. Sodium 162-168 insulin Homo sapiens 31-38 1947721-7 1991 Insulin infusion reduced renal sodium excretion. Sodium 31-37 insulin Homo sapiens 0-7 1852105-1 1991 To determine the mechanism by which vasopressin increases sodium transport in sodium-transporting, tight epithelia, we examined single amiloride-blockable Na channels in membrane patches from cultured distal nephron cells (A6) either before or after treatment with arginine vasopressin. Sodium 58-64 arginine vasopressin Homo sapiens 36-47 1947721-9 1991 Insulin infusion without volume expansion caused a decrease of 24% in the fractional distal sodium excretion. Sodium 92-98 insulin Homo sapiens 0-7 1947721-13 1991 The enhanced GFR is probably a compensatory response to the sodium retention induced by the action of insulin on the distal tubules. Sodium 60-66 insulin Homo sapiens 102-109 1829901-7 1991 Plasma renin activity and plasma angiotensin II levels were significantly lower on LK than on LS or HK, probably reflecting sodium retention. Sodium 124-130 angiotensinogen Homo sapiens 33-47 1852105-1 1991 To determine the mechanism by which vasopressin increases sodium transport in sodium-transporting, tight epithelia, we examined single amiloride-blockable Na channels in membrane patches from cultured distal nephron cells (A6) either before or after treatment with arginine vasopressin. Sodium 78-84 arginine vasopressin Homo sapiens 36-47 2029728-6 1991 In the supraoptic nucleus, vasopressin mRNA levels were significantly decreased in the low-sodium group but were not significantly affected by chloride depletion. Sodium 91-97 arginine vasopressin Rattus norvegicus 27-38 2029014-6 1991 RESULTS: The low sodium diet resulted in a highly significant increase in the plasma renin (2p = 0.0001), aldosterone (2p = 0.0006), and urinary prostaglandin E2 (2p = 0.01) concentrations and the renal potassium excretion (2p = 0.0009), whereas renal sodium excretion was significantly reduced (2p = 0.0001). Sodium 17-23 renin Homo sapiens 85-90 2065475-2 1991 In Gordon"s syndrome (GS; a syndrome of hypertension and hyperkalaemia with normal glomerular filtration rate), excessive proximal sodium reabsorption leads to suppression of renin and aldosterone, hyperkalaemia and hyperchloraemic acidosis. Sodium 131-137 renin Homo sapiens 175-180 1656123-6 1991 Treatment with a vasopressin analogue, desamino-D-arginine vasopressin and forced intake of water restored plasma osmolality and serum sodium levels to normal. Sodium 135-141 arginine vasopressin Homo sapiens 17-28 1656123-6 1991 Treatment with a vasopressin analogue, desamino-D-arginine vasopressin and forced intake of water restored plasma osmolality and serum sodium levels to normal. Sodium 135-141 arginine vasopressin Homo sapiens 59-70 1759997-2 1991 METHODS: Renin profiles, obtained by plotting plasma renin activity against the urinary excretion of sodium, were classified as high (12 percent of the subjects), normal (56 percent), and low (32 percent), and there were expected variations according to age, sex, and race. Sodium 101-107 renin Homo sapiens 9-14 2059912-5 1991 Animals on a high sodium, high chloride diet had a significantly greater increase of blood pressure at 8, 15, 18, and 22 days of AII infusion compared with AII-treated animals on a low sodium, low chloride diet (p less than 0.05). Sodium 18-24 angiotensinogen Rattus norvegicus 129-132 2059912-5 1991 Animals on a high sodium, high chloride diet had a significantly greater increase of blood pressure at 8, 15, 18, and 22 days of AII infusion compared with AII-treated animals on a low sodium, low chloride diet (p less than 0.05). Sodium 185-191 angiotensinogen Rattus norvegicus 156-159 2029728-16 1991 Our results show that chronic sodium, chloride, or potassium depletion differentially affect brain vasopressin mRNA and vasopressin release in young rats. Sodium 30-36 arginine vasopressin Rattus norvegicus 99-110 2029728-16 1991 Our results show that chronic sodium, chloride, or potassium depletion differentially affect brain vasopressin mRNA and vasopressin release in young rats. Sodium 30-36 arginine vasopressin Rattus norvegicus 120-131 2065862-0 1991 Effect of insulin on renal sodium handling in hyperinsulinaemic type 2 (non-insulin-dependent) diabetic patients with peripheral insulin resistance. Sodium 27-33 insulin Homo sapiens 10-17 2065862-0 1991 Effect of insulin on renal sodium handling in hyperinsulinaemic type 2 (non-insulin-dependent) diabetic patients with peripheral insulin resistance. Sodium 27-33 insulin Homo sapiens 51-58 2065862-0 1991 Effect of insulin on renal sodium handling in hyperinsulinaemic type 2 (non-insulin-dependent) diabetic patients with peripheral insulin resistance. Sodium 27-33 insulin Homo sapiens 51-58 1647438-4 1991 When sodium transport was blocked by amiloride, the H+ permeability of the apical membranes of principal cells was negligible but increased dramatically after treatment with antidiuretic hormone (ADH). Sodium 5-11 arginine vasopressin Homo sapiens 174-194 1878323-6 1991 Average reactivities during CONFLICT + SODIUM periods were 11.2/7.9% delta for SBP/DBP (systolic/diastolic blood pressure, mmHg), and -5.65% delta for HR (heart rate, BPM). Sodium 39-45 D-box binding PAR bZIP transcription factor Homo sapiens 83-86 2010543-2 1991 In this study we examine the localization of angiotensinogen mRNA in the blood vessel wall of two rat strains, the Wistar and Wistar Kyoto (WKY), as well as the regulation of vascular angiotensinogen mRNA expression by dietary sodium. Sodium 227-233 angiotensinogen Rattus norvegicus 184-199 2010543-4 1991 In WKY rats fed a 1.6% sodium diet, angiotensinogen mRNA concentration is 2.6-fold higher in the periaortic fat than in the smooth muscle, as analyzed by quantitative slot blot hybridization. Sodium 23-29 angiotensinogen Rattus norvegicus 36-51 2010543-6 1991 After 5 d of a low (0.02%) sodium diet, smooth muscle angiotensinogen mRNA levels increase 3.2-fold (P less than 0.005) as compared with the 1.6% sodium diet. Sodium 27-33 angiotensinogen Rattus norvegicus 54-69 2010543-8 1991 In summary, our data demonstrate regional (smooth muscle vs. periaortic fat) differential regulation of angiotensinogen mRNA levels in the blood vessel wall by sodium. Sodium 160-166 angiotensinogen Rattus norvegicus 104-119 1646259-1 1991 Insulin resistance associated with a hyperinsulinemic response to oral glucose intake has been found in patients with essential hypertension and is believed to play a role in inducing hypertension by causing renal sodium and water retention. Sodium 214-220 insulin Homo sapiens 0-7 1647438-4 1991 When sodium transport was blocked by amiloride, the H+ permeability of the apical membranes of principal cells was negligible but increased dramatically after treatment with antidiuretic hormone (ADH). Sodium 5-11 arginine vasopressin Homo sapiens 196-199 1881501-0 1991 Insulin as a cause of sodium retention and hypertension. Sodium 22-28 insulin Homo sapiens 0-7 1830107-11 1991 However, one explanation for the increase in plasma renin activity and fall in atrial natriuretic peptide is a small reduction in total body sodium. Sodium 141-147 renin Homo sapiens 52-57 1649430-6 1991 C-ANF infusion significantly increased (mean +/- SEM) plasma ANF concentration (437 +/- 45 to 1067 +/- 297 pg/mL), urinary flow rate (0.26 +/- 0.04 to 0.38 +/- 0.07 mL/min/kg), sodium excretion (12.9 +/- 3.5 to 21.7 +/- 6.1 mumol/min/kg), and osmolar clearance (0.14 +/- 0.02 to 0.21 +/- 0.04 mL/min/kg) (p less than 0.05). Sodium 177-183 natriuretic peptide A Homo sapiens 0-5 1649430-6 1991 C-ANF infusion significantly increased (mean +/- SEM) plasma ANF concentration (437 +/- 45 to 1067 +/- 297 pg/mL), urinary flow rate (0.26 +/- 0.04 to 0.38 +/- 0.07 mL/min/kg), sodium excretion (12.9 +/- 3.5 to 21.7 +/- 6.1 mumol/min/kg), and osmolar clearance (0.14 +/- 0.02 to 0.21 +/- 0.04 mL/min/kg) (p less than 0.05). Sodium 177-183 natriuretic peptide A Homo sapiens 2-5 1649430-7 1991 The combined C-ANF/ANF infusion further increased plasma ANF concentration to 2394 +/- 532 pg/mL and resulted in significant increases in urinary flow rate, sodium excretion, osmolar clearance, GFR, and free water clearance compared with C-ANF infusion alone (p less than 0.05). Sodium 157-163 natriuretic peptide A Homo sapiens 13-18 1649430-7 1991 The combined C-ANF/ANF infusion further increased plasma ANF concentration to 2394 +/- 532 pg/mL and resulted in significant increases in urinary flow rate, sodium excretion, osmolar clearance, GFR, and free water clearance compared with C-ANF infusion alone (p less than 0.05). Sodium 157-163 natriuretic peptide A Homo sapiens 15-18 1649430-7 1991 The combined C-ANF/ANF infusion further increased plasma ANF concentration to 2394 +/- 532 pg/mL and resulted in significant increases in urinary flow rate, sodium excretion, osmolar clearance, GFR, and free water clearance compared with C-ANF infusion alone (p less than 0.05). Sodium 157-163 natriuretic peptide A Homo sapiens 19-22 1871041-0 1991 Effects of viscous hyaluronate-sodium solutions on the nasal absorption of vasopressin and an analogue. Sodium 31-37 arginine vasopressin Rattus norvegicus 75-86 1922657-7 1991 Diminishing the sodium in the media, which alters the activity and perhaps the direction of the Na/Ca exchanger, reduced the increase in [Ca2+]i due to hypoxia, but enhanced the KCl response. Sodium 16-22 solute carrier family 8 member A1 Homo sapiens 96-111 2002040-9 1991 Oscillations of intracellular calcium could be observed in +ras cells, if bradykinin was applied at reduced extracellular sodium concentration possibly to impair calcium extrusion via the sodium/calcium exchange. Sodium 122-128 kininogen 1 Homo sapiens 74-84 1828306-1 1991 The circadian variation of plasma atrial natriuretic peptide (ANP) in relation to urinary excretion of sodium (UNa) and potassium (UK) as well as clearance of creatinine (Ccrea) was assessed in 15 juvenile patients with enuresis nocturna and compared with 11 age-, sex-, and weight-matched normal subjects. Sodium 103-109 natriuretic peptide A Homo sapiens 34-60 1828306-8 1991 In conclusion, the study describes the diurnal variation of plasma ANP in relation to urinary excretion of sodium and potassium in a juvenile normal population. Sodium 107-113 natriuretic peptide A Homo sapiens 67-70 2002040-9 1991 Oscillations of intracellular calcium could be observed in +ras cells, if bradykinin was applied at reduced extracellular sodium concentration possibly to impair calcium extrusion via the sodium/calcium exchange. Sodium 188-194 kininogen 1 Homo sapiens 74-84 1996577-7 1991 Thus, the presence of parathyroid hormone (PTH) is necessary for sodium-related alterations in urinary Ca to occur. Sodium 65-71 parathyroid hormone Homo sapiens 22-41 1828349-6 1991 Since a low urinary kallikrein excretion may represent a marker of an impaired production of renal kallikrein, the high levels of ANF found in the LK subgroup could be the result of a compensatory response of the atrium attempting to maintain sodium and volume homeostasis. Sodium 243-249 natriuretic peptide A Homo sapiens 130-133 1828350-4 1991 The combination of head-up tilt and ANP infusion resulted in a less marked decrease in urine flow rate and sodium excretion and a similar increase in plasma renin activity. Sodium 107-113 natriuretic peptide A Homo sapiens 36-39 1847706-10 1991 These results suggest that ANF could play a role in the control of sodium homeostasis in liver cirrhosis with ascites. Sodium 67-73 natriuretic peptide A Homo sapiens 27-30 1850681-5 1991 All three insulin dosages resulted in a marked decline in fractional sodium excretion (actual experiments: basal, 0.95 +/- 0.15%, Ins I, 0.79 +/- 0.10%, Ins II, 0.80 +/- 0.12%, Ins III, 0.84 +/- 0.08%; control experiments: basal, 0.96 +/- 0.10%, Ins I, 1.20 +/- 0.12%, Ins II, 1.53 +/- 0.15%, Ins III, 1.43 +/- 0.10%; means +/- SEM, P less than 0.005, analysis of variance). Sodium 69-75 insulin Homo sapiens 10-17 1850681-6 1991 With the highest insulin dosage, the reduction in fractional sodium excretion tended to be less striking. Sodium 61-67 insulin Homo sapiens 17-24 1999148-6 1991 With sodium restriction, the AII content increased more than 2-fold in the ZG, but not in the decapsulated adrenal tissue. Sodium 5-11 angiotensinogen Rattus norvegicus 29-32 1999148-11 1991 After a lag period, ZG AII increased sharply between 16-48 h of sodium restriction. Sodium 64-70 angiotensinogen Rattus norvegicus 23-26 1999148-12 1991 These data document that sodium intake has a profound effect on the angiotensin content of the ZG, with sodium restriction substantially increasing the levels of AII while reducing the level of its substrate, AI. Sodium 25-31 angiotensinogen Rattus norvegicus 162-165 1999148-12 1991 These data document that sodium intake has a profound effect on the angiotensin content of the ZG, with sodium restriction substantially increasing the levels of AII while reducing the level of its substrate, AI. Sodium 104-110 angiotensinogen Rattus norvegicus 162-165 1999148-14 1991 We conclude that these sodium-mediated changes in tissue AII production may be involved in the increased responsiveness of glomerulosa cells to aldosterone secretagogues during sodium restriction. Sodium 23-29 angiotensinogen Rattus norvegicus 57-60 1999148-14 1991 We conclude that these sodium-mediated changes in tissue AII production may be involved in the increased responsiveness of glomerulosa cells to aldosterone secretagogues during sodium restriction. Sodium 177-183 angiotensinogen Rattus norvegicus 57-60 1829768-0 1991 Attenuated release of atrial natriuretic factor due to sodium loading in salt-sensitive essential hypertension. Sodium 55-61 natriuretic peptide A Homo sapiens 22-47 1989979-3 1991 The largest mRNA induction was observed at day 7 in sodium-depleted rats for P-450(11 beta), with a 4-fold increase, followed by 2.7- and 2.0-fold increases for P-450scc and P-450c21, respectively. Sodium 52-58 cytochrome P450, family 21, subfamily a, polypeptide 1 Rattus norvegicus 174-182 1826997-0 1991 Importance of the renin-angiotensin system in sodium regulation in essential hypertension. Sodium 46-52 renin Homo sapiens 18-23 1826997-8 1991 These results suggest that the state of the renin-angiotensin system is important in renal sodium excretion in EHT. Sodium 91-97 renin Homo sapiens 44-49 1854946-3 1991 The important role in the mechanism of the decrease in the water reabsorption in SHR plays the decrease in the content of vasopressin in the blood and urea in the kidney interstitium while in NR a more marked inhibition of the water reabsorption is caused by the decrease in the concentration of both urea and sodium in the kidney layers. Sodium 310-316 arginine vasopressin Rattus norvegicus 122-133 1830843-4 1991 Plasma renin activity was inversely related to sodium excretion at both proximal (r = -0.145, P less than 0.05) and distal (r = -0.236, P less than 0.001) tubular site, whereas plasma aldosterone was significantly and inversely related to distal sodium excretion only (r = -0.305, P less than 0.001). Sodium 47-53 renin Homo sapiens 7-12 1830843-4 1991 Plasma renin activity was inversely related to sodium excretion at both proximal (r = -0.145, P less than 0.05) and distal (r = -0.236, P less than 0.001) tubular site, whereas plasma aldosterone was significantly and inversely related to distal sodium excretion only (r = -0.305, P less than 0.001). Sodium 246-252 renin Homo sapiens 7-12 1709222-7 1991 ANP (0.005 micrograms/kg/min for 3 h) was administered during maximal water diuresis on both sodium intake levels with and without nitrendipine. Sodium 93-99 natriuretic peptide A Homo sapiens 0-3 1829768-4 1991 There was a significant positive correlation between the plasma ANF and MBP after the high-sodium intake in both SS (r = 0.67, p less than 0.01) and NSS (r = 0.60, p less than 0.01); however, the relation of plasma ANF to MBP shifted apparently to a lower level in SS compared with NSS. Sodium 91-97 natriuretic peptide A Homo sapiens 64-67 1829768-5 1991 These findings not only indicate that there exists a hyporesponsiveness of ANF release by the heart of SS patients in response to high-sodium loading, but also imply that such a response contributes to blood pressure-elevating mechanisms due to sodium loading in this type of human hypertension. Sodium 135-141 natriuretic peptide A Homo sapiens 75-78 1829768-5 1991 These findings not only indicate that there exists a hyporesponsiveness of ANF release by the heart of SS patients in response to high-sodium loading, but also imply that such a response contributes to blood pressure-elevating mechanisms due to sodium loading in this type of human hypertension. Sodium 245-251 natriuretic peptide A Homo sapiens 75-78 1827111-1 1991 Previous studies of atrial natriuretic peptide (ANP) have indicated that its release from the heart and from discrete areas of the central nervous system evokes coordinated physiological and behavioral adjustments that mitigate the adverse hypertensive effects of volume overload and/or acute increases in sodium intake. Sodium 306-312 natriuretic peptide A Homo sapiens 20-46 1827111-1 1991 Previous studies of atrial natriuretic peptide (ANP) have indicated that its release from the heart and from discrete areas of the central nervous system evokes coordinated physiological and behavioral adjustments that mitigate the adverse hypertensive effects of volume overload and/or acute increases in sodium intake. Sodium 306-312 natriuretic peptide A Homo sapiens 48-51 1709222-8 1991 Infusion of ANP increased sodium excretion (mumol/min) from 30 +/- 7 to 81 +/- 12 (LS) and from 316 +/- 27 to 469 +/- 46 (HS). Sodium 26-32 natriuretic peptide A Homo sapiens 12-15 1709222-13 1991 ANP, in physiological concentrations, increases natriuresis mainly by depressing sodium reabsorption in the distal nephron, an effect not enhanced by nitrendipine. Sodium 81-87 natriuretic peptide A Homo sapiens 0-3 1988777-0 1991 Sodium retention by insulin may depend on decreased plasma potassium. Sodium 0-6 insulin Homo sapiens 20-27 1846877-3 1991 They are subject to regulation by circulating levels of ANP in plasma, varying inversely with the latter after high sodium intake, in arterial hypertension and congestive heart failure. Sodium 116-122 natriuretic peptide A Homo sapiens 56-59 1999477-2 1991 PMA or thrombin caused a cytoplasmic alkalinization that required extracellular sodium and was sensitive to 1 mM amiloride, suggesting that the rise in pH was mediated by the Na+/H+ exchanger. Sodium 80-86 coagulation factor II, thrombin Homo sapiens 7-15 1988777-3 1991 We examined whether insulin causes sodium retention through a direct action on the kidney, as is generally assumed, or indirectly through hypokalemia. Sodium 35-41 insulin Homo sapiens 20-27 1988777-5 1991 Without potassium infusion, insulin caused a marked decrease in plasma potassium (-0.75 mmol/L), and decreased urinary sodium and potassium excretions by, approximately 38% and 65%, respectively. Sodium 119-125 insulin Homo sapiens 28-35 1824917-7 1991 These results suggest that production and secretion of both BNP and ANP are concomitantly stimulated by a decreased renal ability to eliminate sodium and water, but this secretion is insufficient to induce effective natriuresis in nephrotic rats. Sodium 143-149 natriuretic peptide B Rattus norvegicus 60-63 1833942-5 1991 ANF appears to play an important physiological role in sodium repleted states, or when the effective plasma volume is increased. Sodium 55-61 natriuretic peptide A Homo sapiens 0-3 1984191-8 1991 Her ratio of plasma renin activity to urinary aldosterone-18-glucuronide excretion was 1.7 after three days of sodium restriction, as compared with a ratio of 4.7 at the age of nine years (normal range, 0.03 to 0.1). Sodium 111-117 renin Homo sapiens 20-25 1833942-6 1991 On the contrary, when the effective plasma volume is decreased or in sodium depleted states, the natriuretic effect of both endogenous and exogenous ANF is severely blunted. Sodium 69-75 natriuretic peptide A Homo sapiens 149-152 1799183-5 1991 Both doses of AII decreased GFR and RPF and increased the filtration fraction (FF); the modifications of these parameters, as well as the reduction of FELi and the fractional excretion of sodium (FENa) and the increase of plasma aldosterone and of plasma atrial natriuretic peptide (ANP), were more evident with pressor doses of AII, which increased the blood pressure from 129/83 to 142/95 mm Hg (p less than 0.01). Sodium 188-194 angiotensinogen Homo sapiens 14-17 1799183-8 1991 These results suggest that, in normal humans, the AII-induced rise of FF may be an important factor, even if not the only one, in enhancing the proximal reabsorption of lithium and thus of sodium, whilst it does not affect the absorption of beta 2M. Sodium 189-195 angiotensinogen Homo sapiens 50-53 2006991-8 1991 These correlations within renin tertiles occurred even though there were no differences in mean blood pressure, plasma ionized calcium, total plasma protein and plasma sodium across renin categories. Sodium 168-174 renin Homo sapiens 26-31 1767729-6 1991 Urinary urea nitrogen and sodium excretion decreased after IGF-I administration. Sodium 26-32 insulin like growth factor 1 Homo sapiens 59-64 2007003-1 1991 There is a growing awareness that the direct intrarenal actions of angiotensin II (ANG II) on both tubular and vascular structures contribute to sodium conservation. Sodium 145-151 angiotensinogen Homo sapiens 67-81 2007003-1 1991 There is a growing awareness that the direct intrarenal actions of angiotensin II (ANG II) on both tubular and vascular structures contribute to sodium conservation. Sodium 145-151 angiotensinogen Homo sapiens 83-89 2007003-9 1991 At these higher doses, the direct hemodynamic actions of ANG II, plus the effects on the glomerular filtration coefficient, will directly reduce filtered sodium load. Sodium 154-160 angiotensinogen Homo sapiens 57-63 2007003-10 1991 Through these synergistic effects on both tubular reabsorptive and hemodynamic function, ANG II can elicit sustained decreases in distal nephron sodium delivery which contribute greatly to its efficacy as a regulator of sodium excretion. Sodium 145-151 angiotensinogen Homo sapiens 89-95 2009143-5 1991 Nevertheless, they are affected adversely by the discordant renin-angiotensin II arising from the ischemic nephrons" presence, which exerts an unwanted sodium-retaining effect on the proximal tubules of the adapting nephrons. Sodium 152-158 renin Homo sapiens 60-65 2009143-5 1991 Nevertheless, they are affected adversely by the discordant renin-angiotensin II arising from the ischemic nephrons" presence, which exerts an unwanted sodium-retaining effect on the proximal tubules of the adapting nephrons. Sodium 152-158 angiotensinogen Homo sapiens 66-80 1668636-2 1991 If the experimental rats are changed to tap water after 15 months of the high sodium diet, the results are partially reversed. Sodium 78-84 nuclear RNA export factor 1 Rattus norvegicus 40-43 1838244-2 1991 Important vasoconstrictor, fluid- and sodium-retaining factors are the renin-angiotensin-aldosterone system, sympathetic nerve activity, and vasopressin; vasodilator, volume, and sodium-eliminating factors are atrial natriuretic peptide, vasodilator prostaglandins like prostacyclin and prostaglandin E2, dopamine, bradykinin, and possibly, endothelial derived relaxing factor (EDRF). Sodium 38-44 renin Homo sapiens 71-76 1838244-5 1991 In more severe heart failure, the renin-angiotensin-aldosterone system is activated, leading to an increase of peripheral and renal vascular resistance and fluid and sodium retention. Sodium 166-172 renin Homo sapiens 34-39 1874031-8 1991 Besides its effects on intrarenal hemodynamics, ANG II directly or indirectly affects renal sodium excretion. Sodium 92-98 angiotensinogen Rattus norvegicus 48-54 1874031-9 1991 Micropuncture and microperfusion studies have shown that ANG II exerts a dose-dependent biphasic effect on proximal tubular sodium reabsorption via apical Na(+)-H+ exchange. Sodium 124-130 angiotensinogen Rattus norvegicus 57-63 1874031-11 1991 The stimulatory effect of ANG II on proximal tubular reabsorption of sodium seems associated with reduction in cAMP and/or activation of protein kinase C, whereas cytosolic free calcium surge activated by ANG II may be part of the cellular message that inhibits proximal tubular reabsorptive function. Sodium 69-75 angiotensinogen Rattus norvegicus 26-32 1874031-15 1991 Furthermore, intracerebroventricular injections of ANG II and ANG III in rats inhibit renal nerve activity and cause a comparable renal effect which can be blocked by Ile7-ANG III and potentiated by bestatin, suggesting that the heptapeptide may also play an active role in the regulation of sodium excretion by actions on renal hemodynamics and tubules. Sodium 292-298 angiotensinogen Rattus norvegicus 51-57 1836424-7 1991 It is not yet clear how important ANP is for the regulation of blood pressure and sodium and water balance during normal pregnancy and pregnancy complicated by pre-eclampsia. Sodium 82-88 natriuretic peptide A Homo sapiens 34-37 1834374-0 1991 Differential effects of angiotensin II and noradrenaline on tubular rejection of sodium produced by ANP in rats. Sodium 81-87 angiotensinogen Rattus norvegicus 24-38 1712268-3 1991 In addition, administration of ACE inhibitors can reduce proximal sodium reabsorption via changes in peritubular hydrostatic and oncotic forces resulting from the fall in postglomerular capillary resistance. Sodium 66-72 angiotensin I converting enzyme Homo sapiens 31-34 1842937-3 1991 Expansion of the extracellular volume stimulates secretion of ANF which consequently contributes to renal excretion of sodium and water. Sodium 119-125 natriuretic peptide A Homo sapiens 62-65 1846120-1 1991 In previous studies we found that vasopressin stimulation of both cyclic AMP (cAMP) formation in cortical collecting tubules (CCT) and sodium reabsorption in isolated perfused kidneys was markedly exaggerated in rats with mineralocorticoid hypertension. Sodium 135-141 arginine vasopressin Rattus norvegicus 34-45 1806484-1 1991 Administration of human growth hormone (GH) is associated with clinically significant sodium retention. Sodium 86-92 growth hormone 1 Homo sapiens 24-38 1725429-1 1991 We assessed whether there is an interaction between angiotensin II (Ang II) and endothelin-1 (ET-1) in the regulation of blood pressure and sodium and water metabolism in rats. Sodium 140-146 angiotensinogen Rattus norvegicus 68-74 1725359-1 1991 This study was conducted to determine the involvement of endogenous endothelin-1 (ET-1), a potent vasoconstricting peptide, in systemic and renal hemodynamics and in the renin-angiotensin system, by inhibiting ET-1 action with an infusion of specific ET-1 antiserum during altered sodium balance. Sodium 281-287 endothelin 1 Rattus norvegicus 68-80 1725359-1 1991 This study was conducted to determine the involvement of endogenous endothelin-1 (ET-1), a potent vasoconstricting peptide, in systemic and renal hemodynamics and in the renin-angiotensin system, by inhibiting ET-1 action with an infusion of specific ET-1 antiserum during altered sodium balance. Sodium 281-287 endothelin 1 Rattus norvegicus 82-86 1725359-2 1991 Infusion of 1:50 diluted ET-1 antiserum, which completely inhibited renal vasoconstriction caused by exogenously administered ET-3 (0.25 to 1.0 nmol/kg), increased urinary sodium excretion (UNaV) and fractional excretion of sodium (FENa), and decreased the plasma renin concentration (PRC) without significant changes in blood pressure, heart rate, GFR, RPF, or urine volume (UV) in conscious rats fed a low-salt diet, but not those on a high-salt diet. Sodium 172-178 endothelin 1 Rattus norvegicus 25-29 1725359-2 1991 Infusion of 1:50 diluted ET-1 antiserum, which completely inhibited renal vasoconstriction caused by exogenously administered ET-3 (0.25 to 1.0 nmol/kg), increased urinary sodium excretion (UNaV) and fractional excretion of sodium (FENa), and decreased the plasma renin concentration (PRC) without significant changes in blood pressure, heart rate, GFR, RPF, or urine volume (UV) in conscious rats fed a low-salt diet, but not those on a high-salt diet. Sodium 224-230 endothelin 1 Rattus norvegicus 25-29 1725429-1 1991 We assessed whether there is an interaction between angiotensin II (Ang II) and endothelin-1 (ET-1) in the regulation of blood pressure and sodium and water metabolism in rats. Sodium 140-146 endothelin 1 Rattus norvegicus 94-98 1725429-1 1991 We assessed whether there is an interaction between angiotensin II (Ang II) and endothelin-1 (ET-1) in the regulation of blood pressure and sodium and water metabolism in rats. Sodium 140-146 endothelin 1 Rattus norvegicus 80-92 1846421-1 1991 Our previous studies have shown that angiotensin II (Ang II) has a dose-dependent biphasic effect on bicarbonate and sodium transport and 4-beta-phorbol-12-myristate-13-acetate can simulate the stimulatory effect of Ang II on Na+/H+ exchange in the proximal convoluted tubules (PCT) of the rat kidney. Sodium 117-123 angiotensinogen Rattus norvegicus 37-51 2043224-5 1991 Acutely, insulin has been shown to stimulate sympathetic nervous system activity and transmembrane electrolyte transport, to promote sodium retention and to cause vascular wall changes, including increased cholesterol biosynthesis and smooth muscle proliferation. Sodium 133-139 insulin Homo sapiens 9-16 1846421-8 1991 These results suggest that PKC and intracellular calcium play a critical role in mediating the biphasic effect of Ang II on bicarbonate and sodium transport in PCT. Sodium 140-146 angiotensinogen Rattus norvegicus 114-120 1846421-1 1991 Our previous studies have shown that angiotensin II (Ang II) has a dose-dependent biphasic effect on bicarbonate and sodium transport and 4-beta-phorbol-12-myristate-13-acetate can simulate the stimulatory effect of Ang II on Na+/H+ exchange in the proximal convoluted tubules (PCT) of the rat kidney. Sodium 117-123 angiotensinogen Rattus norvegicus 53-59 1886454-0 1991 Angiotensin II mediates hyperadrenergic activity evoked by sodium restriction in essential hypertension. Sodium 59-65 angiotensinogen Homo sapiens 0-14 1659877-2 1991 The urinary volume, sodium excretion and cyclic GMP (cGMP) excretion and plasma cGMP were markedly increased by the synthetic alpha-human ANP (alpha-hANP) infusion in healthy volunteers. Sodium 20-26 natriuretic peptide A Homo sapiens 138-141 1921246-2 1991 Restriction of salt intake in the diet lowers blood pressure in many subjects with high blood pressure and this fall in blood pressure is mediated in part by a diminished renin response to sodium restriction as hypertension develops. Sodium 189-195 renin Homo sapiens 171-176 1921246-3 1991 The effect of sodium restriction, like diuretics, is additive to many blood pressure lowering drugs, particularly those that inhibit the renin system such as beta-blockers and angiotensin converting enzyme inhibitors. Sodium 14-20 renin Homo sapiens 137-142 1921253-0 1991 Short-term dietary sodium restriction increases serum lipids and insulin in salt-sensitive and salt-resistant normotensive adults. Sodium 19-25 insulin Homo sapiens 65-72 1886454-1 1991 We examined the possible involvement of angiotensin II in the modulation of circulating norepinephrine produced by acute sodium restriction in essential hypertensive patients (n = 18). Sodium 121-127 angiotensinogen Homo sapiens 40-54 1886454-2 1991 Sodium restriction potentiated plasma level of norepinephrine in parallel with an increased plasma renin activity (r = 0.81, F = 31.2, p less than 0.05 given by the percent changes). Sodium 0-6 renin Homo sapiens 99-104 1886454-3 1991 An intravenous infusion of sarcosine-1, isoleucine-8 angiotensin II produced a significant fall in mean arterial pressure (-6 +/- 2 mmHg, p less than 0.05) in patients on sodium restriction but not before sodium restriction, while the infusion of the antagonist produced a greater decrease (p less than 0.05) in plasma norepinephrine with sodium restriction (-158 +/- 23 pg/ml, p less than 0.05) when compared to that obtained before sodium restriction (-91 +/- 11 pg/ml, p less than 0.05). Sodium 171-177 angiotensinogen Homo sapiens 53-67 1886454-3 1991 An intravenous infusion of sarcosine-1, isoleucine-8 angiotensin II produced a significant fall in mean arterial pressure (-6 +/- 2 mmHg, p less than 0.05) in patients on sodium restriction but not before sodium restriction, while the infusion of the antagonist produced a greater decrease (p less than 0.05) in plasma norepinephrine with sodium restriction (-158 +/- 23 pg/ml, p less than 0.05) when compared to that obtained before sodium restriction (-91 +/- 11 pg/ml, p less than 0.05). Sodium 205-211 angiotensinogen Homo sapiens 53-67 1886454-3 1991 An intravenous infusion of sarcosine-1, isoleucine-8 angiotensin II produced a significant fall in mean arterial pressure (-6 +/- 2 mmHg, p less than 0.05) in patients on sodium restriction but not before sodium restriction, while the infusion of the antagonist produced a greater decrease (p less than 0.05) in plasma norepinephrine with sodium restriction (-158 +/- 23 pg/ml, p less than 0.05) when compared to that obtained before sodium restriction (-91 +/- 11 pg/ml, p less than 0.05). Sodium 205-211 angiotensinogen Homo sapiens 53-67 1886454-3 1991 An intravenous infusion of sarcosine-1, isoleucine-8 angiotensin II produced a significant fall in mean arterial pressure (-6 +/- 2 mmHg, p less than 0.05) in patients on sodium restriction but not before sodium restriction, while the infusion of the antagonist produced a greater decrease (p less than 0.05) in plasma norepinephrine with sodium restriction (-158 +/- 23 pg/ml, p less than 0.05) when compared to that obtained before sodium restriction (-91 +/- 11 pg/ml, p less than 0.05). Sodium 205-211 angiotensinogen Homo sapiens 53-67 1886454-6 1991 It can be interpreted that acute sodium depletion results in a substantial contribution of angiotensin II to the expression of hyperadrenergic activity. Sodium 33-39 angiotensinogen Homo sapiens 91-105 1754319-2 1991 Sodium and water retention in patients with the nephrotic syndrome favours an increase of the content of antidiuretic hormone and plasma renin activity. Sodium 0-6 renin Homo sapiens 137-142 1984626-3 1991 A biracial sample of 159 children and adolescents were classified as having a low, intermediate, or high renin-sodium profile based on the relationship between their plasma renin activity and 24-hour urinary sodium excretion. Sodium 111-117 renin Homo sapiens 105-110 1652115-6 1991 In conclusion, reduced water and sodium excretion after frusemide in the nephrotic syndrome is accompanied by a diminished reduction of blood volume, a delayed decrease in atrial natriuretic peptide, and a blunted increase in angiotensin II and aldosterone compared with healthy subjects. Sodium 33-39 angiotensinogen Homo sapiens 226-240 1659670-4 1991 In both hypertensives and normotensives, serum PTH levels were positively correlated with NcAMP excretion (r = 0.42, p less than 0.05, and r = 0.41, p less than 0.05, respectively) and the ratio of urinary sodium to urinary calcium excretion (r = 0.59, p less than 0.001, and r = 0.75, p less than 0.001), respectively). Sodium 206-212 parathyroid hormone Homo sapiens 47-50 1706107-10 1991 The finding on increased distal sodium reabsorption might point to the existence of an insulin-dependent mechanism. Sodium 32-38 insulin Homo sapiens 87-94 1796634-6 1991 In more severe heart failure vasoconstrictor, sodium and water-retaining mechanisms like the renin-angiotensin-aldosterone system are activated with the consequence of an increase of systemic vascular resistance, a reduction of renal blood flow, and an increased fluid retention. Sodium 46-52 renin Homo sapiens 93-98 1830397-7 1991 ANF may be involved in the understanding of sodium retention during ventilation with PEEP and in the paraneoplastic hyponatraemia of certain bronchial tumours. Sodium 44-50 natriuretic peptide A Homo sapiens 0-3 2078323-7 1990 Sodium-sensitive blood pressure responses in the obese may be secondary to increased cardiac output or fluid volume, and are directly related to circulating insulin levels. Sodium 0-6 insulin Homo sapiens 157-164 1839104-7 1991 Possible mechanisms are a reduced renal perfusion pressure, a receptor down-regulation or an overactivity of sodium-retaining hormones like the renin aldosterone system, and the sympathetic activity. Sodium 109-115 renin Homo sapiens 144-149 2081010-3 1990 In 10 subjects with high renin hypertension, an increase in dietary sodium intake resulted in an increase in urinary calcium excretion (2.5 to 3.4 mmol/L, P = .011) and an increase in serum 1,25-dihydroxyvitamin D (51.2 to 61.0 pmol/L, P = .045). Sodium 68-74 renin Homo sapiens 25-30 2081010-6 1990 It is postulated that the increase in dietary sodium led to an increase in serum 1,25-dihydroxyvitamin D concentration, which may have contributed to an increase in intracellular calcium concentration, a decrease in renal secretion of renin, and a fall in plasma renin activity. Sodium 46-52 renin Homo sapiens 235-240 2081010-6 1990 It is postulated that the increase in dietary sodium led to an increase in serum 1,25-dihydroxyvitamin D concentration, which may have contributed to an increase in intracellular calcium concentration, a decrease in renal secretion of renin, and a fall in plasma renin activity. Sodium 46-52 renin Homo sapiens 263-268 2081010-8 1990 Therefore, 1,25-dihydroxyvitamin D may be a mediator in the response of high renin hypertension to increased sodium intake. Sodium 109-115 renin Homo sapiens 77-82 2244565-2 1990 With an unrestricted sodium diet, plasma renin concentration was inhibited within 10 minutes by intravenous enalkiren and remained essentially undetectable for greater than or equal to 6 hours (11.9 +/- 4 to 1.0 +/- 0.6 ng angiotensin I/ml/hour, p less than 0.05). Sodium 21-27 renin Homo sapiens 41-46 2281947-4 1990 Secondly, in the sodium depleted rat, we find that interference with central, but not peripheral, angiotensin II action suppresses sodium appetite. Sodium 131-137 angiotensinogen Rattus norvegicus 98-112 2281947-5 1990 Together, these data confirm recent evidence which demonstrates that it is angiotensin II of cerebral origin, not angiotensin II of renal origin, that is necessary for the expression of sodium appetite. Sodium 186-192 angiotensinogen Rattus norvegicus 75-89 2076856-5 1990 It has been suggested that hyperinsulinism and insulin resistance may lead to hypertension through altered intracellular calcium metabolism, enhanced renal sodium reabsorption, or through an effect of insulin upon lipid and/or catecholamine metabolism. Sodium 156-162 insulin Homo sapiens 32-39 2076856-5 1990 It has been suggested that hyperinsulinism and insulin resistance may lead to hypertension through altered intracellular calcium metabolism, enhanced renal sodium reabsorption, or through an effect of insulin upon lipid and/or catecholamine metabolism. Sodium 156-162 insulin Homo sapiens 47-54 2079200-1 1990 The capacity of five synthetic analogs of [8-arginine] vasopressin (AVP) to stimulate frog skin sodium transport (natriferic activity) was characterized electrophysiologically using the method of short-circuit current, and compared to that of synthetic AVP. Sodium 96-102 arginine vasopressin Homo sapiens 55-66 1966524-8 1990 On the other hand, the correlation between circulating atriopeptin and sodium excretion exceeded 0.8 in only 3 of 18 experiments and was below 0.6 in 10 experiments. Sodium 71-77 natriuretic peptide A Homo sapiens 55-66 1966524-9 1990 A negative correlation between plasma atriopeptin and renal sodium excretion was observed during left atrial distension in the cardiac-denervated dogs. Sodium 60-66 natriuretic peptide A Homo sapiens 38-49 1962804-0 1990 The effect of the renin inhibitor ES-1005 on the expression of the kidney renin gene in sodium-depleted marmosets. Sodium 88-94 renin Homo sapiens 74-79 1962804-1 1990 The effect of the renin inhibitor ES-1005 or captopril on the expression of the kidney renin gene was investigated in sodium-depleted marmosets. Sodium 118-124 renin Homo sapiens 87-92 1962804-7 1990 These results suggest that the treatment with the renin inhibitor ES-1005 for one week has a paradoxical effect on kidney renin gene expression and renin release from the kidney in sodium-depleted marmosets. Sodium 181-187 renin Homo sapiens 50-55 2151149-7 1990 The results confirm the important role of ANP in the adaptation of reduced kidney mass to the excretion of sodium load. Sodium 107-113 natriuretic peptide A Homo sapiens 42-45 2146863-2 1990 Compared with the placebo, ANF induced an increase in urine volume (p less than 0.05), sodium excretion (p less than 0.05), and chloride excretion (p less than 0.05). Sodium 87-93 natriuretic peptide A Homo sapiens 27-30 2146863-4 1990 The maximal response of urinary sodium excretion rate after ANF infusion was positively correlated with the basal sodium excretion rate (r = 0.579; p less than 0.05) and inversely correlated with basal plasma renin activity (r = -0.623; p less than 0.05). Sodium 32-38 natriuretic peptide A Homo sapiens 60-63 2146863-4 1990 The maximal response of urinary sodium excretion rate after ANF infusion was positively correlated with the basal sodium excretion rate (r = 0.579; p less than 0.05) and inversely correlated with basal plasma renin activity (r = -0.623; p less than 0.05). Sodium 32-38 renin Homo sapiens 209-214 2146863-4 1990 The maximal response of urinary sodium excretion rate after ANF infusion was positively correlated with the basal sodium excretion rate (r = 0.579; p less than 0.05) and inversely correlated with basal plasma renin activity (r = -0.623; p less than 0.05). Sodium 114-120 natriuretic peptide A Homo sapiens 60-63 2148092-7 1990 This study demonstrates a marked sensitivity of the responses of both the ANP and the renin-aldosterone system to small changes in sodium intake and points to their importance in the renal adaptations to small alterations in dietary sodium intake. Sodium 131-137 renin Homo sapiens 86-91 2148092-7 1990 This study demonstrates a marked sensitivity of the responses of both the ANP and the renin-aldosterone system to small changes in sodium intake and points to their importance in the renal adaptations to small alterations in dietary sodium intake. Sodium 233-239 renin Homo sapiens 86-91 2261144-3 1990 By interfering with the formation of angiotensin II, the active agent of the renin system, ACE inhibitors block the system"s vasoconstrictive and sodium-retaining effects, with a consequent reduction in systemic blood pressure. Sodium 146-152 angiotensinogen Homo sapiens 37-51 2261144-3 1990 By interfering with the formation of angiotensin II, the active agent of the renin system, ACE inhibitors block the system"s vasoconstrictive and sodium-retaining effects, with a consequent reduction in systemic blood pressure. Sodium 146-152 renin Homo sapiens 77-82 2261144-3 1990 By interfering with the formation of angiotensin II, the active agent of the renin system, ACE inhibitors block the system"s vasoconstrictive and sodium-retaining effects, with a consequent reduction in systemic blood pressure. Sodium 146-152 angiotensin I converting enzyme Homo sapiens 91-94 2078904-6 1990 These results indicate that ILI in the brain may play a role in the secretion of AVP, and that this mechanism could be operated to control a water-sodium balance. Sodium 147-153 arginine vasopressin Rattus norvegicus 81-84 2079072-3 1990 A mean sodium supplement of 2.2 mmol/kg per day (range 0.5-4.9), double the amount provided with feeds, was required to maintain plasma sodium concentration and plasma renin activity (PRA) in the normal range for age. Sodium 7-13 renin Homo sapiens 168-173 2097166-0 1990 Effect of sodium depletion on the renin-angiotensin-aldosterone system and renal prostaglandins in acromegalic patients. Sodium 10-16 renin Homo sapiens 34-39 2175373-4 1990 A major cellular interaction is apparent in the proximal tubule where inhibition of sodium transport by ANF appears to be Ang II-dependent. Sodium 84-90 natriuretic peptide A Homo sapiens 104-107 2220796-3 1990 ACE inhibitors have similar effects on renal blood flow and glomerular filtration rate in essential hypertension, but they tend to cause sodium retention. Sodium 137-143 angiotensin I converting enzyme Homo sapiens 0-3 2144858-4 1990 On high sodium intake, plasma ANF increased in ONorm, but not in OHyp (to 18.3 +/- 1.7 vs. 11.7 +/- 1.7 fmol/L; P less than 0.001). Sodium 8-14 natriuretic peptide A Homo sapiens 30-33 2144858-11 1990 We postulate a new endocrine syndrome characterized by a relative plasma ANF deficiency during high sodium intake in some hypertension-prone humans. Sodium 100-106 natriuretic peptide A Homo sapiens 73-76 2213375-8 1990 The plasma AVP concentration was significantly lower after 24 hours of maintenance plus replacement fluids than after fluid restriction (p = 0.005), and the change in AVP concentration correlated with the amount of sodium given (p less than 0.02). Sodium 215-221 arginine vasopressin Homo sapiens 167-170 2213375-9 1990 This study supports the hypothesis that serum AVP concentrations are elevated in patients with meningitis because of hypovolemia and become normal when sufficient sodium is given to facilitate reabsorption of water by the proximal tubule of the kidney. Sodium 163-169 arginine vasopressin Homo sapiens 46-49 2145871-3 1990 Peak levels were reached within 2 h declining to control values by 8 h. The rise in ANF was associated with an increase in urine volume and mean urinary sodium excretion rose from 64.9 mmoles/8 h after placebo to 116.1 mmoles/8 h after 10 mg/kg UK 69,578. Sodium 153-159 natriuretic peptide A Homo sapiens 84-87 2148776-6 1990 In the group of 9 diabetic patients, significant (p less than 0.05) reductions in fasting plasma glucose, hematocrit and the urinary excretion of sodium and glucose were seen with insulin treatment. Sodium 146-152 insulin Homo sapiens 180-187 2148776-10 1990 A sodium-retaining effect of insulin and a decrease in osmotic diuresis may have increased the body fluid volume and caused the fall in PRA. Sodium 2-8 insulin Homo sapiens 29-36 2232484-2 1990 Although low sodium diets have been reported to decrease the tissue renin gradient, little information is available on renin release by different areas of the renal cortex or the effect of a low sodium diet. Sodium 13-19 LOW QUALITY PROTEIN: renin Oryctolagus cuniculus 68-73 2164912-0 1990 Prompt inhibition of arginine vasopressin-induced cellular adenosine 3",5"-monophosphate production by extracellular sodium depletion in rat renal inner medullary collecting duct cells in culture. Sodium 117-123 arginine vasopressin Rattus norvegicus 30-41 2150808-2 1990 They were all under constant sodium intake because dietary sodium is known to affect the amount of plasma ANP. Sodium 59-65 natriuretic peptide A Homo sapiens 106-109 2150808-7 1990 In the present study we were able to confirm that under a constant sodium diet, high plasma ANP in patients with Graves" disease was reduced after surgery when they became euthyroid. Sodium 67-73 natriuretic peptide A Homo sapiens 92-95 2150808-8 1990 Results also suggest that high circulating ANP might play an important role in sodium and water metabolism and hemodynamic changes in hyperthyroidism. Sodium 79-85 natriuretic peptide A Homo sapiens 43-46 2222965-2 1990 Recent research provides evidence that parathyroid hormone, calcitonin, 1,25-dihydroxyvitamin D, as well as newly described factors such as calcitonin gene-related peptide (CGRP), exert target-organ-specific actions in cardiac and peripheral vascular tissues, are linked to the renin-aldosterone system, and thus to the control of sodium metabolism, and may directly participate in the hypertensive process, especially in low renin and salt sensitive forms of hypertensive disease. Sodium 331-337 calcitonin related polypeptide alpha Homo sapiens 140-171 2222965-2 1990 Recent research provides evidence that parathyroid hormone, calcitonin, 1,25-dihydroxyvitamin D, as well as newly described factors such as calcitonin gene-related peptide (CGRP), exert target-organ-specific actions in cardiac and peripheral vascular tissues, are linked to the renin-aldosterone system, and thus to the control of sodium metabolism, and may directly participate in the hypertensive process, especially in low renin and salt sensitive forms of hypertensive disease. Sodium 331-337 calcitonin related polypeptide alpha Homo sapiens 173-177 2222965-3 1990 The metabolic set-point of these linked renin and calcium hormone systems, which serve to transduce environmental dietary mineral signals at the cellular level, determines the blood pressure consequences of sodium and calcium loading and/or restriction, and helps to explain the heterogeneous and seemingly inconsistent effects of these dietary maneuvers on blood pressure. Sodium 207-213 renin Homo sapiens 40-45 2147141-4 1990 Similar increase in plasma ANF after saline infusion in both groups was associated with significantly greater urine and sodium excretion in EH than in controls. Sodium 120-126 natriuretic peptide A Homo sapiens 27-30 2166501-3 1990 These results indicate that attenuated glomerular responses to ANF in low-sodium rats might be due to increase of plasma Angiotensin II (Ang II) level, which increases intracellular Ca++ concentration. Sodium 74-80 angiotensinogen Rattus norvegicus 121-135 2174002-4 1990 When substituted with glucocorticoids, patients responded to hANP (100 micrograms) with an increase (p less than 0.025) in diuresis and sodium excretion, whereas no changes in diuresis and sodium excretion were seen following intravenous hANP during glucocorticoid withdrawal. Sodium 136-142 natriuretic peptide A Homo sapiens 61-65 2379945-6 1990 Similarly, sodium restriction caused a 168% elevation of renal renin secretion (p less than 0.05). Sodium 11-17 renin Homo sapiens 63-68 2177369-6 1990 After glycerol or mannitol infusion, the plasma ANF raised significantly (P less than 0.05, paired Student"s test), also the serum osmolarity (P less than 0.05, paired Student"s t test), but the blood pressure and serum sodium kept unchanged. Sodium 220-226 natriuretic peptide A Homo sapiens 48-51 2166501-3 1990 These results indicate that attenuated glomerular responses to ANF in low-sodium rats might be due to increase of plasma Angiotensin II (Ang II) level, which increases intracellular Ca++ concentration. Sodium 74-80 angiotensinogen Rattus norvegicus 137-143 2142862-5 1990 However, chronic oral treatment with the angiotensin-converting-enzyme inhibitor enalapril restored the natriuretic response of sodium-retaining rats with a-v fistula to high doses of ANF. Sodium 128-134 angiotensin I converting enzyme Rattus norvegicus 41-70 2193561-6 1990 The renal vasoconstriction, which accompanies either decreased cardiac output or peripheral arterial vasodilation, causes a decreased distal tubular delivery of sodium and water, thus maximizing the water-retaining effect of vasopressin and impairing normal escape from the sodium-retaining effect of aldosterone. Sodium 161-167 arginine vasopressin Homo sapiens 225-236 2163648-0 1990 Increased sodium-lithium countertransport in black non-insulin-dependent diabetic hypertensives. Sodium 10-16 insulin Homo sapiens 55-62 2375419-1 1990 Initial experiments demonstrated that a 1-h infusion of 10 ng/min angiotensin II (ANG II) into rats causes an increase in plasma aldosterone concentration (PAC) and that chronic administration of aldosterone alone to rats on increased sodium intake causes hypertension. Sodium 235-241 angiotensinogen Rattus norvegicus 66-80 2197881-1 1990 This study was designed to investigate in sodium-depleted monkeys the renal hemodynamic and excretory effects resulting from blockade of the renin-angiotensin system induced by intrarenal infusion of the primate-selective renin inhibitor A-65317. Sodium 42-48 renin Homo sapiens 141-146 2197881-1 1990 This study was designed to investigate in sodium-depleted monkeys the renal hemodynamic and excretory effects resulting from blockade of the renin-angiotensin system induced by intrarenal infusion of the primate-selective renin inhibitor A-65317. Sodium 42-48 renin Homo sapiens 222-227 2375419-1 1990 Initial experiments demonstrated that a 1-h infusion of 10 ng/min angiotensin II (ANG II) into rats causes an increase in plasma aldosterone concentration (PAC) and that chronic administration of aldosterone alone to rats on increased sodium intake causes hypertension. Sodium 235-241 angiotensinogen Rattus norvegicus 82-88 2375419-8 1990 Compared with saline-infused rats, ANG II-infused rats on high sodium intake had normal values for all variables except MAP, which was significantly elevated during ANG II infusion. Sodium 63-69 angiotensinogen Rattus norvegicus 35-41 2148294-11 1990 These data indicate that the fasting natriuresis cannot be explained by changes in ANF levels but that the loss of sodium may contribute to a decline of basal ANF levels, with an attenuation of their physiological postural changes, and to a stimulation of the aldosterone secretion. Sodium 115-121 natriuretic peptide A Homo sapiens 159-162 2083062-1 1990 The study has been performed in an attempt to provide further data on the supposed direct action of insulin on the kidney, based on the assumption that any effect of insulin on sodium reabsorption via co-transport should shift the dose-response curve to the furosemide administration. Sodium 177-183 insulin Homo sapiens 100-107 2083062-1 1990 The study has been performed in an attempt to provide further data on the supposed direct action of insulin on the kidney, based on the assumption that any effect of insulin on sodium reabsorption via co-transport should shift the dose-response curve to the furosemide administration. Sodium 177-183 insulin Homo sapiens 166-173 2167792-0 1990 Role of atrial natriuretic factor in changes in the responsiveness of aldosterone to angiotensin II secondary to sodium loading and depletion in man. Sodium 113-119 angiotensinogen Homo sapiens 85-99 2167792-2 1990 Sodium loading blunts the response of aldosterone to infusion of angiotensin II, whereas sodium depletion leads to an enhanced response. Sodium 0-6 angiotensinogen Homo sapiens 65-79 2147304-7 1990 For the renal response to acute expansion of the ECV thus not only the absolute plasma concentration of ANF is decisive but also its ratio to the activity of the sodium retaining renin-angiotensin-aldosterone system. Sodium 162-168 natriuretic peptide A Homo sapiens 104-107 2206912-6 1990 For instance sodium depletion increases the expression of renal angiotensinogen (as well as renin mRNA), as does high potassium intake and androgen administration. Sodium 13-19 angiotensinogen Rattus norvegicus 64-79 2147304-7 1990 For the renal response to acute expansion of the ECV thus not only the absolute plasma concentration of ANF is decisive but also its ratio to the activity of the sodium retaining renin-angiotensin-aldosterone system. Sodium 162-168 renin Homo sapiens 179-184 2162348-10 1990 In fibroblasts, insulin caused an increase in sodium uptake which was not inhibited by 1 mM amiloride. Sodium 46-52 insulin Homo sapiens 16-23 2383375-1 1990 Sodium loading reduces aldosterone responses to angiotensin II (AII) when compared to the sodium restricted state. Sodium 0-6 angiotensinogen Homo sapiens 48-62 2383375-1 1990 Sodium loading reduces aldosterone responses to angiotensin II (AII) when compared to the sodium restricted state. Sodium 0-6 angiotensinogen Homo sapiens 64-67 2383375-2 1990 Recent investigations suggest that dopamine inhibits the aldosterone secretion and may contribute to the alteration in aldosterone response to AII with sodium intake, since administration of the dopamine antagonist, metoclopramide, enhances the aldosterone responses to AII on a high but not a low salt diet. Sodium 152-158 angiotensinogen Homo sapiens 143-146 2383375-2 1990 Recent investigations suggest that dopamine inhibits the aldosterone secretion and may contribute to the alteration in aldosterone response to AII with sodium intake, since administration of the dopamine antagonist, metoclopramide, enhances the aldosterone responses to AII on a high but not a low salt diet. Sodium 152-158 angiotensinogen Homo sapiens 270-273 2188754-10 1990 Moreover, renin response to sodium depletion appears to be an attribute that additionally characterizes individual hypertensive patients. Sodium 28-34 renin Homo sapiens 10-15 2162795-9 1990 These results suggest that the blunted natriuretic responsiveness to ANP is contributory to the pathogenesis of initial sodium retention in cirrhotics. Sodium 120-126 natriuretic peptide A Homo sapiens 69-72 2190920-11 1990 For example, sodium sensitivity could be mediated by the cation transport mechanism of Na,K-ATPase, or insulin resistance could be induced by an elevated level of adrenergic activity. Sodium 13-19 insulin Homo sapiens 103-110 2347619-3 1990 We have measured red blood cell sodium-lithium counter-transport activity in 36 microalbuminuric insulin-dependent diabetic patients, a group at high risk of progression to clinical nephropathy and cardiovascular disease, and compared it with that of a matched group of 36 normoalbuminuric diabetic patients. Sodium 32-38 insulin Homo sapiens 97-104 2347619-7 1990 In a subset of patients in whom lipoproteins were measured, sodium-lithium countertransport activity was related to total and very low density lipoprotein triglycerides (r = 0.41, p less than 0.05 and r = 0.48, p less than 0.05) and to apolipoprotein B (r = 0.56, p less than 0.05), independently of body mass index, albumin excretion rate, glycemic control, and insulin dose. Sodium 60-66 apolipoprotein B Homo sapiens 236-252 2347619-7 1990 In a subset of patients in whom lipoproteins were measured, sodium-lithium countertransport activity was related to total and very low density lipoprotein triglycerides (r = 0.41, p less than 0.05 and r = 0.48, p less than 0.05) and to apolipoprotein B (r = 0.56, p less than 0.05), independently of body mass index, albumin excretion rate, glycemic control, and insulin dose. Sodium 60-66 insulin Homo sapiens 363-370 2166424-4 1990 The ratio of calcium to sodium clearances (CCa/CNa), a measure of distal tubular calcium transport, was reduced to the same extent by PTH, PTHLP-(1-36), and PTHLP-(1-74) (54.3 +/- 3.9, 52.9 +/- 3.9, and 52.7 +/- 1.3% reductions from control), respectively) at maximal doses (35-50 pM and higher), with half-maximal effects at 10, 18, and 32 pM, respectively. Sodium 24-30 parathyroid hormone Homo sapiens 134-137 2140025-4 1990 Atriopeptin II significantly decreased mean aortic pressure (-12%), GFR (-40%), V (-66%), and the absolute excretion rates of sodium (-47%), potassium (-43%), and total osmolytes (-44%). Sodium 126-132 natriuretic peptide A Homo sapiens 0-11 2159227-5 1990 The apparent dissociation constant (K0.5) of alpha 1 for sodium changed from 12 to 9 mM when going from synaptosomes to membranes. Sodium 57-63 alpha-Tubulin at 84B Drosophila melanogaster 45-52 2159227-8 1990 By comparison, the Na(+)-K(+)-ATPase from the mouse fibroblast cell line, 3T3-F442A cells, expressed only the alpha 1-isozyme, as shown by immunoblotting and by measurement of its ouabain and sodium affinities. Sodium 192-198 alpha-Tubulin at 84B Drosophila melanogaster 110-117 2159228-1 1990 The sensitivity of the synaptosomal Na(+)-K(+)-ATPase to insulin was examined and found to be stimulated by the hormone when physiological intracellular sodium concentrations were present. Sodium 153-159 insulin Homo sapiens 57-64 2159725-0 1990 Effect of vasopressin on sodium transport across inner medullary collecting duct. Sodium 25-31 arginine vasopressin Rattus norvegicus 10-21 2162269-7 1990 In the syndrome of inappropriate secretion of antidiuretic hormone, the fractional excretion of filtered urea was inversely correlated to the fractional excretion of filtered sodium (r = -0.66; P less than 0.001), whereas the fractional excretion of filtered uric acid was not dependent on sodium excretion. Sodium 175-181 arginine vasopressin Homo sapiens 46-66 2162269-7 1990 In the syndrome of inappropriate secretion of antidiuretic hormone, the fractional excretion of filtered urea was inversely correlated to the fractional excretion of filtered sodium (r = -0.66; P less than 0.001), whereas the fractional excretion of filtered uric acid was not dependent on sodium excretion. Sodium 290-296 arginine vasopressin Homo sapiens 46-66 2162269-9 1990 Hypouraemia with high fractional excretion of filtered urea in patients with the syndrome of inappropriate secretion of antidiuretic hormone is related to low urinary sodium excretion and thus reflects low sodium intake. Sodium 167-173 arginine vasopressin Homo sapiens 120-140 2162269-9 1990 Hypouraemia with high fractional excretion of filtered urea in patients with the syndrome of inappropriate secretion of antidiuretic hormone is related to low urinary sodium excretion and thus reflects low sodium intake. Sodium 206-212 arginine vasopressin Homo sapiens 120-140 2188438-8 1990 Treatment of stable congestive heart failure (CHF) with ACE inhibitors can result in enhancement of GFR and reduction of sodium and fluid retention, thus improving the clinical state. Sodium 121-127 angiotensin I converting enzyme Homo sapiens 56-59 2188439-2 1990 This class of agents effectively inhibits the conversion of angiotensin I to the active vasoconstrictor angiotensin II, a hormone that also promotes, via aldosterone stimulation, increased sodium and water retention. Sodium 189-195 angiotensinogen Homo sapiens 60-73 2188439-2 1990 This class of agents effectively inhibits the conversion of angiotensin I to the active vasoconstrictor angiotensin II, a hormone that also promotes, via aldosterone stimulation, increased sodium and water retention. Sodium 189-195 angiotensinogen Homo sapiens 104-118 2185149-0 1990 Angiotensin II: a powerful controller of sodium transport in the early proximal tubule. Sodium 41-47 angiotensinogen Homo sapiens 0-14 2096434-5 1990 Insulin resistance may well be the most important aetiological factor in this type of arterial hypertension as it stimulates both renal sodium reabsorption and sympathetic nervous system activity and reduces vascular Na-K-ATPase activity. Sodium 136-142 insulin Homo sapiens 0-7 2185149-1 1990 Angiotensin II has recently been shown to exert potent control over sodium and water absorption in the proximal convoluted tubule. Sodium 68-74 angiotensinogen Homo sapiens 0-14 2185149-5 1990 These direct tubular transport actions by angiotensin II may participate importantly in various physiological actions of the kidney, including the renal response to change in dietary sodium intake and in extracellular volume, as well as in pathophysiological processes such as hypertension. Sodium 183-189 angiotensinogen Homo sapiens 42-56 1977841-0 1990 Effect of sodium depletion on active renin, inactive renin and prekallikrein in plasma and urinary kallikrein excretion in glomerulonephritic patients. Sodium 10-16 renin Homo sapiens 37-42 1977841-0 1990 Effect of sodium depletion on active renin, inactive renin and prekallikrein in plasma and urinary kallikrein excretion in glomerulonephritic patients. Sodium 10-16 renin Homo sapiens 53-58 2163413-5 1990 Alterations in the responsiveness of the proximal tubule to Ang II in young SHR could contribute to sodium retention observed during development of hypertension in these rats. Sodium 100-106 angiotensinogen Rattus norvegicus 60-66 2352102-4 1990 Fibronectin sorption was reduced when added in conjunction with serum and was inhibited by monovalent ions (such as sodium), but enhanced in the presence of divalent cations (such as calcium). Sodium 116-122 fibronectin 1 Homo sapiens 0-11 2200107-0 1990 Interleukin 1 beta increases the cytosolic free sodium concentration in isolated rat islets of Langerhans. Sodium 48-54 interleukin 1 beta Rattus norvegicus 0-18 2331021-7 1990 Conversely, sodium depletion increased angiotensin II receptors in the zona glomerulosa. Sodium 12-18 angiotensinogen Rattus norvegicus 39-53 2331021-8 1990 In the kidney glomeruli and medulla, angiotensin II receptors were decreased by either sodium or chloride depletion. Sodium 87-93 angiotensinogen Rattus norvegicus 37-51 2331021-0 1990 Different effects of sodium or chloride depletion on angiotensin II receptors in rats. Sodium 21-27 angiotensinogen Rattus norvegicus 53-67 2180817-9 1990 Similarly, a low sodium diet, which led to a slow increase in renal renin content, provoked large oscillations with high initial levels. Sodium 17-23 renin Homo sapiens 68-73 2331021-3 1990 In the brain, subfornical organ angiotensin II receptor concentration was decreased by sodium depletion and increased by chloride depletion. Sodium 87-93 angiotensinogen Rattus norvegicus 32-46 2318519-3 1990 Renin-angiotensin system activation was evident within 24 hours after sodium intake was restricted. Sodium 70-76 renin Homo sapiens 0-5 2159518-0 1990 Characterization of sodium currents in mammalian sensory neurons cultured in serum-free defined medium with and without nerve growth factor. Sodium 20-26 nerve growth factor Homo sapiens 120-139 2145301-4 1990 Sodium retention, possibly induced by hyperinsulinemia, and perhaps glucose-coupled sodium reabsorption in insulin treated patients, seem to play a central role in elevating the blood pressure, but this needs further clarification. Sodium 0-6 insulin Homo sapiens 43-50 2251209-3 1990 Since it was not possible to establish a correlation between plasma renin activity and albumin level, as well as between this activity and aldosterone level, and aldosterone level and sodium excretion it may be surmised that the renin-angiotensin-aldosterone system has no decisive role in the pathogenesis of the nephrotic syndrome. Sodium 184-190 renin Homo sapiens 229-234 2143782-7 1990 Central Ang II administration produced a significant decrease in urine flow, which was associated with elevated plasma AVP, an increase in sodium excretion and a rise in mean arterial blood pressure. Sodium 139-145 angiotensinogen Rattus norvegicus 8-14 2143782-13 1990 These data suggest the possibility of distinct and separate sites within the brain through which Ang II influences vasopressin release and renal sodium handling and elevates blood pressure. Sodium 145-151 angiotensinogen Rattus norvegicus 97-103 2198366-0 1990 [Effect of renin inhibitor (ES-1005) on expression of the kidney renin gene in sodium-depleted marmosets]. Sodium 79-85 renin Homo sapiens 11-16 2198366-0 1990 [Effect of renin inhibitor (ES-1005) on expression of the kidney renin gene in sodium-depleted marmosets]. Sodium 79-85 renin Homo sapiens 65-70 2184915-0 1990 Down-regulation of angiotensin II receptors in subfornical organ of young male rats by chronic dietary sodium depletion. Sodium 103-109 angiotensinogen Rattus norvegicus 19-33 2309737-7 1990 Patients with NIDDM also had augmented blood pressure responses to infused angiotensin II on both sodium diets when compared to control subjects. Sodium 98-104 angiotensinogen Homo sapiens 75-89 2160342-4 1990 Renin was responsive to posture, low sodium diet, saline infusion and frusemide, but relatively unresponsive to raising or lowering circulating levels of angiotensin II. Sodium 37-43 renin Homo sapiens 0-5 2187635-6 1990 Pressor sensitivity to cold and angiotensin II decreased on low sodium diet, associated with a fall in blood pressure. Sodium 64-70 angiotensinogen Homo sapiens 32-46 2187635-10 1990 These findings are consistent with excessive sodium reabsorption as the primary renal lesion in Gordon"s syndrome, leading to volume expansion and suppression of renin and aldosterone. Sodium 45-51 renin Homo sapiens 162-167 2187635-11 1990 Severe dietary sodium restriction leading to volume contraction, by stimulating renin and aldosterone and promoting kaliuresis, corrects the abnormalities. Sodium 15-21 renin Homo sapiens 80-85 2137801-0 1990 Role of insulin and atrial natriuretic peptide in sodium retention in insulin-treated IDDM patients during isotonic volume expansion. Sodium 50-56 insulin Homo sapiens 70-77 2137801-1 1990 Because insulin shows an antinatriuretic effect in healthy humans, insulin therapy resulting in circulating hyperinsulinemia may lead to sodium retention and in turn to hypertension in individuals with insulin-dependent diabetes mellitus (IDDM). Sodium 137-143 insulin Homo sapiens 8-15 2137801-1 1990 Because insulin shows an antinatriuretic effect in healthy humans, insulin therapy resulting in circulating hyperinsulinemia may lead to sodium retention and in turn to hypertension in individuals with insulin-dependent diabetes mellitus (IDDM). Sodium 137-143 insulin Homo sapiens 67-74 2137801-3 1990 This study investigated the relationship between insulin and ANP in modulating sodium metabolism in normotensive and hypertensive IDDM subjects compared with control groups of normotensive and hypertensive nondiabetic subjects. Sodium 79-85 insulin Homo sapiens 49-56 2137801-12 1990 Subcutaneous insulin infusion, resulting in circulating plasma free-insulin levels in normotensive control subjects comparable to those in IDDM patients, inhibited natriuresis, increased proximal tubule sodium reabsorption at the level of the kidney, and inhibited an adequate ANP stimulation by saline challenge. Sodium 203-209 insulin Homo sapiens 13-20 2137801-12 1990 Subcutaneous insulin infusion, resulting in circulating plasma free-insulin levels in normotensive control subjects comparable to those in IDDM patients, inhibited natriuresis, increased proximal tubule sodium reabsorption at the level of the kidney, and inhibited an adequate ANP stimulation by saline challenge. Sodium 203-209 insulin Homo sapiens 68-75 2156654-7 1990 Plasma aldosterone and plasma renin activity increased during the sodium-depleted period but only plasma renin activity was significantly correlated with fractional excretion of filtered sodium. Sodium 187-193 renin Homo sapiens 105-110 2190807-0 1990 Regulation of renal sodium calcium exchange by PTH: alteration with age. Sodium 20-26 parathyroid hormone Rattus norvegicus 47-50 2138597-1 1990 The heart functions as an endocrine organ, releasing atrial natriuretic peptide (ANP), a hormone, in response to sodium and fluid overload. Sodium 113-119 natriuretic peptide A Homo sapiens 53-79 2138597-1 1990 The heart functions as an endocrine organ, releasing atrial natriuretic peptide (ANP), a hormone, in response to sodium and fluid overload. Sodium 113-119 natriuretic peptide A Homo sapiens 81-84 2138597-6 1990 ANP acts to oppose this system by causing vasorelaxation, blocking the secretion and sodium-retaining effects of aldosterone, and inhibiting renal renin secretion. Sodium 85-91 natriuretic peptide A Homo sapiens 0-3 2139694-6 1990 Plasma concentrations of ANP significantly decreased (by 32%) in response to the low sodium regime in both positions. Sodium 85-91 natriuretic peptide A Homo sapiens 25-28 2159502-8 1990 In both hypertensives and controls, plasma concentrations of active renin, angiotensin II and aldosterone decreased with increasing sodium intake, arginine vasopressin did not change, and atrial natriuretic factor and cyclic GMP increased. Sodium 132-138 renin Homo sapiens 68-73 2159509-8 1990 In hypertensive patients, atrial natriuretic factor (ANF) levels were higher at baseline and showed an exaggerated response to sodium loading. Sodium 127-133 natriuretic peptide A Homo sapiens 26-51 2159509-8 1990 In hypertensive patients, atrial natriuretic factor (ANF) levels were higher at baseline and showed an exaggerated response to sodium loading. Sodium 127-133 natriuretic peptide A Homo sapiens 53-56 2159509-9 1990 Changes in angiotensin II (Ang II) or in Ang II binding sites on platelets were similar in patients and controls and changed appropriately with the sodium intake. Sodium 148-154 angiotensinogen Homo sapiens 11-25 2159509-9 1990 Changes in angiotensin II (Ang II) or in Ang II binding sites on platelets were similar in patients and controls and changed appropriately with the sodium intake. Sodium 148-154 angiotensinogen Homo sapiens 27-33 2159509-9 1990 Changes in angiotensin II (Ang II) or in Ang II binding sites on platelets were similar in patients and controls and changed appropriately with the sodium intake. Sodium 148-154 angiotensinogen Homo sapiens 41-47 2138237-8 1990 These findings suggest that ANP increases distal sodium delivery, and decreases sodium reabsorption in distal segments by a mechanism also sensitive to amiloride. Sodium 49-55 natriuretic peptide A Homo sapiens 28-31 2138237-8 1990 These findings suggest that ANP increases distal sodium delivery, and decreases sodium reabsorption in distal segments by a mechanism also sensitive to amiloride. Sodium 80-86 natriuretic peptide A Homo sapiens 28-31 2182930-4 1990 The evidence further suggest that aldosterone and maybe vasopressin, through their effects on the Na+ channels in the late distal tubule and the collecting duct may be of significance in inducing distal Li+ reabsorption, as seen during severe sodium restriction in rats and dogs. Sodium 243-249 arginine vasopressin Rattus norvegicus 56-67 2186360-0 1990 Stimulation of renin synthesis in the hydronephrotic kidney during sodium depletion. Sodium 67-73 renin Homo sapiens 15-20 2153841-7 1990 These findings will be of particular interest if future studies demonstrate that ectopic ANF production can cause sodium abnormalities in patients with small cell lung cancer. Sodium 114-120 natriuretic peptide A Homo sapiens 89-92 2155002-7 1990 Insulin may increase absorption of sodium in the diluting segment of the distal nephron with consequent water retention. Sodium 35-41 insulin Homo sapiens 0-7 2155002-8 1990 Alternatively, insulin might alter sodium/potassium distribution thus causing increased vascular peripheral resistance. Sodium 35-41 insulin Homo sapiens 15-22 2155543-4 1990 Incubation with vasoactive intestinal peptide (VIP) resulted in a dose-dependent (50% maximal dose of 8.8 +/- 3.6 nM) approximately fivefold increase in basal adenosine 3",5"-cyclic monophosphate (cAMP) levels (basal = 14.6 +/- 1.7 pmol.mg protein-1.15 min-1; VIP stimulated = 72.7 +/- 13.2 pmol.mg protein-1.15 min-1), as well as a dose-dependent maximal 32.6 +/- 5.5% decrease in sodium-dependent phosphate uptake (50% maximal decrease of 46.2 +/- 21.2 nM). Sodium 382-388 vasoactive intestinal peptide Homo sapiens 47-50 2317275-0 1990 Dependence of adrenalectomy-induced sodium appetite on the action of angiotensin II in the brain of the rat. Sodium 36-42 angiotensinogen Rattus norvegicus 69-83 2317275-1 1990 Adrenalectomized rats express a robust sodium appetite that is accompanied by high levels of blood-borne angiotensin II and is caused by angiotensin II of cerebral origin. Sodium 39-45 angiotensinogen Rattus norvegicus 105-119 2317275-1 1990 Adrenalectomized rats express a robust sodium appetite that is accompanied by high levels of blood-borne angiotensin II and is caused by angiotensin II of cerebral origin. Sodium 39-45 angiotensinogen Rattus norvegicus 137-151 2306706-8 1990 In two tumor lines DHO-DH activity could be measured and the results are in agreement with the concept that there is a relation between Brequinar sodium sensitivity and enzyme activity. Sodium 146-152 dihydroorotate dehydrogenase (quinone) Homo sapiens 19-25 2183958-0 1990 Sodium intake modulates renal vascular reactivity to endothelin-1 in Dahl rats. Sodium 0-6 endothelin 1 Rattus norvegicus 53-65 2153521-6 1990 The partially purified bovine PTH-RP stimulated cAMP production in UMR106-01 and OK cell lines and elicited a concentration-dependent inhibition of sodium-dependent phosphate transport in OK cells. Sodium 148-154 parathyroid hormone like hormone Bos taurus 30-36 2139449-8 1990 ANF responded to volume expansion, 47.8 +/- 5.1 pg/ml before sodium load and 69.9 +/- 7.0 pg/ml after sodium load, and changed minimally after postural manoeuvres, 47.3 +/- 3.2 pg/ml supine and 41.7 +/- 5.1 pg/ml upright. Sodium 61-67 natriuretic peptide A Homo sapiens 0-3 2139449-8 1990 ANF responded to volume expansion, 47.8 +/- 5.1 pg/ml before sodium load and 69.9 +/- 7.0 pg/ml after sodium load, and changed minimally after postural manoeuvres, 47.3 +/- 3.2 pg/ml supine and 41.7 +/- 5.1 pg/ml upright. Sodium 102-108 natriuretic peptide A Homo sapiens 0-3 2405233-1 1990 Previous studies using human pituitary extracts have not resolved whether the sodium retaining effects of human growth hormone (hGH) are mediated in part by increased aldosterone secretion. Sodium 78-84 growth hormone 1 Homo sapiens 112-126 2405233-8 1990 The results show that Bio-GH-induced retention of sodium involves the activation of the renin-angiotensin system. Sodium 50-56 renin Homo sapiens 88-93 2145724-0 1990 Regulation of proximal tubule sodium reabsorption by angiotensin II (AII) and atrial natriuretic factor (ANF). Sodium 30-36 angiotensinogen Homo sapiens 53-67 2145724-0 1990 Regulation of proximal tubule sodium reabsorption by angiotensin II (AII) and atrial natriuretic factor (ANF). Sodium 30-36 angiotensinogen Homo sapiens 69-72 2145724-0 1990 Regulation of proximal tubule sodium reabsorption by angiotensin II (AII) and atrial natriuretic factor (ANF). Sodium 30-36 natriuretic peptide A Homo sapiens 78-103 2145724-0 1990 Regulation of proximal tubule sodium reabsorption by angiotensin II (AII) and atrial natriuretic factor (ANF). Sodium 30-36 natriuretic peptide A Homo sapiens 105-108 2145726-0 1990 The tenuous relationship between atriopeptin and sodium excretion. Sodium 49-55 natriuretic peptide A Homo sapiens 33-44 2145726-5 1990 It seems unlikely, therefore, that atriopeptin exerts a substantial effect on the regulation of sodium excretion under normal physiological conditions. Sodium 96-102 natriuretic peptide A Homo sapiens 35-46 2220406-0 1990 Different effects of short and longer-term arginine vasopressin (AVP) administration on sodium excretion in Brattleboro rats. Sodium 88-94 arginine vasopressin Rattus norvegicus 52-63 1982809-2 1990 We have examined the relationship between the plasma renin level and serum sodium concentration in our CAPD patients. Sodium 75-81 renin Homo sapiens 53-58 1982809-4 1990 In forty-one patients a statistically significant inverse correlation between serum sodium and plasma renin levels was demonstrated. Sodium 84-90 renin Homo sapiens 102-107 2154103-9 1990 This drop in plasma renin activity and aldosterone by 7 days post partum, in contrast with the unchanged high values of atrial natriuretic factor, may contribute to negative sodium balance after delivery. Sodium 174-180 renin Homo sapiens 20-25 2301649-2 1990 The present study was designed to investigate the role of angiotensin II in the prostaglandin E2-induced stimulation of proximal sodium reabsorption. Sodium 129-135 angiotensinogen Rattus norvegicus 58-72 2405715-6 1990 In addition, the adrenal medullary angiotensin II receptor density was significantly elevated in animals on the low-sodium diet. Sodium 116-122 angiotensinogen Rattus norvegicus 35-49 2405715-7 1990 These results demonstrate that endogenous angiotensin II is capable of providing a positive modulatory influence on neurally mediated release of adrenal epinephrine, an effect that may require a chronic activation of the renin-angiotensin system as occurs naturally with restricted dietary sodium intake. Sodium 290-296 angiotensinogen Rattus norvegicus 42-56 2139554-2 1990 Considered by many investigators to be the putative "third factor" governing sodium excretion, ANF is a peptide actively secreted by the heart, with multiple target organ effectors. Sodium 77-83 natriuretic peptide A Homo sapiens 95-98 2148493-0 1990 Atrial natriuretic peptide (ANP) as a neuropeptide: interaction with angiotensin II on volume control and renal sodium handling. Sodium 112-118 natriuretic peptide A Homo sapiens 0-26 2148493-6 1990 ANP was shown to inhibit ANG II-induced drinking, release of pituitary hormones and natriuresis, and to induce sodium retention when given alone. Sodium 111-117 natriuretic peptide A Homo sapiens 0-3 2110866-5 1990 Oral administration of ES 6864 at 3 mg/kg to conscious, sodium-depleted marmosets inhibited plasma renin activity (PRA) more than 80% after 1 h. Sodium 56-62 renin Homo sapiens 99-104 2184915-1 1990 The effect of a 4-week period of selective dietary sodium depletion on the regulation of peripheral and central angiotensin II receptors was studied in young rats, by quantitative autoradiography. Sodium 51-57 angiotensinogen Rattus norvegicus 112-126 2184915-4 1990 Such sodium depletion corresponded to a down-regulation of kidney angiotensin II receptors, and to an up-regulation of adrenal zona glomerulosa angiotensin II receptors. Sodium 5-11 angiotensinogen Rattus norvegicus 66-80 2141297-5 1990 These findings suggest that ANP not only decreases distal sodium reabsorption, but also proximal fractional tubular sodium reabsorption in man. Sodium 58-64 natriuretic peptide A Homo sapiens 28-31 2184915-4 1990 Such sodium depletion corresponded to a down-regulation of kidney angiotensin II receptors, and to an up-regulation of adrenal zona glomerulosa angiotensin II receptors. Sodium 5-11 angiotensinogen Rattus norvegicus 144-158 2141297-5 1990 These findings suggest that ANP not only decreases distal sodium reabsorption, but also proximal fractional tubular sodium reabsorption in man. Sodium 116-122 natriuretic peptide A Homo sapiens 28-31 2184915-6 1990 In the brain, profound sodium depletion down-regulated angiotensin II receptors in the subfornical organ. Sodium 23-29 angiotensinogen Rattus norvegicus 55-69 2184915-8 1990 Our results indicate a participation of selective central angiotensin II receptors in the regulation of sodium metabolism and suggest that factors other than circulating angiotensin II levels might contribute to regulate the number of angiotensin II receptors in the subfornical organ. Sodium 104-110 angiotensinogen Rattus norvegicus 58-72 2161301-5 1990 The results indicate that enhanced beta-adrenergic receptor function does accompany sympathetic activation during sodium restriction and converting enzyme inhibition and further support studies showing that the renin-angiotensin system plays the dominant role in blood pressure regulation in the sodium depleted state. Sodium 296-302 renin Homo sapiens 211-216 2147579-3 1990 This moderate increase in ANF is not likely to be explained by hypervolemia and is associated with sodium and water retention rather than natriuresis and diuresis. Sodium 99-105 natriuretic peptide A Homo sapiens 26-29 2350986-8 1990 Factors other than those investigated, such as obesity, alterations in sodium homeostasis of refractoriness of the vascular smooth muscle to the vasodilatory effect of PTH may be involved in the pathogenesis of hypertension in PsHP. Sodium 71-77 parathyroid hormone Homo sapiens 168-171 2225723-5 1990 In this review, the authors discuss the hypothesis that, in metabolic diseases such as diabetes mellitus, obesity and acromegaly, the sodium retention and volume expansion, possibly due to exaggerated sodium intake, and/or exogenously induced peripheral hyperinsulinemia and high levels of growth hormone, could trigger a sustained release of EDLF, which in turn increases the blood pressure. Sodium 134-140 growth hormone 1 Homo sapiens 290-304 2191853-2 1990 In patients with moderate to severe heart failure, therapeutic interventions incorporating diuretics, digoxin and selected vasodilators, specifically angiotensin-converting enzyme (ACE) inhibitors, are designed to correct pathophysiological mechanisms such as left ventricular dysfunction, excessive vasoconstriction and renal reabsorption of sodium and water. Sodium 343-349 angiotensin I converting enzyme Homo sapiens 150-179 2191853-2 1990 In patients with moderate to severe heart failure, therapeutic interventions incorporating diuretics, digoxin and selected vasodilators, specifically angiotensin-converting enzyme (ACE) inhibitors, are designed to correct pathophysiological mechanisms such as left ventricular dysfunction, excessive vasoconstriction and renal reabsorption of sodium and water. Sodium 343-349 angiotensin I converting enzyme Homo sapiens 181-184 2143136-4 1990 The effects of acute change in sodium-fluid status on plasma ANF levels was examined in 7 active and 4 inactive acromegalic patients and in 7 healthy subjects. Sodium 31-37 natriuretic peptide A Homo sapiens 61-64 2276581-0 1990 The effect of ADH and insulin on active sodium transport across frog skin in the presence of alternariol mycotoxin. Sodium 40-46 insulin Homo sapiens 22-29 2276581-2 1990 The effect of vasopressin and insulin on active sodium transport across frog skin in the presence of internal alternariol mycotoxin was studied, using the short-circuit technique. Sodium 48-54 arginine vasopressin Homo sapiens 14-25 2276581-4 1990 Vasopressin stimulates sodium transport across frog skin by decreasing the resistance to sodium entry into the epithelial cells, thus partially removing the inhibition on the short-circuit current due to the action of Alternariol mycotoxin. Sodium 23-29 arginine vasopressin Homo sapiens 0-11 2276581-4 1990 Vasopressin stimulates sodium transport across frog skin by decreasing the resistance to sodium entry into the epithelial cells, thus partially removing the inhibition on the short-circuit current due to the action of Alternariol mycotoxin. Sodium 89-95 arginine vasopressin Homo sapiens 0-11 2151773-1 1990 The discovery of atrial natriuretic peptide (ANP) has modified our current understanding of the regulation of sodium metabolism. Sodium 110-116 natriuretic peptide A Homo sapiens 17-43 2155074-6 1990 Sodium excretion during ANF increased 42% vs vehicle (p less than 0.05), in the patients group and remained unchanged in controls. Sodium 0-6 natriuretic peptide A Homo sapiens 24-27 2151773-1 1990 The discovery of atrial natriuretic peptide (ANP) has modified our current understanding of the regulation of sodium metabolism. Sodium 110-116 natriuretic peptide A Homo sapiens 45-48 2143176-1 1990 Low level of plasma atrial natriuretic factor (ANF) under altered dietary sodium and its elevation during bigeminy were found in a 40-year-old woman with idiopathic oedema. Sodium 74-80 natriuretic peptide A Homo sapiens 20-45 2143176-1 1990 Low level of plasma atrial natriuretic factor (ANF) under altered dietary sodium and its elevation during bigeminy were found in a 40-year-old woman with idiopathic oedema. Sodium 74-80 natriuretic peptide A Homo sapiens 47-50 1706037-0 1990 Phosphate as a factor in sodium sensitivity in normal and high renin hypertension. Sodium 25-31 renin Homo sapiens 63-68 2136844-1 1990 Although much experimental evidence is consistent with the concept that atrial natriuretic factor (atriopeptin) is an important physiological regulator of renal sodium excretion, this hypothesis remains unproven. Sodium 161-167 natriuretic peptide A Homo sapiens 99-110 2136844-2 1990 Indeed, a rapidly expanding collection of experimental data appears to be more compatible with the opposite conclusion, namely that circulating atriopeptin exerts only a trivial effect on renal sodium excretion during normal day-to-day living conditions. Sodium 194-200 natriuretic peptide A Homo sapiens 144-155 2136844-3 1990 In this review, the substantial evidence demonstrating that elevations of plasma atriopeptin from threefold to 13-fold produce only a slowly developing and relatively modest natriuresis is reassessed in light of recently published data indicating that the acute intake of food (the pathway by which essentially all sodium enters the body under normal living conditions) does not increase circulating atriopeptin. Sodium 315-321 natriuretic peptide A Homo sapiens 81-92 1697369-7 1990 In hypertensive subjects, we found that ACE inhibition with blood pressure normalization reduces basal and stimulated plasma ANP and blunts the renal sodium excretion in response to saline loading. Sodium 150-156 angiotensin I converting enzyme Homo sapiens 40-43 1706037-3 1990 The response of mean arterial pressure to sodium repletion was directly correlated to the response of plasma renin activity (r = 0.540, p = 0.004) and inversely related to the percent response of serum PO4 concentrations. Sodium 42-48 renin Homo sapiens 109-114 1708021-0 1990 Is atrial natriuretic factor a physiological regulator of sodium excretion? Sodium 58-64 natriuretic peptide A Homo sapiens 3-28 2136743-3 1990 On a high sodium diet there was an increase in urine volume, sodium excretion, osmolal clearance, plasma ANP concentration, and urinary clearance and fractional excretion of AVP, with a decrease in PRA. Sodium 10-16 arginine vasopressin Homo sapiens 174-177 1708021-3 1990 Plasma ANF rises with increased dietary sodium, during intravenous infusion of a saline load, and with change from upright to recumbent posture. Sodium 40-46 natriuretic peptide A Homo sapiens 7-10 1708021-6 1990 These results are consistent with a role for ANF in the physiological regulation of sodium excretion. Sodium 84-90 natriuretic peptide A Homo sapiens 45-48 1708021-7 1990 Factors that clearly modify the natriuretic effect of ANF include volume/sodium status and renal perfusion pressure. Sodium 73-79 natriuretic peptide A Homo sapiens 54-57 1708021-9 1990 Overall, current data favor a role for ANF in the physiological regulation of sodium excretion in humans but more definitive evidence must await the advent of a specific ANF antagonist. Sodium 78-84 natriuretic peptide A Homo sapiens 39-42 1708025-9 1990 Sodium-dependent suppression of renin, angiotension II, aldosterone, and plasma catecholamines was comparable between the two groups. Sodium 0-6 renin Homo sapiens 32-37 2137185-2 1990 This characteristic of the medullary circulation plays an important role in the kidney"s ability to excrete a dilute or concentrated urine in concert with changes in water and sodium transport in the distal nephron secondary to the action of vasopressin, prostaglandins, the renal nerves, and other hormones without significant other renal hemodynamic changes. Sodium 176-182 arginine vasopressin Homo sapiens 242-253 2137185-7 1990 In this regard, activation of the renin-angiotensin system locally reduces blood flow in the papilla which may be necessary before sodium retention is fully expressed in salt retaining states. Sodium 131-137 renin Homo sapiens 34-39 2150207-3 1990 BNP dose-dependently decreased arterial pressure and left atrial pressure and dose-dependently increased heart rate, cardiac output, renal blood flow, urine volume, and sodium excretion. Sodium 169-175 natriuretic peptide B Canis lupus familiaris 0-3 2263162-2 1990 Changes in endogenous ANG II were induced by various sodium intakes (standard-, low-, and high-sodium) or by enalapril treatment. Sodium 53-59 angiotensinogen Rattus norvegicus 22-28 2263162-2 1990 Changes in endogenous ANG II were induced by various sodium intakes (standard-, low-, and high-sodium) or by enalapril treatment. Sodium 95-101 angiotensinogen Rattus norvegicus 22-28 2263162-3 1990 In a low sodium state for 2 weeks, angiotensinogen mRNA levels and plasma ANG II concentration increased 1.3-fold and 1.6-fold compared to those in standard sodium state, respectively. Sodium 9-15 angiotensinogen Rattus norvegicus 35-50 2263162-3 1990 In a low sodium state for 2 weeks, angiotensinogen mRNA levels and plasma ANG II concentration increased 1.3-fold and 1.6-fold compared to those in standard sodium state, respectively. Sodium 9-15 angiotensinogen Rattus norvegicus 74-80 2263162-3 1990 In a low sodium state for 2 weeks, angiotensinogen mRNA levels and plasma ANG II concentration increased 1.3-fold and 1.6-fold compared to those in standard sodium state, respectively. Sodium 157-163 angiotensinogen Rattus norvegicus 35-50 2263162-4 1990 In a high sodium state, angiotensinogen mRNA levels and plasma ANG II concentration decreased by 42% and 56% compared to the standard sodierm state, respectively. Sodium 10-16 angiotensinogen Rattus norvegicus 24-39 2263162-4 1990 In a high sodium state, angiotensinogen mRNA levels and plasma ANG II concentration decreased by 42% and 56% compared to the standard sodierm state, respectively. Sodium 10-16 angiotensinogen Rattus norvegicus 63-69 2141389-0 1990 Change in renal tubular sodium and water handling during progression of polycystic kidney disease: relationship to atrial natriuretic peptide. Sodium 24-30 natriuretic peptide A Homo sapiens 115-141 2074437-7 1990 A sodium and water loss due to inhibition of tubular reabsorption leads to an increase in renin activity and aldosterone concentration in the plasma as seen typically with diuretics. Sodium 2-8 renin Homo sapiens 90-95 2139164-3 1990 Intrarenally infused VP produced a significant decrease of glomerular filtration rate (GFR) and an increase of urinary volume and sodium excretion rate. Sodium 130-136 arginine vasopressin Rattus norvegicus 21-23 2182992-3 1990 In view of the known acute effects of insulin on renal sodium retention, transcellular cation transport and perhaps also on sympathetic system, a possible involvement of insulin resistance in the genesis of essential hypertension deserves consideration. Sodium 55-61 insulin Homo sapiens 38-45 1965738-3 1990 ANP was enhanced in the patients (5.9 to 11.0 pmol/l, P less than 0.01) and the controls (4.9 to 7.1 pmol/l, P less than 0.01), but the elevated level was protracted in the patients simultaneously with a delayed sodium excretion. Sodium 212-218 natriuretic peptide A Homo sapiens 0-3 2348574-5 1990 Because plasma DLI levels correlated with serum IRI, increased levels of insulin could have induced sodium retention leading to increased DLI levels. Sodium 100-106 insulin Homo sapiens 73-80 33770503-1 2021 Neuronal voltage-gated sodium channel NaV1.2 C-terminal domain (CTD) binds calmodulin (CaM) constitutively at its IQ motif. Sodium 23-29 calmodulin 1 Homo sapiens 75-85 2284186-4 1990 Hyperactivity of the renin-aldosterone system determines the newborns" proneness to liquid and sodium retention. Sodium 95-101 renin Homo sapiens 21-26 2377564-3 1990 This case is interesting because after adequate rehydration and normalization of electrolytes we registered a remarkable fall of plasmatic sodium and chloride as a result of hemodilution probably due to a syndrome of inappropriate secretion of antidiuretic hormone, confirmed by values of plasmatic and urinary osmolarity and of urinary electrolytes. Sodium 139-145 arginine vasopressin Homo sapiens 244-264 2151585-6 1990 This decrease in the N-terminus and C-terminus of the ANF prohormone appears to represent a physiologic mechanism for restoration of intravascular volume, secondary to decreased sodium excretion. Sodium 178-184 natriuretic peptide A Homo sapiens 54-57 1707191-1 1990 Blood serum gamma-globulin and albumin were tested for their effect on the sodium currents of voltage clamped internally perfused serum deprived neuroblastoma cells. Sodium 75-81 albumin Homo sapiens 31-38 1707191-5 1990 The data obtained led us to an assumption of the role of albumin as an active substance responsible for the effect of blood serum on the potential-dependent sodium-transporting system of neuroblastoma cell membrane. Sodium 157-163 albumin Homo sapiens 57-64 33766485-10 2021 Aldosterone and insulin both increase the activity of serum and glucocorticoid kinase 1 (SGK-1) which in turn is a major regulator of vascular and renal sodium (Na+) channel activity.The importance of SGK-1 in the pathogenesis of the CMS is highlighted by observations that gain of function mutations in SGK-1 in humans promotes hypertension, insulin resistance and obesity. Sodium 153-159 insulin Homo sapiens 16-23 33774148-0 2021 Persistent sodium conductance contributes to orexin-A-mediated modulation of membrane excitability in neonatal rat mesencephalic V neurons. Sodium 11-17 hypocretin neuropeptide precursor Rattus norvegicus 45-53 33774148-7 2021 A further voltage-clamp experiment demonstrated that Ox-A increased the peak current density of the persistent sodium current (INaP) and shifted its activation curve to the hyperpolarization direction. Sodium 111-117 hypocretin neuropeptide precursor Rattus norvegicus 53-57 33800655-2 2021 An enzyme responsible for this process, sodium-potassium ATPase (NKA), has been currently extensively studied as a potential anticancer target, especially in lung cancer and glioblastoma. Sodium 40-46 tachykinin precursor 1 Homo sapiens 65-68 33794467-1 2021 PURPOSE: Severe hyponatremia, defined as serum sodium concentration ([sNa]) <= 120 mEq/L, requires aggressive treatment to prevent potentially fatal cerebral edema, seizures, and other sequelae, but overcorrection can also result in life-threatening cerebral hemorrhage and demyelination. Sodium 47-53 snail family transcriptional repressor 1 Homo sapiens 70-73 33770503-1 2021 Neuronal voltage-gated sodium channel NaV1.2 C-terminal domain (CTD) binds calmodulin (CaM) constitutively at its IQ motif. Sodium 23-29 calmodulin 1 Homo sapiens 87-90 33778438-0 2021 Low sodium intake increases plasma renin activity. Sodium 4-10 renin Homo sapiens 35-40 33804289-2 2021 These effects arise from the inhibition of two distinct cancer targets: the trypsin-like serine protease urokinase-type plasminogen activator (uPA), a cell-surface mediator of matrix degradation and tumor cell invasiveness, and the sodium-hydrogen exchanger isoform-1 (NHE1), a central regulator of transmembrane pH that supports carcinogenic progression. Sodium 232-238 plasminogen activator, urokinase Homo sapiens 143-146 33234612-2 2021 Dysfunction of NaV1.1 sodium channels, which are chiefly expressed in inhibitory interneurons, explains the epileptic phenotype. Sodium 22-28 sodium channel, voltage-gated, type I, alpha Mus musculus 15-21 33159577-4 2021 IL-6 was involved in the modulation of sodium-potassium-chloride cotransporter (Nkcc) activity. Sodium 39-45 interleukin 6 Rattus norvegicus 0-4 33234612-7 2021 Locally disrupting NaV1.1 expression in the hippocampus or cortex yielded early attenuation of theta-gamma coupling, which in the hippocampus associated with fast ripples, and which was replicated in a computational model when voltage-gated sodium currents were impaired in basket cells. Sodium 241-247 sodium channel, voltage-gated, type I, alpha Mus musculus 19-25 33234612-10 2021 In the present work we show that decreased theta-gamma coupling precedes and associates with seizure activity in a DS mouse model, which could be replicated by brain region-specific ablation of NaV1.1, a sodium channel affected in the majority of DS patients. Sodium 204-210 sodium channel, voltage-gated, type I, alpha Mus musculus 194-200 29027245-0 2018 Epac-induced ryanodine receptor type 2 activation inhibits sodium currents in atrial and ventricular murine cardiomyocytes. Sodium 59-65 Rap guanine nucleotide exchange factor (GEF) 3 Mus musculus 0-4 25431337-8 2015 A second suggestive locus (rs2194437, P = 8.9 x 10(-7) ) located nearby the sodium/calcium exchanger 1 (SLC8A1) was mainly detected in atopic subjects and influenced by inhaled corticosteroid use. Sodium 76-82 solute carrier family 8 member A1 Homo sapiens 104-110 9691010-1 1998 Experiments were performed to investigate vasopressin type 2 receptor (V2)-mediated renal water reabsorption and the renal expression of the vasopressin-regulated water channel aquaporin-2 (AQP-2) in cirrhotic rats with sodium retention but without ascites. Sodium 220-226 arginine vasopressin Rattus norvegicus 141-152 24295739-1 2014 UNLABELLED: Oestrogen-induced uterine fluid sodium (Na(+)) and bicarbonate (HCO3(-)) secretion may involve SLC4A4. Sodium 44-50 solute carrier family 4 member 4 Rattus norvegicus 107-113 24140414-4 2013 Besides being responsible for the regulation of intracellular pH and sodium-calcium inward currents, NHE isoform 1 (NHE-1), which is predominantly expressed in the cardiovascular system, influences the tone of the vessel wall in response to a variety of stimuli, including hypertonic stress. Sodium 69-75 solute carrier family 9 member A1 Homo sapiens 101-114 24140414-4 2013 Besides being responsible for the regulation of intracellular pH and sodium-calcium inward currents, NHE isoform 1 (NHE-1), which is predominantly expressed in the cardiovascular system, influences the tone of the vessel wall in response to a variety of stimuli, including hypertonic stress. Sodium 69-75 solute carrier family 9 member A1 Homo sapiens 116-121 20102298-7 2010 In conclusion, OATP1B3 appears to be a major transport mechanism mediating sodium-independent CGamF accumulation in human liver, and CGamF could be used as a probe substrate for in vitro drug interaction studies. Sodium 75-81 solute carrier organic anion transporter family member 1B3 Homo sapiens 15-22 34794962-9 2022 Additionally, protein abundance of sodium taurocholate co-transporting polypeptide (NTCP) was increased up to 2.0 fold by these three TKIs. Sodium 35-41 solute carrier family 10 member 1 Homo sapiens 84-88 8386485-3 1993 In a first series of experiments, suppression of angiotensin II generation was achieved by chronic (10 days) treatment by the angiotensin-converting-enzyme inhibitor (ACEI) captopril in rats maintained on a low-sodium diet. Sodium 211-217 angiotensinogen Rattus norvegicus 49-63 34875285-1 2022 Dravet Syndrome (DS) is caused by mutations in the Scn1a gene encoding the alpha1 subunit of the sodium channel Nav1.1, which results in febrile seizures that progress to severe tonic-clonic seizures and associated comorbidities. Sodium 97-103 sodium channel, voltage-gated, type I, alpha Mus musculus 51-56 34632703-6 2022 Further, using novel in vivo CoroNa green assay, we show that C2 and C3 blocks sodium channels and reduces inflammatory sodium signals released by peripheral nerve and tissue damage. Sodium 79-85 solute carrier family 22 member 21 Danio rerio 62-71 34632703-6 2022 Further, using novel in vivo CoroNa green assay, we show that C2 and C3 blocks sodium channels and reduces inflammatory sodium signals released by peripheral nerve and tissue damage. Sodium 120-126 solute carrier family 22 member 21 Danio rerio 62-71 34843701-1 2022 Dravet Syndrome (DS) is a severe developmental and epileptic encephalopathy typically caused by loss-of-function de novo mutations in the SCN1A gene which encodes the voltage-gated sodium channel isoform NaV1.1. Sodium 181-187 sodium channel, voltage-gated, type I, alpha Mus musculus 138-143 34843701-1 2022 Dravet Syndrome (DS) is a severe developmental and epileptic encephalopathy typically caused by loss-of-function de novo mutations in the SCN1A gene which encodes the voltage-gated sodium channel isoform NaV1.1. Sodium 181-187 sodium channel, voltage-gated, type I, alpha Mus musculus 204-210 34962430-12 2022 SIGNIFICANCE: Insulin-mediated regulation of Nedd4-2 might impact on inner ear sodium homeostasis with implications for diabetes-induced inner ear damage. Sodium 79-85 insulin Homo sapiens 14-21 34852210-3 2022 PON2 and PON3 are expressed in the aldosterone-sensitive distal nephron of the kidney and have been shown to negatively regulate expression of the epithelial sodium channel (ENaC), a trimeric ion channel that orchestrates salt and water homeostasis. Sodium 158-164 sodium channel epithelial 1 subunit gamma Rattus norvegicus 174-178 34099189-4 2022 RESULTS: Across disorders, genome-wide significant single nucleotide polymorphism-by-sex interaction was detected for a locus encompassing NKAIN2 (rs117780815, p = 3.2 x 10-8), which interacts with sodium/potassium-transporting ATPase (adenosine triphosphatase) enzymes, implicating neuronal excitability. Sodium 198-204 sodium/potassium transporting ATPase interacting 2 Homo sapiens 139-145 34922208-1 2022 BACKGROUND: Sodium/iodide symporter (NIS) acts as a vital role in regulation of iodide uptake in thyroid cancer. Sodium 12-18 solute carrier family 5 member 5 Homo sapiens 37-40 34114611-1 2021 Variants in KCNT1, encoding a sodium-gated potassium channel (subfamily T member 1), have been associated with a spectrum of epilepsies and neurodevelopmental disorders. Sodium 30-36 potassium sodium-activated channel subfamily T member 1 Homo sapiens 12-17 34964123-2 2021 Glucose is taken up by apical sodium-glucose cotransporters SGLT2 and SGLT1 whereas SGLT5 and potentially SGLT4 and GLUT5 have been implicated in apical fructose uptake. Sodium 30-36 solute carrier family 5 member 1 Homo sapiens 70-75 34964123-2 2021 Glucose is taken up by apical sodium-glucose cotransporters SGLT2 and SGLT1 whereas SGLT5 and potentially SGLT4 and GLUT5 have been implicated in apical fructose uptake. Sodium 30-36 solute carrier family 5 member 10 Homo sapiens 84-89 34964123-8 2021 Moreover, renal glucose retention is coupled to sodium retention through SGLT2 and SGLT1, which induces secondary deleterious effects. Sodium 48-54 solute carrier family 5 member 1 Homo sapiens 83-88 34967126-1 2022 This study aimed to evaluate the blood pressure (BP) lowing effect of low-sodium (LS) salt substitution and how the effect influenced by plasma renin concentration (PRC) on middle-aged and elderly hypertensive patients. Sodium 74-80 renin Homo sapiens 144-149 34957475-4 2021 Genetic loss or selective pharmacological inhibition of Nav1.7 in C-LTMRs resulted in a significant reduction in the total sodium current density, an increased mechanical threshold and reduced sensitivity to non-noxious cooling. Sodium 123-129 sodium channel, voltage-gated, type IX, alpha Mus musculus 56-62 34975470-5 2021 Moreover, based on the molecular docking and molecular dynamic simulation, the binding free energies of the constructed systems were calculated, and the binding sites of GAS on the sodium channels (NaV1.7 and NaV1.8) were preliminarily determined. Sodium 181-187 sodium voltage-gated channel alpha subunit 10 Rattus norvegicus 209-215 34975470-6 2021 This study has shown that modulation of NaV1.7 and NaV1.8 sodium channels by GAS contributing to the alleviation of vincristine-induced peripheral neuropathic pain, thus expanding the understanding of complex action of GAS as a neuromodulator. Sodium 58-64 sodium voltage-gated channel alpha subunit 10 Rattus norvegicus 51-57 34904226-2 2022 The purpose of the present study was to determine how the inhibition of basolateral Kir 4.1/Kir 5.1 heteromeric K+ channel affects epithelial sodium channel (ENaC)-mediated Na+ transport in the principal cells of cortical collecting duct (CCD). Sodium 142-148 sodium channel epithelial 1 subunit gamma Rattus norvegicus 158-162 34888757-1 2021 In conventional ethylene carbonate (EC)/propylene carbonate (PC) electrolyte, sodium metal reacts spontaneously and deleteriously with solvent molecules. Sodium 78-90 pyruvate carboxylase Homo sapiens 61-63 34888757-3 2021 Herein, we present a sodium metal alloy strategy via introducing NaIn and Na2In phases in a Na/In/C composite, aiming at boosting Na ion deposition stability in the common EC/PC electrolyte. Sodium 21-33 pyruvate carboxylase Homo sapiens 172-177 34862479-1 2022 Advanced glycation end product (AGE) clearance may cause renal tubular injuries, such as changes in sodium reabsorption. Sodium 100-106 renin binding protein Homo sapiens 0-30 34862479-1 2022 Advanced glycation end product (AGE) clearance may cause renal tubular injuries, such as changes in sodium reabsorption. Sodium 100-106 renin binding protein Homo sapiens 32-35 34862479-7 2022 In a cross-sectional analysis (n = 989), subjects in the top quintile versus quintiles 1-4 of plasma AGE concentration had significantly (P <= 0.004) lower fractional excretion of lithium (18.3% vs. 21.6%) and fractional distal reabsorption rate of sodium (95.0% vs. 95.8%) but similar BP (P >= 0.25). Sodium 249-255 renin binding protein Homo sapiens 101-104 34862479-8 2022 However, there was an interaction between plasma AGE concentration and urinary sodium excretion in relation to diastolic BP (P <= 0.058). Sodium 79-85 renin binding protein Homo sapiens 49-52 34129073-8 2021 Plasma insulin secretion, which potentially enhances renal sodium reabsorption and fluid retention, did not differ between the trials (interaction, P = 0.653). Sodium 59-65 insulin Homo sapiens 7-14 34889274-2 2021 We hypothesize that clinical factors besides albumin and protein in the blood that cause laboratory errors might be associated with sodium ion level difference between the 2 methods in very-low-birth-weight infants during early life after birth. Sodium 132-138 albumin Homo sapiens 45-52 34889274-9 2021 The sodium level difference >4 mmol/L group showed significantly (P < .05) higher sodium level by biochemistry autoanalyzer, lower albumin, lower protein, and higher maximum percent of physiological weight than the sodium level difference <=4 mmol/L group. Sodium 4-10 albumin Homo sapiens 131-138 34551207-2 2021 High sodium consumption may contribute to the development of cardiac impairment in insulin-resistant individuals by promoting inadequate skeletal muscle microvascular perfusion response to insulin. Sodium 5-11 insulin Homo sapiens 83-90 34551207-2 2021 High sodium consumption may contribute to the development of cardiac impairment in insulin-resistant individuals by promoting inadequate skeletal muscle microvascular perfusion response to insulin. Sodium 5-11 insulin Homo sapiens 189-196 34551207-3 2021 We sought to investigate the association of dietary sodium reduction with muscle perfusion, insulin sensitivity, and cardiac function in overweight/obese insulin-resistant (O-IR) normotensive subjects. Sodium 52-58 insulin Homo sapiens 92-99 34551207-10 2021 CONCLUSIONS: The reduction of dietary sodium in the normotensive O-IR population improves cardiac function, and this effect may be associated with the concomitant improvements in skeletal muscle perfusion and insulin resistance. Sodium 38-44 insulin Homo sapiens 209-216 34943879-2 2021 The GH/IGF1 system plays a key role in normal kidney development, glomerular hemodynamic regulation, as well as tubular water, sodium, phosphate, and calcium handling. Sodium 127-133 insulin like growth factor 1 Homo sapiens 7-11 34514854-1 2021 BACKGROUND: Iodide transport defect (ITD) is an uncommon cause of dyshormonogenic congenital hypothyroidism due to homozygous or compound heterozygous pathogenic variants in the SLC5A5 gene, which encodes the sodium/iodide symporter (NIS), causing deficient iodide accumulation in thyroid follicular cells, thus impairing thyroid hormonogenesis. Sodium 209-215 solute carrier family 5 member 5 Homo sapiens 178-184 34837556-1 2022 The human Dietary Approaches to Stop Hypertension-Sodium Trial has shown that beta-aminoisobutyric acid (BAIBA) may prevent the development of salt-sensitive hypertension (SSHT). Sodium 50-56 alanine--glyoxylate aminotransferase 2 Homo sapiens 105-110 34842443-3 2022 Moreover, we determined whether glucose transporter sodium-glucose cotransporter 1 (SGLT1) plays an important role in this process. Sodium 52-58 solute carrier family 5 member 1 Homo sapiens 84-89 34977268-4 2022 Using this assay, we examined the effects of the sodium-dependent glucose cotransporter 1/2 (SGLT1/2) inhibitor drugs phlorizin and sotagliflozin on the basis of our findings that SGLT1 expression is upregulated in CF HLOs and airway epithelial cells compared with their wild-type counterparts. Sodium 49-55 solute carrier family 5 member 1 Homo sapiens 93-100 34843967-0 2022 Mechanistic insights into the interaction of cardiac sodium channel Nav1.5 with MOG1 and a new molecular mechanism for Brugada syndrome. Sodium 53-59 RAN guanine nucleotide release factor Homo sapiens 80-84 34843967-2 2022 MOG1 is a chaperon that binds to Nav1.5, facilitates Nav1.5 trafficking to cell surface, and enhances amplitude of sodium current INa. Sodium 115-121 RAN guanine nucleotide release factor Homo sapiens 0-4 34884494-0 2021 Crosstalk between Sodium-Glucose Cotransporter Inhibitors and Sodium-Hydrogen Exchanger 1 and 3 in Cardiometabolic Diseases. Sodium 18-24 solute carrier family 9 member A1 Homo sapiens 62-95 34884494-5 2021 The mechanism by which these drugs exert their cardioprotective effects is unknown, although recent studies have shown that cardiovascular homeostasis occurs through the interplay of the sodium-hydrogen exchangers (NHE), specifically NHE1 and NHE3, with SGLT2i. Sodium 187-193 solute carrier family 9 member A1 Homo sapiens 234-238 34888232-1 2021 Introduction: Ste20-related protein proline/alanine-rich kinase (SPAK) affects cell proliferation, differentiation, and transformation, and sodium and chloride transport in the gut. Sodium 140-146 serine/threonine kinase 24 Mus musculus 14-19 34977268-4 2022 Using this assay, we examined the effects of the sodium-dependent glucose cotransporter 1/2 (SGLT1/2) inhibitor drugs phlorizin and sotagliflozin on the basis of our findings that SGLT1 expression is upregulated in CF HLOs and airway epithelial cells compared with their wild-type counterparts. Sodium 49-55 solute carrier family 5 member 1 Homo sapiens 180-185 34793577-1 2021 BACKGROUND: Endogenous ouabain (EO) and atrial natriuretic peptide (ANP) are important in regulation of sodium and fluid balance. Sodium 104-110 natriuretic peptide A Homo sapiens 40-66 34633813-6 2021 The number of sodium ions associated with the DNA agrees quantitatively with the experiment for the OPC water model, followed closely by TIP3P+J/C; the largest deviation from the experiment, ~10%, is seen for SPC/E+J/C. Sodium 14-20 surfactant protein C Homo sapiens 209-212 34624234-11 2021 In conclusion, we found that VEGF reduces PV arrhythmogenesis by modulating sodium/calcium homeostasis through VEGFR-1/NOS signaling pathway. Sodium 76-82 vascular endothelial growth factor A Homo sapiens 29-33 34624234-11 2021 In conclusion, we found that VEGF reduces PV arrhythmogenesis by modulating sodium/calcium homeostasis through VEGFR-1/NOS signaling pathway. Sodium 76-82 fms related receptor tyrosine kinase 1 Homo sapiens 111-118 34868940-0 2021 Elevated Sodium Pump alpha3 Subunit Expression Promotes Colorectal Liver Metastasis via the p53-PTEN/IGFBP3-AKT-mTOR Axis. Sodium 9-15 tumor protein p53 Homo sapiens 92-95 34868940-0 2021 Elevated Sodium Pump alpha3 Subunit Expression Promotes Colorectal Liver Metastasis via the p53-PTEN/IGFBP3-AKT-mTOR Axis. Sodium 9-15 AKT serine/threonine kinase 1 Homo sapiens 108-111 34868940-0 2021 Elevated Sodium Pump alpha3 Subunit Expression Promotes Colorectal Liver Metastasis via the p53-PTEN/IGFBP3-AKT-mTOR Axis. Sodium 9-15 mechanistic target of rapamycin kinase Homo sapiens 112-116 34868940-6 2021 Reciprocally, knockdown of the alpha3 subunit or inhibition of the sodium pump dramatically blocked this effect in vitro and in vivo via the downregulation of mTOR activity. Sodium 67-73 mechanistic target of rapamycin kinase Homo sapiens 159-163 34868940-8 2021 Conclusions: Elevated expression of the sodium pump alpha3 subunit promotes CRC liver metastasis via the PTEN/IGFBP3-mediated mTOR pathway, suggesting that sodium pump alpha3 could represent a critical prognostic marker and/or therapeutic target for this disease. Sodium 40-46 mechanistic target of rapamycin kinase Homo sapiens 126-130 34764684-6 2021 Results: On adjustment for traditional risk factors (age, BMI, ALB, ALK, ASP, calcium, cholesterol, potassium, sodium, total protein, uric acid), SHBG could be regarded as an independent predictor for BMD, while fasting blood glucose did not. Sodium 111-117 sex hormone binding globulin Homo sapiens 146-150 34738553-5 2021 In adults with COVID-19, an inverse association between sodium and interleukin-6 levels has been found, indicating that hyponatraemia could be used as a surrogate marker for the risk of cytokine storm and may facilitate the identification of patients who could benefit from immunomodulatory agents. Sodium 56-62 interleukin 6 Homo sapiens 67-80 34544834-6 2021 Aberrantly large persistent sodium currents, a hallmark of SCN8A mutations, were observed and were found to contribute directly to aberrant SST physiology in computational modeling and pharmacological experiments. Sodium 28-34 somatostatin Mus musculus 140-143 34520431-4 2021 RESULTS: Randomization to albumin was associated with a significant increase in sodium; however, there was no interaction between sodium category and treatment for the trial primary end point. Sodium 80-86 albumin Homo sapiens 26-33 34520431-5 2021 DISCUSSION: Targeted intravenous albumin infusions increased serum sodium level in hospitalized hyponatremic patients with cirrhosis, but this did not improve outcome. Sodium 67-73 albumin Homo sapiens 33-40 34263971-3 2021 The dual sodium-glucose transporter 1/2 inhibitor (SGLT1/2i) licogliflozin (LIK066) ameliorates hyperinsulinism in patients with diabetes and obesity. Sodium 9-15 solute carrier family 5 member 1 Homo sapiens 51-59 34853804-1 2021 The sodium-dependent taurocholate co-transporting polypeptide (NTCP)-S267F variant is known to be associated with a reduced risk of hepatitis B virus (HBV) infection and disease progression. Sodium 4-10 solute carrier family 10 member 1 Homo sapiens 63-67 34171450-12 2021 TNF-alpha demonstrated positive association with creatinine (r = 0.4,p = 0.006), BUN (r = 0.63,p = 0.003), sodium (r = 0.44, p = 0.04), potassium (r = 0.41, p = 0.04), and was negatively associated with RVFAC (r = -0.38,p = 0.03) and 6MWT distance (r = -0.54, p = 0.004). Sodium 107-113 tumor necrosis factor Homo sapiens 0-9 34736759-1 2021 INTRODUCTION: Drug-induced block of the hERG potassium channel could predispose to torsade de pointes, depending on occurrence of concomitant blocks of the calcium and/or sodium channels. Sodium 171-177 ETS transcription factor ERG Homo sapiens 40-44 34658111-3 2021 Sodium/potassium ATPase (Na+ K+ -ATPase) is a membrane-bound signaling protein that induces capacitation in bull sperm in response to the steroid hormone ouabain, and its subunit isoforms alpha1, alpha3, beta1, beta2, and beta3 are known in HPM. Sodium 0-6 glycoprotein hormone subunit alpha 2 Homo sapiens 211-216 34658111-3 2021 Sodium/potassium ATPase (Na+ K+ -ATPase) is a membrane-bound signaling protein that induces capacitation in bull sperm in response to the steroid hormone ouabain, and its subunit isoforms alpha1, alpha3, beta1, beta2, and beta3 are known in HPM. Sodium 0-6 T cell immune regulator 1, ATPase H+ transporting V0 subunit a3 Homo sapiens 222-227 34769164-1 2021 Sodium appetite is an innate behavior occurring in response to sodium depletion that induces homeostatic responses such as the secretion of the mineralocorticoid hormone aldosterone from the zona glomerulosa of the adrenal cortex and the stimulation of the peptide hormone angiotensin II (ANG II). Sodium 0-6 angiotensinogen Homo sapiens 273-287 34723976-6 2021 The HSD resulted in increased sodium content in the skin of mice. Sodium 30-36 histidine ammonia lyase Mus musculus 4-7 34622576-1 2021 NiS1.23 Se0.77 nanosheets closely attached to the internal surface of hollow mesoporous carbon sphere (HMCS) to form a NiS1.23 Se0.77 nanosheets embedded in HMCS (NSSNs@HMCS) composite as the anode of sodium ion batteries (SIBs) is reported by a facile synthesis route. Sodium 201-207 MKKS centrosomal shuttling protein Homo sapiens 103-107 34622576-1 2021 NiS1.23 Se0.77 nanosheets closely attached to the internal surface of hollow mesoporous carbon sphere (HMCS) to form a NiS1.23 Se0.77 nanosheets embedded in HMCS (NSSNs@HMCS) composite as the anode of sodium ion batteries (SIBs) is reported by a facile synthesis route. Sodium 201-207 MKKS centrosomal shuttling protein Homo sapiens 157-161 34622576-1 2021 NiS1.23 Se0.77 nanosheets closely attached to the internal surface of hollow mesoporous carbon sphere (HMCS) to form a NiS1.23 Se0.77 nanosheets embedded in HMCS (NSSNs@HMCS) composite as the anode of sodium ion batteries (SIBs) is reported by a facile synthesis route. Sodium 201-207 MKKS centrosomal shuttling protein Homo sapiens 169-173 34769164-1 2021 Sodium appetite is an innate behavior occurring in response to sodium depletion that induces homeostatic responses such as the secretion of the mineralocorticoid hormone aldosterone from the zona glomerulosa of the adrenal cortex and the stimulation of the peptide hormone angiotensin II (ANG II). Sodium 0-6 angiotensinogen Homo sapiens 289-295 34769164-1 2021 Sodium appetite is an innate behavior occurring in response to sodium depletion that induces homeostatic responses such as the secretion of the mineralocorticoid hormone aldosterone from the zona glomerulosa of the adrenal cortex and the stimulation of the peptide hormone angiotensin II (ANG II). Sodium 63-69 angiotensinogen Homo sapiens 273-287 34769164-1 2021 Sodium appetite is an innate behavior occurring in response to sodium depletion that induces homeostatic responses such as the secretion of the mineralocorticoid hormone aldosterone from the zona glomerulosa of the adrenal cortex and the stimulation of the peptide hormone angiotensin II (ANG II). Sodium 63-69 angiotensinogen Homo sapiens 289-295 34769164-3 2021 This narrative review summarizes the main data dealing with the role of mineralocorticoid and ANG II receptors in the central control of sodium appetite. Sodium 137-143 angiotensinogen Homo sapiens 94-100 34769164-6 2021 Several brain areas control sodium appetite, including the nucleus of the solitary tract, which contains aldosterone-sensitive HSD2 neurons, and the organum vasculosum lamina terminalis (OVLT) that contains ANG II-sensitive neurons. Sodium 28-34 angiotensinogen Homo sapiens 207-213 34769164-8 2021 ANG II stimulates salt intake via MAPK, while combined ANG II and aldosterone action induce sodium intake via the IP3 signaling pathway. Sodium 92-98 angiotensinogen Homo sapiens 55-61 34988469-7 2021 We found that furosemide sensitive sodium transport (NKCC2) is only increased during late pregnancy, thiazide sensitive sodium transport (NDCBE/pendrin) is increased in all stages of pregnancy, and that benzamil sensitive sodium transport (ENaC) is increased beginning in mid-pregnancy. Sodium 222-228 sodium channel epithelial 1 subunit gamma Rattus norvegicus 240-244 34652134-1 2021 Sodium reduction of ({SiNDipp}Mg) ({SiNDipp} = {CH2SiMe2N(Dipp)}2; Dipp = 2,6-i-Pr2C6H3) provides the Mg(I) species, ({SiNDipp}MgNa)2, in which the long Mg-Mg bond (>3.2 A) is augmented by persistent Na-aryl interactions. Sodium 0-6 nudix hydrolase 3 Homo sapiens 58-62 34652134-1 2021 Sodium reduction of ({SiNDipp}Mg) ({SiNDipp} = {CH2SiMe2N(Dipp)}2; Dipp = 2,6-i-Pr2C6H3) provides the Mg(I) species, ({SiNDipp}MgNa)2, in which the long Mg-Mg bond (>3.2 A) is augmented by persistent Na-aryl interactions. Sodium 0-6 nudix hydrolase 3 Homo sapiens 67-71 34670899-1 2022 Serum tonicity is defined by the serum concentrations of sodium (sNa) and glucose, which can promote free water movement across intra/extracellular compartments. Sodium 57-63 snail family transcriptional repressor 1 Homo sapiens 65-68 34831067-2 2021 The CFTR protein is known to acts as a chloride (Cl-) channel expressed in the exocrine glands of several body systems where it also regulates other ion channels, including the epithelial sodium (Na+) channel (ENaC) that plays a key role in salt absorption. Sodium 188-194 CF transmembrane conductance regulator Homo sapiens 4-8 34670070-7 2022 After hydration and insulin treatment, the patient"s mental status and serum glucose and sodium levels improved, and no neurological complications were observed. Sodium 89-95 insulin Homo sapiens 20-27 34733169-12 2021 We hypothesize that the obtained upregulation of cardiac and renal PCSK6/corin in rats with compensated CHF may represent a compensatory response aiming at maintaining normal Na+ balance, whereas the decline in these two enzymes may contribute to the pathogenesis of avid sodium retention, cardiac hypertrophy, and blunted atrial natriuretic peptide/brain natriuretic peptide actions in decompensated CHF. Sodium 272-278 proprotein convertase subtilisin/kexin type 6 Rattus norvegicus 67-72 34533476-7 2021 Lower sodium levels at admission were correlated with higher CRP (p=0.039) and serum lactate levels (p= 0.019), but not IL-6. Sodium 6-12 C-reactive protein Homo sapiens 61-64 34647168-5 2021 Furthermore, CBF prevented vascular smooth muscle cell (VSMC) transdifferentiation into osteoblast-like cells within the vascular wall via the sodium-dependent phosphate transporter PIT-1 and by inhibition of NF-kappaB activation and the subsequent BMP2/p-SMAD pathway. Sodium 143-149 POU class 1 homeobox 1 Homo sapiens 182-187 34692745-6 2021 In the group receiving PN under the supervision of a surgeon, the level of blood glucose (207 vs. 182, P < 0.01), sodium (138 vs. 136, P = 0.01), potassium (3.97 vs. 3.53, P < 0.01), and white blood cell count (9.83 vs. 9.28, P < 0.01) increased significantly at the end of the PN compared to baseline. Sodium 114-120 U6 snRNA biogenesis phosphodiesterase 1 Homo sapiens 23-25 34692745-6 2021 In the group receiving PN under the supervision of a surgeon, the level of blood glucose (207 vs. 182, P < 0.01), sodium (138 vs. 136, P = 0.01), potassium (3.97 vs. 3.53, P < 0.01), and white blood cell count (9.83 vs. 9.28, P < 0.01) increased significantly at the end of the PN compared to baseline. Sodium 114-120 U6 snRNA biogenesis phosphodiesterase 1 Homo sapiens 278-280 34605855-4 2022 The gene encodes SNAT3, a sodium-coupled neutral amino acid transporter and a principal transporter of the amino acids asparagine, histidine, and glutamine, the latter being the precursor for the neurotransmitters GABA and glutamate. Sodium 26-32 solute carrier family 38 member 3 Homo sapiens 17-22 34324871-3 2021 Here, we performed RNA sequencing (RNA-seq) to examine the transcriptional profiles changes in mice in response to MIA and identified that the expression of Scn1a gene, encoding the pore-forming alpha-subunit of the brain voltage-gated sodium channel type-1 (NaV1.1) primarily in fast-spiking inhibitory interneurons, was significantly decreased in the medial prefrontal cortex (mPFC) of juvenile offspring after MIA. Sodium 236-242 sodium channel, voltage-gated, type I, alpha Mus musculus 157-162 34324871-3 2021 Here, we performed RNA sequencing (RNA-seq) to examine the transcriptional profiles changes in mice in response to MIA and identified that the expression of Scn1a gene, encoding the pore-forming alpha-subunit of the brain voltage-gated sodium channel type-1 (NaV1.1) primarily in fast-spiking inhibitory interneurons, was significantly decreased in the medial prefrontal cortex (mPFC) of juvenile offspring after MIA. Sodium 236-242 sodium channel, voltage-gated, type I, alpha Mus musculus 259-265 34223773-1 2021 PURPOSE: Liddle syndrome is a hereditary form of arterial hypertension caused by mutations in the genes coding of the epithelial sodium channel - SCNN1A, SCNN1B and SCNN1G. Sodium 129-135 sodium channel epithelial 1 subunit alpha Homo sapiens 146-152 34236307-10 2021 CONCLUSION: Daily variations in solute output affect urine volume in NDI/CDI/SIADH/NSIAD, this could affect serum sodium (SNa) despite no variation in fluid intake. Sodium 114-120 snail family transcriptional repressor 1 Homo sapiens 122-125 34375627-0 2021 Regulation of the voltage-dependent sodium channel NaV1.1 by AKT1. Sodium 36-42 AKT serine/threonine kinase 1 Homo sapiens 61-65 34293127-3 2021 OBJECTIVES: We hypothesized that a low-sodium DASH diet improves (lowers) biomarkers of inflammation (C-reactive protein (CRP) and soluble urokinase plasminogen activator receptor (suPAR)) and mineral metabolism (phosphorus and fibroblast growth factor-23 (FGF23)). Sodium 39-45 C-reactive protein Homo sapiens 102-120 34293127-3 2021 OBJECTIVES: We hypothesized that a low-sodium DASH diet improves (lowers) biomarkers of inflammation (C-reactive protein (CRP) and soluble urokinase plasminogen activator receptor (suPAR)) and mineral metabolism (phosphorus and fibroblast growth factor-23 (FGF23)). Sodium 39-45 C-reactive protein Homo sapiens 122-125 34684456-0 2021 Association of Sodium, Potassium and Sodium-to-Potassium Ratio with Urine Albumin Excretion among the General Chinese Population. Sodium 15-21 albumin Homo sapiens 74-81 34684456-0 2021 Association of Sodium, Potassium and Sodium-to-Potassium Ratio with Urine Albumin Excretion among the General Chinese Population. Sodium 37-43 albumin Homo sapiens 74-81 34584093-2 2021 The previously solved structures of the outward facing (OF) conformation for AE1 (SLC4A1) and NBCe1 (SLC4A4) transporters revealed an identical overall fold despite their different transport modes (chloride/bicarbonate exchange versus sodium-carbonate cotransport). Sodium 235-241 solute carrier family 4 member 4 Homo sapiens 101-107 34561392-4 2021 Using the sodium channel blocker TTX (1-10microM) to inhibit Nav1.7 and other TTX-S sodium channels along the sciatic nerve, we first showed that around 2/3rds of nociceptive L4 DRG neurons innervating the skin, but a lower proportion innervating the muscle (45%), are blocked by TTX. Sodium 10-16 sodium channel, voltage-gated, type IX, alpha Mus musculus 61-67 34632152-4 2021 Exposure of HUVEC to elevated sodium within the physiological range up to 24 h is accompanied by changes in monovalent cations fluxes and Na,K-ATPase activation, and, in turn, results in a significant decrease in the content of PTGS2, IL6 and IL1LR1 mRNAs. Sodium 30-36 prostaglandin-endoperoxide synthase 2 Homo sapiens 228-233 34632152-4 2021 Exposure of HUVEC to elevated sodium within the physiological range up to 24 h is accompanied by changes in monovalent cations fluxes and Na,K-ATPase activation, and, in turn, results in a significant decrease in the content of PTGS2, IL6 and IL1LR1 mRNAs. Sodium 30-36 interleukin 6 Homo sapiens 235-238 34630093-12 2021 Mechanically, FGF21 can ameliorate the electrophysiological function of AC16 cells, which is characterized by rescuing the expression and dysfunction of cardiac sodium current (I Na) and inward rectifier potassium (I k1) in AC16 cells induced by hydrogen peroxide. Sodium 161-167 fibroblast growth factor 21 Homo sapiens 14-19 34630137-3 2021 Urinary sodium, potassium, and chloride concentrations as well as urinary osmolality were lower in hAAT-Tg mice maintained on a high salt diet during both the active and inactive cycles. Sodium 8-14 serpin family A member 1 Homo sapiens 99-103 34567798-1 2021 We describe a Chinese family with severe autosomal-dominant nocturnal frontal lobe epilepsy (ADNFLE) and psychiatric problems in whom whole-exome family trio sequencing identified a heterozygous mutation in the potassium channel subfamily T, member 1 (KCNT1), a sodium-gated potassium channel gene, which was a novel missense mutation c.2153A>T (p. Asp718Val). Sodium 262-268 potassium sodium-activated channel subfamily T member 1 Homo sapiens 211-250 34621749-11 2021 The dermal eGC/ED markers UEA1, VEGFR2, and vWF all associated with plasma levels of NT-proBNP and sodium (all R 2 > 0.29 and P < 0.01), except for vWF that only associated with plasma NT-proBNP. Sodium 99-105 von Willebrand factor Homo sapiens 44-47 34535765-4 2021 We showed that immature IQSEC2 mutant dentate gyrus (DG) granule neurons were extremely hyperexcitable, exhibiting increased sodium and potassium currents compared to those of CRISPR-Cas9-corrected isogenic controls, and displayed dysregulation of genes involved in differentiation and development. Sodium 125-131 IQ motif and Sec7 domain ArfGEF 2 Homo sapiens 24-30 34575961-0 2021 Calmodulin Interactions with Voltage-Gated Sodium Channels. Sodium 43-49 calmodulin 1 Homo sapiens 0-10 34575961-3 2021 CaM modulates the voltage-gated sodium channel gating process, alters sodium current density, and regulates sodium channel protein trafficking and expression. Sodium 32-38 calmodulin 1 Homo sapiens 0-3 34575961-3 2021 CaM modulates the voltage-gated sodium channel gating process, alters sodium current density, and regulates sodium channel protein trafficking and expression. Sodium 70-76 calmodulin 1 Homo sapiens 0-3 34575961-3 2021 CaM modulates the voltage-gated sodium channel gating process, alters sodium current density, and regulates sodium channel protein trafficking and expression. Sodium 108-114 calmodulin 1 Homo sapiens 0-3 34575961-5 2021 In the present review, we discuss CaM interactions with the voltage-gated sodium channel and modulators involved in CaM regulation, as well as summarize CaM-binding IQ domain mutations associated with human diseases in the voltage-gated sodium channel family. Sodium 74-80 calmodulin 1 Homo sapiens 34-37 34575961-5 2021 In the present review, we discuss CaM interactions with the voltage-gated sodium channel and modulators involved in CaM regulation, as well as summarize CaM-binding IQ domain mutations associated with human diseases in the voltage-gated sodium channel family. Sodium 237-243 calmodulin 1 Homo sapiens 153-156 34499251-3 2022 Our objective was to investigate if plasma renin activity and serum aldosterone are associated with urine sodium and potassium in youth referred for hypertensive disorders. Sodium 106-112 renin Homo sapiens 43-48 34499251-6 2022 We used multivariable generalized linear models to estimate the associations of renin and aldosterone with urine sodium and potassium. Sodium 113-119 renin Homo sapiens 80-85 34567798-1 2021 We describe a Chinese family with severe autosomal-dominant nocturnal frontal lobe epilepsy (ADNFLE) and psychiatric problems in whom whole-exome family trio sequencing identified a heterozygous mutation in the potassium channel subfamily T, member 1 (KCNT1), a sodium-gated potassium channel gene, which was a novel missense mutation c.2153A>T (p. Asp718Val). Sodium 262-268 potassium sodium-activated channel subfamily T member 1 Homo sapiens 252-257 34370712-7 2021 Furthermore, preliminary data show an inverse association between serum sodium and interleukin-6 levels, suggesting that hyponatraemia might be used as a surrogate marker for the risk of a cytokine storm and the need for treatment with interleukin antagonists. Sodium 72-78 interleukin 6 Homo sapiens 83-96 34076854-0 2021 Growth Differentiation Factor-15 Produces Analgesia by Inhibiting Tetrodotoxin-Resistant Nav1.8 Sodium Channel Activity in Rat Primary Sensory Neurons. Sodium 96-102 growth differentiation factor 15 Rattus norvegicus 0-32 34076854-0 2021 Growth Differentiation Factor-15 Produces Analgesia by Inhibiting Tetrodotoxin-Resistant Nav1.8 Sodium Channel Activity in Rat Primary Sensory Neurons. Sodium 96-102 sodium voltage-gated channel alpha subunit 10 Rattus norvegicus 89-95 34076854-6 2021 Furthermore, GDF-15 concentration-dependently suppressed tetrodotoxin-resistant sodium channel Nav1.8 currents, and shifted the steady-state inactivation curves of Nav1.8 in a hyperpolarizing direction. Sodium 80-86 growth differentiation factor 15 Rattus norvegicus 13-19 34076854-6 2021 Furthermore, GDF-15 concentration-dependently suppressed tetrodotoxin-resistant sodium channel Nav1.8 currents, and shifted the steady-state inactivation curves of Nav1.8 in a hyperpolarizing direction. Sodium 80-86 sodium voltage-gated channel alpha subunit 10 Rattus norvegicus 95-101 34622607-5 2021 In addition, baseline eGFR-CysC was negatively correlated with the model for end-stage liver disease (MELD) score ( r=-0.439, P<0.001), MELD plus sodium (MELD-Na) score ( r=-0.481, P<0.001) and Chronic Liver Failure Consortium ACLF (CLIF-C ACLF) score ( r=-0.340, P<0.001). Sodium 146-152 epidermal growth factor receptor Homo sapiens 22-26 34353268-8 2022 These mechanisms lead to activation of the renin-angiotensin-aldosterone system, sodium and water retention, activation of neprilysin, of the sodium-glucose-2 transporter, which promote interstitial fibrosis, ventricular remodeling and a consequent increase in cardiac output >8L/min. Sodium 142-148 membrane metalloendopeptidase Homo sapiens 123-133 1961256-5 1991 Following high sodium intake, both angiotensin II (100 nmol/l) and angiotensin I (1 mumol/l) caused a marked increase of the electrically evoked noradrenaline overflow. Sodium 15-21 angiotensinogen Rattus norvegicus 35-49 1961256-12 1991 The results are in keeping with a sodium-dependent intracardiac formation of angiotensin II which facilitates noradrenaline release from sympathetic nerve terminals. Sodium 34-40 angiotensinogen Rattus norvegicus 77-91 1961256-13 1991 Following low sodium intake, cardiac angiotensin II formation is active, as indicated by the suppression of noradrenaline release by angiotensin-converting enzyme inhibitors and the ineffectiveness of exogenous application of angiotensin II. Sodium 14-20 angiotensinogen Rattus norvegicus 37-51 34404133-10 2021 After adjusting for confounding factors including age, systolic blood pressure, diabetes, urinary protein excretion, serum albumin, serum sodium, serum chlorine, urinary calcium excretion, urinary phosphorus excretion and use of diuretics, multivariate logistic regression analysis demonstrated that higher level of urinary sodium excretion was associated with increased risk of FO in patients with CKD (OR=1.005, 95%CI: 1.000-1.011, P=0.048). Sodium 324-330 albumin Homo sapiens 117-130 34414225-8 2021 Additionally, the phosphorylation levels of three membrane proteins, the zinc transporter SLC39A7, the sodium-dependent neutral amino acid transporters SLC1A5 and SLC38A7, and three translation initiation factors, eukaryotic initiation factor (eIF)5B, eIF4G, and eIF3C, were positively regulated by amino acid signals. Sodium 103-109 solute carrier family 38 member 7 Homo sapiens 163-170 34422415-11 2021 The combination of IV Furosemide with Vasopressin infusion resulted in tailored diuresis and more controlled titration of serum sodium levels than adjustment in Vasopressin and fluids alone. Sodium 128-134 arginine vasopressin Homo sapiens 38-49 34458695-2 2021 Using ex vivo blood vessels and primary endothelial cells from human brain microvessels, we show that patient-derived Abeta assemblies, termed amylospheroids (ASPD), exist on the microvascular surface in patients" brains and inhibit vasorelaxation through binding to the alpha3 subunit of sodium, potassium-ATPase (NAKalpha3) in caveolae on endothelial cells. Sodium 289-295 amyloid beta precursor protein Homo sapiens 118-123 34196428-0 2021 The PDZ protein SCRIB regulates sodium/iodide symporter (NIS) expression at the basolateral plasma membrane. Sodium 32-38 solute carrier family 5 member 5 Homo sapiens 57-60 34103689-1 2021 Voltage-gated sodium channel Nav1.7 robustly expressed in peripheral nociceptive neurons has been considered as a therapeutic target for chronic pain, but there is no selective Nav1.7 inhibitor available for therapy of chronic pain. Sodium 14-20 sodium channel, voltage-gated, type IX, alpha Mus musculus 29-35 34232678-7 2021 We describe our findings that sodium, entering antigen-presenting cells via an epithelial sodium channel, triggers a PKC (protein kinase C)- and SGK1 (serum/glucocorticoid kinase 1)-stimulated activation of nicotinamide adenine dinucleotide phosphate oxidase, which, in turn, enhances lipid oxidation with generation of highly reactive isolevuglandins. Sodium 30-36 dual oxidase 2 Homo sapiens 207-258 34232678-7 2021 We describe our findings that sodium, entering antigen-presenting cells via an epithelial sodium channel, triggers a PKC (protein kinase C)- and SGK1 (serum/glucocorticoid kinase 1)-stimulated activation of nicotinamide adenine dinucleotide phosphate oxidase, which, in turn, enhances lipid oxidation with generation of highly reactive isolevuglandins. Sodium 90-96 dual oxidase 2 Homo sapiens 207-258 34334139-5 2021 These actions of sodium, potassium and magnesium and other minerals, trace elements and vitamins are likely to be secondary to their action on pro-inflammatory cytokines IL-6, TNF-alpha and IL-17 and metabolism of essential fatty acids that may account for their involvement in the pathobiology of insulin resistance, T2DM, HTN and autoimmune diseases. Sodium 17-23 interleukin 6 Homo sapiens 170-174 34334139-5 2021 These actions of sodium, potassium and magnesium and other minerals, trace elements and vitamins are likely to be secondary to their action on pro-inflammatory cytokines IL-6, TNF-alpha and IL-17 and metabolism of essential fatty acids that may account for their involvement in the pathobiology of insulin resistance, T2DM, HTN and autoimmune diseases. Sodium 17-23 tumor necrosis factor Homo sapiens 176-185 34334139-5 2021 These actions of sodium, potassium and magnesium and other minerals, trace elements and vitamins are likely to be secondary to their action on pro-inflammatory cytokines IL-6, TNF-alpha and IL-17 and metabolism of essential fatty acids that may account for their involvement in the pathobiology of insulin resistance, T2DM, HTN and autoimmune diseases. Sodium 17-23 insulin Homo sapiens 298-305 34143299-4 2021 The GH/IGF-1 system regulates glomerular hemodynamics, renal gluconeogenesis, tubular sodium and water, phosphate, and calcium handling, as well as renal synthesis of 1,25 (OH)2 vitamin D3 and the antiaging hormone Klotho. Sodium 86-92 insulin like growth factor 1 Homo sapiens 7-12 34310861-9 2021 It is suggested that both COX isoforms play opposing roles in renal function, with natriuresis increased by COX-1 inhibition followed by a drop in a blood pressure, whereas COX-2 inhibition increases blood pressure and promotes sodium retention. Sodium 228-234 mitochondrially encoded cytochrome c oxidase II Homo sapiens 173-178 34337896-8 2021 However, despite similar changes in AP and renal hemodynamics, AngII induced increases (p < 0.05) in urinary sodium excretion in WT (3916 +- 942%) were less in the KO strains, more or less in TNFR1KO (473 +- 170%) than in TNFR2KO (1176 +- 168%). Sodium 109-115 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 63-68 34131037-11 2021 We find that CBD interacts with TTX-resistant sodium channels in a state-dependent manner suggesting particularly tight binding to slow inactivated states of Nav1.8 channels, which dominate overall inactivation of Nav1.8 channels for small maintained depolarizations from the resting potential. Sodium 46-52 sodium channel, voltage-gated, type X, alpha Mus musculus 158-164 34131037-11 2021 We find that CBD interacts with TTX-resistant sodium channels in a state-dependent manner suggesting particularly tight binding to slow inactivated states of Nav1.8 channels, which dominate overall inactivation of Nav1.8 channels for small maintained depolarizations from the resting potential. Sodium 46-52 sodium channel, voltage-gated, type X, alpha Mus musculus 214-220 34166227-0 2021 A variant of ASIC2 mediates sodium retention in nephrotic syndrome. Sodium 28-34 acid sensing ion channel subunit 2 Homo sapiens 13-18 34166227-2 2021 This Na retention is usually attributed to epithelial sodium channel (ENaC) activation following plasma aldosterone increase. Sodium 54-60 sodium channel epithelial 1 subunit gamma Rattus norvegicus 70-74 34166227-5 2021 We, then, identified a truncated variant of acid sensing ion channel 2b (ASIC2b) that induced sustained acid-stimulated sodium currents when co-expressed with ASIC2a. Sodium 120-126 acid sensing ion channel subunit 2 Homo sapiens 159-165 34349262-1 2021 MFSD2A is a sodium-dependent lysophosphatidylcholine symporter that is responsible for the uptake of docosahexaenoic acid into the brain1,2, which is crucial for the development and performance of the brain3. Sodium 12-18 major facilitator superfamily domain containing 2A Mus musculus 0-6 34349262-7 2021 The structure-together with our functional studies and molecular dynamics simulations-identifies a conserved sodium-binding site, reveals a potential lipid entry pathway and helps to rationalize MFSD2A mutations that underlie microcephaly syndromes. Sodium 109-115 major facilitator superfamily domain containing 2A Mus musculus 195-201 34196428-1 2021 The sodium/iodide symporter (NIS) expresses at the basolateral plasma membrane of the thyroid follicular cell and mediates iodide accumulation required for normal thyroid hormonogenesis. Sodium 4-10 solute carrier family 5 member 5 Homo sapiens 29-32 34294776-8 2021 In multivariate analysis, compared to the GPS 0 group, the GPS 2 group was associated with high mortality (hazard ratio 2.92, 95% confidence interval 1.77-4.81, p < 0.001) after adjustment for age, sex, blood pressure, HF history, HF severity, hemoglobin, renal function, sodium, BNP, left ventricular ejection fraction, and anti-HF medications. Sodium 272-278 G protein pathway suppressor 2 Homo sapiens 59-64 34357973-0 2021 Identification and Characterization of Novel Proteins from Arizona Bark Scorpion Venom That Inhibit Nav1.8, a Voltage-Gated Sodium Channel Regulator of Pain Signaling. Sodium 124-130 sodium channel, voltage-gated, type X, alpha Mus musculus 100-106 34357973-1 2021 The voltage-gated sodium channel Nav1.8 is linked to neuropathic and inflammatory pain, highlighting the potential to serve as a drug target. Sodium 18-24 sodium channel, voltage-gated, type X, alpha Mus musculus 33-39 34180110-9 2021 He-CTD of the (M + 2Na)2+ and the (M + 2 K)2+ precursors generated singly charged product ions from the loss of a sodium ion and potassium ion, respectively. Sodium 114-120 CTD Homo sapiens 3-6 34305821-7 2021 CB1R could also participate to water and sodium balance and to blood pressure regulation but its precise role remains to decipher. Sodium 41-47 cannabinoid receptor 1 Homo sapiens 0-4 34132028-11 2021 Spearman correlation analysis indicated that urinary sodium excretion positively correlated with urinary protein excretion (r = .178, p .001), SBP (r = .109, p = .002), and DBP (r = .086, p = .015). Sodium 53-59 D-box binding PAR bZIP transcription factor Homo sapiens 175-178 34132028-12 2021 After adjusting for age, gender, BMI, eGFR, urinary protein excretion, and history of taking antihypertensive drug, multivariate linear regression demonstrated that higher level of urinary sodium excretion associated with increased level of SBP, DBP, and MAP (beta = 0.020, p = .049; beta = 0.015, p = .040; beta = 0.016, p = .025, respectively). Sodium 189-195 D-box binding PAR bZIP transcription factor Homo sapiens 246-249 34180640-5 2021 It will specifically emphasize the "yin-yang" nature of Ang II signaling by comparing and contrasting the effects and activity of various systems, pathways and components found in hypertension to those found in Gitelman"s and Bartter"s syndromes (GS/BS), two rare autosomal recessive tubulopathies characterized by electrolytic imbalance, metabolic alkalosis, sodium wasting and prominent activation of the renin-angiotensin-aldosterone system. Sodium 360-366 angiotensinogen Homo sapiens 56-62 34238463-9 2021 Finally, we report on the effects of drugs such as AVP analogues and/or oxytocin, another neuropeptide that increases sodium excretion in animal models and humans with CDI, and sildenafil, a compound that increases the expression and function of AQP2 channels in animal models and humans with NDI. Sodium 118-124 arginine vasopressin Homo sapiens 51-54 34110521-1 2021 PURPOSE OF REVIEW: The sodium (Na+) and hydrogen (H+) exchanger 3 (NHE3), known as solute carrier family 9 member 3 (SLC9A3), mediates active transcellular Na+ and bicarbonate reabsorption in the small intestine of the gut and proximal tubules of the kidney. Sodium 23-29 solute carrier family 9 (sodium/hydrogen exchanger), member 3 Mus musculus 67-71 34110521-1 2021 PURPOSE OF REVIEW: The sodium (Na+) and hydrogen (H+) exchanger 3 (NHE3), known as solute carrier family 9 member 3 (SLC9A3), mediates active transcellular Na+ and bicarbonate reabsorption in the small intestine of the gut and proximal tubules of the kidney. Sodium 23-29 solute carrier family 9 (sodium/hydrogen exchanger), member 3 Mus musculus 117-123 34163352-1 2021 The cardiac sodium-calcium exchanger (NCX1) is important for normal Na+- and Ca2+-homeostasis and cardiomyocyte relaxation and contraction. Sodium 12-18 solute carrier family 8 member A1 Rattus norvegicus 38-42 34290819-2 2021 HypoPP is a rare disease caused by genetic mutations related to expression of sodium or calcium ion channels. Sodium 78-84 calcium voltage-gated channel subunit alpha1 S Homo sapiens 0-6 34045018-12 2021 In contrast, lowering sodium from high to low levels reduced NT-proBNP independently of diet (19%; 95% CI: -24% to -14%), but did not alter hs-cTnI and mildly increased hs-CRP (9%; 95% CI: 0.4% to 18%). Sodium 22-28 C-reactive protein Homo sapiens 172-175 34045018-13 2021 Combining DASH with sodium reduction lowered hs-cTnI by 20% (95% CI: -31% to -7%) and NT-proBNP by 23% (95% CI: -32% to -12%), whereas hs-CRP was not significantly changed (-7%; 95% CI: -22% to 9%) compared with the high sodium-control diet. Sodium 20-26 C-reactive protein Homo sapiens 138-141 34072568-5 2021 Three transporters were identified, one that was sodium-dependent, PROT (SLC6A7), and two others that were sodium-independent, PAT1 (SLC36A1) and PAT2 (SLC36A2). Sodium 49-55 solute carrier family 6 (neurotransmitter transporter, L-proline), member 7 Mus musculus 73-79 34079337-2 2021 The angiotensin I-converting enzyme (ACE1), angiotensin-converting enzyme 2 (ACE2), angiotensinogen (AGT) and receptors angiotensin II receptor type 1 (AGTR1) are key factors for SARS-CoV-2 entering in the cells, sodium and water retention with an increase blood pressure, promotion of fibrotic and inflammatory phenomena resulting in a cytokine storm. Sodium 213-219 angiotensin I converting enzyme Homo sapiens 4-35 34079337-2 2021 The angiotensin I-converting enzyme (ACE1), angiotensin-converting enzyme 2 (ACE2), angiotensinogen (AGT) and receptors angiotensin II receptor type 1 (AGTR1) are key factors for SARS-CoV-2 entering in the cells, sodium and water retention with an increase blood pressure, promotion of fibrotic and inflammatory phenomena resulting in a cytokine storm. Sodium 213-219 angiotensinogen Homo sapiens 84-99 34122084-2 2021 We have previously shown that CsA increases the activity of the epithelial sodium channel (ENaC) in cultured distal nephron cells. Sodium 75-81 sodium channel epithelial 1 subunit gamma Rattus norvegicus 91-95 34113255-0 2021 ANG II and Aldosterone Acting Centrally Participate in the Enhanced Sodium Intake in Water-Deprived Renovascular Hypertensive Rats. Sodium 68-74 angiotensinogen Rattus norvegicus 0-6 34113255-4 2021 Therefore, the purpose of this study was to investigate whether angiotensin II (ANG II) and/or aldosterone participates in the increased sodium intake in 2K1C rats under WD. Sodium 137-143 angiotensinogen Rattus norvegicus 64-78 34113255-4 2021 Therefore, the purpose of this study was to investigate whether angiotensin II (ANG II) and/or aldosterone participates in the increased sodium intake in 2K1C rats under WD. Sodium 137-143 angiotensinogen Rattus norvegicus 80-86 34113255-13 2021 These results suggest the participation of ANG II and aldosterone acting centrally in the enhanced sodium intake in WD 2K1C rats, and not in the maintenance of hypertension in satiated and fluid-replete 2K1C rats. Sodium 99-105 angiotensinogen Rattus norvegicus 43-49 34103922-4 2021 GRK4 plays an important role in regulation of renal sodium excretion. Sodium 52-58 G protein-coupled receptor kinase 4 Homo sapiens 0-4 34847569-2 2021 Enterocyte ACE2 is coexpressed as the apical membrane trafficking partner obligatory for expression and activity of the B0AT1 sodium-dependent neutral amino acid transporter. Sodium 126-132 solute carrier family 38 member 7 Homo sapiens 151-173 34065042-3 2021 Excitatory amino acid carrier 1 (EAAC1), a sodium-dependent glutamate/cysteine transporter that is selectively present in neurons, plays a central role in the regulation of neuronal GSH production. Sodium 43-49 solute carrier family 1 member 1 Homo sapiens 0-31 34065042-3 2021 Excitatory amino acid carrier 1 (EAAC1), a sodium-dependent glutamate/cysteine transporter that is selectively present in neurons, plays a central role in the regulation of neuronal GSH production. Sodium 43-49 solute carrier family 1 member 1 Homo sapiens 33-38 34219841-0 2021 Photoionization Loss of Mercury"s Sodium Exosphere: Seasonal Observations by MESSENGER and the THEMIS Telescope. Sodium 34-40 thymocyte selection associated Homo sapiens 95-101 35258103-6 2022 Finally, pharmacoepidemiological-pharmacodynamic analysis revealed a significant correlation between the decrease in serum sodium levels and binding affinity for serotonin transporter (SERT; r=-0.84, P=0.02), suggesting that lower binding affinity of mirtazapine, fluvoxamine, and milnacipran against SERT is responsible for the above difference. Sodium 123-129 solute carrier family 6 member 4 Homo sapiens 162-183 34320496-9 2021 CONCLUSIONS: Our data demonstrated that the synergy between 20-HETE and HFD could decrease NKCC2 protein via posttranslational ubiquitination, which was thought to be the main mechanism underlying the short-term effect in response to HFD and might be responsible for the adaptive modulation of renal NKCC2 to resist sodium retention. Sodium 316-322 solute carrier family 12, member 1 Mus musculus 91-96 34320496-9 2021 CONCLUSIONS: Our data demonstrated that the synergy between 20-HETE and HFD could decrease NKCC2 protein via posttranslational ubiquitination, which was thought to be the main mechanism underlying the short-term effect in response to HFD and might be responsible for the adaptive modulation of renal NKCC2 to resist sodium retention. Sodium 316-322 solute carrier family 12, member 1 Mus musculus 300-305 34644706-3 2021 In this study, we aimed to explore another potential effect modifier: the predialysis serum sodium (SNa) and related proxies of plasma tonicity. Sodium 92-98 snail family transcriptional repressor 1 Homo sapiens 100-103 35514008-1 2022 BACKGROUND: Bulevirtide (BLV) blocks the uptake of the hepatitis D virus (HDV) into hepatocytes via the sodium/bile acid cotransporter NTCP. Sodium 104-110 solute carrier family 10 member 1 Homo sapiens 135-139 35506380-2 2022 Although aldosterone activates MR to increase epithelial sodium channel (ENaC) activity, glucocorticoids also activate MR but are metabolized by 11betaHSD2 (11beta-hydroxysteroid dehydrogenase type 2). Sodium 57-63 hydroxysteroid 11-beta dehydrogenase 2 Mus musculus 145-155 35506380-2 2022 Although aldosterone activates MR to increase epithelial sodium channel (ENaC) activity, glucocorticoids also activate MR but are metabolized by 11betaHSD2 (11beta-hydroxysteroid dehydrogenase type 2). Sodium 57-63 hydroxysteroid 11-beta dehydrogenase 2 Mus musculus 157-199 35525869-0 2022 Two adjacent phosphorylation sites in the C-terminus of the channel"s alpha-subunit have opposing effects on epithelial sodium channel (ENaC) activity. Sodium 120-126 sodium channel epithelial 1 subunit gamma Rattus norvegicus 136-140 35525869-1 2022 How phosphorylation of the epithelial sodium channel (ENaC) contributes to its regulation is incompletely understood. Sodium 38-44 sodium channel epithelial 1 subunit gamma Rattus norvegicus 54-58 35453033-1 2022 Defects of the cystic fibrosis (CF) transmembrane conductance regulator (CFTR) protein affect the homeostasis of chloride, bicarbonate, sodium, and water in the airway surface liquid, influencing the mucus composition and viscosity, which induces a severe condition of infection and inflammation along the whole life of CF patients. Sodium 136-142 CF transmembrane conductance regulator Homo sapiens 15-71 35453033-1 2022 Defects of the cystic fibrosis (CF) transmembrane conductance regulator (CFTR) protein affect the homeostasis of chloride, bicarbonate, sodium, and water in the airway surface liquid, influencing the mucus composition and viscosity, which induces a severe condition of infection and inflammation along the whole life of CF patients. Sodium 136-142 CF transmembrane conductance regulator Homo sapiens 73-77 35435735-2 2022 SCN1A encodes for the alpha subunit of the voltage-gated type I sodium channel (NaV1.1), the primary voltage-gated sodium channel responsible for generation of action potentials in GABAergic inhibitory interneurons. Sodium 64-70 sodium channel, voltage-gated, type I, alpha Mus musculus 0-5 35435735-2 2022 SCN1A encodes for the alpha subunit of the voltage-gated type I sodium channel (NaV1.1), the primary voltage-gated sodium channel responsible for generation of action potentials in GABAergic inhibitory interneurons. Sodium 64-70 sodium channel, voltage-gated, type I, alpha Mus musculus 80-86 35435735-2 2022 SCN1A encodes for the alpha subunit of the voltage-gated type I sodium channel (NaV1.1), the primary voltage-gated sodium channel responsible for generation of action potentials in GABAergic inhibitory interneurons. Sodium 115-121 sodium channel, voltage-gated, type I, alpha Mus musculus 0-5 35435735-2 2022 SCN1A encodes for the alpha subunit of the voltage-gated type I sodium channel (NaV1.1), the primary voltage-gated sodium channel responsible for generation of action potentials in GABAergic inhibitory interneurons. Sodium 115-121 sodium channel, voltage-gated, type I, alpha Mus musculus 80-86 35296155-0 2022 Na+-Retaining Action of COX-2 (Cyclooxygenase-2)/EP1 Pathway in the Collecting Duct via Activation of Intrarenal Renin-Angiotensin-Aldosterone System and Epithelial Sodium Channel. Sodium 165-171 prostaglandin E receptor 1 (subtype EP1) Mus musculus 49-52 35296155-8 2022 CONCLUSIONS: The study for the first time reports that CD COX-2/EP1 pathway might play a key role in maintenance of Na+ homeostasis in the face of Na+ depletion, at least in part, through activation of intrarenal renin-angiotensin-aldosterone-system and epithelial sodium channel. Sodium 265-271 prostaglandin E receptor 1 (subtype EP1) Mus musculus 64-67 35608043-4 2022 Here, we have exploited this effect in the investigation of conformational differences in the molten globule states of cyt c induced by different sodium anions, namely sulfate, chloride and perchlorate. Sodium 146-152 cytochrome c, somatic Homo sapiens 119-124 35621227-2 2022 We have identified a novel drug for hyperphosphatemia, EOS789, that interacts with several sodium-dependent phosphate transporters (NaPi-IIb, PiT-1, and PiT-2) known to contribute to intestinal phosphate absorption. Sodium 91-97 POU class 1 homeobox 1 Rattus norvegicus 142-147 35635440-0 2022 Inhibition of the sodium-dependent HCO3- transporter SLC4A4, produces a cystic fibrosis-like airway disease phenotype. Sodium 18-24 solute carrier family 4 member 4 Homo sapiens 53-59 35635440-7 2022 We report herein that the electrogenic, sodium-dependent, bicarbonate cotransporter, SLC4A4, is expressed in the basolateral membrane of human and mouse airways, and that it"s pharmacological inhibition or genetic silencing reduces bicarbonate secretion. Sodium 40-46 solute carrier family 4 member 4 Homo sapiens 85-91 35624145-3 2022 Thirteen kinases were found to activate sodium/hydrogen exchanger (NHE1) in normal hematopoietic progenitors, of which FLT3-ITD, KRASG12D, and BTK phosphorylated NHE1 maintained alkaline intracellular pH (pHi) and supported survival of AML cells. Sodium 40-46 solute carrier family 9 member A1 Homo sapiens 67-71 35624145-3 2022 Thirteen kinases were found to activate sodium/hydrogen exchanger (NHE1) in normal hematopoietic progenitors, of which FLT3-ITD, KRASG12D, and BTK phosphorylated NHE1 maintained alkaline intracellular pH (pHi) and supported survival of AML cells. Sodium 40-46 fms related receptor tyrosine kinase 3 Homo sapiens 119-123 35624145-3 2022 Thirteen kinases were found to activate sodium/hydrogen exchanger (NHE1) in normal hematopoietic progenitors, of which FLT3-ITD, KRASG12D, and BTK phosphorylated NHE1 maintained alkaline intracellular pH (pHi) and supported survival of AML cells. Sodium 40-46 solute carrier family 9 member A1 Homo sapiens 162-166 34308420-1 2021 Dravet Syndrome (DS) is a severe childhood epilepsy caused by heterozygous loss-of-function mutations in the SCN1A gene encoding brain type-I voltage-gated sodium channel Nav1.1. Sodium 156-162 sodium channel, voltage-gated, type I, alpha Mus musculus 109-114 34308420-1 2021 Dravet Syndrome (DS) is a severe childhood epilepsy caused by heterozygous loss-of-function mutations in the SCN1A gene encoding brain type-I voltage-gated sodium channel Nav1.1. Sodium 156-162 sodium channel, voltage-gated, type I, alpha Mus musculus 171-177 35487063-2 2022 Solute carrier family 1 member 5 (SLC1A5) is a sodium channel that functions as a glutamine transporter. Sodium 47-53 solute carrier family 1 (neutral amino acid transporter), member 5 Mus musculus 0-32 35487063-2 2022 Solute carrier family 1 member 5 (SLC1A5) is a sodium channel that functions as a glutamine transporter. Sodium 47-53 solute carrier family 1 (neutral amino acid transporter), member 5 Mus musculus 34-40 35607818-1 2022 Background: This study aims to elucidate the associations among dietary seaweed (gim and miyeok/dashima) and iodine intakes, the rs77277498 polymorphism of the SLC5A5 gene codifying the sodium/iodine symporter, and thyroid cancer risk in a Korean population. Sodium 186-192 solute carrier family 5 member 5 Homo sapiens 160-166 35258103-6 2022 Finally, pharmacoepidemiological-pharmacodynamic analysis revealed a significant correlation between the decrease in serum sodium levels and binding affinity for serotonin transporter (SERT; r=-0.84, P=0.02), suggesting that lower binding affinity of mirtazapine, fluvoxamine, and milnacipran against SERT is responsible for the above difference. Sodium 123-129 solute carrier family 6 member 4 Homo sapiens 185-189 35258103-6 2022 Finally, pharmacoepidemiological-pharmacodynamic analysis revealed a significant correlation between the decrease in serum sodium levels and binding affinity for serotonin transporter (SERT; r=-0.84, P=0.02), suggesting that lower binding affinity of mirtazapine, fluvoxamine, and milnacipran against SERT is responsible for the above difference. Sodium 123-129 solute carrier family 6 member 4 Homo sapiens 301-305 35603785-1 2022 Loss-of-function (LOF) variants in SCN1B, encoding the voltage-gated sodium channel beta1/beta1B subunits, are linked to neurological and cardiovascular diseases. Sodium 69-75 sodium channel, voltage-gated, type I, beta Mus musculus 35-40 35255185-3 2022 An X-ray diffraction study of the sodium derivative shows that the complex features two unreduced HOAd1 donors as well as the reduced alkoxide (OAd1), with the Ad1 fragments clustered together on the same side of the NaO3 plane, contrary to steric considerations. Sodium 34-40 amyloid beta precursor protein Homo sapiens 160-163 35580629-2 2022 Establishment of HBV infection requires a molecular interaction between the virus envelope glycoprotein L (LHBs) and the host entry receptor sodium-taurocholate co-transporting polypeptide (NTCP), a sodium-dependent bile acid transporter from blood to hepatocytes 3. Sodium 141-147 solute carrier family 10 member 1 Homo sapiens 190-194 35580629-2 2022 Establishment of HBV infection requires a molecular interaction between the virus envelope glycoprotein L (LHBs) and the host entry receptor sodium-taurocholate co-transporting polypeptide (NTCP), a sodium-dependent bile acid transporter from blood to hepatocytes 3. Sodium 199-205 solute carrier family 10 member 1 Homo sapiens 190-194 35574842-2 2022 In diabetes, IL (interleukin)-6 induces salt sensitivity through a dysregulation of the epithelial sodium channel. Sodium 99-105 interleukin 6 Mus musculus 13-31 35600585-2 2022 ITD is an autosomal recessive disorder caused by loss-of-function variants in the sodium/iodide symporter (NIS)-coding SLC5A5 gene. Sodium 82-88 solute carrier family 5 member 5 Homo sapiens 119-125 35430873-11 2022 CONCLUSIONS: Our results identified the role of activated CD8Ts in contributing to increased sodium retention in DCTS through the IFN-gamma-PDL1 pathway. Sodium 93-99 interferon gamma Mus musculus 130-139 35430873-11 2022 CONCLUSIONS: Our results identified the role of activated CD8Ts in contributing to increased sodium retention in DCTS through the IFN-gamma-PDL1 pathway. Sodium 93-99 CD274 antigen Mus musculus 140-144 35625445-0 2022 Corin: A Key Mediator in Sodium Homeostasis, Vascular Remodeling, and Heart Failure. Sodium 25-31 corin, serine peptidase Homo sapiens 0-5 35625445-4 2022 In addition to the heart, corin is expressed in other tissues, including those of the kidney, skin, and uterus, where corin-mediated ANP production and signaling act locally to promote sodium excretion and vascular remodeling. Sodium 185-191 corin, serine peptidase Homo sapiens 26-31 35625445-4 2022 In addition to the heart, corin is expressed in other tissues, including those of the kidney, skin, and uterus, where corin-mediated ANP production and signaling act locally to promote sodium excretion and vascular remodeling. Sodium 185-191 corin, serine peptidase Homo sapiens 118-123 35625445-4 2022 In addition to the heart, corin is expressed in other tissues, including those of the kidney, skin, and uterus, where corin-mediated ANP production and signaling act locally to promote sodium excretion and vascular remodeling. Sodium 185-191 natriuretic peptide A Homo sapiens 133-136 35625445-7 2022 In this review, we discuss most recent findings regarding the role of corin in non-cardiac tissues, including the kidney and skin, in regulating sodium homeostasis and body fluid excretion. Sodium 145-151 corin, serine peptidase Homo sapiens 70-75 35523577-2 2022 In heart transplant recipients, angiotensin-converting enzyme inhibitors have been demonstrated to be a keystone for the treatment of hypertension with a wide spectrum of pleiotropic molecular effects ranging from improvement of the peripheral vascular system to regulation of the fluid and sodium balance. Sodium 291-297 angiotensin I converting enzyme Homo sapiens 32-61 35150131-4 2022 In the present study, we found that human immortalized podocytes express messenger RNA and protein of phosphate transporters, including NaPi 2c (SLC34A3), Pit 1 (SLC20A1), and Pit 2 (SLC20A2), which are sodium-dependent and mediate intracellular phosphate (Pi) transport, and XPR1, which is responsible for extracellular Pi transport. Sodium 203-209 solute carrier family 34 member 3 Homo sapiens 136-143 35353937-7 2022 In the presence of Abeta oligomers, knockdown of Nav1.6 reduces intracellular calcium overload by suppressing reverse sodium-calcium exchange channel, consequently increasing inactive NFAT1 (the nuclear factor of activated T cells) levels and thus reducing BACE1 transcription. Sodium 118-124 nuclear factor of activated T cells, cytoplasmic, calcineurin dependent 2 Mus musculus 184-189 35150131-4 2022 In the present study, we found that human immortalized podocytes express messenger RNA and protein of phosphate transporters, including NaPi 2c (SLC34A3), Pit 1 (SLC20A1), and Pit 2 (SLC20A2), which are sodium-dependent and mediate intracellular phosphate (Pi) transport, and XPR1, which is responsible for extracellular Pi transport. Sodium 203-209 solute carrier family 34 member 3 Homo sapiens 145-152 35601958-3 2022 TIP peptide, AP301) is a 17-mer cyclic peptide that mimics the LLD of human TNF which activates the amiloride-sensitive epithelial sodium channel (ENaC) and, as such, recapitulates the capacity of TNF to enhance alveolar fluid clearance, as demonstrated in numerous preclinical studies. Sodium 131-137 tumor necrosis factor Homo sapiens 76-79 35285452-2 2022 We hypothesized that sodium-glucose cotransporter 2 (SGLT2) inhibition and angiotensin II type 1 receptor (AT1R) blockade can synergistically reduce renal sodium reabsorption by beneficially effects on these transporters, leading to lower BP and ameliorating renal and cardiac damage. Sodium 155-161 angiotensin II receptor, type 1b Rattus norvegicus 75-105 35285452-2 2022 We hypothesized that sodium-glucose cotransporter 2 (SGLT2) inhibition and angiotensin II type 1 receptor (AT1R) blockade can synergistically reduce renal sodium reabsorption by beneficially effects on these transporters, leading to lower BP and ameliorating renal and cardiac damage. Sodium 155-161 angiotensin II receptor, type 1b Rattus norvegicus 107-111 35573729-3 2022 The sodium-dependent organic anion transporter Soat (Slc10a6) is a plasma membrane uptake transporter for sulfated steroids. Sodium 4-10 solute carrier family 10 (sodium/bile acid cotransporter family), member 6 Mus musculus 53-60 35601958-3 2022 TIP peptide, AP301) is a 17-mer cyclic peptide that mimics the LLD of human TNF which activates the amiloride-sensitive epithelial sodium channel (ENaC) and, as such, recapitulates the capacity of TNF to enhance alveolar fluid clearance, as demonstrated in numerous preclinical studies. Sodium 131-137 tumor necrosis factor Homo sapiens 197-200 35462606-1 2022 The pathogenic mechanism of cystic fibrosis (CF) includes the functional interaction of the cystic fibrosis transmembrane conductance regulator (CFTR) protein with the epithelial sodium channel (ENaC). Sodium 179-185 CF transmembrane conductance regulator Homo sapiens 92-143 35414109-1 2022 Supressed plasma renin in patients with primary hypertension is thought to be an indirect marker of sodium-induced volume expansion which is associated with more severe hypertension and hypertension-mediated organ damage. Sodium 100-106 renin Homo sapiens 17-22 35414109-10 2022 These results suggests that sodium retention in hypertension characterised by a low-renin state is associated with cell membrane damage reflected by eGCSS. Sodium 28-34 renin Homo sapiens 84-89 35620081-12 2022 Higher plasma total renin remained significantly associated with lower sodium output per doubling of diuretic dose (beta = -0.41 (-0.76, -0.059) per SD change) with adjustment; higher plasma total and active renin were significantly associated with lower fractional excretion of sodium per doubling of diuretic dose (beta = -0.48 (-0.83, -0.14) and beta = -0.51 (-0.95, -0.08), respectively) in adjusted models. Sodium 71-77 renin Homo sapiens 20-25 35620081-12 2022 Higher plasma total renin remained significantly associated with lower sodium output per doubling of diuretic dose (beta = -0.41 (-0.76, -0.059) per SD change) with adjustment; higher plasma total and active renin were significantly associated with lower fractional excretion of sodium per doubling of diuretic dose (beta = -0.48 (-0.83, -0.14) and beta = -0.51 (-0.95, -0.08), respectively) in adjusted models. Sodium 279-285 renin Homo sapiens 20-25 35048187-5 2022 In addition, Slc7a5 is a transporter for the first-line anti-allodynic gabapentinoid drugs and binds to ion channels implicated in nociception and chronic pain including the voltage-gated sodium channel Nav1.7 and the voltage-gated potassium channels Kv1.1 and Kv1.2. Sodium 188-194 sodium channel, voltage-gated, type IX, alpha Mus musculus 203-209 35194979-3 2022 Here, we describe the in vivo effects of a novel potent inhibitor of the intestinal sodium-dependent phosphate cotransporter NPT2b, LY3358966. Sodium 84-90 solute carrier family 34 (sodium phosphate), member 2 Mus musculus 125-130 35409270-3 2022 Sodium proton exchanger 1 (NHE1) is an important factor in SC acidification. Sodium 0-6 solute carrier family 9 member A1 Homo sapiens 27-31 35453560-5 2022 Mechanistic investigation from both in vivo and in vitro data suggested that disruption of cytoskeleton induced by excessive reactive oxygen species defected intracellular transport of aquaporin 1, this likely resulted in the disappearance of sodium sieving upon PET. Sodium 243-249 aquaporin 1 (Colton blood group) Homo sapiens 185-196 35504352-0 2022 Transmembrane serine protease 2 (TMPRSS2) proteolytically activates the epithelial sodium channel (ENaC) by cleaving the channel"s gamma-subunit. Sodium 83-89 transmembrane serine protease 2 Homo sapiens 0-31 35504352-0 2022 Transmembrane serine protease 2 (TMPRSS2) proteolytically activates the epithelial sodium channel (ENaC) by cleaving the channel"s gamma-subunit. Sodium 83-89 transmembrane serine protease 2 Homo sapiens 33-40 35137522-1 2022 In the present study we describe and explain an aberrant behavior in terms of receptor binding profile of a fluorescein-based multimodal imaging agent for gastrin releasing peptide receptor (GRPR) visualization by elucidating a chelating mechanism on sodium ions of its fluorescent dye moiety. Sodium 251-257 gastrin releasing peptide receptor Homo sapiens 155-189 35137522-1 2022 In the present study we describe and explain an aberrant behavior in terms of receptor binding profile of a fluorescein-based multimodal imaging agent for gastrin releasing peptide receptor (GRPR) visualization by elucidating a chelating mechanism on sodium ions of its fluorescent dye moiety. Sodium 251-257 gastrin releasing peptide receptor Homo sapiens 191-195 35438852-1 2022 OBJECTIVES: Iodide transport defect (ITD) is one of the principal causes of congenital hypothyroidism (CH) and its primary molecular mechanism is a mutation of the sodium/iodide symporter (NIS) gene. Sodium 164-170 solute carrier family 5 member 5 Homo sapiens 189-192 35514347-1 2022 The sodium (Na+)/hydrogen (H+) exchanger 3 (NHE3) is one of the most important Na+/H+ antiporters in the small intestines of the gastrointestinal tract and the proximal tubules of the kidney. Sodium 4-10 solute carrier family 9 (sodium/hydrogen exchanger), member 3 Mus musculus 44-48 35447164-7 2022 For instance, central infusion of IL-1beta or TNF-alpha can directly affect sodium and water consumption in animal models. Sodium 76-82 tumor necrosis factor Homo sapiens 46-55 35419655-0 2022 Simulations suggest double sodium binding induces unexpected conformational changes in thrombin. Sodium 27-33 coagulation factor II, thrombin Homo sapiens 87-95 35419655-6 2022 The correlation matrices for different binding modes suggest regions that may play an important role in thrombin"s allosteric response and provide us a possible allosteric pathway for the sodium binding. Sodium 188-194 coagulation factor II, thrombin Homo sapiens 104-112 35419655-8 2022 Principal component analysis (PCA) shows us how the different regions of thrombin change conformation together with sodium binding. Sodium 116-122 coagulation factor II, thrombin Homo sapiens 73-81 35462606-1 2022 The pathogenic mechanism of cystic fibrosis (CF) includes the functional interaction of the cystic fibrosis transmembrane conductance regulator (CFTR) protein with the epithelial sodium channel (ENaC). Sodium 179-185 CF transmembrane conductance regulator Homo sapiens 145-149 35475027-8 2022 Following oral sodium suppression, the aldosterone-to-renin ratio was 4-fold higher using immunoassay (27.2 (19.7, 62.4) vs 6.4 (3.5, 19.1) ng/dL per ng/mL/hour; P < .001). Sodium 15-21 renin Homo sapiens 54-59 35191472-0 2022 The yin and yang of Tbx5 variant effects on sodium channel function. Sodium 44-50 T-box transcription factor 5 Homo sapiens 20-24 35303888-5 2022 We postulate that cardiac benefit modulated by SGLT2i"s can be commonly attributed to their inhibition of sodium-loaders in the plasma membrane (NHE-1, Nav1.5, SGLT) affecting intracellular sodium-homeostasis (the sodium-interactome), thereby providing a unifying view on the various effects reported in separate studies. Sodium 106-112 solute carrier family 9 member A1 Homo sapiens 145-150 35303888-5 2022 We postulate that cardiac benefit modulated by SGLT2i"s can be commonly attributed to their inhibition of sodium-loaders in the plasma membrane (NHE-1, Nav1.5, SGLT) affecting intracellular sodium-homeostasis (the sodium-interactome), thereby providing a unifying view on the various effects reported in separate studies. Sodium 190-196 solute carrier family 9 member A1 Homo sapiens 145-150 35303888-5 2022 We postulate that cardiac benefit modulated by SGLT2i"s can be commonly attributed to their inhibition of sodium-loaders in the plasma membrane (NHE-1, Nav1.5, SGLT) affecting intracellular sodium-homeostasis (the sodium-interactome), thereby providing a unifying view on the various effects reported in separate studies. Sodium 214-220 solute carrier family 9 member A1 Homo sapiens 145-150 35370551-1 2022 Dravet syndrome is severe childhood-onset epilepsy, caused by loss of function mutations in the SCN1A gene, encoding for the voltage-gated sodium channel NaV1.1. Sodium 139-145 sodium channel, voltage-gated, type I, alpha Mus musculus 96-101 35370551-1 2022 Dravet syndrome is severe childhood-onset epilepsy, caused by loss of function mutations in the SCN1A gene, encoding for the voltage-gated sodium channel NaV1.1. Sodium 139-145 sodium channel, voltage-gated, type I, alpha Mus musculus 154-160 35256591-0 2022 mTORC1 induces plasma membrane depolarization and promotes preosteoblast senescence by regulating the sodium channel Scn1a. Sodium 102-108 sodium channel, voltage-gated, type I, alpha Mus musculus 117-122 35256591-5 2022 We further identified the sodium channel Scn1a as a mediator of membrane depolarization in senescent preosteoblasts. Sodium 26-32 sodium channel, voltage-gated, type I, alpha Mus musculus 41-46 35131865-0 2022 The anti-diabetic drug metformin regulates voltage-gated sodium channel NaV1.7 via the ubiquitin-ligase NEDD4-2. Sodium 57-63 sodium channel, voltage-gated, type IX, alpha Mus musculus 72-78 35175729-7 2022 A NaF layer, on top of the sodium metal, leads to a much more uniform deposition of sodium and greatly enhanced cyclability. Sodium 27-39 C-X-C motif chemokine ligand 8 Homo sapiens 2-5 35157443-0 2022 Histamine Sensitization of the Voltage-Gated Sodium Channel Nav1.7 Contributes to Histaminergic Itch in Mice. Sodium 45-51 itchy, E3 ubiquitin protein ligase Mus musculus 96-100 35175729-7 2022 A NaF layer, on top of the sodium metal, leads to a much more uniform deposition of sodium and greatly enhanced cyclability. Sodium 84-90 C-X-C motif chemokine ligand 8 Homo sapiens 2-5 34714114-0 2022 Renal NOXA1/NOX1 Signaling Regulates Epithelial Sodium Channel and Sodium Retention in Angiotensin II-induced Hypertension. Sodium 67-73 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 87-101 35124009-0 2022 Oxidized alkyl phospholipids stimulate sodium transport in proximal tubules via a non-genomic PPARgamma-dependent pathway. Sodium 39-45 peroxisome proliferator activated receptor gamma Homo sapiens 94-103 35402583-12 2022 Epithelial sodium channel alpha subunit (alpha-ENaC) was revealed as a direct target gene of miR-432-5p and expressed on both human peritoneum and MeT-5A cells. Sodium 11-17 sodium channel epithelial 1 subunit alpha Homo sapiens 41-51 35015304-0 2022 The T1-tetramerization Domain of Kv1.2 Rescues Expression and Preserves Function of a Truncated NaChBac Sodium Channel. Sodium 104-110 potassium voltage-gated channel subfamily A member 2 Homo sapiens 33-38 35453332-2 2022 In this study, the interaction between resveratrol and whey protein isolate (WPI), sodium caseinate (SC) and soy protein isolate (SPI) during storage were systematically investigated from the aspects of polyphenol loading, antioxidant activity and oxidability. Sodium 83-89 chromogranin A Homo sapiens 130-133 35124009-3 2022 Although it has been reported that PPARgamma agonists including thiazolidinediones can induce plasma volume expansion by enhancing renal sodium and water retention, the role of azPC in renal transport functions is unknown. Sodium 137-143 peroxisome proliferator activated receptor gamma Homo sapiens 35-44 35535075-11 2022 Short-term use of Vasopressin (V2) receptor antagonists may also be used to normalize sodium levels prior to LT. Sodium 86-92 arginine vasopressin receptor 2 Homo sapiens 18-43 35150739-5 2022 Here, we demonstrate that Major Facilitator Superfamily Domain containing 2a (Mfsd2a), a sodium-dependent lysophosphatidylcholine (LPC) transporter, is expressed at the apical surface of AT2 cells. Sodium 89-95 major facilitator superfamily domain containing 2A Mus musculus 26-76 35150739-5 2022 Here, we demonstrate that Major Facilitator Superfamily Domain containing 2a (Mfsd2a), a sodium-dependent lysophosphatidylcholine (LPC) transporter, is expressed at the apical surface of AT2 cells. Sodium 89-95 major facilitator superfamily domain containing 2A Mus musculus 78-84 35228649-4 2022 High salt intake under reduced NO production overactivated the angiotensin II-SPAK (STE20/SPS1-related proline-alanine-rich protein kinase)-NCC (sodium chloride co-transporter) pathway in the kidney, resulting in the insufficient excretion of sodium during the day and its excessive excretion at night. Sodium 145-151 solute carrier family 12, member 3 Mus musculus 140-143 35228649-4 2022 High salt intake under reduced NO production overactivated the angiotensin II-SPAK (STE20/SPS1-related proline-alanine-rich protein kinase)-NCC (sodium chloride co-transporter) pathway in the kidney, resulting in the insufficient excretion of sodium during the day and its excessive excretion at night. Sodium 243-249 solute carrier family 12, member 3 Mus musculus 140-143 35269829-2 2022 Reduced CFTR protein results in decreased Cl- secretion and excessive sodium reabsorption in epithelial cells, which consequently leads to epithelial dehydration and the accumulation of thick mucus within the affected organs, such as the lungs, pancreas, gastrointestinal (GI) tract, reproductive system and sweat glands. Sodium 70-76 CF transmembrane conductance regulator Homo sapiens 8-12 35371779-10 2022 Theoretically, treatment of hydrocephalus-related hyponatremia with CSF-diversion procedures should relieve the pressure on the hypothalamus, mitigating ADH production, which in turn will decrease sodium excretion and ameliorate the hyponatremia. Sodium 197-203 arginine vasopressin Homo sapiens 153-156 35212623-1 2022 Dravet syndrome (DS) is a neurodevelopmental disorder due to pathogenic variants in SCN1A encoding the Nav1.1 sodium channel subunit, characterized by treatment-resistant epilepsy, temperature-sensitive seizures, developmental delay/intellectual disability with features of autism spectrum disorder, and increased risk of sudden death. Sodium 110-116 sodium channel, voltage-gated, type I, alpha Mus musculus 84-89 35212623-1 2022 Dravet syndrome (DS) is a neurodevelopmental disorder due to pathogenic variants in SCN1A encoding the Nav1.1 sodium channel subunit, characterized by treatment-resistant epilepsy, temperature-sensitive seizures, developmental delay/intellectual disability with features of autism spectrum disorder, and increased risk of sudden death. Sodium 110-116 sodium channel, voltage-gated, type I, alpha Mus musculus 103-109 35252404-10 2022 In KoGES, urine sodium was correlated with BP in both groups after adjusting for age, sex, and eGFR; however, the correlation coefficient was lower in older participants. Sodium 16-22 renin binding protein Homo sapiens 81-84 35252404-1 2022 Background: Age-related alterations in renal sodium handling affect blood pressure (BP). Sodium 45-51 renin binding protein Homo sapiens 12-15 35203314-8 2022 Mechanistically, ZO-1 deficient myocytes displayed a reduction in sodium current density (INa) and an increased sensitivity to isoproterenol stimulation. Sodium 66-72 tight junction protein 1 Mus musculus 17-21 35237171-0 2022 Sodium, Glucose and Dysregulated Glucagon Secretion: The Potential of Sodium Glucose Transporters. Sodium 70-76 glucagon Homo sapiens 33-41 35237171-10 2022 Under hyperglycaemic conditions, SGLT1 mediated accumulation of sodium results in alpha cell dysregulation due to altered cellular acidification and ATP production. Sodium 64-70 solute carrier family 5 member 1 Homo sapiens 33-38 35062349-11 2022 A whole-cell patch-clamp analysis suggested that HERV-W ENV enhanced sodium influx through DRD2. Sodium 69-75 endogenous retrovirus group W member 1, envelope Homo sapiens 49-59 35113855-4 2022 Single-nucleotide polymorphisms (SNPs) in ACE, ADRB1, and SLC12A3 associated (P < 5.0 x 10-8) with systolic blood pressure (SBP) in genome-wide association studies (GWAS) were used to proxy inhibition of angiotensin-converting enzyme (ACE), beta-1 adrenergic receptor (ADRB1), and sodium-chloride symporter (NCC), respectively. Sodium 281-287 angiotensin I converting enzyme Homo sapiens 42-45 35022275-5 2022 HBV/HCV coinfection and HBx, HBV preS2, HCV Core, and HCV NS2/3 overexpression increased TGF-beta1 mRNA levels in sodium taurocholate cotransporting polypeptide-Huh7.5.1 cells compared with controls. Sodium 114-120 NS2 Homo sapiens 58-63 35022275-5 2022 HBV/HCV coinfection and HBx, HBV preS2, HCV Core, and HCV NS2/3 overexpression increased TGF-beta1 mRNA levels in sodium taurocholate cotransporting polypeptide-Huh7.5.1 cells compared with controls. Sodium 114-120 transforming growth factor beta 1 Homo sapiens 89-98 35124009-10 2022 These results suggest that azPC stimulates renal PT sodium-coupled bicarbonate transport via a CD36/PPARgamma/MEK/ERK pathway. Sodium 52-58 peroxisome proliferator activated receptor gamma Homo sapiens 100-109 35124009-10 2022 These results suggest that azPC stimulates renal PT sodium-coupled bicarbonate transport via a CD36/PPARgamma/MEK/ERK pathway. Sodium 52-58 Eph receptor B1 Rattus norvegicus 114-117 35013561-6 2022 The epithelial sodium-hydrogen exchanger, NHE1, is a ubiquitous plasma membrane protein tasked with the maintenance of cytoplasmic pH at neutrality. Sodium 15-21 solute carrier family 9 member A1 Homo sapiens 42-46 35053371-0 2022 Sodium Binding Stabilizes the Outward-Open State of SERT by Limiting Bundle Domain Motions. Sodium 0-6 solute carrier family 6 member 4 Homo sapiens 52-56 35012534-3 2022 METHODS: To investigate whether monocarboxylate transporter 1 (MCT1) and sodium-coupled MCT1 (SMCT1) are altered in ALS cell and mouse models, a cellular uptake study, quantitative real time polymerase chain reaction and western blot parameters were used. Sodium 73-79 solute carrier family 16 (monocarboxylic acid transporters), member 1 Mus musculus 88-92 34999954-1 2022 SLC10A7, encoded by the so-called SLC10A7 gene, is the seventh member of a human sodium/bile acid cotransporter family, known as the SLC10 family. Sodium 81-87 solute carrier family 10 member 7 Homo sapiens 0-7 35083300-5 2021 Overall, miR-190a-5p suppressed the increase in SCN3B sodium current caused by endogenous IL-2, whereas miR-190a-5p inhibitor significantly reversed this effect. Sodium 54-60 interleukin 2 Homo sapiens 90-94 34999954-1 2022 SLC10A7, encoded by the so-called SLC10A7 gene, is the seventh member of a human sodium/bile acid cotransporter family, known as the SLC10 family. Sodium 81-87 solute carrier family 10 member 7 Homo sapiens 34-41 34980259-1 2022 BACKGROUND: Dravet Syndrome is a severe childhood pharmaco-resistant epileptic disorder mainly caused by mutations in the SCN1A gene, which encodes for the alpha1 subunit of the type I voltage-gated sodium channel (NaV1.1), that causes imbalance between excitation and inhibition in the brain. Sodium 199-205 sodium channel, voltage-gated, type I, alpha Mus musculus 122-127 34980259-1 2022 BACKGROUND: Dravet Syndrome is a severe childhood pharmaco-resistant epileptic disorder mainly caused by mutations in the SCN1A gene, which encodes for the alpha1 subunit of the type I voltage-gated sodium channel (NaV1.1), that causes imbalance between excitation and inhibition in the brain. Sodium 199-205 sodium channel, voltage-gated, type I, alpha Mus musculus 215-221 34986694-1 2022 INTRODUCTION: Disorders of serum sodium (SNa) are common in hospitalized patients with COVID-19 and may reflect underlying disease severity. Sodium 33-39 snail family transcriptional repressor 1 Homo sapiens 41-44 34995919-11 2022 Furthermore, canonical transient receptor potential channel 6 (TRPC6) was identified as the mechanism mediating local increase of sodium (Na+) useful to drive NCX1 reverse mode and, therefore, NCX1-mediated Ca2+ refilling. Sodium 130-136 solute carrier family 8 member A1 Rattus norvegicus 159-163 34995919-11 2022 Furthermore, canonical transient receptor potential channel 6 (TRPC6) was identified as the mechanism mediating local increase of sodium (Na+) useful to drive NCX1 reverse mode and, therefore, NCX1-mediated Ca2+ refilling. Sodium 130-136 solute carrier family 8 member A1 Rattus norvegicus 193-197 35024498-3 2022 The voltage-gated sodium channel NaV1.7 is expressed at high levels in peripheral nerve tissues and has been implicated in the development of CIPN. Sodium 18-24 sodium channel, voltage-gated, type IX, alpha Mus musculus 33-39 2690611-6 1989 To maintain glomerular filtration rate and an adequate excretion of sodium, the ischemic nephrons require a higher rate of renin secretion than they are actually receiving, because at low perfusion pressures maximal angiotensin II-induced efferent arteriolar constriction is needed to maintain glomerular filtration rate. Sodium 68-74 angiotensinogen Homo sapiens 216-230 2559720-17 1989 Sodium and GTP inhibited neurotensin binding in a concentration-dependent manner. Sodium 0-6 neurotensin Homo sapiens 25-36 2532691-7 1989 In the hANP only experiment, in both groups hANP resulted in increased urinary volume and both sodium and chloride excretion (P less than 0.05 vs placebo only experiment). Sodium 95-101 natriuretic peptide A Homo sapiens 44-48 2558573-4 1989 CT, on the other hand, did not affect the diastolic blood pressure, but the stimulation of diuresis and of the FE of sodium and chloride was more pronounced with CT than with CGRP (P less than 0.01). Sodium 117-123 calcitonin related polypeptide alpha Homo sapiens 175-179 2697460-0 1989 Effect of dietary sodium intake on the pressor reactivity to angiotensin II in rats with experimental cirrhosis of the liver. Sodium 18-24 angiotensinogen Rattus norvegicus 61-75 2697460-7 1989 Upon injection of angiotensin II, control rats show a dose-dependent increase in mean arterial pressure which is higher in high sodium than in normal sodium rats. Sodium 128-134 angiotensinogen Rattus norvegicus 18-32 2532579-11 1989 Renal vein plasma renin activity increased by 56% with sodium restriction (P less than 0.01), whereas arterial ANP concentrations fell by 39% (P less than 0.05). Sodium 55-61 renin Homo sapiens 18-23 2531762-7 1989 In contrast, TIVCC with similar reductions in CO and MAP but without increases in ANF resulted in decreases in UNaV and RBF and increases in PRA and PA. Exogenous administration of ANF in TIVCC to mimic levels in acute CHF prevented sodium retention, renal vasoconstriction, and activation of renin and aldosterone. Sodium 233-239 natriuretic peptide A Homo sapiens 181-184 2531762-8 1989 These studies demonstrate that endogenous ANF serves as an important physiologic volume regulator in acute CHF to maintain sodium excretion and possibly participate in the suppression of activation of the renin-angiotensin-aldosterone system despite the stimulus of arterial hypotension. Sodium 123-129 natriuretic peptide A Homo sapiens 42-45 2534404-2 1989 Plasma ANF was positively and significantly related to sodium excretion at the distal nephron, indicating that this hormone interacts with a distal renal tubular site to influence the control of sodium excretion in man. Sodium 55-61 natriuretic peptide A Homo sapiens 7-10 2534404-2 1989 Plasma ANF was positively and significantly related to sodium excretion at the distal nephron, indicating that this hormone interacts with a distal renal tubular site to influence the control of sodium excretion in man. Sodium 195-201 natriuretic peptide A Homo sapiens 7-10 2607517-8 1989 The relationships of DBP with body mass index and with the urinary sodium: potassium ratio were also 0.2 mmHg/kg/m2 and 0.8 mmHg/unit steeper (P less than 0.05) in post- than in pre-menopausal subjects. Sodium 67-73 D-box binding PAR bZIP transcription factor Homo sapiens 21-24 2531832-9 1989 These results demonstrate that weight loss while ingesting a controlled low sodium diet is accompanied by changes in ANF that directly correlate with changes in blood pressure and inversely correlate with changes in the renin-aldosterone axis, which ANF is known to inhibit. Sodium 76-82 natriuretic peptide A Homo sapiens 117-120 2531832-9 1989 These results demonstrate that weight loss while ingesting a controlled low sodium diet is accompanied by changes in ANF that directly correlate with changes in blood pressure and inversely correlate with changes in the renin-aldosterone axis, which ANF is known to inhibit. Sodium 76-82 natriuretic peptide A Homo sapiens 250-253 2532366-1 1989 The role of peptides from the N terminus and C terminus of the 126 amino acid atrial natriuretic factor (ANF) prohormone in modulating renal sodium and water handling has not been defined. Sodium 141-147 natriuretic peptide A Homo sapiens 78-103 2532366-1 1989 The role of peptides from the N terminus and C terminus of the 126 amino acid atrial natriuretic factor (ANF) prohormone in modulating renal sodium and water handling has not been defined. Sodium 141-147 natriuretic peptide A Homo sapiens 105-108 2554807-1 1989 Direct dose-dependent effects of angiotensin II on renal tubular sodium reabsorption have been demonstrated. Sodium 65-71 angiotensinogen Rattus norvegicus 33-47 2554807-8 1989 We conclude that angiotensin II infusion is associated with a decrease in the K1/2 of renal cortical Na,K-ATPase activity for sodium. Sodium 126-132 angiotensinogen Rattus norvegicus 17-31 2684484-7 1989 The reasons for the association of insulin resistance and essential hypertension can be sought in at least four general types of mechanisms--sodium retention, sympathetic nervous system overactivity, disturbed membrane ion transport, and altered muscle fiber composition. Sodium 141-147 insulin Homo sapiens 35-42 2533223-0 1989 Impact of acute and chronic sodium loading on atrial natriuretic peptide and renin in man. Sodium 28-34 renin Homo sapiens 77-82 2533223-1 1989 The relationship between the renin-angiotensin system and the atrial natriuretic peptide and its contributions to the control of sodium balance is not clarified. Sodium 129-135 renin Homo sapiens 29-34 2690611-8 1989 This angiotensin II impairs sodium excretion (adaptive hypernatriuresis) from unaffected, adapting nephrons by promoting proximal sodium reabsorption and by inducing afferent constriction. Sodium 28-34 angiotensinogen Homo sapiens 5-19 2690611-8 1989 This angiotensin II impairs sodium excretion (adaptive hypernatriuresis) from unaffected, adapting nephrons by promoting proximal sodium reabsorption and by inducing afferent constriction. Sodium 130-136 angiotensinogen Homo sapiens 5-19 2512459-3 1989 The release of renin is followed by an increase in angiotensin II in the renal interstitium, which is responsible for adjusting the vascular tone of the efferent arterioles and vasa recta and for stimulating proximal tubular reabsorption of sodium. Sodium 241-247 renin Homo sapiens 15-20 2512459-3 1989 The release of renin is followed by an increase in angiotensin II in the renal interstitium, which is responsible for adjusting the vascular tone of the efferent arterioles and vasa recta and for stimulating proximal tubular reabsorption of sodium. Sodium 241-247 angiotensinogen Homo sapiens 51-65 2512459-4 1989 Variations in medullary circulation induced by angiotensin II could alter medullary interstitial pressure and the medullary production of prostaglandins E2 and I2 and, ultimately, could modulate sodium reabsorption in the medullary thick ascending limbs and the collecting ducts. Sodium 195-201 angiotensinogen Homo sapiens 47-61 2533297-8 1989 These results suggest that the balance between aldosterone and ANP may be a useful index in understanding sodium homeostasis in these settings. Sodium 106-112 natriuretic peptide A Homo sapiens 63-66 2530666-10 1989 However, plasma ANF concentration was related to allograft fractional sodium excretion (r = 0.687, p less than 0.001). Sodium 70-76 natriuretic peptide A Homo sapiens 16-19 2558135-0 1989 Antihypertensive contribution of sodium depletion and the sympathetic axis during chronic angiotensin II converting enzyme inhibition. Sodium 33-39 angiotensinogen Homo sapiens 90-104 2530666-12 1989 Circulating plasma ANF may also have a direct effect on allograft sodium excretion. Sodium 66-72 natriuretic peptide A Homo sapiens 19-22 2553328-0 1989 Alterations in cerebrospinal fluid angiotensin II by sodium intake in patients with essential hypertension. Sodium 53-59 angiotensinogen Homo sapiens 35-49 2531299-7 1989 In the 6 patients in whom serum ANP level alone was elevated, a near linear relationship was observed between serum ANP levels and urine sodium excretion (r = 0.851). Sodium 137-143 natriuretic peptide A Homo sapiens 32-35 2531299-7 1989 In the 6 patients in whom serum ANP level alone was elevated, a near linear relationship was observed between serum ANP levels and urine sodium excretion (r = 0.851). Sodium 137-143 natriuretic peptide A Homo sapiens 116-119 2679144-4 1989 Insulin also increased fractional sodium reabsorption and diminished the natriuretic effect of ANG II. Sodium 34-40 insulin Homo sapiens 0-7 2529059-11 1989 Urinary sodium excretion increased significantly (p less than 0.02) by the end of phase 2 under ANF infusion (+38 +/- 15%), whereas it decreased (-10 +/- 6%) under placebo infusion by the end of phase 2. Sodium 8-14 natriuretic peptide A Homo sapiens 96-99 2534066-6 1989 Plasma renin activity suppressed to a lesser extent in the acromegalic group after 4 h. The facts that basal plasma ANF was not raised in acromegalic subjects and did not respond to saline stimulation demonstrate that an abnormality of ANF control may be an important factor in the aetiology of the expanded sodium status of patients with acromegaly and hence may contribute to the hypertension seen in patients with growth hormone excess. Sodium 308-314 natriuretic peptide A Homo sapiens 236-239 2677101-6 1989 Supine plasma renin activity and plasma aldosterone were significantly lower during the high sodium diet. Sodium 93-99 renin Homo sapiens 14-19 2794053-5 1989 A pronounced enrichment of EPO was observed in cysts with sodium concentrations greater than 100 mmol/liter, suggesting an association with proximal tubular malformations. Sodium 58-64 erythropoietin Homo sapiens 27-30 2685117-0 1989 Effect of angiotensin converting enzyme inhibition on cardiovascular regulation during reflex sympathetic activation in sodium-replete patients with essential hypertension. Sodium 120-126 angiotensin I converting enzyme Homo sapiens 10-39 2685117-6 1989 These findings suggest that even in the sodium-replete state, Ang II exerts a facilitatory action on adrenergic function that is physiologically relevant for the regulation of forearm blood flow and the maintenance of blood pressure during the application of gravitational stresses. Sodium 40-46 angiotensinogen Homo sapiens 62-68 2812277-0 1989 Angiotensin II receptor binding in the rat hypothalamus and circumventricular organs during dietary sodium deprivation. Sodium 100-106 angiotensinogen Rattus norvegicus 0-14 2682342-5 1989 These results suggest that reduced salt intake in response to manipulations of the body sodium and renin-angiotensin system in hypophysectomized rats may result from decreased angiotensinogen mRNA levels. Sodium 88-94 angiotensinogen Rattus norvegicus 176-191 2529543-7 1989 These effects were accompanied by significant increases in urinary volume and sodium excretion, two well-established renal responses to ANF peptides. Sodium 78-84 natriuretic peptide A Homo sapiens 136-139 2528914-9 1989 These data indicate that the low dosage of ANP causes natriuresis by reducing sodium absorption in a distal nephron target segment; enalapril impairs this effect, perhaps by enhancing ANP-induced vasoconstriction, which decreases delivery to this target segment. Sodium 78-84 natriuretic peptide A Homo sapiens 43-46 2812277-1 1989 The effect of dietary sodium intake on angiotensin II (Ang II) receptor binding in the rat brain was studied using quantitative in vitro autoradiography. Sodium 22-28 angiotensinogen Rattus norvegicus 39-53 2812277-1 1989 The effect of dietary sodium intake on angiotensin II (Ang II) receptor binding in the rat brain was studied using quantitative in vitro autoradiography. Sodium 22-28 angiotensinogen Rattus norvegicus 55-61 2812277-5 1989 Ang II binding in the area postrema was significantly suppressed in the sodium-deprived rats (60% of control; p less than 0.05). Sodium 72-78 angiotensinogen Rattus norvegicus 0-6 2812277-8 1989 In the hypothalamic paraventricular nucleus, there was a small (9%) but significant (p less than 0.001) increase in Ang II receptor binding in the sodium-deprived group. Sodium 147-153 angiotensinogen Rattus norvegicus 116-122 2812277-10 1989 These results suggest that only a limited subset of brain Ang II receptors respond to sodium deprivation and do so in a region-specific manner. Sodium 86-92 angiotensinogen Rattus norvegicus 58-64 2676669-4 1989 Sodium clearance declined with increasing plasma insulin concentrations (1.3 +/- 0.4, 1.0 +/- 0.3 and 0.5 +/- 0.2 ml.min-1.1.73 m-2, p less than 0.001), while glomerular filtration rate (108 +/- 21, 104 +/- 21 and 108 +/- 20 ml.min-1. Sodium 0-6 insulin Homo sapiens 49-56 2574629-8 1989 In heart failure, cGMP continues to reflect augmented ANF levels, suggesting that in this disease, the lack of an ANF effect on sodium excretion is due to a defect distal to cGMP generation. Sodium 128-134 natriuretic peptide A Homo sapiens 114-117 2527819-2 1989 During ANF infusions, the patients excreted 11.8 +/- 2.0 mmol (mean +/- SEM) sodium more than during the time-matched placebo phase natriuresis (p less than 0.001, mean increase of 53% above placebo values). Sodium 77-83 natriuretic peptide A Homo sapiens 7-10 2547581-0 1989 Sodium-mediated modulation of aldosterone secretion: impact of converting enzyme inhibition on rat glomerulosa cell response to angiotensin-II. Sodium 0-6 angiotensinogen Rattus norvegicus 128-142 2591876-5 1989 Mechanism of carpal tunnel syndrome in acromegaly is that edematous synovial tissues compress the median nerve because oversecretion of growth hormone causes increase of sodium and water retention in the extracellular fluid. Sodium 170-176 growth hormone 1 Homo sapiens 136-150 2530268-8 1989 Angiotensin II, but not norepinephrine or glucose solution administration, was associated with a significant increase in urine volume and sodium excretion. Sodium 138-144 angiotensinogen Rattus norvegicus 0-14 2681604-3 1989 Acute renal failure induced by ACE inhibition may develop without a reduction in systemic blood pressure it is enhanced by prior sodium depletion and is reversible when treatment is withdrawn. Sodium 129-135 angiotensin I converting enzyme Homo sapiens 31-34 2810118-6 1989 In the frog skin epithelium, benzylimidazole (10(-4) M) inhibited the vasopressin-stimulated (100 mU/ml) sodium transport and in the toad bladder it decreased the vasopressin-stimulated (5 mU/ml) hydroosmotic flow. Sodium 105-111 arginine vasopressin Rattus norvegicus 70-81 2668763-3 1989 The variables that best predicted the degree of sodium sensitivity were the fasting plasma insulin level, the plasma aldosterone level while the low-salt diet was being given, the plasma norepinephrine level while the high-salt diet was being given, and the percentage of body weight made up by fat. Sodium 48-54 insulin Homo sapiens 91-98 2548784-3 1989 At the early phase of the disease, plasma ANF was also correlated with the excreted fraction of filtered sodium (FENa) (r = 0.95). Sodium 105-111 natriuretic peptide A Homo sapiens 42-45 2480537-0 1989 Influence of vasopressin level on osmotic pressure and sodium concentration in plasma and cerebrospinal fluid in patients with intracranial lesions. Sodium 55-61 arginine vasopressin Homo sapiens 13-24 2480537-1 1989 To study the influence of the vasopressin level on osmotic pressure and sodium concentration in plasma and cerebrospinal fluid (CSF), plasma and CSF were sampled simultaneously in 27 patients with central nervous system lesions. Sodium 72-78 arginine vasopressin Homo sapiens 30-41 2673301-11 1989 These results suggest that the modulation of the vascular responsiveness to Ang II by prostaglandins is altered by sodium balance and salt sensitivity in EH. Sodium 115-121 angiotensinogen Homo sapiens 76-82 2546751-7 1989 The binding of [125I]alpha IR-3, a monoclonal antibody to the human type I IGF receptor, to monolayers and suspensions of HSF also depends on the sodium ion concentration; it is 5- to 7-fold higher in the absence of sodium chloride. Sodium 146-152 interleukin 6 Homo sapiens 122-125 2546751-11 1989 Sodium ions (and other ions) may induce a conformational change in the receptor and BPs and cause decreased availability of both the IGF-I-binding site and the alpha IR-3 epitope on the receptor and the IGF-binding site on the BP. Sodium 0-6 insulin like growth factor 1 Homo sapiens 133-138 2527200-0 1989 Effect of plasma sodium on aldosterone secretion during angiotensin II stimulation in normal humans. Sodium 17-23 angiotensinogen Homo sapiens 56-70 2527200-11 1989 We conclude that small physiological elevations of plasma sodium concentrations can signal substantial decreases of plasma aldosterone in normal human subjects in situations where plasma angiotensin II is moderately elevated. Sodium 58-64 angiotensinogen Homo sapiens 187-201 2550696-7 1989 Thus, the antiproteinuric effect of the ACE inhibitor lisinopril appears to be dose and time related, and is strongly dependent on dietary sodium restriction, whereas it does not depend on initial proteinuria, BP, or GFR. Sodium 139-145 angiotensin I converting enzyme Homo sapiens 40-43 2730914-0 1989 Effects of sodium removal on calcium mobilization and dense granule secretion induced by thrombin in human platelets. Sodium 11-17 coagulation factor II, thrombin Homo sapiens 89-97 2553806-5 1989 Infusion of synthetic alpha-hANP caused a greater increase in the rate of sodium excretion in patients with Cushing"s syndrome and primary aldosteronism compared with normal volunteers. Sodium 74-80 natriuretic peptide A Homo sapiens 28-32 2528702-1 1989 High affinity, sodium-dependent binding of [3H]mazindol is associated with the noradrenergic transporter while the binding of [3H]imipramine and [3H]paroxetine are associated with the serotonin transporter, e.g. in human platelets. Sodium 15-21 solute carrier family 6 member 4 Homo sapiens 184-205 2534930-5 1989 An increase in 1-minute urine output and 1-minute sodium excretion with the urine significantly correlated with plasma ANP decrease during 90 minutes following furosemide administration. Sodium 50-56 natriuretic peptide A Homo sapiens 119-122 2546667-5 1989 Drug sensitivity correlated with this residual DHO-DH activity; DHO-DH activity was only slightly inhibited by Brequinar Sodium in the most resistant lines, and almost completely in the most sensitive. Sodium 121-127 dihydroorotate dehydrogenase (quinone) Homo sapiens 64-70 2527107-11 1989 The changes in urinary osmolality and sodium excretion both correlated with the changes in plasma ANP levels. Sodium 38-44 natriuretic peptide A Homo sapiens 98-101 2527107-14 1989 Our results suggest a role for ANP-induced (intra)renal haemodynamic changes in ANP-induced natriuresis, possibly through an increase in the filtered load of sodium into a washed-out medullary interstitium. Sodium 158-164 natriuretic peptide A Homo sapiens 31-34 2527107-14 1989 Our results suggest a role for ANP-induced (intra)renal haemodynamic changes in ANP-induced natriuresis, possibly through an increase in the filtered load of sodium into a washed-out medullary interstitium. Sodium 158-164 natriuretic peptide A Homo sapiens 80-83 2767407-4 1989 It is concluded that tilapia are able to acclimate to acid water by successful control--probably via prolactin--of diffusional sodium losses across the integument, in particular the gill surface. Sodium 127-133 prolactin Sus scrofa 101-110 2745911-6 1989 Sodium content ranged from 2 mg to 2,180 mg/tsp and sodium:potassium ratio from 0.07 to 2,460. Sodium 0-6 thrombospondin 1 Homo sapiens 44-47 2549153-0 1989 Effect of sodium intake on phosphoinositides and inositol trisphosphate response to angiotensin II, K+ and ACTH in rat glomerulosa cells. Sodium 10-16 angiotensinogen Rattus norvegicus 84-98 2813560-0 1989 Effects of central and peripheral neuropeptide Y on sodium and water excretion in the rat. Sodium 52-58 neuropeptide Y Rattus norvegicus 34-48 2813560-3 1989 Accordingly, we examined the effects of intracerebroventricular (ICV) or intrarenal administration of NPY on sodium and water excretion in the barbiturate anesthetized rat. Sodium 109-115 neuropeptide Y Rattus norvegicus 102-105 2813560-6 1989 The results showed that the intrarenal infusion of NPY at 1 microgram/kg/min increased sodium and water excretion relative to the saline control group without altering blood pressure or creatinine clearance. Sodium 87-93 neuropeptide Y Rattus norvegicus 51-54 2813560-7 1989 Similarly, ICV administration of NPY at 10 micrograms in a 5 microliters volume increased the excretion of sodium and water without altering blood pressure as compared to the artificial CSF group. Sodium 107-113 neuropeptide Y Rattus norvegicus 33-36 2813560-8 1989 These findings suggest that both central and peripheral NPY may contribute to the regulation of sodium and water excretion in the rat. Sodium 96-102 neuropeptide Y Rattus norvegicus 56-59 2730914-1 1989 Removal of extracellular sodium decreased calcium mobilization from intracellular stores induced by thrombin in aspirin-treated human platelets. Sodium 25-31 coagulation factor II, thrombin Homo sapiens 100-108 2730914-7 1989 These results suggest that the presence of external sodium is required for normal thrombin-induced calcium release from the intracellular stores and hence for dense granule secretion. Sodium 52-58 coagulation factor II, thrombin Homo sapiens 82-90 2525347-5 1989 This marked sensitivity in the responses of both the ANP and the renin-aldosterone system to small increases in sodium intake clearly points to their importance in the renal adaptations to alterations in dietary sodium intake. Sodium 112-118 renin Homo sapiens 65-70 2525347-5 1989 This marked sensitivity in the responses of both the ANP and the renin-aldosterone system to small increases in sodium intake clearly points to their importance in the renal adaptations to alterations in dietary sodium intake. Sodium 212-218 renin Homo sapiens 65-70 2757896-2 1989 The renin-angiotensin-aldosterone-system is important for the maintenance of sodium balance in man. Sodium 77-83 renin Homo sapiens 4-9 2736884-6 1989 Compared with placebo, ANG II caused a significant fall in urinary sodium excretion (113 +/- 13 to 82 +/- 10 mumol/min). Sodium 67-73 angiotensinogen Homo sapiens 23-29 2736884-12 1989 ANG II also reduced fractional distal delivery [(sodium clearance plus free water clearance) divided by creatinine clearance], another measure of proximal tubular outflow. Sodium 49-55 angiotensinogen Homo sapiens 0-6 2553424-1 1989 Atrial natriuretic peptide (ANP) increases renal sodium and water excretion in several species including man. Sodium 49-55 natriuretic peptide A Homo sapiens 0-26 2553424-1 1989 Atrial natriuretic peptide (ANP) increases renal sodium and water excretion in several species including man. Sodium 49-55 natriuretic peptide A Homo sapiens 28-31 2670663-2 1989 Insulin applied to the basolateral side of the epithelium stimulated the sodium transport as shown by both increased short-circuit current, Isc, (P less than 0.02) and transepithelial potential difference, Voc, (P less than 0.002). Sodium 73-79 insulin Homo sapiens 0-7 2757896-4 1989 We have investigated the possible interaction of physiological doses of angiotensin II and noradrenaline on sodium excretion in man. Sodium 108-114 angiotensinogen Homo sapiens 72-86 2757896-12 1989 Angiotensin II when infused with placebo caused a 37% fall in absolute sodium excretion and a 32% fall when infused with noradrenaline (no significant difference between the 2 days). Sodium 71-77 angiotensinogen Homo sapiens 0-14 2527992-0 1989 Relationship between basal and sodium-stimulated plasma atrial natriuretic factor, age, sex and blood pressure in normal man. Sodium 31-37 natriuretic peptide A Homo sapiens 56-81 2670663-4 1989 The driving force of sodium ions, ENa, increased after insulin (P less than 0.005). Sodium 21-27 insulin Homo sapiens 55-62 2670663-6 1989 The effects of insulin were compared with those of a vasopressin analog (dDAVP), known to stimulate transepithelial sodium transport by increasing the permeability of the apical cell membrane for sodium ions. Sodium 116-122 arginine vasopressin Homo sapiens 53-64 2732947-1 1989 Phospholipase A2 (PLA2) treatment has been shown previously to stimulate the sodium-dependent high-affinity choline uptake system as assessed by both the specific binding of [3H]hemicholinium-3 ([ 3H]HCh-3) and the uptake of [3H]choline. Sodium 77-83 phospholipase A2 group IB Homo sapiens 0-16 2732947-1 1989 Phospholipase A2 (PLA2) treatment has been shown previously to stimulate the sodium-dependent high-affinity choline uptake system as assessed by both the specific binding of [3H]hemicholinium-3 ([ 3H]HCh-3) and the uptake of [3H]choline. Sodium 77-83 phospholipase A2 group IB Homo sapiens 18-22 2732947-11 1989 These results support the hypothesis that PLA2 might be involved in the regulation of the sodium-dependent high-affinity choline uptake. Sodium 90-96 phospholipase A2 group IB Homo sapiens 42-46 2666829-10 1989 The large variety of functions of PRL, in particular the regulation of the transport of sodium and chloride across epithelial membranes, and the regulation of mucus production, can be matched to the major disease symptomatology. Sodium 88-94 prolactin Homo sapiens 34-37 2532741-4 1989 ANF infusion increased sodium excretion rate by a mean of 68% compared with a fall of 40% in a placebo group, and significant increases in urinary albumin excretion occurred during the peptide infusion. Sodium 23-29 natriuretic peptide A Homo sapiens 0-3 2673301-6 1989 The mean blood pressure (MBP) response to Ang II was significantly higher on high sodium intake than on low sodium intake in NSS and NT, but not in SS. Sodium 82-88 angiotensinogen Homo sapiens 42-48 2673301-6 1989 The mean blood pressure (MBP) response to Ang II was significantly higher on high sodium intake than on low sodium intake in NSS and NT, but not in SS. Sodium 108-114 angiotensinogen Homo sapiens 42-48 2673301-7 1989 IND significantly increased the MBP response to Ang II on low sodium intake in NSS and NT, but not in SS. Sodium 62-68 angiotensinogen Homo sapiens 48-54 2673301-8 1989 IND significantly increased the TPR response to Ang II on low sodium intake, remarkably in NSS and NT compared with SS. Sodium 62-68 angiotensinogen Homo sapiens 48-54 2673301-9 1989 Salt sensitivity (% decrease in MBP from high to low sodium intake) highly correlated with the increase in the TPR response to Ang II by IND on low sodium intake (r = -0.90). Sodium 53-59 angiotensinogen Homo sapiens 127-133 2673301-9 1989 Salt sensitivity (% decrease in MBP from high to low sodium intake) highly correlated with the increase in the TPR response to Ang II by IND on low sodium intake (r = -0.90). Sodium 148-154 angiotensinogen Homo sapiens 127-133 2673301-10 1989 After captopril administration, IND still increased the MBP and TPR response to Ang II on low sodium intake. Sodium 94-100 angiotensinogen Homo sapiens 80-86 2532741-5 1989 Thus, the high levels of plasma ANF found in CRF may have a role in the maintenance of sodium balance. Sodium 87-93 natriuretic peptide A Homo sapiens 32-35 2667598-0 1989 Pharmacological investigations of a new renin inhibitor in normal sodium-unrestricted volunteers. Sodium 66-72 renin Homo sapiens 40-45 2660287-7 1989 We speculate that normotensive subjects with low plasma renin activity present significant changes in the relationship between the renin-angiotensin-aldosterone system and sodium and calcium levels, and that this group is at risk for hypertension. Sodium 172-178 renin Homo sapiens 56-61 2660287-7 1989 We speculate that normotensive subjects with low plasma renin activity present significant changes in the relationship between the renin-angiotensin-aldosterone system and sodium and calcium levels, and that this group is at risk for hypertension. Sodium 172-178 renin Homo sapiens 131-136 2720433-2 1989 injections of angiotensin II (ANG II, 10 pg, 100 pg and 10 ng) on renal sodium excretion were investigated in conscious rats instrumented with a chronic urethral catheter. Sodium 72-78 angiotensinogen Rattus norvegicus 14-28 2720433-3 1989 ANG II increased renal sodium excretion dose-dependently with a threshold i.c.v. Sodium 23-29 angiotensinogen Rattus norvegicus 0-6 2498609-7 1989 Sodium excretory rate decreased during insulin infusion in lean subjects by 2.2 mEq/h but increased in obese by 5.3 mEq/h (difference in response between groups, P = .024). Sodium 0-6 insulin Homo sapiens 39-46 2670657-7 1989 Sodium clearance decreased (from 1.4 +/- 0.6 to 1.1 +/- 0.5 ml/min 1.73 sqm with perindopril, p less than 0.05, and from 0.97 +/- 0.44 to 0.88 +/- 0.51 with captopril, n.s.). Sodium 0-6 CD59 molecule (CD59 blood group) Homo sapiens 63-68 2472523-4 1989 During the control infusion of ANP, urinary sodium excretion rose from 4.5 +/- 0.8 to 11.2 +/- 2.2 mEq/min and urine volume from 32 +/- 14 to 115 +/- 34 ml/30 min. Sodium 44-50 natriuretic peptide A Homo sapiens 31-34 2472523-5 1989 This increment in urinary volume and sodium output during ANP infusion was almost completely reduced by ACE inhibition. Sodium 37-43 natriuretic peptide A Homo sapiens 58-61 2532253-15 1989 It is proposed that disruption of glomerulo-tubular balance occurred in these experiments from inhibition of endogenous angiotensin II-stimulated proximal sodium reabsorption by ANF. Sodium 155-161 angiotensinogen Rattus norvegicus 120-134 2540021-6 1989 Internally applied bradykinin produces a frequency-dependent block of the sodium current. Sodium 74-80 kininogen 1 Homo sapiens 19-29 2495728-3 1989 We raised a series of monoclonal antibodies (MAb) to these proteins and, using light and electron immunohistochemistry, localized the higher Mr glycoproteins (GP70) to the apical plasma membrane and subapical granules of the sodium-transporting cell of the TUB epithelium, the granular cell. Sodium 225-231 embigin Homo sapiens 159-163 2705532-2 1989 Previous studies in the rat have suggested that NPY influences renal sodium reabsorption and renin release. Sodium 69-75 neuropeptide Y Rattus norvegicus 48-51 2673748-0 1989 Effects of sodium depletion and orthostasis on plasma and urinary vasopressin in normal subjects. Sodium 11-17 arginine vasopressin Homo sapiens 66-77 2655479-4 1989 The depressor response to neither agent changed over the next 40 h. The pressor response to angiotensin II was blunted significantly by 8 h and also did not change over the next 40 h. The findings indicate that the rapid tempo of sodium homeostasis in the rat is matched by an equally rapid tempo of activation of the renin-angiotensin system, although the factors responsible for aldosterone release are probably more complex. Sodium 230-236 angiotensinogen Rattus norvegicus 92-106 2490815-8 1989 The second, sodium-volume-related vasoconstriction, is marked by a reciprocally subnormal renin level and involves abnormal sodium retention and calcium transport. Sodium 12-18 renin Homo sapiens 90-95 2546843-2 1989 At 22 degrees C, a 45 min incubation of the total tissue with 10(-6) M insulin significantly decreased both the initial rate and the peak of sodium-dependent phosphate uptake by the corresponding brush border membranes. Sodium 141-147 insulin Homo sapiens 71-78 2663528-2 1989 Endothelin, 1 nmol/kg body weight given as a bolus, induced a transient decrease in glomerular filtration rate (72%) and in renal plasma flow (76%) as well as in sodium excretion, accompanied by a sustained increase in renal vascular resistance. Sodium 162-168 endothelin 1 Rattus norvegicus 0-13 2565086-8 1989 Thus, in patients with congestive heart failure, low dose ANF boluses may produce an increase in urine flow rate and sodium excretion rate that is independent of renal plasma flow or glomerular filtration rate. Sodium 117-123 natriuretic peptide A Homo sapiens 58-61 2538313-7 1989 This increase in pHi induced by AII was dependent upon the extracellular sodium concentration (ED50 values = 2.8 mM) and was blunted in sodium-free medium. Sodium 73-79 glucose-6-phosphate isomerase Bos taurus 17-20 2538313-7 1989 This increase in pHi induced by AII was dependent upon the extracellular sodium concentration (ED50 values = 2.8 mM) and was blunted in sodium-free medium. Sodium 136-142 glucose-6-phosphate isomerase Bos taurus 17-20 2673748-1 1989 We investigated the effects of sodium depletion and orthostasis on the plasma concentration and urinary excretion of vasopressin (AVP) in eight normal female subjects. Sodium 31-37 arginine vasopressin Homo sapiens 117-128 2673748-4 1989 A significant (p less than 0.05) increase in plasma AVP and a significant (p less than 0.05) decrease in 24-h urinary excretion of AVP were observed during sodium depletion. Sodium 156-162 arginine vasopressin Homo sapiens 52-55 2673748-4 1989 A significant (p less than 0.05) increase in plasma AVP and a significant (p less than 0.05) decrease in 24-h urinary excretion of AVP were observed during sodium depletion. Sodium 156-162 arginine vasopressin Homo sapiens 131-134 2673748-5 1989 One-hour ambulation significantly increased plasma AVP in both control and sodium depleted phases (p less than 0.01). Sodium 75-81 arginine vasopressin Homo sapiens 51-54 2673748-7 1989 The present results suggest that AVP may play an important role in the maintenance of blood pressure during orthostasis in the sodium depleted state. Sodium 127-133 arginine vasopressin Homo sapiens 33-36 2567677-2 1989 A 7-day infusion of dopamine or somatostatin, at a rate which was found to exert a maximum inhibition of aldosterone secretion in 12 h, only partially reversed the effects of sodium deprivation. Sodium 175-181 somatostatin Rattus norvegicus 32-44 2527302-2 1989 The change from a low (25 mmol/day) to a high (241 mmol/day) sodium intake was associated with a 2.5 fold increase in circulating immunoreactive ANF. Sodium 61-67 natriuretic peptide A Homo sapiens 145-148 2527302-3 1989 On both sodium diets, an infusion of synthetic ANF (99-126) given at two different rates caused a progressive decrease of arterial pressure. Sodium 8-14 natriuretic peptide A Homo sapiens 47-50 2527302-7 1989 On a low sodium intake ANF caused a progressive fall of glomerular filtration rates and effective renal plasma flow. Sodium 9-15 natriuretic peptide A Homo sapiens 23-26 2527302-9 1989 In patients with uncomplicated diabetes mellitus, circulating ANF responds physiologically to variations in sodium intake. Sodium 108-114 natriuretic peptide A Homo sapiens 62-65 2527302-10 1989 A low sodium diet could predispose to arterial hypotension and renal functional impairment during infusion of ANF (99-126). Sodium 6-12 natriuretic peptide A Homo sapiens 110-113 2545963-3 1989 A small dose of ANF (0.03 micrograms/kg/min) increased sodium clearance (CNa) significantly without any appreciable changes in NcGMP, creatinine clearance (Ccr) or renal blood flow (RBF). Sodium 55-61 natriuretic peptide A Homo sapiens 16-19 2542401-2 1989 Plasma ANF and cGMP concentrations were less on the low than on the high sodium intake. Sodium 73-79 natriuretic peptide A Homo sapiens 7-10 2542401-3 1989 Values for ANF on the medium sodium intake were intermediate. Sodium 29-35 natriuretic peptide A Homo sapiens 11-14 2554261-4 1989 The above results suggest that a decrease in sympathetic system activity and intracellular sodium concentration may play a role in the hypotensive action of enalapril maleate related to the inhibition of angiotensin II formation. Sodium 91-97 angiotensinogen Homo sapiens 204-218 2525071-2 1989 The comparable rise of plasma ANF concentration during infusion of saline was associated with a significantly higher renal excretion of urine and sodium in EH, as compared with controls. Sodium 146-152 natriuretic peptide A Homo sapiens 30-33 2522705-9 1989 Thus, patients with primary hyperparathyroidism have elevated plasma levels of angiotensin II and arginine vasopressin which may be compensatory phenomena counteracting volume depletion owing to a decreased renal concentrating ability induced by hypercalcemia, and owing to PTH-induced inhibition of renal sodium reabsorption. Sodium 306-312 angiotensinogen Homo sapiens 79-93 2522705-9 1989 Thus, patients with primary hyperparathyroidism have elevated plasma levels of angiotensin II and arginine vasopressin which may be compensatory phenomena counteracting volume depletion owing to a decreased renal concentrating ability induced by hypercalcemia, and owing to PTH-induced inhibition of renal sodium reabsorption. Sodium 306-312 arginine vasopressin Homo sapiens 107-118 2522287-2 1989 Increasing doses of vasopressin potentiated AP-induced natriuresis in a dose-dependent manner, e.g., sodium excretion during AP administration (290 ng/min) was 0.66 +/- 0.16, 2.02 +/- 0.68, 5.21 +/- 1.38 and 7.08 +/- 1.96 mu eq/min during infusion of 0.00, 0.78, 1.56, and 3.12 ng.kg-1.min-1 of vasopressin, respectively. Sodium 101-107 arginine vasopressin Rattus norvegicus 20-31 2645916-5 1989 Peak serum insulin levels after glucose correlated inversely with the decline in sodium excretion (r = .67, P less than .10). Sodium 81-87 insulin Homo sapiens 11-18 2645916-8 1989 Insulin may modulate renal sodium metabolism directly, or through a yet unknown mechanism. Sodium 27-33 insulin Homo sapiens 0-7 2645917-0 1989 Blood pressure and serum calcium responses to altered sodium intake in high renin hypertension. Sodium 54-60 renin Homo sapiens 76-81 2645917-1 1989 Subjects with high renin hypertension tend to be sodium-resistant showing paradoxical blood pressure responses to alterations in sodium intake. Sodium 49-55 renin Homo sapiens 19-24 2645917-1 1989 Subjects with high renin hypertension tend to be sodium-resistant showing paradoxical blood pressure responses to alterations in sodium intake. Sodium 129-135 renin Homo sapiens 19-24 2645917-6 1989 The blood pressure response to increased sodium intake in high renin hypertension would appear to be divergent and related not only to the suppression of plasma renin activity, but also to changes in circulating calcium. Sodium 41-47 renin Homo sapiens 63-68 2645917-6 1989 The blood pressure response to increased sodium intake in high renin hypertension would appear to be divergent and related not only to the suppression of plasma renin activity, but also to changes in circulating calcium. Sodium 41-47 renin Homo sapiens 161-166 2646952-0 1989 Altered sodium regulation of renal angiotensinogen mRNA in the spontaneously hypertensive rat. Sodium 8-14 angiotensinogen Rattus norvegicus 35-50 2646952-5 1989 Mild sodium depletion stimulated angiotensinogen mRNA in WKY kidneys by almost 50% compared with normal salt diet (P less than 0.01). Sodium 5-11 angiotensinogen Rattus norvegicus 33-48 2646952-9 1989 Thus the SHR exhibits an alteration in the sodium regulation of intrarenal angiotensinogen mRNA expression. Sodium 43-49 angiotensinogen Rattus norvegicus 75-90 2923250-4 1989 Plasma sodium was lower during the hyperglycemic study, but elevation in plasma sodium concentration by infusion of saline caused progressive linear increases in both thirst and plasma vasopressin concentrations in both studies. Sodium 80-86 arginine vasopressin Homo sapiens 185-196 2923250-5 1989 Linear regression analysis defined lowered plasma sodium thresholds for both thirst appreciation and vasopressin release during the hyperglycemic study, although the sensitivity of the osmoreceptors remained unchanged. Sodium 50-56 arginine vasopressin Homo sapiens 101-112 2923250-8 1989 These results show that insulin-dependent diabetic patients osmoregulate appropriately when moderately hyperglycemic but that the threshold plasma sodium for vasopressin secretion and thirst appreciation is lowered by an unknown mechanism. Sodium 147-153 arginine vasopressin Homo sapiens 158-169 2526071-2 1989 During chronic sodium loading, which increased mean body weight by 1.5 kg and markedly reduced plasma renin and aldosterone levels, plasma IR-ANP increased from 21 +/- 3 to 36 +/- 7 pmol/l (P less than 0.02). Sodium 15-21 renin Homo sapiens 102-107 2646216-0 1989 Renin regulation in type II diabetes mellitus: influence of dietary sodium. Sodium 68-74 renin Homo sapiens 0-5 2646216-10 1989 Inactive renin levels changed in a similar direction and magnitude as PRA in response to sodium intake and posture in the three study groups. Sodium 89-95 renin Homo sapiens 9-14 2535228-6 1989 Urine sodium excretion was positively correlated with plasma hANP in patients without ascites, but not in patients with ascites. Sodium 6-12 natriuretic peptide A Homo sapiens 61-65 2708819-2 1989 The sodium chloride sensitivity was independently correlated with the change in erythrocyte sodium concentration (r = 0.47) and with the change in plasma renin activity (r = 0.29); but it was not related to basal blood pressure, the change in plasma volume of the change in plasma norepinephrine concentration. Sodium 4-10 renin Homo sapiens 154-159 2527458-6 1989 The plasma hANP correlated significantly with the fractional excretion of sodium (p less than 0.05) and the 24-hour urinary excretion of sodium (p less than 0.01) in normotensives. Sodium 74-80 natriuretic peptide A Homo sapiens 11-15 2527458-6 1989 The plasma hANP correlated significantly with the fractional excretion of sodium (p less than 0.05) and the 24-hour urinary excretion of sodium (p less than 0.01) in normotensives. Sodium 137-143 natriuretic peptide A Homo sapiens 11-15 2527458-9 1989 In regard to the effects of hANP on renal function, hANP may contribute to the regulation of sodium handling in normotensive adolescents, whereas other regulatory mechanisms need to be considered in the case of hypertensives. Sodium 93-99 natriuretic peptide A Homo sapiens 52-56 2784056-5 1989 Also acute renal hCGRP induced effects were observed, as a significant increase in urinary volume and in the urinary calcium, sodium, potassium, and chloride excretion. Sodium 126-132 calcitonin related polypeptide alpha Homo sapiens 17-22 2537029-1 1989 Activators of protein kinase C (PKC) inhibit sodium transport in proximal tubules (PT) (M. Baum and S. R. Hays. Sodium 45-51 proline rich transmembrane protein 2 Homo sapiens 14-30 2537029-1 1989 Activators of protein kinase C (PKC) inhibit sodium transport in proximal tubules (PT) (M. Baum and S. R. Hays. Sodium 45-51 proline rich transmembrane protein 2 Homo sapiens 32-35 2920003-1 1989 In neurosurgical patients with hyponatraemia (plasma sodium less than 130 mmol/l) and natriuresis, increased antidiuretic hormone (ADH) secretion may be appropriate rather than inappropriate. Sodium 53-59 arginine vasopressin Homo sapiens 109-129 2923672-7 1989 Plasma concentrations of angiotensin II and aldosterone, which are markedly elevated by each episode of sodium depletion, return to basal levels between and after depletions, and are not the cause of the chronically increased need-free salt intake of the multi-depleted rat. Sodium 104-110 angiotensinogen Rattus norvegicus 25-39 2523767-8 1989 ANP infusion alone caused increases in the urine volume (from 96 +/- 23 to 229 +/- 44 mL/h, P less than 0.05) and urinary sodium excretion (from 11.5 +/- 1.6 to 20.9 +/- 4.2 mEq/h, P less than 0.05). Sodium 122-128 natriuretic peptide A Homo sapiens 0-3 2523767-13 1989 The antinatriuretic effects of exogenous AII were reversed by superimposed ANP infusion (urinary sodium excretion: from 4.8 +/- 1.0 to 24.3 +/- 5.2 mEq/h, P less than 0.01). Sodium 97-103 angiotensinogen Homo sapiens 41-44 2523767-13 1989 The antinatriuretic effects of exogenous AII were reversed by superimposed ANP infusion (urinary sodium excretion: from 4.8 +/- 1.0 to 24.3 +/- 5.2 mEq/h, P less than 0.01). Sodium 97-103 natriuretic peptide A Homo sapiens 75-78 2523767-15 1989 In addition the increased tubular sodium reabsorption induced by AII was inhibited by concomitant ANP infusion (fractional proximal tubular sodium reabsorption: from 90.7 +/- 3.5 to 80.3 +/- 16.6%, P less than 0.05, fractional post-proximal tubular sodium reabsorption: from 91.5 +/- 9.8 to 87.6 +/- 8.8%, P less than 0.05). Sodium 34-40 angiotensinogen Homo sapiens 65-68 2523767-15 1989 In addition the increased tubular sodium reabsorption induced by AII was inhibited by concomitant ANP infusion (fractional proximal tubular sodium reabsorption: from 90.7 +/- 3.5 to 80.3 +/- 16.6%, P less than 0.05, fractional post-proximal tubular sodium reabsorption: from 91.5 +/- 9.8 to 87.6 +/- 8.8%, P less than 0.05). Sodium 34-40 natriuretic peptide A Homo sapiens 98-101 2523767-15 1989 In addition the increased tubular sodium reabsorption induced by AII was inhibited by concomitant ANP infusion (fractional proximal tubular sodium reabsorption: from 90.7 +/- 3.5 to 80.3 +/- 16.6%, P less than 0.05, fractional post-proximal tubular sodium reabsorption: from 91.5 +/- 9.8 to 87.6 +/- 8.8%, P less than 0.05). Sodium 140-146 angiotensinogen Homo sapiens 65-68 2523767-15 1989 In addition the increased tubular sodium reabsorption induced by AII was inhibited by concomitant ANP infusion (fractional proximal tubular sodium reabsorption: from 90.7 +/- 3.5 to 80.3 +/- 16.6%, P less than 0.05, fractional post-proximal tubular sodium reabsorption: from 91.5 +/- 9.8 to 87.6 +/- 8.8%, P less than 0.05). Sodium 140-146 natriuretic peptide A Homo sapiens 98-101 2523767-15 1989 In addition the increased tubular sodium reabsorption induced by AII was inhibited by concomitant ANP infusion (fractional proximal tubular sodium reabsorption: from 90.7 +/- 3.5 to 80.3 +/- 16.6%, P less than 0.05, fractional post-proximal tubular sodium reabsorption: from 91.5 +/- 9.8 to 87.6 +/- 8.8%, P less than 0.05). Sodium 140-146 angiotensinogen Homo sapiens 65-68 2523767-15 1989 In addition the increased tubular sodium reabsorption induced by AII was inhibited by concomitant ANP infusion (fractional proximal tubular sodium reabsorption: from 90.7 +/- 3.5 to 80.3 +/- 16.6%, P less than 0.05, fractional post-proximal tubular sodium reabsorption: from 91.5 +/- 9.8 to 87.6 +/- 8.8%, P less than 0.05). Sodium 140-146 natriuretic peptide A Homo sapiens 98-101 2643635-3 1989 Stimulation of renin secretion with prolonged dietary sodium restriction or amiloride resulted in marked increases in the plasma levels of prorenin, active renin, and plasma renin activity (PRA); suppression of renin secretion with indomethacin resulted in parallel decreases in prorenin, active renin, and PRA. Sodium 54-60 renin Homo sapiens 15-20 2643635-3 1989 Stimulation of renin secretion with prolonged dietary sodium restriction or amiloride resulted in marked increases in the plasma levels of prorenin, active renin, and plasma renin activity (PRA); suppression of renin secretion with indomethacin resulted in parallel decreases in prorenin, active renin, and PRA. Sodium 54-60 renin Homo sapiens 142-147 2643635-3 1989 Stimulation of renin secretion with prolonged dietary sodium restriction or amiloride resulted in marked increases in the plasma levels of prorenin, active renin, and plasma renin activity (PRA); suppression of renin secretion with indomethacin resulted in parallel decreases in prorenin, active renin, and PRA. Sodium 54-60 renin Homo sapiens 142-147 2643635-3 1989 Stimulation of renin secretion with prolonged dietary sodium restriction or amiloride resulted in marked increases in the plasma levels of prorenin, active renin, and plasma renin activity (PRA); suppression of renin secretion with indomethacin resulted in parallel decreases in prorenin, active renin, and PRA. Sodium 54-60 renin Homo sapiens 142-147 2643635-3 1989 Stimulation of renin secretion with prolonged dietary sodium restriction or amiloride resulted in marked increases in the plasma levels of prorenin, active renin, and plasma renin activity (PRA); suppression of renin secretion with indomethacin resulted in parallel decreases in prorenin, active renin, and PRA. Sodium 54-60 renin Homo sapiens 142-147 2566711-2 1989 Adequate secretion of vasopressin and aldosterone in response to the changes in sodium concentration and plasma osmolality point to the absence of significant functional disorders of the corresponding glands. Sodium 80-86 arginine vasopressin Homo sapiens 22-33 2654438-4 1989 Percent increases in mean blood pressure and intracellular sodium concentration in erythrocytes and in lymphocytes after salt loading were greater in low renin hypertensive patients than in normal renin hypertensives. Sodium 59-65 renin Homo sapiens 154-159 2654438-4 1989 Percent increases in mean blood pressure and intracellular sodium concentration in erythrocytes and in lymphocytes after salt loading were greater in low renin hypertensive patients than in normal renin hypertensives. Sodium 59-65 renin Homo sapiens 197-202 2576635-2 1989 Six NHS, acting in CHF, have presently been identified: three of them induce vasoconstriction and sodium retention (sympathetic nervous systems, renin-angiotensin-aldosterone system and arginine-vasopressine system); the remaining three offset or balance the former ones, acting, therefore as "counterregulators" (prostaglandins--PGE2 and PGI2--, dopaminergic system and atrial natriuretic factor). Sodium 98-104 renin Homo sapiens 145-150 2521270-2 1989 It has been speculated that ANF is a counterregulatory hormone that influences regional blood flow and sodium balance in human patients by either direct vasorelaxation or by inhibiting the release of other vasoconstrictor neurohormones. Sodium 103-109 natriuretic peptide A Homo sapiens 28-31 2678894-3 1989 The variables threshold pressure and slope of the "renal baroreceptor"--mechanism of renin release serve different physiological functions: changes in slope (sensitivity) counteract short term changes in sodium balance whereas threshold pressure ensures a minimal systemic blood pressure associated with normal glomerular filtration. Sodium 204-210 renin Homo sapiens 85-90 2558506-8 1989 These findings suggested that 1) NEP may play a major role in the catabolism of renal KIN in human, 2) NEP is accelerated in PA, 3) unknown K-ase, different from K-ase I, II or NEP, may exist in PA, and 4) accelerated renal K-ase activity may play some role on the disorder of renal water-sodium metabolism and high blood pressure in PA. Sodium 289-295 membrane metalloendopeptidase Homo sapiens 33-36 2524162-5 1989 In normal hydrated subjects undergoing WI, the increases in ANP correlate with the magnitude of the natriuresis, suggesting that ANP constitutes an important determinant of renal sodium handling in humans. Sodium 179-185 natriuretic peptide A Homo sapiens 60-63 2524162-5 1989 In normal hydrated subjects undergoing WI, the increases in ANP correlate with the magnitude of the natriuresis, suggesting that ANP constitutes an important determinant of renal sodium handling in humans. Sodium 179-185 natriuretic peptide A Homo sapiens 129-132 2525878-0 1989 Relationship between plasma ANF responsiveness and renal sodium handling in cirrhotic humans. Sodium 57-63 natriuretic peptide A Homo sapiens 28-31 2643968-8 1989 In contrast, plasma renin activity was greater in sickle cell patients at all levels of sodium intake in both supine and upright positions. Sodium 88-94 renin Homo sapiens 20-25 2524978-7 1989 Our results indicate that ANP/CDD may play a role in the regulation of sodium secretion in the salt gland of aquatic birds. Sodium 71-77 natriuretic peptide A Homo sapiens 26-29 2547039-2 1989 After acute intravenous administration to normotensive sodium-depleted marmosets, renin inhibitors of different structural types induced a maximum hypotensive response of a magnitude similar to that induced after angiotensin converting enzyme (ACE) inhibition. Sodium 55-61 renin Homo sapiens 82-87 2524978-7 1989 Our results indicate that ANP/CDD may play a role in the regulation of sodium secretion in the salt gland of aquatic birds. Sodium 71-77 natriuretic peptide A Homo sapiens 30-33 2912378-5 1989 Dissociation constants obtained for apo-alpha-lactalbumin were about 80 microM for ANS and 4.7 microM for bis-ANS in the absence of sodium ion. Sodium 132-138 lactalbumin alpha Homo sapiens 40-57 2552973-3 1989 The patient showed persistent hyponatremia accompanied with continuous loss of sodium in the urine, which resulted from inappropriate secretion of antidiuretic hormone (ADH). Sodium 79-85 arginine vasopressin Homo sapiens 147-167 2699788-0 1989 [Effect of sodium depletion on the renin-angiotensin-aldosterone system and prostaglandins in patients with insulin-dependent diabetes mellitus]. Sodium 11-17 renin Homo sapiens 35-40 2655608-2 1989 Angiotensin II (AII) acts as a potent pressor agent directly, by virtue of its vasoconstrictor activity and indirectly, by the volume expansion resulting from stimulation of aldosterone release from the adrenal cortex, leading to sodium and water retention. Sodium 230-236 angiotensinogen Homo sapiens 0-14 2655608-2 1989 Angiotensin II (AII) acts as a potent pressor agent directly, by virtue of its vasoconstrictor activity and indirectly, by the volume expansion resulting from stimulation of aldosterone release from the adrenal cortex, leading to sodium and water retention. Sodium 230-236 angiotensinogen Homo sapiens 16-19 2552973-3 1989 The patient showed persistent hyponatremia accompanied with continuous loss of sodium in the urine, which resulted from inappropriate secretion of antidiuretic hormone (ADH). Sodium 79-85 arginine vasopressin Homo sapiens 169-172 2523227-4 1989 ANP increased sodium excretion and urine flow rate but did not alter blood pressure or plasma renin activity. Sodium 14-20 natriuretic peptide A Homo sapiens 0-3 2478241-4 1989 Our findings suggest that monensin uncouples the vasopressin-receptor-G protein-adenylate cyclase sequence at some early step, by a mechanism that remains unknown, but that may directly or indirectly involve intracellular sodium. Sodium 222-228 arginine vasopressin Homo sapiens 49-60 2558792-3 1989 In patients, baseline urine volume and sodium output were similar, however, rise in urine volume and urinary sodium was greatly reduced during the infusion of hANP. Sodium 109-115 natriuretic peptide A Homo sapiens 159-163 2529065-4 1989 Only in post-partum women was ANF significantly directly related to sodium excretion. Sodium 68-74 natriuretic peptide A Homo sapiens 30-33 2558819-5 1989 The plasma AII of rats fed a sodium deficient diet was 300.0 +/- 100.6 pg/ml, while that of rats given oral Enalapril, an angiotensin converting enzyme (ACE) inhibitor, for 1 week was 35.7 +/- 28.0 pg/ml. Sodium 29-35 angiotensinogen Rattus norvegicus 11-14 2533110-3 1989 Thus it can be postulated that insulin therapy resulting in circulating hyperinsulinemia can lead to sodium retention and in turn to hypertension in insulin dependent diabetes. Sodium 101-107 insulin Homo sapiens 31-38 2533110-5 1989 The aim of the present study was to investigate the relationship between insulin and ANP in modulating sodium metabolism in seven insulin dependent diabetic patients in comparison with eight normal control subjects at baseline and during a saline infusion (2 mmol/kg/90 min) at euglycemic blood levels. Sodium 103-109 insulin Homo sapiens 73-80 2693146-4 1989 Insulin may stimulate sodium reabsorption in man through an effect on the distal nephron segment. Sodium 22-28 insulin Homo sapiens 0-7 2693148-2 1989 Possible reasons for this phenomenon include the presence of the insulin resistance/hyperinsulinaemia syndrome in EH, leading to sodium retention, stimulation of the sympathetic nervous system and impaired glucose tolerance. Sodium 129-135 insulin Homo sapiens 65-72 2524388-6 1989 It is concluded that with those doses of ANF the changes in renal haemodynamics and sodium handling were essentially similar after bolus injections and a constant infusion. Sodium 84-90 natriuretic peptide A Homo sapiens 41-44 2663759-4 1989 Transplanted kidneys show a preserved reaction pattern of renin secretion to sodium deprivation and upright position. Sodium 77-83 renin Homo sapiens 58-63 2558792-6 1989 In the controls, angiotensin I-converting-enzyme (ACE) inhibition by enalapril significantly reduced the urinary output of sodium and water after ANP infusion. Sodium 123-129 angiotensin I converting enzyme Homo sapiens 17-48 2558792-6 1989 In the controls, angiotensin I-converting-enzyme (ACE) inhibition by enalapril significantly reduced the urinary output of sodium and water after ANP infusion. Sodium 123-129 angiotensin I converting enzyme Homo sapiens 50-53 2483440-3 1989 Dopamine, which has no significant effects on Ang II-induced aldosterone secretion in sodium-replete subjects, inhibits the hormonal response to Ang II infusion in sodium-depleted normal subjects, suggesting that the sodium balance state may be an important factor in the dopaminergic mechanisms controlling aldosterone secretion. Sodium 164-170 angiotensinogen Rattus norvegicus 145-151 2541089-3 1989 Only the high-affinity, sodium-dependent binding was found to be associated with the serotonin transporter complex. Sodium 24-30 solute carrier family 6 member 4 Homo sapiens 85-106 2541089-6 1989 It is suggested that the sodium-dependent [3H]IMI binding or a more selective ligand (e.g. [3H]paroxetine) should be used in future studies of serotonin transporter function in depression. Sodium 25-31 solute carrier family 6 member 4 Homo sapiens 143-164 2483420-8 1989 The reversal of hypertensive cardiovascular structural changes as well as the enhancement of renal sodium excretion by ACE inhibitors are important mechanisms of their long-term antihypertensive action. Sodium 99-105 angiotensin I converting enzyme Homo sapiens 119-122 2483424-6 1989 The synthesis of renin is initiated when the cAMP concentration increases under the influence of hormones (parathyroid hormone, catecholamines), of mediators (e.g., prostanoids), or of changes in composition of tubular fluid (in sodium, chlorine, or calcium) detected by the macula densa. Sodium 229-235 renin Homo sapiens 17-22 2474103-2 1989 Homeostatic mechanisms, including activation of the renin-aldosterone system, may counteract the effects of sodium restriction. Sodium 108-114 renin Homo sapiens 52-57 2474103-4 1989 The combination of dietary sodium restriction with blockade of the renin system by an ACE inhibitor is a particularly effective way to improve blood pressure control. Sodium 27-33 angiotensin I converting enzyme Homo sapiens 86-89 2529408-0 1989 Effect of sodium intake on fasting and postprandial levels of atrial natriuretic factor in humans. Sodium 10-16 natriuretic peptide A Homo sapiens 62-87 2473351-4 1989 These findings confirm, in a random sample of untreated male workers, the importance of age and renal function in predicting ANP levels in the plasma and emphasize the potential importance of ANP in the control of sodium excretion in humans under free living conditions. Sodium 214-220 natriuretic peptide A Homo sapiens 192-195 2473352-4 1989 ANP infusion alone caused increases in urinary volume, urinary sodium excretion, and glomerular filtration rate (GFR). Sodium 63-69 natriuretic peptide A Homo sapiens 0-3 2473352-7 1989 The anti-natriuretic effects of exogenous Ang II were reversed by concomitant ANP infusion, which inhibited both proximal and postproximal sodium reabsorption induced by Ang II without changing the GFR. Sodium 139-145 angiotensinogen Homo sapiens 42-48 2473352-7 1989 The anti-natriuretic effects of exogenous Ang II were reversed by concomitant ANP infusion, which inhibited both proximal and postproximal sodium reabsorption induced by Ang II without changing the GFR. Sodium 139-145 natriuretic peptide A Homo sapiens 78-81 2473352-7 1989 The anti-natriuretic effects of exogenous Ang II were reversed by concomitant ANP infusion, which inhibited both proximal and postproximal sodium reabsorption induced by Ang II without changing the GFR. Sodium 139-145 angiotensinogen Homo sapiens 170-176 2473352-8 1989 These results indicate that endogenous Ang II plays an obligatory role in the natriuretic response to ANP and also suggested that ANP inhibits Ang II-stimulated tubular reabsorption of sodium. Sodium 185-191 angiotensinogen Homo sapiens 39-45 2473352-8 1989 These results indicate that endogenous Ang II plays an obligatory role in the natriuretic response to ANP and also suggested that ANP inhibits Ang II-stimulated tubular reabsorption of sodium. Sodium 185-191 natriuretic peptide A Homo sapiens 130-133 2473352-8 1989 These results indicate that endogenous Ang II plays an obligatory role in the natriuretic response to ANP and also suggested that ANP inhibits Ang II-stimulated tubular reabsorption of sodium. Sodium 185-191 angiotensinogen Homo sapiens 143-149 2473355-1 1989 In initial studies of human atrial natriuretic factor (ANF) administered to man, 100 microns intravenous bolus doses infused in normal volunteers and patients with essential hypertension resulted in clear increases in urinary excretion of sodium (four- to sixfold), urine volume, calcium, magnesium, and phosphorous. Sodium 239-245 natriuretic peptide A Homo sapiens 28-53 2473355-1 1989 In initial studies of human atrial natriuretic factor (ANF) administered to man, 100 microns intravenous bolus doses infused in normal volunteers and patients with essential hypertension resulted in clear increases in urinary excretion of sodium (four- to sixfold), urine volume, calcium, magnesium, and phosphorous. Sodium 239-245 natriuretic peptide A Homo sapiens 55-58 2474096-6 1989 Angiotensin II, by its hemodynamic and tubular effects, modulates renal sodium and water excretion and has an important role in blood pressure regulation. Sodium 72-78 angiotensinogen Homo sapiens 0-14 2474096-9 1989 This suggests that local angiotensin concentrations in the vascular and renin tissues may be more important in determining sodium and water excretion. Sodium 123-129 renin Homo sapiens 72-77 2651516-6 1989 In contrast, severe sodium restriction blunted or prevented the development of hypertension in SHR and was associated with (1) marked increases in plasma renin activity (2) increased maintenance of blood pressure by the renin-angiotensin system (as assessed by captopril), and (3) a marked decrease in the blood pressure response to angiotensin II. Sodium 20-26 angiotensinogen Rattus norvegicus 333-347 2918302-6 1989 The monovalent cations, potassium and sodium, activated NAT by a similar mechanism which differed from the caused by the divalent cations. Sodium 38-44 N-acetyltransferase 1 Rattus norvegicus 56-59 2529408-1 1989 The effect of chronic dietary sodium intake on fasting and postprandial plasma atrial natriuretic factor (ANF) levels was examined in 2 studies of normal humans. Sodium 30-36 natriuretic peptide A Homo sapiens 79-104 2529408-6 1989 In contrast, when blood samples were obtained postprandially, significant increases in plasma ANF were observed in the group maintained on high sodium diet. Sodium 144-150 natriuretic peptide A Homo sapiens 94-97 2529408-10 1989 However, plasma ANF is significantly elevated during chronic high sodium intake, when measured postprandially. Sodium 66-72 natriuretic peptide A Homo sapiens 16-19 2593764-0 1989 Effects of intraarterial, intravenous, and intraluminal neurotensin on canine ileal sodium and water absorption and blood flow. Sodium 84-90 neurotensin Canis lupus familiaris 56-67 2593764-4 1989 Intravenous and intraarterial infusion of neurotensin increased net sodium, potassium, and water secretion, due to increased secretory fluxes, and increased hematocrits. Sodium 68-74 neurotensin Canis lupus familiaris 42-53 2593764-6 1989 Neurotensin increased potassium secretion at 0.075 micrograms/min IA, increased sodium and water secretion at 0.75 micrograms/min IA and IV, and increased hematocrit at 7.5 micrograms/min IA and and IV. Sodium 80-86 neurotensin Canis lupus familiaris 0-11 2593764-9 1989 Neurotensin can increase potassium secretion at physiologic levels by a local effect and can increase sodium and water secretion at high physiological-pathological levels through a hormonal mechanism. Sodium 102-108 neurotensin Canis lupus familiaris 0-11 2521696-2 1989 Animal work suggests that part of the natriuretic effect of ANF may be due to inhibition of proximal and distal nephron sodium reabsorption and we now present evidence for similar effects of ANF in man. Sodium 120-126 natriuretic peptide A Homo sapiens 60-63 2521696-7 1989 These findings suggest that ANF inhibits whole-kidney fractional proximal tubular sodium reabsorption in man. Sodium 82-88 natriuretic peptide A Homo sapiens 28-31 2521696-8 1989 Evidence is also presented to show that ANF depresses distal nephron fractional sodium reabsorption as evaluated both by the lithium method and by estimation of solute-free water clearance. Sodium 80-86 natriuretic peptide A Homo sapiens 40-43 2533973-5 1989 In healthy volunteers, however, the same dose of ANF increased urinary excretion of sodium, potassium, calcium, chloride and phosphorus as well as water, and creatinine clearances, and decreased plasma aldosterone. Sodium 84-90 natriuretic peptide A Homo sapiens 49-52 2712937-7 1989 The average serum sodium in the group with other febrile illnesses was higher (146 +/- 5 mEq/L; p less than 0.05) and could represent an appropriate stimulus for antidiuretic hormone release. Sodium 18-24 arginine vasopressin Homo sapiens 162-182 2701770-3 1989 Renin and aldosterone levels significantly increased in group C. A significant correlation was observed between plasma aldosterone concentration and urinary sodium excretion, and between plasma renin activity and aldosterone levels. Sodium 157-163 renin Homo sapiens 0-5 3063116-7 1988 The PTH-vitamin D axis as modulated by the serum ionized calcium level controls adaptation to alterations in dietary calcium and sodium intake and to changes in skeletal turnover based on the level of physical activity. Sodium 129-135 parathyroid hormone Homo sapiens 4-7 2473351-3 1989 In a multivariate analysis, plasma ANP was independently and positively related to age (p less than 0.001), urinary sodium excretion (p less than 0.01), and inversely related to creatinine clearance (p less than 0.02).These variables explained more than 12% of the variability of plasma levels of ANP. Sodium 116-122 natriuretic peptide A Homo sapiens 35-38 2974245-5 1988 The change in ANP induced by VE was inversely correlated with the percent fall in hematocrit and the increment in the fractional excretion of sodium in both groups. Sodium 142-148 natriuretic peptide A Homo sapiens 14-17 2849322-3 1988 An infusion of ACTH (600 micrograms/day) for 7 days, superimposed upon the NE, caused a further rise in AP to a plateau of 143 +/- 9 mmHg after 5 days while cumulative sodium balance fell to -149 +/- 41 meq by the 7th day. Sodium 168-174 proopiomelanocortin Canis lupus familiaris 15-19 2847885-6 1988 The removal of adenomas in the patients with primary aldosteronism significantly lowered both plasma levels of ANP and cyclic guanosine 2",3"-monophosphate and reduced an increase in sodium excretion during ANP infusion, whereas the responses of blood pressure and plasma aldosterone to ANP infusion were not altered by the operation. Sodium 183-189 natriuretic peptide A Homo sapiens 207-210 2847885-6 1988 The removal of adenomas in the patients with primary aldosteronism significantly lowered both plasma levels of ANP and cyclic guanosine 2",3"-monophosphate and reduced an increase in sodium excretion during ANP infusion, whereas the responses of blood pressure and plasma aldosterone to ANP infusion were not altered by the operation. Sodium 183-189 natriuretic peptide A Homo sapiens 207-210 2918302-8 1989 At high potassium or sodium concentration the affinity of acetyl coenzyme A for NAT begins to decrease suggesting that excess monovalent cations can be inhibitory and may represent an endogenous regulatory mechanism controlling in vivo NAT activity. Sodium 21-27 N-acetyltransferase 1 Rattus norvegicus 80-83 2918302-8 1989 At high potassium or sodium concentration the affinity of acetyl coenzyme A for NAT begins to decrease suggesting that excess monovalent cations can be inhibitory and may represent an endogenous regulatory mechanism controlling in vivo NAT activity. Sodium 21-27 N-acetyltransferase 1 Rattus norvegicus 236-239 2847885-5 1988 However, an increase in urinary sodium excretion caused by ANP was higher in the hypertensive than in the normotensive patients (+250% vs. +70%, p less than 0.01) and correlated positively with mean blood pressure during ANP infusion (r = 0.47, p less than 0.001). Sodium 32-38 natriuretic peptide A Homo sapiens 59-62 2847885-5 1988 However, an increase in urinary sodium excretion caused by ANP was higher in the hypertensive than in the normotensive patients (+250% vs. +70%, p less than 0.01) and correlated positively with mean blood pressure during ANP infusion (r = 0.47, p less than 0.001). Sodium 32-38 natriuretic peptide A Homo sapiens 221-224 2849322-5 1988 In contrast, when ACTH infusion was repeated during NE infusion while RAP was prevented from increasing using a servo-controlled aortic occluder, cumulative sodium balance increased to 197 +/- 35 meq and AP rose from 108 +/- 5 to 168 +/- 5 mmHg after 7 days and did not plateau. Sodium 157-163 proopiomelanocortin Canis lupus familiaris 18-22 2849322-8 1988 However, when RAP is not allowed to rise, ACTH is associated with sodium retention and severe systemic hypertension, suggesting that the natriuretic effects of ACTH are caused by increased RAP and that the natriuresis blunts the chronic hypertensive effects of ACTH. Sodium 66-72 proopiomelanocortin Canis lupus familiaris 42-46 2977171-7 1988 These findings are consistent with a renal tubular avidity for sodium, leading to volume expansion, suppression of renin, and, depending on dietary sodium intake, hypertension. Sodium 63-69 renin Homo sapiens 115-120 2975995-1 1988 The possible interaction between arginine vasopressin (AVP) and atrial natriuretic factor (ANF) in the control of urinary sodium and water excretion was investigated in man. Sodium 122-128 arginine vasopressin Homo sapiens 33-53 2975995-1 1988 The possible interaction between arginine vasopressin (AVP) and atrial natriuretic factor (ANF) in the control of urinary sodium and water excretion was investigated in man. Sodium 122-128 arginine vasopressin Homo sapiens 55-58 2975995-1 1988 The possible interaction between arginine vasopressin (AVP) and atrial natriuretic factor (ANF) in the control of urinary sodium and water excretion was investigated in man. Sodium 122-128 natriuretic peptide A Homo sapiens 64-89 2852237-6 1988 However, in sodium-depleted subjects, and perhaps also in other circumstances where circulating concentrations of Ang I are elevated, local ACE may significantly affect vascular tone. Sodium 12-18 angiotensin I converting enzyme Homo sapiens 140-143 2852238-2 1988 In treated animals, the amount of sodium lost during the 6-day observation period was higher than that found in untreated rats, but only at doses that significantly inhibited the circulating angiotensin converting enzyme (ACE). Sodium 34-40 angiotensin I converting enzyme Rattus norvegicus 191-220 2852238-2 1988 In treated animals, the amount of sodium lost during the 6-day observation period was higher than that found in untreated rats, but only at doses that significantly inhibited the circulating angiotensin converting enzyme (ACE). Sodium 34-40 angiotensin I converting enzyme Rattus norvegicus 222-225 2977165-5 1988 Angiotensinogen mRNA levels in the liver, kidney and brain were altered by varying sodium intake. Sodium 83-89 angiotensinogen Rattus norvegicus 0-15 2977165-6 1988 In the high-sodium state angiotensinogen mRNA decreased, but in the low-sodium state it increased. Sodium 12-18 angiotensinogen Rattus norvegicus 25-40 3071591-2 1988 The cerebrospinal fluid concentration of angiotensin II (Ang II) from the patients on a normal-sodium diet was 1.36 +/- 0.41 fmol/ml (n = 5). Sodium 95-101 angiotensinogen Homo sapiens 41-55 3071591-6 1988 The circulating renin-angiotensin system was stimulated by sodium depletion, and the cerebrospinal fluid concentration of Ang II also increased significantly. Sodium 59-65 renin Homo sapiens 16-21 3071591-7 1988 Sodium depletion may stimulate the brain Ang-II forming system, as it does the circulating renin-angiotensin system. Sodium 0-6 renin Homo sapiens 91-96 2977198-5 1988 Plasma ANP concentration increased with the high-sodium diet in both the SS and NSS patients, but the mean increment was significantly greater in the SS than the NSS patients. Sodium 49-55 natriuretic peptide A Homo sapiens 7-10 2977198-7 1988 These findings suggest that an increased level of circulating ANP in hypertensive patients represents a compensatory mechanism to offset further elevation of blood pressure and sodium retention. Sodium 177-183 natriuretic peptide A Homo sapiens 62-65 2975995-1 1988 The possible interaction between arginine vasopressin (AVP) and atrial natriuretic factor (ANF) in the control of urinary sodium and water excretion was investigated in man. Sodium 122-128 natriuretic peptide A Homo sapiens 91-94 2975995-4 1988 Atrial natriuretic factor caused a significant increase in sodium excretion (UNaV) [+56%], urinary flow rate (V) [+17%] and free water clearance (CH2O) [+23%]; creatinine clearance (Ccr) did not change. Sodium 59-65 natriuretic peptide A Homo sapiens 0-25 2853752-2 1988 Since angiotensin II (Ang II) directly stimulates proximal tubular sodium transport, we investigated age-related changes in proximal reabsorption (Jv), using shrinking split-drop micropuncture before and after enalaprilat in SHR at 5, 7 and 12 weeks of age and in age-matched Wistar-Kyoto rats (WKY). Sodium 67-73 angiotensinogen Rattus norvegicus 6-20 2853752-2 1988 Since angiotensin II (Ang II) directly stimulates proximal tubular sodium transport, we investigated age-related changes in proximal reabsorption (Jv), using shrinking split-drop micropuncture before and after enalaprilat in SHR at 5, 7 and 12 weeks of age and in age-matched Wistar-Kyoto rats (WKY). Sodium 67-73 angiotensinogen Rattus norvegicus 22-28 3071599-0 1988 Norepinephrine and calcium responses to altered sodium intake in modulating and non-modulating high-renin hypertension. Sodium 48-54 renin Homo sapiens 100-105 3071599-1 1988 Sodium sensitivity in subjects with high-renin hypertension has been associated with non-modulation of cardiovascular and biochemical responses to alteration in sodium intake. Sodium 0-6 renin Homo sapiens 41-46 3071599-2 1988 Using the percentage suppression of plasma renin activity in response to an increase in dietary sodium intake, high-renin hypertensive subjects were categorized in two groups. Sodium 96-102 renin Homo sapiens 43-48 3071599-3 1988 In association with the increase in sodium intake, modulators showed greater than 58% suppression of plasma renin activity, and significant reductions in mean arterial pressure, plasma aldosterone, norepinephrine and serum calcium concentration. Sodium 36-42 renin Homo sapiens 108-113 3071599-5 1988 The blood pressure response to an increase in dietary sodium intake may be a composite of responses of the renin-angiotensin-aldosterone axis, the adrenergic nervous system and calcium regulatory system. Sodium 54-60 renin Homo sapiens 107-112 3241258-4 1988 The urinary sodium to potassium ratio was significantly and positively correlated with SBP and DBP in both males and females. Sodium 12-18 D-box binding PAR bZIP transcription factor Homo sapiens 95-98 3196359-1 1988 We have examined the effects of exogenous phospholipase A2 (PLA2) on the sodium-dependent high-affinity choline uptake mechanism as assessed by the specific binding of [3H]hemicholinium-3 ([3H]HCh-3). Sodium 73-79 phospholipase A2 group IB Homo sapiens 42-58 3196359-1 1988 We have examined the effects of exogenous phospholipase A2 (PLA2) on the sodium-dependent high-affinity choline uptake mechanism as assessed by the specific binding of [3H]hemicholinium-3 ([3H]HCh-3). Sodium 73-79 phospholipase A2 group IB Homo sapiens 60-64 2470415-1 1988 Injection of cAMP induces in snail neurons generator potential, which is related to an increase of sodium and decrease of potassium permeability of the neuron outer membrane. Sodium 99-105 cathelicidin antimicrobial peptide Homo sapiens 13-17 3154627-4 1988 A low-sodium diet or a high-potassium diet, or nephrectomy markedly increases the adrenal renin concentration in the zona glomerulosa cells without any effect on the fasciculata-medullary cells. Sodium 6-12 renin Homo sapiens 90-95 3073072-9 1988 It has recently been suggested that hyperinsulinemia and insulin resistance may also contribute to the maintenance of an elevated blood pressure because insulin is known to promote sodium retention and enhance sympathetic nervous system activity. Sodium 181-187 insulin Homo sapiens 41-48 3073072-9 1988 It has recently been suggested that hyperinsulinemia and insulin resistance may also contribute to the maintenance of an elevated blood pressure because insulin is known to promote sodium retention and enhance sympathetic nervous system activity. Sodium 181-187 insulin Homo sapiens 57-64 2850819-1 1988 In a previous paper, we showed that during a long-term, moderate restriction in sodium intake, sympathetic nervous system activity was only transiently stimulated, whereas a sustained rise of plasma renin activity occurred. Sodium 80-86 renin Homo sapiens 199-204 3053797-9 1988 Documented mechanisms include insulin-like actions on carbohydrate and fat metabolism, polydipsia, and sodium retention. Sodium 103-109 insulin Homo sapiens 30-37 2973849-5 1988 hANP increased urine flow rate, sodium, calcium and magnesium excretion without significant changes in potassium and phosphate excretion, heart rate or blood pressure. Sodium 32-38 natriuretic peptide A Homo sapiens 0-4 2973849-7 1988 hANP caused a small change in fractional lithium clearance, and larger changes in distal nephron handling of sodium and water. Sodium 109-115 natriuretic peptide A Homo sapiens 0-4 2973849-11 1988 The data suggest that hANP inhibits the reabsorption of sodium and water by an action on distal segments of the nephron and perhaps the proximal tubule. Sodium 56-62 natriuretic peptide A Homo sapiens 22-26 3181734-4 1988 After acute acidification of the water, which leads to a substantial fall in plasma osmolarity and plasma electrolyte levels, the activation of the prolactin cells is less marked than after gradual acidification of the water, when plasma osmolarity, plasma sodium, and plasma total and ionic calcium levels are not noticeably affected. Sodium 257-263 prolactin Sus scrofa 148-157 2465448-2 1988 Total exchangeable sodium was measured by an isotopic dilution technique to quantitate the effects of the low salt diet and ACE inhibitor on body sodium and extracellular fluid. Sodium 146-152 angiotensin I converting enzyme Rattus norvegicus 124-127 2848091-6 1988 These data confirm previous reports of increased adrenal sensitivity to alpha-MSH and angiotensin II in sodium depletion, and also suggest the existence of intraglandular mechanisms for signal amplification which may be involved in mediating the adrenal response to very small concentrations of stimulant. Sodium 104-110 angiotensinogen Rattus norvegicus 86-100 3058795-8 1988 These adaptive responses provide a basis for the observation that the inhibition of renin activity with converting enzyme inhibitors in essential hypertension increases renal blood flow and sodium excretion. Sodium 190-196 renin Homo sapiens 84-89 3058795-9 1988 They also explain why converting enzyme inhibitors can effectively reduce blood pressure, even when renin levels are not absolutely elevated, since any circulating renin imposed upon the adapting hypernatriuretic nephrons inappropriately impairs their sodium excretion. Sodium 252-258 renin Homo sapiens 164-169 3058795-12 1988 The net effect of this uncoordinated response is to shift total renal function so that systemic arterial hypertension is sustained by abnormal sodium retention for the inappropriately high plasma renin level, or vice versa. Sodium 143-149 renin Homo sapiens 196-201 2458353-1 1988 Arginine vasopressin (antidiuretic hormone, ADH) stimulation of sodium transport in high electrical resistance epithelia is accompanied by adenylate cyclase stimulation and cAMP accumulation. Sodium 64-70 arginine vasopressin Homo sapiens 9-20 3414540-3 1988 When a volume deficit occurs, e.g., by restriction of sodium intake or through hemorrhage, a substantial part of the renal vasoconstriction that occurs is due to angiotensin II. Sodium 54-60 angiotensinogen Homo sapiens 162-176 3046266-3 1988 Because of changes in the renin-aldosterone system, the elderly may have problems maintaining sodium and potassium balance. Sodium 94-100 renin Homo sapiens 26-31 3046823-12 1988 In CCl4 rats included in protocol B, there was a close chronological relationship between the activation of the renin-aldosterone system, as estimated by urinary aldosterone excretion, the onset of sodium retention and the increase in urinary excretion of 6-keto-PGF1 alpha and TXB2. Sodium 198-204 C-C motif chemokine ligand 4 Rattus norvegicus 3-7 3054233-8 1988 Low-renin vasoconstriction is correctable by sodium depletion or by calcium channel or alpha adrenergic blockade. Sodium 45-51 renin Homo sapiens 4-9 2974940-3 1988 Recent in vitro and in vivo studies indicate that ANF secretion also may be stimulated by increased plasma osmolality and/or sodium concentration. Sodium 125-131 natriuretic peptide A Homo sapiens 50-53 2973331-1 1988 Atrial natriuretic factor (ANF) is a peptide hormone of cardiac origin, released in response to atrial distention, that increases sodium excretion, inhibits the renin-angiotensin-aldosterone (RAA) system, and decreases arterial pressure. Sodium 130-136 natriuretic peptide A Homo sapiens 0-25 2973331-1 1988 Atrial natriuretic factor (ANF) is a peptide hormone of cardiac origin, released in response to atrial distention, that increases sodium excretion, inhibits the renin-angiotensin-aldosterone (RAA) system, and decreases arterial pressure. Sodium 130-136 natriuretic peptide A Homo sapiens 27-30 2970795-3 1988 At a perfusion pressure of 130 mmHg 50 pmol/l ANP produced an increase of 3.13 +/- 0.68 mumol/min in sodium excretion (UNa V), compared with a fall of 0.33 +/- 1.04 mumol/min in controls (P less than 0.02); fractional excretion of sodium (FENa) rose by 1.45 +/- 0.36% vs. -0.12 +/- 0.47% (P less than 0.05); glomerular filtration rate (GFR) was unchanged. Sodium 101-107 natriuretic peptide A Homo sapiens 46-49 2970795-3 1988 At a perfusion pressure of 130 mmHg 50 pmol/l ANP produced an increase of 3.13 +/- 0.68 mumol/min in sodium excretion (UNa V), compared with a fall of 0.33 +/- 1.04 mumol/min in controls (P less than 0.02); fractional excretion of sodium (FENa) rose by 1.45 +/- 0.36% vs. -0.12 +/- 0.47% (P less than 0.05); glomerular filtration rate (GFR) was unchanged. Sodium 231-237 natriuretic peptide A Homo sapiens 46-49 3231703-0 1988 Sodium-depletion-induced contractures in isolated rat vas deferens: possible role of endogenous catecholamines. Sodium 0-6 arginine vasopressin Rattus norvegicus 54-57 3413684-5 1988 HSL produced significant increases in serum sodium and osmolality, which resolved within 48 hours. Sodium 44-50 lipase E, hormone sensitive type Sus scrofa 0-3 3044668-8 1988 Sodium loading resulted in a significant increase in ANG II binding by glomeruli from NTR, whereas a decrease in binding occurred in glomeruli from SHR. Sodium 0-6 angiotensinogen Rattus norvegicus 53-59 2970225-0 1988 Sodium balance effects on renin, angiotensinogen, and atrial natriuretic polypeptide mRNA levels. Sodium 0-6 angiotensinogen Rattus norvegicus 33-48 2970225-7 1988 The angiotensinogen mRNA level in the liver and kidney decreased in the high-sodium and increased in the low-sodium state to similar extents. Sodium 77-83 angiotensinogen Rattus norvegicus 4-19 2970225-7 1988 The angiotensinogen mRNA level in the liver and kidney decreased in the high-sodium and increased in the low-sodium state to similar extents. Sodium 109-115 angiotensinogen Rattus norvegicus 4-19 2970225-10 1988 These results demonstrate that sodium intake affects the expression of the renin and angiotensinogen genes and slightly alters the expression of ANP gene. Sodium 31-37 angiotensinogen Rattus norvegicus 85-100 2970434-5 1988 Basal, predict ANF concentrations decreased and increased after low and high sodium intakes, respectively. Sodium 77-83 natriuretic peptide A Homo sapiens 15-18 2970434-6 1988 Furthermore, highly significant postural ANF decrements after 1 hour of standing occurred with each diet, although they were lower after the low than after the high sodium diet. Sodium 165-171 natriuretic peptide A Homo sapiens 41-44 2841357-2 1988 Physiologic concentrations of angiotensin II stimulate sodium transport by intestinal and renal early (S1) and late (S2) proximal tubule epithelial cells. Sodium 55-61 angiotensinogen Rattus norvegicus 30-44 2841357-5 1988 The mechanism by which angiotensin II regulates intestinal sodium transport is by potentiating sympathetic nerve activity and norepinephrine release. Sodium 59-65 angiotensinogen Rattus norvegicus 23-37 2905268-0 1988 Disparate effects of neuropeptide Y and clonidine on the excretion of sodium and water in the rat. Sodium 70-76 neuropeptide Y Rattus norvegicus 21-35 2905268-2 1988 We therefore compared the effects of clonidine and NPY on the excretion of sodium and water in anesthetized rats which were unilaterally nephrectomized (right kidney) 10 days prior to the experiment. Sodium 75-81 neuropeptide Y Rattus norvegicus 51-54 2905268-6 1988 Only NPY increased sodium excretion and osmolar clearance. Sodium 19-25 neuropeptide Y Rattus norvegicus 5-8 2970360-5 1988 Compared with the placebo infusion, atrial natriuretic peptide (ANP) produced a 43% greater sodium excretion and a 34% greater urinary volume in the subsequent hour. Sodium 92-98 natriuretic peptide A Homo sapiens 36-62 2970360-5 1988 Compared with the placebo infusion, atrial natriuretic peptide (ANP) produced a 43% greater sodium excretion and a 34% greater urinary volume in the subsequent hour. Sodium 92-98 natriuretic peptide A Homo sapiens 64-67 3294177-7 1988 In patients with essential hypertension, intracellular sodium and free calcium concentrations were negatively correlated with plasma renin activity (r = -0.66, p less than 0.001; r = -0.60, p less than 0.001, plasma norepinephrine concentration. Sodium 55-61 renin Homo sapiens 133-138 3294177-8 1988 These results suggest that a considerable relationship exists between intracellular sodium and free calcium in lymphocytes and that, in essential hypertension, the alteration in cellular metabolism of sodium and calcium may be linked to the renin system but not to blood pressure, age, or adrenergic activity. Sodium 84-90 renin Homo sapiens 241-246 3294177-8 1988 These results suggest that a considerable relationship exists between intracellular sodium and free calcium in lymphocytes and that, in essential hypertension, the alteration in cellular metabolism of sodium and calcium may be linked to the renin system but not to blood pressure, age, or adrenergic activity. Sodium 201-207 renin Homo sapiens 241-246 3263237-3 1988 This prospective study of 17 consecutive patients receiving parenteral high dose IL-2 documents a reversible syndrome of hypotension, oliguria, fluid retention, azotemia and very low urinary excretion of sodium (median FeNa of 0.04%). Sodium 204-210 interleukin 2 Homo sapiens 81-85 3044668-10 1988 Although a high sodium intake caused a reduction in the response of glomeruli from both NTR and SHR to exogenous ANG II, these changes were not statistically significant. Sodium 16-22 angiotensinogen Rattus norvegicus 113-119 2971131-9 1988 Thus, there is evidence for a decreased responsiveness to hANP exclusively of renal fluid, sodium, and chloride excretion in uncomplicated type 1 diabetes mellitus. Sodium 91-97 natriuretic peptide A Homo sapiens 58-62 2968054-2 1988 Intravascular volume expansion over 30 min with donor blood equal to 3% body weight increased plasma ANF concentration from a base line of 216 +/- 28 to 1,590 +/- 240 pg/ml (P less than 0.001) in sodium-replete rats. Sodium 196-202 natriuretic peptide A Homo sapiens 101-104 2973295-5 1988 The change in ANP induced by VE was inversely correlated with the fall in hematocrit and the variation in fractional excretion of sodium in both groups. Sodium 130-136 natriuretic peptide A Homo sapiens 14-17 2973296-4 1988 Intravenous infusion of ANF for 2 h (1 microgram/mn) induced the expected increases in urinary flow rate, and sodium and potassium excretions (+226, +307 and +171 p. 100, respectively). Sodium 110-116 natriuretic peptide A Homo sapiens 24-27 2841075-10 1988 Furthermore, pHi backregulation was inhibited by removing sodium from the extracellular solution. Sodium 58-64 glucose-6-phosphate isomerase Bos taurus 13-16 3286047-9 1988 They also show a blunted rate of renin suppression after a sodium load, although plasma renin activity falls to the same low level at steady state. Sodium 59-65 renin Homo sapiens 33-38 3292416-8 1988 During sodium restriction, PRA was significantly lower (p less than 0.01) in the sodium-sensitive subsets (2.56 +/- 1.6 vs 4.04 +/- 2.6; 2.65 +/- 2.1 vs 3.88 +/- 2.6 ng angiotensin I/ml/hr). Sodium 81-87 angiotensinogen Homo sapiens 169-182 3292417-8 1988 Interstitial angiotensin II could influence sodium tubular reabsorption directly by stimulating sodium transport in proximal renal tubules and indirectly by altering medullary blood flow and, thereby, medullary interstitial pressure. Sodium 44-50 angiotensinogen Homo sapiens 13-27 3292417-8 1988 Interstitial angiotensin II could influence sodium tubular reabsorption directly by stimulating sodium transport in proximal renal tubules and indirectly by altering medullary blood flow and, thereby, medullary interstitial pressure. Sodium 96-102 angiotensinogen Homo sapiens 13-27 3411123-0 1988 The effects of intravenous angiotensin II upon blood pressure and sodium and urate excretion in human pregnancy. Sodium 66-72 angiotensinogen Homo sapiens 27-41 3411123-6 1988 Angiotensin II evoked a dose-dependent pressor response, a graded increase in PAC and a reduction in sodium and urate excretion in both pregnant and non-pregnant women. Sodium 101-107 angiotensinogen Homo sapiens 0-14 3411123-7 1988 The administration of Ang II had a proportionately greater effect on sodium and urate excretion in non-pregnant than in pregnant women; the pressor response to Ang II was also decreased in the pregnant women. Sodium 69-75 angiotensinogen Homo sapiens 22-28 2834967-0 1988 Enhanced vasopressin (V2-receptor)-induced sodium retention in mineralocorticoid hypertension. Sodium 43-49 arginine vasopressin receptor 2 Rattus norvegicus 9-33 2976977-3 1988 After sodium infusion ANP was unchanged in the patients but significantly increased in the controls. Sodium 6-12 natriuretic peptide A Homo sapiens 22-25 2976977-10 1988 It is suggested that the increased level of ANP can be viewed as a compensatory phenomenon to an abnormal sodium or volume homeostasis in the early stages of chronic glomerulonephritis. Sodium 106-112 natriuretic peptide A Homo sapiens 44-47 3390713-1 1988 Angiotensin II (Ang II) and aldosterone levels increase with sodium deficiency, promoting sodium conservation and arousing a salt appetite in rats. Sodium 61-67 angiotensinogen Rattus norvegicus 0-14 3390713-1 1988 Angiotensin II (Ang II) and aldosterone levels increase with sodium deficiency, promoting sodium conservation and arousing a salt appetite in rats. Sodium 61-67 angiotensinogen Rattus norvegicus 16-22 3390713-1 1988 Angiotensin II (Ang II) and aldosterone levels increase with sodium deficiency, promoting sodium conservation and arousing a salt appetite in rats. Sodium 90-96 angiotensinogen Rattus norvegicus 0-14 3390713-1 1988 Angiotensin II (Ang II) and aldosterone levels increase with sodium deficiency, promoting sodium conservation and arousing a salt appetite in rats. Sodium 90-96 angiotensinogen Rattus norvegicus 16-22 2966574-6 1988 These results support the concept that decreased effective circulating volume plays a role in pathogenesis of cirrhotic ascites, and that a relative deficiency of ANP plays a role in the sodium retention of decompensated cirrhosis. Sodium 187-193 natriuretic peptide A Homo sapiens 163-166 2966770-4 1988 Human ANF-(99-126) infusion for 45 minutes at 0.034 microgram/kg/min augmented (p less than 0.05-0.01) diuresis and urinary sodium, chloride, calcium, phosphate, and magnesium excretion. Sodium 124-130 natriuretic peptide A Homo sapiens 6-9 3284388-7 1988 Our observations suggest that the abnormally elevated glomerular blood flow and filtration rate of early IDDM can be corrected by a low-sodium diet via stimulation of endogenous ANG II. Sodium 136-142 angiotensinogen Rattus norvegicus 178-184 2965633-7 1988 ANP caused a significant increase in urine flow and sodium excretion. Sodium 52-58 natriuretic peptide A Homo sapiens 0-3 3401630-0 1988 Effects of atropine and tetrodotoxin on neurotensin-induced ileal sodium transport in the dog. Sodium 66-72 neurotensin Canis lupus familiaris 40-51 3401630-6 1988 Neurotensin caused a transient increase in net sodium absorption which was not associated with significant changes in unidirectional fluxes. Sodium 47-53 neurotensin Canis lupus familiaris 0-11 3064608-2 1988 Because the kidney is both the source of circulating renin and the final determinant of the state of sodium balance, which in turn defines responsiveness to angiotensin II, one might have anticipated substantial interest in the impact of converting enzyme inhibitors on the kidney when these agents were developed. Sodium 101-107 angiotensinogen Homo sapiens 157-171 3284356-5 1988 Sodium-sensitive individuals were characterized by significantly increased forearm vascular resistance and decreased plasma renin activity and aldosterone concentration. Sodium 0-6 renin Homo sapiens 124-129 3260620-9 1988 We conclude: (1) IL-2 induces an increase in vascular permeability causing the development of edema, sodium avidity, and prerenal azotemia as occurs during endotoxemia; (2) IL-2 therapy induces respiratory alkalosis with the subsequent intracellular shift of phosphorous accompanied by increased renal phosphorous reabsorption; and (3) there is no evidence of renal tubular dysfunction (renal tubular acidosis [RTA], renal leak of glucose, phosphorous, or magnesium). Sodium 101-107 interleukin 2 Homo sapiens 17-21 3260620-9 1988 We conclude: (1) IL-2 induces an increase in vascular permeability causing the development of edema, sodium avidity, and prerenal azotemia as occurs during endotoxemia; (2) IL-2 therapy induces respiratory alkalosis with the subsequent intracellular shift of phosphorous accompanied by increased renal phosphorous reabsorption; and (3) there is no evidence of renal tubular dysfunction (renal tubular acidosis [RTA], renal leak of glucose, phosphorous, or magnesium). Sodium 101-107 interleukin 2 Homo sapiens 173-177 3259932-4 1988 These results suggest that sodium-dependent [3H]imipramine sites relevant for serotonin uptake may be the same as the substrate recognition sites on the serotonin transporter. Sodium 27-33 solute carrier family 6 member 4 Rattus norvegicus 153-174 2975458-8 1988 These data confirm that atrial natriuretic peptide inhibits renin secretion in a dose-related manner and suggest that this action of the peptide is modified by both the baseline sodium status and renal function of the recipient. Sodium 178-184 renin Homo sapiens 60-65 2975463-4 1988 Plasma renin activity was related to 24-hour urinary sodium excretion. Sodium 53-59 renin Homo sapiens 7-12 3279770-4 1988 Although insulin has complex actions on the circulation, plausible mechanisms by which insulin might raise blood pressure include renal sodium retention and stimulation of the sympathetic nervous system. Sodium 136-142 insulin Homo sapiens 87-94 2964780-5 1988 The increment of urinary sodium excretion rate was significantly correlated with that of plasma ANF. Sodium 25-31 natriuretic peptide A Homo sapiens 96-99 2978738-2 1988 Evidence from numerous experiments incorporating central blood volume expansion and changes in sodium status supports atrial stretch as the prime determinant of ANF release. Sodium 95-101 natriuretic peptide A Homo sapiens 161-164 3342932-6 1988 Finally, we provide evidence indicating that FGF can combine with endogenously occurring heparin-like components: immobilized FGF binds sodium-[35S]sulfate labeled components secreted in muscle culture conditioned medium, an interaction inhibited by anti-HeSPG antibodies or heparin, but not by other sulfated glycosaminoglycans. Sodium 136-144 fibroblast growth factor 10 Gallus gallus 45-48 2851654-7 1988 Plasma renin was increased by enalapril and lowered by increased sodium intake. Sodium 65-71 renin Homo sapiens 7-12 3361121-1 1988 Enhanced renal vasoconstriction and renal tubular sodium reabsorption mediated by noradrenaline and angiotensin II (Ang II) have been implicated in the pathogenesis of essential hypertension. Sodium 50-56 angiotensinogen Homo sapiens 100-114 3361121-1 1988 Enhanced renal vasoconstriction and renal tubular sodium reabsorption mediated by noradrenaline and angiotensin II (Ang II) have been implicated in the pathogenesis of essential hypertension. Sodium 50-56 angiotensinogen Homo sapiens 116-122 3353502-14 1988 (5) In sodium-free reconstructed McCoy"s 5a medium, pHi was 0.25-0.1 pH units lower than that in the sodium-containing counterpart at pHe 6.3-7.2, and heat sensitization increased accordingly; however, heat survival plotted versus pHi was identical for the two types of media. Sodium 7-13 glucose-6-phosphate isomerase Cricetulus griseus 52-55 3353502-14 1988 (5) In sodium-free reconstructed McCoy"s 5a medium, pHi was 0.25-0.1 pH units lower than that in the sodium-containing counterpart at pHe 6.3-7.2, and heat sensitization increased accordingly; however, heat survival plotted versus pHi was identical for the two types of media. Sodium 7-13 glucose-6-phosphate isomerase Cricetulus griseus 231-234 3126665-1 1988 Angiotensin II (ANG II) is believed to stimulate sodium and water absorption from the small intestine by enhancing sympathetic nerve transmission. Sodium 49-55 angiotensinogen Rattus norvegicus 0-14 3126665-1 1988 Angiotensin II (ANG II) is believed to stimulate sodium and water absorption from the small intestine by enhancing sympathetic nerve transmission. Sodium 49-55 angiotensinogen Rattus norvegicus 16-22 3342932-6 1988 Finally, we provide evidence indicating that FGF can combine with endogenously occurring heparin-like components: immobilized FGF binds sodium-[35S]sulfate labeled components secreted in muscle culture conditioned medium, an interaction inhibited by anti-HeSPG antibodies or heparin, but not by other sulfated glycosaminoglycans. Sodium 136-144 fibroblast growth factor 10 Gallus gallus 126-129 2967239-4 1988 Sodium loading increased resting supine plasma IR-ANP (P less than 0.037) and suppressed plasma renin and aldosterone, including the renin-aldosterone response to exercise. Sodium 0-6 renin Homo sapiens 96-101 2967239-4 1988 Sodium loading increased resting supine plasma IR-ANP (P less than 0.037) and suppressed plasma renin and aldosterone, including the renin-aldosterone response to exercise. Sodium 0-6 renin Homo sapiens 133-138 3389028-4 1988 This fall appears to be mediated in part by a diminished renin response to the sodium restriction as blood pressure becomes more severe. Sodium 79-85 renin Homo sapiens 57-62 3130264-3 1988 Infusion of vasopressin in normal subjects was associated with an increase in fractional excretion of sodium by the kidney, which continued during the day after the infusion was stopped. Sodium 102-108 arginine vasopressin Homo sapiens 12-23 3130264-5 1988 Infusion of vasopressin in patients lacking adrenocortical function was associated with a smaller increase in fractional excretion of sodium by the kidney in comparison with that seen in normal subjects, and the increase in sodium excretion was confined to the period of the infusion. Sodium 134-140 arginine vasopressin Homo sapiens 12-23 3130264-5 1988 Infusion of vasopressin in patients lacking adrenocortical function was associated with a smaller increase in fractional excretion of sodium by the kidney in comparison with that seen in normal subjects, and the increase in sodium excretion was confined to the period of the infusion. Sodium 224-230 arginine vasopressin Homo sapiens 12-23 3130264-7 1988 We conclude that changes in mineralocorticoid activity are the main factors contributing to the increase in renal sodium excretion seen during, and after, the continuous infusion of vasopressin in salt- and water-restricted man. Sodium 114-120 arginine vasopressin Homo sapiens 182-193 2827465-7 1988 The changes in ANP following PVS were positively correlated with changes in right atrial pressure (p less than 0.05), urinary cyclic guanosine monophosphate (p less than 0.05), urinary sodium excretion (p less than 0.05), and urine volume (p less than 0.01). Sodium 185-191 natriuretic peptide A Homo sapiens 15-18 3228647-0 1988 Effects of intracerebroventricular infusion of angiotensin II and related peptides on water and sodium ingestion and excretion. Sodium 96-102 angiotensinogen Rattus norvegicus 47-61 2455613-0 1988 In vitro action of insulin on erythrocyte sodium transport mechanisms: its possible role in the pathogenesis of arterial hypertension. Sodium 42-48 insulin Homo sapiens 19-26 2455613-1 1988 The effects of insulin on sodium and potassium metabolism have been well known for many years; clinical observation and laboratory experience showed different results about the insulin effect on the sodium-potassium pump. Sodium 26-32 insulin Homo sapiens 15-22 2964952-5 1988 Changes in the plasma hANP level were correlated positively with those of urinary sodium excretion and negatively with those of plasma renin activity on days 7 and 14 of salt repletion. Sodium 82-88 natriuretic peptide A Homo sapiens 22-26 2964952-7 1988 These findings indicate that the plasma hANP level is closely related to sodium intake in patients with essential hypertension. Sodium 73-79 natriuretic peptide A Homo sapiens 40-44 2966021-4 1988 There was a dissociation between ANP response and urinary sodium excretion. Sodium 58-64 natriuretic peptide A Homo sapiens 33-36 2827942-3 1988 The density of these binding sites for ANP on platelets is decreased after increased dietary sodium intake, when plasma ANP levels increase. Sodium 93-99 natriuretic peptide A Homo sapiens 39-42 2970767-4 1988 Transient increases in plasma ANP, in four cardiac recipients 3-10-fold their basal levels, could neither be related to rejection episodes nor to cardiac dysfunction, but rather to signs of fluid and sodium retention. Sodium 200-206 natriuretic peptide A Homo sapiens 30-33 3076742-0 1988 Plasma renin activity in patients with sodium-sensitive and sodium-resistant symptomatic arterial hypertension. Sodium 39-45 renin Homo sapiens 7-12 3076742-0 1988 Plasma renin activity in patients with sodium-sensitive and sodium-resistant symptomatic arterial hypertension. Sodium 60-66 renin Homo sapiens 7-12 3285861-5 1988 The hyperinsulinemia of obesity may, therefore, increase blood pressure by 1) direct effects of insulin to stimulate renal sodium reabsorption, and 2) sympathetic stimulation of the heart, blood vessels, and kidney. Sodium 123-129 insulin Homo sapiens 9-16 2856049-2 1988 The converting enzyme inhibitors, captopril (SQ14 225, Squibb) or enalaprilic acid (MK 422, Merck Sharp and Dohme), were used to evaluate the role of angiotensin II in sodium (Na) appetite of Na-deplete rats given a choice of water and 0.5 mol/l NaCl to drink. Sodium 168-174 angiotensinogen Rattus norvegicus 150-164 2902974-2 1988 Vasopressin induces a rapid increase in water permeability and stimulates net sodium transport in responsive epithelia through the mediation of cAMP. Sodium 78-84 arginine vasopressin Homo sapiens 0-11 11538849-1 1988 Angiotensin II (Ang II) induces a marked reduction in renal blood flow at doses well below those required to induce a pressor response, and as blood flow falls there is a decline in glomerular filtration rate and sodium excretion. Sodium 213-219 angiotensinogen Homo sapiens 0-14 11538849-1 1988 Angiotensin II (Ang II) induces a marked reduction in renal blood flow at doses well below those required to induce a pressor response, and as blood flow falls there is a decline in glomerular filtration rate and sodium excretion. Sodium 213-219 angiotensinogen Homo sapiens 16-22 11537094-3 1988 We have now measured atrial natriuretic factor (ANF), a hormone recently shown to regulate sodium and water excretion, in blood specimens obtained during flight. Sodium 91-97 natriuretic peptide A Homo sapiens 21-46 11537094-3 1988 We have now measured atrial natriuretic factor (ANF), a hormone recently shown to regulate sodium and water excretion, in blood specimens obtained during flight. Sodium 91-97 natriuretic peptide A Homo sapiens 48-51 2900130-1 1988 In this paper the different aspects of the role played by alpha-adrenoceptors in the control of renin secretion from the juxtaglomerular apparatus and renal sodium and water reabsorption, and the effects of alpha-adrenoceptor antagonists on systemic haemodynamics, will be investigated. Sodium 157-163 renin Homo sapiens 96-101 3240918-3 1988 In the first group (N = 10), a single 20-mg dose of the slow-release formulation caused an increase in 8-h sodium excretion (P less than 0.025) and urine volume (P less than 0.005). Sodium 107-113 nuclear receptor subfamily 4 group A member 1 Homo sapiens 20-26 3072177-2 1988 The first is renin-independent, requires antecedent sodium retention, and appears related to abnormal membrane transport of calcium. Sodium 52-58 renin Homo sapiens 13-18 3283072-7 1988 In addition, patients of both groups showed normal response of the renin-aldosterone system following diuretic and dietary induced sodium and volume depletion. Sodium 131-137 renin Homo sapiens 67-72 2973989-0 1988 Frusemide pretreatment blunts the inhibition of renal tubular sodium reabsorption by ANF in man. Sodium 62-68 natriuretic peptide A Homo sapiens 85-88 3386276-0 1988 Interaction between aldosterone and vasopressin on vascular smooth muscle permeability to sodium. Sodium 90-96 arginine vasopressin Homo sapiens 36-47 3060296-6 1988 The link between plasma AVP and hypertension remains unclear, but it appears likely that it has an important permissive action in the development of sodium-dependent forms of hypertension. Sodium 149-155 arginine vasopressin Rattus norvegicus 24-27 2832471-0 1988 Haemodynamic, hormonal and renal effects of adrenocorticotrophic hormone in sodium-restricted man. Sodium 76-82 proopiomelanocortin Homo sapiens 44-72 2832471-1 1988 The effect of a dietary sodium restriction (15 mmol/day) on the development of adrenocorticotrophic hormone (ACTH) hypertension was examined in six normal male subjects. Sodium 24-30 proopiomelanocortin Homo sapiens 79-107 2832471-1 1988 The effect of a dietary sodium restriction (15 mmol/day) on the development of adrenocorticotrophic hormone (ACTH) hypertension was examined in six normal male subjects. Sodium 24-30 proopiomelanocortin Homo sapiens 109-113 2832471-2 1988 When ACTH (1 mg/day) was given for 5 days to subjects on a sodium-restricted diet, systolic blood pressure rose (116 +/- 4 to 125 +/- 4 mmHg, P less than 0.001), while diastolic blood pressure was unchanged. Sodium 59-65 proopiomelanocortin Homo sapiens 5-9 2975718-3 1988 On the contrary, aldosterone increased and vasopressin decreased in the low sodium period but did not change between the control and high sodium periods. Sodium 76-82 arginine vasopressin Homo sapiens 43-54 2832823-3 1988 (1) Regulation of pHi after induction of an acid load by removal of NH4Cl could be blocked either totally by removal of extracellular sodium, or subtotally (about 90%) by application of amiloride (1 mmol/l). Sodium 134-140 glucose-6-phosphate isomerase Bos taurus 18-21 3227050-0 1988 Enhanced pressor responses to angiotensin II caused by excessive sodium loading in the pithed rat. Sodium 65-71 angiotensinogen Rattus norvegicus 30-44 3227050-1 1988 The influence of changes in the sodium balance on angiotensin II-induced pressor responses were studied in the pithed rat preparation, which is characterized by a highly activated renin-angiotensin-aldosterone system (RAAS) with high plasma renin and angiotensin II concentrations. Sodium 32-38 angiotensinogen Rattus norvegicus 50-64 3227050-2 1988 The pressor response to angiotensin II was enhanced by excessive sodium loading only, as induced by a high sodium diet combined with a mineralocorticoid, but not by a high salt diet as such. Sodium 65-71 angiotensinogen Rattus norvegicus 24-38 3227050-2 1988 The pressor response to angiotensin II was enhanced by excessive sodium loading only, as induced by a high sodium diet combined with a mineralocorticoid, but not by a high salt diet as such. Sodium 107-113 angiotensinogen Rattus norvegicus 24-38 3227050-6 1988 Our finding that in this preparation excessive sodium loading still appears to enhance pressor responses to angiotensin II supports the conclusion that increased sodium load directly sensitizes vascular angiotensin II receptors. Sodium 47-53 angiotensinogen Rattus norvegicus 108-122 3227050-6 1988 Our finding that in this preparation excessive sodium loading still appears to enhance pressor responses to angiotensin II supports the conclusion that increased sodium load directly sensitizes vascular angiotensin II receptors. Sodium 47-53 angiotensinogen Rattus norvegicus 203-217 3227050-6 1988 Our finding that in this preparation excessive sodium loading still appears to enhance pressor responses to angiotensin II supports the conclusion that increased sodium load directly sensitizes vascular angiotensin II receptors. Sodium 162-168 angiotensinogen Rattus norvegicus 108-122 3227050-6 1988 Our finding that in this preparation excessive sodium loading still appears to enhance pressor responses to angiotensin II supports the conclusion that increased sodium load directly sensitizes vascular angiotensin II receptors. Sodium 162-168 angiotensinogen Rattus norvegicus 203-217 3287122-0 1988 [Plasma renin activity in relation to sodium excretion. Sodium 38-44 renin Homo sapiens 8-13 3420302-2 1988 Chronic prolactin administration significantly furthered the effects of sodium restriction. Sodium 72-78 prolactin Rattus norvegicus 8-17 2977818-1 1988 Atrial natriuretic peptide (ANP) and the renin-angiotensin-aldosterone system are important regulatory hormones in sodium homeostasis. Sodium 115-121 renin Homo sapiens 41-46 3509745-2 1987 The IL-2 regimen produced progressive hypotension, azotemia, and sodium avidity (fractional excretion of sodium = 0.20 +/- 0.07 percent) despite massive fluid administration (mean: 18.4 liter per five days) and weight gain (mean: 4.0 kg). Sodium 65-71 interleukin 2 Homo sapiens 4-8 2970171-5 1988 P-ANP increased during high sodium intake to 134 +/- 9 pg/ml, compared to 55 +/- 7 pg/ml during low sodium intake. Sodium 28-34 natriuretic peptide A Homo sapiens 2-5 2970179-12 1988 A less pronounced, but significant increase of absolute sodium excretion of the LK was observed in both groups after AT II infusion. Sodium 56-62 angiotensinogen Homo sapiens 117-122 2970180-2 1988 While high sodium loading caused an increase of plasma ANP levels and a concomitant decrease of plasma renin and aldosterone concentrations, low sodium loading caused the opposite pattern of ANP and renin/aldosterone secretion. Sodium 11-17 natriuretic peptide A Homo sapiens 55-58 2970180-2 1988 While high sodium loading caused an increase of plasma ANP levels and a concomitant decrease of plasma renin and aldosterone concentrations, low sodium loading caused the opposite pattern of ANP and renin/aldosterone secretion. Sodium 11-17 renin Homo sapiens 103-108 2970180-2 1988 While high sodium loading caused an increase of plasma ANP levels and a concomitant decrease of plasma renin and aldosterone concentrations, low sodium loading caused the opposite pattern of ANP and renin/aldosterone secretion. Sodium 145-151 natriuretic peptide A Homo sapiens 191-194 2970180-2 1988 While high sodium loading caused an increase of plasma ANP levels and a concomitant decrease of plasma renin and aldosterone concentrations, low sodium loading caused the opposite pattern of ANP and renin/aldosterone secretion. Sodium 145-151 renin Homo sapiens 199-204 2970180-3 1988 Some patients with essential hypertension with highly elevated plasma ANP levels (10-20-fold above the normal range) showed an only moderate decrease of ANP and a slight increase of renin under a low sodium diet. Sodium 200-206 natriuretic peptide A Homo sapiens 70-73 2970180-3 1988 Some patients with essential hypertension with highly elevated plasma ANP levels (10-20-fold above the normal range) showed an only moderate decrease of ANP and a slight increase of renin under a low sodium diet. Sodium 200-206 renin Homo sapiens 182-187 2970180-5 1988 We speculate that high levels of plasma ANP in patients with essential hypertension might be interpreted as a compensatory mechanism either for an insufficient excretion of sodium or for myocardial dysfunction. Sodium 173-179 natriuretic peptide A Homo sapiens 40-43 3509745-2 1987 The IL-2 regimen produced progressive hypotension, azotemia, and sodium avidity (fractional excretion of sodium = 0.20 +/- 0.07 percent) despite massive fluid administration (mean: 18.4 liter per five days) and weight gain (mean: 4.0 kg). Sodium 105-111 interleukin 2 Homo sapiens 4-8 3326859-0 1987 Relationship between plasma renin activity and distal nephron sodium delivery and reabsorption in man. Sodium 62-68 renin Homo sapiens 28-33 3062959-2 1988 In general, ACE-inhibition does not affect normal glomerular filtration rate (GFR) but may increase GFR in patients on a low sodium intake prior to treatment. Sodium 125-131 angiotensin I converting enzyme Homo sapiens 12-15 3062959-4 1988 In contrast to other vasodilator drugs, the decrease in blood pressure induced by ACE-inhibition is not accompanied by sodium retention, but rather by an initial natriuresis. Sodium 119-125 angiotensin I converting enzyme Homo sapiens 82-85 3347628-0 1988 Influence of recombinant IGF-I (somatomedin C) on sodium-dependent phosphate transport in cultured renal epithelium. Sodium 50-56 insulin like growth factor 1 Homo sapiens 32-45 2965232-1 1987 There is now much evidence that atrial natriuretic peptide (ANP) is important in the control of sodium balance. Sodium 96-102 natriuretic peptide A Homo sapiens 32-58 2965232-1 1987 There is now much evidence that atrial natriuretic peptide (ANP) is important in the control of sodium balance. Sodium 96-102 natriuretic peptide A Homo sapiens 60-63 3326859-1 1987 The relationship between plasma renin activity and distal tubular sodium delivery and reabsorption was examined in man. Sodium 66-72 renin Homo sapiens 32-37 3326859-3 1987 The maximal water diuresis method and the lithium clearance method both showed a negative correlation between plasma renin activity and distal sodium delivery and reabsorption. Sodium 143-149 renin Homo sapiens 117-122 2961274-1 1987 We studied the effect of alpha-human natriuretic peptide (ANP, 100 micrograms iv) on renal sodium handling in eight healthy subjects before and after 7 days of indomethacin (50 mg 3 times a day). Sodium 91-97 natriuretic peptide A Homo sapiens 25-56 2965232-4 1987 In normal male volunteers, ANP caused urinary sodium excretion to rise significantly from baseline (+80 +/- 44 mumol/min) whereas ANG II was potently antinatriuretic (-125 +/- 36 mumol/min). Sodium 46-52 natriuretic peptide A Homo sapiens 27-30 2965232-5 1987 When ANP was administered against a nonpressor background infusion of ANG II, urinary sodium excretion rose from a new lower level (-93 +/- 22 mumol/min) to a rate not significantly different from control (-22 +/- 25 mumol/min). Sodium 86-92 natriuretic peptide A Homo sapiens 5-8 2965232-5 1987 When ANP was administered against a nonpressor background infusion of ANG II, urinary sodium excretion rose from a new lower level (-93 +/- 22 mumol/min) to a rate not significantly different from control (-22 +/- 25 mumol/min). Sodium 86-92 angiotensinogen Homo sapiens 70-76 3426122-4 1987 The diagnosis of HA1 is based on simple examinations, especially systematic measurement of kaliemia in every hypertensive patient with a normal sodium diet before treatment. Sodium 144-150 Rho GTPase activating protein 45 Homo sapiens 17-20 2835134-8 1987 These data suggest that when endogenous AII levels are elevated without a concurrent increase in blood pressure, as occurs during hypovolemia or sodium depletion, AII may have a significant influence on ACTH secretion. Sodium 145-151 proopiomelanocortin Canis lupus familiaris 203-207 2961274-1 1987 We studied the effect of alpha-human natriuretic peptide (ANP, 100 micrograms iv) on renal sodium handling in eight healthy subjects before and after 7 days of indomethacin (50 mg 3 times a day). Sodium 91-97 natriuretic peptide A Homo sapiens 58-61 2961274-3 1987 Prior to indomethacin, ANP caused a fourfold rise in sodium excretion over the first 20 min and a threefold rise in fractional sodium excretion. Sodium 53-59 natriuretic peptide A Homo sapiens 23-26 2961274-3 1987 Prior to indomethacin, ANP caused a fourfold rise in sodium excretion over the first 20 min and a threefold rise in fractional sodium excretion. Sodium 127-133 natriuretic peptide A Homo sapiens 23-26 2961274-11 1987 Indomethacin and ANP appear to have opposite effects on sodium excretion, maximal free water clearance, and lithium clearance. Sodium 56-62 natriuretic peptide A Homo sapiens 17-20 2824371-0 1987 Humoral sodium transport inhibitor in acute volume expansion and low renin hypertension. Sodium 8-14 renin Homo sapiens 69-74 2960617-9 1987 Infusion of ANF in humans that produced plasma levels in the upper physiological range caused increased sodium excretion and decreased plasma renin activity. Sodium 104-110 natriuretic peptide A Homo sapiens 12-15 3480991-0 1987 Sodium sensitivity and resistance of blood pressure: the role of the kidney and the renin-aldosterone axis. Sodium 0-6 renin Homo sapiens 84-89 3326697-3 1987 Evidence is presented that the renin-angiotensin-aldosterone system and the adrenergic nervous system are important determinants of the blood pressure response to sodium depletion and sodium loading, respectively. Sodium 163-169 renin Homo sapiens 31-36 3326697-3 1987 Evidence is presented that the renin-angiotensin-aldosterone system and the adrenergic nervous system are important determinants of the blood pressure response to sodium depletion and sodium loading, respectively. Sodium 184-190 renin Homo sapiens 31-36 3314453-3 1987 The first mechanism is renin independent, requires antecedent sodium retention and appears related to abnormal membrane transport of calcium. Sodium 62-68 renin Homo sapiens 23-28 3314453-4 1987 This vasoconstriction is identified by low plasma renin and ionized calcium and is correctable by sodium depletion or calcium channel or alpha blockade. Sodium 98-104 renin Homo sapiens 50-55 2889370-9 1987 It is suggested that vasopressin acts as a vasoconstrictor hormone in conscious sodium-depleted rats when either the renin-angiotensin system or alpha-adrenergic system is inhibited but not when both systems are blocked. Sodium 80-86 arginine vasopressin Rattus norvegicus 21-32 3308701-1 1987 We have reported that 50% of subjects with normal renin essential hypertension have both delayed suppression of the renin-angiotensin-aldosterone axis following sodium infusion and a delayed rate of excretion of an acute salt load. Sodium 161-167 renin Homo sapiens 116-121 2821056-10 1987 alpha hANP also increased urine volume [176 +/- 31 (+/- SEM) vs. 113 +/- 19 mL/mmol creatinine with placebo; P less than 0.03] and sodium excretion (2.14 +/- 0.48 vs. 0.58 +/- 0.22 mmol/mmol creatinine with placebo; P less than 0.004) on the ACTH infusion days. Sodium 131-137 natriuretic peptide A Homo sapiens 6-10 2821056-11 1987 With angiotensin II, urine volume was also significantly increased by alpha hANP (150 +/- 27 vs. 81 +/- 15 mL/mmol creatinine with placebo; P less than 0.03), and urine sodium excretion doubled. Sodium 169-175 angiotensinogen Homo sapiens 5-19 2963166-9 1987 Thus, under salt loading and water diuresis conditions, hANP infusion did not alter GFR, but reduced proximal reabsorption of sodium, and markedly enhanced the fraction of sodium escaping distal tubular reabsorption, suggesting that hANP-induced natriuresis is due, for an important part, to inhibition of sodium reabsorption in the distal nephron. Sodium 126-132 natriuretic peptide A Homo sapiens 56-60 2963166-9 1987 Thus, under salt loading and water diuresis conditions, hANP infusion did not alter GFR, but reduced proximal reabsorption of sodium, and markedly enhanced the fraction of sodium escaping distal tubular reabsorption, suggesting that hANP-induced natriuresis is due, for an important part, to inhibition of sodium reabsorption in the distal nephron. Sodium 172-178 natriuretic peptide A Homo sapiens 56-60 2963166-9 1987 Thus, under salt loading and water diuresis conditions, hANP infusion did not alter GFR, but reduced proximal reabsorption of sodium, and markedly enhanced the fraction of sodium escaping distal tubular reabsorption, suggesting that hANP-induced natriuresis is due, for an important part, to inhibition of sodium reabsorption in the distal nephron. Sodium 172-178 natriuretic peptide A Homo sapiens 56-60 2960480-10 1987 Changes in plasma ANP concentrations both within the diurnal study period and during sodium deprivation were closely and positively correlated with concomitant changes in cumulative sodium balance. Sodium 85-91 natriuretic peptide A Homo sapiens 18-21 2960480-10 1987 Changes in plasma ANP concentrations both within the diurnal study period and during sodium deprivation were closely and positively correlated with concomitant changes in cumulative sodium balance. Sodium 182-188 natriuretic peptide A Homo sapiens 18-21 3310771-0 1987 The effects of angiotensin-converting enzyme inhibition on sodium handling in patients with advanced chronic obstructive pulmonary disease. Sodium 59-65 angiotensin I converting enzyme Homo sapiens 15-44 3310771-5 1987 Thus, the mechanism by which angiotensin-converting enzyme inhibition induces an acute sodium diuresis in these patients remains to be elucidated. Sodium 87-93 angiotensin I converting enzyme Homo sapiens 29-58 3078193-0 1987 [Plasma renin activity in patients with sodium-responsive and unresponsive essential hypertension]. Sodium 40-46 renin Homo sapiens 8-13 3631062-0 1987 A possible mechanism of increased sodium influx in red cells with abnormal membrane lipid levels induced by phospholipase A2. Sodium 34-40 phospholipase A2 group IB Homo sapiens 108-124 3653973-0 1987 Association of haptoglobin with sodium sensitivity and resistance of blood pressure. Sodium 32-38 haptoglobin Homo sapiens 15-26 3653973-3 1987 Both hypertensive and normotensive subjects with haptoglobin 1-1 phenotype were significantly more (p less than 0.05) likely to be sodium-sensitive than were those with 2-1 or 2-2 phenotypes, and subjects with 2-2 phenotypes were more apt to be sodium-resistant. Sodium 131-137 haptoglobin Homo sapiens 49-60 3653973-3 1987 Both hypertensive and normotensive subjects with haptoglobin 1-1 phenotype were significantly more (p less than 0.05) likely to be sodium-sensitive than were those with 2-1 or 2-2 phenotypes, and subjects with 2-2 phenotypes were more apt to be sodium-resistant. Sodium 245-251 haptoglobin Homo sapiens 49-60 2960551-2 1987 Intrarenal infusion of alpha-hANP at a rate of 0.05 microgram/kg per min resulted in a significant increase in renal blood flow, urine flow and urinary excretion of sodium with no change in renal perfusion pressure. Sodium 165-171 natriuretic peptide A Homo sapiens 29-33 2960551-4 1987 A significant correlation was observed during alpha-hANP infusion between changes in both urine flow and sodium excretion and inner cortical blood flow; changes in inner cortical blood flow may reflect changes in medullary blood flow. Sodium 105-111 natriuretic peptide A Homo sapiens 52-56 3626762-0 1987 Parathyroid hormone in sodium-dependent hypertension. Sodium 23-29 parathyroid hormone Rattus norvegicus 0-19 3626762-12 1987 Rather, elevation of circulating PTH levels may be a response to prolonged increases in sodium consumption. Sodium 88-94 parathyroid hormone Rattus norvegicus 33-36 3626763-0 1987 Influence of sodium intake on circulating levels of neuropeptide Y. Sodium 13-19 neuropeptide Y Rattus norvegicus 52-66 3626763-4 1987 The purpose of this study was therefore to assess whether there exists a relationship between dietary sodium intake and the levels of circulating NPY. Sodium 102-108 neuropeptide Y Rattus norvegicus 146-149 3626763-10 1987 These findings are therefore compatible with the hypothesis that sodium balance might to some extent influence blood pressure regulation via changes in circulating NPY levels which in turn modify blood pressure responsiveness. Sodium 65-71 neuropeptide Y Rattus norvegicus 164-167 2958207-11 1987 Our results are compatible with the concept that increased ANP secretion may play a role in the immediate increase in sodium excretion after a saline load. Sodium 118-124 natriuretic peptide A Homo sapiens 59-62 3037881-4 1987 These results suggest that the increased plasma levels of atrial natriuretic peptide, which appear to be associated with an increase in plasma renin activity and with hepatic dysfunction, may participate in maintaining homeostasis of sodium and fluid volume in patients with chronic liver disease. Sodium 234-240 renin Homo sapiens 143-148 3623678-1 1987 To study the role of calcium movements in mediating the effects of sodium chloride on the response of blood pressure to angiotensin II (ANG II), we infused ANG II before and after giving calcium channel blocking drugs (nifedipine and diltiazem) and calcium infusions to normal subjects during high and low sodium intakes. Sodium 67-73 angiotensinogen Homo sapiens 120-134 3623678-1 1987 To study the role of calcium movements in mediating the effects of sodium chloride on the response of blood pressure to angiotensin II (ANG II), we infused ANG II before and after giving calcium channel blocking drugs (nifedipine and diltiazem) and calcium infusions to normal subjects during high and low sodium intakes. Sodium 67-73 angiotensinogen Homo sapiens 136-142 3623678-2 1987 ANG II was also in nine patients with essential hypertension eating a low sodium diet. Sodium 74-80 angiotensinogen Homo sapiens 0-6 3623678-9 1987 The results suggest that in normal subjects increased DBP responses to ANG II, induced by an increase in sodium intake, are partially mediated by increased extracellular to intracellular calcium movements, since they are blocked by the structurally different calcium channel blocking drugs nifedipine and diltiazem. Sodium 105-111 angiotensinogen Homo sapiens 71-77 3623678-10 1987 In hypertensive patients on a low sodium diet, increased DBP responses to ANG II infusion were blocked by nifedipine, indicating they are at least partly mediated by increased extracellular to intracellular calcium flux. Sodium 34-40 angiotensinogen Homo sapiens 74-80 2956609-11 1987 The data of the urinary sodium excretion showed the escape from sodium-retaining effect of aldosterone, and this escape could be explained by the increase in plasma ANP. Sodium 24-30 natriuretic peptide A Homo sapiens 165-168 3121240-3 1987 Increased concentrations of antidiuretic hormone (ADH) result in retention of free water, increased excretion of sodium, and hyponatremia. Sodium 113-119 arginine vasopressin Homo sapiens 28-48 3121240-3 1987 Increased concentrations of antidiuretic hormone (ADH) result in retention of free water, increased excretion of sodium, and hyponatremia. Sodium 113-119 arginine vasopressin Homo sapiens 50-53 2445661-7 1987 These results show that the drugs interact differently with the different cell populations involved in T cell proliferation: increase of an amiloride-dependent sodium influx is an obligatory step required to induce the early increase of the ouabain-dependent potassium influx which is needed for the expression of IL 2 receptors. Sodium 160-166 interleukin 2 Homo sapiens 314-318 3476800-2 1987 Despite some empirical and theoretical objections, linear regression analysis of the relationship between plasma vasopressin and plasma osmolality or sodium continues to provide a simple and useful way to describe the major functional properties of the osmoregulatory system. Sodium 150-156 arginine vasopressin Homo sapiens 113-124 3323041-0 1987 Urinary sodium & plasma renin activity following renal transplantation. Sodium 8-14 renin Homo sapiens 28-33 3037888-3 1987 These are patients with essential hypertension who fail to modulate their renal blood flow and aldosterone responsiveness to angiotensin II when dietary sodium is changed. Sodium 153-159 angiotensinogen Homo sapiens 125-139 3658129-6 1987 By its presumed reduction of central and peripheral vasopressin release through lowering the cerebrospinal fluid sodium concentration, it may help in decreasing the brain water content. Sodium 113-119 arginine vasopressin Rattus norvegicus 52-63 3037888-5 1987 On a high sodium load only nonmodulators have a decrease in BP in response to short-term treatment with an angiotensin-converting enzyme (ACE) inhibitor, which indicates an abnormality in intrarenal angiotensin II levels or in the renal angiotensin II receptor. Sodium 10-16 angiotensin I converting enzyme Homo sapiens 107-136 3037888-5 1987 On a high sodium load only nonmodulators have a decrease in BP in response to short-term treatment with an angiotensin-converting enzyme (ACE) inhibitor, which indicates an abnormality in intrarenal angiotensin II levels or in the renal angiotensin II receptor. Sodium 10-16 angiotensin I converting enzyme Homo sapiens 138-141 3037891-2 1987 Angiotensin II supported systemic BP by direct systemic vasoconstriction, by facilitating the central and peripheral effects of the sympathetic nervous system, by promoting renal sodium retention by the production of aldosterone, and by increasing total body water by enhancing thirst and the synthesis of vasopressin. Sodium 179-185 angiotensinogen Homo sapiens 0-14 3037892-8 1987 This action of ANP is thought to contribute to the enhanced renal excretion of sodium-rich urine in response to ANP. Sodium 79-85 natriuretic peptide A Homo sapiens 15-18 3037892-8 1987 This action of ANP is thought to contribute to the enhanced renal excretion of sodium-rich urine in response to ANP. Sodium 79-85 natriuretic peptide A Homo sapiens 112-115 3037892-9 1987 Finally, in two models of chronic extracellular volume expansion, namely, mineralocorticoid excess and a reduction in nephron number with a high sodium intake, endogenous plasma ANP levels increased significantly above control levels. Sodium 145-151 natriuretic peptide A Homo sapiens 178-181 3037893-6 1987 In addition, the direct renal tubular influence of angiotensin II and aldosterone contribute to sodium retention. Sodium 96-102 angiotensinogen Homo sapiens 51-65 3300326-4 1987 Upright plasma renin activity was suppressed in cyclosporine-treated patients (cyclosporine 2.9 +/- 0.9, azathioprine 4.7 +/- 0.9, renal insufficiency 5.2 +/- 1.9 ng/ml/hour) but could be stimulated by a four-day period of dietary sodium restriction and diuretic administration (cyclosporine 15.8 +/- 4.4 ng/ml/hour). Sodium 231-237 renin Homo sapiens 15-20 3300326-7 1987 It is concluded that suppression of plasma renin activity by cyclosporine is physiologic and may reflect expansion of extracellular fluid volume, which can be reversed by sodium depletion. Sodium 171-177 renin Homo sapiens 43-48 3037340-2 1987 The p21-induced pH change was inhibited by amiloride treatment or growth of cells in medium low in sodium, suggesting a role for the Na+/H+ antiporter. Sodium 99-105 solute carrier family 9 (sodium/hydrogen exchanger), member 1 Mus musculus 133-150 3039766-6 1987 The increase in plasma AII levels in the 4 patients was larger than that observed in a previous study in normal subjects after rigorous dietary sodium restriction. Sodium 144-150 angiotensinogen Homo sapiens 23-26 3039766-8 1987 Rises in PRA, AII, and plasma potassium were partially reversed by increased sodium intake and further suppressed by resumption of fludrocortisone therapy. Sodium 77-83 angiotensinogen Homo sapiens 14-17 3115635-2 1987 During an in-patient metabolic balance study she required 1.0 mg fludrocortisone daily and dietary sodium supplementation to make plasma renin activity and serum potassium normal, and to abolish postural hypotension. Sodium 99-105 renin Homo sapiens 137-142 3305466-6 1987 At rest as well as during exercise, Aldo rose with increasing ANG II, but the stimulatory effect of ANG II on Aldo was attenuated with higher sodium intake, as estimated from UVNa. Sodium 142-148 angiotensinogen Homo sapiens 100-106 2957643-10 1987 The natriuretic action of hANP is related to increases in glomerular filtration rate and proximal tubular rejection of sodium (as assessed by fractional reabsorption of lithium). Sodium 119-125 natriuretic peptide A Homo sapiens 26-30 2950290-3 1987 Infusion of ANF into the avian renal portal system increased urine flow rate and sodium excretion by as much as 300% and 100%, respectively. Sodium 81-87 natriuretic peptide A Gallus gallus 12-15 2822310-0 1987 Effect of sodium depletion on pressor responsiveness in ACTH-induced hypertension in man. Sodium 10-16 proopiomelanocortin Homo sapiens 56-60 2889551-0 1987 Interaction of vasopressin, angiotensin and alpha-adrenergic system in sodium depletion in the rat. Sodium 71-77 arginine vasopressin Rattus norvegicus 15-26 2889551-6 1987 In sodium depletion, endogenous vasopressin acts as a vasoconstrictor hormone, particularly in the kidney, when either the renin-angiotensin or alpha-adrenergic system is inhibited. Sodium 3-9 arginine vasopressin Rattus norvegicus 32-43 3028957-5 1987 Conversely, enalapril substantially altered the blood pressure response to ANG II with sodium restriction, completely preventing the reduction in responsiveness. Sodium 87-93 angiotensinogen Homo sapiens 75-81 3033389-1 1987 It has been suggested that AII-mediated renal mechanisms limit the efficacy of moderate sodium restriction in the lowering of blood pressure (BP) in hypertension. Sodium 88-94 NLR family pyrin domain containing 3 Homo sapiens 27-30 3033389-10 1987 This blunting may contribute to the increased sodium sensitivity of BP during ACE-inhibition. Sodium 46-52 angiotensin I converting enzyme Homo sapiens 78-81 3103761-0 1987 Moderate sodium restriction with angiotensin converting enzyme inhibitor in essential hypertension: a double blind study. Sodium 9-15 angiotensin I converting enzyme Homo sapiens 33-62 3569605-11 1987 However, the increment in sodium excretion was greater in low-renin EH than that in normal-renin EH (0.05 less than p less than 0.10), high-renin EH (p less than 0.05) and NT (p less than 0.05). Sodium 26-32 renin Homo sapiens 62-67 3569605-11 1987 However, the increment in sodium excretion was greater in low-renin EH than that in normal-renin EH (0.05 less than p less than 0.10), high-renin EH (p less than 0.05) and NT (p less than 0.05). Sodium 26-32 renin Homo sapiens 91-96 3569605-11 1987 However, the increment in sodium excretion was greater in low-renin EH than that in normal-renin EH (0.05 less than p less than 0.10), high-renin EH (p less than 0.05) and NT (p less than 0.05). Sodium 26-32 renin Homo sapiens 91-96 3812735-2 1987 The time course of angiotensin II (ANG II) binding in the presence of a NaCl gradient (medium greater than intravesicular) demonstrated an "overshoot" characteristic of electrogenic sodium-dependent D-glucose uptake. Sodium 182-188 angiotensinogen Rattus norvegicus 19-33 3812735-2 1987 The time course of angiotensin II (ANG II) binding in the presence of a NaCl gradient (medium greater than intravesicular) demonstrated an "overshoot" characteristic of electrogenic sodium-dependent D-glucose uptake. Sodium 182-188 angiotensinogen Rattus norvegicus 35-41 3549504-6 1987 We confirmed the inverse correlation between serum sodium and serum renin. Sodium 51-57 renin Homo sapiens 68-73 3818012-5 1987 Acetylcholine, adenosine 5"-diphosphate, and thrombin induced endothelium-dependent relaxations that were significantly depressed in the aorta of DS fed a high sodium diet. Sodium 160-166 coagulation factor II Rattus norvegicus 45-53 3323202-5 1987 However, in other animals maintained on a high salt intake but given a constant infusion of angiotensin II (20 ng/kg/min), renal nerve stimulation caused minimal changes in renal haemodynamics but significantly reduced urine flow by 41%, absolute sodium excretion by 54% and fractional sodium excretion by 49%. Sodium 247-253 angiotensinogen Rattus norvegicus 92-106 3323202-5 1987 However, in other animals maintained on a high salt intake but given a constant infusion of angiotensin II (20 ng/kg/min), renal nerve stimulation caused minimal changes in renal haemodynamics but significantly reduced urine flow by 41%, absolute sodium excretion by 54% and fractional sodium excretion by 49%. Sodium 286-292 angiotensinogen Rattus norvegicus 92-106 2955962-2 1987 Plasma levels (mean +/- SEM) of ANP in healthy subjects on a normal sodium intake were 8.4 +/- 1.4 pg/ml and could be modified by changes in sodium intake with increases in sodium intake being associated with higher levels. Sodium 68-74 natriuretic peptide A Homo sapiens 32-35 2955962-2 1987 Plasma levels (mean +/- SEM) of ANP in healthy subjects on a normal sodium intake were 8.4 +/- 1.4 pg/ml and could be modified by changes in sodium intake with increases in sodium intake being associated with higher levels. Sodium 141-147 natriuretic peptide A Homo sapiens 32-35 2955962-2 1987 Plasma levels (mean +/- SEM) of ANP in healthy subjects on a normal sodium intake were 8.4 +/- 1.4 pg/ml and could be modified by changes in sodium intake with increases in sodium intake being associated with higher levels. Sodium 141-147 natriuretic peptide A Homo sapiens 32-35 2955962-5 1987 These results suggest that circulating ANP corresponds to the biologically active peptide and point to an important role of the atrial peptides in the control of sodium balance. Sodium 162-168 natriuretic peptide A Homo sapiens 39-42 3035942-2 1987 Exposure of isolated toad bladders to quinidine, calcium ionophores (A23187, X537A), or low-sodium or potassium-free serosal solutions resulted in a dose-dependent decrease in the hydrosmotic response to vasopressin or exogenous adenosine 3",5"-cyclic monophosphate (cAMP). Sodium 92-98 arginine vasopressin Homo sapiens 204-215 3035964-2 1987 Plasma renin activity, its response to sodium depletion, and the renal vein renin ratio during sodium depletion were greater in unilateral than in bilateral stenosis. Sodium 95-101 renin Homo sapiens 76-81 3035964-3 1987 A fall in diastolic blood pressure induced by analog infusion during sodium depletion was correlated with the preinfusion plasma renin activity and with the renal vein renin ratio. Sodium 69-75 renin Homo sapiens 129-134 3035964-3 1987 A fall in diastolic blood pressure induced by analog infusion during sodium depletion was correlated with the preinfusion plasma renin activity and with the renal vein renin ratio. Sodium 69-75 renin Homo sapiens 168-173 2882875-3 1987 When sodium intake is restricted or a diuretic is used, the reactive increase in plasma renin activity makes a substantial contribution to limiting the decrease in blood pressure. Sodium 5-11 renin Homo sapiens 88-93 3552505-4 1987 Using univariate analysis, all the patients with poor sodium excretion had abnormally high levels of plasma renin activity, plasma aldosterone, and arginine vasopressin. Sodium 54-60 renin Homo sapiens 108-113 3552505-4 1987 Using univariate analysis, all the patients with poor sodium excretion had abnormally high levels of plasma renin activity, plasma aldosterone, and arginine vasopressin. Sodium 54-60 arginine vasopressin Homo sapiens 157-168 2442543-1 1987 Inhibitors of the angiotensin-converting enzyme (ACE) acutely increase sodium excretion. Sodium 71-77 angiotensin I converting enzyme Homo sapiens 18-47 2442543-1 1987 Inhibitors of the angiotensin-converting enzyme (ACE) acutely increase sodium excretion. Sodium 71-77 angiotensin I converting enzyme Homo sapiens 49-52 3298415-1 1987 Blockade of angiotensin-converting enzyme has been variously reported to increase or to decrease sodium excretion in patients with cirrhosis and ascites. Sodium 97-103 angiotensin I converting enzyme Homo sapiens 12-41 3298415-6 1987 The antinatriuretic effect of captopril may be mediated by reduced angiotensin II-mediated sodium excretion, by decreased prostaglandin production, and/or by indirect effects of reduced blood pressure. Sodium 91-97 angiotensinogen Homo sapiens 67-81 3036130-5 1987 Diferric transferrin induced proton release depends on external sodium and is inhibited by amiloride. Sodium 64-70 transferrin Homo sapiens 9-20 3555119-4 1987 In the present work, we have studied whether human recombinant interleukin-1 beta (hrIL-1) could affect the renal handling of sodium and thus, could be implicated in natriuretic response to pyrogens or endotoxins. Sodium 126-132 interleukin 1 beta Homo sapiens 63-81 3578531-0 1987 Adrenergic and angiotensin II influences on renal vascular tone in chronic sodium depletion. Sodium 75-81 angiotensinogen Rattus norvegicus 15-29 3578531-3 1987 The results indicate that both angiotensin II and adrenergic activity contribute to the maintenance of renal vascular resistance during chronic sodium depletion. Sodium 144-150 angiotensinogen Rattus norvegicus 31-45 3578531-7 1987 The findings indicate that the glomerular hemodynamic changes that characterize chronic sodium depletion are primarily due to the activity of angiotensin II. Sodium 88-94 angiotensinogen Rattus norvegicus 142-156 2953526-2 1987 Mean plasma ANP on a fixed sodium intake before fludrocortisone was 6.5 +/- SEM 1.1 pg/ml. Sodium 27-33 natriuretic peptide A Homo sapiens 12-15 2953526-4 1987 The rise in plasma ANP was closely related to the amount of sodium retained during the fludrocortisone treatment and the sodium "escape" occurred by days 4 to 7. Sodium 60-66 natriuretic peptide A Homo sapiens 19-22 2953526-4 1987 The rise in plasma ANP was closely related to the amount of sodium retained during the fludrocortisone treatment and the sodium "escape" occurred by days 4 to 7. Sodium 121-127 natriuretic peptide A Homo sapiens 19-22 2953526-5 1987 These results support the concept that ANP could play an important hormonal role in over-coming the sodium-retaining effects of mineralocorticoids in man. Sodium 100-106 natriuretic peptide A Homo sapiens 39-42 3555966-2 1987 Sodium restriction, over a 15-day period, reduced daily urinary PGE2 and TXB2 in concordance with urinary flow (V) and sodium excretion (UNa+V), but increased plasma renin activity (PRA) and plasma aldosterone concentration (PAC). Sodium 0-6 LOW QUALITY PROTEIN: renin Oryctolagus cuniculus 166-171 3555966-5 1987 It is concluded that chronic sodium intake produces opposite changes in the renal prostaglandin and the renin-angiotensin systems. Sodium 29-35 LOW QUALITY PROTEIN: renin Oryctolagus cuniculus 104-109 3301353-4 1987 This fall appears to be mediated in part by a diminished renin response to the sodium restriction as blood pressure becomes more severe. Sodium 79-85 renin Homo sapiens 57-62 3034033-7 1987 The present results show that ACE inhibition with ramipril in sodium-replete healthy volunteers induces a decrease in blood pressure that is not accompanied by changes in heart rate, pressor sensitivity to exogenous norepinephrine or baroreceptor sensitivity. Sodium 62-68 angiotensin I converting enzyme Homo sapiens 30-33 2951575-1 1987 The sympathetic nervous system and atrial natriuretic factor (ANF) are intimately involved in sodium, volume and blood pressure homeostasis, particularly in response to volume and pressure overloads. Sodium 94-100 natriuretic peptide A Homo sapiens 35-60 2951575-1 1987 The sympathetic nervous system and atrial natriuretic factor (ANF) are intimately involved in sodium, volume and blood pressure homeostasis, particularly in response to volume and pressure overloads. Sodium 94-100 natriuretic peptide A Homo sapiens 62-65 2882685-7 1987 As in humans, active and inactive plasma renin increased during sodium depletion and inactive renin increased during beta-adrenergic blockade, while active renin decreased. Sodium 64-70 renin Homo sapiens 41-46 3551628-3 1987 When intravenous insulin infusion was stopped, plasma vasopressin, osmolality, and glucose increased over the ensuing 5 h, whereas plasma sodium decreased, and blood volume and pressure did not change. Sodium 138-144 insulin Homo sapiens 17-24 3551628-4 1987 This increase in vasopressin was not due to a loss of osmoregulation, because changes in plasma osmolality and sodium, induced by infusion of hypertonic saline or water loading, induced appropriate vasopressin responses under insulin deplete as well as replete conditions. Sodium 111-117 arginine vasopressin Homo sapiens 17-28 3551628-4 1987 This increase in vasopressin was not due to a loss of osmoregulation, because changes in plasma osmolality and sodium, induced by infusion of hypertonic saline or water loading, induced appropriate vasopressin responses under insulin deplete as well as replete conditions. Sodium 111-117 arginine vasopressin Homo sapiens 198-209 3030698-0 1987 Liver angiotensinogen synthesis and release during captopril treatment in sodium-depleted rats. Sodium 74-80 angiotensinogen Rattus norvegicus 6-21 3030698-10 1987 The angiotensinogen liver content and in vitro angiotensinogen release were decreased in sodium-depleted rats treated with a converting enzyme inhibitor, and these parameters were negatively correlated to in vivo plasma levels of renin, angiotensin I, and des-angiotensin I-angiotensinogen. Sodium 89-95 angiotensinogen Rattus norvegicus 4-19 3030698-10 1987 The angiotensinogen liver content and in vitro angiotensinogen release were decreased in sodium-depleted rats treated with a converting enzyme inhibitor, and these parameters were negatively correlated to in vivo plasma levels of renin, angiotensin I, and des-angiotensin I-angiotensinogen. Sodium 89-95 angiotensinogen Rattus norvegicus 47-62 3030698-10 1987 The angiotensinogen liver content and in vitro angiotensinogen release were decreased in sodium-depleted rats treated with a converting enzyme inhibitor, and these parameters were negatively correlated to in vivo plasma levels of renin, angiotensin I, and des-angiotensin I-angiotensinogen. Sodium 89-95 angiotensinogen Rattus norvegicus 47-62 3546565-2 1987 Sodium restriction augmented plasma renin activity (PRA), which was associated with a rise in basal renal PGE2 synthesis and urinary excretion, whereas sodium supplementation attenuated PRA with a decrease in renal PGE2 synthesis and urinary excretion. Sodium 0-6 LOW QUALITY PROTEIN: renin Oryctolagus cuniculus 36-41 3585223-1 1987 Infusion of dopamine is reported to reduce the response of aldosterone to infused angiotensin II in sodium-deplete but not sodium-replete man. Sodium 100-106 angiotensinogen Homo sapiens 82-96 3585223-3 1987 The responses of both aldosterone and 18-hydroxycorticosterone to infusion of angiotensin II appeared to be reduced by dopamine in sodium-deplete, but not sodium-replete, subjects. Sodium 131-137 angiotensinogen Homo sapiens 78-92 3035468-7 1987 Renal effects of angiotensin II and aldosterone are responsible for sodium and water retention. Sodium 68-74 angiotensinogen Homo sapiens 17-31 3032326-0 1987 Moderate sodium restriction with angiotensin converting enzyme inhibitor in essential hypertension. Sodium 9-15 angiotensin I converting enzyme Homo sapiens 33-62 3029119-5 1987 At saturating concentrations, both rIL-1 alpha and rIL-1 beta induce a simultaneous rise in intracellular pH and sodium concentration. Sodium 113-119 interleukin 1 alpha Rattus norvegicus 35-46 3029119-5 1987 At saturating concentrations, both rIL-1 alpha and rIL-1 beta induce a simultaneous rise in intracellular pH and sodium concentration. Sodium 113-119 interleukin 1 beta Rattus norvegicus 51-61 2952835-2 1987 In the controls, plasma levels of hANP at 8:00 a.m. were lowered from 73 +/- 11 to 49 +/- 7 pg/ml during low sodium diet and increased to 128 +/- 37 pg/ml after high salt intake. Sodium 109-115 natriuretic peptide A Homo sapiens 34-38 2952835-3 1987 Plasma ANP levels were significantly lower after 4 h of upright posture during unrestricted, low and high sodium intake. Sodium 106-112 natriuretic peptide A Homo sapiens 7-10 2952835-4 1987 In the hypertensive group, plasma ANP levels were elevated during unrestricted diet (203 +/- 43 pg/ml), during the low sodium period (139 +/- 31 pg/ml), and after high sodium intake (267 +/- 63 pg/ml) compared to the controls. Sodium 119-125 natriuretic peptide A Homo sapiens 34-37 2952835-4 1987 In the hypertensive group, plasma ANP levels were elevated during unrestricted diet (203 +/- 43 pg/ml), during the low sodium period (139 +/- 31 pg/ml), and after high sodium intake (267 +/- 63 pg/ml) compared to the controls. Sodium 168-174 natriuretic peptide A Homo sapiens 34-37 2948754-3 1987 Plasma renin activity and aldosterone decreased significantly with increasing sodium intake whereas plasma vasopressin was highest on the high sodium intake. Sodium 78-84 renin Homo sapiens 7-12 3027576-3 1987 The data we present here indicate that inhibition of this transport by ethylisopropyl-amiloride or by lowering extracellular sodium reduces or even completely suppresses the rise in cytoplasmic free Ca2+ concentration that is essential for platelet aggregation in response to thrombin. Sodium 125-131 coagulation factor II, thrombin Homo sapiens 276-284 2948754-3 1987 Plasma renin activity and aldosterone decreased significantly with increasing sodium intake whereas plasma vasopressin was highest on the high sodium intake. Sodium 143-149 arginine vasopressin Homo sapiens 107-118 2948755-0 1987 Atrial natriuretic peptide inhibits the effect of endogenous angiotensin II on plasma aldosterone in conscious sodium-depleted rats. Sodium 111-117 angiotensinogen Rattus norvegicus 61-75 2948755-4 1987 During sodium depletion, the rise in plasma renin activity which determines an increment in the circulating concentration of angiotensin II was accompanied by a rise in aldosterone secretion as expected. Sodium 7-13 angiotensinogen Rattus norvegicus 125-139 3789043-5 1986 Increased fetal plasma and urine arginine vasopressin concentrations were associated with significant increases in fetal urine osmolality (146 +/- 12 to 262 +/- 30 mosm) and sodium concentration (35.8 +/- 2.8 to 76.5 +/- 20 mu Eq/ml), but fetal urine production rates did not change (0.68 +/- 0.11 to 0.62 +/- 0.15 ml/min). Sodium 174-180 arginine vasopressin Homo sapiens 42-53 3580257-0 1987 The importance of the response of the renin-angiotensin system in determining blood pressure changes with sodium restriction. Sodium 106-112 renin Homo sapiens 38-43 3580257-3 1987 This lack of response of blood pressure to sodium restriction appears to be due, at least in part, to a reactive rise in renin and angiotensin II. Sodium 43-49 renin Homo sapiens 121-145 3580257-5 1987 With sodium restriction there is less of a rise in renin and angiotensin II compared with normotensive subjects and patients have a greater fall in blood pressure compared with normotensive subjects but the effect is less in mild compared to severe hypertension. Sodium 5-11 renin Homo sapiens 51-56 3580257-5 1987 With sodium restriction there is less of a rise in renin and angiotensin II compared with normotensive subjects and patients have a greater fall in blood pressure compared with normotensive subjects but the effect is less in mild compared to severe hypertension. Sodium 5-11 angiotensinogen Homo sapiens 61-75 3319647-4 1987 Hyperreninaemia after captopril was inversely related to the prevailing plasma sodium level (r = -0.66, p less than 0.01), and the changes in both systolic and diastolic blood pressure were correlated with baseline plasma renin activity (r = 0.49, p less than 0.05 for systolic and r = 0.71, p less than 0.01 for diastolic blood pressure). Sodium 79-85 renin Homo sapiens 5-10 2485062-7 1987 Hypotension can occur with the first dose of ACE inhibitor, especially in sodium-depleted subjects; in patients on prior antihypertensive therapy, particularly if this includes a diuretic; and in the elderly. Sodium 74-80 angiotensin I converting enzyme Homo sapiens 45-48 2955161-3 1987 Moreover the role of alpha-hANP is of particular interest in chronic renal failure, since in this pathological condition increased sodium and water retention plays a major pathogenetic role in the development of hypertension and altered secretion and/or metabolism of alpha-hANP may contribute to fluid volume and BP regulation. Sodium 131-137 natriuretic peptide A Homo sapiens 27-31 2955161-3 1987 Moreover the role of alpha-hANP is of particular interest in chronic renal failure, since in this pathological condition increased sodium and water retention plays a major pathogenetic role in the development of hypertension and altered secretion and/or metabolism of alpha-hANP may contribute to fluid volume and BP regulation. Sodium 131-137 natriuretic peptide A Homo sapiens 274-278 2964567-1 1987 In six patients with nephrotic syndrome of various aetiology, the increase in absolute and fractional sodium excretion (FENa) after a bolus injection of 100 micrograms alpha-human atrial natriuretic peptide (ANP) was not different from the effect in normal healthy subjects at comparable sodium levels. Sodium 288-294 natriuretic peptide A Homo sapiens 208-211 3028957-0 1987 Role of angiotensin II in the hormonal, renal, and electrolyte response to sodium restriction. Sodium 75-81 angiotensinogen Homo sapiens 8-22 3028957-1 1987 Adrenal responses to angiotensin II (ANG II) are enhanced with restriction of sodium intake. Sodium 78-84 angiotensinogen Homo sapiens 21-35 3028957-1 1987 Adrenal responses to angiotensin II (ANG II) are enhanced with restriction of sodium intake. Sodium 78-84 angiotensinogen Homo sapiens 37-43 3126454-0 1987 The renin-angiotensin-aldosterone system during haemodialysis with acetate or bicarbonate at different dialysate sodium concentrations. Sodium 113-119 renin Homo sapiens 4-9 3126454-3 1987 At lower dialysate sodium concentrations, plasma renin activity (acetate dialysis and bicarbonate dialysis) and aldosterone concentration (only acetate dialysis) were higher than they were at higher dialysate sodium concentrations. Sodium 19-25 renin Homo sapiens 49-54 3306849-3 1987 Long-term MTC administration was found to significantly potentiate both the rise in the plasma level of aldosterone and the hypertrophy of the zona glomerulosa and its parenchymal cells induced by a prolonged treatment with angiotensin II (AII), but not those evoked by a chronic sodium deprivation alone or combined with AII infusion. Sodium 280-286 angiotensinogen Rattus norvegicus 224-238 3536587-2 1986 Recent studies, however, have demonstrated that in several forms of chronic hypertension caused by aldosterone, angiotensin II (AngII), vasopressin, or norepinephrine and adrenocorticotropin, increased renal arterial pressure is essential for maintaining normal excretion of sodium and water in the face of reduced renal excretory capability. Sodium 275-281 angiotensinogen Homo sapiens 128-133 3039093-8 1986 It is concluded that acute ANG II blockade has no influence on the vascular resistance in the human forearm, but increases basal SBF in sodium depleted subjects and "paralyses" the vasoconstrictor response to LBNP. Sodium 136-142 angiotensinogen Homo sapiens 27-33 3553473-0 1986 Natriuresis and the renin axis in sodium-sensitive man. Sodium 34-40 renin Homo sapiens 20-25 3553473-3 1986 Sodium-sensitive individuals had lower renin values than those who were resistant to sodium. Sodium 0-6 renin Homo sapiens 39-44 3553473-5 1986 Sodium-sensitive subjects exhibited greater aldosterone responses to renin stimulation after volume depletion than resistant subjects. Sodium 0-6 renin Homo sapiens 69-74 3553473-6 1986 Sodium sensitivity is associated with exaggerated natriuresis as well as tighter coupling between renin and aldosterone. Sodium 0-6 renin Homo sapiens 98-103 2946838-0 1986 Role of atrial natriuretic peptide in sodium homeostasis in premature infants. Sodium 38-44 natriuretic peptide A Homo sapiens 8-34 3793196-0 1986 Regulation of primate angiotensin II receptors during altered sodium intake. Sodium 62-68 angiotensinogen Rattus norvegicus 22-36 3793196-1 1986 In the rat, angiotensin II receptors of the adrenal glomerulosa and smooth muscle undergo reciprocal regulatory changes that parallel the changes in target cell sensitivity to angiotensin II during altered sodium intake. Sodium 206-212 angiotensinogen Rattus norvegicus 12-26 3793196-1 1986 In the rat, angiotensin II receptors of the adrenal glomerulosa and smooth muscle undergo reciprocal regulatory changes that parallel the changes in target cell sensitivity to angiotensin II during altered sodium intake. Sodium 206-212 angiotensinogen Rattus norvegicus 176-190 2946839-2 1986 Changes in the plasma concentration of ANF were then correlated with postnatal age, severity of respiratory distress, and water and sodium balance. Sodium 132-138 natriuretic peptide A Homo sapiens 39-42 3793196-2 1986 In primates, the relative importance of angiotensin II receptor regulation during sodium-induced changes in angiotensin II sensitivity is not clear. Sodium 82-88 angiotensinogen Rattus norvegicus 108-122 3793196-4 1986 Consistent with the decreased pressor response to angiotensin II, smooth muscle angiotensin II receptors were fewer in sodium-restricted monkeys (93 +/- 17 fmol/mg) than in sodium-loaded monkeys (171 +/- 6 fmol/mg). Sodium 119-125 angiotensinogen Rattus norvegicus 80-94 3625541-15 1986 Arginine vasopressin administered at 12 mu u./min induced plasma hormone levels of 1.54 +/- 0.09 mu u./ml and produced a large antidiuresis and small increase in the rate of sodium excretion. Sodium 174-180 arginine vasopressin Rattus norvegicus 9-20 3793196-5 1986 However, in contrast to the rat, changes in zona glomerulosa angiotensin II receptors in monkey adrenal were similar to those in smooth muscle, decreasing with sodium restriction and increasing with sodium loading (344 +/- 64 and 660 +/- 68 fmol/mg, respectively). Sodium 160-166 angiotensinogen Rattus norvegicus 61-75 3793196-5 1986 However, in contrast to the rat, changes in zona glomerulosa angiotensin II receptors in monkey adrenal were similar to those in smooth muscle, decreasing with sodium restriction and increasing with sodium loading (344 +/- 64 and 660 +/- 68 fmol/mg, respectively). Sodium 199-205 angiotensinogen Rattus norvegicus 61-75 3625542-0 1986 A synergistic effect of oxytocin and vasopressin on sodium excretion in the neurohypophysectomized rat. Sodium 52-58 arginine vasopressin Rattus norvegicus 37-48 3625542-14 1986 Arginine vasopressin administration (12 microunits/min) inducing plasma levels of 1.24 +/- 0.08 microunit/ml, reduced urine flow by 80% and produced a small increase in sodium excretion. Sodium 169-175 arginine vasopressin Rattus norvegicus 9-20 3625542-18 1986 Combined hormone administration at the lower rate of 5 microunits/min oxytocin and 4 microunits/min vasopressin produced a similar large increment in sodium excretion. Sodium 150-156 arginine vasopressin Rattus norvegicus 100-111 3532893-6 1986 Calcium-regulating hormones and the renin-aldosterone system may coordinately mediate the blood pressure effects of differing dietary calcium and sodium intakes at the cellular level by altering cellular handling of monovalent and divalent ions. Sodium 146-152 renin Homo sapiens 36-41 3792454-0 1986 Arginine vasopressin innoculates against age-related increases in sodium-dependent high affinity choline uptake and discrepancies in the content of temporal memory. Sodium 66-72 arginine vasopressin Rattus norvegicus 9-20 2948752-0 1986 Effect of dietary sodium on plasma concentration of immunoreactive atrial natriuretic factor in normal humans. Sodium 18-24 natriuretic peptide A Homo sapiens 67-92 2948752-5 1986 Plasma immunoreactive ANF was 47.9 +/- 4.8 pg/ml on the low-sodium diet and rose to 68.1 +/- 5.9 pg/ml on the high-sodium diet (p less than 0.01). Sodium 60-66 natriuretic peptide A Homo sapiens 22-25 2948752-5 1986 Plasma immunoreactive ANF was 47.9 +/- 4.8 pg/ml on the low-sodium diet and rose to 68.1 +/- 5.9 pg/ml on the high-sodium diet (p less than 0.01). Sodium 115-121 natriuretic peptide A Homo sapiens 22-25 2948752-6 1986 These results demonstrate that secretion of ANF by the heart may be modulated by the changes produced by extreme variations in sodium intake. Sodium 127-133 natriuretic peptide A Homo sapiens 44-47 2945832-4 1986 In NL, ANF infusion of 0.10 microgram/kg per min (40 pmol/kg per min) induced increases (P less than 0.05) of absolute (from 160 +/- 23 to 725 +/- 198 mueq/min) and fractional (1-4%) sodium excretion, urine flow rate (from 10 +/- 1.6 to 20 +/- 2.6 ml/min), osmolar (from 3.2 +/- 0.6 to 6.8 +/- 1.2 ml/min) and free water (from 6.8 +/- 1.6 to 13.6 +/- 1.6 ml/min) clearances, and filtration fraction (from 20 +/- 1 to 26 +/- 2%). Sodium 183-189 natriuretic peptide A Homo sapiens 7-10 3021923-2 1986 Abnormally high ambulatory plasma renin activity was seen in 14 of 19 patients with 24-hour urine sodium excretion greater than 50 mEq. Sodium 98-104 renin Homo sapiens 34-39 3481117-1 1987 The effect of vasoactive intestinal peptide (VIP), secretin, and VIP-secretin (Ala4, Val5-secretin) on the net movements of sodium, potassium, fluid, and mucus was investigated in the rat colon perfused in vivo. Sodium 124-130 vasoactive intestinal peptide Rattus norvegicus 65-68 3760114-1 1986 To study the role of calcium movements in mediating the effects of sodium chloride on the response of plasma aldosterone to angiotensin II (AII), we administered calcium channel-blocking drugs (nifedipine and diltiazem) and calcium infusions to normal subjects during high and low sodium intakes before and after AII infusion. Sodium 67-73 angiotensinogen Homo sapiens 124-138 3760114-1 1986 To study the role of calcium movements in mediating the effects of sodium chloride on the response of plasma aldosterone to angiotensin II (AII), we administered calcium channel-blocking drugs (nifedipine and diltiazem) and calcium infusions to normal subjects during high and low sodium intakes before and after AII infusion. Sodium 67-73 angiotensinogen Homo sapiens 140-143 3760114-2 1986 AII was also infused in 13 patients with essential hypertension eating a high sodium diet. Sodium 78-84 angiotensinogen Homo sapiens 0-3 3760114-9 1986 Calcium infusion increased the aldosterone sensitivity to AII during the low sodium diet, but not during the high sodium diet. Sodium 77-83 angiotensinogen Homo sapiens 58-61 3760114-10 1986 The results suggest that in normal subjects, increased plasma aldosterone responses to AII induced by reduction in sodium intake are partially mediated by increased extracellular to intracellular calcium movements, since they are blocked by the structurally different calcium channel-blocking drugs nifedipine and diltiazem. Sodium 115-121 angiotensinogen Homo sapiens 87-90 3760114-11 1986 In hypertensive patients eating a high sodium diet, increased aldosterone responses to AII infusion were blocked by nifedipine, indicating that they are at least partly mediated by increased extracellular to intracellular calcium flux. Sodium 39-45 angiotensinogen Homo sapiens 87-90 3794328-0 1986 Plasma vasopressin concentration in high sodium renal hypertension. Sodium 41-47 arginine vasopressin Rattus norvegicus 7-18 2950253-2 1986 Experimental subjects were rats with hypertension made by chronic infusion of vasopressin on regular intakes of sodium or on sodium loading with 1% NaCl as drinking water. Sodium 112-118 arginine vasopressin Rattus norvegicus 78-89 3794328-7 1986 These results provide further evidence for a contribution of vasopressin to sodium-dependent hypertension. Sodium 76-82 arginine vasopressin Rattus norvegicus 61-72 3533999-0 1986 Sodium regulation of angiotensinogen mRNA expression in rat kidney cortex and medulla. Sodium 0-6 angiotensinogen Rattus norvegicus 21-36 3533999-4 1986 Densitometric analysis of Northern blots demonstrated that renal cortical angiotensinogen mRNA concentrations increased 3.5-fold (P less than 0.001) and medulla, 1.5-fold (P less than 0.005) on low sodium compared with high sodium diet, whereas renal cortex renin mRNA levels increased 6.8-fold (P less than 0.0005). Sodium 198-204 angiotensinogen Rattus norvegicus 74-89 3533999-4 1986 Densitometric analysis of Northern blots demonstrated that renal cortical angiotensinogen mRNA concentrations increased 3.5-fold (P less than 0.001) and medulla, 1.5-fold (P less than 0.005) on low sodium compared with high sodium diet, whereas renal cortex renin mRNA levels increased 6.8-fold (P less than 0.0005). Sodium 224-230 angiotensinogen Rattus norvegicus 74-89 3533999-6 1986 These findings provide evidence for sodium regulation of renal renin and angiotensinogen mRNA expressions, which supports potential existence of an intrarenally regulated RAS and suggest that different factors regulate renal and hepatic angiotensinogen. Sodium 36-42 angiotensinogen Rattus norvegicus 73-88 3533999-6 1986 These findings provide evidence for sodium regulation of renal renin and angiotensinogen mRNA expressions, which supports potential existence of an intrarenally regulated RAS and suggest that different factors regulate renal and hepatic angiotensinogen. Sodium 36-42 angiotensinogen Rattus norvegicus 237-252 3795712-5 1986 Changes in renin-angiotensin-aldosterone activity showed close correlation with changes in sodium balance. Sodium 91-97 renin Homo sapiens 11-16 2878464-6 1986 However, enhancement of the plasma renin activity and plasma aldosterone concentration responses by prior sodium depletion of the sheep by furosemide administration or suppression of the plasma renin activity and plasma aldosterone concentration responses by prior salt loading did not influence the magnitude of the hypotension-induced hypokalaemia. Sodium 106-112 renin Ovis aries 35-40 2441907-7 1986 These findings may explain the hypokalaemic and sodium retaining effects of insulin in man; they may also partially explain the raised Na+ efflux rate constants in obesity. Sodium 48-54 insulin Homo sapiens 76-83 2945562-0 1986 Inhibitory roles of the hypothalamic atrial natriuretic polypeptide on the vasopressin release in the sodium-loaded rats. Sodium 102-108 arginine vasopressin Rattus norvegicus 75-86 2945562-2 1986 Sodium loading increased not only the blood pressure but also the urinary output of vasopressin significantly. Sodium 0-6 arginine vasopressin Rattus norvegicus 84-95 2945562-7 1986 These results indicate that the vasopressin production in the hypothalamus is increased, but the release is relatively suppressed in the sodium-loaded rats, and that increased hypothalamic atrial natriuretic polypeptide is involved in the suppression of the vasopressin release and in decreasing their sodium appetite to avoid the high sodium environment. Sodium 137-143 arginine vasopressin Rattus norvegicus 258-269 2945562-7 1986 These results indicate that the vasopressin production in the hypothalamus is increased, but the release is relatively suppressed in the sodium-loaded rats, and that increased hypothalamic atrial natriuretic polypeptide is involved in the suppression of the vasopressin release and in decreasing their sodium appetite to avoid the high sodium environment. Sodium 302-308 arginine vasopressin Rattus norvegicus 32-43 2875660-6 1986 When the ganglionic blocker pentolinium tartrate was given to sodium-depleted rats the pressor response to AVP was restored to control levels. Sodium 62-68 arginine vasopressin Rattus norvegicus 107-110 2875660-0 1986 Pressor resistance to vasopressin in sodium depletion, potassium depletion, and cirrhosis. Sodium 37-43 arginine vasopressin Rattus norvegicus 22-33 3022372-1 1986 Angiotensin I converting enzyme inhibition by captopril and enalapril may influence sodium and potassium homeostasis. Sodium 84-90 angiotensin I converting enzyme Homo sapiens 0-31 2875660-10 1986 We conclude that resistance to the pressor action of AVP in sodium depletion was secondary to resetting of the baroreceptors. Sodium 60-66 arginine vasopressin Rattus norvegicus 53-56 2875660-1 1986 Resistance to the pressor effects of angiotensin II, but not norepinephrine, has been observed in sodium depletion, potassium depletion, and cirrhosis. Sodium 98-104 angiotensinogen Rattus norvegicus 37-51 2875660-4 1986 In conscious rats, the pressor response to graded doses of AVP was reduced in sodium depletion by 27-43% compared with control rats. Sodium 78-84 arginine vasopressin Rattus norvegicus 59-62 2944381-6 1986 The renin-angiotensin-aldosterone system and the sympathetic nervous system, which are activated in most cirrhotic patients with ascites, and a nonosmotic hypersecretion of antidiuretic hormone are important mechanisms of sodium and water retention. Sodium 222-228 renin Homo sapiens 4-9 2947978-5 1986 Toward the other end of the spectrum, revealed by the finding of low plasma renin, a sodium-volume-induced form of vasoconstriction operates. Sodium 85-91 renin Homo sapiens 76-81 2944688-2 1986 We have investigated whether this enhanced sodium excretion could be mediated by the recently discovered natriuretic factor, atrial natriuretic peptide (ANP). Sodium 43-49 natriuretic peptide A Homo sapiens 125-151 2944688-2 1986 We have investigated whether this enhanced sodium excretion could be mediated by the recently discovered natriuretic factor, atrial natriuretic peptide (ANP). Sodium 43-49 natriuretic peptide A Homo sapiens 153-156 2943848-6 1986 The increase in concentration of ANP in plasma between dialyses, at a time when many patients are susceptible to sodium and water overload, and its return towards normal after dialysis supports the putative role of ANP as a circulating factor released in response to sodium and water accumulation. Sodium 113-119 natriuretic peptide A Homo sapiens 33-36 2943356-4 1986 Concentrations of both atrial natriuretic peptide and renin showed significant inverse relations with serum sodium concentrations. Sodium 108-114 renin Homo sapiens 54-59 2943848-6 1986 The increase in concentration of ANP in plasma between dialyses, at a time when many patients are susceptible to sodium and water overload, and its return towards normal after dialysis supports the putative role of ANP as a circulating factor released in response to sodium and water accumulation. Sodium 267-273 natriuretic peptide A Homo sapiens 33-36 2943848-6 1986 The increase in concentration of ANP in plasma between dialyses, at a time when many patients are susceptible to sodium and water overload, and its return towards normal after dialysis supports the putative role of ANP as a circulating factor released in response to sodium and water accumulation. Sodium 267-273 natriuretic peptide A Homo sapiens 215-218 3014903-8 1986 More interestingly, the number of spleen vasopressin binding sites was always lower in Dahl salt-resistant animals than in the Dahl salt-sensitive animals receiving either a sodium deficient or a 1% NaCl or an 8% NaCl-containing diet. Sodium 174-180 arginine vasopressin Rattus norvegicus 41-52 3531301-7 1986 Fetal plasma renin activity was inversely related to fetal plasma sodium levels (P less than 0.01). Sodium 66-72 renin Homo sapiens 13-18 2874211-0 1986 Development of high sodium renal hypertension during chronic blockade of the vascular effects of vasopressin. Sodium 20-26 arginine vasopressin Rattus norvegicus 97-108 3017033-11 1986 This may be different in states of sodium depletion with reduced vascular effects of AII. Sodium 35-41 angiotensinogen Homo sapiens 85-88 3026272-9 1986 These receptors are modulated by sodium intake and the difference in receptor number between S and R rats could explain the increased vascular reactivity of S animals to vasopressin. Sodium 33-39 arginine vasopressin Rattus norvegicus 170-181 2874211-1 1986 Studies in sodium-dependent models of hypertension have shown that arginine-vasopressin (AVP) plays an important role in the maintenance of blood pressure, predominantly through its vasoconstrictor action. Sodium 11-17 arginine vasopressin Rattus norvegicus 76-87 3521337-0 1986 Control of sodium excretion by angiotensin II: intrarenal mechanisms and blood pressure regulation. Sodium 11-17 angiotensinogen Homo sapiens 31-45 3457670-7 1986 A significant increase in fractional sodium clearance of approximately 50% occurred during the AVP infusions, which was abolished after pretreatment with indomethacin. Sodium 37-43 arginine vasopressin Homo sapiens 95-98 3531413-4 1986 Moderate reduction of sodium intake is additive to the effect of blood-pressure-lowering drugs, particularly those that block the renin-angiotensin system such as beta-blockers and converting enzyme inhibitors. Sodium 22-28 renin Homo sapiens 130-135 3099713-0 1986 [Effects of aldosterone and vasopressin on transmembrane efflux of sodium from the arterial wall]. Sodium 67-73 arginine vasopressin Rattus norvegicus 28-39 3522418-8 1986 In both groups sodium-sensitive individuals were significantly older (p less than 0.001) and had lower baseline renin values than sodium-resistant subjects. Sodium 15-21 renin Homo sapiens 112-117 2941538-2 1986 In this endocrine control, the renin axis provides the primary defence against sodium volume depletion and hypotension while atrial hormone plays an increasingly active counter-role for coping with situations that involve a sodium-volume surfeit or rising blood volume or blood pressure levels. Sodium 79-85 renin Homo sapiens 31-36 2425177-6 1986 This facilitation by angiotensin II in SHR can be altered by placement of the rats (5-6, 10-11 week-old) on a sodium-restricted diet. Sodium 110-116 angiotensinogen Rattus norvegicus 21-35 3517066-5 1986 Both renin-angiotensin system and sympathetic nervous system activity were greater during the 10 meq diet, and suppressed with the 100 meq sodium diet. Sodium 139-145 renin Homo sapiens 5-10 3517066-6 1986 For both diets, plasma renin and urinary aldosterone excretion were correlated with urinary sodium excretion (r = -0.768, r = -0.726, respectively; P less than 0.005). Sodium 92-98 renin Homo sapiens 23-28 3735922-7 1986 Therefore, blood Prl decrease leads to sodium retention in hyperprolactinemic hypertensive patients that may have an adverse pathogenetic significance. Sodium 39-45 prolactin Homo sapiens 17-20 3013653-0 1986 Angiotensin-converting enzyme responses following enalapril in the sodium deficient rat. Sodium 67-73 angiotensin I converting enzyme Rattus norvegicus 0-29 3013653-6 1986 Thus it appears that inhibition of ACE activity in both plasma and tissue contributes to the blood pressure lowering activity of enalapril in the sodium deficient normotensive rat. Sodium 146-152 angiotensin I converting enzyme Rattus norvegicus 35-38 3518053-7 1986 Thus, in cirrhotic alcoholic patients with ascites the determination of daily urinary sodium excretion, which is inversely related to the activity of the renin-angiotensin system, provides a useful prognostic index for the response to salt restriction and longterm survival. Sodium 86-92 renin Homo sapiens 154-159 3007502-0 1986 Parathyroid hormone increases sodium/calcium exchange activity in renal cells and the blunting of the response in aging. Sodium 30-36 parathyroid hormone Rattus norvegicus 0-19 3514280-0 1986 Regulation of glomerular filtration rate and sodium excretion by angiotensin II. Sodium 45-51 angiotensinogen Homo sapiens 65-79 3011198-0 1986 Sodium increases angiotensin II receptors in neuronal cultures from brains of normotensive and hypertensive rats. Sodium 0-6 angiotensinogen Rattus norvegicus 17-31 3011198-4 1986 Neuronal cultures from SH rat brains showed a similar sodium-stimulated increase in Ang II binding; however this increase was 150% greater than that observed in neuronal cultures from WKY rat brain. Sodium 54-60 angiotensinogen Rattus norvegicus 84-90 3011198-5 1986 Kinetic studies of the effects of sodium ions on both WKY and SH neuronal cultures showed an increase in the dissociation of 125I-Ang II from its receptors in the presence of sodium ions. Sodium 34-40 angiotensinogen Rattus norvegicus 130-136 3011198-5 1986 Kinetic studies of the effects of sodium ions on both WKY and SH neuronal cultures showed an increase in the dissociation of 125I-Ang II from its receptors in the presence of sodium ions. Sodium 175-181 angiotensinogen Rattus norvegicus 130-136 3011198-6 1986 In addition, Scatchard analysis revealed that the increase in binding caused by sodium was due to an increase in the number of Ang II receptors. Sodium 80-86 angiotensinogen Rattus norvegicus 127-133 3011198-7 1986 These observations indicate that sodium ions increase the number of Ang II specific receptors in intact neuronal cells and that this stimulation was more pronounced in neuronal cells from SH rat brains compared with WKY controls. Sodium 33-39 angiotensinogen Rattus norvegicus 68-74 2938871-4 1986 Sodium excretion trebled (P = less than 0.005) during the infusion of a calculated dose of 15 pmol of alpha-h-ANP min-1 kg-1 and there was an accompanying diuresis; radioimmunoassay of plasma alpha-h-ANP during the natriuresis indicated a mean peak incremental concentration of 203 +/- 78 (SEM) pmol/l. Sodium 0-6 CD59 molecule (CD59 blood group) Homo sapiens 114-124 3963083-0 1986 Sodium excretion in human pregnancy: a role for arginine vasopressin. Sodium 0-6 arginine vasopressin Homo sapiens 57-68 3963083-2 1986 A significant rise in plasma arginine vasopressin was observed only in second-trimester subjects following sodium loading (5.6 +/- 0.5 to 6.6 +/- 0.5 pg/ml; p less than 0.05). Sodium 107-113 arginine vasopressin Homo sapiens 38-49 3963083-5 1986 It is suggested that arginine vasopressin secretion increases to assist natriuresis following dietary sodium loading in the second trimester of human pregnancy. Sodium 102-108 arginine vasopressin Homo sapiens 30-41 3524920-5 1986 The basic abnormality is excessive renal sodium retention, leading to chronic suppression of renin and aldosterone; the latter is then hyporesponsive to the hyperkalaemic stimulus. Sodium 41-47 renin Homo sapiens 93-98 3514728-3 1986 Plasma vasopressin concentration correlated with the percent decrease of systemic vascular resistance (r = 0.70, p less than 0.025), serum sodium (r = 0.72, p less than 0.02) and serum creatinine (r = 0.85, p less than 0.005). Sodium 139-145 arginine vasopressin Homo sapiens 7-18 3514728-6 1986 Levels of plasma renin activity ranged between 1 and 46 ng/ml per h (average 14.7 +/- 5.7) and correlated with serum sodium (r = 0.77, p less than 0.025), serum creatinine (r = 0.73, p less than 0.025) and right atrial pressure (r = 0.67, p less than 0.05). Sodium 117-123 renin Homo sapiens 17-22 3514280-4 1986 The sodium-retaining action of AngII may be due, in part, to constriction of efferent arterioles and to subsequent changes in peritubular capillary physical forces. Sodium 4-10 angiotensinogen Homo sapiens 31-36 3514280-5 1986 However, AngII may also directly stimulate sodium reabsorption in proximal and distal tubules, although the exact site at which AngII increases distal tubular transport is still uncertain. Sodium 43-49 angiotensinogen Homo sapiens 9-14 3082358-0 1986 Insulin-stimulated sodium transport in toad urinary bladder. Sodium 19-25 insulin Homo sapiens 0-7 3514280-7 1986 Thus, the intrarenal effects of AngII provide a mechanism for stabilizing the GFR and excretion of metabolic waste products while causing sodium and water retention, thereby helping to regulate body fluid volumes and arterial pressure. Sodium 138-144 angiotensinogen Homo sapiens 32-37 3519007-1 1986 To clarify age-related changes in the plasma renin activity (PRA)-aldosterone (ALDO) system in relation to urinary sodium (Na) excretion in pseudohypoaldosteronism type I (PHA), we followed a patient with PHA serially by measuring the hormonal balance and urinary electrolyte excretion for 5 years. Sodium 115-121 renin Homo sapiens 45-50 3007237-4 1986 We have recently demonstrated that sodium ions are essential for dopaminergic inhibitory action on PRL secretion. Sodium 35-41 prolactin Rattus norvegicus 99-102 3004605-1 1986 Previous studies by other investigators have shown that sodium depletion causes down-regulation of angiotensin II receptors in renal glomeruli, which is ascribed to elevation of circulating angiotensin II levels. Sodium 56-62 angiotensinogen Rattus norvegicus 99-113 3004605-1 1986 Previous studies by other investigators have shown that sodium depletion causes down-regulation of angiotensin II receptors in renal glomeruli, which is ascribed to elevation of circulating angiotensin II levels. Sodium 56-62 angiotensinogen Rattus norvegicus 190-204 3511737-0 1986 Interference with central actions of angiotensin II suppresses sodium appetite. Sodium 63-69 angiotensinogen Rattus norvegicus 37-51 3511737-1 1986 We have proposed that sodium appetite is aroused by a synergy in the brain of angiotensin II and aldosterone. Sodium 22-28 angiotensinogen Rattus norvegicus 78-92 3513604-0 1986 Sodium requirement for insulin release: putative role in regulation of intracellular pH. Sodium 0-6 insulin Homo sapiens 23-30 3511737-6 1986 These results offer compelling evidence for the idea that angiotensin II action in the brain is necessary for expression of sodium appetite. Sodium 124-130 angiotensinogen Rattus norvegicus 58-72 3950526-0 1986 Vasopressin secretion in normotensive black and white men and women on normal and low sodium diets. Sodium 86-92 arginine vasopressin Homo sapiens 0-11 3002660-6 1986 This interaction between serum sodium concentration, drug treatment, and long-term outcome suggests that the renin-angiotensin system may exert a deleterious effect on the survival of some patients with chronic heart failure, which can be antagonized by converting enzyme inhibition, and provides a clinical counterpart for the similar prognostic role that has been postulated for angiotensin II in experimental preparations of heart failure. Sodium 31-37 renin Homo sapiens 109-114 3002660-6 1986 This interaction between serum sodium concentration, drug treatment, and long-term outcome suggests that the renin-angiotensin system may exert a deleterious effect on the survival of some patients with chronic heart failure, which can be antagonized by converting enzyme inhibition, and provides a clinical counterpart for the similar prognostic role that has been postulated for angiotensin II in experimental preparations of heart failure. Sodium 31-37 angiotensinogen Homo sapiens 381-395 3950526-2 1986 During the normal sodium diet, the 24-h urinary excretion of vasopressin was significantly (P less than 0.05) higher in men than in women and higher (P less than 0.05) in black than in white subjects. Sodium 18-24 arginine vasopressin Homo sapiens 61-72 3950526-5 1986 Reduction in sodium intake resulted in a significantly (P less than 0.01) decreased excretion of vasopressin in all groups except black women, but had no effect on plasma vasopressin concentrations. Sodium 13-19 arginine vasopressin Homo sapiens 97-108 2943142-2 1986 Renin release may result from one of several different stimuli: renal tubular sodium delivery and sensing by the macula densa, sympathetic nervous system activity, and baroreceptor to changes in renal blood flow. Sodium 78-84 renin Homo sapiens 0-5 3703019-0 1986 Sodium-dependence of the saturability of carrier-mediated noradrenaline efflux from noradrenergic neurones in the rat vas deferens. Sodium 0-6 arginine vasopressin Rattus norvegicus 118-121 3017059-13 1986 Low serum sodium values increase and azotemia may be corrected, if ACE inhibitor doses are carefully titrated to avoid severe hypotension. Sodium 10-16 angiotensin I converting enzyme Homo sapiens 67-70 2870138-2 1986 Our results show that L-Glu is taken up by a sodium-dependent, high-affinity uptake system with a Km = 8 +/- 3.5 X 10(-6) M and a Vmax = 48 +/- 14 X 10(-12) mol/min/mg protein; 3H-L-Glu or 3H-L- and D-Asp are taken up and accumulated by rod somata and inner segments in retinas incubated at 37 degrees C or at ambient temperature; cones accumulate 3H-L-Glu at ambient temperature but not at 37 degrees C. Neither 3H-L-Asp nor D-Asp is accumulated by cones at either temperature; rods and cones show the same labeling pattern irrespective of whether they are located in the central or peripheral retina; and antiserum to AAT preferentially stains the cone somata, inner segments, and synaptic pedicles, while the outer segments are negative. Sodium 45-51 serpin family A member 1 Homo sapiens 620-623 2943142-9 1986 In an analysis of the factors that may result in renin release, tubular delivery of sodium to the macula densa may emerge as the most important regulator of renin release. Sodium 84-90 renin Homo sapiens 49-54 2943142-9 1986 In an analysis of the factors that may result in renin release, tubular delivery of sodium to the macula densa may emerge as the most important regulator of renin release. Sodium 84-90 renin Homo sapiens 157-162 3535395-4 1986 Plasma renin concentration increased four-fold during sodium depletion (p less than 0.001). Sodium 54-60 renin Homo sapiens 7-12 3953317-3 1986 AII and Aldo were normal before sodium loading and suppressed after saline in PKD patients and controls. Sodium 32-38 angiotensinogen Homo sapiens 0-3 3535395-8 1986 Thus, during sodium restriction in middle-aged hypertensive men, blood pressure reduction occurs concomitantly with inhibited vasopressin release, despite enhanced renin and catecholamine release. Sodium 13-19 arginine vasopressin Homo sapiens 126-137 3766163-5 1986 After sodium loading significant decrease of PRA (-83%), prostaglandin excretion (-34%), insignificant decrease of aldosterone and kallikrein excretion and significant increase of vasopressin (134%) were established. Sodium 6-12 arginine vasopressin Rattus norvegicus 180-191 3947689-3 1986 Plasma PRL proved to be significantly higher in the edematous group (11.0 +/- 1.9 vs. 4.2 +/- 3.1 U/l, p less than 0.01) but it remained unaltered by furosemide challenge (8.5 +/- 1.5 U/l) in spite of the marked elevation of urine flow and sodium excretion. Sodium 240-246 prolactin Homo sapiens 7-10 2939792-7 1986 In this construction the renin system acts primarily to defend sodium balance and blood pressure, with the atrial hormone playing an increasingly active counterpart in situations involving sodium-volume surfeit and/or high blood pressure. Sodium 63-69 renin Homo sapiens 25-30 3006712-5 1986 showed an increase in urinary excretion of bradykinin accompanied by increases in urinary water and sodium excretion. Sodium 100-106 kininogen 1 Canis lupus familiaris 43-53 3530563-9 1986 Patients who responded to sodium restriction had a lower initial renin value than other patients. Sodium 26-32 renin Homo sapiens 65-70 3530563-10 1986 This study emphasises the importance of the interaction between sodium, potassium and renin in the determination of blood pressure levels. Sodium 64-70 renin Homo sapiens 86-91 2946586-3 1986 The constant ANP infusion caused a delayed and prolonged excretion of sodium, chloride and calcium, no change in potassium or phosphate excretion or in glomerular filtration rate but a marked decrease in renal plasma flow. Sodium 70-76 natriuretic peptide A Homo sapiens 13-16 3957560-2 1986 Plasma renin activity was very high (median 29.0 ng/ml/hr) at admission, decreased after equilibration with a normal sodium diet (9.9 ng/ml/hr) and was negatively correlated with urinary sodium excretion. Sodium 117-123 renin Homo sapiens 7-12 3957560-2 1986 Plasma renin activity was very high (median 29.0 ng/ml/hr) at admission, decreased after equilibration with a normal sodium diet (9.9 ng/ml/hr) and was negatively correlated with urinary sodium excretion. Sodium 187-193 renin Homo sapiens 7-12 2434767-1 1986 Vasopressin increases the permeability of responsive epithelia for a variety of chemical species, such as sodium, urea, water, and lipophilic molecules. Sodium 106-112 arginine vasopressin Homo sapiens 0-11 3554904-5 1986 Thus, vasopressin was the only pressor hormone which varied directly with sodium intake, blood pressure and body weight during sodium depletion. Sodium 74-80 arginine vasopressin Homo sapiens 6-17 3554904-5 1986 Thus, vasopressin was the only pressor hormone which varied directly with sodium intake, blood pressure and body weight during sodium depletion. Sodium 127-133 arginine vasopressin Homo sapiens 6-17 3716879-6 1986 The decrease in urinary sodium excretion was associated with increases in plasma renin activity and urinary aldosterone excretion, while a sympathetic nervous natriuretic index (urinary dopamine to noradrenaline excretion ratio) decreased. Sodium 24-30 renin Homo sapiens 81-86 3716879-11 1986 We conclude that moderate sodium restriction lowered the blood pressure and affected the renin-aldosterone and sympathetic nervous system to retain sodium which might explain the constancy of the plasma volume. Sodium 26-32 renin Homo sapiens 89-94 3716879-11 1986 We conclude that moderate sodium restriction lowered the blood pressure and affected the renin-aldosterone and sympathetic nervous system to retain sodium which might explain the constancy of the plasma volume. Sodium 148-154 renin Homo sapiens 89-94 3828578-4 1986 Sodium-depleted rats required 3.5 and 2.4 times larger dose of norepinephrine and angiotensin II, respectively, than the control rats to produce an increase in MAP of 20-25 mmHg. Sodium 0-6 angiotensinogen Rattus norvegicus 82-96 2952486-17 1986 However, since peripheral resistance was not changed, another non-renin, sodium-related mechanism must take over to sustain increased arterial constriction. Sodium 73-79 renin Homo sapiens 66-71 2422491-10 1986 We conclude that enalapril in essential hypertension alleviates the angiotensin-II-mediated abnormalities in renal hemodynamics and sodium excretion. Sodium 132-138 angiotensinogen Homo sapiens 68-82 2422494-4 1986 Because of the activation of the renin-angiotensin system, angiotensin-mediated vasoconstriction and aldosterone-mediated sodium retention can be suppressed and, in some individuals, completely blocked by converting enzyme inhibitors. Sodium 122-128 renin Homo sapiens 33-38 2438484-7 1986 Tissue-specific regulation of angiotensinogen mRNA is also observed when rats are placed on a low-sodium diet. Sodium 98-104 angiotensinogen Rattus norvegicus 30-45 2438484-8 1986 Sodium depletion stimulates renin angiotensinogen mRNA expression but does not influence hepatic angiotensinogen mRNA levels. Sodium 0-6 angiotensinogen Rattus norvegicus 34-49 2438485-2 1986 Addition of ANG II to the serosal surface of isolated segments of rat jejunum significantly increased sodium and water absorption. Sodium 102-108 angiotensinogen Rattus norvegicus 12-18 2948056-5 1986 After initiation of pulsatile nocturnal treatment (5 pulses of 30 micrograms ANP every 3 h), diuresis increased, leading to a persistent normalization of sodium and chloride excretion. Sodium 154-160 natriuretic peptide A Homo sapiens 77-80 3080471-2 1986 Our previous studies in cortical collecting ducts isolated from rat kidneys have shown that vasopressin increases both sodium absorption and potassium secretion, while bradykinin inhibits sodium absorption without affecting potassium transport. Sodium 119-125 arginine vasopressin Rattus norvegicus 92-103 2948064-8 1986 ANP-secretion is stimulated during sodium retention induced by mineralocorticoids, however ANP does not seem to trigger the escape mechanism. Sodium 35-41 natriuretic peptide A Homo sapiens 0-3 3944536-5 1986 We conclude that, in man, AVP is selectively secreted in response to both dehydration and high sodium intake, whilst even after the stimulus of rapidly increasing plasma osmolality during intravenous infusion of hypertonic saline the rise in oxytocin is not statistically significant. Sodium 95-101 arginine vasopressin Homo sapiens 26-29 2425102-2 1986 Recently, we have shown that aprotinin, a kallikrein inhibitor, inhibits the stimulation of plasma renin activity (PRA) by either furosemide or a low sodium diet. Sodium 150-156 renin Homo sapiens 99-104 2425102-9 1986 These results suggest that both renal kallikrein and prostaglandins play an important role in the control of renin release under sodium depletion. Sodium 129-135 renin Homo sapiens 109-114 3866691-7 1985 PGE2-induced sodium and chloride secretion were also significantly reduced by NPY at an infusion rate of 0.4 but not of 0.04 pmol X min-1. Sodium 13-19 neuropeptide Y Rattus norvegicus 78-81 3765573-6 1986 The changes in plasma sodium of the subgroups of patients with essential hypertension are accompanied by certain deviations in hemodynamics, in plasma aldosterone and in plasma renin activity. Sodium 22-28 renin Homo sapiens 177-182 2866706-3 1985 When sodium intake is restricted or a diuretic is used, the reactive increase in plasma renin activity makes a substantial contribution to limiting the blood pressure fall. Sodium 5-11 renin Homo sapiens 88-93 2866707-1 1985 The renin-angiotensin-aldosterone system regulates blood pressure and volume homeostasis in addition to sodium and potassium metabolism, and may be linked to divalent cation metabolism as well as hypertensive disease. Sodium 104-110 renin Homo sapiens 4-9 4073288-3 1985 AVP secretion in response to osmotic stimuli also was significantly blunted, although sufficient increases in plasma AVP levels did occur, in association with an abnormally high range of plasma sodium concentrations, to allow urinary concentration comparable to control animals. Sodium 194-200 arginine vasopressin Rattus norvegicus 0-3 3635150-5 1986 The principal effectors of renal sodium retention and vasoconstriction are stimulation of the renin-angiotensin-aldosterone axis and augmentation of renal sympathetic nerve activity. Sodium 33-39 renin Homo sapiens 94-99 3907740-2 1985 The pressor-response curve to angiotensin II in rats previously on a high sodium intake was shifted to the left of that found in rats previously on a low sodium intake. Sodium 74-80 angiotensinogen Rattus norvegicus 30-44 3907740-2 1985 The pressor-response curve to angiotensin II in rats previously on a high sodium intake was shifted to the left of that found in rats previously on a low sodium intake. Sodium 154-160 angiotensinogen Rattus norvegicus 30-44 4092777-1 1985 Effect of calcitonin (CT) upon the AP of contractile cardiomyocytes was absent under conditions of blockade of beta-adrenoreceptors with inderal which reduced the level of intracellular sodium and ionized calcium. Sodium 186-192 calcitonin related polypeptide alpha Homo sapiens 10-20 2856753-6 1985 The sodium retaining properties of growth hormone may cause a rise of blood pressure in a susceptible minority of acromegalics. Sodium 4-10 growth hormone 1 Homo sapiens 35-49 3006895-3 1985 After sodium depletion, mesenteric artery angiotensin II receptors were down-regulated as expected. Sodium 6-12 angiotensinogen Rattus norvegicus 42-56 4085913-1 1985 An infusion with Ornipressin (8-ornithin vasopressin) in a patient with decompensated alcoholic liver cirrhosis increased urinary volume from 30 ml/h to 500 ml/h, creatinine clearance from 24 to 65 ml/min, and fractional sodium excretion from 0.86% to 11.1%. Sodium 221-227 arginine vasopressin Homo sapiens 41-52 2856715-2 1985 This study employs an in vitro system to examine the relationship between sodium intake and dopamine-induced renin release. Sodium 74-80 renin Ovis aries 109-114 2856760-0 1985 Role of vasopressin in cardiovascular adaptation to sodium depletion in the conscious rat. Sodium 52-58 arginine vasopressin Rattus norvegicus 8-19 2856726-0 1985 The effect of human atrial natriuretic peptide on urinary sodium and urinary dopamine excretion in man. Sodium 58-64 natriuretic peptide A Homo sapiens 20-46 2856726-4 1985 High dose ANP infusion (15 pmol/kg per min) produced an increase in plasma immunoreactive ANP levels of 203 +/- 78 pmol/l and caused the urinary sodium excretion to increase from 3.5 +/- 1.6 to 11.0 +/- 7.4 mmol/30 min period (P < 0.05). Sodium 145-151 natriuretic peptide A Homo sapiens 10-13 2856760-1 1985 The hypothesis that vasopressin participates in cardiovascular adaptation to sodium depletion was examined in male Sprague-Dawley rats studied after 6 days (n = 28) or 4 weeks (n = 28) of low sodium diet. Sodium 77-83 arginine vasopressin Rattus norvegicus 20-31 2856729-7 1985 During sodium restriction, plasma renin activity and urinary aldosterone excretion significantly increased. Sodium 7-13 renin Homo sapiens 34-39 2856760-9 1985 Vasopressin appears to contribute to early but not late cardiovascular adaptation to sodium depletion. Sodium 85-91 arginine vasopressin Rattus norvegicus 0-11 2856782-3 1985 We studied calcium metabolism in essential hypertension and used renin-sodium profiling, which reveals the biochemical heterogeneity of clinical hypertension. Sodium 71-77 renin Homo sapiens 65-70 4095364-0 1985 D-galactose uptake by snail intestine: competitive inhibition by phlorizin and sodium dependence. Sodium 79-85 snail family transcriptional repressor 1 Homo sapiens 22-27 3005558-7 1985 They also demonstrated that in the rat the action of the renal nerves to decrease sodium excretion was dependent on angiotensin II. Sodium 82-88 angiotensinogen Rattus norvegicus 116-130 3003304-5 1985 These individuals have a defect in the way that sodium intake modifies adrenal and renal vascular responses to angiotensin II, resulting in an abnormality in sodium handling. Sodium 48-54 angiotensinogen Homo sapiens 111-125 2932646-1 1985 The renin-angiotensin-aldosterone axis exerts major control over sodium and potassium balance and arterial blood pressure. Sodium 65-71 renin Homo sapiens 4-9 2932646-2 1985 These three functions are continuously regulated by changes in angiotensin II and aldosterone levels in response to wide variations in dietary intake of sodium and potassium. Sodium 153-159 angiotensinogen Homo sapiens 63-77 2932646-3 1985 In addition, changes in intrarenal physical factors cause changes in the supply of distal tubular sodium that, in turn, work to determine sodium and potassium excretion and to modulate the release of renal renin. Sodium 98-104 renin Homo sapiens 206-211 2932646-10 1985 In this construction the renin system primarily defends sodium balance and blood pressure, with the atrial hormone having an increasing counter-influence in situations involving high blood pressure or sodium surfeit. Sodium 56-62 renin Homo sapiens 25-30 4052780-0 1985 Modulation of salt appetite by lateral ventricular infusions of angiotensin II and carbachol during sodium depletion. Sodium 100-106 angiotensinogen Rattus norvegicus 64-78 4052780-1 1985 Infusions of angiotensin II (AII) or carbachol (CBC) into the lateral ventricles of rats which had been depleted of sodium 4 h previously with either furosemide or polyethylene glycol produced significant changes in salt appetite and sodium and water balances relative to rats infused with saline vehicle. Sodium 116-122 angiotensinogen Rattus norvegicus 13-27 4052780-1 1985 Infusions of angiotensin II (AII) or carbachol (CBC) into the lateral ventricles of rats which had been depleted of sodium 4 h previously with either furosemide or polyethylene glycol produced significant changes in salt appetite and sodium and water balances relative to rats infused with saline vehicle. Sodium 234-240 angiotensinogen Rattus norvegicus 13-27 4052780-2 1985 Infusions of AII enhanced the salt appetite and led to rapid retention of both sodium and water. Sodium 79-85 angiotensinogen Rattus norvegicus 13-16 3908312-6 1985 Following a 1-hour infusion of angiotensin II in sodium-depleted and captopril-treated rats, plasma renin concentration decreased by 84% whereas no significant changes in either renal renin concentration or renin mRNA content were observed. Sodium 49-55 angiotensinogen Rattus norvegicus 31-45 3908322-2 1985 Insulin-stimulated renal sodium reabsorption induces expansion of the extracellular volume, increase in cardiac output, and ultimately, hypertension. Sodium 25-31 insulin Homo sapiens 0-7 3003304-5 1985 These individuals have a defect in the way that sodium intake modifies adrenal and renal vascular responses to angiotensin II, resulting in an abnormality in sodium handling. Sodium 158-164 angiotensinogen Homo sapiens 111-125 2865701-3 1985 The high catecholamine values in cirrhotic patients and the activation of the renin angiotensin-aldosterone system suggest the use of beta-blockers to reduce sodium-water retention. Sodium 158-164 renin Homo sapiens 78-83 2864856-1 1985 Relationship to blood pressure, renin-sodium profiles, and antihypertensive therapy. Sodium 38-44 renin Homo sapiens 32-37 3931553-9 1985 This process had an approximate K 1/2 for sodium of 10-20 mM and an approximate maximal rate of 50 nmol Ca mg-1 min-1. Sodium 42-48 CD59 molecule (CD59 blood group) Homo sapiens 112-117 2932471-3 1985 Plasma levels of ANF in healthy volunteers on a low sodium diet were 9.8 +/- 1.4 pmol/liter and increased to 21.9 +/- 3.0 on a high sodium diet. Sodium 52-58 natriuretic peptide A Homo sapiens 17-20 2932471-3 1985 Plasma levels of ANF in healthy volunteers on a low sodium diet were 9.8 +/- 1.4 pmol/liter and increased to 21.9 +/- 3.0 on a high sodium diet. Sodium 132-138 natriuretic peptide A Homo sapiens 17-20 2932471-4 1985 The levels of atrial natriuretic factor correlated directly with urinary sodium and inversely with plasma renin activity and plasma aldosterone levels. Sodium 73-79 natriuretic peptide A Homo sapiens 14-39 2932471-6 1985 These results suggest that atrial natriuretic factor plays an important role in the adaptation to increased sodium intake. Sodium 108-114 natriuretic peptide A Homo sapiens 27-52 2413014-5 1985 The binding of LqTx in vesicles of PC/PE (65:35) is sensitive to both the membrane potential formed by sodium gradients across the reconstituted vesicle membrane and the cation concentration in the extravesicular medium. Sodium 103-109 procollagen C-endopeptidase enhancer Rattus norvegicus 35-40 3902012-6 1985 Angiotensin II was increased by a low sodium diet while a high sodium diet did not affect its content. Sodium 38-44 angiotensinogen Rattus norvegicus 0-14 2864682-8 1985 ACE inhibition reduces symptoms, enhances exercise capacity, and favorably affects sodium, water, and potassium homeostasis in patients with heart failure. Sodium 83-89 angiotensin I converting enzyme Homo sapiens 0-3 2997540-5 1985 In 50-60% of normal or high-renin patients with essential hypertension ACE-inhibitors induce a potentiated acute renal response: renal blood flow and sodium excretion increase more than they do in the remainder of the hypertensives or in normal subjects. Sodium 150-156 angiotensin I converting enzyme Homo sapiens 71-74 2997540-8 1985 ACE-inhibition reverses this failure of the renal blood supply to respond to sodium loading. Sodium 77-83 angiotensin I converting enzyme Homo sapiens 0-3 4064572-7 1985 A ten-fold increase in vasopressin depressed the papillary sodium concentration to a level similar to that in the control group and produced a marked natriuresis. Sodium 59-65 arginine vasopressin Rattus norvegicus 23-34 3898868-3 1985 During osmotic stimulation with hypertonic saline, plasma vasopressin increased in close linear correlation with plasma osmolality or sodium in both groups. Sodium 134-140 arginine vasopressin Homo sapiens 58-69 4030040-7 1985 Although confirmatory data are needed, our findings suggest that moderate sodium restriction enhances aldosterone responsiveness to endogenous angiotensin II and adrenocorticotropic hormone without diminishing the pressor activity of endogenous angiotensin II. Sodium 74-80 angiotensinogen Homo sapiens 143-157 3897045-6 1985 In the patients, equilibrium after raised sodium intake was accompanied by a marked increase in blood pressure and blood volume, a moderate fall in plasma renin activity and levels of aldosterone and norepinephrine, and only little expansion of the interstitial space. Sodium 42-48 renin Homo sapiens 155-160 4055233-0 1985 Equilibrium and kinetic study of sodium- and potassium-induced conformational changes of apo-alpha-lactalbumin. Sodium 33-39 lactalbumin alpha Homo sapiens 93-110 3897045-9 1985 In the normal volunteers, increasing the sodium intake from 20 to 1128 mEq/day evoked no consistent change in blood pressure but caused a comparable rise in blood volume, considerable suppression of plasma renin activity, aldosterone, and norepinephrine, and a much larger increase in interstitial volume. Sodium 41-47 renin Homo sapiens 206-211 2992406-4 1985 Studies with these agents have clearly shown that the renin-angiotensin system plays an important role in the defense of body balance and blood pressure in hypovolemic state, including sodium deficiency and hemorrhage. Sodium 185-191 renin Homo sapiens 54-59 3012004-6 1985 The log of the initial plasma renin activity correlated with the changes in blood pressure (r = 0.59, p less than 0.05) in effective renal plasma flow (r = 0.59, p less than 0.05) and in sodium excretion (r = 0.65, p less than 0.01). Sodium 187-193 renin Homo sapiens 30-35 2998811-3 1985 Sodium ion (140 mM) induced a 2 fold increase in the affinity of adrenal angiotensin II receptors for the agonist (Ka = 2.15 nM-1, vs. 1.01 nM-1 for controls), but decreased antagonist binding by reducing the number of available receptors by up to 50% in both adrenal and uterine membrane particles. Sodium 0-6 angiotensinogen Rattus norvegicus 73-87 4025567-0 1985 Sodium-dependent hypertension produced by chronic central angiotensin II infusion. Sodium 0-6 angiotensinogen Rattus norvegicus 58-72 4025567-6 1985 Hypertension was found to be sodium dependent, with high sodium intake augmenting the increase in arterial pressure in response to chronic ICV ANG II. Sodium 29-35 angiotensinogen Rattus norvegicus 143-149 4025567-6 1985 Hypertension was found to be sodium dependent, with high sodium intake augmenting the increase in arterial pressure in response to chronic ICV ANG II. Sodium 57-63 angiotensinogen Rattus norvegicus 143-149 4025567-8 1985 This study demonstrates that chronic selective stimulation of brain ANG II receptors by means of continuous ICV infusion of ANG II produces sodium-sensitive increases in arterial pressure associated with, but not dependent on, increased fluid intake. Sodium 140-146 angiotensinogen Rattus norvegicus 68-74 4025567-8 1985 This study demonstrates that chronic selective stimulation of brain ANG II receptors by means of continuous ICV infusion of ANG II produces sodium-sensitive increases in arterial pressure associated with, but not dependent on, increased fluid intake. Sodium 140-146 angiotensinogen Rattus norvegicus 124-130 2990759-1 1985 Renal alpha 2-adrenoceptor stimulation by epinephrine infusion reverses cyclic adenosine monophosphate-mediated effects of vasopressin on sodium and water excretion. Sodium 138-144 arginine vasopressin Rattus norvegicus 123-134 2990759-3 1985 In the presence of alpha 1-adrenoceptor blockade with prazosin (30 nM) alpha 2-adrenoceptor stimulation with epinephrine reversed the cyclic adenosine monophosphate-mediated effects of vasopressin on sodium (P less than 0.05) and water (P less than 0.05) excretion. Sodium 200-206 arginine vasopressin Rattus norvegicus 185-196 3909580-7 1985 At this late stage of renal hypertension renin may play a contributory role.Thus, the primary abnormality in the chain of events leading eventually to hypertension is a renal inability to maintain a proper balance between sodium intake and output. Sodium 222-228 renin Homo sapiens 41-46 4006354-4 1985 Sodium and potassium chloride supplementation lead to improved growth and strength, partial correction of his electrolyte abnormalities, and a decrease in markedly elevated plasma renin activity. Sodium 0-6 renin Homo sapiens 180-185 3893156-2 1985 At low doses, ANG II stimulates sodium (Na) and water absorption from all intestinal areas. Sodium 32-38 angiotensinogen Homo sapiens 14-20 3901077-0 1985 The renin-angiotensin-aldosterone system in decompensated cirrhosis: its activity in relation to sodium balance. Sodium 97-103 renin Homo sapiens 4-9 4019771-6 1985 Arginine vasopressin (10(-10) M in the bath) caused a sustained fourfold increase in net sodium absorption and a sustained threefold increase in net potassium secretion. Sodium 89-95 arginine vasopressin Rattus norvegicus 9-20 4019771-10 1985 Arginine vasopressin causes a reversible increase in net potassium secretion and net sodium absorption. Sodium 85-91 arginine vasopressin Rattus norvegicus 9-20 4003573-9 1985 Finally, the effects on thirst and vasopressin secretion were observed at plasma sodium concentration and osmolality changes that are well within the physiological range. Sodium 81-87 arginine vasopressin Homo sapiens 35-46 2988346-0 1985 Alpha 2-adrenoceptor antagonism of vasopressin-induced changes in sodium excretion. Sodium 66-72 arginine vasopressin Rattus norvegicus 35-46 2988346-5 1985 Vasopressin (10 microU/ml) produced a significant (P less than 0.05) decrease in both water and sodium excretion. Sodium 96-102 arginine vasopressin Rattus norvegicus 0-11 2988346-7 1985 Alpha 2-Adrenoceptor stimulation with l-epinephrine (28 nM) reversed (P less than 0.05) the effects of vasopressin on water and sodium excretion. Sodium 128-134 arginine vasopressin Rattus norvegicus 103-114 2988346-11 1985 Thus alpha 2-adrenoceptor stimulation antagonized the effects of vasopressin on both water and sodium excretion at the renal level. Sodium 95-101 arginine vasopressin Rattus norvegicus 65-76 3915319-0 1985 Dietary sodium intake increases vasopressin secretion in man. Sodium 8-14 arginine vasopressin Homo sapiens 32-43 3915319-2 1985 Urinary vasopressin excretion decreased from 6.7 +/- 1.0 ng/hr (control) to 3.9 +/- 0.3 ng/hr (p less than 0.01) when sodium excretion decreased from 188 +/ 18 to 16 +/- 2 mmol/24 hr. Sodium 118-124 arginine vasopressin Homo sapiens 8-19 3915319-3 1985 During the first day of high sodium intake, the urinary vasopressin excretion increased to 10.0 +/- 1.2 ng/hr (p less than 0.01) compared with control and remained high throughout the sodium repletion. Sodium 29-35 arginine vasopressin Homo sapiens 56-67 3915319-3 1985 During the first day of high sodium intake, the urinary vasopressin excretion increased to 10.0 +/- 1.2 ng/hr (p less than 0.01) compared with control and remained high throughout the sodium repletion. Sodium 184-190 arginine vasopressin Homo sapiens 56-67 3915319-4 1985 Through all collection periods at low, normal, and high sodium intake, vasopressin excretion increased concomitantly with serum sodium concentration and osmolality. Sodium 56-62 arginine vasopressin Homo sapiens 71-82 3915319-4 1985 Through all collection periods at low, normal, and high sodium intake, vasopressin excretion increased concomitantly with serum sodium concentration and osmolality. Sodium 128-134 arginine vasopressin Homo sapiens 71-82 3915319-5 1985 After low sodium intake for 7 days, the serum vasopressin concentration averaged 2.7 +/- 0.6 ng/l, and this level was maintained throughout the sodium repletion period. Sodium 10-16 arginine vasopressin Homo sapiens 46-57 3915319-5 1985 After low sodium intake for 7 days, the serum vasopressin concentration averaged 2.7 +/- 0.6 ng/l, and this level was maintained throughout the sodium repletion period. Sodium 144-150 arginine vasopressin Homo sapiens 46-57 3915319-6 1985 These results are compatible with a stimulatory effect of dietary sodium intake on pituitary vasopressin secretion in man. Sodium 66-72 arginine vasopressin Homo sapiens 93-104 3915319-7 1985 Dietary sodium may stimulate vasopressin secretion through extracellular osmolality or even by a direct effect of extracellular sodium on periventricular receptors. Sodium 8-14 arginine vasopressin Homo sapiens 29-40 2991371-4 1985 Over a range of sodium intakes from 15 to 200 mmol/day there was a negative correlation between plasma concentration of angiotensin II and receptor site concentration (rs = 0.57, P less than 0.01). Sodium 16-22 angiotensinogen Homo sapiens 120-147 3926508-0 1985 Active and acid-activable inactive renin during inhibition by indomethacin of prostaglandin synthesis in sodium-replete man. Sodium 105-111 renin Homo sapiens 35-40 2991371-9 1985 Angiotensin II receptors in platelets respond to changes in sodium intake like receptors in arterial muscle. Sodium 60-66 angiotensinogen Homo sapiens 0-14 3927201-3 1985 Our data indicate that transmitter release induced by both increased intraterminal sodium levels and by the calcium entry into the nerve endings during depolarization might be mediated by calmodulin-dependent processes. Sodium 83-89 calmodulin 1 Homo sapiens 188-198 3894515-0 1985 Sodium restriction lowers high blood pressure through a decreased response of the renin system--direct evidence using saralasin. Sodium 0-6 renin Homo sapiens 82-87 3894515-4 1985 A highly significant negative correlation was found between the fall in blood pressure on sodium restriction and the change in blood pressure with saralasin (r = -0.52; P less than 0.005); this correlation was still significant when corrected for the severity of the hypertension (r = -0.41; P = 0.03) while it became non-significant if controlled for plasma renin activity on the low sodium diet (r = -033; NS). Sodium 90-96 renin Homo sapiens 359-364 3894515-5 1985 These results provide direct evidence that the fall in blood pressure which is seen on reducing sodium intake in many patients with essential hypertension is, at least in part, directly mediated by the reactivity of the renin angiotensin system. Sodium 96-102 renin Homo sapiens 220-225 3887946-1 1985 Angiotensin II (ANG II) is a powerful effector agent in the regulation of extracellular volume and exerts an important influence on renal sodium excretion. Sodium 138-144 angiotensinogen Homo sapiens 0-14 3887946-1 1985 Angiotensin II (ANG II) is a powerful effector agent in the regulation of extracellular volume and exerts an important influence on renal sodium excretion. Sodium 138-144 angiotensinogen Homo sapiens 16-22 3887946-2 1985 In addition to its effects on aldosterone secretion, ANG II acts directly on the kidney causing retention of sodium at low (physiological) doses and enhanced sodium excretion at high doses. Sodium 109-115 angiotensinogen Homo sapiens 53-59 3887946-2 1985 In addition to its effects on aldosterone secretion, ANG II acts directly on the kidney causing retention of sodium at low (physiological) doses and enhanced sodium excretion at high doses. Sodium 158-164 angiotensinogen Homo sapiens 53-59 3887946-4 1985 Micropuncture and microperfusion studies have demonstrated that proximal tubular sodium and water transport are stimulated by physiological concentrations (10(-12) to 10(-10) M) of ANG II on the peritubular side, whereas higher doses (10(-7) M) cause inhibition. Sodium 81-87 angiotensinogen Homo sapiens 181-187 3887946-8 1985 The data indicate that ANG II binds to receptors on the basolateral cell membrane and alters the rate of entry of sodium through the luminal membrane to increase or decrease, depending on the concentration of peptide. Sodium 114-120 angiotensinogen Homo sapiens 23-29 2992854-1 1985 ACTH 1 mg/day for 5 days raises systolic blood pressure (SBP) in normotensive and hypertensive subjects on a fixed electrolyte intake of 100 mmol/day sodium (Na) and potassium (K) (Whitworth et al. Sodium 150-156 proopiomelanocortin Homo sapiens 0-4 3894761-7 1985 Dietary sodium depletion resulted in a significantly greater arteriolar renin content (86.1 +/- 17.5 ngAI X hr-1/arteriole) compared with that from rabbits on a normal sodium diet (26.8 +/- 2.51 ngAI X hr-1/arteriole). Sodium 8-14 LOW QUALITY PROTEIN: renin Oryctolagus cuniculus 72-77 3894761-8 1985 However, sodium depletion did not alter the basal renin release rate suggesting that sodium depletion increased renin content in a storage pool rather than a pool contributing to basal release. Sodium 85-91 LOW QUALITY PROTEIN: renin Oryctolagus cuniculus 112-117 2988106-2 1985 The concentration of AVP in plasma increased 2-4 fold, osmolality in serum increased 12-16 mosmol/kg, and urinary excretion of cAMP increased 20-40% during sodium loading to the same extent in all three groups. Sodium 156-162 arginine vasopressin Homo sapiens 21-24 2988106-7 1985 In conclusion, the increase in cAMP excretion in urine during the sodium loading might be explained by an AVP-induced stimulation of renal cAMP production. Sodium 66-72 arginine vasopressin Homo sapiens 106-109 2992892-3 1985 Sodium restriction amplifies the circadian rhythms of PRA and PA, whereas propranolol loading inhibits these same rhythms on a unrestricted sodium intake, but much less so under conditions of sodium deprivation. Sodium 0-6 S100 calcium binding protein A6 Homo sapiens 54-57 2985655-11 1985 Thus, short-term converting enzyme inhibition corrected abnormalities in sodium-mediated modulation of renal vascular responsiveness to AII. Sodium 73-79 angiotensinogen Homo sapiens 136-139 3890387-1 1985 In rabbits with standard diet, in cholesterolaemic rabbits, in pregnant women with physiological hyperinsulinism and in a control group with lower peripheral insulin concentrations after glucose load negative correlations were found between the intracellular sodium content and the KG-value of the intravenous glucose tolerance test. Sodium 259-265 insulin Homo sapiens 102-109 3899461-5 1985 The correlation of initial pressure with plasma insulin remained significant even when allowing for age, surface area, BMI, and plasma concentrations of glucose, urea, creatinine, sodium and urate. Sodium 180-186 insulin Homo sapiens 48-55 3881995-4 1985 ANG II caused a significant fall of glomerular filtration rate, renal plasma flow (with an increase in filtration fraction), fractional sodium excretion, and urine output in both studies. Sodium 136-142 angiotensinogen Homo sapiens 0-6 3918465-5 1985 However, when given together with 600 mM NaCl, ANG II (8 micrograms X 2 ml-1 X 100 g-1) significantly potentiated the plasma ADH response to the vehicle at 15, 30, and 60 min, without affecting those of plasma osmolality, sodium, and hematocrit. Sodium 222-228 angiotensinogen Rattus norvegicus 47-53 3994548-3 1985 However, as a consequence of the high sodium load during SNa-HDA, volume was shifted from the extra- to the intravascular space. Sodium 38-44 snail family transcriptional repressor 1 Homo sapiens 57-60 3890393-10 1985 A second possibility is a decrease in sodium content of the arteriolar wall with the consequent decrease in vascular response to pressor agents (angiotensin II, catecholamines). Sodium 38-44 angiotensinogen Homo sapiens 145-159 3900253-3 1985 Regulation of water and sodium metabolism: urine-concentrating mechanisms and action of vasopressin]. Sodium 24-30 arginine vasopressin Homo sapiens 88-99 3846407-5 1985 The infusion of vasopressin induced significant increases in circulating levels of vasopressin (248.1 +/- 35.2 pg/ml in vasopressin-infused rats (n = 7) compared to 95.5 +/- 14.6 pg/ml in vehicle-infused rats (n = 7), p less than 0.001) and in weight gain (39.6 +/- 1.3 g in vasopressin-infused rats (n = 7) compared to 29.1 +/- 3.3 g in vehicle-infused rats (n = 7), p less than 0.05), and also sustained decreases in water intake and urine volume, but it did not induce any change in urinary sodium excretion. Sodium 494-500 arginine vasopressin Rattus norvegicus 16-27 3846407-5 1985 The infusion of vasopressin induced significant increases in circulating levels of vasopressin (248.1 +/- 35.2 pg/ml in vasopressin-infused rats (n = 7) compared to 95.5 +/- 14.6 pg/ml in vehicle-infused rats (n = 7), p less than 0.001) and in weight gain (39.6 +/- 1.3 g in vasopressin-infused rats (n = 7) compared to 29.1 +/- 3.3 g in vehicle-infused rats (n = 7), p less than 0.05), and also sustained decreases in water intake and urine volume, but it did not induce any change in urinary sodium excretion. Sodium 494-500 arginine vasopressin Rattus norvegicus 83-94 3846407-5 1985 The infusion of vasopressin induced significant increases in circulating levels of vasopressin (248.1 +/- 35.2 pg/ml in vasopressin-infused rats (n = 7) compared to 95.5 +/- 14.6 pg/ml in vehicle-infused rats (n = 7), p less than 0.001) and in weight gain (39.6 +/- 1.3 g in vasopressin-infused rats (n = 7) compared to 29.1 +/- 3.3 g in vehicle-infused rats (n = 7), p less than 0.05), and also sustained decreases in water intake and urine volume, but it did not induce any change in urinary sodium excretion. Sodium 494-500 arginine vasopressin Rattus norvegicus 83-94 3846407-5 1985 The infusion of vasopressin induced significant increases in circulating levels of vasopressin (248.1 +/- 35.2 pg/ml in vasopressin-infused rats (n = 7) compared to 95.5 +/- 14.6 pg/ml in vehicle-infused rats (n = 7), p less than 0.001) and in weight gain (39.6 +/- 1.3 g in vasopressin-infused rats (n = 7) compared to 29.1 +/- 3.3 g in vehicle-infused rats (n = 7), p less than 0.05), and also sustained decreases in water intake and urine volume, but it did not induce any change in urinary sodium excretion. Sodium 494-500 arginine vasopressin Rattus norvegicus 83-94 2981464-1 1985 The renin-angiotension system is activated in many patients with congestive heart failure (CHF), resulting in angiotensin-mediated vasoconstriction and aldosterone-mediated sodium and water retention. Sodium 173-179 renin Homo sapiens 4-9 2982239-9 1985 However, the marked suppression of aldosterone secretion observed in sodium-replete individuals during prolonged ACTH treatment was not seen in this study. Sodium 69-75 proopiomelanocortin Homo sapiens 113-117 2982239-10 1985 Angiotensin II or a different factor associated with sodium depletion may, therefore, partly protect the zona glomerulosa from adverse effects of ACTH observed in the sodium-replete state. Sodium 53-59 angiotensinogen Homo sapiens 0-14 2982239-10 1985 Angiotensin II or a different factor associated with sodium depletion may, therefore, partly protect the zona glomerulosa from adverse effects of ACTH observed in the sodium-replete state. Sodium 53-59 proopiomelanocortin Homo sapiens 146-150 2982239-10 1985 Angiotensin II or a different factor associated with sodium depletion may, therefore, partly protect the zona glomerulosa from adverse effects of ACTH observed in the sodium-replete state. Sodium 167-173 angiotensinogen Homo sapiens 0-14 2982239-10 1985 Angiotensin II or a different factor associated with sodium depletion may, therefore, partly protect the zona glomerulosa from adverse effects of ACTH observed in the sodium-replete state. Sodium 167-173 proopiomelanocortin Homo sapiens 146-150 3904334-0 1985 The sodium intake modifies the renin-aldosterone and blood pressure changes associated with moderately low energy diets. Sodium 4-10 renin Homo sapiens 31-36 3911719-9 1985 Almost in every patient with a serum sodium concentration lower or equal 132 mmol/l the plasma renin activity was markedly elevated. Sodium 37-43 renin Homo sapiens 95-100 3911719-10 1985 Patients with normal serum sodium concentrations exhibited only slightly elevated plasma renin activity. Sodium 27-33 renin Homo sapiens 89-94 4013686-1 1985 The concentration of prolactin in amniotic fluid from 91 pregnant women (Group I: 51 specimens obtained at 15th-20th week of gestation; Group II: 40 specimens at term) has been correlated with the amniotic fluid concentrations of calcium, of the ions sodium, chloride, and potassium, and with the clinical data. Sodium 251-257 prolactin Homo sapiens 21-30 4013686-2 1985 When the week of gestation in multiple regression analyses was predetermined for inclusion in the first step, the amniotic prolactin concentration was found to be significantly correlated with sodium or chloride in both groups and the correlation coefficients in the two groups were alike. Sodium 193-199 prolactin Homo sapiens 123-132 4013686-4 1985 The results indicate that the amniotic sodium and chloride concentrations could be of importance for the regulation of the amniotic prolactin concentration. Sodium 39-45 prolactin Homo sapiens 132-141 3881978-3 1985 Acute intrarenal infusion of BK also increased urine volume (UV) from 0.255 +/- 0.044 to 0.523 +/- 0.103 ml/min and urinary sodium excretion (UNaV) from 5.72 +/- 1.5 to 13.7 +/- 3.4 mueq/min. Sodium 124-130 kininogen 1 Canis lupus familiaris 29-31 4050888-9 1985 The limited effect on blood pressure and the renin system of a marked sodium removal during salt subtraction suggests that sodium must still be present in excess in these patients. Sodium 70-76 renin Homo sapiens 45-50 3884028-4 1985 This subpressor dose of angiotensin II significantly decreased urine volume, urinary excretion of sodium, chloride and phosphate and distal delivery [(CH2O + CCl)/GFR X 100] in the absence of changes in GFR or distal fractional chloride absorption [CH2O/(CH2O + CCl)]. Sodium 98-104 angiotensinogen Homo sapiens 24-38 3899597-3 1985 The complete analysis of the role of angiotensin II has to take into account the prevailing sodium balance for a given level of angiotensin II and also its indirect action upon the sympathetic nervous system as well as other hormonal systems. Sodium 92-98 angiotensinogen Homo sapiens 37-51 3899597-3 1985 The complete analysis of the role of angiotensin II has to take into account the prevailing sodium balance for a given level of angiotensin II and also its indirect action upon the sympathetic nervous system as well as other hormonal systems. Sodium 92-98 angiotensinogen Homo sapiens 128-142 3005182-8 1985 ACE inhibitors seem, at the moment, contraindicated in pregnancy and in hyperkalaemic syndromes and must be used with caution in patients with collagen disease (mainly associated with renal failure), with severe bilateral renal artery stenosis (and with severe artery stenosis of a solitary kidney) and with severe sodium depletion. Sodium 315-321 angiotensin I converting enzyme Homo sapiens 0-3 3894477-1 1985 Eight normotensive obese subjects participated in an inpatient study designed to determine the effect of a constant sodium intake (150 mEq) on the renin-aldosterone axis during 12 weeks of weight reduction. Sodium 116-122 renin Homo sapiens 147-152 2412009-4 1985 The action may be due to (a) a change in glomerular filtration rate and/or renal blood flow; (b) interference with renin release; (c) interference with aldosterone secretion and/or aldosterone action on distal tubule; (d) interference with adrenergic sodium handling; (e) a direct tubular action. Sodium 251-257 renin Homo sapiens 115-120 2412013-1 1985 Infusion of H.261, the inhibitor of human renin in the baboon, lowered blood angiotensin I, plasma angiotensin II, and arterial pressure suggesting that in the sodium-depleted state angiotensin II contributes to the maintenance of arterial pressure. Sodium 160-166 angiotensinogen Homo sapiens 182-196 2412016-9 1985 The results of these comparative studies suggest that, in states of sodium depletion, the acute hypotensive effects of renin- or CE-inhibitors are entirely due to their interference with the renin-angiotensin system. Sodium 68-74 renin Homo sapiens 119-125 2412016-9 1985 The results of these comparative studies suggest that, in states of sodium depletion, the acute hypotensive effects of renin- or CE-inhibitors are entirely due to their interference with the renin-angiotensin system. Sodium 68-74 renin Homo sapiens 119-124 2412019-2 1985 The administration of saralasin or captopril and, in the near future, of renin inhibitors induces a fall in blood pressure that is variable from one subject to the other according to the sodium balance and the level of activation of the system. Sodium 187-193 renin Homo sapiens 73-78 2984453-6 1985 Vasopressin-stimulated sodium transport, as reflected by short circuit current (SCC), was inhibited by 18 +/- 6% in the presence of bilirubin (N = 10; P less than 0.02). Sodium 23-29 arginine vasopressin Rattus norvegicus 0-11 2984453-11 1985 These findings show that short-term exposure to bilirubin exerts a tissue-specific effect on the vasopressin-stimulated active transport of sodium but has no effect on the vasopressin-induced fluxes of water and urea. Sodium 140-146 arginine vasopressin Rattus norvegicus 97-108 2983148-3 1985 Renin and aldosterone measurements showed that changes in the sodium and potassium excretion were produced by a lower activity of the renin-angiotensin-aldosterone system in the first 1.5 hour of hypokinesia. Sodium 62-68 renin Homo sapiens 0-5 2983148-3 1985 Renin and aldosterone measurements showed that changes in the sodium and potassium excretion were produced by a lower activity of the renin-angiotensin-aldosterone system in the first 1.5 hour of hypokinesia. Sodium 62-68 renin Homo sapiens 134-139 3873575-1 1985 Eluates from a Sephadex G-25 column through which dog renal homogenate was passed contained a factor that inhibited lactoperoxidase (LPO)-catalyzed iodination of tyrosine as well as the short circuit current (active absorptive sodium flux) in isolated skin of the bullfrog (Rana catesbeiana). Sodium 227-233 lactoperoxidase Canis lupus familiaris 116-131 3873575-1 1985 Eluates from a Sephadex G-25 column through which dog renal homogenate was passed contained a factor that inhibited lactoperoxidase (LPO)-catalyzed iodination of tyrosine as well as the short circuit current (active absorptive sodium flux) in isolated skin of the bullfrog (Rana catesbeiana). Sodium 227-233 lactoperoxidase Canis lupus familiaris 133-136 2983253-0 1985 Effect of the angiotensin converting enzyme inhibitor, captopril (SQ14,225), on orthostatic sodium and water retention in patients with idiopathic edema. Sodium 92-98 angiotensin I converting enzyme Homo sapiens 14-43 3001754-7 1985 The regulated release of gamma MSH peptides may contribute to CNS regulation of renal sodium excretion. Sodium 86-92 proopiomelanocortin Homo sapiens 25-34 6100739-1 1984 Previous studies have demonstrated that dopamine inhibits the aldosterone response to angiotensin II in the sodium deplete state in man, but not in the normal sodium balance state. Sodium 108-114 angiotensinogen Homo sapiens 86-100 3906991-4 1985 In patients with renal failure, diuresis also increased, however sodium excretion with urine dramatically reduced which was accompanied by inhibition of plasma renin activity. Sodium 65-71 renin Homo sapiens 160-165 6391132-7 1984 The renin-angiotensin system is activated in these patients, in part to preserve sodium homeostasis. Sodium 81-87 renin Homo sapiens 4-9 6599675-1 1984 The present study was undertaken to examine the possible relationship between dietary sodium intake and arginine vasopressin (AVP). Sodium 86-92 arginine vasopressin Homo sapiens 113-124 6599675-1 1984 The present study was undertaken to examine the possible relationship between dietary sodium intake and arginine vasopressin (AVP). Sodium 86-92 arginine vasopressin Homo sapiens 126-129 6599675-2 1984 In 12 normotensive men (aged 23-26 years) urinary AVP excretion decreased from 6.7 +/- 1.0 to 3.9 +/- 0.3 ng/h (P less than 0.01) when sodium excretion by dietary intervention for one week was reduced from 188 +/- 18 to 16 +/- 2 mmol/24 h. At a high sodium intake (300 mmol/day), AVP excretion increased to 10.0 +/- 1.2 ng/h during the first day (P less than 0.01) and remained high throughout one week of sodium load. Sodium 135-141 arginine vasopressin Homo sapiens 50-53 6599675-2 1984 In 12 normotensive men (aged 23-26 years) urinary AVP excretion decreased from 6.7 +/- 1.0 to 3.9 +/- 0.3 ng/h (P less than 0.01) when sodium excretion by dietary intervention for one week was reduced from 188 +/- 18 to 16 +/- 2 mmol/24 h. At a high sodium intake (300 mmol/day), AVP excretion increased to 10.0 +/- 1.2 ng/h during the first day (P less than 0.01) and remained high throughout one week of sodium load. Sodium 250-256 arginine vasopressin Homo sapiens 50-53 6599675-2 1984 In 12 normotensive men (aged 23-26 years) urinary AVP excretion decreased from 6.7 +/- 1.0 to 3.9 +/- 0.3 ng/h (P less than 0.01) when sodium excretion by dietary intervention for one week was reduced from 188 +/- 18 to 16 +/- 2 mmol/24 h. At a high sodium intake (300 mmol/day), AVP excretion increased to 10.0 +/- 1.2 ng/h during the first day (P less than 0.01) and remained high throughout one week of sodium load. Sodium 250-256 arginine vasopressin Homo sapiens 50-53 6599675-3 1984 These results are compatible with a major physiological role of sodium in AVP secretion in man. Sodium 64-70 arginine vasopressin Homo sapiens 74-77 6528215-5 1984 In the patients but not in the control subjects the increase of sodium excretion correlated positively with pre-infusion value of AII and negatively with change in AII during the sodium loading. Sodium 64-70 angiotensinogen Homo sapiens 130-133 6528215-5 1984 In the patients but not in the control subjects the increase of sodium excretion correlated positively with pre-infusion value of AII and negatively with change in AII during the sodium loading. Sodium 64-70 angiotensinogen Homo sapiens 164-167 6528215-5 1984 In the patients but not in the control subjects the increase of sodium excretion correlated positively with pre-infusion value of AII and negatively with change in AII during the sodium loading. Sodium 179-185 angiotensinogen Homo sapiens 164-167 6496761-4 1984 Blockade of angiotensin II receptors with [Sar1-Ala8]angiotensin II caused a greater decrease in arterial pressure in the sodium-depleted, renal-wrapped animals compared with sham-operated rats. Sodium 122-128 angiotensinogen Rattus norvegicus 12-26 6496761-4 1984 Blockade of angiotensin II receptors with [Sar1-Ala8]angiotensin II caused a greater decrease in arterial pressure in the sodium-depleted, renal-wrapped animals compared with sham-operated rats. Sodium 122-128 angiotensinogen Rattus norvegicus 53-67 6100873-6 1984 The renin-angiotensin system plays a role in the regulation of blood pressure levels in normal experimental animals and man--its importance depending on the state of sodium balance. Sodium 166-172 renin Homo sapiens 4-9 6100876-10 1984 Thus, in nearly half of the patients with essential hypertension, ACE inhibition appears to correct an abnormality in the sodium-mediated modulation of adrenal responses to angiotensin II, suggesting that this abnormality reflects an alteration in the interaction of angiotensin II and its receptor. Sodium 122-128 angiotensin I converting enzyme Homo sapiens 66-69 6100876-10 1984 Thus, in nearly half of the patients with essential hypertension, ACE inhibition appears to correct an abnormality in the sodium-mediated modulation of adrenal responses to angiotensin II, suggesting that this abnormality reflects an alteration in the interaction of angiotensin II and its receptor. Sodium 122-128 angiotensinogen Homo sapiens 173-187 6100876-10 1984 Thus, in nearly half of the patients with essential hypertension, ACE inhibition appears to correct an abnormality in the sodium-mediated modulation of adrenal responses to angiotensin II, suggesting that this abnormality reflects an alteration in the interaction of angiotensin II and its receptor. Sodium 122-128 angiotensinogen Homo sapiens 267-281 6240442-0 1984 Contribution of vasopressin and the sympathetic nervous system in the early phase of high sodium one-kidney renal hypertension. Sodium 90-96 arginine vasopressin Rattus norvegicus 16-27 6084759-6 1984 As expected, rats maintained on the low-sodium regimen for either 5 or 21 days had marked stimulation of plasma renin activity and increased angiotensin I, angiotensin II, and aldosterone formation. Sodium 40-46 angiotensinogen Rattus norvegicus 156-170 6084790-1 1984 This study investigated the ability of angiotensin II (Ang II) to facilitate the stimulation-induced release of [3H]norepinephrine [( 3H]NE) from two cardiovascular regulatory areas in normal and sodium-restricted rats. Sodium 196-202 angiotensinogen Rattus norvegicus 55-61 6084790-3 1984 Placement of rats on a sodium-restricted diet abolished the facilitation of [3H]NE release due to Ang II. Sodium 23-29 angiotensinogen Rattus norvegicus 98-104 6084790-7 1984 These results suggest that low sodium diets may alter the facilitation of [3H]NE release by Ang II by interactions with the renin-angiotensin system. Sodium 31-37 angiotensinogen Rattus norvegicus 92-98 6094612-7 1984 The time course of sodium regulation of glomerular angiotensin II receptors was studied in rats switched from a moderate sodium to either a high sodium diet or a low sodium diet plus furosemide. Sodium 19-25 angiotensinogen Rattus norvegicus 51-65 6094612-8 1984 Receptor density was unchanged at 24 h, varied directly with sodium intake for 1-5 d when induction was maximal, and remained constant for at least 21 d. The time course of receptor regulation closely paralleled changes in plasma angiotensin II. Sodium 61-67 angiotensinogen Rattus norvegicus 230-244 6094612-13 1984 The infusion of angiotensin II (100 mg/min) for 15 min or 2 h into anesthetized rats maintained on moderate sodium intake resulted in a 50% reduction in specific angiotensin binding that could not be reversed by the dissociation of endogenous angiotensin. Sodium 108-114 angiotensinogen Rattus norvegicus 16-30 6094854-0 1984 Effects of sodium, potassium, ACTH and nephrectomy on adrenal renin. Sodium 11-17 renin Homo sapiens 62-67 6085418-5 1984 Somatostatin (SST) decreased the output of hepatic bile, bile acids, sodium, potassium, and bicarbonate by about 25%. Sodium 69-75 somatostatin Canis lupus familiaris 0-12 6495367-8 1984 The administration of low-dose (2-10 microU/kg/min) vasopressin by continuous infusion maintained plasma sodium and osmolality in the normal range over the course of the experiments (24 hr) in the experimental group. Sodium 105-111 arginine vasopressin Homo sapiens 52-63 6598066-5 1984 This was attributed to thorough biochemical evaluation of the underlying metabolic state by measurement of renal potassium handling and by determining the responses of the renin-aldosterone axis to changes in sodium balance. Sodium 209-215 renin Homo sapiens 172-177 6090837-0 1984 Biological action and binding sites for vasopressin on the mesenteric artery from normal and sodium-depleted rats. Sodium 93-99 arginine vasopressin Rattus norvegicus 40-51 6090837-5 1984 In sodium-depleted rats we have observed an increase (27%) of the maximal response to AVP with no significant change in ED50 (from 2.8 +/- 1.0 X 10(-8) M to 1.3 +/- 0.2 X 10(-8) M). Sodium 3-9 arginine vasopressin Rattus norvegicus 86-89 6090837-6 1984 On the membrane preparation, the number of binding sites for 3H-AVP was increased from 71 +/- 17 fmole/mg protein (Kd 3.5 +/- 0.5 nM) to 115 +/- 10 fmole/mg protein (Kd 4.8 +/- 0.3 nM) in the sodium-depleted rat by comparison to control animals. Sodium 192-198 arginine vasopressin Rattus norvegicus 64-67 6090837-8 1984 Receptors for AVP are increased in the mesenteric vascular bed by sodium depletion. Sodium 66-72 arginine vasopressin Rattus norvegicus 14-17 6391571-1 1984 Monensin, a specific sodium ionophore, has been shown to reduce glucose-induced proinsulin biosynthesis by 30% and to completely inhibit the intracellular conversion of proinsulin to insulin. Sodium 21-27 insulin Homo sapiens 80-90 6391571-1 1984 Monensin, a specific sodium ionophore, has been shown to reduce glucose-induced proinsulin biosynthesis by 30% and to completely inhibit the intracellular conversion of proinsulin to insulin. Sodium 21-27 insulin Homo sapiens 169-179 6092173-0 1984 Solubilized adrenal angiotensin II receptors: studies on the site of action of sodium and calcium ions, and on the role of disulfide bridges. Sodium 79-85 angiotensinogen Rattus norvegicus 20-34 6389240-5 1984 Insulin delivered to the latter sites stimulates several important processes, including reabsorption of sodium, phosphate, and glucose. Sodium 104-110 insulin Homo sapiens 0-7 6208488-0 1984 The outward transport of axoplasmic noradrenaline induced by a rise of the sodium concentration in the adrenergic nerve endings of the rat vas deferens. Sodium 75-81 arginine vasopressin Rattus norvegicus 139-142 6746861-5 1984 Both assays gave almost identical results in normal subjects whereas in three different conditions characterized by a high renin level (severe hypertension plus low sodium diet, converting enzyme inhibition, and adrenal insufficiency) higher results were obtained by the direct assay. Sodium 165-171 renin Homo sapiens 123-128 6086642-11 1984 The correlation of rapid changes in cGMP levels with changes in membrane current leave open the possibility that changes in cGMP concentration may be an obligatory step in the reaction sequence linking rhodopsin activation by light and the resultant decrease in sodium permeability of the plasma membrane. Sodium 262-268 rhodopsin Homo sapiens 202-211 6489442-0 1984 GABA agonists inhibit central sodium-induced vasopressin-dependent increases in arterial pressure. Sodium 30-36 arginine vasopressin Rattus norvegicus 45-56 6476882-2 1984 With insulin treatment alone plasma sodium concentrations in two children returned to normal. Sodium 36-42 insulin Homo sapiens 5-12 6380316-0 1984 Sodium appetite during captopril blockade of endogenous angiotensin II formation. Sodium 0-6 angiotensinogen Rattus norvegicus 56-70 6380316-1 1984 Angiotensin II and aldosterone increase in response to sodium deficiency to promote sodium and water conservation. Sodium 55-61 angiotensinogen Rattus norvegicus 0-14 6380316-1 1984 Angiotensin II and aldosterone increase in response to sodium deficiency to promote sodium and water conservation. Sodium 84-90 angiotensinogen Rattus norvegicus 0-14 6393932-8 1984 These chronic elevations of angiotensin II directly increase blood pressure and decrease the kidney"s ability to excrete sodium by either a direct renal effect or indirectly by stimulating aldosterone-dependent sodium retention. Sodium 121-127 angiotensinogen Homo sapiens 28-42 6086885-4 1984 A renal alpha-2 adrenoceptor response was demonstrated by showing that epinephrine could reverse the effect of vasopressin on water and sodium in the presence of beta blockade and alpha-1 destruction by POB. Sodium 136-142 arginine vasopressin Rattus norvegicus 111-122 6379373-3 1984 Since sodium deficiency is associated with a reduction in renal dopamine formation, we investigated the effect of dopamine on angiotensin II-induced aldosterone secretion in the sodium-depleted state. Sodium 178-184 angiotensinogen Homo sapiens 126-140 6328965-6 1984 Both converting enzyme inhibition with captopril and sodium repletion, factors known to decrease endogenous angiotensin II activity, provoked agonist responses to saralasin infusion. Sodium 53-59 angiotensinogen Homo sapiens 108-122 6394181-3 1984 The greatest fall in blood pressure with sodium restriction was seen in those patients with the least rise in renin. Sodium 41-47 renin Homo sapiens 110-115 6329658-5 1984 Infusion of a high dose of angiotensin II into potassium-deficient rats stimulated aldosterone biosynthesis depending upon the concurrent sodium intake. Sodium 138-144 angiotensinogen Rattus norvegicus 27-41 6329658-7 1984 Angiotensin II seems to be essential for the induction but not for the maintenance of a high activity of the enzyme(s) involved in the conversion of corticosterone to aldosterone during combined sodium and potassium restriction. Sodium 195-201 angiotensinogen Rattus norvegicus 0-14 6329658-8 1984 The sensitivity of the zona glomerulosa to the long term stimulatory action of angiotensin II varies with the sodium intake and appears to be regulated by the plasma potassium concentration and unknown other mediators. Sodium 110-116 angiotensinogen Rattus norvegicus 79-93 6385344-0 1984 Angiotensin II analogue infusion test in renovascular hypertension under low sodium intake and under spironolactone administration: is angiotensin II analogue infusion test useful in determining the mode of treatment? Sodium 77-83 angiotensinogen Homo sapiens 0-14 6383842-1 1984 Dietary sodium intake alters pressor responsiveness to angiotensin II (AII) as well as altering prostaglandin production. Sodium 8-14 angiotensinogen Rattus norvegicus 55-69 6383842-1 1984 Dietary sodium intake alters pressor responsiveness to angiotensin II (AII) as well as altering prostaglandin production. Sodium 8-14 angiotensinogen Rattus norvegicus 71-74 6383842-3 1984 Prostaglandin synthesis inhibition with meclofenamate (5 mg/kg) or indomethacin (5 mg/kg) significantly enhanced the pressor response for AII at infusion rates of 0.10, 0.30 and 1.0 microgram/kg per min (P less than 0.05) in rats previously on a low sodium intake but had no effect in rats previously on a high sodium intake. Sodium 250-256 angiotensinogen Rattus norvegicus 138-141 6383842-3 1984 Prostaglandin synthesis inhibition with meclofenamate (5 mg/kg) or indomethacin (5 mg/kg) significantly enhanced the pressor response for AII at infusion rates of 0.10, 0.30 and 1.0 microgram/kg per min (P less than 0.05) in rats previously on a low sodium intake but had no effect in rats previously on a high sodium intake. Sodium 311-317 angiotensinogen Rattus norvegicus 138-141 6383842-6 1984 These results suggest that prostaglandin synthetase inhibition may enhance the pressor response for angiotensin II in situations where endogenous angiotensin II levels are elevated (i.e. low sodium intake). Sodium 191-197 angiotensinogen Rattus norvegicus 100-114 6144625-11 1984 In addition, the serum sodium concentration was significantly reduced by vasopressin (from 134.3 +/- 1.6 to 128.3 +/- 1.4 mEq per liter, p less than 0.001) but not by somatostatin (134.6 +/- 1.1 vs. 133.2 +/- 1.1 mEq per liter). Sodium 23-29 arginine vasopressin Homo sapiens 73-84 6202963-9 1984 A significant decrease in renal sodium and water excretion occurred only during administration of the highest dose of 50 mg t.i.d., when reduction in blood pressure was pronounced and there were reflex increases in plasma renin activity and plasma aldosterone. Sodium 32-38 renin Homo sapiens 222-227 6323514-1 1984 Human platelets possess angiotensin II (AII) receptors which increase in number in response to sodium loading, a response similar to that reported for animal smooth muscle and renal AII receptors. Sodium 95-101 angiotensinogen Homo sapiens 24-38 6323514-1 1984 Human platelets possess angiotensin II (AII) receptors which increase in number in response to sodium loading, a response similar to that reported for animal smooth muscle and renal AII receptors. Sodium 95-101 angiotensinogen Homo sapiens 40-43 6328346-0 1984 Restricted dietary sodium intake alters peripheral but not central angiotensin II receptors. Sodium 19-25 angiotensinogen Rattus norvegicus 67-81 6328346-6 1984 In contrast, both the 125I-Ang II binding density and dissociation constant in the adrenal gland were significantly elevated, while the binding density of 125-I-Ang II in the bladder smooth muscle was significantly decreased in the sodium-restricted group. Sodium 232-238 angiotensinogen Rattus norvegicus 27-33 6328346-6 1984 In contrast, both the 125I-Ang II binding density and dissociation constant in the adrenal gland were significantly elevated, while the binding density of 125-I-Ang II in the bladder smooth muscle was significantly decreased in the sodium-restricted group. Sodium 232-238 angiotensinogen Rattus norvegicus 161-167 6328142-0 1984 Plasma prolactin during the body fluid and electrolyte changes of dehydration and sodium depletion in steers. Sodium 82-88 prolactin Homo sapiens 7-16 6328142-1 1984 The effect of dehydration and sodium depletion on plasma prolactin levels in steer calves is very different from the changes seen in the rat and possibly in man. Sodium 30-36 prolactin Bos taurus 57-66 6328142-11 1984 The means whereby both divergent physiological processes of dehydration and sodium depletion generate stimuli which inhibit prolactin secretion and the relevance of this response in fluid balance homeostasis requires further research. Sodium 76-82 prolactin Homo sapiens 124-133 6143083-8 1984 Responsiveness of the renin-angiotensin system may limit the fall in blood-pressure induced by sodium restriction. Sodium 95-101 renin Homo sapiens 22-27 6741439-4 1984 Plasma ADH markedly increased after NaCl administration and was significantly correlated with plasma sodium (r = 0.67, P less than 0.005) when the patients were awake, whereas it did not change over 30 min and was not correlated with plasma sodium (r = 0.18, P greater than 0.05) under fentanyl anaesthesia. Sodium 101-107 arginine vasopressin Homo sapiens 7-10 6693420-2 1984 The dose-dependent depolarization of the platelet"s negative membrane potential by thrombin is in large part due to a rapid uptake of sodium. Sodium 134-140 coagulation factor II, thrombin Homo sapiens 83-91 6693420-5 1984 It is thus apparent that: 1) the change in the membrane potential induced by thrombin is directly dependent upon the transmembrane sodium gradient and is primarily due to a dose-dependent sodium uptake by the platelets; and 2) the thrombin-induced secretory processes are dependent upon maintenance of the transmembrane potassium gradients. Sodium 131-137 coagulation factor II, thrombin Homo sapiens 77-85 6693420-5 1984 It is thus apparent that: 1) the change in the membrane potential induced by thrombin is directly dependent upon the transmembrane sodium gradient and is primarily due to a dose-dependent sodium uptake by the platelets; and 2) the thrombin-induced secretory processes are dependent upon maintenance of the transmembrane potassium gradients. Sodium 131-137 coagulation factor II, thrombin Homo sapiens 231-239 6693420-5 1984 It is thus apparent that: 1) the change in the membrane potential induced by thrombin is directly dependent upon the transmembrane sodium gradient and is primarily due to a dose-dependent sodium uptake by the platelets; and 2) the thrombin-induced secretory processes are dependent upon maintenance of the transmembrane potassium gradients. Sodium 188-194 coagulation factor II, thrombin Homo sapiens 77-85 6693420-5 1984 It is thus apparent that: 1) the change in the membrane potential induced by thrombin is directly dependent upon the transmembrane sodium gradient and is primarily due to a dose-dependent sodium uptake by the platelets; and 2) the thrombin-induced secretory processes are dependent upon maintenance of the transmembrane potassium gradients. Sodium 188-194 coagulation factor II, thrombin Homo sapiens 231-239 6696107-6 1984 These results indicate that exogenous vasopressin may stimulate the release of endogenous AVP, an effect that appears to be enhanced by sodium depletion and is virtually absent in the elderly. Sodium 136-142 arginine vasopressin Homo sapiens 38-49 6398959-0 1984 Effects of insulin on plasma concentration and renal excretion of sodium and potassium. Sodium 66-72 insulin Homo sapiens 11-18 6398960-0 1984 Influence of electrolyte depletion and aldosterone on insulin induced changes in plasma concentration and renal excretion of sodium and potassium. Sodium 125-131 insulin Homo sapiens 54-61 3907374-7 1985 Major changes in plasma renin activity, aldosterone, and, to a lesser extent, norepinephrine accompanied these changes in kidney function, displaying inverse and exponential correlations with daily sodium excretion and ECFV. Sodium 198-204 renin Homo sapiens 24-29 6326599-9 1984 DOCA infusion into sodium-depleted rats partially corrected the down-regulation of vascular ANG II receptors independent of changes in PRA. Sodium 19-25 angiotensinogen Rattus norvegicus 92-98 6428366-1 1984 The renin-aldosterone system contributes to the regulation of arterial pressure and to the maintenance of sodium and potassium balance. Sodium 106-112 renin Homo sapiens 4-9 6721932-5 1984 These findings support previous suggestions that whereas AII normally contributes little to thirst, it may help to mediate sodium appetite in rats when aldosterone is abundant. Sodium 123-129 angiotensinogen Rattus norvegicus 57-60 6721932-7 1984 These findings suggest that whereas septal lesions may sensitize the rat"s brain to the sodium-appetite-eliciting effects of AII as well as to its dipsogenic effects, sodium appetite emerges only if the induced thirst is not too pronounced. Sodium 88-94 angiotensinogen Rattus norvegicus 125-128 6423371-5 1984 Basal PRL release was slightly but significantly reduced by replacing sodium by choline in the incubation medium and was almost completely suppressed when isoosmolar concentrations of glucose were substituted for sodium. Sodium 70-76 prolactin Rattus norvegicus 6-9 6423371-5 1984 Basal PRL release was slightly but significantly reduced by replacing sodium by choline in the incubation medium and was almost completely suppressed when isoosmolar concentrations of glucose were substituted for sodium. Sodium 213-219 prolactin Rattus norvegicus 6-9 6423371-8 1984 Of two antidopaminergic drugs, haloperidol and l-sulpiride, only the first inhibited the release of PRL at high doses (10(-5) - 10(-4) M) in the presence of sodium but became stimulatory at 10(-4) M in the absence of the ion. Sodium 157-163 prolactin Rattus norvegicus 100-103 6423371-12 1984 They also clearly show that sodium intervenes in dopaminergic agonist and antagonist inhibition of PRL release through a mechanism which appears independent of either dopaminergic receptor, Ca2+ or Na+ channel, or Na+/K+ pump. Sodium 28-34 prolactin Rattus norvegicus 99-102 6323565-4 1984 The changes in mean arterial pressure and left ventricular filling pressure seen with first doses of the drug varied linearly and inversely with the pretreatment serum sodium concentration (r = -0.58 and r = -0.53, respectively); this was likely related to the finding that, before administration of captopril, the serum sodium concentration varied linearly and inversely with the logarithm of the plasma renin activity (r = -0.78). Sodium 168-174 renin Homo sapiens 405-410 6425093-0 1984 Different sodium requirements for 86Rb efflux and for growth hormone and prolactin secretion from bovine anterior pituitary cells. Sodium 10-16 prolactin Bos taurus 73-82 6425093-1 1984 The sodium dependence of growth hormone and prolactin secretion and of 86Rb efflux from bovine anterior pituitary cells in response to acetylcholine and TRH was examined. Sodium 4-10 prolactin Bos taurus 44-53 6374767-3 1984 The renin proportionate response to PGI2 was not altered by sodium restriction but blunted by sodium depletion, compatible with the hypothesis that endogenous PGI2 is high in Na depletion. Sodium 94-100 renin Ovis aries 4-9 6199985-11 1984 In normotensive marmosets the renin-angiotensin system participates in the maintenance of blood pressure, to a degree depending on the state of sodium balance. Sodium 144-150 renin Homo sapiens 30-35 6373591-10 1984 Dopamine inhibits AII-induced aldosterone secretion during sodium deficiency in humans. Sodium 59-65 angiotensinogen Homo sapiens 18-21 6715111-5 1984 Increased fractional sodium excretion in cases of recent onset might indicate inadequate adaptation of the proximal tubules to the increased filtered load or to inadequate insulin therapy. Sodium 21-27 insulin Homo sapiens 172-179 6328407-1 1984 We examined effects of osmolality or sodium concentration on vasopressin induced cyclic AMP generation in the medullary thick ascending limbs isolated from collagenase treated rat kidneys. Sodium 37-43 arginine vasopressin Rattus norvegicus 61-72 6372072-7 1984 Measurement of renin and aldosterone levels should be used for evaluation of the severity of a sodium deficiency. Sodium 95-101 renin Homo sapiens 15-20 6361570-5 1984 Individual serum sodium concentrations were inversely correlated with levels of prostaglandin E2 metabolites (r = -0.92, P less than 0.001) and plasma renin activity (r = -0.69, P less than 0.02). Sodium 17-23 renin Homo sapiens 151-156 6741563-8 1984 A negative correlation between renal PG production and VP plasma levels and excretion was demonstrated during the changes of dietary sodium intake. Sodium 133-139 arginine vasopressin Homo sapiens 55-57 6097382-4 1984 Plasma renin activity increased after ACTH infusion only on the lower sodium intake. Sodium 70-76 renin Homo sapiens 7-12 6321067-3 1984 In this context, it is potentially important that stress causing ACTH release, as well as other neurohumoral effects, causes increased salt appetite and can impair renal sodium excretion. Sodium 170-176 proopiomelanocortin Homo sapiens 65-69 6097382-5 1984 Blood pressure response to angiotensin II was greater on the higher sodium intake. Sodium 68-74 angiotensinogen Homo sapiens 27-41 6097382-7 1984 Kaliuresis was increased on the day of the 4-h infusion of angiotensin II on the higher sodium intake but no significant changes were apparent during the administration of angiotensin II. Sodium 88-94 angiotensinogen Homo sapiens 59-73 6325055-2 1984 ACTH administration produced hypokalaemia, initial urinary sodium retention, a fall in active plasma renin concentration, a transient rise in plasma aldosterone concentration and sustained rises in plasma deoxycorticosterone concentration and urinary kallikrein activity. Sodium 59-65 proopiomelanocortin Homo sapiens 0-4 6083400-3 1984 However, the AII receptors in adrenal zona glomerulosa and vascular smooth muscle undergo reciprocal regulatory changes during alterations in sodium intake. Sodium 142-148 angiotensinogen Rattus norvegicus 13-16 6368215-9 1984 Prolonged hypovolemic hypotension or sodium depletion increases renin levels. Sodium 37-43 renin Homo sapiens 64-69 6703422-6 1984 This sodium resistance may be related to a relative hypokalemia (3.4 mmol X 1(-1) ). Sodium 5-11 amyloid beta precursor protein binding family A member 1 Homo sapiens 74-81 6714651-5 1984 The prolactin character of the purified protein was established by its lactogenic activity in the rabbit mammary gland in vitro and its sodium-retaining activity in hypophysectomized Fundulus heteroclitus. Sodium 136-142 prolactin Oryctolagus cuniculus 4-13 6083400-9 1984 The increase in subfornical-organ receptors is analogous to the up-regulation of AII sites in the adrenal cortex during sodium deficiency and may have a potentiating action upon the dipsogenic role of AII during dehydration. Sodium 120-126 angiotensinogen Rattus norvegicus 81-84 6399317-4 1984 Fluharty and I have found (Behavioral Neuroscience, 1983) that treatment of salt replete rats with low doses of both angiotensin (Ang II) and a mineralocorticoid (DOCA) evokes a rapid, reliable, and specific appetite for sodium solutions, and we have proposed that the hormones of renal sodium conservation are also the hormones for the behavioral defense against sodium deficiency. Sodium 221-227 angiotensinogen Rattus norvegicus 117-128 6399313-1 1984 Intracranial renin is a potent stimulus to sodium appetite and thirst, the effects being mediated by local generation of angiotensin II. Sodium 43-49 angiotensinogen Rattus norvegicus 121-135 6399317-4 1984 Fluharty and I have found (Behavioral Neuroscience, 1983) that treatment of salt replete rats with low doses of both angiotensin (Ang II) and a mineralocorticoid (DOCA) evokes a rapid, reliable, and specific appetite for sodium solutions, and we have proposed that the hormones of renal sodium conservation are also the hormones for the behavioral defense against sodium deficiency. Sodium 221-227 angiotensinogen Rattus norvegicus 130-136 6399317-4 1984 Fluharty and I have found (Behavioral Neuroscience, 1983) that treatment of salt replete rats with low doses of both angiotensin (Ang II) and a mineralocorticoid (DOCA) evokes a rapid, reliable, and specific appetite for sodium solutions, and we have proposed that the hormones of renal sodium conservation are also the hormones for the behavioral defense against sodium deficiency. Sodium 287-293 angiotensinogen Rattus norvegicus 117-128 6399317-4 1984 Fluharty and I have found (Behavioral Neuroscience, 1983) that treatment of salt replete rats with low doses of both angiotensin (Ang II) and a mineralocorticoid (DOCA) evokes a rapid, reliable, and specific appetite for sodium solutions, and we have proposed that the hormones of renal sodium conservation are also the hormones for the behavioral defense against sodium deficiency. Sodium 287-293 angiotensinogen Rattus norvegicus 130-136 6399317-4 1984 Fluharty and I have found (Behavioral Neuroscience, 1983) that treatment of salt replete rats with low doses of both angiotensin (Ang II) and a mineralocorticoid (DOCA) evokes a rapid, reliable, and specific appetite for sodium solutions, and we have proposed that the hormones of renal sodium conservation are also the hormones for the behavioral defense against sodium deficiency. Sodium 287-293 angiotensinogen Rattus norvegicus 117-128 6399317-4 1984 Fluharty and I have found (Behavioral Neuroscience, 1983) that treatment of salt replete rats with low doses of both angiotensin (Ang II) and a mineralocorticoid (DOCA) evokes a rapid, reliable, and specific appetite for sodium solutions, and we have proposed that the hormones of renal sodium conservation are also the hormones for the behavioral defense against sodium deficiency. Sodium 287-293 angiotensinogen Rattus norvegicus 130-136 6399317-6 1984 That is, sodium replete rats that have been primed for 3 days with DOCA (500 micrograms/day), which does not produce an appetite for salt, and are then given a pulse intracerebroventricular (ICV) injection of Ang II (60 ng), which by itself does not produce an appetite for salt, will run in an alleyway in order to ingest small drops of 3% NaCl. Sodium 9-15 angiotensinogen Rattus norvegicus 209-215 6323866-6 1984 In supine, sodium repleted states, ACTH is a potent stimulus of aldosterone at 000-0600 h and 1700-1900 h clocktime, whereas during daytime renin-angiotensin is an additional regulator. Sodium 11-17 proopiomelanocortin Homo sapiens 35-39 6699780-8 1984 A 30 mV, mucosa-positive voltage clamp, applied near the peak of the response to vasopressin, further increased both sodium transport and carbon dioxide production. Sodium 117-123 arginine vasopressin Homo sapiens 81-92 6699780-14 1984 Sodium transport was increased by approximately 35% more when aldosterone-treated hemibladders were voltage clamped after vasopressin, the control paired hemibladders being exposed to vasopressin and voltage clamping alone. Sodium 0-6 arginine vasopressin Homo sapiens 122-133 6204138-6 1984 Pharmacologic interruption of the renin-angiotensin system is proving useful not only for blood pressure control in patients with hypertension but also because of its influence on the kidney in some or all of these conditions--at least in part attributable to restoration of more normal renal sodium handling. Sodium 293-299 renin Homo sapiens 34-39 6204139-10 1984 Thus AVP may act as an impormediator of volume changes associated with alterations in sodium intake or excretion and thereby affect blood pressure. Sodium 86-92 arginine vasopressin Rattus norvegicus 5-8 6382488-0 1984 Expression of plasma renin activity in terms of urinary sodium excretion and posture in normal subjects on free sodium intake. Sodium 56-62 renin Homo sapiens 21-26 6321936-4 1984 PTH administration increased urinary excretion of cyclic AMP, sodium, potassium, bicarbonate, phosphate clearance, and reabsorption of calcium. Sodium 62-68 parathyroid hormone Homo sapiens 0-3 6196232-12 1983 Studies with monkeys show that a peptide renin inhibitors may cause hypotension after sodium depletion and normalize blood pressure in Goldblatt hypertension to the same degree as a converting-enzyme inhibitor. Sodium 86-92 renin Homo sapiens 41-46 6699780-14 1984 Sodium transport was increased by approximately 35% more when aldosterone-treated hemibladders were voltage clamped after vasopressin, the control paired hemibladders being exposed to vasopressin and voltage clamping alone. Sodium 0-6 arginine vasopressin Homo sapiens 184-195 6371561-2 1984 Recent evidence has shown that many patients with the nephrotic syndrome have a normal or low plasma renin activity suggesting that there might be an intrarenal cause for their sodium retention. Sodium 177-183 renin Homo sapiens 101-106 6358261-0 1983 Defect in the sodium-modulated tissue responsiveness to angiotensin II in essential hypertension. Sodium 14-20 angiotensinogen Homo sapiens 56-70 6382488-2 1984 Supine and upright plasma renin activities were then related to the 24-hour urinary sodium or the 2-hour urinary sodium excretion, measured in the morning after overnight fasting. Sodium 84-90 renin Homo sapiens 26-31 6358261-1 1983 In normal subjects, dietary sodium intake modulates renovascular, adrenal, and pressor responses to infused angiotensin II (AII). Sodium 28-34 angiotensinogen Homo sapiens 108-122 6358261-1 1983 In normal subjects, dietary sodium intake modulates renovascular, adrenal, and pressor responses to infused angiotensin II (AII). Sodium 28-34 angiotensinogen Homo sapiens 124-127 6358261-9 1983 Renal blood flow responses to all AII doses were statistically greater on a high-vs.-low salt diet in the NR (P less than 0.001, chi-square) and normotensives (P = 0.004, chi-square) but sodium intake had no effect on this response in the AbR. Sodium 187-193 angiotensinogen Homo sapiens 34-37 6382488-2 1984 Supine and upright plasma renin activities were then related to the 24-hour urinary sodium or the 2-hour urinary sodium excretion, measured in the morning after overnight fasting. Sodium 113-119 renin Homo sapiens 26-31 6309884-0 1983 Endogenous angiotensin II as a determinant of sodium-modulated changes in tissue responsiveness to angiotensin II in normal man. Sodium 46-52 angiotensinogen Homo sapiens 11-25 6418847-5 1983 Insulin significantly increased sodium transport in aldosterone-treated skin and lowered the resistance. Sodium 32-38 insulin Homo sapiens 0-7 6400115-3 1983 At the same time there was attenuation of the expected increase in plasma renin activity appropriate for such a sodium loss. Sodium 112-118 renin Homo sapiens 74-79 6360917-0 1983 Renin-aldosterone axis in ethanol intoxication during sodium and fluid repletion versus depletion. Sodium 54-60 renin Homo sapiens 0-5 6360917-3 1983 In sodium-depleted subjects starting levels of plasma renin activity (PRA) and plasma aldosterone were increased as expected. Sodium 3-9 renin Homo sapiens 54-59 6639745-5 1983 Conversely, sodium appetite was enhanced in PEG-treated rats when angiotensin II (AII) was produced in unusually large amounts in the brain, owing to the systemic administration of captopril. Sodium 12-18 angiotensinogen Rattus norvegicus 66-80 6639745-5 1983 Conversely, sodium appetite was enhanced in PEG-treated rats when angiotensin II (AII) was produced in unusually large amounts in the brain, owing to the systemic administration of captopril. Sodium 12-18 angiotensinogen Rattus norvegicus 82-85 6309884-0 1983 Endogenous angiotensin II as a determinant of sodium-modulated changes in tissue responsiveness to angiotensin II in normal man. Sodium 46-52 angiotensinogen Homo sapiens 99-113 6354522-8 1983 On the low sodium intake, the enhanced PA response to MCP probably reflects both a direct adrenal effect and an indirect effect mediated via activation of the renin-angiotensin system. Sodium 11-17 renin Homo sapiens 159-164 6309884-1 1983 Dietary sodium restriction reduces vascular smooth muscle, particularly renovascular, responsiveness to infused angiotensin II (AII), while the responsiveness of the adrenal and the AII-renin short feedback loop to AII is enhanced. Sodium 8-14 angiotensinogen Homo sapiens 112-126 6309884-1 1983 Dietary sodium restriction reduces vascular smooth muscle, particularly renovascular, responsiveness to infused angiotensin II (AII), while the responsiveness of the adrenal and the AII-renin short feedback loop to AII is enhanced. Sodium 8-14 angiotensinogen Homo sapiens 128-131 6309884-5 1983 In sodium-restricted subjects, preinfusion AII and aldosterone levels were significantly reduced, (P less than 0.001) to the range found in sodium-replete subjects, after 75 h of MK421 administration, whereas blood pressure and PAH responses to infused AII were significantly enhanced (P less than 0.01). Sodium 3-9 angiotensinogen Homo sapiens 43-46 6309884-6 1983 Blood pressure and PAH responses to infused AII in sodium-replete subjects were not significantly modified by MK421 treatment, confirming that the drug effect was specific. Sodium 51-57 angiotensinogen Homo sapiens 44-47 6309884-8 1983 Thus, sodium-modulated changes in PAH and blood pressure responsiveness to infused AII depend on circulating AII levels. Sodium 6-12 angiotensinogen Homo sapiens 83-86 6309884-8 1983 Thus, sodium-modulated changes in PAH and blood pressure responsiveness to infused AII depend on circulating AII levels. Sodium 6-12 angiotensinogen Homo sapiens 109-112 6309884-10 1983 Two different mechanisms determine sodium modulation of tissue responsiveness to AII; in one, circulating AII via a receptor mechanism is the mediator, and in the other, some other factor(s) also linked to sodium intake must be responsible. Sodium 35-41 angiotensinogen Homo sapiens 81-84 6309884-10 1983 Two different mechanisms determine sodium modulation of tissue responsiveness to AII; in one, circulating AII via a receptor mechanism is the mediator, and in the other, some other factor(s) also linked to sodium intake must be responsible. Sodium 35-41 angiotensinogen Homo sapiens 106-109 6400108-2 1983 The renin-angiotensin system, renal kinins and prostaglandins are all implicated in the regulation of glomerular filtration rate (GRF), renal blood flow (RBF) and urinary sodium excretion. Sodium 171-177 renin Homo sapiens 4-9 6085835-9 1983 We have also found that plasma renin values in heart failure are dependent on sodium intake. Sodium 78-84 renin Homo sapiens 31-36 6100600-1 1983 Sodium intake has a substantial effect on target tissue responsiveness to angiotensin II (AII). Sodium 0-6 angiotensinogen Homo sapiens 74-88 6100600-1 1983 Sodium intake has a substantial effect on target tissue responsiveness to angiotensin II (AII). Sodium 0-6 angiotensinogen Homo sapiens 90-93 6100600-3 1983 In a substantial number of patients with essential hypertension this normal sodium-mediated modulation of tissue responsiveness to AII is absent. Sodium 76-82 angiotensinogen Homo sapiens 131-134 6100600-6 1983 The elevated blood pressure may result either from an alteration in renal sodium handling or inappropriate increases in AII levels, depending on ambient sodium intake. Sodium 153-159 angiotensinogen Homo sapiens 120-123 6100608-1 1983 Plasma angiotensinogen was measured by two different methods in three groups of sodium-depleted rats: control rats, captopril-treated rats and enalapril-treated rats. Sodium 80-86 angiotensinogen Rattus norvegicus 7-22 6100609-2 1983 Previous work in rats has shown that the prodrug ACE inhibitor, enalapril (MK-421), lowered blood pressure most effectively when PRA was elevated [sodium deficiency, two-kidney, one figure 8 hypertension, diuretic-treated spontaneously hypertensive rats (SHR)]. Sodium 147-153 angiotensin I converting enzyme Rattus norvegicus 49-52 6417325-12 1983 The increases in fetal plasma sodium levels were also associated with reductions in fetal plasma renin activity. Sodium 30-36 renin Ovis aries 97-102 6639745-7 1983 These and other findings raise the possibility that the normal secretion of aldosterone in rats after PEG treatment might permit physiological amounts of AII to be effective in stimulating sodium appetite. Sodium 189-195 angiotensinogen Rattus norvegicus 154-157 6639746-0 1983 Sodium appetite elicited by intracerebroventricular infusion of angiotensin II in the rat: I. Sodium 0-6 angiotensinogen Rattus norvegicus 64-78 6639746-2 1983 Intracerebroventricular infusion of angiotensin II (Ang II) elicits a substantial sodium appetite in the rat. Sodium 82-88 angiotensinogen Rattus norvegicus 36-50 6639746-2 1983 Intracerebroventricular infusion of angiotensin II (Ang II) elicits a substantial sodium appetite in the rat. Sodium 82-88 angiotensinogen Rattus norvegicus 52-58 6639746-4 1983 The larger and more sustained bouts of sodium ingestion occurring 8-12 hr after the start of the Ang II infusion appear to represent a behavioral compensation for this incurred sodium deficit. Sodium 39-45 angiotensinogen Rattus norvegicus 97-103 6639746-4 1983 The larger and more sustained bouts of sodium ingestion occurring 8-12 hr after the start of the Ang II infusion appear to represent a behavioral compensation for this incurred sodium deficit. Sodium 177-183 angiotensinogen Rattus norvegicus 97-103 6639746-5 1983 These results confirm the arousal of a sodium appetite by action of Ang II on the brain but indicate the need for caution in assigning to it a direct and exclusive role in the neuroendocrine control of sodium intake. Sodium 39-45 angiotensinogen Rattus norvegicus 68-74 6639747-0 1983 Sodium appetite elicited by intracerebroventricular infusion of angiotensin II in the rat: II. Sodium 0-6 angiotensinogen Rattus norvegicus 64-78 6400108-4 1983 Locally synthetized vasodilatory hormones (kinins, prostaglandins) modulate the effects of angiotensin II (AII), norepinephrine and alpha-adrenergic stimuli on renal vasculature and sodium excretion. Sodium 182-188 angiotensinogen Homo sapiens 91-105 6366501-0 1983 A comparison of biological effects of three angiotensin II antagonists in sodium depleted hypertensive patients. Sodium 74-80 angiotensinogen Homo sapiens 44-58 6371683-3 1983 Sheep subjected to rapid sodium depletion in response to parotid cannula drainage showed features indicating increased activity of the renin-angiotensin system with a rise in plasma renin concentration, an increase in the juxtaglomerular index and morphological evidence of increased renin granule production in arteriolar myoepithelioid cells. Sodium 25-31 renin Ovis aries 135-140 6371683-3 1983 Sheep subjected to rapid sodium depletion in response to parotid cannula drainage showed features indicating increased activity of the renin-angiotensin system with a rise in plasma renin concentration, an increase in the juxtaglomerular index and morphological evidence of increased renin granule production in arteriolar myoepithelioid cells. Sodium 25-31 renin Ovis aries 182-187 6371683-3 1983 Sheep subjected to rapid sodium depletion in response to parotid cannula drainage showed features indicating increased activity of the renin-angiotensin system with a rise in plasma renin concentration, an increase in the juxtaglomerular index and morphological evidence of increased renin granule production in arteriolar myoepithelioid cells. Sodium 25-31 renin Ovis aries 182-187 6371683-4 1983 In contrast, in sheep subjected to dietary sodium loading, there was evidence of decreased activity of the renin-angiotensin system with a fall in plasma renin concentration and relatively poor myoepithelioid cell granulation. Sodium 43-49 renin Ovis aries 107-112 6371683-4 1983 In contrast, in sheep subjected to dietary sodium loading, there was evidence of decreased activity of the renin-angiotensin system with a fall in plasma renin concentration and relatively poor myoepithelioid cell granulation. Sodium 43-49 renin Ovis aries 154-159 6689137-4 1983 No significant differences (NSD) were found except for greater sodium in Hyp milk. Sodium 63-69 phosphate regulating endopeptidase homolog, X-linked Mus musculus 73-76 6135874-6 1983 During moderate sodium restriction, plasma renin activity was low or low-normal in five of the seven patients. Sodium 16-22 renin Homo sapiens 43-48 6345048-5 1983 The usual two- to three-fold rise in plasma renin activity and angiotensin II observed in normal subjects on assumption of the upright posture after ingestion of 200 mg of sodium/day failed to occur in the kininogen-deficient individual. Sodium 172-178 renin Homo sapiens 44-49 6140085-0 1983 Effects of actinomycin D and cycloheximide on the activities of catalase and D-amino acid oxidase in the rat kidney cortex during sodium restriction. Sodium 130-136 catalase Rattus norvegicus 64-72 6140085-0 1983 Effects of actinomycin D and cycloheximide on the activities of catalase and D-amino acid oxidase in the rat kidney cortex during sodium restriction. Sodium 130-136 D-amino-acid oxidase Rattus norvegicus 77-97 6136631-2 1983 During sodium restriction, the rise in aldosterone one secretion was accompanied by trophic changes in the adrenal glomerulosa zone including increased angiotensin II receptors and enzymes of early and late steps in the aldosterone biosynthetic pathway. Sodium 7-13 angiotensinogen Rattus norvegicus 152-166 6883736-7 1983 A significant inverse relationship existed between sodium intake and bioactive angiotensin II in 5 normal subjects studied on low, normal and high sodium diets. Sodium 51-57 angiotensinogen Homo sapiens 79-93 6378223-0 1983 [Nyctohemeral values of plasma renin and aldosterone in relation to age, sex and sodium intake and posture]. Sodium 81-87 renin Homo sapiens 31-36 6310234-6 1983 Angiotensin II infusion in both sodium replete and deplete states also caused variable aldosterone responses. Sodium 32-38 angiotensinogen Homo sapiens 0-14 6136631-3 1983 All these effects of sodium restriction were reproduced by infusion of angiotensin II, and could be prevented by administration of the converting enzyme inhibitor, SQ 14,225. Sodium 21-27 angiotensinogen Rattus norvegicus 71-85 6136631-4 1983 These findings indicate that the adrenal secretory and trophic responses to sodium restriction are mediated by angiotensin II. Sodium 76-82 angiotensinogen Rattus norvegicus 111-125 6363775-0 1983 [Effects of vasopressin and insulin on sodium transport in the cultured renal cells]. Sodium 39-45 arginine vasopressin Homo sapiens 12-23 6655806-9 1983 The relative bioavailabilities of KS-R1, calculated on the basis of AUC and urinary recovery after parenteral administration of ABPC sodium, were 81.0 to 87.5% in mice, 37.6 to 45.9% in rats and 75.6 to 101% in rabbits, which were 1.5 to 2.8 times higher than those of ABPC orally administered. Sodium 133-139 kinase suppressor of ras 1 Mus musculus 34-39 6363775-0 1983 [Effects of vasopressin and insulin on sodium transport in the cultured renal cells]. Sodium 39-45 insulin Homo sapiens 28-35 6303176-1 1983 Recent studies suggest that sodium-dependent low-renin hypertension in animals results at least in part from sodium-potassium pump inhibition in blood vessels and heart by a humoral agent released from or influenced by the anteroventral third ventricular area of the brain. Sodium 28-34 renin Homo sapiens 49-54 6303410-0 1983 Lactoperoxidase-catalyzed iodination of sodium and potassium ion-activated adenosine triphosphatase in the Madin-Darby canine kidney epithelial cell line and canine renal membranes. Sodium 40-46 lactoperoxidase Canis lupus familiaris 0-15 6341220-6 1983 The increase in RVR in response to AII was positively correlated to sodium intake and plasma aldosterone concentration, indicating that these two factors might modulate the renal vascular reactivity. Sodium 68-74 angiotensinogen Homo sapiens 35-38 6866010-4 1983 Of the four mcAbs studies only mcAb 5.5, which is directed against the cholinergic site in Torpedo AChR, blocks the binding of alpha-bungarotoxin (alpha-Bgt) to AChR in chick muscle cultures and inhibits carbamylcholine-induced sodium transport in these cells. Sodium 228-234 cholinergic receptor nicotinic delta subunit Gallus gallus 99-103 6369515-1 1983 The relationship of the renin-angiotensin-aldosterone system to blood pressure and sodium homeostasis and to renal function was investigated serially in 12 patients with fulminant hepatic failure. Sodium 83-89 renin Homo sapiens 24-29 6357769-0 1983 Hypokalemia and sodium retention in patients with diabetes and chronic hepatitis receiving insulin and glycyrrhizin. Sodium 16-22 insulin Homo sapiens 91-98 6404909-0 1983 Role of sodium in ADP- and thrombin-induced megakaryocyte spreading. Sodium 8-14 coagulation factor II, thrombin Homo sapiens 27-35 6404909-1 1983 We investigated the role of sodium in megakaryocyte spreading induced by thrombin and ADP. Sodium 28-34 coagulation factor II, thrombin Homo sapiens 73-81 6404909-12 1983 These results indicate that megakaryocyte spreading induced by ADP and thrombin depends on an increase in sodium conductance. Sodium 106-112 coagulation factor II, thrombin Homo sapiens 71-79 6348254-2 1983 Injection of pig renin or purified renin from the mouse submaxillary gland into the preoptic region or third ventricle of the rat caused thirst within a minute or so of injection followed shortly afterwards by increased sodium appetite. Sodium 220-226 renin Sus scrofa 17-22 6348254-2 1983 Injection of pig renin or purified renin from the mouse submaxillary gland into the preoptic region or third ventricle of the rat caused thirst within a minute or so of injection followed shortly afterwards by increased sodium appetite. Sodium 220-226 renin Sus scrofa 35-40 6345888-3 1983 The results were compared with those of patients with primary aldosteronism and with essential hypertension where renin activity can be stimulated under similar sodium balance conditions. Sodium 161-167 renin Homo sapiens 114-119 6337910-5 1983 Subsequently, a small but significant decrease in serum arginine vasopressin levels to 3.04 +/- 0.65 microU/ml (p less than 0.05) was associated with a further rise in serum sodium levels above baseline values (138 +/- 1.4 mEq/L, p less than 0.01) and in serum osmolality. Sodium 174-180 arginine vasopressin Homo sapiens 65-76 6136631-6 1983 However, sodium restriction for 6 days significantly increased adrenal glomerulosa angiotensin II receptors and enzymes of the early and late aldosterone biosynthetic pathway, indicating that the pituitary gland is not necessary for the adrenal effects of angiotensin II. Sodium 9-15 angiotensinogen Rattus norvegicus 83-97 6136631-6 1983 However, sodium restriction for 6 days significantly increased adrenal glomerulosa angiotensin II receptors and enzymes of the early and late aldosterone biosynthetic pathway, indicating that the pituitary gland is not necessary for the adrenal effects of angiotensin II. Sodium 9-15 angiotensinogen Rattus norvegicus 256-270 6136631-7 1983 In contrast to the prominent glomerulotropic actions of angiotensin II in rats on normal or low sodium intake, infusion of angiotensin II during high sodium intake did not increase blood aldosterone, angiotensin II receptors, or 18-hydroxylase activity, indicating that the trophic actions of the octapeptide are determined by the state of sodium balance. Sodium 150-156 angiotensinogen Rattus norvegicus 123-137 6136631-7 1983 In contrast to the prominent glomerulotropic actions of angiotensin II in rats on normal or low sodium intake, infusion of angiotensin II during high sodium intake did not increase blood aldosterone, angiotensin II receptors, or 18-hydroxylase activity, indicating that the trophic actions of the octapeptide are determined by the state of sodium balance. Sodium 150-156 angiotensinogen Rattus norvegicus 123-137 6136631-7 1983 In contrast to the prominent glomerulotropic actions of angiotensin II in rats on normal or low sodium intake, infusion of angiotensin II during high sodium intake did not increase blood aldosterone, angiotensin II receptors, or 18-hydroxylase activity, indicating that the trophic actions of the octapeptide are determined by the state of sodium balance. Sodium 150-156 angiotensinogen Rattus norvegicus 123-137 6136631-7 1983 In contrast to the prominent glomerulotropic actions of angiotensin II in rats on normal or low sodium intake, infusion of angiotensin II during high sodium intake did not increase blood aldosterone, angiotensin II receptors, or 18-hydroxylase activity, indicating that the trophic actions of the octapeptide are determined by the state of sodium balance. Sodium 150-156 angiotensinogen Rattus norvegicus 123-137 6136631-9 1983 The ability of such factors to influence the effects of angiotensin II could serve as a protective mechanism to modulate aldosterone responses to angiotensin II when elevations in the circulating level of the peptide occur in the absence of sodium deficiency. Sodium 241-247 angiotensinogen Rattus norvegicus 56-70 6136631-9 1983 The ability of such factors to influence the effects of angiotensin II could serve as a protective mechanism to modulate aldosterone responses to angiotensin II when elevations in the circulating level of the peptide occur in the absence of sodium deficiency. Sodium 241-247 angiotensinogen Rattus norvegicus 146-160 6295691-5 1983 Further incremental and percentage changes of 18-OHB in response to graded dose infusions of angiotensin II and adrenocorticotropic hormone (ACTH) were greater during the 40 mmol of sodium intake period. Sodium 182-188 angiotensinogen Homo sapiens 93-139 6297212-3 1983 However, if the sodium-loaded dexamethasone-treated rats were given maintenance doses of ACTH, angiotensin II exerted a strong adrenoglomerulotrophic effect. Sodium 16-22 angiotensinogen Rattus norvegicus 95-109 6138931-2 1983 Stimulation or inhibition of renin at least during a normal sodium intake seems to depend mostly on the sympathetic nervous system and be mediated through beta 1-adrenoceptors. Sodium 60-66 renin Homo sapiens 29-34 6185006-9 1983 These studies suggest that intrarenal angiotensin II may mediate this reduction in LpA during chronic sodium depletion, but an effect of adrenergic nerve activity has not been excluded. Sodium 102-108 angiotensinogen Rattus norvegicus 38-52 6625420-4 1983 Sodium inflation is likely to be responsible for abnormal responses to angiotensin II and its antagonists in normotensive acromegalics, which make the use of these agents inappropriate for the study of the renin-angiotensin-aldosterone system. Sodium 0-6 angiotensinogen Homo sapiens 71-85 6367845-6 1983 The resulting fall in insulin levels may lead to decreased sodium absorption in the kidney. Sodium 59-65 insulin Homo sapiens 22-29 6626630-1 1983 The role of prolactin in the adaptation of premature infants to the alterations of sodium balance was investigated by measuring plasma prolactin levels serially in 7 low birth weight, premature infants with (group I) and without (group II) NaCl supplementation. Sodium 83-89 prolactin Homo sapiens 12-21 6626630-5 1983 When supplemental sodium was given, the plasma prolactin level declined with age at a steady rate to the mean value of 3,516 +/- 502 mU/l by the end of 5th week. Sodium 18-24 prolactin Homo sapiens 47-56 6626630-7 1983 It is concluded that physiological sodium depletion may account for the prolonged hyperprolactinemia and prolactin might have some importance in the control of sodium homeostasis in low birth weight, premature infants. Sodium 35-41 prolactin Homo sapiens 87-96 6303639-2 1983 ACTH administration was associated with urinary sodium retention, hypokalaemia, elevation of fasting blood glucose, lymphopaenia and eosinopaenia. Sodium 48-54 proopiomelanocortin Homo sapiens 0-4 6315266-6 1983 The increase in subfornical organ receptors resembles the up-regulation of AII sites which occurs in the adrenal cortex during sodium deficiency, and could play a role in potentiating the dipsogenic effect of AII in dehydration. Sodium 127-133 angiotensinogen Rattus norvegicus 75-78 6315274-5 1983 If this is so, our results suggest that the renin system is an important control of both normal and high blood pressure when on a normal sodium intake. Sodium 137-143 renin Homo sapiens 44-49 6357558-2 1983 The renin concentration of these cells is influenced by changes in sodium balance and after nephrectomy, while the renin of the fasciculata-medullary tissue is not. Sodium 67-73 renin Homo sapiens 4-9 6357565-0 1983 The renin system for long-term control over vasoconstriction and sodium-volume homeostasis in the spectrum of hypertension: three new frontiers in research. Sodium 65-71 renin Homo sapiens 4-9 6667558-0 1983 Influence of sodium diet and deoxycorticosterone on the response to norepinephrine, lysine-vasopressin and angiotensin II of isolated perfused rat mesenteric arteries. Sodium 13-19 angiotensinogen Rattus norvegicus 107-121 6137317-7 1983 Vasopressin failed to increase SCC in vivo when the external sodium concentration was 115 mM, being effective only when the sodium concentration was low (5 mM). Sodium 124-130 arginine vasopressin Homo sapiens 0-11 6671385-6 1983 Low NA and A may participate in lowering the plasma renin activity which in PA in suppressed, sometimes disproportionately to the actual body sodium content. Sodium 142-148 renin Homo sapiens 52-57 6129161-7 1983 It is suggested that the positive inotropic effect of ATX II is caused by a delayed inactivation of the fast sodium current, which leads to an increase of the sodium transient and of the pump activity of Na+,K+-ATPase. Sodium 109-115 ectonucleotide pyrophosphatase/phosphodiesterase 2 Homo sapiens 54-57 6129161-7 1983 It is suggested that the positive inotropic effect of ATX II is caused by a delayed inactivation of the fast sodium current, which leads to an increase of the sodium transient and of the pump activity of Na+,K+-ATPase. Sodium 159-165 ectonucleotide pyrophosphatase/phosphodiesterase 2 Homo sapiens 54-57 6129161-8 1983 In contrast to the presynaptic mode of action on crustacean and frog nerve-muscle preparations, ATX II has a direct effect on mammalian skeletal muscle fiber membranes and induces a sodium-dependent increase of twitch responses and duration of the action potential. Sodium 182-188 ectonucleotide pyrophosphatase/phosphodiesterase 2 Homo sapiens 96-99 6294273-1 1983 Vasopressin enhances osmotic water flow and sodium transport across the toad urinary bladder by mechanisms involving cyclic AMP and calcium. Sodium 44-50 arginine vasopressin Homo sapiens 0-11 6664426-5 1983 In conclusion, the benefit of HDB is not remarkable when HDA is performed not only in standard conditions but also with a bath rich in sodium and with control of ultrafiltration. Sodium 135-141 integrator complex subunit 6 Homo sapiens 30-33 6343958-8 1983 A marked increase of the production of Angiotensin-I with increasing sodium concentrations at a low Potassium range was observed and the opposite was true at high Potassium concentrations. Sodium 69-75 angiotensinogen Homo sapiens 39-52 6128546-2 1982 The other 8 patients had a high plasma renin activity which may have caused the sodium retention. Sodium 80-86 renin Homo sapiens 39-44 6756162-1 1982 The role of angiotensin II in the stimulation of aldosterone biosynthesis by sodium sequestration in potassium-deficient rats was assessed by experiments involving 1-day angiotensin II infusion, converting enzyme inhibition, and bilateral nephrectomy. Sodium 77-83 angiotensinogen Rattus norvegicus 12-26 6756162-5 1982 According to these results, angiotensin II is an essential mediator in the stimulation of aldosterone biosynthesis by sodium sequestration. Sodium 118-124 angiotensinogen Rattus norvegicus 28-42 6292538-0 1982 Effects of dietary sodium on brain angiotensin II receptors in spontaneously hypertensive rats. Sodium 19-25 angiotensinogen Rattus norvegicus 35-49 6822640-0 1983 Dopaminergic modulation of aldosterone responsiveness to angiotensin II with changes in sodium intake. Sodium 88-94 angiotensinogen Homo sapiens 57-71 6822640-1 1983 The aldosterone response to infused angiotensin II (AII) is blunted by sodium (Na) loading. Sodium 71-77 angiotensinogen Homo sapiens 36-50 6822640-1 1983 The aldosterone response to infused angiotensin II (AII) is blunted by sodium (Na) loading. Sodium 71-77 angiotensinogen Homo sapiens 52-55 6822640-10 1983 These results suggest that dopamine may be an important regulator of the alterations in aldosterone responsiveness to AII that occur during changes in dietary sodium intake. Sodium 159-165 angiotensinogen Homo sapiens 118-121 6292538-7 1982 The secretion of arginine vasopressin (AVP) increased significantly in SHR with high sodium intake. Sodium 85-91 arginine vasopressin Rattus norvegicus 26-37 6757970-2 1982 In each renin subgroup, the administration of furosemide and 2 hours upright posture induced marked increases in urinary excretion of PGE and sodium, and in plasma renin activity. Sodium 142-148 renin Homo sapiens 8-13 6751073-4 1982 On restricted sodium intake, diabetics, compared to normotensives, had reduced urinary kallikrein activity (p less than 0.01) and reduced ambulatory plasma renin activity (p less than 0.01). Sodium 14-20 renin Homo sapiens 156-161 7124963-1 1982 We investigated the systemic and regional hemodynamic alterations induced in normotensive anephric rats by stimulation of endogenous vasopressin with an acute sodium and fluid load and following vasopressin inhibition with a specific antagonist of its vasoconstricting action. Sodium 159-165 arginine vasopressin Rattus norvegicus 133-144 7172121-4 1982 AII increased the glomerular filtration rate (GFR) by 155%, increased sodium reabsorption by 157%, and decreased the urine sodium concentration by 34% without affecting sodium excretion. Sodium 70-76 angiotensinogen Rattus norvegicus 0-3 7172121-4 1982 AII increased the glomerular filtration rate (GFR) by 155%, increased sodium reabsorption by 157%, and decreased the urine sodium concentration by 34% without affecting sodium excretion. Sodium 123-129 angiotensinogen Rattus norvegicus 0-3 7172121-4 1982 AII increased the glomerular filtration rate (GFR) by 155%, increased sodium reabsorption by 157%, and decreased the urine sodium concentration by 34% without affecting sodium excretion. Sodium 123-129 angiotensinogen Rattus norvegicus 0-3 7172121-6 1982 In these experiments, AII had no effect on sodium reabsorption or excretion and decreased the urine sodium concentration by 7%. Sodium 100-106 angiotensinogen Rattus norvegicus 22-25 7143552-4 1982 Bumetanide, given intravenously, spironolactone, frusemide and ADH increased urinary sodium and all except frusemide intravenously decreased faecal sodium regardless of route of administration. Sodium 85-91 arginine vasopressin Homo sapiens 63-66 6286278-0 1982 Vasopressin resistance induced by low sodium and high mannitol in toad bladder. Sodium 38-44 arginine vasopressin Homo sapiens 0-11 6286477-0 1982 Modulation of brain angiotensin-converting enzyme by dietary sodium and chronic intravenous and intracerebroventricular fusion of angiotensin II. Sodium 61-67 angiotensin I converting enzyme Rattus norvegicus 20-49 6286477-3 1982 Sodium-loaded rats had lower activity of ACE in hypothalamus, striatum, and midbrain, and higher activity in spinal cord compared to controls. Sodium 0-6 angiotensin I converting enzyme Rattus norvegicus 41-44 6286477-4 1982 In sodium-restricted rats, ACE was elevated in pituitary and depressed in spinal cord. Sodium 3-9 angiotensin I converting enzyme Rattus norvegicus 27-30 6286477-7 1982 These results show that ACE in several brain regions is sensitive to dietary sodium intake and support the hypothesis that angiotensin-containing neurons in these areas might be responsive to NaCl status of the animal. Sodium 77-83 angiotensin I converting enzyme Rattus norvegicus 24-27 7132236-1 1982 There is accumulating evidence that acetylcholinesterase (AChE might be involved in the transport of sodium across biological membranes. Sodium 101-107 acetylcholinesterase (Cartwright blood group) Homo sapiens 36-56 7132236-1 1982 There is accumulating evidence that acetylcholinesterase (AChE might be involved in the transport of sodium across biological membranes. Sodium 101-107 acetylcholinesterase (Cartwright blood group) Homo sapiens 58-62 7132236-6 1982 Sodium inhibited AChE at low substrate concentrations, whereas the enzyme was activated by sodium at moderate and high substrate levels. Sodium 0-6 acetylcholinesterase (Cartwright blood group) Homo sapiens 17-21 6813454-24 1982 This paper supports the hypothesis that release of inactive renin by the kidney is controlled by a sodium-sensitive mechanism. Sodium 99-105 LOW QUALITY PROTEIN: renin Oryctolagus cuniculus 60-65 7091310-8 1982 Taken together, these data affirm in diabetic rats, as in humans, the occurrence of 1) elevated steady-state levels of AVP in serum; 2) abnormal sensitivity of AVP secretion to changes in serum sodium and osmolality; and 3) an apparently intact end-organ responsiveness to AVP. Sodium 194-200 arginine vasopressin Homo sapiens 119-122 7091310-8 1982 Taken together, these data affirm in diabetic rats, as in humans, the occurrence of 1) elevated steady-state levels of AVP in serum; 2) abnormal sensitivity of AVP secretion to changes in serum sodium and osmolality; and 3) an apparently intact end-organ responsiveness to AVP. Sodium 194-200 arginine vasopressin Homo sapiens 160-163 7091310-8 1982 Taken together, these data affirm in diabetic rats, as in humans, the occurrence of 1) elevated steady-state levels of AVP in serum; 2) abnormal sensitivity of AVP secretion to changes in serum sodium and osmolality; and 3) an apparently intact end-organ responsiveness to AVP. Sodium 194-200 arginine vasopressin Homo sapiens 160-163 6809473-3 1982 During the initial 30 min period a maximum additional excretion rate of sodium of 3.3 mmol min-1 was reached at an excretion rate of 0.8 mg furosemide min-1. Sodium 72-78 CD59 molecule (CD59 blood group) Homo sapiens 91-96 6809473-3 1982 During the initial 30 min period a maximum additional excretion rate of sodium of 3.3 mmol min-1 was reached at an excretion rate of 0.8 mg furosemide min-1. Sodium 72-78 CD59 molecule (CD59 blood group) Homo sapiens 151-156 6281293-1 1982 Escape from the sodium-retaining action of mineralocorticoids coincides with the suppression of plasma renin and angiotensin II levels. Sodium 16-22 renin Homo sapiens 103-127 6753495-7 1982 The study supports the view that sodium sensitive receptors close to the cerebral ventricular system participate in the regulation of renal sodium excretion and renin release, it also suggests that renal sodium excretion is affected by an unknown hormonal factor of cerebral origin, while the release of renin seen in response to a reduction in CSF [Na] is mediated by the renal nerves. Sodium 33-39 renin Ovis aries 161-166 6753495-7 1982 The study supports the view that sodium sensitive receptors close to the cerebral ventricular system participate in the regulation of renal sodium excretion and renin release, it also suggests that renal sodium excretion is affected by an unknown hormonal factor of cerebral origin, while the release of renin seen in response to a reduction in CSF [Na] is mediated by the renal nerves. Sodium 33-39 renin Ovis aries 304-309 7044119-7 1982 In the normotensive relatives of hypertensive patients, the renin system may be responsible for the decreased sodium excretory capacity. Sodium 110-116 renin Homo sapiens 60-65 7037818-8 1982 Gross changes in sodium intake during pregnancy result in changes in active and inactive renin concentrations parallel to those observed in nonpregnant controls. Sodium 17-23 renin Homo sapiens 89-94 6280473-2 1982 On the sodium-restricted diet, the hypotensive response to captopril was accompanied by significant increments in the metabolite of prostaglandin E2 (PGE2-M) and bradykinin and by significant decrements in angiotensin II. Sodium 7-13 kininogen 1 Homo sapiens 162-172 6280473-2 1982 On the sodium-restricted diet, the hypotensive response to captopril was accompanied by significant increments in the metabolite of prostaglandin E2 (PGE2-M) and bradykinin and by significant decrements in angiotensin II. Sodium 7-13 angiotensinogen Homo sapiens 206-220 7072743-5 1982 The elevated ADH levels occurred despite significantly lower plasma sodium concentration (133 +/- 1 meq/liter versus 138 +/- 2 meq/liter, p less than 0.05) compared wit control values. Sodium 68-74 arginine vasopressin Homo sapiens 13-16 7041843-0 1982 Racial difference in salivary sodium-potassium ratio in low renin essential hypertension. Sodium 30-36 renin Homo sapiens 60-65 6807681-2 1982 Renin (PRA) increased significantly after low sodium diet and the increase was inversely related to urinary sodium excretion. Sodium 46-52 renin Homo sapiens 0-5 6807681-2 1982 Renin (PRA) increased significantly after low sodium diet and the increase was inversely related to urinary sodium excretion. Sodium 46-52 S100 calcium binding protein A6 Homo sapiens 7-10 6807681-2 1982 Renin (PRA) increased significantly after low sodium diet and the increase was inversely related to urinary sodium excretion. Sodium 108-114 renin Homo sapiens 0-5 6807681-2 1982 Renin (PRA) increased significantly after low sodium diet and the increase was inversely related to urinary sodium excretion. Sodium 108-114 S100 calcium binding protein A6 Homo sapiens 7-10 6807681-4 1982 PRA decrements after either oxprenolol or indomethacin were significantly related to PRA values after low sodium diet while no correlation was present between PRA values after oxprenolol and indomethacin. Sodium 106-112 S100 calcium binding protein A6 Homo sapiens 0-3 6807681-4 1982 PRA decrements after either oxprenolol or indomethacin were significantly related to PRA values after low sodium diet while no correlation was present between PRA values after oxprenolol and indomethacin. Sodium 106-112 S100 calcium binding protein A6 Homo sapiens 85-88 6807681-4 1982 PRA decrements after either oxprenolol or indomethacin were significantly related to PRA values after low sodium diet while no correlation was present between PRA values after oxprenolol and indomethacin. Sodium 106-112 S100 calcium binding protein A6 Homo sapiens 85-88 6807681-5 1982 Aldosterone excretion showed a trend similar to that of PRA, being related to PRA on normal and low sodium diet, and to a lesser extent after drug treatment. Sodium 100-106 S100 calcium binding protein A6 Homo sapiens 56-59 7044934-0 1982 Interaction between effects of insulin and vasopressin on renal excretion of water and sodium in rats. Sodium 87-93 arginine vasopressin Rattus norvegicus 43-54 6285371-0 1982 Beta-endorphin: opiate receptor binding activities of six naturally occurring beta-endorphin homologs studied by using tritiated human hormone and naloxone as primary ligands--effects of sodium ion. Sodium 187-193 proopiomelanocortin Homo sapiens 0-14 6175971-0 1982 Intracerebroventricular infusions of angiotensin II increases sodium excretion. Sodium 62-68 angiotensinogen Homo sapiens 37-51 7066698-6 1982 Sodium accumulation, in the presence of NGF, increases from E6 to E10. Sodium 0-6 nerve growth factor Gallus gallus 40-43 7068178-4 1982 These results suggest that angiotensinogen participates in the regulation of blood pressure in normotensive rats, even in the sodium-replete state. Sodium 126-132 angiotensinogen Rattus norvegicus 27-42 7068180-2 1982 In the patients with essential hypertension, the rate constant for total sodium efflux was significantly lower than in the normotensives (5.96.10(-3) +/- 0.45.10(-3) min-1 vs 6.69.10(-3) +/- 0.49.10(-3) min-1; p less than 0.005), which was due to a reduced ouabain-sensitive sodium efflux rate constant. Sodium 73-79 CD59 molecule (CD59 blood group) Homo sapiens 166-171 7068180-2 1982 In the patients with essential hypertension, the rate constant for total sodium efflux was significantly lower than in the normotensives (5.96.10(-3) +/- 0.45.10(-3) min-1 vs 6.69.10(-3) +/- 0.49.10(-3) min-1; p less than 0.005), which was due to a reduced ouabain-sensitive sodium efflux rate constant. Sodium 73-79 CD59 molecule (CD59 blood group) Homo sapiens 203-208 7068188-3 1982 Plasma renin activity became high in the low sodium group and low in the high sodium group at the end of the treatment. Sodium 45-51 LOW QUALITY PROTEIN: renin Oryctolagus cuniculus 7-12 7068188-3 1982 Plasma renin activity became high in the low sodium group and low in the high sodium group at the end of the treatment. Sodium 78-84 LOW QUALITY PROTEIN: renin Oryctolagus cuniculus 7-12 7061705-1 1982 The administration of vasodilating agents such as bradykinin and acetylcholine cause an increase in urinary sodium excretion. Sodium 108-114 kininogen 1 Canis lupus familiaris 50-60 7061705-5 1982 Bradykinin increased renal blood flow from 222 to 342 ml/min, urine volume from 0.2 to 1.2 ml/min, and urine sodium excretion from 28 to 115 mueq/min. Sodium 109-115 kininogen 1 Canis lupus familiaris 0-10 7061705-9 1982 Control papillary plasma flow was 29 ml/min per 100 g. Bradykinin increased urinary sodium excretion 108 mueq/min and decreased urinary osmolality from 1,254 to 516 mosmol/kg in association with a rise in papillary plasma flow to 62 ml/min per 100 g. Urine sodium excretion, urinary osmolality, and urine flow rate, as well as papillary plasma flow rate (32 ml/min per 100 g) were unchanged from control when secretin was administered. Sodium 84-90 kininogen 1 Canis lupus familiaris 55-65 7061705-9 1982 Control papillary plasma flow was 29 ml/min per 100 g. Bradykinin increased urinary sodium excretion 108 mueq/min and decreased urinary osmolality from 1,254 to 516 mosmol/kg in association with a rise in papillary plasma flow to 62 ml/min per 100 g. Urine sodium excretion, urinary osmolality, and urine flow rate, as well as papillary plasma flow rate (32 ml/min per 100 g) were unchanged from control when secretin was administered. Sodium 257-263 kininogen 1 Canis lupus familiaris 55-65 7043493-2 1982 A low sodium intake increased urinary excretion of PGF2 alpha MUM (p less than 0.05), but failed to change urinary excretion of PGE and PGF2 alpha. Sodium 6-12 latexin Homo sapiens 62-65 7043493-3 1982 In contrast, a high sodium intake increased urinary excretion of PGE (p less than 0.01) and decreased urinary excretion of PGF2 alpha MUM (p less than 0.02). Sodium 20-26 latexin Homo sapiens 134-137 7043493-4 1982 A low sodium intake decreased the ratio of urinary PGE/PGF2 alpha MUM and high sodium increased it (both p less than 0.001). Sodium 6-12 latexin Homo sapiens 66-69 7036728-5 1982 A decrease in sodium and water delivery to the ascending limb or in NaCl reabsorption by the ascending limb will impair urinary diluting ability, as will the presence of ADH. Sodium 14-20 arginine vasopressin Homo sapiens 170-173 7039342-4 1982 Absolute and fractional sodium excretion were increased sixfold during ANG II blockade. Sodium 24-30 angiotensinogen Rattus norvegicus 71-77 7037024-6 1982 It is concluded that serum sodium can be used to identify those patients with congestive heart failure who have a high plasma renin activity. Sodium 27-33 renin Homo sapiens 126-131 6758385-0 1982 [Correlation of erythrocyte sodium concentration and the KG-value in variable peripheral insulin levels]. Sodium 28-34 insulin Homo sapiens 89-96 6758385-4 1982 A conception was presented issuing from the fact that the negative correlation between the KG-value and the sodium concentration is based on properties of the cell membrane which influence the intracellular sodium concentration as well as the effect of insulin in the cell. Sodium 108-114 insulin Homo sapiens 253-260 6750618-0 1982 The role of the adrenal glands in sodium excretion evoked by centrally administered renin. Sodium 34-40 renin Homo sapiens 84-89 7126762-2 1982 Choline glycerophospholipids with diacyl residues and also alk-1"-enyl and acyl residues gave the readily interpretable field desorption mass spectra in which a sodium cluster ion [M+NA]+ was a base peak. Sodium 161-167 secretory leukocyte peptidase inhibitor Homo sapiens 59-64 7200346-6 1982 The data confirm the hypothesis that the principal determinant of pressor responsiveness to A II during pregnancy is arteriolar response; this seems to be modulated by alterations in the sodium content of the vessel wall. Sodium 187-193 NLR family pyrin domain containing 3 Homo sapiens 92-96 6220764-0 1982 [Relations between the renin-angiotensin-aldosterone system and urinary elimination of sodium: study of healthy subjects in clinostatism and on a sodium-free diet]. Sodium 87-93 renin Homo sapiens 23-28 6220764-0 1982 [Relations between the renin-angiotensin-aldosterone system and urinary elimination of sodium: study of healthy subjects in clinostatism and on a sodium-free diet]. Sodium 146-152 renin Homo sapiens 23-28 7055905-1 1982 Results obtained with a potentiometric analyzer, NOVA 1, specific for sodium and potassium, were compared with those by flame photometry. Sodium 70-76 NOVA alternative splicing regulator 1 Homo sapiens 49-55 7055905-4 1982 There may be a small interaction between sodium and albumin. Sodium 41-47 albumin Homo sapiens 52-59 6183031-1 1982 Animal data suggest that angiotensin II may directly affect renal sodium retention independent of aldosterone (4,6). Sodium 66-72 angiotensinogen Homo sapiens 25-39 6183031-3 1982 We describe here experiments designed to elucidate the role of angiotensin II in renal sodium retention in normal man. Sodium 87-93 angiotensinogen Homo sapiens 63-77 6291809-1 1982 It is well established that the response of plasma aldosterone to ACTH is enhanced in the sodium depleted state. Sodium 90-96 proopiomelanocortin Homo sapiens 66-70 6291809-11 1982 Thus, endogenous prostaglandins appear to be of far greater importance than the renin-angiotensin system in mediating the increased aldosterone response to ACTH administration during the sodium depleted state in man. Sodium 187-193 proopiomelanocortin Homo sapiens 156-160 6291819-6 1982 When the renin system is depressed, sodium loss may prevent a large drop in aldosterone levels. Sodium 36-42 renin Homo sapiens 9-14 6307553-4 1982 ACE was inversely related to systolic and mean arterial blood pressures, inversely to serum sodium and urinary potassium and directly to serum potassium levels. Sodium 92-98 angiotensin I converting enzyme Homo sapiens 0-3 6749346-8 1982 The mechanism of this sustained renin response several days after cessation of diuretic therapy may be best explained by a prolonged action of furosemide or by partial ongoing volume depletion with reduced sodium load to the distal nephron. Sodium 206-212 renin Homo sapiens 32-37 6754152-1 1982 A nomogram based on the relationship between plasma renin activity and urinary sodium excretion in normal subjects has been used to classify 956 patients with essential hypertension into low, medium and high renin subgroups. Sodium 79-85 renin Homo sapiens 52-57 6754154-0 1982 The salivary sodium/potassium ratio in hypertension: relation to race and plasma renin activity. Sodium 13-19 renin Homo sapiens 81-86 6756698-11 1982 At the physiological level the activation and/or release of renin appears to be primarily determined by sodium-volume changes perceived by a distal tubular mechanism. Sodium 104-110 renin Homo sapiens 60-65 7047005-0 1982 Aldosterone responsiveness to angiotensin II after sodium restriction in subjects with low renin essential hypertension. Sodium 51-57 renin Homo sapiens 91-96 7047005-2 1982 The PA response to sodium restriction in relation to changes in plasma renin activity (PRA) was estimated by the ratio of PA increment to PRA increment after sodium restriction (delta PA/delta PRA). Sodium 19-25 renin Homo sapiens 71-76 7047005-5 1982 Apparently some LREH subjects, whose delta PA/delta PRA ratios after sodium restriction were high, have an abnormally enhanced aldosterone responsiveness to AII under the condition of low sodium intake. Sodium 69-75 angiotensinogen Homo sapiens 157-160 7047005-5 1982 Apparently some LREH subjects, whose delta PA/delta PRA ratios after sodium restriction were high, have an abnormally enhanced aldosterone responsiveness to AII under the condition of low sodium intake. Sodium 188-194 angiotensinogen Homo sapiens 157-160 7105437-4 1982 Thus, two vasopressor mechanisms were stimulated by sodium excess: an acute, transient, partly vasopressin-mediated phase seemed to be followed by a chronic phase mediated through stimulation of central sympathetic neurons. Sodium 52-58 arginine vasopressin Rattus norvegicus 95-106 6764472-4 1982 Sodium loading was associated with marked suppression of plasma renin activity, aldosterone and norepinephrine, and increases in cardiac index. Sodium 0-6 renin Homo sapiens 64-69 7033264-0 1982 Influence of sodium homeostasis on dopaminergic modulation of aldosterone, renin, and prolactin secretion in man. Sodium 13-19 prolactin Homo sapiens 86-95 7033264-7 1982 The proportion of total renin which was inactive was greater with the higher sodium intake. Sodium 77-83 renin Homo sapiens 24-29 7033264-8 1982 These data suggest that sodium homeostasis may influence dopaminergic modulation of renin, aldosterone, and PRL secretion and may effect the interrelationship between active and inactive renin. Sodium 24-30 renin Homo sapiens 84-89 7033264-8 1982 These data suggest that sodium homeostasis may influence dopaminergic modulation of renin, aldosterone, and PRL secretion and may effect the interrelationship between active and inactive renin. Sodium 24-30 renin Homo sapiens 187-192 6290664-0 1982 Enhanced sensitivity to stimulation of sodium transport and cyclic AMP by antidiuretic hormone after Ca2+ depletion of isolated frog skin epithelium. Sodium 39-45 arginine vasopressin Homo sapiens 74-94 6290664-1 1982 The role of Ca2+ in the stimulation by antidiuretic hormone (ADH) of active sodium transport across the isolated epithelium of frog skin was investigated. Sodium 76-82 arginine vasopressin Homo sapiens 39-59 6290664-1 1982 The role of Ca2+ in the stimulation by antidiuretic hormone (ADH) of active sodium transport across the isolated epithelium of frog skin was investigated. Sodium 76-82 arginine vasopressin Homo sapiens 61-64 6223136-1 1982 CaATPase of human erythrocyte membranes exists in both a basal and a calmodulin-activated form, each of which can be further activated by monovalent ions such as sodium, potassium or lithium. Sodium 162-168 calmodulin 1 Homo sapiens 69-79 7069622-9 1982 In the first hour of prolactin administration (in comparison with the control group), urine flow, sodium output and osmolal output were all significantly reduced (P less than 0.02); there was also a reduction (P less than 0.05) in renal plasma flow (p-amino-hippurate clearance), but the filtration fraction did not alter. Sodium 98-104 prolactin Rattus norvegicus 21-30 7077947-1 1982 Changes in renal hemodynamics and sodium excretion induced by an angiotensin II (AII) infusion were correlated with urinary prostaglandin E2 (PGE2) excretion in 15 patients with cirrhosis and ascites. Sodium 34-40 angiotensinogen Homo sapiens 65-79 7077947-1 1982 Changes in renal hemodynamics and sodium excretion induced by an angiotensin II (AII) infusion were correlated with urinary prostaglandin E2 (PGE2) excretion in 15 patients with cirrhosis and ascites. Sodium 34-40 angiotensinogen Homo sapiens 81-84 7077947-10 1982 We conclude that in patients with hepatic cirrhosis, the sodium excretion pattern induced by an exogenous AII challenge may depend on the prior state of intrarenal prostaglandin activity. Sodium 57-63 angiotensinogen Homo sapiens 106-109 6757778-0 1982 Is the renin-angiotensin-aldosterone system involved in the sodium retention in the nephrotic syndrome? Sodium 60-66 renin Homo sapiens 7-12 6280212-1 1982 The effects of diazoxide and hydrochlorothiazide on vasopressin-induced increments in osmotic water flow and sodium transport across the frog bladder were studied. Sodium 109-115 arginine vasopressin Homo sapiens 52-63 7079557-2 1982 Renal arterial infusion of BK (3 micrograms/min) in control dogs produced a sustained increase in urine flow rate (V), sodium excretion (UNaV), potassium excretion (UKV), and renal plasma flow (RPF) without a consistent change in glomerular filtration rate (GFR) or renin secretion rate (RSR). Sodium 119-125 kininogen 1 Canis lupus familiaris 27-29 7028367-17 1981 These data support our previous suggestion that activation of inactive renin is regulated by a sodium-sensitive intrarenal mechanism. Sodium 95-101 LOW QUALITY PROTEIN: renin Oryctolagus cuniculus 71-76 6171420-1 1981 We previously found that the sustained rise in active sodium transport by the toad urinary bladder after exposure to insulin is associated with the synthesis of a membrane protein with a molecular weight of 25,000. Sodium 54-60 insulin Homo sapiens 117-124 7033970-0 1981 Effect of furosemide and dietary sodium on kidney and plasma big and small renin. Sodium 33-39 renin Homo sapiens 75-80 7036720-0 1981 Sodium intake alters the effects of norepinephrine on the renin system and the kidney. Sodium 0-6 renin Homo sapiens 58-63 7026131-0 1981 Plasma angiotensin II concentration regulates vascular but not adrenal responsiveness to restriction of sodium intake in normal man. Sodium 104-110 angiotensinogen Homo sapiens 7-21 7026131-2 1981 Sodium restriction increases adrenal and decreases vascular sensitivity to angiotensin II (ANG II). Sodium 0-6 angiotensinogen Homo sapiens 75-89 7026131-2 1981 Sodium restriction increases adrenal and decreases vascular sensitivity to angiotensin II (ANG II). Sodium 0-6 angiotensinogen Homo sapiens 91-97 7026131-9 1981 In the ANG II infusion studies the slope of the aldosterone--ANG II regression line on low sodium intake was significantly steeper than that on high sodium intake. Sodium 91-97 angiotensinogen Homo sapiens 7-13 7026131-9 1981 In the ANG II infusion studies the slope of the aldosterone--ANG II regression line on low sodium intake was significantly steeper than that on high sodium intake. Sodium 91-97 angiotensinogen Homo sapiens 61-67 7026131-9 1981 In the ANG II infusion studies the slope of the aldosterone--ANG II regression line on low sodium intake was significantly steeper than that on high sodium intake. Sodium 149-155 angiotensinogen Homo sapiens 7-13 7026131-12 1981 In the ANG II infusion studies the slope of the mean blood pressure--ANG II regression line on high sodium intake was significantly steeper than that on low sodium intake. Sodium 100-106 angiotensinogen Homo sapiens 7-13 7026131-12 1981 In the ANG II infusion studies the slope of the mean blood pressure--ANG II regression line on high sodium intake was significantly steeper than that on low sodium intake. Sodium 100-106 angiotensinogen Homo sapiens 69-75 7026131-12 1981 In the ANG II infusion studies the slope of the mean blood pressure--ANG II regression line on high sodium intake was significantly steeper than that on low sodium intake. Sodium 157-163 angiotensinogen Homo sapiens 69-75 7026131-13 1981 The addition of captopril to sodium-restricted subjects caused the slope of the regression relationship to increase significantly, consistent with an enhanced vascular responsiveness when endogenous ANG II levels were lowered. Sodium 29-35 angiotensinogen Homo sapiens 199-205 6795033-1 1981 Insulin-stimulated sodium transport in the toad urinary bladder consists of two components, a brief element of rapid onset that is independent of protein synthesis, and a sustained increase, slower in onset, that is dependent upon RNA and protein synthesis. Sodium 19-25 insulin Homo sapiens 0-7 7028610-6 1981 Sodium retention correlated significantly with the percent fall in urinary aldosterone only in the low-renin essential hypertension group. Sodium 0-6 renin Homo sapiens 103-108 7026596-5 1981 The significance of the plasma sodium rise was assessed by observing the vasopressin response to hypoglycemia in a patient shown previously to have a selective loss of the vasopressin response to osmotic stimulation. Sodium 31-37 arginine vasopressin Homo sapiens 73-84 7158367-6 1982 infusion of indomethacin bradykinin was infused into the left renal artery, RBFdir, urine flow and sodium excretion increased to the control values in the left kidney while remained lower in the right kidney. Sodium 99-105 kininogen 1 Canis lupus familiaris 25-35 7026596-5 1981 The significance of the plasma sodium rise was assessed by observing the vasopressin response to hypoglycemia in a patient shown previously to have a selective loss of the vasopressin response to osmotic stimulation. Sodium 31-37 arginine vasopressin Homo sapiens 172-183 6800358-1 1981 Insulin increases active sodium transport by the toad urinary bladder within 15 min, an effect which persists for an least 20 h. In tissues pre-treated with inhibitors of transcription or translation, sodium transport briefly increases after insulin addition but returns to basal levels within 60-90 min. Sodium 25-31 insulin Homo sapiens 0-7 6800358-1 1981 Insulin increases active sodium transport by the toad urinary bladder within 15 min, an effect which persists for an least 20 h. In tissues pre-treated with inhibitors of transcription or translation, sodium transport briefly increases after insulin addition but returns to basal levels within 60-90 min. Sodium 25-31 insulin Homo sapiens 242-249 6800358-4 1981 The time course and dose-response relationship of the induction of protein synthesis by insulin suggest that these proteins may play a role in the sustained elevation of sodium transport by insulin. Sodium 170-176 insulin Homo sapiens 88-95 6800358-4 1981 The time course and dose-response relationship of the induction of protein synthesis by insulin suggest that these proteins may play a role in the sustained elevation of sodium transport by insulin. Sodium 170-176 insulin Homo sapiens 190-197 6800812-6 1981 It is suggested that the responsiveness of the renin-aldosterone system is abnormal during exercise in young patients with mild essential hypertension, both without and with previous intravenous sodium loading. Sodium 195-201 renin Homo sapiens 47-52 7026126-5 1981 Significant rises in plasma renin activity, plasma aldosterone concentration and renal aldosterone excretion occurred by day 2 of sodium deprivation. Sodium 130-136 renin Homo sapiens 28-33 7282947-16 1981 Thus, the slow pressure effect of ANG II develops at a lower and more nearly physiological plasma concentration of the peptide than do the direct pressor effect and the effects on drinking, eating, and urinary sodium excretion. Sodium 210-216 angiotensinogen Rattus norvegicus 34-40 7295860-2 1981 In two normaldosteronemic insulin-dependent diabetic patients during high sodium intake and insulin withdrawal infusion of hypertonic glucose induced a paradoxical elevation of serum potassium levels, while no such abnormalities were found in two other diabetics despite of lower plasma aldosterone levels. Sodium 74-80 insulin Homo sapiens 26-33 7295860-4 1981 PGIH was elicited when given 100 g of glucose orally to further three patients with normaldosteronemic diabetes in whom a complete reversal of PGIH was obtained l glucose-induced hyperkalemia (PGIH) was abolished during insulin withdrawal by sodium restriction associated with a dramatic increase in plasma aldosterone. Sodium 242-248 insulin Homo sapiens 220-227 7295860-5 1981 PGIH was elicited when given 100 g of glucose orally to further three patients with normaldosteronemic diabetes in whom a complete reversal of PGIH was obtained l glucose-induced hyperkalemia (PGIH) was abolished during insulin withdrawal by sodium restriction associated with a dramatic increase in plasma aldosterone. Sodium 242-248 insulin Homo sapiens 220-227 7028550-0 1981 The effect of insulin on renal sodium metabolism. Sodium 31-37 insulin Homo sapiens 14-21 7028550-2 1981 Data are discussed which demonstrate that insulin plays an important role in sodium metabolism. Sodium 77-83 insulin Homo sapiens 42-49 7028550-3 1981 The primary action of insulin on sodium balance is exerted on the kidney. Sodium 33-39 insulin Homo sapiens 22-29 7028550-4 1981 Increases in plasma insulin concentration within the physiological range stimulate sodium reabsorption by the distal nephron segments and this effect is independent of changes in circulating metabolites or other hormones. Sodium 83-89 insulin Homo sapiens 20-27 7028550-5 1981 Several clinical situations are reviewed: sodium wasting in poorly controlled diabetics, natriuresis of starvation, anti-natriuresis of refeeding and hypertension of obesity, in which insulin-mediated changes in sodium balance have been shown to play an important pathophysiological role. Sodium 42-48 insulin Homo sapiens 184-191 7028550-5 1981 Several clinical situations are reviewed: sodium wasting in poorly controlled diabetics, natriuresis of starvation, anti-natriuresis of refeeding and hypertension of obesity, in which insulin-mediated changes in sodium balance have been shown to play an important pathophysiological role. Sodium 212-218 insulin Homo sapiens 184-191 7261551-12 1981 The reduced plasma concentration of vasopressin may account for the decreased plasma and blood volume and the slightly elevated plasma sodium concentration observed in young SHRSP rats. Sodium 135-141 arginine vasopressin Rattus norvegicus 36-47 7300021-4 1981 The lack of the adjusting control system in the brain angiotensin II receptors for sodium balance may be, at least in a part, responsible for the enhancement of vasopressin secretion in the hypertensive rats compared to that in the control rats with high salt intake. Sodium 83-89 angiotensinogen Rattus norvegicus 54-68 7300021-4 1981 The lack of the adjusting control system in the brain angiotensin II receptors for sodium balance may be, at least in a part, responsible for the enhancement of vasopressin secretion in the hypertensive rats compared to that in the control rats with high salt intake. Sodium 83-89 arginine vasopressin Rattus norvegicus 161-172 6266576-6 1981 It strongly suggested that the renin system plays an important part in maintaining blood pressure in normotensive subjects receiving normal sodium intake. Sodium 140-146 renin Homo sapiens 31-36 6266727-1 1981 It has been suggested that an inappropriate relationship between renin and exchangeable sodium is responsible for the hypertension of patients with chronic renal failure. Sodium 88-94 renin Homo sapiens 65-70 6114434-2 1981 Angiotensin II also mediates the adrenal effects of altered sodium balance, and is essential for the aldosterone response to sodium restriction. Sodium 60-66 angiotensinogen Homo sapiens 0-14 6114434-2 1981 Angiotensin II also mediates the adrenal effects of altered sodium balance, and is essential for the aldosterone response to sodium restriction. Sodium 125-131 angiotensinogen Homo sapiens 0-14 6114434-3 1981 However, the adrenal effects of angiotensin II are attenuated during sodium loading, suggesting that other local or humoral factors modulate its actions on adrenal glomerulosa function. Sodium 69-75 angiotensinogen Homo sapiens 32-46 6789950-0 1981 Relation between arterial pressure, dietary sodium intake, and renin system in essential hypertension. Sodium 44-50 renin Homo sapiens 63-68 6266543-3 1981 The side chain of arginine, n-propylguanidinium (nPG), reversibly decreases peak sodium conductance and increases the speed of sodium current decay, when perfused internally. Sodium 81-87 OPA1 mitochondrial dynamin like GTPase Homo sapiens 49-52 6266543-3 1981 The side chain of arginine, n-propylguanidinium (nPG), reversibly decreases peak sodium conductance and increases the speed of sodium current decay, when perfused internally. Sodium 127-133 OPA1 mitochondrial dynamin like GTPase Homo sapiens 49-52 6266543-10 1981 Results show that at - 70 mV, nPG leaves sodium channels rapidly (less than 500 microseconds) in normal sodium gradient, but more slowly (greater than 1 ms) in reversed sodium gradient. Sodium 41-47 OPA1 mitochondrial dynamin like GTPase Homo sapiens 30-33 6266543-10 1981 Results show that at - 70 mV, nPG leaves sodium channels rapidly (less than 500 microseconds) in normal sodium gradient, but more slowly (greater than 1 ms) in reversed sodium gradient. Sodium 104-110 OPA1 mitochondrial dynamin like GTPase Homo sapiens 30-33 6266544-5 1981 Testing several nPG concentrations we find that peak sodium current declines sharply with [nPG] at all levels, but the decay time constant approaches an asymptote above 4 mM. Sodium 53-59 OPA1 mitochondrial dynamin like GTPase Homo sapiens 16-19 6266544-5 1981 Testing several nPG concentrations we find that peak sodium current declines sharply with [nPG] at all levels, but the decay time constant approaches an asymptote above 4 mM. Sodium 53-59 OPA1 mitochondrial dynamin like GTPase Homo sapiens 91-94 7030526-0 1981 Sodium, potassium and age: possible determinants of plasma renin activity and aldosterone during childhood (age 4-16). Sodium 0-6 renin Homo sapiens 59-64 7030526-3 1981 Significant negative correlation was obtained between plasma renin activity and the 24-h urinary sodium excretion; r = -0.40, P less than 0.01. Sodium 97-103 renin Homo sapiens 61-66 7018813-11 1981 The parallel fall in blood pressure and ANG II levels in salt-depleted normal subjects is consistent with maintenance of blood pressure by increased levels of ANG II in sodium depletion. Sodium 169-175 angiotensinogen Homo sapiens 159-165 7016959-0 1981 Plasma aldosterone response to angiotensin II in sodium-restricted elderly subjects with essential hypertension. Sodium 49-55 angiotensinogen Homo sapiens 31-45 7016959-7 1981 Apparently some subjects with essential hypertension, whose PRAs response subnormally to sodium restriction, have an abnormally enhanced adrenal responsiveness to AII under the conditions of low-sodium intake. Sodium 89-95 angiotensinogen Homo sapiens 163-166 7016959-7 1981 Apparently some subjects with essential hypertension, whose PRAs response subnormally to sodium restriction, have an abnormally enhanced adrenal responsiveness to AII under the conditions of low-sodium intake. Sodium 195-201 angiotensinogen Homo sapiens 163-166 7016891-7 1981 Dietary sodium restriction resulted in a further rise in plasma renin activity and a rise in urinary pH 1 aldo and 18-OH-corticosterone. Sodium 8-14 renin Homo sapiens 64-69 7024616-4 1981 The above alterations are characterized by the loss of the adequate response of the renin-angiotensin system and the adrenal cortex to the increased sodium concentration, and extracellular fluid volume in the body, as well as by the separation of the functions of these two humoral systems. Sodium 149-155 renin Homo sapiens 84-89 7036014-0 1981 [Effects of changes in the sodium balance on plasma catecholamines and renin activity at rest and on their response to orthostatic stimulation in arterial hypertension]. Sodium 27-33 renin Homo sapiens 71-76 7240147-3 1981 System ASC, identified by its sodium ion dependency and intolerance of N-methylation of substrates, was found to be relatively insensitive to external pH and nutrient limitation. Sodium 30-36 PYD and CARD domain containing Homo sapiens 7-10 7020728-1 1981 The response of the renin-angiotensin system to high and low sodium diets, to standing, and to saralasin infusion was assessed before and after surgical correction of aortic coarctation in a 27-year-old man. Sodium 61-67 renin Homo sapiens 20-25 6271208-0 1981 Effects of antidiuretic hormone on kinetic and energetic determinants of active sodium transport in frog skin. Sodium 80-86 arginine vasopressin Homo sapiens 11-31 7017596-4 1981 During sodium depletion, the plasma renin activity was higher in the right renal artery (17.8 ng/ml/h) than in the left artery (9.4 ng/ml/h) and the infra-renal portion of the inferior vena cava (8.7 ng/ml/h). Sodium 7-13 renin Homo sapiens 36-41 6787081-5 1981 VIP reduced the lumen-to-plasma unidirectional sodium and chloride flux rates, while the plasma-to-lumen flux rates were decreased to a lesser extent or remained unchanged. Sodium 47-53 vasoactive intestinal peptide Homo sapiens 0-3 6787206-10 1981 It is concluded that the predominant effect of vasopressin on transepithelial sodium transport is to increase the sodium conductance of the mucosal plasma membrane. Sodium 78-84 arginine vasopressin Homo sapiens 47-58 6792863-9 1981 The study supports the view that sodium sensitive receptors close to the cerebral ventricular system participate in the regulation of ADH secretion, water intake, renin release, and renal sodium excretion. Sodium 33-39 renin Ovis aries 163-168 7018237-9 1981 A significant difference between the slopes of the regression lines relating renin activity and sodium excretion for the two renin subgroups indicates that renin release in low renin patients is less sensitive to alterations in sodium balance. Sodium 96-102 renin Homo sapiens 125-130 7018237-9 1981 A significant difference between the slopes of the regression lines relating renin activity and sodium excretion for the two renin subgroups indicates that renin release in low renin patients is less sensitive to alterations in sodium balance. Sodium 96-102 renin Homo sapiens 125-130 7018237-9 1981 A significant difference between the slopes of the regression lines relating renin activity and sodium excretion for the two renin subgroups indicates that renin release in low renin patients is less sensitive to alterations in sodium balance. Sodium 96-102 renin Homo sapiens 125-130 6266960-4 1981 In response to dietary sodium restriction for 12 days, plasma renin activity (PRA) increased fivefold in patients with pituitary insufficiency, while plasma aldosterone concentration failed to increase significantly, averaging 11.0 +/- 3.1 before and 12.3 +/- 3.7 ng/dl (ns, p greater than 0.05) after sodium deficiency. Sodium 23-29 renin Homo sapiens 62-67 6266960-7 1981 Although the adrenal glomerulosa cells were markedly sensitive to ACTH during sodium deficiency, they remained almost totally refractory to AII since aldosterone secretion failed to increase significantly in response to continuous infusion of a pressor dose of AII for 1 hour. Sodium 78-84 proopiomelanocortin Homo sapiens 66-70 6266960-9 1981 These data demonstrate that some non-ACTH pituitary factor(s) is essential for a normal aldosterone response to ACTH, AII, and sodium deficiency. Sodium 127-133 proopiomelanocortin Homo sapiens 37-41 7262983-0 1981 Vasopressin elevation in essential hypertension and increased responsiveness to sodium intake. Sodium 80-86 arginine vasopressin Homo sapiens 0-11 6784808-2 1981 The rate constant for total leucocyte sodium efflux measured during a normal diet was significantly correlated with the plasma renin activity measured during a low sodium diet. Sodium 38-44 renin Homo sapiens 127-132 6269554-5 1981 The use of these inhibitors, especially captopril (so far the most studied), has made it clear that renin plays a part in experimental and human essential hypertension and participates in the control of arterial blood pressure in subjects with normal sodium intake. Sodium 251-257 renin Homo sapiens 100-105 6784808-2 1981 The rate constant for total leucocyte sodium efflux measured during a normal diet was significantly correlated with the plasma renin activity measured during a low sodium diet. Sodium 164-170 renin Homo sapiens 127-132 6784808-3 1981 Impairment of leucocyte sodium transport was significantly greater in eight patients whose plasma renin activity failed to rise into the normal range during the low sodium diet as compared with the 14 other patients, whose renin system responded normally to sodium restriction. Sodium 24-30 renin Homo sapiens 98-103 6784808-3 1981 Impairment of leucocyte sodium transport was significantly greater in eight patients whose plasma renin activity failed to rise into the normal range during the low sodium diet as compared with the 14 other patients, whose renin system responded normally to sodium restriction. Sodium 24-30 renin Homo sapiens 223-228 7018795-12 1981 Some form of sodium-sensitive mechanism may control the activation of inactive renin. Sodium 13-19 LOW QUALITY PROTEIN: renin Oryctolagus cuniculus 79-84 7018406-5 1981 A significant inverse relationship was found between both plasma renin activity and angiotensin II, and serum sodium in the girls; a similar, although not statistically significant, relationship was seen with plasma renin activity in the boys. Sodium 110-116 renin Homo sapiens 65-70 7204574-2 1981 At low physiological doses, angiotensin II (AII) stimulates jejunal sodium and water absorption, while at high doses peptide inhibits absorption and/or stimulates secretion. Sodium 68-74 angiotensinogen Rattus norvegicus 28-42 7204574-2 1981 At low physiological doses, angiotensin II (AII) stimulates jejunal sodium and water absorption, while at high doses peptide inhibits absorption and/or stimulates secretion. Sodium 68-74 angiotensinogen Rattus norvegicus 44-47 7211097-5 1981 In both groups, the response of P-aldo to A II infusion was greater in the sodium deplete than in the replete state, although "sensitization" was slightly less marked in H than in N. This may be due to the blunted rise of plasma-A II after sodium loss in H, which may also account for abnormalities in the blood pressure response in the H group. Sodium 75-81 angiotensinogen Homo sapiens 42-46 7028855-1 1981 In eight fetal sheep the factors influencing renal sodium excretion were determined and related to the activity of the renin-angiotensin system. Sodium 51-57 renin Ovis aries 119-124 7028855-6 1981 There was however an inverse relationship between urinary sodium excretion and plasma renin activity, similar to that seen in adult animals (Vander & Miller, 1964) and between log plasma renin activity and GFR (P less than 0.001). Sodium 58-64 renin Ovis aries 86-91 7028855-8 1981 However they do show that the fetal renin-angiotensin system like the adult renin-angiotensin system is closely linked to those renal factors that influence renal sodium excretion. Sodium 163-169 renin Ovis aries 36-41 7028855-8 1981 However they do show that the fetal renin-angiotensin system like the adult renin-angiotensin system is closely linked to those renal factors that influence renal sodium excretion. Sodium 163-169 renin Ovis aries 76-81 7211097-2 1981 We investigated whether the "sensitization" of the zona glomerulosa against angiotensin II (A II) by sodium deficiency was mediated by the pituitary gland. Sodium 101-107 angiotensinogen Homo sapiens 76-90 7211097-2 1981 We investigated whether the "sensitization" of the zona glomerulosa against angiotensin II (A II) by sodium deficiency was mediated by the pituitary gland. Sodium 101-107 angiotensinogen Homo sapiens 92-96 7013593-2 1981 Sodium restriction alone had no effect on renal clearances but did increase plasma renin activity and urinary prostaglandin E excretion. Sodium 0-6 renin Homo sapiens 83-88 7348020-3 1981 During the 12-25 minute long dipsogenic action of AII, sodium intake was significantly increased as compared to the control group. Sodium 55-61 angiotensinogen Rattus norvegicus 50-53 6258416-3 1981 Plasma renin activity increased with sodium depletion (30 mEq sodium intake for 3 days after furosemide treatment) from 1.26 +/- 0.07 to 3.26 +/- 0.48 ng/ml/hr (p less than 0.001). Sodium 37-43 renin Homo sapiens 7-12 6258416-3 1981 Plasma renin activity increased with sodium depletion (30 mEq sodium intake for 3 days after furosemide treatment) from 1.26 +/- 0.07 to 3.26 +/- 0.48 ng/ml/hr (p less than 0.001). Sodium 62-68 renin Homo sapiens 7-12 6258416-6 1981 The results indicate that the renin-angiotensin system participates in the regulation of blood pressure in essential hypertension, even in the sodium-repleted state. Sodium 143-149 renin Homo sapiens 30-35 6258416-7 1981 This role of the renin-angiotensin system in blood pressure regulation becomes more crucial during sodium depletion. Sodium 99-105 renin Homo sapiens 17-22 6258080-3 1981 The positive regulatory action of angiotensin II on its adrenal receptors occurs with elevations of the circulating peptide concentration within the physiological range and probably contributes to the increased sensitivity of the adrenal during sodium deficiency. Sodium 245-251 angiotensinogen Homo sapiens 34-48 6455045-10 1981 HNS released AVP in dose related manner to the osmotic challenge of sodium or glucose, and AVP release was stimulated from HNS by prostaglandin E2, but not by dopamine. Sodium 68-74 arginine vasopressin Rattus norvegicus 13-16 6257881-3 1981 Amrinone enhanced the effect of vasopressin and cyclic AMP on water and urea permeabilities, as well as the effect of vasopressin on sodium transport. Sodium 133-139 arginine vasopressin Homo sapiens 118-129 7348020-5 1981 At the same time, AII significantly increased the rate of sodium intake and the sodium appetite when a choice of water and NaCl was offered, and the basis of comparison was the water depleted group. Sodium 58-64 angiotensinogen Rattus norvegicus 18-21 6280547-0 1981 Effects of insulin on sodium transport by the amphibian urinary bladder. Sodium 22-28 insulin Homo sapiens 11-18 7457608-1 1981 At low doses, angiotensin II (AII) stimulates jejunal sodium and water absorption in the pentobarbital sodium-anesthetized rat. Sodium 54-60 angiotensinogen Rattus norvegicus 14-28 7457608-1 1981 At low doses, angiotensin II (AII) stimulates jejunal sodium and water absorption in the pentobarbital sodium-anesthetized rat. Sodium 54-60 angiotensinogen Rattus norvegicus 30-33 6803642-0 1981 Role of induced proteins in insulin-stimulated sodium transport. Sodium 47-53 insulin Homo sapiens 28-35 6803642-1 1981 Insulin increases active sodium transport by the toad urinary bladder, an effect that begins with 15 minutes and persists for at least 20 hours. Sodium 25-31 insulin Homo sapiens 0-7 6803642-3 1981 To examine the relationship of protein synthesis to the sustained increase in sodium transport elicited by insulin, we have studied the effects of the hormone upon the incorporation of radioactive amino acids into mucosal cell proteins. Sodium 78-84 insulin Homo sapiens 107-114 6803642-6 1981 Thus the effects of insulin upon sodium transport appear to be the result of two separate mechanisms, (1) a short-term response that is independent of protein synthesis and (2) a long-term response that is expressed after the first hour of hormone treatment and that requires the synthesis of one or more specific proteins in the granular cell. Sodium 33-39 insulin Homo sapiens 20-27 7007090-0 1981 [Effect of insulin and hydrocortisone on the concentration of sodium and potassium ions in nucleated and non-nucleated erythrocytes of chickens and rats]. Sodium 62-68 insulin Gallus gallus 11-18 7037337-9 1981 Basal plasma renin activity was 1.0 approximately 1.5 ng/ml/hr and increased by sodium depletion. Sodium 80-86 renin Homo sapiens 13-18 6973460-6 1981 The relation between the duration of both antidiuresis and sodium excretion and the way of administration was, however, more pronounced in the case of [8-lysine]vasopressin. Sodium 59-65 arginine vasopressin Rattus norvegicus 161-172 7004991-10 1981 On this diet the mean creatinine clearance was 104.3 +/- 6.4 ml/min, and the mean plasma renin activity and serum aldosterone levels had decreased physiologically with the higher sodium intake. Sodium 179-185 renin Homo sapiens 89-94 7037589-0 1981 Circadian rhythms of plasma renin, aldosterone and cortisol on habitual and low dietary sodium intake. Sodium 88-94 renin Homo sapiens 28-33 7009425-2 1981 Significant increase of active renin concentration (p less than 0.01) and decrease of the percentage of inactive renin concentration (p less than 0.01) after sodium depletion was observed in 15 essential hypertensive subjects with normal plasma renin activity. Sodium 158-164 renin Homo sapiens 113-118 7009425-2 1981 Significant increase of active renin concentration (p less than 0.01) and decrease of the percentage of inactive renin concentration (p less than 0.01) after sodium depletion was observed in 15 essential hypertensive subjects with normal plasma renin activity. Sodium 158-164 renin Homo sapiens 113-118 7009425-3 1981 In eight of 15 patients, significant increase of inactive renin concentration (p less than 0.01) was observed after sodium depletion. Sodium 116-122 renin Homo sapiens 58-63 7016790-3 1981 An attempt is made to relate the effects of insulin on sodium metabolism to four common clinical situations: (a) hypertension and obesity, (b) sodium wasting in diabetes mellitus, (c) natriuresis of starvation, and (d) sodium retention and edema following refeeding. Sodium 55-61 insulin Homo sapiens 44-51 7016790-3 1981 An attempt is made to relate the effects of insulin on sodium metabolism to four common clinical situations: (a) hypertension and obesity, (b) sodium wasting in diabetes mellitus, (c) natriuresis of starvation, and (d) sodium retention and edema following refeeding. Sodium 143-149 insulin Homo sapiens 44-51 7016790-3 1981 An attempt is made to relate the effects of insulin on sodium metabolism to four common clinical situations: (a) hypertension and obesity, (b) sodium wasting in diabetes mellitus, (c) natriuresis of starvation, and (d) sodium retention and edema following refeeding. Sodium 143-149 insulin Homo sapiens 44-51 7009425-5 1981 A small increase of active and inactive renin concentration was observed following sodium depletion in six essential hypertensive subjects with low plasma renin activity (PRA). Sodium 83-89 renin Homo sapiens 40-45 7009427-1 1981 Relationship between angiotensin II and body sodium and potassium on correction of hypertension by captopril and subsequent surgery. Sodium 45-51 angiotensinogen Homo sapiens 21-35 7009428-2 1981 Plasma renin activity (PRA) measured supine and after 4 hours of quiet ambulation, both on an ad libitum diet and on Day 4 of a 10 mEq low sodium diet, was always lower in the diabetics (31%-56% of control values). Sodium 139-145 renin Homo sapiens 7-12 6258970-0 1980 Effect of prolactin on human red cell sodium transport. Sodium 38-44 prolactin Homo sapiens 10-19 7266710-6 1981 With hypovolemia or heart failure, angiotensin II is a mediator of efferent arteriolar constriction promoting a proportionately greater fall in renal plasma flow than in glomerular filtration rate, thereby augmenting sodium reabsorption. Sodium 217-223 angiotensinogen Homo sapiens 35-49 6256111-0 1980 Effects of variations in sodium intake on the acute vasodepressor response to kininase II inhibition in rats with mild two-kidney, one-clip hypertension. Sodium 25-31 angiotensin I converting enzyme Rattus norvegicus 78-89 6256111-2 1980 Unilateral renal artery constriction in rats maintained on a sodium-deplete, but not sodium-replete, diet induced an augmented acute vasodepressor response to kininase II inhibition produced by an intravenous injection of the dipeptidyl carboxypeptidase inhibitor captopril (250 microgram) during continuous saralasin-induced angiotensin II blockade (10 microgram/min). Sodium 61-67 angiotensin I converting enzyme Rattus norvegicus 159-170 6256111-8 1980 The augmented acute vasodepressor response to kininase II inhibition in sodium-depleted rats with benign two-kidney, one-clip hypertension is probably due to bradykinin potentiation and secondary to an increased activity of the kallikrein-kinin system. Sodium 72-78 angiotensin I converting enzyme Rattus norvegicus 46-57 7428699-0 1980 Stimulation of intestinal sodium and water transport in vivo by angiotensin II and analogs. Sodium 26-32 angiotensinogen Homo sapiens 64-78 6780545-9 1980 Sodium ion stimulated serine transport in the presence of NADH, NADH plus cytochrome c or succinate plus PMS, but had no stimulatory effect on the corresponding dehydrogenase activities. Sodium 0-6 cytochrome c, somatic Homo sapiens 74-86 6258970-1 1980 Incubation of red cells with higher concentrations of prolactin in vitro enhanced the cellular sodium level and produced a significant reduction in erythrocyte membrane adenosine triphosphatase activity. Sodium 95-101 prolactin Homo sapiens 54-63 7001899-1 1980 This review considers the mechanism, prevention and therapy of sodium-dependent, low-renin, presumably volume-expanded, hypertension. Sodium 63-69 renin Homo sapiens 85-90 7436645-6 1980 These data suggest that sodium deprivation enhances the sympathetic nervous system activity and the orthostatic stimulation of renin release. Sodium 24-30 renin Homo sapiens 127-132 6254355-5 1980 Plasma ACTH concentrations were significantly higher in patients with sodium-losing CAH than in patients with non-sodium-losing CAH. Sodium 70-76 proopiomelanocortin Homo sapiens 7-11 6254355-5 1980 Plasma ACTH concentrations were significantly higher in patients with sodium-losing CAH than in patients with non-sodium-losing CAH. Sodium 114-120 proopiomelanocortin Homo sapiens 7-11 6254355-6 1980 These findings support the concepts that patients with the sodium-losing condition have a more severe enzyme deficiency and that ACTH stimulation may be affected by sodium balance. Sodium 165-171 proopiomelanocortin Homo sapiens 129-133 6254360-3 1980 Only in the state of considerable sodium depletion does blockade of the renin system produce any untoward effect, i.e. hypotension. Sodium 34-40 renin Homo sapiens 72-77 7193170-6 1980 These findings are tentatively explained by two mechanisms: 1) Angiotensin II has a "trophic" effect on the adrenal cortex, thus causing a progressive increase of secretion of corticosteroids in the normal sodium as well as in the low sodium state. Sodium 206-212 angiotensinogen Homo sapiens 63-77 6780460-8 1980 Inactive renin was usually increased in amount in plasma of sodium-depleted normal men, but the elution volume did not change with sodium intake. Sodium 60-66 renin Homo sapiens 9-14 7438475-3 1980 Hypertension with low plasma renin is consistent with sodium retention. Sodium 54-60 renin Homo sapiens 29-34 6780460-10 1980 Inactive renin in plasma was usually increased after sodium depletion, but the elution volume did not change. Sodium 53-59 renin Homo sapiens 9-14 6252230-1 1980 The role of the renin-angiotensin system in enhancing aldosterone responsiveness to ACTH during acute sodium depletion was studied in 14 healthy medical students. Sodium 102-108 proopiomelanocortin Homo sapiens 84-88 6252230-5 1980 The administration of ACTH, but not of vehicle, produced significant increases in plasma aldosterone in both control and acute sodium-depleted subjects. Sodium 127-133 proopiomelanocortin Homo sapiens 22-26 6252230-6 1980 However, the ACTH-induced increases in plasma aldosterone and their maximal net and percent increments during acute sodium depletion were significantly greater than control values. Sodium 116-122 proopiomelanocortin Homo sapiens 13-17 6252231-8 1980 The results demonstrate that in normal males on a sodium-restricted diet, baseline aldosterone levels are controlled in part by ACTH. Sodium 50-56 proopiomelanocortin Homo sapiens 128-132 6903427-8 1980 In the rat vasopressin-induced changes in kallikrein excretion were positively correlated with changes in sodium and potassium excretion and negatively correlated with changes in free water clearance. Sodium 106-112 arginine vasopressin Rattus norvegicus 11-22 7002566-3 1980 Both AIIA had agonistic pressor activities in subjects on high and regular sodium diets, [Sar, Ile]-AII being more potent than [Sar, Ala]-AII. Sodium 75-81 NLR family pyrin domain containing 3 Homo sapiens 5-8 6253591-9 1980 The demonstration of specific binding sites for prolactin localized primarily in the proximal tubules was consistent with renal action of prolactin, predominantly on sodium metabolism. Sodium 166-172 prolactin Rattus norvegicus 48-57 7002566-5 1980 Both AIIA strongly antagonized the rise in BP, the increase in PAC and the reduction of Ccr induced by AII administration in subjects on all three sodium diets. Sodium 147-153 NLR family pyrin domain containing 3 Homo sapiens 5-8 6253591-9 1980 The demonstration of specific binding sites for prolactin localized primarily in the proximal tubules was consistent with renal action of prolactin, predominantly on sodium metabolism. Sodium 166-172 prolactin Rattus norvegicus 138-147 6255463-3 1980 Scatchard analysis of the binding data shows heterogeneity of the binding sites that can be resolved into two populations with apparent dissociation constants of 3.0 (+/-2.0) X 10(-10) and 3.3 (+/- 0.5) X 10(-9) M. Sodium ions decrease the binding of human beta-endorphin to spinal cord to the same extent as found in rat brain. Sodium 215-221 proopiomelanocortin Homo sapiens 257-271 7022539-5 1980 Plasma renin activity was higher in hypertensive patients despite higher exchangeable sodium levels. Sodium 86-92 renin Homo sapiens 7-12 7410380-8 1980 Sodium-dependent binding to the soluble extract is insensitive to K+, suggesting that separate sites on the serotonin transporter mediate the effects of effects of Na+ and K+. Sodium 0-6 solute carrier family 6 member 4 Homo sapiens 108-129 6253796-2 1980 Elevation of circulating angiotensin II levels by sodium depletion or renal artery stenosis is associated with a diminished pressor response to infused angiotensin II (refs 1-3). Sodium 50-56 angiotensinogen Homo sapiens 25-39 6253796-2 1980 Elevation of circulating angiotensin II levels by sodium depletion or renal artery stenosis is associated with a diminished pressor response to infused angiotensin II (refs 1-3). Sodium 50-56 angiotensinogen Homo sapiens 152-166 6253796-3 1980 Conversely, the vasocontrictor response to the hormone is enhanced when endogenous angiotensin II levels are reduced by sodium loading or nephrectomy. Sodium 120-126 angiotensinogen Homo sapiens 83-97 7398582-0 1980 The effects of hemorrhage and sodium depletion on plasma concentrations of angiotensin II and [des-Asp1]angiotensin II in the rat. Sodium 30-36 angiotensinogen Rattus norvegicus 75-89 7000955-0 1980 Increased sodium appetite in adrenalectomized or hypophysectomized rats after intracranial injections of renin or angiotensin II. Sodium 10-16 angiotensinogen Rattus norvegicus 114-128 7000955-6 1980 These results demonstrated that the delayed sodium appetite induced by renin or angiotensin II is not secondary to the stimulation of release of hormones from the pituitary gland or adrenal cortex. Sodium 44-50 angiotensinogen Rattus norvegicus 80-94 6159648-0 1980 Specific inhibition of renin by an angiotensinogen analog: studies in sodium depletion and renin-dependent hypertension. Sodium 70-76 renin Homo sapiens 23-28 7408898-0 1980 Sodium-23 nuclear magnetic resonance as an indicator of sodium binding to calmodulin and tryptic fragments, in relation to calcium content. Sodium 0-6 calmodulin 1 Homo sapiens 74-84 16592871-1 1980 Between dipolar aprotic solvents S(1) and S(2), the transfer activity coefficients, (S(1) )gamma(S(2) ), of complexed sodium, potassium, thallium(I), and silver ions with cryptand 2.2.2 have been found to be equal to that of the cryptand. Sodium 118-124 proteasome 26S subunit, non-ATPase 1 Homo sapiens 84-89 16592871-1 1980 Between dipolar aprotic solvents S(1) and S(2), the transfer activity coefficients, (S(1) )gamma(S(2) ), of complexed sodium, potassium, thallium(I), and silver ions with cryptand 2.2.2 have been found to be equal to that of the cryptand. Sodium 118-124 ribosomal protein S2 Homo sapiens 91-101 7408898-0 1980 Sodium-23 nuclear magnetic resonance as an indicator of sodium binding to calmodulin and tryptic fragments, in relation to calcium content. Sodium 56-62 calmodulin 1 Homo sapiens 74-84 6162600-0 1980 Immunoreactive substance P in human plasma: response to changes in posture and sodium balance. Sodium 79-85 tachykinin precursor 1 Homo sapiens 15-26 6249864-0 1980 Reduced aldosterone secretory response to acute ACTH stimulation in sodium-restricted elderly subjects. Sodium 68-74 proopiomelanocortin Homo sapiens 48-52 6162600-8 1980 In eight healthy subjects plasma immunoreactive substance P rose only slightly from 169 +/0 41 pmol/l, on a sodium intake ad lib., to 244 +/- 45 pmol/l by day 4 of dietary sodium restriction (35 mmol/day) and significantly fell to 51 +/- 20 pmol/l (P less than 0.001) by day 4 of high sodium intake (350 mmol/day). Sodium 108-114 tachykinin precursor 1 Homo sapiens 48-59 6162600-8 1980 In eight healthy subjects plasma immunoreactive substance P rose only slightly from 169 +/0 41 pmol/l, on a sodium intake ad lib., to 244 +/- 45 pmol/l by day 4 of dietary sodium restriction (35 mmol/day) and significantly fell to 51 +/- 20 pmol/l (P less than 0.001) by day 4 of high sodium intake (350 mmol/day). Sodium 172-178 tachykinin precursor 1 Homo sapiens 48-59 6162600-8 1980 In eight healthy subjects plasma immunoreactive substance P rose only slightly from 169 +/0 41 pmol/l, on a sodium intake ad lib., to 244 +/- 45 pmol/l by day 4 of dietary sodium restriction (35 mmol/day) and significantly fell to 51 +/- 20 pmol/l (P less than 0.001) by day 4 of high sodium intake (350 mmol/day). Sodium 172-178 tachykinin precursor 1 Homo sapiens 48-59 6995299-4 1980 Since renin and fractional sodium excretion values were inversely correlated in all subject groups, it is possible that the heritable influences we observed on sodium excretion were mediated by the renin-angiotensin-aldosterone system. Sodium 27-33 renin Homo sapiens 198-203 6156899-3 1980 With restriction of sodium intake, an increase in renal blood flow occurs; because a quantitatively similar response occurs to the angiotensin II analogs it is likely that the response reflects reversal of the local action of angiotensin II. Sodium 20-26 angiotensinogen Homo sapiens 226-240 6249735-0 1980 Central actions and brain receptor binding of angiotensin II: Influence of sodium intake. Sodium 75-81 angiotensinogen Rattus norvegicus 46-60 6249735-5 1980 In sodium-depleted rats, water intake was lower than in controls after AII given i.v.t. Sodium 3-9 angiotensinogen Rattus norvegicus 71-74 6249735-10 1980 This hyperresponsiveness to central AII was abolished by feeding a low-sodium diet. Sodium 71-77 angiotensinogen Rattus norvegicus 36-39 6249735-11 1980 Specific 125I-AII binding in vitro to brain membranes was consistently lower in sodium-depleted rats. Sodium 80-86 angiotensinogen Rattus norvegicus 14-17 6249735-12 1980 The results suggest that sodium depletion modifies the central actions of AII. Sodium 25-31 angiotensinogen Rattus norvegicus 74-77 6995299-4 1980 Since renin and fractional sodium excretion values were inversely correlated in all subject groups, it is possible that the heritable influences we observed on sodium excretion were mediated by the renin-angiotensin-aldosterone system. Sodium 160-166 renin Homo sapiens 6-11 6995299-4 1980 Since renin and fractional sodium excretion values were inversely correlated in all subject groups, it is possible that the heritable influences we observed on sodium excretion were mediated by the renin-angiotensin-aldosterone system. Sodium 160-166 renin Homo sapiens 198-203 6102949-0 1980 Somatostatin stimulates sodium and chloride absorption in the rabbit ileum. Sodium 24-30 somatostatin Oryctolagus cuniculus 0-12 7443613-5 1980 The sodium retention was associated with suppression of plasma levels of renin and aldosterone. Sodium 4-10 renin Homo sapiens 73-78 6247919-2 1980 Progressive sodium depletion was associated with progressive increased in basal (pre-ACTH) plasma levels of renin, angiotensin II, aldosterone, 18-hydroxycorticosterone (18-OH-B), and 18-hydroxy-11-deoxycorticosterone (18-OH-DOC). Sodium 12-18 proopiomelanocortin Canis lupus familiaris 85-89 6247919-4 1980 The threshold dose of ACTH required to elicit an aldosterone response during low-sodium intake was similar to that for cortisol, but was higher during normal or high-sodium intake. Sodium 81-87 proopiomelanocortin Canis lupus familiaris 22-26 6247919-4 1980 The threshold dose of ACTH required to elicit an aldosterone response during low-sodium intake was similar to that for cortisol, but was higher during normal or high-sodium intake. Sodium 166-172 proopiomelanocortin Canis lupus familiaris 22-26 6247919-6 1980 Whereas the slopes of ACTH/aldosterone and ACTH/18-OH-B dose-response curves were steepened by lower sodium diets, the ACTH/cortisol response was significantly flattened by severe sodium depletion. Sodium 101-107 proopiomelanocortin Canis lupus familiaris 22-26 6247919-6 1980 Whereas the slopes of ACTH/aldosterone and ACTH/18-OH-B dose-response curves were steepened by lower sodium diets, the ACTH/cortisol response was significantly flattened by severe sodium depletion. Sodium 101-107 proopiomelanocortin Canis lupus familiaris 43-47 6247919-6 1980 Whereas the slopes of ACTH/aldosterone and ACTH/18-OH-B dose-response curves were steepened by lower sodium diets, the ACTH/cortisol response was significantly flattened by severe sodium depletion. Sodium 101-107 proopiomelanocortin Canis lupus familiaris 43-47 6247919-7 1980 We conclude that ACTH is a potent and direct-acting short-term regulator of aldosterone secretion, subject to modification by altered sodium balance. Sodium 134-140 proopiomelanocortin Canis lupus familiaris 17-21 6247216-5 1980 Prolactin seems able to cause a prolonged reduction in water, sodium, and potassium excretion, a pattern that is imitated by no other hormone with the possible exception of growth hormone. Sodium 62-68 prolactin Homo sapiens 0-9 6247218-5 1980 Subsequent actions of prolactin may involve the following: a) an increased intracellular concentration of potassium and a reduced level of sodium, b) an increased level of cGMP and a reduced level of cAMP, c) an enhanced rate of prostaglandin biosyntheesis mediated by a stimulation of phospholipase A2 activity, and d) a stimulation of polyamine synthesis. Sodium 139-145 prolactin Homo sapiens 22-31 6154896-1 1980 Intracranial injection of angiotensin II (AII) or activation of the cerebral isorenin-angiotensin system with intracranial renin causes an immediate thirst and a delayed sodium appetite in the rat. Sodium 170-176 angiotensinogen Rattus norvegicus 26-40 6154896-1 1980 Intracranial injection of angiotensin II (AII) or activation of the cerebral isorenin-angiotensin system with intracranial renin causes an immediate thirst and a delayed sodium appetite in the rat. Sodium 170-176 angiotensinogen Rattus norvegicus 42-45 6154896-5 1980 We report here that NGF-induced thirst and sodium appetite, as well as increased blood pressure and increase ornithine decarboxylase activity in the brain and liver, depend on the formation of AII (see also ref. Sodium 43-49 angiotensinogen Rattus norvegicus 193-196 7386120-0 1980 Potentiation of sulpiride-induced prolactin secretion by sodium deprivation in man. Sodium 57-63 prolactin Homo sapiens 34-43 7400708-6 1980 The molecular configuration of monosaccharides which have the ability to stimulate GIP release agreed well with the structural requirements for active transport by the sodium-dependent hexose pathway. Sodium 168-174 gastric inhibitory polypeptide Rattus norvegicus 83-86 7411437-0 1980 Arousal of a specific and persistent sodium appetite in the rat with continuous intracerebroventricular infusion of angiotensin II. Sodium 37-43 angiotensinogen Rattus norvegicus 116-130 7000394-0 1980 Renin and aldosterone in hypothyroidism: relation to excretion of sodium and potassium. Sodium 66-72 renin Homo sapiens 0-5 7353759-7 1980 At these levels VIP caused a dose-dependent decrease of water and sodium absorption. Sodium 66-72 vasoactive intestinal peptide Homo sapiens 16-19 6988802-2 1980 For a daily sodium intake of 120 mmol plasma angiotensinogen was abnormally increased, plasma renin activity (PRA) remained normal, but without significant diurnal variation. Sodium 12-18 angiotensinogen Homo sapiens 45-60 6106414-5 1980 Basal serum prolactin levels of women correlate negative significant with serum sodium levels and positive significant with the sodium concentration of red blood cells and basal TSH values. Sodium 80-86 prolactin Homo sapiens 12-21 6106414-5 1980 Basal serum prolactin levels of women correlate negative significant with serum sodium levels and positive significant with the sodium concentration of red blood cells and basal TSH values. Sodium 128-134 prolactin Homo sapiens 12-21 6998681-1 1980 The responses of renin release to three different stimuli, such as 1) head-up tilt, 2) administration of loop diuretics(bumetanide) and 3) low sodium diet + administration of bumetanide + ambulation were examined in essential hypertensive patients and normotensive subjects. Sodium 143-149 renin Homo sapiens 17-22 6987895-6 1980 These results provide further evidence that the synthesis of angiotensinogen may be increased by angiotensin II, but indicate that the circulating level of angiotensin II in sodium-deficient animals is not sufficiently high to produce this response. Sodium 174-180 angiotensinogen Rattus norvegicus 156-170 6243671-4 1980 ACTH infusion produced natriuresis, suggesting the need for additional sodium supplementation during the stress of illness, with a resultant increase in ACTH secretion. Sodium 71-77 proopiomelanocortin Homo sapiens 0-4 6243671-4 1980 ACTH infusion produced natriuresis, suggesting the need for additional sodium supplementation during the stress of illness, with a resultant increase in ACTH secretion. Sodium 71-77 proopiomelanocortin Homo sapiens 153-157 7396399-0 1980 [Effects of low, normal and high sodium diet on antidiuretic hormone and prolactin (author"s transl)]. Sodium 33-39 prolactin Homo sapiens 73-82 7011150-0 1980 Insulin-stimulated sodium transport in the toad urinary bladder: role of specific protein synthesis. Sodium 19-25 insulin Homo sapiens 0-7 6251761-4 1980 The development of hypotension was related to the prevailing plasma renin level, which was partly determined by the degree of sodium-depletion and the aetiology of hypertension. Sodium 126-132 renin Homo sapiens 68-73 6992515-6 1980 After 4 months, renin was inversely correlated with serum sodium. Sodium 58-64 renin Homo sapiens 16-21 7470759-5 1980 The falls in absolute and fractional sodium excretions caused by this manoeuvre were of similar magnitude to those obtained in the absence of drug.5 The results obtained using the 1-Sar, 8-Ile angiotensin II are consistent with angiotensin II having an important intra-renal site of action to regulate glomerular filtration rate, possibly via an action at the efferent arteriole. Sodium 37-43 angiotensinogen Homo sapiens 228-242 7000473-0 1980 Dissociated renin-aldosterone response to acute sodium depletion in patients with a previous history of pregnancy-associated hypertension. Sodium 48-54 renin Homo sapiens 12-17 7011672-11 1980 In unusual circumstances, vasopressin levels can occur that are capable of producing a diuresis and increased urine sodium excretion. Sodium 116-122 arginine vasopressin Homo sapiens 26-37 6993099-0 1980 Effect of an intravenous fluid load on urinary sodium excretion and its relation to blood pressure, blood volume and renin in hypertensive and normotensive man. Sodium 47-53 renin Homo sapiens 117-122 6253243-4 1980 With the renin system neutralized, blood pressure becomes exquisitely sensitive to changes in sodium balance. Sodium 94-100 renin Homo sapiens 9-14 7440260-0 1980 Quantitation of glucose-6-phosphate dehydrogenase activity in cortical fractions of the nephron in sodium-depleted and sodium-loaded rabbits. Sodium 99-105 glucose-6-phosphate 1-dehydrogenase Oryctolagus cuniculus 16-49 7440260-0 1980 Quantitation of glucose-6-phosphate dehydrogenase activity in cortical fractions of the nephron in sodium-depleted and sodium-loaded rabbits. Sodium 119-125 glucose-6-phosphate 1-dehydrogenase Oryctolagus cuniculus 16-49 7440260-1 1980 Glucose-6-phosphate dehydrogenase activity was measured quantitatively in isolated cortical fractions of the nephron in sodium-depleted and sodium-loaded rabbits. Sodium 120-126 glucose-6-phosphate 1-dehydrogenase Oryctolagus cuniculus 0-33 7440260-1 1980 Glucose-6-phosphate dehydrogenase activity was measured quantitatively in isolated cortical fractions of the nephron in sodium-depleted and sodium-loaded rabbits. Sodium 140-146 glucose-6-phosphate 1-dehydrogenase Oryctolagus cuniculus 0-33 7440260-5 1980 However, using conventional histochemical incubation methods semiquantitative estimation of glucose-6-phosphate dehydrogenase showed a slight decrease in enzyme activity in the macula densa and distal convoluted tubule, and a slight increase in the proximal convoluted tubule during sodium-depletion. Sodium 283-289 glucose-6-phosphate 1-dehydrogenase Oryctolagus cuniculus 92-125 7001263-0 1980 Influence of age and sodium intake on plasma renin activity of normal subjects. Sodium 21-27 renin Homo sapiens 45-50 7367456-3 1980 Angiotensin II (50, 100 and 200 microgram/kg, IP) increased urine output and urinary sodium excretion rate in a graded fashion with increasing doses in both control and estrogen-treated rats. Sodium 85-91 angiotensinogen Rattus norvegicus 0-14 6259658-1 1980 Calcitonin in pharmacologic doses influences the renal handling of electrolytes, especially phosphate and sodium. Sodium 106-112 calcitonin related polypeptide alpha Homo sapiens 0-10 7368628-5 1980 Glycosaminoglycans appear to be not only important participants in the effect of the antidiuretic hormone on the permeability of intersticial structures; they also play a certain role in the increase of osmolality of the renal papillar intersticium under the conditions of the antidiuresis, providing the release of loosely bound sodium. Sodium 330-336 arginine vasopressin Homo sapiens 85-105 7027063-3 1980 Time-course of plasma ADH following hypertonic saline administration and sensitivity of the response (increase of plasma ADH related to increase of plasma sodium) were not modified. Sodium 155-161 arginine vasopressin Homo sapiens 121-124 510563-1 1979 The enzyme renin is the initiator of a series of steps that ultimately leads to the generation of angiotensin II, a potent pressor peptide that also has both a direct and indirect role in renal sodium conservation. Sodium 194-200 renin Homo sapiens 11-16 232024-7 1979 Prior sodium depletion abolished the specificity of the renin and depressor responses to angiotensin blockage for renovascular hypertension. Sodium 6-12 renin Homo sapiens 56-61 119504-4 1979 Some renin hypertensive, hypersecretion of renin is the main factor in these cases but its effect is aggravated by the sodium overload. Sodium 119-125 renin Homo sapiens 5-10 119504-4 1979 Some renin hypertensive, hypersecretion of renin is the main factor in these cases but its effect is aggravated by the sodium overload. Sodium 119-125 renin Homo sapiens 43-48 496101-0 1979 Nephrotic syndrome: vasoconstriction and hypervolemic types indicated by renin-sodium profiling. Sodium 79-85 renin Homo sapiens 73-78 510563-1 1979 The enzyme renin is the initiator of a series of steps that ultimately leads to the generation of angiotensin II, a potent pressor peptide that also has both a direct and indirect role in renal sodium conservation. Sodium 194-200 angiotensinogen Homo sapiens 98-112 232088-1 1979 Previous studies have suggested that angiotensin II and sodium can act as alternative mechanisms in maintaining high blood pressure in chronic renovascular hypertension, In the present study, exchangeable sodium was measured in rats in which angiotensin II has been confirmed or excluded as the main cause of the hypertension. Sodium 56-62 angiotensinogen Rattus norvegicus 242-256 232088-1 1979 Previous studies have suggested that angiotensin II and sodium can act as alternative mechanisms in maintaining high blood pressure in chronic renovascular hypertension, In the present study, exchangeable sodium was measured in rats in which angiotensin II has been confirmed or excluded as the main cause of the hypertension. Sodium 205-211 angiotensinogen Rattus norvegicus 37-51 232088-1 1979 Previous studies have suggested that angiotensin II and sodium can act as alternative mechanisms in maintaining high blood pressure in chronic renovascular hypertension, In the present study, exchangeable sodium was measured in rats in which angiotensin II has been confirmed or excluded as the main cause of the hypertension. Sodium 205-211 angiotensinogen Rattus norvegicus 242-256 490250-7 1979 It is suggested that the rapid improvement of distal tubular sodium reabsorption in premature infants might result from forced stimulation by the excessively activated renin-angiotensin-aldosterone system. Sodium 61-67 renin Homo sapiens 168-173 395185-0 1979 Glucose-induced paradoxical hyperkalemia in patients with suppression of the renin-aldosterone system: prevention by sodium depletion. Sodium 117-123 renin Homo sapiens 77-82 522241-0 1979 Renin response to upright posture in varying sodium balance in normal young Japanese men. Sodium 45-51 renin Homo sapiens 0-5 395185-2 1979 Sodium restriction induced a dramatic increase in plasma renin activity (PRA) and/or plasma aldosterone (PA) in every patient, a substantial fall in the elevated serum potassium levels in 4 out of the 6 patients and a marked increase in fractional potassium excretion. Sodium 0-6 renin Homo sapiens 57-62 397605-2 1979 Converting hormone located on vascular endothelium converts the decapeptide to an octapeptide, angiotensin II, which effects vasoconstriction, the secretion of aldosterone by the adrenal cortex, and retention of sodium by the kidney. Sodium 212-218 angiotensinogen Homo sapiens 95-109 397605-7 1979 Renin"s part in chronic renovascular hypertension depends on whether or not sodium is permitted to accumulate. Sodium 76-82 renin Homo sapiens 0-5 397605-8 1979 If sodium intake is restricted or if sodium excretion is unimpaired (such as in two-kidney renovascular hypertension models), renin continues to play a significant role during the chronic phase. Sodium 3-9 renin Homo sapiens 126-131 494268-4 1979 1)Resting PRA (pre-dialysis PRA) was positively correlated to delta PRA/removed-sodium, delta PRA/removed-water, serum osmolality, and diastolic blood pressure, but negatively to serum sodium concentration, age, and pulse pressure/diastolic blood pressure. Sodium 80-86 S100 calcium binding protein A6 Homo sapiens 10-13 494268-4 1979 1)Resting PRA (pre-dialysis PRA) was positively correlated to delta PRA/removed-sodium, delta PRA/removed-water, serum osmolality, and diastolic blood pressure, but negatively to serum sodium concentration, age, and pulse pressure/diastolic blood pressure. Sodium 80-86 S100 calcium binding protein A6 Homo sapiens 28-31 494268-4 1979 1)Resting PRA (pre-dialysis PRA) was positively correlated to delta PRA/removed-sodium, delta PRA/removed-water, serum osmolality, and diastolic blood pressure, but negatively to serum sodium concentration, age, and pulse pressure/diastolic blood pressure. Sodium 80-86 S100 calcium binding protein A6 Homo sapiens 28-31 494268-4 1979 1)Resting PRA (pre-dialysis PRA) was positively correlated to delta PRA/removed-sodium, delta PRA/removed-water, serum osmolality, and diastolic blood pressure, but negatively to serum sodium concentration, age, and pulse pressure/diastolic blood pressure. Sodium 80-86 S100 calcium binding protein A6 Homo sapiens 28-31 494268-4 1979 1)Resting PRA (pre-dialysis PRA) was positively correlated to delta PRA/removed-sodium, delta PRA/removed-water, serum osmolality, and diastolic blood pressure, but negatively to serum sodium concentration, age, and pulse pressure/diastolic blood pressure. Sodium 185-191 S100 calcium binding protein A6 Homo sapiens 10-13 494268-4 1979 1)Resting PRA (pre-dialysis PRA) was positively correlated to delta PRA/removed-sodium, delta PRA/removed-water, serum osmolality, and diastolic blood pressure, but negatively to serum sodium concentration, age, and pulse pressure/diastolic blood pressure. Sodium 185-191 S100 calcium binding protein A6 Homo sapiens 28-31 494268-4 1979 1)Resting PRA (pre-dialysis PRA) was positively correlated to delta PRA/removed-sodium, delta PRA/removed-water, serum osmolality, and diastolic blood pressure, but negatively to serum sodium concentration, age, and pulse pressure/diastolic blood pressure. Sodium 185-191 S100 calcium binding protein A6 Homo sapiens 28-31 494268-4 1979 1)Resting PRA (pre-dialysis PRA) was positively correlated to delta PRA/removed-sodium, delta PRA/removed-water, serum osmolality, and diastolic blood pressure, but negatively to serum sodium concentration, age, and pulse pressure/diastolic blood pressure. Sodium 185-191 S100 calcium binding protein A6 Homo sapiens 28-31 494268-5 1979 Statistically significant factors controlling the resting PRA were delta PRA/removed-sodium, delta PRA//removed-water, and serum sodium concentration. Sodium 85-91 S100 calcium binding protein A6 Homo sapiens 58-61 494268-5 1979 Statistically significant factors controlling the resting PRA were delta PRA/removed-sodium, delta PRA//removed-water, and serum sodium concentration. Sodium 129-135 S100 calcium binding protein A6 Homo sapiens 58-61 494268-7 1979 2)Post-dialysis PRA was significantly correlated to the resting PRA, delta PRA/removed-sodium, delta PRA/removed-water, serum sodium concentration, and age, but not to the blood pressure indices. Sodium 87-93 S100 calcium binding protein A6 Homo sapiens 16-19 494268-7 1979 2)Post-dialysis PRA was significantly correlated to the resting PRA, delta PRA/removed-sodium, delta PRA/removed-water, serum sodium concentration, and age, but not to the blood pressure indices. Sodium 126-132 S100 calcium binding protein A6 Homo sapiens 16-19 90271-2 1979 Plasma angiotensin II was disproportionately high in relation to exchangeable sodium. Sodium 78-84 angiotensinogen Homo sapiens 7-21 474758-4 1979 Before meclofenamate administration, bradykinin augmented the urinary output of a "PGE"-like substance from 1.00 +/- 0.25 to 3.88 +/- 1.09 ng/min (P less than 0.05) and increased renal blood flow by 65 +/- 9 ml/min (P less than 0.001), urine flow by 0.55 +/- 0.23 ml/min (P less than 0.05), and sodium excretion by 64.8 +/- 18.0 mueq/min (P less than 0.01). Sodium 295-301 kininogen 1 Canis lupus familiaris 37-47 315865-7 1979 Changes in urinary excretion of sodium and potassium are considered to be consequence of direct renal action of MSH. Sodium 32-38 proopiomelanocortin Homo sapiens 112-115 469152-7 1979 The age-related decrease of plasma renin activity is discussed on the light of the age-related impairment in the ability of the kidney to excrete sodium and water. Sodium 146-152 renin Homo sapiens 35-40 501929-8 1979 The renin-aldosterone axis in response to changes in dietary sodium and posture must be individually assessed. Sodium 61-67 renin Homo sapiens 4-9 531273-7 1979 This observation indicates that S, like angiotensin II, has a direct effect upon the renal tubules evoking an increase of sodium reabsorption. Sodium 122-128 angiotensinogen Homo sapiens 40-54 466476-0 1979 Sodium dependence of the nerve growth factor--regulated hexose uptake in chick embryo ganglionic cells. Sodium 0-6 nerve growth factor Gallus gallus 25-44 466476-9 1979 These results indicate that availability of major energy substrates to NGF-dependent dorsal root ganglionic neurons is controlled by sodium gradients across their membranes. Sodium 133-139 nerve growth factor Gallus gallus 71-74 466476-10 1979 It is conceivable that NGF provides for maintenance and development of its target neurons by acting on such sodium gradients and, consequently, regulating the intake of essential nutrients. Sodium 108-114 nerve growth factor Gallus gallus 23-26 477875-3 1979 This suggests that only the proximal colon region, where most of the fluid and sodium absorption takes place, is responsive to prolactin. Sodium 79-85 prolactin Rattus norvegicus 127-136 464098-4 1979 Fractional sodium excretion was also increased by angiotensin II and norepinephrine in the dexamethasone-treated rats, but not in the aldosterone-treated rats. Sodium 11-17 angiotensinogen Rattus norvegicus 50-64 464461-2 1979 All 32 renovascular patients on normal sodium intake had high renin-sodium profiles and renin values greater than or equal to 5 ng angiotensin I/mL.h, as compared to 20 of 64 with essential hypertension. Sodium 39-45 renin Homo sapiens 88-93 464461-2 1979 All 32 renovascular patients on normal sodium intake had high renin-sodium profiles and renin values greater than or equal to 5 ng angiotensin I/mL.h, as compared to 20 of 64 with essential hypertension. Sodium 68-74 renin Homo sapiens 62-67 477254-0 1979 Evidence for the local occurrence of angiotensin II in rat kidney and its modulation by dietary sodium intake and converting enzyme blockade. Sodium 96-102 angiotensinogen Rattus norvegicus 37-51 477254-8 1979 Animals fed on a sodium-deficient diet for 8 days had markedly higher concentrations of intrarenal ANG II, plasma renin activity and kidney renin concentration than sodium-replete animals. Sodium 17-23 angiotensinogen Rattus norvegicus 99-105 457865-9 1979 The role of angiotensin II (AII) in maintaining glomerular and proximal tubular adaptations to chronic sodium depletion was assessed in subsets of groups 1 and 2 by the infusion of the AII antagonist Saralasin at a rate of 1 mug/kg per min. Sodium 103-109 angiotensinogen Rattus norvegicus 28-31 457865-20 1979 The marked changes observed during Saralasin infusion in the chronically sodium-depleted rat reveal important modifying effects of endogenously generated AII on both the glomerulus and proximal tubule. Sodium 73-79 angiotensinogen Rattus norvegicus 154-157 493037-0 1979 [Variations in urinary antidiuretic hormone levels related to sodium intake (author"s transl)]. Sodium 62-68 arginine vasopressin Homo sapiens 23-43 465171-7 1979 Natriuresis with a higher % of the filtered sodium excretion was observed in the malnourished groups and in normal children with 0.5 mU of vasopressin. Sodium 44-50 arginine vasopressin Homo sapiens 139-150 396242-7 1979 These findings indicate that although renin and aldosterone secretion respond to change in sodium intake in pregnancy, the cause of the increased renin secretion of pregnancy may be secondary to the increase that occurs in prostaglandin synthesis. Sodium 91-97 renin Homo sapiens 38-43 221530-5 1979 ACTH induced sodium retention and weight gain. Sodium 13-19 proopiomelanocortin Homo sapiens 0-4 490371-6 1979 Decreased sodium excretion was observed in both urine and faeces during sodium depletion and the physiological control of these changes is discussed in relation to the renin-angiotensin-aldosterone system. Sodium 10-16 LOW QUALITY PROTEIN: renin Oryctolagus cuniculus 168-173 490374-4 1979 Active renin increased by 97% during sodium depletion and returned to control levels on repletion. Sodium 37-43 LOW QUALITY PROTEIN: renin Oryctolagus cuniculus 7-12 490374-7 1979 During dietary sodium depletion inactive renin levels initially fell to zero and then increased until, after 13 days, inactive renin was again 10% of total renin levels, a proportion comparable to the control values. Sodium 15-21 LOW QUALITY PROTEIN: renin Oryctolagus cuniculus 41-46 490374-9 1979 Sodium repletion caused plasma inactive renin to return to control levels over about 13 days, a quite different time course to active renin. Sodium 0-6 LOW QUALITY PROTEIN: renin Oryctolagus cuniculus 40-45 514119-4 1979 The hypothesis is developed which states that elevated levels of lead exposure will not interact with sodium to enhance the development of renin angiotensin aldosterone related hypertension but in fact may even diminish the effects of exposure to elevated amounts of sodium on blood pressure through a depression of plasma renin activity. Sodium 267-273 renin Homo sapiens 323-328 573458-0 1979 Stimulation of proximal tubular sodium reabsorption by ile5 angiotensin II in the rat kidney. Sodium 32-38 angiotensinogen Rattus norvegicus 60-74 573458-1 1979 A direct dose-dependent stimulation or inhibition by val5-angiotensin II of sodium reabsorption in the rat proximal nephron has been shown using stationary microperfusion combined with perfusion of the peritubular capilaries. Sodium 76-82 angiotensinogen Rattus norvegicus 58-72 481942-0 1979 Plasma renin activity related to sodium balance, renal function and urinary vasopressin in the newborn infant. Sodium 33-39 renin Homo sapiens 7-12 481942-4 1979 Plasma renin activity (log values) was inversely correlated with sodium intake (r = -0.58) or with urinary sodium (r = -0.44), and positively with urinary osmolality (r = 0.67). Sodium 65-71 renin Homo sapiens 7-12 481942-4 1979 Plasma renin activity (log values) was inversely correlated with sodium intake (r = -0.58) or with urinary sodium (r = -0.44), and positively with urinary osmolality (r = 0.67). Sodium 107-113 renin Homo sapiens 7-12 465054-0 1979 Nerve growth factor influences sodium ion extrusion from chick embryonic dorsal root ganglionic neurons. Sodium 31-37 nerve growth factor Gallus gallus 0-19 220228-0 1979 The role of cytochrome P-450 in the action of sodium depletion on aldosterone biosynthesis in rats. Sodium 46-52 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 12-28 454584-0 1979 Effect of the sodium/potassium ratio on glyceraldehyde 3-phosphate dehydrogenase interaction with red cell vesicles. Sodium 14-20 glyceraldehyde-3-phosphate dehydrogenase Homo sapiens 40-80 454584-12 1979 The sodium/potassium concentration dependence of this process in red cells is mimicked by 31P resonance shifts in the (glyceraldehyde 3-phosphate/glyceraldehyde-3-phosphate dehydrogenase/inside out vesicle) system. Sodium 4-10 glyceraldehyde-3-phosphate dehydrogenase Homo sapiens 146-186 35288-0 1979 Evaluation of an instrument (Nova-1) for direct potentiometric analysis of sodium and potassium in blood and their indirect potentiometric determination in urine. Sodium 75-81 NOVA alternative splicing regulator 1 Homo sapiens 29-35 393503-8 1979 Plasma renin activity and plasma aldosterone responded subnormally to sodium restriction. Sodium 70-76 renin Homo sapiens 7-12 219653-5 1979 A 24-h angiotensin II infusion into sodium- and potassium-replete rats induced significant increases in both the serum aldosterone and the conversion. Sodium 36-42 angiotensinogen Rattus norvegicus 7-21 36191-0 1979 Biosynthetic processes related to the stimulation by insulin of sodium transport in the toad bladder. Sodium 64-70 insulin Homo sapiens 53-60 465980-4 1979 A further period of more severe sodium depletion increased plasma renin levels and the depressor effect of saralasin, but did not help to differentiate renal artery stenosis from other forms of hypertension. Sodium 32-38 renin Homo sapiens 66-71 477223-2 1979 This study was done to examine the possibility that escape from the sodium retention produced by aldosterone may be associated with an inhibition of prolactin secretion. Sodium 68-74 prolactin Homo sapiens 149-158 467373-1 1979 In a group of four young patients with stable chronic renal failure and hyperkalemia sodium restriction induced a remarkable increase in plasma renin activity (PRA) and plasma aldosterone (PA), a decrease in the elevated serum potassium (SK) and a rise in potassium excretion. Sodium 85-91 renin Homo sapiens 144-149 467373-2 1979 During high sodium intake the levels of PRA and PA were lower than those found in the healthy control group suggesting that enhanced suppressibility of the renin-angiotensin-aldosterone system (RAAS) was the main cause of hyperkalemia. Sodium 12-18 renin Homo sapiens 156-161 457984-4 1979 Milk yield and sodium and magnesium concentrations of the milk varied with days of the estrous cycle. Sodium 15-21 Weaning weight-maternal milk Bos taurus 58-62 457984-6 1979 However, sodium concentration of the milk was the only component that varied significantly during the 3 days centered on estrus (days -1, 0, and 1). Sodium 9-15 Weaning weight-maternal milk Bos taurus 37-41 218456-4 1979 Administration of adrenocorticotropic hormone (ACTH) to women during the third trimester of pregnancy was noted previously to result in marked sodium retention, while aldosterone excretion declined. Sodium 143-149 proopiomelanocortin Homo sapiens 18-45 218456-4 1979 Administration of adrenocorticotropic hormone (ACTH) to women during the third trimester of pregnancy was noted previously to result in marked sodium retention, while aldosterone excretion declined. Sodium 143-149 proopiomelanocortin Homo sapiens 47-51 218456-5 1979 Since urinary tetrahydrodesoxycorticosterone increased substantially, sodium retention resulting from ACTH was ascribed to enhanced DOC secretion. Sodium 70-76 proopiomelanocortin Homo sapiens 102-106 313658-0 1979 Correlation between the mechanism of insulin and vasopressin actions on sodium transport across isolated frog skin. Sodium 72-78 insulin Homo sapiens 37-44 313658-0 1979 Correlation between the mechanism of insulin and vasopressin actions on sodium transport across isolated frog skin. Sodium 72-78 arginine vasopressin Homo sapiens 49-60 455738-3 1979 It is concluded that angiotensin II plays a major part in stimulating aldosterone secretion during sodium depletion in man. Sodium 99-105 angiotensinogen Homo sapiens 21-35 399937-3 1979 However, the BH group exhibited greater responses in terms of plasma catecholamines and plasma renin activity in response to sodium deprivation and treadmill exercise. Sodium 125-131 renin Homo sapiens 95-100 94387-0 1979 Sodium intake and plasma angiotensin level as modulators of adrenal and uterine angiotensin II receptors in the rat. Sodium 0-6 angiotensinogen Rattus norvegicus 80-94 94387-4 1979 However, a more markedly positive sodium balance, such as that observed in deoxycorticosterone acetate (DOCA) hypertension and in one-kidney Goldblatt hypertension, resulted in a reduction of the adrenocortical angiotensin II binding capacity. Sodium 34-40 angiotensinogen Rattus norvegicus 212-226 94387-6 1979 It is proposed that the number of angiotensin II receptors is determined by the combined influences of sodium status and angiotensin II concentration. Sodium 103-109 angiotensinogen Rattus norvegicus 34-48 289865-0 1979 Angiotensin II blockade: evidence for baroreceptor-mediated renin release and the role of sodium balance. Sodium 90-96 angiotensinogen Homo sapiens 0-14 110603-7 1979 These results suggest that in non-azotaemic cirrhosis with ascites the renin-angiotensin-aldosterone system is an important factor influencing sodium excretion, increased plasma renin and aldosterone concentrations are mainly due to an increased secretion rate, and total renal perfusion is not a major factor influencing renin secretion. Sodium 143-149 renin Homo sapiens 71-76 285563-0 1979 Effect of sodium loading on the renin-aldosterone system in essential hypertension. Sodium 10-16 renin Homo sapiens 32-37 474181-3 1979 AII was then correlated statistically to PRA, PA and 24-hour urinary excretions of aldosterone (Aldo-U), sodium and potassium and to the blood pressure (BP) levels. Sodium 105-111 angiotensinogen Homo sapiens 0-3 397714-4 1979 Moderately elevated values of plasma renin activity in older salt-losers normalized after increasing the dietary sodium intake. Sodium 113-119 renin Homo sapiens 37-42 454855-0 1979 The role of sodium and potassium ions in the contractile response and development of tachyphylaxis to angiotensin II on vascular smooth muscle. Sodium 12-18 angiotensinogen Rattus norvegicus 102-116 454855-4 1979 On the rat aorta increased medium sodium concentrations potentiated the response to angiotensin II and inhibited the development of tachyphylaxis. Sodium 34-40 angiotensinogen Rattus norvegicus 84-98 214254-6 1979 Therefore, the amplitude of the elevation is predictably diminished by the rise in plasma renin consequent to prior sodium restriction, and also by preliminary receptor exposure to low dose nonpressor infusions of saralasin itself (0.01-0.1 microgram/kg per min). Sodium 116-122 renin Homo sapiens 90-95 428287-0 1979 Renal hemodynamics and the renin--angiotensin system in cirrhosis: relationship to sodium retention. Sodium 83-89 renin Homo sapiens 27-32 391545-2 1979 There is a parallel between water intake and plasma renin activity (PRA) in states like hypovolemia, hemorrhagia, hypotension, sodium loss, etc. Sodium 127-133 renin Homo sapiens 52-57 232724-11 1979 This sensitivity to the inhibitor of the fast sodium carrying mechanism appears to be an element of the pleiotypic response of the cells in culture to serum or to insulin. Sodium 46-52 insulin Homo sapiens 163-170 226768-8 1979 The effect of ACTH alone as compared to the effect of ACTH and indomethacin showed: plasma sodium concentration, 139 +/- 1 vs. 131 +/ 3 mEg/liter (P less than 0.01, mean +/- SEM); plasma osmolality, 287 +/- 3 vs. 270 +/- 3 mOsm/liter (P less than 0.01); free water clearance, 97 +/- 66 vs. -1100 +/- 380 ml/24hr (P less than 0.01); urine volume, 2,000 +/- 60 vs. 950 +/- 200 ml/day (P less than 0.01); and urine osmolality 282 +/- 12 vs. 720 +/- 144 mOsm/liter (P less than 0.01). Sodium 91-97 proopiomelanocortin Homo sapiens 14-18 226768-8 1979 The effect of ACTH alone as compared to the effect of ACTH and indomethacin showed: plasma sodium concentration, 139 +/- 1 vs. 131 +/ 3 mEg/liter (P less than 0.01, mean +/- SEM); plasma osmolality, 287 +/- 3 vs. 270 +/- 3 mOsm/liter (P less than 0.01); free water clearance, 97 +/- 66 vs. -1100 +/- 380 ml/24hr (P less than 0.01); urine volume, 2,000 +/- 60 vs. 950 +/- 200 ml/day (P less than 0.01); and urine osmolality 282 +/- 12 vs. 720 +/- 144 mOsm/liter (P less than 0.01). Sodium 91-97 proopiomelanocortin Homo sapiens 54-58 156392-3 1979 Serum sodium levels decreased significantly in hypertensive patients one or two days before the peak of the hypertensive crisis and, in the Center where it was measured, plasma renin activity increased in an opposite trend to the fall of sodium. Sodium 6-12 renin Homo sapiens 177-182 384510-7 1979 The results also suggest that an increased activity of the renin-angiotensin system may be counterbalanced by sodium and fluid retention in hypertension following an acute renal allograft reaction. Sodium 110-116 renin Homo sapiens 59-64 215372-0 1978 Alterations of adrenal and uterine angiotensin II receptors during variation of sodium intake and/or experimental hypertension. Sodium 80-86 angiotensinogen Rattus norvegicus 35-49 215372-2 1978 Angiotensin II receptors from rat adrenal gland and myometrium were studied during variation of sodium intake. Sodium 96-102 angiotensinogen Rattus norvegicus 0-14 744810-3 1978 Milk from cows with evidence of udder infection had higher sodium and chloride and lower potassium than cows free of mastitis. Sodium 59-65 Weaning weight-maternal milk Bos taurus 0-4 364155-7 1978 Finally, the major functions of the renin-angiotensin system in the control of blood pressure, of sodium and water balance, and of intrarenal events, are summarized. Sodium 98-104 renin Homo sapiens 36-41 102471-8 1978 Plasma renin activity, but not plasma aldosterone correlated with the fluid and sodium retention over the initial 24 h treatment period, but not with potassium requirements. Sodium 80-86 renin Homo sapiens 7-12 30650-4 1978 Recently, it has been shown that angiotensin II, infused intravenously or through the carotid artery at rates that produce increases in plasma angiotensin II levels similar to those that occur in mild sodium depletion, causes the water-replete animal to drink. Sodium 201-207 angiotensinogen Homo sapiens 33-47 30650-4 1978 Recently, it has been shown that angiotensin II, infused intravenously or through the carotid artery at rates that produce increases in plasma angiotensin II levels similar to those that occur in mild sodium depletion, causes the water-replete animal to drink. Sodium 201-207 angiotensinogen Homo sapiens 143-157 744170-10 1978 These results indicate taht pretreatment of sodium depletion is necessary to prevent the side effect caused by the agonistic pressor action of AII analogue, and also to predict renin depency in hypertensive patients efficiently. Sodium 44-50 renin Homo sapiens 177-182 400731-0 1978 Adrenal responses to pharmacological interruption of the renin-angiotensin system in sodium-restricted normal man. Sodium 85-91 renin Homo sapiens 57-62 400731-1 1978 We assessed the role of the renin-angiotensin system in the control of aldosterone secretion in response to sodium restriction in 62 normal subjects. Sodium 108-114 renin Homo sapiens 28-33 400731-2 1978 Both saralasin, an angiotensin II antagonist, and SQ 20881, a converting enzyme inhibitor, induced a dose-related decrease in plasma aldosterone levels when the renin-angiotensin system was activated by restriction of sodium intake. Sodium 218-224 renin Homo sapiens 161-166 701125-6 1978 Angiotensin II may thus have a role in the maintenance of P- in the supine sodium-deplete normal subjects, and stimulation of the renin angiotensin system during physical exercise contributes to a minor extent to the increase in P- in these conditions. Sodium 75-81 angiotensinogen Homo sapiens 0-14 713415-2 1978 After sodium-depletion of short duration mean arterial pressure dropped more than 10 mm Hg in 9 of 25 patients with essential and in 7 of 9 patients with renin-induced hypertension. Sodium 6-12 renin Homo sapiens 154-159 713415-3 1978 After long-lasting sodium depletion the fall of mean arterial pressure exceeded 10 mm Hg in 11 of 16 patients with essential and in 8 of 9 patients with renin-induced hypertension. Sodium 19-25 renin Homo sapiens 153-158 219051-7 1979 This decrease of PGE in turn causes a reduction of plasma renin activity, possibly either by accelerating the retention of sodium and water or by failing to stimulate renin synthesis. Sodium 123-129 renin Homo sapiens 58-63 699348-3 1978 Deprivation of sodium without bromocriptine resulted in progressive and highly significant increases in the plasma concentration of aldosterone from 230 +/- 50 to 418 +/- 44 (SEM) pmol/l, 18-hydroxycorticosterone from 627 +/- 138 to 1420 +/- 478 pmol/l, PRC from 108 +/- 38 to 166 +/- 14 muU/ml and AII from 16 +/- 3 to 29 +/- 4 pmol/l. Sodium 15-21 angiotensinogen Homo sapiens 299-302 699348-5 1978 Sodium deprivation together with bromocriptine resulted in increases in the plasma concentrations of aldosterone from 230 +/- 47 to 416 +/- 72 pmol/l, 18-hydroxycorticosterone from 630 +/- 99 to 1629 +/- 552 pmol/l, PRC from 105 +/- 12 muU/ml and AII from 14 +/- 3 to 26 +/- 5 pmol/l. Sodium 0-6 angiotensinogen Homo sapiens 247-250 233670-1 1978 A study was performed to determine the possible role of angiotensin II (AII) in mediating the increased adrenal aldosterone response to infused alpha 1-24-ACTH, induced by sodium deprivation. Sodium 172-178 angiotensinogen Homo sapiens 56-70 233670-1 1978 A study was performed to determine the possible role of angiotensin II (AII) in mediating the increased adrenal aldosterone response to infused alpha 1-24-ACTH, induced by sodium deprivation. Sodium 172-178 angiotensinogen Homo sapiens 72-75 233670-1 1978 A study was performed to determine the possible role of angiotensin II (AII) in mediating the increased adrenal aldosterone response to infused alpha 1-24-ACTH, induced by sodium deprivation. Sodium 172-178 proopiomelanocortin Homo sapiens 155-159 233670-5 1978 ACTH infusion produced an increase in the plasma aldosterone concentration which was significantly greater during sodium restriction than when sodium intake was unlimited. Sodium 114-120 proopiomelanocortin Homo sapiens 0-4 233670-5 1978 ACTH infusion produced an increase in the plasma aldosterone concentration which was significantly greater during sodium restriction than when sodium intake was unlimited. Sodium 143-149 proopiomelanocortin Homo sapiens 0-4 211515-1 1978 The role of angiotensin II as mediator of the aldosterone response to short periods of sodium restriction was studied in rats by administration of a converting enzyme inhibitor to block formation of the octapeptide throughout the duration of decreased sodium intake. Sodium 87-93 angiotensinogen Rattus norvegicus 12-26 211515-2 1978 In control animals, short-term sodium restriction caused increased levels of adrenal receptors for angiotensin II, with enhancement of early and late steps in aldosterone biosynthesis and elevation of plasma aldosterone concentration. Sodium 31-37 angiotensinogen Rattus norvegicus 99-113 211515-3 1978 Each of these changes induced by sodium deficiency was abolished during blockade of angiotensin II formation by continuous infusion of the converting enzyme inhibitor, SQ 14,225. Sodium 33-39 angiotensinogen Rattus norvegicus 84-98 744066-7 1978 The response to A-II may provide an explanation for the reported increase in 18-OH-DOC production after sodium restriction. Sodium 104-110 angiotensinogen Rattus norvegicus 16-20 690322-1 1978 Insulin glucose therapy can correct hyponatraemia and renal sodium retention in burns, sepsis and circulatory failure. Sodium 60-66 insulin Homo sapiens 0-7 670429-3 1978 When serum sodium decreased to 110 mEq/liter, plasma antidiuretic hormone (ADH) was elevated at 30 pg/ml. Sodium 11-17 arginine vasopressin Homo sapiens 53-73 670429-3 1978 When serum sodium decreased to 110 mEq/liter, plasma antidiuretic hormone (ADH) was elevated at 30 pg/ml. Sodium 11-17 arginine vasopressin Homo sapiens 75-78 78048-0 1978 Big renin in plasma of healthy subjects on high sodium intake. Sodium 48-54 renin Homo sapiens 4-9 78048-2 1978 When healthy volunteers were given first a diet containing 400 mmol sodium and then a diet containing 10 mmol sodium for 4 days the changes in salt intake stimulated large changes in active plasma-renin and smaller changes in inactive renin. Sodium 110-116 renin Homo sapiens 197-202 78048-2 1978 When healthy volunteers were given first a diet containing 400 mmol sodium and then a diet containing 10 mmol sodium for 4 days the changes in salt intake stimulated large changes in active plasma-renin and smaller changes in inactive renin. Sodium 110-116 renin Homo sapiens 235-240 672437-0 1978 Comparison of the biological effects of two angiotensin II analogues in hypertensive patients with sodium depletion. Sodium 99-105 angiotensinogen Homo sapiens 44-58 666132-2 1978 In normal subjects, three components of renin release, "basal," "neural," and "sodium-sensitive," could be delineated. Sodium 79-85 renin Homo sapiens 40-45 639240-6 1978 The net effect of sodium depletion was to reduce the pressor response to saralasin in all renin subgroups by 9 to 12 mm Hg. Sodium 18-24 renin Homo sapiens 90-95 28952-8 1978 The normal-sodium group showed an immediate but temporary rise of the renin and aldosterone levels; in the low-sodium group renin and aldosterone increased more slowly but remained elevated. Sodium 11-17 renin Homo sapiens 70-75 28952-9 1978 It is concluded that dietary sodium restriction increases diuretic-induced potassium loss, presumably by an increased activity of the renin-angiotensin-aldosterone system, while sodium delivery to the distal renal tubules remains sufficiently high to allow increased potassium secretion. Sodium 29-35 renin Homo sapiens 134-139 353767-3 1978 PRA fell steadily as renal function improved and plasma sodium rose following transplantation and when rejection episodes were excluded an inverse relationship between PRA and renal function could be seen. Sodium 56-62 S100 calcium binding protein A6 Homo sapiens 168-171 418180-0 1978 Vasopressin-like effects of a hallucinogenic drug--harmaline--on sodium and water transport. Sodium 65-71 arginine vasopressin Homo sapiens 0-11 642412-5 1978 Plasma sodium was inversely correlated to PRA, PRC, AT II and aldosterone, but no relationship was detected between these parameters of the RAAS and plasma potassium. Sodium 7-13 angiotensinogen Homo sapiens 52-57 645884-1 1978 Under inactin anesthesia, intravenous infusion of [Sar1,Thr8]angiotensin II produced a hypotensive effect in young spontaneously hypertensive rats (SHR) treated with furosemide and in mature SH rats fed a low-sodium diet. Sodium 209-215 angiotensinogen Rattus norvegicus 61-75 638887-0 1978 Effect of the external concentrations of potassium and sodium on the release of (--)-[3H]noradrenaline from the adrenergic nerves of the rat vas deferens. Sodium 55-61 arginine vasopressin Rattus norvegicus 141-144 638887-1 1978 The effect of the external concentrations of sodium and potassium on the nerve-induced release of (--)-[3H]noradrenaline from the adrenergic nerves of the rat vas deferens has been investigated. Sodium 45-51 arginine vasopressin Rattus norvegicus 159-162 639473-6 1978 During treatment with carbamazepine plasma sodium increased wheras plasma and urine arginine-vasopressin and urine osmolality decreased. Sodium 43-49 arginine vasopressin Homo sapiens 93-104 688983-3 1978 However, when the renin-angiotensin-aldosterone system was stimulated by sodium depletion the glucose-induced paradoxical hyperkalemia was abolished and the governing role of potassium became less evident. Sodium 73-79 renin Homo sapiens 18-23 148727-0 1978 The influence of different sodium loads on renin release in hypertensive and normotensive states of chronic renal failure. Sodium 27-33 renin Homo sapiens 43-48 148727-1 1978 The purpose of the present study was to examine the influence of different sodium loads on renin release in the hypertensive and normotensive state of chronic renal failure. Sodium 75-81 renin Homo sapiens 91-96 148727-8 1978 This alteration in renin release may contribute to the maintenance of hypertension in chronic renal failure, PRC being "inappropriately" increased in relationship to the sodium excess. Sodium 170-176 renin Homo sapiens 19-24 221518-0 1978 Prolonged infusions of Ile5-angiotensin-II in sodium replete and deplete man: effects on aldosterone, ACTH, cortisol, blood pressure, and electrolyte balance. Sodium 46-52 angiotensinogen Homo sapiens 28-42 221518-1 1978 Angiotensin II (Ile5) was infused for 72 h into 4 sodium replete (3 ng/kg/min) and 8 sodium deplete (3 or 6 ng/kg/min) healthy young men after appropriate control periods, and the effects on aldosterone secretion, plasma cortisol, ACTH, renin activity, plasma and urinary electrolytes, and blood pressure were assessed. Sodium 50-56 angiotensinogen Homo sapiens 0-14 221518-2 1978 Sustained contrived elevation of plasma angiotensin II levels in sodium replete subjects to the range of moderate sodium depletion led to a sustained increase in plasma and urinary aldosterone levels, which further and significantly increased between the 1st and 2nd days of angiotensin II infusion, when gross sodium retention during infusion was prevented. Sodium 65-71 angiotensinogen Homo sapiens 40-54 221518-4 1978 In the sodium deplete state, the absolute increment of aldosterone secretion for a given elevation of angiotensin II levels diring infusion was larger than in sodium replete subjects. Sodium 7-13 angiotensinogen Homo sapiens 102-116 221518-5 1978 This confirms the conclusions from previous short-term angiotensin II infusion experiments that sodium deficiency sensitizes the zona glomerulosa against angiotensin II. Sodium 96-102 angiotensinogen Homo sapiens 55-69 221518-5 1978 This confirms the conclusions from previous short-term angiotensin II infusion experiments that sodium deficiency sensitizes the zona glomerulosa against angiotensin II. Sodium 96-102 angiotensinogen Homo sapiens 154-168 221518-9 1978 The opposite shifts in sensitivity against angiotensin II of the zona glomerulosa and of resistance blood vessels with changes in the sodium state seem to be an effective and important means in the regulation of body sodium. Sodium 134-140 angiotensinogen Homo sapiens 43-57 641142-8 1978 Administration of bradykinin to chronically sodium-depleted dogs also lowered the MABP and increased RBF but had no effect on the RVR to AII. Sodium 44-50 kininogen 1 Canis lupus familiaris 18-28 633780-3 1978 It is suggested that renal hypotension after acute losses of sodium and extracellular fluid may also develop in patients with chronically depressed renin-angiotensin system. Sodium 61-67 renin Homo sapiens 148-153 750607-1 1978 Previous studies from this laboratory have demonstrated that the redistribution of blood volume and concomitant central hypervolemia induced by water immersion to the neck (NI), produces a prompt and profound suppression of plasma renin activity (PRA) and plasma aldosterone concentration (PA) without concomitant alterations in serum sodium and potassium concentrations. Sodium 335-341 renin Homo sapiens 231-236 205561-1 1978 In the toad urinary bladder 8-p-chlorophenylthio-cyclic AMP mimics the stimulatory effects of antidiuretic hormone on osmotic water permeability, 3H2O diffusion, and transepithelial sodium transport; but unlike the hormone does not cause an increase in urea permeability. Sodium 182-188 adenine phosphoribosyltransferase Homo sapiens 56-59 633132-0 1978 Sodium and water metabolism under the influence of prolactin, aldosterone, and antidiuretic hormone. Sodium 0-6 prolactin Oryctolagus cuniculus 51-60 633132-13 1978 Prolactin (200 i.u./day) caused a reduction in urine volume and in renal sodium excretion and since there were no compensatory changes in water and sodium intake, this led to substantial accumulation of both water and sodium. Sodium 73-79 prolactin Oryctolagus cuniculus 0-9 204942-1 1978 The mechanism of increased adrenal sensitivity to angiotensin II during the aldosterone response to sodium restriction was investigated in the rat. Sodium 100-106 angiotensinogen Rattus norvegicus 50-64 204942-2 1978 Sodium restriction for 36 hr markedly increased the aldosterone-stimulating effect of low-dose (1 ng/min) infusion of angiotensin II and caused enhanced binding of (125)I-labeled angiotensin II to the zona glomerulosa in vivo. Sodium 0-6 angiotensinogen Rattus norvegicus 118-132 204942-2 1978 Sodium restriction for 36 hr markedly increased the aldosterone-stimulating effect of low-dose (1 ng/min) infusion of angiotensin II and caused enhanced binding of (125)I-labeled angiotensin II to the zona glomerulosa in vivo. Sodium 0-6 angiotensinogen Rattus norvegicus 179-193 204942-3 1978 Conversely, in vivo binding of (125)I-labeled angiotensin II was significantly decreased after 36 hr of high-sodium intake. Sodium 109-115 angiotensinogen Rattus norvegicus 46-60 204942-4 1978 In isolated glomerulosa cells, the increased binding of angiotensin II after sodium restriction was shown to result from a significant increase in receptor affinity (+80%) and a smaller increase in receptor concentration (+25%). Sodium 77-83 angiotensinogen Rattus norvegicus 56-70 204942-7 1978 During sodium loading for 36 hr and 4 days, the converse effects on adrenal angiotensin II receptors and aldosterone production were observed. Sodium 7-13 angiotensinogen Rattus norvegicus 76-90 204942-8 1978 Also, in contrast to the consistent increase in angiotensin II receptors in the adrenal glands of sodium-restricted animals, the angiotensin II binding capacity of uterine smooth muscle was decreased by 40% after 7 days of sodium restriction.The rapid regulation of receptor affinity and concentration during changes in sodium intake provides a basis for the dynamic modulation of aldosterone responses by dietary sodium content. Sodium 223-229 angiotensinogen Rattus norvegicus 129-143 204942-8 1978 Also, in contrast to the consistent increase in angiotensin II receptors in the adrenal glands of sodium-restricted animals, the angiotensin II binding capacity of uterine smooth muscle was decreased by 40% after 7 days of sodium restriction.The rapid regulation of receptor affinity and concentration during changes in sodium intake provides a basis for the dynamic modulation of aldosterone responses by dietary sodium content. Sodium 223-229 angiotensinogen Rattus norvegicus 129-143 204942-8 1978 Also, in contrast to the consistent increase in angiotensin II receptors in the adrenal glands of sodium-restricted animals, the angiotensin II binding capacity of uterine smooth muscle was decreased by 40% after 7 days of sodium restriction.The rapid regulation of receptor affinity and concentration during changes in sodium intake provides a basis for the dynamic modulation of aldosterone responses by dietary sodium content. Sodium 223-229 angiotensinogen Rattus norvegicus 129-143 204942-9 1978 During sodium restriction, the sequential changes in receptor affinity and concentration account for the enhanced binding and steroidogenic actions of angiotensin II in vivo and in vitro. Sodium 7-13 angiotensinogen Rattus norvegicus 151-165 204942-11 1978 The opposite finding in smooth muscle-that sodium restriction decreases the concentration of angiotensin II receptors-is consistent with the divergent effects of changing sodium balance upon vascular and adrenal responses to angiotensin II. Sodium 43-49 angiotensinogen Rattus norvegicus 93-107 204942-11 1978 The opposite finding in smooth muscle-that sodium restriction decreases the concentration of angiotensin II receptors-is consistent with the divergent effects of changing sodium balance upon vascular and adrenal responses to angiotensin II. Sodium 43-49 angiotensinogen Rattus norvegicus 225-239 204942-11 1978 The opposite finding in smooth muscle-that sodium restriction decreases the concentration of angiotensin II receptors-is consistent with the divergent effects of changing sodium balance upon vascular and adrenal responses to angiotensin II. Sodium 171-177 angiotensinogen Rattus norvegicus 93-107 204942-11 1978 The opposite finding in smooth muscle-that sodium restriction decreases the concentration of angiotensin II receptors-is consistent with the divergent effects of changing sodium balance upon vascular and adrenal responses to angiotensin II. Sodium 171-177 angiotensinogen Rattus norvegicus 225-239 202988-9 1978 The concomitant increase in plasma PRL might synergize with ALDO in influencing the renal retention of sodium, but PRL alone has little apparent effect on human kidney function. Sodium 103-109 prolactin Homo sapiens 35-38 735881-8 1978 Angiotensin II appears to be of importance for the maintenance of BP in sodium replete hypertensive patients with normal or high PRA. Sodium 72-78 angiotensinogen Homo sapiens 0-14 754782-0 1978 [Effect of sodium depletion on plasma renin activity in blood reflux from the renal veins in essential and nephrovascular hypertension]. Sodium 11-17 renin Homo sapiens 38-43 699587-3 1978 Conceivably saralasin exerts different sodium-dependent effects on peripheral angiotensin II and specific intrarenal vascular receptors. Sodium 39-45 angiotensinogen Homo sapiens 78-92 699588-1 1978 1-Sar-8-ala-angiotensin II did not change intra-arterial pressure in 25 sodium replete hypertensive patients, whilst the pressure changes were closely related to the plasma renin level during sodium depletion (r = -0.87; n = 32). Sodium 192-198 renin Homo sapiens 173-178 699588-3 1978 Plasma renin is unaffected in sodium replete subjects, but increases during saralasin in sodium deplete conditions. Sodium 30-36 renin Homo sapiens 7-12 624393-1 1978 In experimental dystrophy of the liver in rats provoked by introduction of CCL4 the enlargement of the extracellular space is followed by a diminished excretion of sodium. Sodium 164-170 C-C motif chemokine ligand 4 Rattus norvegicus 75-79 640577-1 1978 The changes in plasma renin activity (PRA) and plasma aldosterone concentration (PA) in response to dietary sodium restriction and upright posture were evaluated in 7 patients with juvenile-type, insulin-dependent, uncomplicated diabetes mellitus and in 5 healthy volunteers. Sodium 108-114 renin Homo sapiens 22-27 731678-2 1978 Changes in cellular sodium produced by amiloride, vasopressin, aldosterone, hypoxia, ouabain, and sodium-free media are consistent with a cellular sodium transport pool. Sodium 20-26 arginine vasopressin Homo sapiens 50-61 625013-5 1978 injections of renin nor intravenous infusions of angiotensin II stimulated sodium appetite in normal rats or sodium-replete adrenalectomized rats.4. Sodium 75-81 angiotensinogen Rattus norvegicus 49-63 215819-12 1978 Although aldo and DOC and sodium retention may contribute to the ACTH induced blood pressure elevation, other factors must play a role. Sodium 26-32 proopiomelanocortin Homo sapiens 65-69 366278-4 1978 The excess of sodium-retaining corticoids (DOC or aldosterone) together with sodium suppress the secretion of renin, while a deficiency of cortical hormones (adrenalectomy, morbus Addison) increase it." Sodium 14-20 renin Homo sapiens 110-115 366278-4 1978 The excess of sodium-retaining corticoids (DOC or aldosterone) together with sodium suppress the secretion of renin, while a deficiency of cortical hormones (adrenalectomy, morbus Addison) increase it." Sodium 77-83 renin Homo sapiens 110-115 628191-0 1978 Effect of prolonged low-dose infusions of ile5-angiotensin ii on blood pressure, aldosterone and electrolyte excretion in sodium replete man. Sodium 122-128 angiotensinogen Homo sapiens 47-61 628191-2 1978 Plasma angiotensin II levels were therby raised to the range of moderate sodium depletion. Sodium 73-79 angiotensinogen Homo sapiens 7-21 628191-8 1978 Blood pressure increased gradually during angiotensin II infusion, reflecting changes in sodium balance. Sodium 89-95 angiotensinogen Homo sapiens 42-56 622601-6 1978 The increase in plasma renin activity expected with sodium depletion and diuretic therapy was not blunted by propranolol. Sodium 52-58 renin Homo sapiens 23-28 341466-2 1978 Unstimulated plasma renin and aldosterone levels were within control range in all patients and rose significantly in response to sodium depletion. Sodium 129-135 renin Homo sapiens 20-25 742128-0 1978 [Effect of oral sodium load on the renin and aldosterone secretion in essential hypertension. Sodium 16-22 renin Homo sapiens 35-40 599483-0 1977 Active and inactive renin in rabbit plasma during sodium depletion and repletion [proceedings]. Sodium 50-56 LOW QUALITY PROTEIN: renin Oryctolagus cuniculus 20-25 920808-0 1977 Effects of endogenous angiotensin II on renal sodium excretion and renal hemodynamics. Sodium 46-52 angiotensinogen Homo sapiens 22-36 603306-2 1977 Bradykinin, when injected into the renal artery of the dog, reduced the proximal reabsorption of sodium and water and decreased the secretion of p-aminohippuric acid (PAH). Sodium 97-103 kininogen 1 Canis lupus familiaris 0-10 603306-4 1977 This enabled us to conclude that Bk decreased the transport efficiency of sodium and PAH. Sodium 74-80 kininogen 1 Canis lupus familiaris 33-35 601775-6 1977 The present data suggest that angiotensin II influences the synthesis or release of renal PG in patients with essential hypertension on normal sodium diet, but not when they are on low sodium diet. Sodium 143-149 angiotensinogen Homo sapiens 30-44 211000-0 1977 The effect of parathyroid hormone (PTH) and dietary phosphate on the sodium-dependent phosphate transport system located in the rat renal brush border membrane. Sodium 69-75 parathyroid hormone Rattus norvegicus 14-33 71600-8 1977 Thus, sodium depletion stimulates total renin release, while propranolol and clonidine produce divergent responses of active renin and prorenin, the changes in prorenin depending on the changes induced in blood-pressure. Sodium 6-12 renin Homo sapiens 40-45 578621-1 1977 The relation between plasma prolactin (PRL) and sodium metabolism was studied in adult male rats. Sodium 48-54 prolactin Rattus norvegicus 28-37 578621-1 1977 The relation between plasma prolactin (PRL) and sodium metabolism was studied in adult male rats. Sodium 48-54 prolactin Rattus norvegicus 39-42 599839-1 1977 We assessed the role of the renin-angiotensin system in the response of the renal circulation to restriction of sodium intake in 38 normal patients. Sodium 112-118 renin Homo sapiens 28-33 563937-8 1977 To choose the most rational therapy regimen it may be useful to calculate the renin-sodium index that reflects the relationship between the plasma renin activity and the urine excretion of sodium. Sodium 84-90 renin Homo sapiens 78-83 599962-0 1977 The influence of upright position and sodium restriction in the diet on plasma renin activity (PRA) and aldosteronemia in patients with chronic nephritis. Sodium 38-44 renin Homo sapiens 79-84 563937-8 1977 To choose the most rational therapy regimen it may be useful to calculate the renin-sodium index that reflects the relationship between the plasma renin activity and the urine excretion of sodium. Sodium 84-90 renin Homo sapiens 147-152 902688-7 1977 Thus, a bradykinin-induced increase in free water clearance may be accounted for by other than an inhibition of proximal tubular sodium reabsorption. Sodium 129-135 kininogen 1 Canis lupus familiaris 8-18 561647-0 1977 The effect of prolactin on sodium flux through the isolated amniotic membrane of the guinea pig. Sodium 27-33 prolactin Cavia porcellus 14-23 902672-0 1977 Hypotensive effects of sodium volume depletion and 1-sar-8-ala-angiotensin II in relation to plasma renin in hypertensive patients. Sodium 23-29 renin Homo sapiens 100-105 902672-1 1977 The hypotensive effect of acute sodium volume depletion, produced by chlorthalidone and a low sodium diet, was inversely related to the plasma renin concentration (PRC) in 13 hypertensive patients of varying aetiology (r = 0.61; p less than 0.05); weight reduction induced by this therapy was not related to PRC (r = 0.12; p greater than 0.1). Sodium 32-38 renin Homo sapiens 143-148 902672-1 1977 The hypotensive effect of acute sodium volume depletion, produced by chlorthalidone and a low sodium diet, was inversely related to the plasma renin concentration (PRC) in 13 hypertensive patients of varying aetiology (r = 0.61; p less than 0.05); weight reduction induced by this therapy was not related to PRC (r = 0.12; p greater than 0.1). Sodium 94-100 renin Homo sapiens 143-148 914228-0 1977 [Effects of acute sodium depletion on blood pressure and renin-angiotensin-aldosterone system in patients with benign essential hypertension (author"s transl)]. Sodium 18-24 renin Homo sapiens 57-62 902672-3 1977 The combined hypotensive response to acute sodium volume depletion and to angiotensin II blockade during sodium volume depletion was not related to PRC (r = 0.15; p greater than 0.1). Sodium 105-111 angiotensinogen Homo sapiens 74-88 902672-4 1977 The results demonstrate that acute sodium volume depletion caused similar weight loss in patients with high and low PRC values, and it would have had similar hypotensive effects but for angiotensin-induced vasoconstriction in the high renin patients. Sodium 35-41 renin Homo sapiens 235-240 909130-11 1977 Furthermore, the change in mean arterial pressure induced by infusion of angiotensin II analogue seemed to correlate with DBH activity change by sodium depletion. Sodium 145-151 angiotensinogen Homo sapiens 73-87 886216-0 1977 Effects of potassium chloride on plasma renin activity during sodium restriction in normal man. Sodium 62-68 renin Homo sapiens 40-45 872524-9 1977 There was a significant positive correlation between exchangeable sodium and plasma growth hormone. Sodium 66-72 growth hormone 1 Homo sapiens 84-98 907802-5 1977 These results demonstrate that the inhibitory effect of two different betablocking agents on renin release is not related to their cardio-selectivity and is independent of sodium balance. Sodium 172-178 renin Homo sapiens 93-98 907802-6 1977 The influence of the renin decrease on aldosterone is dependent on sodium balance and on the initial state of the renin angiotensin system. Sodium 67-73 renin Homo sapiens 21-26 872524-13 1977 We conclude that (a) suppression of plasma renin activity in acromegaly can be explained by sodium retention, (b) hypersecretion of growth hormone is probably responsible for the increased exchangeable sodium, and (c) sodium overload cannot be directly related to blood pressure but may contribute to the increased occurrence of hypertension in acromegaly. Sodium 92-98 renin Homo sapiens 43-48 872524-13 1977 We conclude that (a) suppression of plasma renin activity in acromegaly can be explained by sodium retention, (b) hypersecretion of growth hormone is probably responsible for the increased exchangeable sodium, and (c) sodium overload cannot be directly related to blood pressure but may contribute to the increased occurrence of hypertension in acromegaly. Sodium 202-208 growth hormone 1 Homo sapiens 132-146 872524-13 1977 We conclude that (a) suppression of plasma renin activity in acromegaly can be explained by sodium retention, (b) hypersecretion of growth hormone is probably responsible for the increased exchangeable sodium, and (c) sodium overload cannot be directly related to blood pressure but may contribute to the increased occurrence of hypertension in acromegaly. Sodium 202-208 growth hormone 1 Homo sapiens 132-146 874078-7 1977 Plasma renin activity showed similar increments after sodium restriction in all groups. Sodium 54-60 renin Homo sapiens 7-12 862554-0 1977 Effect of prolactin on sodium and potassium concentrations in mammary alveolar tissue. Sodium 23-29 prolactin Homo sapiens 10-19 874056-2 1977 Significant angiotensin II-dependence of blood pressure was found only after the combined stimulus of sodium restriction (10 mEq daily for 4 days) and ambulation. Sodium 102-108 angiotensinogen Homo sapiens 12-26 877126-0 1977 Effect of vasopressin administration on sodium excretion and plasma phosphate concentration. Sodium 40-46 arginine vasopressin Homo sapiens 10-21 17257-7 1977 It is suggested that serum prolactin may possible participate in sodium retention in man as has been demonstrated in studies on animals. Sodium 65-71 prolactin Homo sapiens 27-36 407362-8 1977 These observations are in accord with the theory of Leaf and his associates, that the predominant effect of vasopressin is to enhance sodium entry into the transporting epithelial cells of the toad urinary bladder. Sodium 134-140 arginine vasopressin Homo sapiens 108-119 17257-0 1977 Increased serum prolactin in diabetic ketoacidosis; correlation between serum sodium and serum prolacting concentration. Sodium 78-84 prolactin Homo sapiens 16-25 17257-6 1977 However, a significant negative correlation between log serum prolactin concentration and serum sodium concentration was demonstrated (r = -0.61, P less than 0.01). Sodium 96-102 prolactin Homo sapiens 62-71 407360-0 1977 Interrelationships of sodium transport and carbon dioxide production by the toad bladder: response to changes in mucosal sodium concentration, to vasopressin and to availability of metabolic substrate. Sodium 22-28 arginine vasopressin Homo sapiens 146-157 407360-2 1977 The rate of sodium transport was varied by changing the concentration of sodium in the mucosal bath (substitution with choline), by adding vasopressin, by adding metabolic substrates and by adding malonate, and the ratio of the change of sodium transport and CO2 production was determined Mean values for deltaNa/deltaCO2 (equiv/mole) were: Na in equilibrium choline 18.3 +/- 1.1; vasopressin 15.5 +/- 2.8; and pyruvate (corrected for the increment in "nontransport" CO2) 15.4 +/- 3.5. Sodium 12-18 arginine vasopressin Homo sapiens 139-150 407360-2 1977 The rate of sodium transport was varied by changing the concentration of sodium in the mucosal bath (substitution with choline), by adding vasopressin, by adding metabolic substrates and by adding malonate, and the ratio of the change of sodium transport and CO2 production was determined Mean values for deltaNa/deltaCO2 (equiv/mole) were: Na in equilibrium choline 18.3 +/- 1.1; vasopressin 15.5 +/- 2.8; and pyruvate (corrected for the increment in "nontransport" CO2) 15.4 +/- 3.5. Sodium 12-18 arginine vasopressin Homo sapiens 381-392 18271-0 1977 Effect of parathyroid hormone on renal excretion of sodium and hydrogen ions. Sodium 52-58 parathyroid hormone Homo sapiens 10-29 884929-0 1977 The effect of dietary sodium intake on the blood pressure and cardiac output responses to angiotensin II in unanaesthetized rats. Sodium 22-28 angiotensinogen Rattus norvegicus 90-104 20666-2 1977 According to the results of the plasma renin activity, we noted variations in blood volume and exchangeable sodium in order to determine the best possible treatment based on these data. Sodium 108-114 renin Homo sapiens 39-44 858175-8 1977 Renin fell during the phase of sodium gain, and remained low afterwards. Sodium 31-37 renin Homo sapiens 0-5 858175-14 1977 The long-term effects of mineralocorticoid excess on the interrelations between pressure, volume, and renin bear some resemblance to the pattern observed in patients with established essential hypertension, i.e., pressure remains elevated despite a decrease of volume, and renin is "inappropriately" suppressed in relation to the sodium and volume status. Sodium 330-336 renin Homo sapiens 102-107 858972-0 1977 Effect of pharmacologic doses of vasopressin on sodium reabsorption in the rat kidney. Sodium 48-54 arginine vasopressin Rattus norvegicus 33-44 858972-5 1977 To reduce the influence of the pressor effect of these doses of vasopressin on the kidney, the aorta was constricted proximal to the renal arteries and this resulted in a decrease in urinary sodium excretion to 2.87 +/- 0.57 micronEq/min. Sodium 191-197 arginine vasopressin Rattus norvegicus 64-75 858972-9 1977 It is concluded that pharmacologic doses of vasopressin inhibit sodium reabsorption in the proximal convoluted tubule as well as in distal portions of the nephron. Sodium 64-70 arginine vasopressin Rattus norvegicus 44-55 858972-10 1977 The magnitude of sodium excretion observed is a function both of vasopressin inhibition of sodium reabsorption and the pressor effect of vasopressin. Sodium 17-23 arginine vasopressin Rattus norvegicus 65-76 858972-10 1977 The magnitude of sodium excretion observed is a function both of vasopressin inhibition of sodium reabsorption and the pressor effect of vasopressin. Sodium 17-23 arginine vasopressin Rattus norvegicus 137-148 858972-10 1977 The magnitude of sodium excretion observed is a function both of vasopressin inhibition of sodium reabsorption and the pressor effect of vasopressin. Sodium 91-97 arginine vasopressin Rattus norvegicus 65-76 874867-0 1977 On the question of body fluid volume or sodium status influencing renin release. Sodium 40-46 renin Ovis aries 66-71 870773-9 1977 In a separate study, the adrenal response to infused angiotensin II was determined in 12 hypertensive patients who were on a sodium intake of 200 meq. Sodium 125-131 angiotensinogen Homo sapiens 53-67 870773-12 1977 Thus, some patients with normal-renin essential hypertension may have either enhanced or reduced adrenal responsiveness to angiotensin II, depending on the conditions of dietary intake of sodium. Sodium 188-194 angiotensinogen Homo sapiens 123-137 191300-3 1977 This subgroup includes nearly all patients with high or "normal" renin--sodium profiles. Sodium 72-78 renin Homo sapiens 65-70 191300-7 1977 Meanwhile the validation provided by these three different pharmacologic probes portends a burgeoning clinical role for renin--sodium profiling not only in screening for renal and adrenal cortical hypertensions but also for characterizing the vasoconstrictor and volume elements involved in various individual patients and thus enabling more specific treatments of the various subtypes of essential hypertension. Sodium 127-133 renin Homo sapiens 120-125 845699-1 1977 Four lactating Holstein cows were used in a 4 X 4 Latin Square design to determine the effects of postruminally administering sodium caseinate and/or glucose on milk production, milk composition, nitrogen utilization, amino acid utilization by the lactating mammary gland and glucose turnover rate. Sodium 126-132 Weaning weight-maternal milk Bos taurus 161-165 845699-2 1977 An 8.5% increase in milk yield and a 13.3% increase in milk protein production were obtained during infusion of sodium caseinate. Sodium 112-118 Weaning weight-maternal milk Bos taurus 20-24 845699-2 1977 An 8.5% increase in milk yield and a 13.3% increase in milk protein production were obtained during infusion of sodium caseinate. Sodium 112-118 casein beta Bos taurus 55-67 14160-2 1977 The renin-angiotensin system appears to play a major role in the regulation of sodium excretion and fluid intake in a wide variety of animal species from mammals to teleosts. Sodium 79-85 renin Homo sapiens 4-9 558584-14 1977 This implies that a high sodium concentration at the macula densa stimulates renin release. Sodium 25-31 renin Homo sapiens 77-82 190265-0 1977 Effects of ionophore A23187 on base-line and vasopressin-stimulated sodium transport in the toad bladder. Sodium 68-74 arginine vasopressin Homo sapiens 45-56 846069-2 1977 In group, I, normal salt animals hypotonically expanded with antidiuretic hormone (ADH) (using a protocol known to stimulate aldosterone) presented large amounts of sodium to the distal tubule and excreted an acute HCl load much more efficiently than did animals pretreated with either a normal (NL) or low (LO) salt diet alone. Sodium 165-171 arginine vasopressin Homo sapiens 61-81 846069-2 1977 In group, I, normal salt animals hypotonically expanded with antidiuretic hormone (ADH) (using a protocol known to stimulate aldosterone) presented large amounts of sodium to the distal tubule and excreted an acute HCl load much more efficiently than did animals pretreated with either a normal (NL) or low (LO) salt diet alone. Sodium 165-171 arginine vasopressin Homo sapiens 83-86 846069-4 1977 Acid excretion was maximized (ADH) when distal sodium avidity was stimulated in the presence of adequate distal sodium delivery and minimized (F) when distal sodium delivery was limited (despite possible augmentation of distal sodium avidity). Sodium 47-53 arginine vasopressin Homo sapiens 30-33 846071-10 1977 These results suggest that angiotensin II plays an active role in sustaining normal blood pressure only under conditions of considerable sodium-depletion. Sodium 137-143 angiotensinogen Homo sapiens 27-41 844248-9 1977 It is suggested that inhibition of prostaglandin synthesis by indomethacin, in the presence of a stimulated renin-angiotensin system and hyperaldosteronism, may cause this strong tendency to sodium retention. Sodium 191-197 renin Homo sapiens 108-113 30731547-11 1977 Literature data suggest the following changes in the milk composition from quarters definitely positive to mastitis screening tests based on somatic cell counts compared to normal quarters (values represent percent of normal): total solids (92), lactose (85), fat (88), total protein (100), caseins (82), whey protein (162), chloride (161), sodium (136), potassium (91), pH (105), lipase activity (116), and acid degree value (183). Sodium 341-347 Weaning weight-maternal milk Bos taurus 53-57 846064-1 1977 The role of the renin-angiotensin system in mediating the aldosterone response to sodium depletion was examined by administration of propranolol during dietary sodium restriction. Sodium 82-88 renin Homo sapiens 16-21 846064-2 1977 The beta-adrenergic antagonist prevented the expected increase of plasma renin activity in response to sodium restriction in six of twelve studies. Sodium 103-109 renin Homo sapiens 73-78 846064-6 1977 It is suggested that the aldosterone response to sodium restriction is mediated not only by increased plasma renin activity and angiotensin II concentration, but also another mechanism, possibly related to increased adrenal sensitivity to angiotensin during sodium depletion. Sodium 49-55 renin Homo sapiens 109-114 846064-6 1977 It is suggested that the aldosterone response to sodium restriction is mediated not only by increased plasma renin activity and angiotensin II concentration, but also another mechanism, possibly related to increased adrenal sensitivity to angiotensin during sodium depletion. Sodium 49-55 angiotensinogen Homo sapiens 128-142 556854-0 1977 Dose-dependent stimulation and inhibition of proximal tubular sodium reabsorption by angiotensin II in the rat kidney. Sodium 62-68 angiotensinogen Rattus norvegicus 85-99 837964-3 1977 The effect of ASA on urinary sodium excretion was most prominent during day time (8 a.m.-10 p.m.) and on days with low sodium intake, as confirmed by control sodium excretion and plasma renin activity. Sodium 29-35 renin Homo sapiens 186-191 339673-6 1977 The results indicate that sodium retention is involved in the pathogenesis of posttransplant hypertension and suggest that an increased activity of the renin--angiotensin system is counterbalanced by an accumulation of sodium in TRAS. Sodium 219-225 renin Homo sapiens 152-157 899932-4 1977 Stimulation of endogenous PTH secretion by calcium-poor hyperoncotic albumin resulted in a similar decrease in net calcium, sodium, and water absorption. Sodium 124-130 parathyroid hormone Rattus norvegicus 26-29 899932-5 1977 It is suggested that PTH has a direct inhibitory effect on jejunal calcium, sodium, and water absorption. Sodium 76-82 parathyroid hormone Rattus norvegicus 21-24 833263-9 1977 These observations suggest that estrogen-induced increases in renin substrate do not alone account for the increases in the renin-angiotensin-aldosterone system observed during pregnancy, but rather such increases appear to represent a physiological response to increased sodium need during pregnancy. Sodium 272-278 renin Homo sapiens 62-67 846042-0 1977 Responses of plasma renin to sodium load in two types of experimental renal hypertension. Sodium 29-35 LOW QUALITY PROTEIN: renin Oryctolagus cuniculus 20-25 857177-6 1977 It is concluded that the renin-angiotensin system in patients on chronic hemodialysis still functions as one of the adjustment mechanisms for the circulatory homeostasis, when challenged by volume loss or volume and sodium loading. Sodium 216-222 renin Homo sapiens 25-30 917179-0 1977 Concentrations of antidiuretic hormone in plasma during human sodium restriction. Sodium 62-68 arginine vasopressin Homo sapiens 18-38 895996-1 1977 Plasma prolactin was determined in a longitudinal study, where -9 manic-depressive patients were examined before lithium treatment and at various times during the treatment with the aim of unravelling a possible association between initial changes in water and sodium balance during lithium treatment and changes in plasma prolactin level. Sodium 261-267 prolactin Homo sapiens 7-16 886604-0 1977 Influence of insulin on sodium efflux in barnacle muscle fibers. Sodium 24-30 insulin Homo sapiens 13-20 341139-1 1977 Interrelationship between blood pressure, kidney function, renin-aldosterone system and body sodium content. Sodium 93-99 renin Homo sapiens 59-64 341139-5 1977 It is suggested that sodium retention may counterbalance increased activity of the renin system in KTAS. Sodium 21-27 renin Homo sapiens 83-88 583991-3 1977 Circulating vasopressin levels were also markedly increased, the size of these increases being the same as those seen in other pigs given exogenous vasopressin in amounts which were shown to increase urinary sodium excretion. Sodium 208-214 vasopressin Sus scrofa 148-159 583991-4 1977 This suggests that vasopressin was probably contributing to the increase in renal sodium excretion seen in those pigs given the intravenous salt loads. Sodium 82-88 vasopressin Sus scrofa 19-30 613576-0 1977 [Regulation of renin secretion in saluretic-induced sodium loss]. Sodium 52-58 renin Homo sapiens 15-20 1013701-2 1976 Using this approach it was possible to show that renin via angiotensin participates actively in blood pressure maintenace, particularly following sodium depletion. Sodium 146-152 renin Homo sapiens 49-54 980059-3 1976 Patients from all three renin subgroups exhibited a fall in blood pressure when sufficiently sodium depleted, and an elevation in blood pressure when sodium replete or insufficiently depleted. Sodium 93-99 renin Homo sapiens 24-29 980059-3 1976 Patients from all three renin subgroups exhibited a fall in blood pressure when sufficiently sodium depleted, and an elevation in blood pressure when sodium replete or insufficiently depleted. Sodium 150-156 renin Homo sapiens 24-29 980059-4 1976 However, those with low renin required loss of substantially more sodium (sufficient to elicit compensatory stimulation of renin) before depletion could be achieved. Sodium 66-72 renin Homo sapiens 24-29 980059-4 1976 However, those with low renin required loss of substantially more sodium (sufficient to elicit compensatory stimulation of renin) before depletion could be achieved. Sodium 66-72 renin Homo sapiens 123-128 980059-5 1976 In patients with essential hypertension of all three renin subgroups, sodium balance determines the degree of participation of the renin-angiotensin system in sustaining high blood pressure. Sodium 70-76 renin Homo sapiens 53-58 980059-5 1976 In patients with essential hypertension of all three renin subgroups, sodium balance determines the degree of participation of the renin-angiotensin system in sustaining high blood pressure. Sodium 70-76 renin Homo sapiens 131-136 980059-6 1976 Even the low-renin type can become renin dependent with sufficient sodium depletion. Sodium 67-73 renin Homo sapiens 13-18 980059-6 1976 Even the low-renin type can become renin dependent with sufficient sodium depletion. Sodium 67-73 renin Homo sapiens 35-40 791534-4 1976 The role of angiotensin II in feedback control of renin secretion is confirmed as is its importance in aldosterone stimulation both in relation to posture and sodium depletion. Sodium 159-165 angiotensinogen Homo sapiens 12-26 1000801-2 1976 The most commonly used preservative, NaF, makes analysis of other serum constituents such as sodium and calcium and urea difficult or impossible, an especially serious limitation when sample size must be restricted. Sodium 93-99 C-X-C motif chemokine ligand 8 Homo sapiens 37-40 799552-4 1976 The renin-angiotensin system appeared to behave in a normal fashion in response to alterations in sodium intake and posture. Sodium 98-104 renin Homo sapiens 4-9 1071606-6 1976 These findings suggest that: (a) standing blood pressure in sodium-deprived normal subjects is angiotensin II dependent; (b)normal-renin hypertensive patients when sodium deprived by diet alone do not appear to be angiotensin II dependent (angiotensin II is unlikely therefore to be directly maintaining their blood pressure on their normal sodium intake);(c) the rise in blood pressure seen in low-renin hypertensive patients with saralasin may be a further way of distinguishing this group of patients. Sodium 60-66 angiotensinogen Homo sapiens 95-109 1071607-2 1976 In all three renin sub-groups of essential hypertension, the state of sodium balance determines the degree of participation of the renin-angiotensin system in sustaining high blood pressure. Sodium 70-76 renin Homo sapiens 13-18 1071607-2 1976 In all three renin sub-groups of essential hypertension, the state of sodium balance determines the degree of participation of the renin-angiotensin system in sustaining high blood pressure. Sodium 70-76 renin Homo sapiens 131-136 1071607-4 1976 Even the low-renin type can become renin-dependent when sufficient sodium depletion has bee achieved. Sodium 67-73 renin Homo sapiens 13-18 1071607-4 1976 Even the low-renin type can become renin-dependent when sufficient sodium depletion has bee achieved. Sodium 67-73 renin Homo sapiens 35-40 1002819-3 1976 Sodium lactate (75 mEq sodium/hr) also significantly reduced renin levels at 20-30 min (P less than 0.01). Sodium 23-29 renin Homo sapiens 61-66 1002819-4 1976 The infusion of 1/3 normal saline (25 mEq sodium/h for 2 h) produced a significant reduction (P less than 0.01) in plasma renin activity (from control levels of 5.2 +/- 0.8 to 3.1 +/- 0.6 ng/ml/h at 90 min). Sodium 42-48 renin Homo sapiens 122-127 1002819-6 1976 The observed effects of the hydrogen and calcium ions on suppressing renin release may be secondary to their known actions on renal sodium excretion. Sodium 132-138 renin Homo sapiens 69-74 1002819-7 1976 Since the infusions of calcium and hydrogen ions both result in an increased delivery of sodium to the distal segment of the nephron, the results may reflect the regulation of renin by the macula densa, a sensitive intrarenal sensor of renal tubular sodium. Sodium 89-95 renin Homo sapiens 176-181 1002819-7 1976 Since the infusions of calcium and hydrogen ions both result in an increased delivery of sodium to the distal segment of the nephron, the results may reflect the regulation of renin by the macula densa, a sensitive intrarenal sensor of renal tubular sodium. Sodium 250-256 renin Homo sapiens 176-181 995500-9 1976 A II infusion induced an increase in urinary sodium excretion only in the two patients with renal sodium wastage (from 80-90 to 265-230 muEq/min in 30 min). Sodium 45-51 angiotensinogen Homo sapiens 0-4 995500-9 1976 A II infusion induced an increase in urinary sodium excretion only in the two patients with renal sodium wastage (from 80-90 to 265-230 muEq/min in 30 min). Sodium 98-104 angiotensinogen Homo sapiens 0-4 10725-0 1976 Effect of sodium depletion on plasma renin concentration before and during adrenergic beta-receptor blockade with propranolol in normotensive man. Sodium 10-16 renin Homo sapiens 37-42 10725-2 1976 Sodium depletion stimulates renin release. Sodium 0-6 renin Homo sapiens 28-33 10725-3 1976 Evaluation of plasma renin would, therefore seem possible only in relation to sodium balance. Sodium 78-84 renin Homo sapiens 21-26 10725-5 1976 A well-defined hyperbolic relationship was found between the two variables indicating that the physiologic level of plasma renin concentration depends on the state of sodium balance. Sodium 167-173 renin Homo sapiens 123-128 10725-8 1976 In 20 healthy normotensive subjects in whom beta-receptor blockade was verified by a significant reduction in pulse rate, the same hyperbolic relationship was found between plasma renin concentration and sodium excretion as in the control group showing that sodium depletion stimulates renin release independent of sympathetic nervous activity. Sodium 204-210 renin Homo sapiens 180-185 10725-8 1976 In 20 healthy normotensive subjects in whom beta-receptor blockade was verified by a significant reduction in pulse rate, the same hyperbolic relationship was found between plasma renin concentration and sodium excretion as in the control group showing that sodium depletion stimulates renin release independent of sympathetic nervous activity. Sodium 258-264 renin Homo sapiens 180-185 10725-8 1976 In 20 healthy normotensive subjects in whom beta-receptor blockade was verified by a significant reduction in pulse rate, the same hyperbolic relationship was found between plasma renin concentration and sodium excretion as in the control group showing that sodium depletion stimulates renin release independent of sympathetic nervous activity. Sodium 258-264 renin Homo sapiens 286-291 185902-2 1976 A reciprocal relationship exists between sodium balance and the circulating levels of renin and angiotensin II. Sodium 41-47 renin Homo sapiens 86-91 185902-2 1976 A reciprocal relationship exists between sodium balance and the circulating levels of renin and angiotensin II. Sodium 41-47 angiotensinogen Homo sapiens 96-110 185902-3 1976 The vascular responsiveness to angiotensin II, the major vasconstrictor component of the renal pressor system, can be impaired by numerous factors including sodium depletion or a reduction in effective plasma volume. Sodium 157-163 angiotensinogen Homo sapiens 31-45 185902-8 1976 These observations support the view that the decrease in vascular response to angiotensin II during sodium deprivation or when body fluid volumes are reduced is the result of prior occupancy of the receptor sites by endogenous hormone generated both in the plasma and locally within blood vessel walls. Sodium 100-106 angiotensinogen Homo sapiens 78-92 976493-3 1976 An important incidental finding after angiotensin II blockade in both sodium-depleted dogs and dogs with thoracic caval constriction was the striking drop in arterial pressure. Sodium 70-76 angiotensinogen Rattus norvegicus 38-52 976493-5 1976 In the rat, both the nonapeptide converting enzyme inhibitor and [Sar1, Ala8]-angiotensin II produced a marked decrease in aldosterone secretion in hypophysectomized, sodium-depleted animals. Sodium 167-173 angiotensinogen Rattus norvegicus 78-92 1053468-6 1976 There was a general upward shift of plasma renin levels in terms of 24-hour renal sodium excretion in those who demonstrated an antihypertensive response to the drug. Sodium 82-88 renin Homo sapiens 43-48 11039-3 1976 An angiotensin inhibitor (1,sarcosine-8,valine angiotensin II) decreased sodium excretion. Sodium 73-79 angiotensinogen Rattus norvegicus 47-61 975494-5 1976 A significant (p less than 0.05 increase in 24 h urinary aldosterone, plasma aldosterone and plasma renin activity resulted with decreased dietary sodium intake and conversely, a significant (p less than 0.05) decrease in each hormone occurred with increased dietary sodium intake. Sodium 147-153 renin Homo sapiens 100-105 976606-1 1976 Plasma renin activity (PRA) was determined in 48 patients with diabetes mellitus in sodium balance on a 10-20 mEq. Sodium 84-90 renin Homo sapiens 7-12 965491-1 1976 The binding affinity and concentration of specific angiotensin II receptor sites of rat adrenal cortical cells and homogenates were determined after 1 and 6 wk of altered sodium and potassium intake. Sodium 171-177 angiotensinogen Rattus norvegicus 51-65 965491-2 1976 Sodium deprivation caused marked increases in plasma renin, blood angiotensin II, and plasma aldosterone, and was accompanied by a significant increase (+74%) in the number of specific angiotensin II receptor sites per adrenal cortical cell. Sodium 0-6 angiotensinogen Rattus norvegicus 66-80 965491-2 1976 Sodium deprivation caused marked increases in plasma renin, blood angiotensin II, and plasma aldosterone, and was accompanied by a significant increase (+74%) in the number of specific angiotensin II receptor sites per adrenal cortical cell. Sodium 0-6 angiotensinogen Rattus norvegicus 185-199 965491-4 1976 Sodium loading and potassium deprivation were followed by the opposite effect upon adrenal receptors, with reduction of the angiotensin II-binding capacity. Sodium 0-6 angiotensinogen Rattus norvegicus 124-138 965491-9 1976 These studies have demonstrated that chronic changes in sodium or potassium balance and acute changes in blood angiotensin II levels can exert modulating effects upon the adrenal content and/or affinity of specific receptor sites for angiotensin II. Sodium 56-62 angiotensinogen Rattus norvegicus 234-248 988054-0 1976 The effects of dietary sodium on the diurnal activity of the renin-angiotensin-aldosterone system and the excretion of urinary electrolytes. Sodium 23-29 renin Homo sapiens 61-66 990387-0 1976 Effect of acute sodium or potassium depletion on plasma renin activity in haemodialysed patients. Sodium 16-22 renin Homo sapiens 56-61 821964-2 1976 The effect of TRH induced acute elevation of endogenous serum prolactin on renal water, sodium, potassium and total solute excretion was investigated during metabolic balance conditions and during escape form mineralocorticoid excess in 8 normal volunteers (6 males, 2 females)... Sodium 88-94 prolactin Homo sapiens 62-71 999213-6 1976 Plasma renin activity values correlated positively with 12-hour urinary VMA excretion (p less than 0.01) and negatively with 6-hour urinary sodium excretion (p less than 0.05) before and after Sauna, suggesting the role of catecholamines and sodium depletion in renin response in Sauna. Sodium 140-146 renin Homo sapiens 7-12 999213-6 1976 Plasma renin activity values correlated positively with 12-hour urinary VMA excretion (p less than 0.01) and negatively with 6-hour urinary sodium excretion (p less than 0.05) before and after Sauna, suggesting the role of catecholamines and sodium depletion in renin response in Sauna. Sodium 242-248 renin Homo sapiens 7-12 939003-2 1976 Angiotensin II, infused intravenously, increased plasma aldosterone concentration in two of six anephric subjects taking their usual dietary quantities of sodium. Sodium 155-161 angiotensinogen Homo sapiens 0-14 939003-3 1976 After 3 days of dietary sodium restriction and weight-reducing hemodialysis, the aldosterone response to infused angiotensin II in the two previously reactive subjects was enhanced, while the four previously unreactive subjects also showed a rise in plasma aldosterone. Sodium 24-30 angiotensinogen Homo sapiens 113-127 954369-0 1976 Letter: Sodium balance and responsiveness to angiotensin II. Sodium 8-14 angiotensinogen Homo sapiens 45-59 181394-2 1976 High exchangeable sodium (56.7 meq/kg vs. 45-55 meq/kg in controls) was associated with a low plasma renin activity (6 ng/1/min vs. 26 +/- 3.1 in controls) and reduced aldosterone secretion rate (5.56 mug/day; normal: 50-150 mug per day)). Sodium 18-24 renin Homo sapiens 101-106 783200-8 1976 In the presently studied patients, the impairment in renal conservation of sodium appeared to be in part the consequence of an impaired ability of the vasopressin-responsive segments of the distal nephron to generate and maintain appropriately steep transepithelial sodium concentration gradients. Sodium 266-272 arginine vasopressin Homo sapiens 151-162 940019-0 1976 Plasma renin activity in normal children: its relationship to age and rates of excretion of sodium and potassium. Sodium 92-98 renin Homo sapiens 7-12 965879-5 1976 After the first dose of frusemide in study A, the mean plasma prolactin concentration correlated negatively with the urinary Na and K excretion over 5 h. After 38 h sodium depletion, the plasma prolactin concentration correlated positively with urinary Na excretion following the second dose of frusemide. Sodium 165-171 prolactin Homo sapiens 194-203 939234-2 1976 A reciprocal correlation was found demonstrating that the hyperactivity of the renin-angiotensin-aldosterone system is stimulated in infants by a low sodium intake. Sodium 150-156 renin Homo sapiens 79-84 937361-3 1976 Studies of his renal function suggest that the basic pathophysiologic defect was an abnormality in proximal tubular sodium reabsorption which led to extracellular fluid volume depletion and consequent stimulation of the renin-angiotensin-aldosterone axis. Sodium 116-122 renin Homo sapiens 220-225 180059-7 1976 Patients with normal and low renin hypertension had similar changes in plasma 18-OH DOC levels with sodium restriction. Sodium 100-106 renin Homo sapiens 29-34 180059-8 1976 However, the mean high sodium level in the normal renin essential hypertension group (11.6+/-1.6 ng/dl) was significantly greater (P is less than 0.001) than in the control group (5.4+/-0.7 ng/dl). Sodium 23-29 renin Homo sapiens 50-55 182957-0 1976 The number of sodium ion pumping sites in skeletal muscle and its modification by insulin. Sodium 14-20 insulin Homo sapiens 82-89 940907-2 1976 This study suggests that emotional stimuli, which produce cardioacceleration, may also cause increased renin secretion, thus providing a mechanism by which factors operating through the mind and sodium intake could summate in the production of hypertension. Sodium 195-201 renin Homo sapiens 103-108 183180-0 1976 Disappearance of insulin response after enzymatic treatment of sodium-transporting amphibian epithelia. Sodium 63-69 insulin Homo sapiens 17-24 183180-1 1976 Amphibian epithelia specialized in trans-cellular sodium transport lose their capacity to react to insulin by a stimulation of this process upon treatment with collagenase; baseline activity and responsiveness to other hormones (vasopressin, aldosterone) bringing about such a stimulation are preserved. Sodium 50-56 insulin Homo sapiens 99-106 178461-2 1976 Patients with essential hypertension had been previously studied and known to have normal responses of plasma renin activity to sodium restriction and upright posture. Sodium 128-134 renin Homo sapiens 110-115 178463-4 1976 Renal clearance data suggest that the suppression of renin activity was not a consequence of renal hemodynamic change or altered sodium transport, but of direct inhibition through a receptor mediating a short feedback loop. Sodium 129-135 LOW QUALITY PROTEIN: renin Oryctolagus cuniculus 53-58 178464-1 1976 The restriction of dietary sodium intake is known to depress the cardiovascular responses to angiotensin II and increase the sensitivity of the adrenal zona glomerulosa to this steroidogenic octapeptide. Sodium 27-33 angiotensinogen Rattus norvegicus 93-107 178464-4 1976 In nephrectomized rats, angiotensin III had one-third of the pressor activity relative to angiotensin II when either normal or sodium-deprived animals were compared. Sodium 127-133 angiotensinogen Rattus norvegicus 24-38 178464-9 1976 In cells dispersed from adrenal capsules of sodium-deprived rats, the maximal steroidogenic response to angiotensin II occurred at 3 X 10(-8) M, whereas angiotensin III was maximal at 1 X 10(-9) M. Aldosterone synthesis induced by both peptides was increased approximately 45% in adrenal cells from low salt rats. Sodium 44-50 angiotensinogen Rattus norvegicus 104-118 1278105-0 1976 Influence of sodium intake on vascular and adrenal angiotensin II receptors. Sodium 13-19 angiotensinogen Rattus norvegicus 51-65 1278105-1 1976 The restriction of sodium intake reduces the sensitivity of vascular smooth muscle to angiotensin II, but enhances its influence on the adrenal glomerulosa cell. Sodium 19-25 angiotensinogen Rattus norvegicus 86-100 1020762-5 1976 Sodium depletion abolished pressor responses and resulted in depressor responses in 64 per cent of the patients with normal renin values. Sodium 0-6 renin Homo sapiens 124-129 791534-3 1976 These studies indicate that angiotensin II does not have an obligatory role in blood pressure maintenance in the normal, sodium replete individual, but it is essential following sodium depletion. Sodium 178-184 angiotensinogen Homo sapiens 28-42 57453-12 1976 It is concluded that sodium depletion induced "renin dependency" of B.P. Sodium 21-27 renin Homo sapiens 47-52 932525-7 1976 Response of renin activity to sodium restriction and standing was 73 per cent of that of the younger age group. Sodium 30-36 renin Homo sapiens 12-17 179329-0 1976 Angiotensin II binding to renal glomeruli from sodium-loaded and sodium-depleted rats. Sodium 47-53 angiotensinogen Rattus norvegicus 0-14 179329-0 1976 Angiotensin II binding to renal glomeruli from sodium-loaded and sodium-depleted rats. Sodium 65-71 angiotensinogen Rattus norvegicus 0-14 818786-2 1976 Exogenous prolactin caused a significant increase in frequency and severity of the lesions, with accompanying sodium retention. Sodium 110-116 prolactin Rattus norvegicus 10-19 177880-0 1976 Insulin stimulates active sodium transport in toad bladder by two mechanisms. Sodium 26-32 insulin Homo sapiens 0-7 1261208-2 1976 Suppression of the renin-aldosterone system by expansion of the extracellular fluid volume with extra sodium and mineralocorticoid for 6 days was studied in nine young men with very mild essential hypertension and in ten normotensive young men. Sodium 102-108 renin Homo sapiens 19-24 1261210-0 1976 The influence of sodium intake on the pressor response to angiotensin II in the unanaesthetized rat. Sodium 17-23 angiotensinogen Rattus norvegicus 58-72 1278538-0 1976 [Sodium release from tissue paracellular space under the influence of angiotensin II]. Sodium 1-7 angiotensinogen Rattus norvegicus 70-84 1278538-1 1976 Angiotensin II added in vitro in concentration 3-10(-10) M increased the sodium release from the aorta wall, myocardium, and skin in the rat. Sodium 73-79 angiotensinogen Rattus norvegicus 0-14 987139-0 1976 [The mechanism of paradoxical response of plasma renin activity to sodium in patients with edema]. Sodium 67-73 renin Homo sapiens 49-54 943925-5 1976 Hypertensive children with low and high plasma renin activity were found to have an inappropriately high level of urinary aldosterone excretion in relation to urinary sodium excretion. Sodium 167-173 renin Homo sapiens 47-52 817031-10 1976 However, stimulation of transepithelial sodium transport by vasopressin appeared not to affect the rate of potassium uptake. Sodium 40-46 arginine vasopressin Homo sapiens 60-71 174834-5 1976 When converting enzyme inhibitor was administered, which blocked the generation of angiotensin II, sodium replete subjects were able to compensate for an upright tilt, despite the absence of angiotensin II, without significant hemodynamic change when compared to control state. Sodium 99-105 angiotensinogen Homo sapiens 83-97 1024254-3 1976 Sodium supply was proved to influence significantly the pressor response to angiotensin II and not that to noradrenaline thus implying the presence of arterial receptors which bind angiotensin specifically. Sodium 0-6 angiotensinogen Homo sapiens 76-90 174834-8 1976 Both plasma aldosterone concentration and plasma renin activity rose on tilting in both sodium replete and sodium depleted subjects. Sodium 88-94 renin Homo sapiens 49-54 174834-12 1976 These results indicate that angiotensin II is essential for blood pressure maintenance in sodium depleted individuals, that angiotensin II exerts a direct feedback control on renin secretion, and that angiotensin II is the primary stimulus to aldosterone secretion in response to both sodium depletion and to posture. Sodium 90-96 angiotensinogen Homo sapiens 28-42 1249473-10 1976 Plasma renin activity and urinary aldosterone excretion rose progressively with the two levels of sodium restriction. Sodium 98-104 renin Homo sapiens 7-12 1255070-0 1976 Proceedings: Relationship between angiotensin II and sodium status in the control of blood pressure: studies in anephric subjects and in subjects with renal hypertension. Sodium 53-59 angiotensinogen Homo sapiens 34-48 940271-1 1976 Inverse interrelations between plasma renin activity and exchangeable sodium or blood volume were found in both normotensive (N = 23) and hypertensive (N =29) hemodialysis patients (r= 0.47; P less than 0.005); however, mean plasma renin for any given sodium/volume state was at least two-fold higher in hypertensive than in normotensive hemodialysis patients or normal subjects (N =31). Sodium 70-76 renin Homo sapiens 38-43 1255073-0 1976 Proceedings: Water and sodium accumulation in rabbits after administration of prolactin. Sodium 23-29 prolactin Oryctolagus cuniculus 78-87 948620-9 1976 Pressor infusions of angiotensin II raise peripheral levels of IR-PGA, and this response is exaggerated by a low sodium diet and blocked by either acute or chronic indomethacin administration. Sodium 113-119 angiotensinogen Homo sapiens 21-35 940271-1 1976 Inverse interrelations between plasma renin activity and exchangeable sodium or blood volume were found in both normotensive (N = 23) and hypertensive (N =29) hemodialysis patients (r= 0.47; P less than 0.005); however, mean plasma renin for any given sodium/volume state was at least two-fold higher in hypertensive than in normotensive hemodialysis patients or normal subjects (N =31). Sodium 252-258 renin Homo sapiens 38-43 187379-3 1976 Sodium and water permeability effects of vasopressin have been shown in toad bladder to have different dose response characteristics. Sodium 0-6 arginine vasopressin Rattus norvegicus 41-52 10715-1 1976 The relationship between blood pressure, plasma renin, plasma renin substrate and exchangeable sodium in chronic hemodialysis patients. Sodium 95-101 renin Homo sapiens 62-67 10715-8 1976 These results strongly suggest that the renin-angiotensin system is the most important factor involved in the pathogenesis of hypertension in end-stage renal disease, when sodium balance is adequately controlled. Sodium 172-178 renin Homo sapiens 40-45 1244226-1 1976 An interaction between oral contraceptive agents, sodium intake, and the renin-angiotensin system in healthy young women. Sodium 50-56 renin Homo sapiens 73-78 187379-4 1976 Maximum sodium transport occurs at a lower dose of vasopressin (2 mU/ml) and is believed to be associated with direct permeability effects of the hormone. Sodium 8-14 arginine vasopressin Rattus norvegicus 51-62 1244226-3 1976 There was also significant activation of the renin-angiotensin system: renin substrate was increased approximately 3-fold in association with a striking increase in the circulating renin activity and angiotensin II levels in relation to sodium intake and excretion. Sodium 237-243 renin Homo sapiens 45-50 1244226-3 1976 There was also significant activation of the renin-angiotensin system: renin substrate was increased approximately 3-fold in association with a striking increase in the circulating renin activity and angiotensin II levels in relation to sodium intake and excretion. Sodium 237-243 renin Homo sapiens 71-76 195885-4 1976 Prolactin injection caused a transient decrease in urinary sodium excretion, but proximal tubular sodium reabsorption, estimated by lissamine green transit time, was unaffected. Sodium 59-65 prolactin Rattus norvegicus 0-9 1244226-3 1976 There was also significant activation of the renin-angiotensin system: renin substrate was increased approximately 3-fold in association with a striking increase in the circulating renin activity and angiotensin II levels in relation to sodium intake and excretion. Sodium 237-243 renin Homo sapiens 71-76 1244226-3 1976 There was also significant activation of the renin-angiotensin system: renin substrate was increased approximately 3-fold in association with a striking increase in the circulating renin activity and angiotensin II levels in relation to sodium intake and excretion. Sodium 237-243 angiotensinogen Homo sapiens 200-214 1244226-6 1976 Moreover, the oral contraceptive agents modified the basic relationship between sodium balance and vascular responsiveness to angiotensin II, suggesting that the agents acted through some mechanism other than alteration in the state of sodium balance. Sodium 80-86 angiotensinogen Homo sapiens 126-140 7705-6 1976 We would conclude from these studies that the effect of vasopressin on the luminal cell membrane is a widespread one, modifying both lipid components and components involved in amide, sodium and water transport. Sodium 184-190 arginine vasopressin Homo sapiens 56-67 69276-1 1976 Administration of pituitrin, vasopressin, and oxytocin to rats during spontaneous micturition increases diuresis and sodium excretion by reducing tubular reabsorption. Sodium 117-123 arginine vasopressin Rattus norvegicus 29-40 188010-7 1976 Despite the increased level of activity of the renin-angiotensin system in normal pregnancy, sodium homeostasis is maintained. Sodium 93-99 renin Homo sapiens 47-52 787950-1 1976 When plasma renin activity is related to sodium balance as evaluated from urinary sodium excretion, a physiological index of normality is obtained along with the ability to detect subtle variations in renin secretion. Sodium 41-47 renin Homo sapiens 12-17 787950-1 1976 When plasma renin activity is related to sodium balance as evaluated from urinary sodium excretion, a physiological index of normality is obtained along with the ability to detect subtle variations in renin secretion. Sodium 41-47 renin Homo sapiens 201-206 787950-1 1976 When plasma renin activity is related to sodium balance as evaluated from urinary sodium excretion, a physiological index of normality is obtained along with the ability to detect subtle variations in renin secretion. Sodium 82-88 renin Homo sapiens 12-17 787950-1 1976 When plasma renin activity is related to sodium balance as evaluated from urinary sodium excretion, a physiological index of normality is obtained along with the ability to detect subtle variations in renin secretion. Sodium 82-88 renin Homo sapiens 201-206 798202-1 1976 In anaesthetized dogs that were sodium-depleted or subjected to thoracic caval constriction, Sar1-Ala8-angiotensin II produced a striking decrease in aldosterone secretion; also, arterial pressure fell while plasma renin activity (PRA) increased. Sodium 32-38 angiotensinogen Rattus norvegicus 103-117 798202-3 1976 In the rat, sodium depletion produced a marked increase in PRA and aldosterone secretion; studies with angiotensin II blockade during administration of the nonapeptide converting enzyme inhibitor or Sar1-Ala8-angiotensin II demonstrated an important role for angiotensin II in mediating the increase in aldosterone secretion during sodium depletion in the rat. Sodium 12-18 angiotensinogen Rattus norvegicus 103-117 798202-3 1976 In the rat, sodium depletion produced a marked increase in PRA and aldosterone secretion; studies with angiotensin II blockade during administration of the nonapeptide converting enzyme inhibitor or Sar1-Ala8-angiotensin II demonstrated an important role for angiotensin II in mediating the increase in aldosterone secretion during sodium depletion in the rat. Sodium 12-18 angiotensinogen Rattus norvegicus 209-223 798202-3 1976 In the rat, sodium depletion produced a marked increase in PRA and aldosterone secretion; studies with angiotensin II blockade during administration of the nonapeptide converting enzyme inhibitor or Sar1-Ala8-angiotensin II demonstrated an important role for angiotensin II in mediating the increase in aldosterone secretion during sodium depletion in the rat. Sodium 12-18 angiotensinogen Rattus norvegicus 209-223 798204-6 1976 (a) Prevention of AII generation by nephrectomy or converting enzyme inhibition increases the pressor response to AII which then becomes independent of sodium balance. Sodium 152-158 angiotensinogen Homo sapiens 18-21 1019161-3 1976 2) In standing normotensive volunteers, angiotensin II inhibition induced significant hypotension if previously a cumulative sodium loss of at least 160-200 mEq had been induced. Sodium 125-131 angiotensinogen Homo sapiens 40-54 1019161-5 1976 4) Following vigorous and prolonged sodium depletion induced by low sodium diet, with chlorthalidone and spironolactone, blood pressure became renin-dependent even in those patients who initially had exhibited a hypertensive response to saralasin, suggesting that under appropriate conditions, renin can play an active pressure role in all patients with essential hypertension. Sodium 36-42 renin Homo sapiens 143-148 1019161-5 1976 4) Following vigorous and prolonged sodium depletion induced by low sodium diet, with chlorthalidone and spironolactone, blood pressure became renin-dependent even in those patients who initially had exhibited a hypertensive response to saralasin, suggesting that under appropriate conditions, renin can play an active pressure role in all patients with essential hypertension. Sodium 36-42 renin Homo sapiens 294-299 1019161-5 1976 4) Following vigorous and prolonged sodium depletion induced by low sodium diet, with chlorthalidone and spironolactone, blood pressure became renin-dependent even in those patients who initially had exhibited a hypertensive response to saralasin, suggesting that under appropriate conditions, renin can play an active pressure role in all patients with essential hypertension. Sodium 68-74 renin Homo sapiens 143-148 1019166-3 1976 They also emphasize the importance of the renin-angiotensin system in the control of aldosterone in sodium depletion and in renal hypertension. Sodium 100-106 renin Homo sapiens 42-47 1019167-3 1976 In 12 tests performed after sodium depletion, the decrease in mean arterial pressure ranged from 13 to 76 mm Hg and showed a significant correlation with the plasma renin concentration prevailing immediately before the infusion of the drug (r = 0.81; p less than 0.001). Sodium 28-34 renin Homo sapiens 165-170 1215976-1 1975 Plasma renin activity was found to correlate inversely with exchangeable sodium or blood volume in both normotensive and hypertensive hemodialysis patients. Sodium 73-79 renin Homo sapiens 7-12 1192571-4 1975 Intravenous infusion of an angiotensin II antagonist, 1-Sar-8-Ala-angiotensin II, caused a significant reduction of arterial blood pressure in sodium-depleted rats but not in normal rats. Sodium 143-149 angiotensinogen Rattus norvegicus 27-41 1192571-4 1975 Intravenous infusion of an angiotensin II antagonist, 1-Sar-8-Ala-angiotensin II, caused a significant reduction of arterial blood pressure in sodium-depleted rats but not in normal rats. Sodium 143-149 angiotensinogen Rattus norvegicus 66-80 1192571-8 1975 The data presented in this paper are consistent with the conclusion that clonidine acts at some site in the sympathetic nervous system of sodium-depleted rats to inhibit renal nerve activity with a resultant suppression of renin secretion and a reduction of the angiotensin II-maintained arterial blood pressure. Sodium 138-144 angiotensinogen Rattus norvegicus 262-276 1208596-0 1975 The relationship between sodium excretion and renin secretion by the perfused kidney. Sodium 25-31 renin Homo sapiens 46-51 1208596-6 1975 These results provide new evidence for the hypothesis that the rate at which sodium is delivered to the macula densa is an important determinant of the rate of renin secretion. Sodium 77-83 renin Homo sapiens 160-165 1215619-0 1975 Sodium dependence of intestinal active transport of sugars in snail (Cryptomphalus hortensis Muller). Sodium 0-6 snail family transcriptional repressor 1 Homo sapiens 62-67 1215619-4 1975 Sodium seems to play a specific and important but not indispensable role in sugar active transport by snail intestine. Sodium 0-6 snail family transcriptional repressor 1 Homo sapiens 102-107 1192047-6 1975 The findings emphasise the need to relate data from patients to age-matched control values before attempting interpretation and suggest that sodium depletion is a more potent stimulator of renin-aldosterone release than renovascular disease or renal scarring in children. Sodium 141-147 renin Homo sapiens 189-194 1239966-4 1975 The increase of renin and plasma aldosterone was correlated inversely to urinary sodium-potassium-ratio. Sodium 81-87 renin Homo sapiens 16-21 1082005-0 1975 Proceedings: Effect of prolactin on sodium transport across frog skin in vitro. Sodium 36-42 prolactin Homo sapiens 23-32 1185036-5 1975 Significant increments of PRA and A II on either sodium intake occurred within 5 to 20 minutes; the peak values occurred within 90 minutes and tended to plateau until the end of the study (240 minutes). Sodium 49-55 S100 calcium binding protein A6 Homo sapiens 26-29 1185036-5 1975 Significant increments of PRA and A II on either sodium intake occurred within 5 to 20 minutes; the peak values occurred within 90 minutes and tended to plateau until the end of the study (240 minutes). Sodium 49-55 NLR family pyrin domain containing 3 Homo sapiens 34-38 1185036-12 1975 Specifically, the slope of the regression relationship between PRA and PA was more than 4-fold steeper in the sodium-restricted than sodium-loaded subjects. Sodium 110-116 S100 calcium binding protein A6 Homo sapiens 63-66 1185036-12 1975 Specifically, the slope of the regression relationship between PRA and PA was more than 4-fold steeper in the sodium-restricted than sodium-loaded subjects. Sodium 133-139 S100 calcium binding protein A6 Homo sapiens 63-66 538-4 1975 Inverse renin-blood pressure interrelations were noted during two of four study conditions involving normal sodium intake or mild sodium depletion (r = --0.44 and --0.47, respectively), but not during progressive sodium depletion. Sodium 108-114 renin Homo sapiens 8-13 538-4 1975 Inverse renin-blood pressure interrelations were noted during two of four study conditions involving normal sodium intake or mild sodium depletion (r = --0.44 and --0.47, respectively), but not during progressive sodium depletion. Sodium 130-136 renin Homo sapiens 8-13 538-4 1975 Inverse renin-blood pressure interrelations were noted during two of four study conditions involving normal sodium intake or mild sodium depletion (r = --0.44 and --0.47, respectively), but not during progressive sodium depletion. Sodium 130-136 renin Homo sapiens 8-13 1190091-2 1975 Plasma renin activity during standing was referred to a standard renin-urinary sodium nomogram derived from 18 normal subjects. Sodium 79-85 renin Homo sapiens 7-12 1166859-9 1975 In contrast, suppression of the renin level to normal was demonstrated by sodium loading. Sodium 74-80 renin Homo sapiens 32-37 1192694-2 1975 Intravenous frusemide produced in normal subjects a prompt rise of plasma renin concentration which correlated with urinary sodium. Sodium 124-130 renin Homo sapiens 74-79 453-11 1975 (3) In the outer segments of vertebrate receptors, absorption of light by rhodopsin causes the plasma membrane to hyperpolarize due to a decrease in sodium conductance, possibly mediated by calcium ions. Sodium 149-155 rhodopsin Homo sapiens 74-83 1220728-0 1975 [Effect of beta-adrenergic block on the response of plasma renin activity to acute sodium depletion in the rabbit]. Sodium 83-89 LOW QUALITY PROTEIN: renin Oryctolagus cuniculus 59-64 168714-9 1975 Our results indicate that in normal supine man the influence of ACTH and renin on PA may vary with different sodium intakes. Sodium 109-115 proopiomelanocortin Homo sapiens 64-68 168714-9 1975 Our results indicate that in normal supine man the influence of ACTH and renin on PA may vary with different sodium intakes. Sodium 109-115 renin Homo sapiens 73-78 168714-10 1975 Under normal sodium intake ACTH seems to be the dominant factor controlling PA, whereas under sodium restriction changes in PA are mediated through the renin angiotensin system. Sodium 94-100 renin Homo sapiens 152-157 168714-11 1975 When the secretion of ACTH is suppressed by dexamethasone, renin controls PA both under normal and low sodium intake. Sodium 103-109 proopiomelanocortin Homo sapiens 22-26 168714-11 1975 When the secretion of ACTH is suppressed by dexamethasone, renin controls PA both under normal and low sodium intake. Sodium 103-109 renin Homo sapiens 59-64 1157223-0 1975 Selective inhibition by des-1-Asp-8-lle-angiotensin ii of the steroidogenic response to restricted sodium intake in the rat. Sodium 99-105 angiotensinogen Rattus norvegicus 40-54 1157223-7 1975 At the doses studied, however, 7-Ile-angiotensin III caused a marked decrease (50%) in aldosterone excretion in sodium-deprived rats, but 1-Sar-8-Ile-angiotensin II had no effect on aldosterone excretion. Sodium 112-118 angiotensinogen Rattus norvegicus 37-51 1157223-8 1975 In the sodium-deprived rats, the administration of 7-Ile-angiotensin Ile was not associated with an acute increase in plasma renin activity, but treatment with 1-Sar-8-Ile-angiotensin II resulted in a sixfold increase in plasma renin activity, but otensin III was not associated with an acute increase in plasma renin activity, but treatment with 1-Sar-8-Ile-angiotensin II resulted in a sixfold increase in plasma renin activity. Sodium 7-13 angiotensinogen Rattus norvegicus 172-186 1214319-0 1975 [Proceedings: Effect of parathyroid hormone on the renal excretion of sodium and bicarbonate ions]. Sodium 70-76 parathyroid hormone Homo sapiens 24-43 6288486-8 1982 It is suggested that the origin of urinary angiotensin I-converting enzyme is the kidney, and that the enzyme might regulate sodium excretion in cooperation with renal kallikrein-kinin system. Sodium 125-131 angiotensin I converting enzyme Homo sapiens 43-74 1171939-5 1975 During infusion of sodium caseinate, milk production, milk protein (N times 6.38) production, and efficiency of nitrogen utilization for milk crude protein production were increased. Sodium 19-25 Weaning weight-maternal milk Bos taurus 37-41 1171939-5 1975 During infusion of sodium caseinate, milk production, milk protein (N times 6.38) production, and efficiency of nitrogen utilization for milk crude protein production were increased. Sodium 19-25 casein beta Bos taurus 54-66 1171939-5 1975 During infusion of sodium caseinate, milk production, milk protein (N times 6.38) production, and efficiency of nitrogen utilization for milk crude protein production were increased. Sodium 19-25 Weaning weight-maternal milk Bos taurus 54-58 3076-4 1975 The localization of AChE, BuChE products of cytochemical reaction on sodium suggests that the cholinergic mechanism may take part in the process of synaptic transmission. Sodium 69-75 acetylcholinesterase (Cartwright blood group) Homo sapiens 20-24 1149403-8 1975 Reduction in glomerular filtration rate contributed to changes in sodium excretion produced by bradykinin and eledoisin. Sodium 66-72 kininogen 1 Canis lupus familiaris 95-105 1162906-0 1975 [Relationship of plasma renin activity and exchangeable sodium in various types of hypertension]. Sodium 56-62 renin Homo sapiens 24-29 1166770-4 1975 The calculated values of rate constant of transmembranal sodium fluxes are 0.0282+/-0.0052 min-1 and the half-time of the exchange of sodium between intracellular compartments is 24.27+/-4.53 min. Sodium 57-63 CD59 molecule (CD59 blood group) Homo sapiens 91-96 167999-4 1975 Bradykinin caused a dose-related increase in renal blood flow, urine flow, sodium excretion, and kinin content of renal venous blood. Sodium 75-81 kininogen 1 Canis lupus familiaris 0-10 1147438-1 1975 Effects of potassium and sodium replacement on the renin-angiotensin-aldosterone system. Sodium 25-31 renin Homo sapiens 51-56 168229-1 1975 The brief (60-min) infusion of a small amount (1.25 mug) of ACTH into 7 normal subjects on an unrestricted sodium intake resulted in a vigorous plasma aldosterone response in each case. Sodium 107-113 proopiomelanocortin Homo sapiens 60-64 1177406-0 1975 [Metabolism of angiotensin II during angiotensin infusion and following sodium depletion]. Sodium 72-78 angiotensinogen Homo sapiens 15-29 1177406-9 1975 Sodium depletion increased arterial and venous concentrations of A II and H. Sodium 0-6 NLR family pyrin domain containing 3 Homo sapiens 65-75 1177406-10 1975 During infusion of angiotensin II-amide the arterial and venous concentrations of A II and H increased approximately parallel to the concentrations before sodium depletion. Sodium 155-161 angiotensinogen Homo sapiens 19-33 1177406-10 1975 During infusion of angiotensin II-amide the arterial and venous concentrations of A II and H increased approximately parallel to the concentrations before sodium depletion. Sodium 155-161 NLR family pyrin domain containing 3 Homo sapiens 82-92 172005-7 1975 These results confirm that acute sodium depletion stimulates aldosterone secretion by the way of renin angiotensin system then ACTH acts directly on the adrenal cortex. Sodium 33-39 renin Homo sapiens 97-102 1168128-4 1975 Bovine growth hormone and ovine prolactin produce essentially similar effects in intact rats: significant increases in fluid, sodium and calcium transport in the duodenum; in fluid, sodium and potassium transport in the jejunum; in sodium, chloride, potassium and calcium transport in the ileum. Sodium 126-132 prolactin Bos taurus 32-41 1168128-4 1975 Bovine growth hormone and ovine prolactin produce essentially similar effects in intact rats: significant increases in fluid, sodium and calcium transport in the duodenum; in fluid, sodium and potassium transport in the jejunum; in sodium, chloride, potassium and calcium transport in the ileum. Sodium 182-188 prolactin Bos taurus 32-41 1168128-4 1975 Bovine growth hormone and ovine prolactin produce essentially similar effects in intact rats: significant increases in fluid, sodium and calcium transport in the duodenum; in fluid, sodium and potassium transport in the jejunum; in sodium, chloride, potassium and calcium transport in the ileum. Sodium 182-188 prolactin Bos taurus 32-41 1128229-8 1975 Blood pressure showed a negative correlation with PRA, but a positive one with body weight and cumulative sodium balance, and with plasma and extracellular volumes.it is suggested that whereas renin and aldosterone are involved in the maintenance of circulatory homeostasis during sodium loss, sodium retention causes an increase in blood pressure by concomitant changes in body fluids. Sodium 106-112 renin Homo sapiens 193-198 1128229-8 1975 Blood pressure showed a negative correlation with PRA, but a positive one with body weight and cumulative sodium balance, and with plasma and extracellular volumes.it is suggested that whereas renin and aldosterone are involved in the maintenance of circulatory homeostasis during sodium loss, sodium retention causes an increase in blood pressure by concomitant changes in body fluids. Sodium 281-287 renin Homo sapiens 193-198 1128229-8 1975 Blood pressure showed a negative correlation with PRA, but a positive one with body weight and cumulative sodium balance, and with plasma and extracellular volumes.it is suggested that whereas renin and aldosterone are involved in the maintenance of circulatory homeostasis during sodium loss, sodium retention causes an increase in blood pressure by concomitant changes in body fluids. Sodium 281-287 renin Homo sapiens 193-198 235559-18 1975 Thus, in sodium-depleted individuals, saline infusion produces a rapid fall of plasma bradykinin at a rate similar to that observed for a II and PRA. Sodium 9-15 kininogen 1 Homo sapiens 86-96 235559-19 1975 Conversely, in sodium-loaded individuals, assumption of upright posture leads to a parallel rise in A II, TPRA, and bradykinin. Sodium 15-21 angiotensinogen Homo sapiens 100-104 235559-19 1975 Conversely, in sodium-loaded individuals, assumption of upright posture leads to a parallel rise in A II, TPRA, and bradykinin. Sodium 15-21 kininogen 1 Homo sapiens 116-126 235559-20 1975 These studies indicate that there is a close correlation of bradykinin levels with renin activity and angiotensin II, in both acute sodium loading and assumption of upright posture, suggesting that these two systems may be physiologically interrelated. Sodium 132-138 kininogen 1 Homo sapiens 60-70 235559-20 1975 These studies indicate that there is a close correlation of bradykinin levels with renin activity and angiotensin II, in both acute sodium loading and assumption of upright posture, suggesting that these two systems may be physiologically interrelated. Sodium 132-138 renin Homo sapiens 83-88 235559-20 1975 These studies indicate that there is a close correlation of bradykinin levels with renin activity and angiotensin II, in both acute sodium loading and assumption of upright posture, suggesting that these two systems may be physiologically interrelated. Sodium 132-138 angiotensinogen Homo sapiens 102-116 234604-10 1975 4) Infusion of angiotensin II in sub- or pauci-pressor doses causes an isosmotic sodium saving, since it reduced the glomerular filtrate and increases the fraction of filtrate reabsorbed by the proximal tubules; the tubular effect is likely secondary to increased vascular, especially postglomerular resistance. Sodium 81-87 angiotensinogen Homo sapiens 15-29 1135521-0 1975 Marked elevation of plasma renin activity during post diuretic sodium conservation in furosemide stimulated subjects. Sodium 63-69 renin Homo sapiens 27-32 1116335-3 1975 First, renin activity was measured in hospital patients after 5 days of sodium restriction and 3 h ambulation. Sodium 72-78 renin Homo sapiens 7-12 817563-6 1975 During the course of intravenous infusion therapy, a progressive increase in mena osmolality was observed, accompanied by a rise in blood glucose, sodium and urea levels. Sodium 147-153 ENAH actin regulator Homo sapiens 77-81 234677-8 1975 Three criteria, derived from four renin measurements, identify this situation: (1) Hypersecretion of renin is reflected by a high peripheral level when indexed against sodium excretion. Sodium 168-174 renin Homo sapiens 101-106 172003-3 1975 The sodium depletion induced by furosemide during continuous ACTH infusion increases plasma renin activity but does not change PA. Sodium 4-10 proopiomelanocortin Homo sapiens 61-65 172003-3 1975 The sodium depletion induced by furosemide during continuous ACTH infusion increases plasma renin activity but does not change PA. Sodium 4-10 renin Homo sapiens 92-97 1232875-3 1975 Several factors take a part in the regulation of renin secretion (mean arterial pressure, introduction of sodium and potassium, the sympathetic nervous system, ADH and concentration of angiotensin II in plasma). Sodium 107-113 renin Homo sapiens 50-55 165438-3 1975 Five of six patients with hyperkalemia had diminished function of the renin-angiotensin-aldosterone system; their ability to conserve sodium during salt depletion was less than that of normokalemic patients. Sodium 134-140 renin Homo sapiens 70-75 170550-1 1975 Calcitonin, whatever its origin, produces a decrease in the renal tubular reabsorption of sodium, phosphate and calcium in man and in the rat. Sodium 90-96 calcitonin related polypeptide alpha Homo sapiens 0-10 4547907-0 1974 The effect of insulin on active sodium transport in the frog skin. Sodium 32-38 insulin Homo sapiens 14-21 4367700-0 1974 [Influence of angiotensin II-infusion on the sodium- and potassium level in plasma and erythrocytes of normotensive persons and patients with essential hypertension (author"s transl)]. Sodium 45-51 angiotensinogen Homo sapiens 14-28 4209873-0 1974 Effects of vasopressin on toad bladder membrane proteins: relationship to transport of sodium and water. Sodium 87-93 arginine vasopressin Homo sapiens 11-22 4363070-0 1974 Intradiem changes of plasma aldosterone, cortisol, corticosterone and growth hormone in sodium restriction. Sodium 88-94 growth hormone 1 Homo sapiens 70-84 4362400-0 1974 ACTH-induced sodium retention in pregnancy. Sodium 13-19 proopiomelanocortin Homo sapiens 0-4 4360859-0 1974 A specific role for saline or the sodium ion in the regulation of renin and aldosterone secretion. Sodium 34-40 renin Homo sapiens 66-71 4360859-2 1974 The present study was performed to determine whether sodium has an action apart from volume in the regulation of the secretion of renin and aldosterone. Sodium 53-59 renin Homo sapiens 130-135 4360859-13 1974 The data support a specific role for volume expansion with saline or the sodium ion per se in the regulation of renin and aldosterone. Sodium 73-79 renin Homo sapiens 112-117 4828272-0 1974 Effect of growth hormone on sodium transport and osmotic water flow across toad skin. Sodium 28-34 growth hormone 1 Homo sapiens 10-24 4359751-0 1974 Proceedings: Pressor sensitivity to angiotensin II in relation to sodium. Sodium 66-72 angiotensinogen Homo sapiens 36-50 4361937-0 1974 Pressor effect of angiotensin II in sodium replete and deplete rats. Sodium 36-42 angiotensinogen Rattus norvegicus 18-32 4375892-0 1974 The relationship between the plasma concentrations of renin and angiotensin with total exchangeable sodium in hypertension. Sodium 100-106 renin Homo sapiens 54-59 4759606-0 1973 Effect of sodium deprivation and pinealectomy on pituitary and plasma prolactin in the rat. Sodium 10-16 prolactin Rattus norvegicus 70-79 4752309-3 1973 Plasma renin concentration was inversely related to exchangeable sodium in the responsive group but was inappropriately high for the level of exchangeable sodium in the resistant group. Sodium 65-71 renin Homo sapiens 7-12 4752309-3 1973 Plasma renin concentration was inversely related to exchangeable sodium in the responsive group but was inappropriately high for the level of exchangeable sodium in the resistant group. Sodium 155-161 renin Homo sapiens 7-12 4752309-4 1973 There was a better correlation between mean blood pressure and the product of plasma renin concentration and exchangeable sodium than with renin concentration alone.These results indicate that a severely diseased kidney can respond to changes in exchangeable sodium by alterations in renin secretion and they also support the concept that the potential pressor effect of renin is modified by exchangeable sodium. Sodium 259-265 renin Homo sapiens 85-90 4752309-4 1973 There was a better correlation between mean blood pressure and the product of plasma renin concentration and exchangeable sodium than with renin concentration alone.These results indicate that a severely diseased kidney can respond to changes in exchangeable sodium by alterations in renin secretion and they also support the concept that the potential pressor effect of renin is modified by exchangeable sodium. Sodium 259-265 renin Homo sapiens 139-144 4752309-4 1973 There was a better correlation between mean blood pressure and the product of plasma renin concentration and exchangeable sodium than with renin concentration alone.These results indicate that a severely diseased kidney can respond to changes in exchangeable sodium by alterations in renin secretion and they also support the concept that the potential pressor effect of renin is modified by exchangeable sodium. Sodium 259-265 renin Homo sapiens 139-144 4752309-4 1973 There was a better correlation between mean blood pressure and the product of plasma renin concentration and exchangeable sodium than with renin concentration alone.These results indicate that a severely diseased kidney can respond to changes in exchangeable sodium by alterations in renin secretion and they also support the concept that the potential pressor effect of renin is modified by exchangeable sodium. Sodium 259-265 renin Homo sapiens 139-144 4752309-4 1973 There was a better correlation between mean blood pressure and the product of plasma renin concentration and exchangeable sodium than with renin concentration alone.These results indicate that a severely diseased kidney can respond to changes in exchangeable sodium by alterations in renin secretion and they also support the concept that the potential pressor effect of renin is modified by exchangeable sodium. Sodium 259-265 renin Homo sapiens 85-90 4752309-4 1973 There was a better correlation between mean blood pressure and the product of plasma renin concentration and exchangeable sodium than with renin concentration alone.These results indicate that a severely diseased kidney can respond to changes in exchangeable sodium by alterations in renin secretion and they also support the concept that the potential pressor effect of renin is modified by exchangeable sodium. Sodium 259-265 renin Homo sapiens 139-144 4752309-4 1973 There was a better correlation between mean blood pressure and the product of plasma renin concentration and exchangeable sodium than with renin concentration alone.These results indicate that a severely diseased kidney can respond to changes in exchangeable sodium by alterations in renin secretion and they also support the concept that the potential pressor effect of renin is modified by exchangeable sodium. Sodium 259-265 renin Homo sapiens 139-144 4752309-4 1973 There was a better correlation between mean blood pressure and the product of plasma renin concentration and exchangeable sodium than with renin concentration alone.These results indicate that a severely diseased kidney can respond to changes in exchangeable sodium by alterations in renin secretion and they also support the concept that the potential pressor effect of renin is modified by exchangeable sodium. Sodium 259-265 renin Homo sapiens 139-144 4542709-0 1973 Effect of antidiuretic hormone on sodium uptake across outer surface of frog skin. Sodium 34-40 arginine vasopressin Homo sapiens 10-30 4542270-0 1973 Somatotropic and sodium-retaining effects of human growth hormone and placental lactogen in lower vertebrates. Sodium 17-23 growth hormone 1 Homo sapiens 51-65 4355704-1 1973 An abnormal relation between sodium and the renin-angiotensin system. Sodium 29-35 renin Homo sapiens 44-49 4799902-1 1973 Release of sodium ions from the surface of rhodopsin molecules on illumination (author"s transl)]. Sodium 11-17 rhodopsin Homo sapiens 43-52 4542575-14 1973 Insulin also increased (22)Na efflux and net sodium efflux into Li-Ringer. Sodium 45-51 insulin Homo sapiens 0-7 4349529-0 1973 Control of vasopressin stimulation of sodium transport in the toad bladder. Sodium 38-44 arginine vasopressin Homo sapiens 11-22 4349531-0 1973 Angiotensin I conversion in the kidney and its modulation by sodium balance. Sodium 61-67 angiotensinogen Homo sapiens 0-13 4700008-1 1973 Plasma renin levels, measured in 39 untreated patients in 1967, under conditions of sodium loading and sodium depletion have been related to the incidence of stroke and myocardial infarction. Sodium 84-90 renin Homo sapiens 7-12 4700008-1 1973 Plasma renin levels, measured in 39 untreated patients in 1967, under conditions of sodium loading and sodium depletion have been related to the incidence of stroke and myocardial infarction. Sodium 103-109 renin Homo sapiens 7-12 4155453-0 1973 [The influence of catecholamines and synthetic derivatives of vasopressin on the active transport of sodium ions and other bioelectrical properties of the cell membrane (author"s transl)]. Sodium 101-107 arginine vasopressin Homo sapiens 62-73 4117201-0 1972 Raised plasma angiotensin II and aldosterone during dietary sodium restriction in man. Sodium 60-66 angiotensinogen Homo sapiens 14-28 4347443-0 1972 Effect of chlorothiazide and sodium on vascular responsiveness to angiotensin II. Sodium 29-35 angiotensinogen Homo sapiens 66-80 4643745-0 1972 [Effect of antidiuretic hormone on energy-coupled transport of sodium in renal epithelial mitochondria]. Sodium 63-69 arginine vasopressin Homo sapiens 11-31 4343575-0 1972 Renin, angiotensin II, and adrenal corticosteroid relationships during sodium deprivation and angiotensin infusion in normotensive and hypertensive man. Sodium 71-77 renin Homo sapiens 0-5 4655969-0 1972 Further evaluation of the role of insulin in sodium retention associated with carbohydrate administration after a fast in the obese. Sodium 45-51 insulin Homo sapiens 34-41 5056660-12 1972 From these studies, it is concluded that plasma renin activity is the dominant factor controlling plasma aldosterone when sodium-depleted normal subjects are acutely repleted. Sodium 122-128 renin Homo sapiens 48-53 4671214-0 1972 Effect of vasopressin on sodium transport in renal cortical collecting tubules. Sodium 25-31 arginine vasopressin Homo sapiens 10-21 4338644-0 1972 [Regulation of the renin-angiotensin system in congestive heart failure: indications for a total body sodium-dependent regulation of the renin secretion]. Sodium 102-108 renin Homo sapiens 19-24 4338644-0 1972 [Regulation of the renin-angiotensin system in congestive heart failure: indications for a total body sodium-dependent regulation of the renin secretion]. Sodium 102-108 renin Homo sapiens 137-142 5008533-0 1972 The effects of sodium loading and deprivation on plasma renin and plasma and urinary aldosterone in hypertension. Sodium 15-21 renin Homo sapiens 56-61 4331800-0 1972 Angiotensin II vascular receptors: their avidity in relationship to sodium balance, the autonomic nervous system, and hypertension. Sodium 68-74 angiotensinogen Rattus norvegicus 0-14 5116048-0 1971 Electrically evoked release of vasopressin from isolated neurohypophyses in sodium-free media. Sodium 76-82 arginine vasopressin Homo sapiens 31-42 5560670-0 1971 The effect of sodium and calcium on renin release in vitro. Sodium 14-20 renin Homo sapiens 36-41 4399668-0 1971 Glycine-amide effect on the vasopressin stimulated sodium and water transport across toad bladder. Sodium 51-57 arginine vasopressin Homo sapiens 28-39 4322475-0 1971 The dissociation of aldosterone secretion and systemic renin and angiotensin II levels during the correction of sodium deficiency. Sodium 112-118 angiotensinogen Homo sapiens 65-79 5539024-0 1971 The relative effects of serum sodium concentration and the state of body fluid balance on renin secretion. Sodium 30-36 renin Homo sapiens 90-95 4319970-8 1970 However, the results do suggest that in various situations, the influence of potassium on plasma renin activity may be either amplified or preempted by changes in sodium balance. Sodium 163-169 renin Homo sapiens 97-102 4319970-12 1970 The effects of potassium ions on renin secretion might also be mediated indirectly via an induced change in tubular sodium transport. Sodium 116-122 renin Homo sapiens 33-38 5523457-0 1970 [The possibility of stimulation and suppression of renin secretion by sodium deprivation and sodium loading in primary and renal hypertension]. Sodium 70-76 renin Homo sapiens 51-56 4915450-1 1970 Phase microscopy of toad urinary bladder has demonstrated that vasopressin can cause an enlargement of the epithelial intercellular spaces under conditions of no net transfer of water or sodium. Sodium 187-193 arginine vasopressin Homo sapiens 63-74 4317384-4 1970 On a 10 mEq sodium intake, the increase in excretion and secretion rates of aldosterone in the hypertensive patients could be correlated with plasma renin activity (PRA). Sodium 12-18 renin Homo sapiens 149-154 4317871-0 1970 Effect of change of sodium balance on the corticosteroid response to angiotensin II. Sodium 20-26 angiotensinogen Homo sapiens 69-83 4187459-8 1969 It is concluded that the rapid transfer of sodium and water from the circulation to the rumen via the saliva during ingestion of dry feed is sufficient to activate the renin/angiotensin system. Sodium 43-49 renin Ovis aries 168-173 5821919-0 1969 Effect of vasopressin on sodium and potassium reabsorption by the renal tubules in man. Sodium 25-31 arginine vasopressin Homo sapiens 10-21 5762042-7 1969 The effects of ADH have been interpreted in terms of the formation of water-filled sodium-permselective pores in the outer facing membranes which occupy, at most, 0.3% of the skin surface. Sodium 83-89 arginine vasopressin Homo sapiens 15-18 5773772-0 1969 Effect of vasopressin on the entry of sodium into the renal tubule. Sodium 38-44 arginine vasopressin Homo sapiens 10-21 5773783-0 1969 Effect of prolactin on the active transport of sodium by the isolated toad bladder. Sodium 47-53 prolactin Homo sapiens 10-19 4307191-0 1969 Micropuncture study of the action of angiotensin-II on tubular sodium and water reabsorption in the rat. Sodium 63-69 angiotensinogen Rattus norvegicus 37-51 4306624-0 1969 [Effect of angiotensin II on tubular sodium and water reabsorption in the rat]. Sodium 37-43 angiotensinogen Rattus norvegicus 11-25 4302904-0 1968 Effect of angiotensin II on urinary sodium excretion in normal subjects and in cirrhotic patients. Sodium 36-42 angiotensinogen Homo sapiens 10-24 5751263-2 1968 Effect of the plasma sodium reduction on renin secretion]. Sodium 21-27 renin Homo sapiens 41-46 5730691-0 1968 [Regulation of renin secretion in sodium deficiency]. Sodium 34-40 renin Homo sapiens 15-20 5736238-0 1968 [Effects of various doses of insulin on potassium and sodium content in the brain tissue and blood serum]. Sodium 54-60 insulin Homo sapiens 29-36 5665176-0 1968 Seasonal changes of antidiuretic hormone action on sodium transport across frog skin. Sodium 51-57 arginine vasopressin Homo sapiens 20-40 4299011-8 1968 This observation suggests that the hyper-aldosteronism is secondary to a tendency to sodium loss in the patient whose ACTH production is not suppressed. Sodium 85-91 proopiomelanocortin Homo sapiens 118-122 4297478-10 1968 Stimulation at this site can explain, at least in part, the increased effectiveness of adrenocorticotropin (ACTH) on aldosterone biogenesis during sodium depletion. Sodium 147-153 proopiomelanocortin Canis lupus familiaris 108-112 4970225-8 1968 Sodium ion appeared to suppress l-asparaginase production. Sodium 0-6 asparaginase and isoaspartyl peptidase 1 Homo sapiens 32-46 4300463-0 1968 [Relation between the blood-pressure effect of angiotensin II and the mean arterial pressure, serum sodium, serum potassium, serum angiotensinase and plasma renin in man]. Sodium 100-106 angiotensinogen Homo sapiens 47-61 5689335-0 1968 Action of insulin on sodium efflux from the toad cocyte. Sodium 21-27 insulin Homo sapiens 10-17 4890788-0 1968 [Regulation of renin secretion in sodium deficiency]. Sodium 34-40 renin Homo sapiens 15-20 5599903-0 1967 [Effect of sodium ions on the activity of acetylcholinesterase of erythrocytes]. Sodium 11-17 acetylcholinesterase (Cartwright blood group) Homo sapiens 42-62 6021207-4 1967 In normal subjects the stimuli of upright posture and of sodium depletion both resulted in increases in urinary catecholamines, plasma renin activity, and urinary aldosterone. Sodium 57-63 renin Homo sapiens 135-140 5971033-1 1966 Experiments are described which indicate that iodinated human serum albumin underestimates the amount of extracellular sodium trapped in the packed layer of red blood cells, when cells and plasma are separated by centrifugation. Sodium 119-125 albumin Homo sapiens 62-75 5971034-2 1966 When human serum albumin(-131)I is used to measure the percentage of plasma trapped in the packed red blood cells after centrifugation, approximately 30 % of red blood cell sodium is found to equilibrate immediately with plasma. Sodium 173-179 albumin Homo sapiens 17-24 5971034-3 1966 It is concluded that this immediately exchangeable compartment of red blood cell sodium is an experimental artefact, associated with the use of labeled albumin for measuring plasma trapping. Sodium 81-87 albumin Homo sapiens 152-159 5926083-0 1966 Changes in plasma aldosterone, cortisol, corticosterone, and renin concentration in a patient with sodium-losing renal disease. Sodium 99-105 renin Homo sapiens 61-66 5937540-0 1966 Relation of plasma renin to sodium balance and arterial pressure in experimental renal hypertension. Sodium 28-34 renin Homo sapiens 19-24 5948254-0 1966 The effect of small amounts of antidiuretic hormone on sodium and urate excretion in pregnancy. Sodium 55-61 arginine vasopressin Homo sapiens 31-51 5938558-0 1966 Effects of bradykinin on the movement of water and sodium in some isolated living membranes. Sodium 51-57 kininogen 1 Homo sapiens 11-21 4285879-0 1966 [Influence of intravenous perfusion of angiotensin II on the urinary elimination of sodium in edematous cardiac patients]. Sodium 84-90 angiotensinogen Homo sapiens 39-53 4286529-0 1965 Effect of angiotensin II on active transport of sodium by toad bladder and skin. Sodium 48-54 angiotensinogen Homo sapiens 10-24 4284773-0 1965 Effect of variations of plasma sodium concentration on the adrenal response to angiotensin II. Sodium 31-37 angiotensinogen Homo sapiens 79-93 5860051-0 1965 [Effect of the antidiuretic hormone on the renal excretion of sodium during pregnancy]. Sodium 62-68 arginine vasopressin Homo sapiens 15-35 14101494-0 1963 THE MECHANISM OF INCREASED SODIUM EXCRETION DURING WATER LOADING WITH 2-5 PERCENT DEXTROSE AND VASOPRESSIN. Sodium 27-33 arginine vasopressin Homo sapiens 96-107 14485417-0 1962 Influence of hydration on renal function and medullary sodium during vasopressin infusion. Sodium 55-61 arginine vasopressin Homo sapiens 69-80 13983844-0 1962 [Comparisons between sodium excretion in the ACTH-electrolyte test and eosinopenia after ACTH administration in rheumatics]. Sodium 21-27 proopiomelanocortin Homo sapiens 45-49 13778410-0 1961 The reduction of insulin and its benzyl derivatives by sodium in liquid ammonia and the regeneration of activity from the reduced products. Sodium 55-61 insulin Homo sapiens 17-24 13752638-0 1961 Stimulation of active transport of sodium from sodium-rich frog muscle by insulin and lactate. Sodium 35-41 insulin Homo sapiens 74-81 14414942-0 1960 Some effects of mammalian neurohypophyseal hormones on metabolism and active transport of sodium by the isolated toad bladder. Sodium 90-96 arginine vasopressin Homo sapiens 26-42 14444029-0 1960 Further observations on hyponatremia and renal sodium loss probably resulting from inappropriate secretion of antidiuretic hormone. Sodium 47-53 arginine vasopressin Homo sapiens 110-130 13797479-0 1960 Urinary sodium retention after ACTH stimulation: a rapid, simple screening test for adrenal cortical insufficiency. Sodium 8-14 proopiomelanocortin Homo sapiens 31-35 14437815-0 1959 The syndrome of hyponatremia and renal sodium loss probably resulting from inappropriate secretion of antidiuretic hormone. Sodium 39-45 arginine vasopressin Homo sapiens 102-122 13607824-0 1958 [Effect of insulin on plasma sodium and potassium in pigeons]. Sodium 29-35 insulin Homo sapiens 11-18 13541450-0 1958 Effect of insulin on sodium in muscle. Sodium 21-27 insulin Homo sapiens 10-17 13561335-0 1958 [Effect of vasopressin on the elimination of water load, sodium and potassium in weanling rats]. Sodium 57-63 arginine vasopressin Rattus norvegicus 11-22 13448105-0 1957 [Study of clinical aspects and water, sodium and potassium excretion during treatment with ACTH, cortisone and related compounds]. Sodium 38-44 proopiomelanocortin Homo sapiens 91-95 13424324-0 1957 Effect of purified vasopressin and oxytocin on water and sodium excretion in hypophysectomized rats. Sodium 57-63 arginine vasopressin Rattus norvegicus 19-30 13250792-0 1955 [Variations of plasma sodium, potassium and magnesium under the effect of insulin]. Sodium 22-28 insulin Homo sapiens 74-81 13221777-0 1955 Active sodium uptake by the toad and its response to the antidiuretic hormone. Sodium 7-13 arginine vasopressin Homo sapiens 57-77 13181026-0 1954 [Clinical study of renal tubular resorption of potassium and sodium under the action of ACTH and cortisone. Sodium 61-67 proopiomelanocortin Homo sapiens 88-92 13108985-0 1953 The prevention of ACTH-induced sodium retention by the use of potassium salts: a quantitative study. Sodium 31-37 proopiomelanocortin Homo sapiens 18-22 13086766-0 1953 [Insulin hypoglycemia as element of different serum-erythrocyte distributions of potassium and sodium]. Sodium 95-101 insulin Homo sapiens 1-8 13035064-26 1953 In interpreting the experimental results on theoretical grounds, it is suggested (a) that in normal skin, it is the variation in the electric conductance in skin of chloride ions which essentially, although not exclusively, determines the rate of net uptake of sodium chloride, (b) that a factor in the ACTH preparation used, possibly ACTH itself, may have lowered the electric conductance in skin of sodium ions either truly or apparently, (c) that potassium ions are treated by the skin primarily as passive ions. Sodium 261-267 proopiomelanocortin Homo sapiens 303-307 13035064-26 1953 In interpreting the experimental results on theoretical grounds, it is suggested (a) that in normal skin, it is the variation in the electric conductance in skin of chloride ions which essentially, although not exclusively, determines the rate of net uptake of sodium chloride, (b) that a factor in the ACTH preparation used, possibly ACTH itself, may have lowered the electric conductance in skin of sodium ions either truly or apparently, (c) that potassium ions are treated by the skin primarily as passive ions. Sodium 261-267 proopiomelanocortin Homo sapiens 335-339 13016143-0 1952 The influence of ACTH on the sodium and potassium concentrations of human saliva. Sodium 29-35 proopiomelanocortin Homo sapiens 17-21 13016806-0 1952 Sodium, potassium and chloride retention produced by growth hormone in the absence of the adrenals. Sodium 0-6 growth hormone 1 Homo sapiens 53-67 14927720-0 1952 The influence of ACTH on the sodium and potassium concentration of human mixed saliva. Sodium 29-35 proopiomelanocortin Homo sapiens 17-21 14917842-0 1952 The effect of ACTH and cortisone on the sodium and potassium levels of human saliva. Sodium 40-46 proopiomelanocortin Homo sapiens 14-18 14867963-0 1951 Effect of vasopressin (pitressin)-induced water retention on sodium excretion. Sodium 61-67 arginine vasopressin Homo sapiens 10-21 14795066-0 1950 The effects of sodium and potassium on the metabolic and physiologic responses to ACTH. Sodium 15-21 proopiomelanocortin Homo sapiens 82-86 14795090-0 1950 The effect of ACTH on tubular reabsorption of sodium and potassium. Sodium 46-52 proopiomelanocortin Homo sapiens 14-18 15436808-0 1950 The effect of sodium intake on the action of ACTH in uncomplicated essential hypertension. Sodium 14-20 proopiomelanocortin Homo sapiens 45-49 19872676-12 1932 The internal composition depends on permeability, e.g., sodium penetrates less rapidly than potassium and in consequence potassium predominates over sodium in the "artificial sap." Sodium 56-62 SH2 domain containing 1A Homo sapiens 175-178 19872676-12 1932 The internal composition depends on permeability, e.g., sodium penetrates less rapidly than potassium and in consequence potassium predominates over sodium in the "artificial sap." Sodium 149-155 SH2 domain containing 1A Homo sapiens 175-178 33581669-3 2021 This study aimed at exploring the role of sodium or other fluorides (NaF), which are intentionally added to flux-cored wire electrodes for stainless steel welding, on the solubility (in phosphate buffered saline) and toxicity of the generated welding fume particles. Sodium 42-48 C-X-C motif chemokine ligand 8 Homo sapiens 69-72 34051803-5 2021 The discovery of the bile-acid pump sodium-taurocholate co-transporting polypeptide (NTCP) as the receptor of HBV has advanced our understanding of HBV biology. Sodium 36-42 solute carrier family 10 member 1 Homo sapiens 85-89 34037494-0 2021 Association of Cystic Fibrosis Transmembrane Conductance Regulator with Epithelial Sodium Channel Subunits Carrying Liddle"s Syndrome Mutations. Sodium 83-89 CF transmembrane conductance regulator Homo sapiens 15-66 34034251-1 2021 BACKGROUND: Angiotensin II (Ang II) and the renal sympathetic nervous system exert a strong influence on renal sodium and water excretion. Sodium 111-117 angiotensinogen Rattus norvegicus 12-26 34034251-1 2021 BACKGROUND: Angiotensin II (Ang II) and the renal sympathetic nervous system exert a strong influence on renal sodium and water excretion. Sodium 111-117 angiotensinogen Rattus norvegicus 28-34 34024121-7 2021 The hypertensive response of PRRR279V/L282V to AngII infusion was blunted in parallel with attenuated response of intrarenal renin and renal medullary alpha-epithelial sodium channel expression. Sodium 168-174 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 47-52 34024121-8 2021 By using Ussing chamber technique, primary collecting duct cells from PRRR279V/L282V mice exhibited blunted response of epithelial sodium channel activity to AngII as compared to wild-type cells. Sodium 131-137 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 158-163 33324992-12 2021 A potentially pathogenic role of the novel ANK3 variant is suggested by the direct interaction of Ankyrin-G with the cardiac sodium channel, however, more patients with ANK3 variants and ERS would be required to establish ANK3 as novel ERS susceptibility gene. Sodium 125-131 ankyrin 3 Homo sapiens 43-47 33324992-12 2021 A potentially pathogenic role of the novel ANK3 variant is suggested by the direct interaction of Ankyrin-G with the cardiac sodium channel, however, more patients with ANK3 variants and ERS would be required to establish ANK3 as novel ERS susceptibility gene. Sodium 125-131 ankyrin 3 Homo sapiens 98-107 33979795-5 2021 Sodium retention was calculated using our formula: eRNa+ = DeltaBW x (SNa+)t2 - total body water (TBW)t1 x ([SNa+]t1 - [SNa+]t2), where TBW represents the calculated volume of the total body water and (SNa+)t1 and (SNa+)t2 represent the sodium concentration at the beginning and at the end of the IDI, respectively. Sodium 0-6 snail family transcriptional repressor 1 Homo sapiens 70-73 33979795-5 2021 Sodium retention was calculated using our formula: eRNa+ = DeltaBW x (SNa+)t2 - total body water (TBW)t1 x ([SNa+]t1 - [SNa+]t2), where TBW represents the calculated volume of the total body water and (SNa+)t1 and (SNa+)t2 represent the sodium concentration at the beginning and at the end of the IDI, respectively. Sodium 0-6 snail family transcriptional repressor 1 Homo sapiens 109-112 33979795-5 2021 Sodium retention was calculated using our formula: eRNa+ = DeltaBW x (SNa+)t2 - total body water (TBW)t1 x ([SNa+]t1 - [SNa+]t2), where TBW represents the calculated volume of the total body water and (SNa+)t1 and (SNa+)t2 represent the sodium concentration at the beginning and at the end of the IDI, respectively. Sodium 0-6 snail family transcriptional repressor 1 Homo sapiens 109-112 33979795-5 2021 Sodium retention was calculated using our formula: eRNa+ = DeltaBW x (SNa+)t2 - total body water (TBW)t1 x ([SNa+]t1 - [SNa+]t2), where TBW represents the calculated volume of the total body water and (SNa+)t1 and (SNa+)t2 represent the sodium concentration at the beginning and at the end of the IDI, respectively. Sodium 0-6 snail family transcriptional repressor 1 Homo sapiens 109-112 33979795-5 2021 Sodium retention was calculated using our formula: eRNa+ = DeltaBW x (SNa+)t2 - total body water (TBW)t1 x ([SNa+]t1 - [SNa+]t2), where TBW represents the calculated volume of the total body water and (SNa+)t1 and (SNa+)t2 represent the sodium concentration at the beginning and at the end of the IDI, respectively. Sodium 0-6 snail family transcriptional repressor 1 Homo sapiens 109-112 33969697-1 2021 A major pathway in hypertension pathogenesis involves direct activation of Ang II (AT1) receptors in the kidney, stimulating sodium reabsorption. Sodium 125-131 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 75-97 34040506-0 2021 Investigating the Mechanism of Sodium Binding to SERT Using Direct Simulations. Sodium 31-37 solute carrier family 6 member 4 Homo sapiens 49-53 34040506-4 2021 Transport of serotonin by SERT is energized by the transmembrane electrochemical gradient of sodium. Sodium 93-99 solute carrier family 6 member 4 Homo sapiens 26-30 34040506-5 2021 We used extensive molecular dynamics simulations to investigate the process of sodium binding to SERT, which is the first step in the transport cycle that leads to serotonin uptake. Sodium 79-85 solute carrier family 6 member 4 Homo sapiens 97-101 33377278-12 2021 Angiotensin II antagonism alleviates CsA nephrotoxicity via the COX-2-dependent normalization of creatinine clearance and sodium excretion. Sodium 122-128 angiotensinogen Rattus norvegicus 0-14 33085785-1 2021 AIM: Plasma renin activity (PRA) is regarded as a marker of sodium and fluid homeostasis in patients with primary hypertension. Sodium 60-66 renin Homo sapiens 12-17 33462806-5 2021 SLC9C1 encodes a sperm-specific sodium/proton exchanger, which in mouse regulates pH homeostasis and interacts with the soluble Adenylyl Cyclase (sAC), a key regulator of the signalling pathways involved in sperm motility and capacitation. Sodium 32-38 solute carrier family 9, subfamily C (Na+-transporting carboxylic acid decarboxylase), member 1 Mus musculus 0-6 33615880-2 2021 There is a large body of evidence for the fact that sodium-glucose co-transporter 2 inhibitors may significantly improve all-cause mortality, cardiovascular mortality and hospitalization for HF in patients with HFrEF who received renin-angiotensin system blockers including angiotensin receptor neprilysin inhibitors, beta-blockers and mineralocorticoid receptor antagonists. Sodium 52-58 membrane metalloendopeptidase Homo sapiens 295-305 32693647-5 2021 Although SUR2B level was elevated, the level of sodium-calcium exchanger NCX1 and inducible nitric oxide synthase were reduced and increased, respectively. Sodium 48-54 solute carrier family 8 member A1 Rattus norvegicus 73-77 33028070-1 2021 Background/Aims: This study aimed to investigate whether urinary angiotensinogen (UAGT) excretion was associated with elevated blood pressure in patients with chronic kidney disease (CKD) and to evaluate the relationship among blood pressure, intra-renal renin-angiotensin system (RAS) activity, and dietary sodium in patients with CKD. Sodium 308-314 angiotensinogen Homo sapiens 65-80 33910361-1 2021 Background: Genetic variants in SCN10A, encoding the neural voltage-gated sodium channel NaV1.8, are strongly associated with atrial fibrillation, Brugada syndrome, cardiac conduction velocities and heart rate. Sodium 74-80 sodium channel, voltage-gated, type X, alpha Mus musculus 32-38 33910361-1 2021 Background: Genetic variants in SCN10A, encoding the neural voltage-gated sodium channel NaV1.8, are strongly associated with atrial fibrillation, Brugada syndrome, cardiac conduction velocities and heart rate. Sodium 74-80 sodium channel, voltage-gated, type X, alpha Mus musculus 89-95 33910361-11 2021 In patch-clamp transfection experiments, expression of Scn10a-short-encoded NaV1.8-short increased NaV1.5-mediated sodium current. Sodium 115-121 sodium channel, voltage-gated, type X, alpha Mus musculus 55-61 33910361-11 2021 In patch-clamp transfection experiments, expression of Scn10a-short-encoded NaV1.8-short increased NaV1.5-mediated sodium current. Sodium 115-121 sodium channel, voltage-gated, type X, alpha Mus musculus 76-82 33910361-12 2021 We propose that non-coding genetic variation modulates transcriptional regulation of Scn10a-short in cardiomyocytes that impacts on NaV1.5-mediated sodium current and heart rhythm. Sodium 148-154 sodium channel, voltage-gated, type X, alpha Mus musculus 85-91 33912899-1 2021 CONTEXT: Iodide transport defect (ITD) (Online Mendelian Inheritance in Man #274400) is an uncommon cause of dyshormonogenic congenital hypothyroidism due to loss-of-function variants in the SLC5A5 gene, which encodes the sodium/iodide symporter (NIS), causing deficient iodide accumulation in thyroid follicular cells. Sodium 222-228 solute carrier family 5 member 5 Homo sapiens 191-197 33651714-1 2021 The excitability of interneurons requires Nav1.1, the alpha subunit of voltage-gated sodium channel. Sodium 85-91 sodium channel, voltage-gated, type I, alpha Mus musculus 42-48 33857948-5 2021 Using flow cytometric methods, we determined that the IL-8-induced cellular activity was largely dependent on specific ion channels and transporters, such as the sodium-proton exchanger 1 (NHE1) and non-NHE1-dependent sodium flux. Sodium 162-168 C-X-C motif chemokine ligand 8 Homo sapiens 54-58 33857948-5 2021 Using flow cytometric methods, we determined that the IL-8-induced cellular activity was largely dependent on specific ion channels and transporters, such as the sodium-proton exchanger 1 (NHE1) and non-NHE1-dependent sodium flux. Sodium 162-168 solute carrier family 9 member A1 Homo sapiens 189-193 33857948-5 2021 Using flow cytometric methods, we determined that the IL-8-induced cellular activity was largely dependent on specific ion channels and transporters, such as the sodium-proton exchanger 1 (NHE1) and non-NHE1-dependent sodium flux. Sodium 218-224 C-X-C motif chemokine ligand 8 Homo sapiens 54-58 33864813-13 2021 The increased urine excretion of glucose and sodium was mediated by decreased renal SGLT2 expression due to inactivation of the IKKalpha/beta/NF-kappaB-induced inflammatory response. Sodium 45-51 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 142-151 33658306-1 2021 Advances in genome sequencing have identified over 1300 mutations in the SCN1A sodium channel gene that result in genetic epilepsies. Sodium 79-85 sodium channel, voltage-gated, type I, alpha Mus musculus 73-78 33845849-13 2021 A high concentration of urine sodium in AIS patients was found to be correlated with lower TREM2 expression and detrimental stroke outcomes. Sodium 30-36 triggering receptor expressed on myeloid cells 2 Homo sapiens 91-96 33921209-0 2021 NFAT5 Is Involved in GRP-Enhanced Secretion of GLP-1 by Sodium. Sodium 56-62 gastrin releasing peptide Mus musculus 21-24 33921209-1 2021 Gastrin, secreted by G-cells, and glucagon-like peptide-1 (GLP-1), secreted by L-cells, may participate in the regulation of sodium balance. Sodium 125-131 gastrin Mus musculus 0-7 33921209-5 2021 GRP enhances the high sodium-induced increase in GLP-1 secretion. Sodium 22-28 gastrin releasing peptide Mus musculus 0-3 33921209-7 2021 Silencing NFAT5 in L-cells abrogates the stimulatory effect of GRP on the high sodium-induced GLP-1 secretion and protein expression, and the sodium-induced increase in GRPR expression. Sodium 79-85 gastrin releasing peptide Mus musculus 63-66 33921515-3 2021 The present study aimed to identify more virus-selective inhibitors of NTCP by screening of 87 propanolamine derivatives from the former development of intestinal bile acid reabsorption inhibitors (BARIs), which interact with the NTCP-homologous intestinal apical sodium-dependent bile acid transporter (ASBT). Sodium 264-270 solute carrier family 10 member 1 Homo sapiens 230-234 33921515-3 2021 The present study aimed to identify more virus-selective inhibitors of NTCP by screening of 87 propanolamine derivatives from the former development of intestinal bile acid reabsorption inhibitors (BARIs), which interact with the NTCP-homologous intestinal apical sodium-dependent bile acid transporter (ASBT). Sodium 264-270 solute carrier family 10 member 1 Homo sapiens 71-75 33920088-0 2021 Regulation of Serum Sodium Levels during Chemotherapy Using Selective Arginine Vasopressin V2-Receptor Antagonist Tolvaptan in a Four-Year-Old Girl with a Suprasellar Germ Cell Tumor. Sodium 20-26 arginine vasopressin receptor 2 Homo sapiens 79-102 33824491-1 2021 The intrarenal renin-angiotensin system is critical for the regulation of tubule sodium reabsorption, renal haemodynamics and blood pressure. Sodium 81-87 renin Homo sapiens 15-20 33824491-7 2021 Furthermore, binding of prorenin and renin to the prorenin receptor in the collecting duct evokes a number of responses, including the non-proteolytic enzymatic activation of prorenin to produce ANGI from proximal tubule-derived angiotensinogen, which is then converted into ANGII by luminal angiotensin-converting enzyme; stimulation of the epithelial sodium channel (ENaC) in principal cells; and activation of intracellular pathways linked to the upregulation of cyclooxygenase 2 and profibrotic genes. Sodium 353-359 renin Homo sapiens 27-32 33824491-7 2021 Furthermore, binding of prorenin and renin to the prorenin receptor in the collecting duct evokes a number of responses, including the non-proteolytic enzymatic activation of prorenin to produce ANGI from proximal tubule-derived angiotensinogen, which is then converted into ANGII by luminal angiotensin-converting enzyme; stimulation of the epithelial sodium channel (ENaC) in principal cells; and activation of intracellular pathways linked to the upregulation of cyclooxygenase 2 and profibrotic genes. Sodium 353-359 angiotensinogen Homo sapiens 195-199 33824491-8 2021 These findings suggest that dysregulation of the renin-angiotensin system in the collecting duct contributes to the development of hypertension by enhancing sodium reabsorption and the progression of kidney injury. Sodium 157-163 renin Homo sapiens 49-54 1147060-8 1975 Prolactin may be counteracting the effects of physical factors on the regulation of sodium reabsorption in the proximal tubule. Sodium 84-90 prolactin Rattus norvegicus 0-9 1132118-5 1975 Simultaneous plasma renin activities were elevated and comparable to those of civilized subjects placed for brief periods on 10 mEq sodium diets. Sodium 132-138 renin Homo sapiens 20-25 1149189-4 1975 In normal rats, sodium depletion reduced the volume of antiserum required to prevent a pressor response to 50 ng of angiotensin II from 0.32 to 0.22 ml; sodium loading increased the volume required to 0.65 ml. Sodium 16-22 angiotensinogen Rattus norvegicus 116-130 1149189-8 1975 These observations indicate that sodium-induced changes in the vascular response to angiotensin II require the presence of kidney tissue. Sodium 33-39 angiotensinogen Rattus norvegicus 84-98 1148527-0 1975 Proceedings: Sodium and the response of rat descending colon and rat uterus to angiotensin II. Sodium 13-19 angiotensinogen Rattus norvegicus 79-93 802649-12 1975 This study suggests that the decrease in plasma renin activity was related to the lowering of the heart rate rather than to sodium retention and that adrenergic-blocking agents can impair the normal relationship between stroke index and plasma volume, between plasma volume and plasma renin activity, and between plasma renin activity and plasma aldosterone. Sodium 124-130 renin Homo sapiens 48-53 1056284-6 1975 Reduction and redistribution of renal blood flow in response to a low sodium diet appears to be mediated by a beta-receptor mechanism and may be a consequence of intrarenal release of renin. Sodium 70-76 LOW QUALITY PROTEIN: renin Oryctolagus cuniculus 184-189 1077790-8 1975 These results indicate that: (a) angiotensin II is essential for blood pressure control in the sodium-depleted individual; (b) angiotensin II exerts direct feedback control on renin secretion; (c) angiotensin II is the primary stimulus to aldosterone secretion in response to both sodium depletion and posture. Sodium 95-101 angiotensinogen Homo sapiens 33-47 1077790-8 1975 These results indicate that: (a) angiotensin II is essential for blood pressure control in the sodium-depleted individual; (b) angiotensin II exerts direct feedback control on renin secretion; (c) angiotensin II is the primary stimulus to aldosterone secretion in response to both sodium depletion and posture. Sodium 95-101 angiotensinogen Homo sapiens 127-141 1077790-8 1975 These results indicate that: (a) angiotensin II is essential for blood pressure control in the sodium-depleted individual; (b) angiotensin II exerts direct feedback control on renin secretion; (c) angiotensin II is the primary stimulus to aldosterone secretion in response to both sodium depletion and posture. Sodium 95-101 angiotensinogen Homo sapiens 127-141 1077790-8 1975 These results indicate that: (a) angiotensin II is essential for blood pressure control in the sodium-depleted individual; (b) angiotensin II exerts direct feedback control on renin secretion; (c) angiotensin II is the primary stimulus to aldosterone secretion in response to both sodium depletion and posture. Sodium 281-287 angiotensinogen Homo sapiens 33-47 1077790-8 1975 These results indicate that: (a) angiotensin II is essential for blood pressure control in the sodium-depleted individual; (b) angiotensin II exerts direct feedback control on renin secretion; (c) angiotensin II is the primary stimulus to aldosterone secretion in response to both sodium depletion and posture. Sodium 281-287 angiotensinogen Homo sapiens 127-141 1077790-8 1975 These results indicate that: (a) angiotensin II is essential for blood pressure control in the sodium-depleted individual; (b) angiotensin II exerts direct feedback control on renin secretion; (c) angiotensin II is the primary stimulus to aldosterone secretion in response to both sodium depletion and posture. Sodium 281-287 angiotensinogen Homo sapiens 127-141 166090-6 1975 These findings suggest that beta-adrenergic receptors have a role in mediating the effects of sodium depletion upon renin secretion and adenyl cyclase activity. Sodium 94-100 renin Homo sapiens 116-121 1098253-7 1975 Three criteria, derived from four renin measurements, identify this situation: (1) Hypersecretion of renin is reflected by a high peripheral level when referenced against sodium excretion. Sodium 171-177 renin Homo sapiens 101-106 1173310-0 1975 Effects of calcium and sodium on vasopressin release in vitro induced by a prolonged potassium stimulation. Sodium 23-29 arginine vasopressin Rattus norvegicus 33-44 1173310-10 1975 In addition they show that a considerable fraction of the vasopressin present in the neurohypophysis can be mobilized during a continued strong stimulation if sodium is omitted from the medium. Sodium 159-165 arginine vasopressin Rattus norvegicus 58-69 1122880-2 1975 Prolactin administration significantly stimulated fluid, sodium,potassium, calcium, magnesium and chloride transport across everted jejunal sacs. Sodium 57-63 prolactin Rattus norvegicus 0-9 1122880-5 1975 Prolactin action on fluid and sodium absorption showed a dose-dependent tendency, maximal stimulation resulting from administration of 1.0 to 2.0 mg prolactin daily; higher doses failed to elicit significant response. Sodium 30-36 prolactin Rattus norvegicus 0-9 1122880-10 1975 These results suggest that the effects of prolactin on intestinal transport may be dependent on increased movement of sodium. Sodium 118-124 prolactin Rattus norvegicus 42-51 1102803-0 1975 Inter-relationships between plasma angiotensin II, arterial pressure, aldosterone and exchangeable sodium in normotensive and hypertensive man. Sodium 99-105 angiotensinogen Homo sapiens 35-49 1120786-5 1975 Urinary sodium excretion (UNaV) decreased from 401 plus or minus 46 (SEM) to 213 plus or minus 18 mueq/min during insulin administration, the change becoming significant (P smaller than 0.02) within the 30-60 min collection period. Sodium 8-14 insulin Homo sapiens 114-121 1120786-13 1975 The effect of insulin on CH2O suggests that insulin"s effect on sodium excretion is due to enhancement of sodium reabsorption in the diluting segment of the distal nephron. Sodium 64-70 insulin Homo sapiens 14-21 1120786-13 1975 The effect of insulin on CH2O suggests that insulin"s effect on sodium excretion is due to enhancement of sodium reabsorption in the diluting segment of the distal nephron. Sodium 64-70 insulin Homo sapiens 44-51 1120786-13 1975 The effect of insulin on CH2O suggests that insulin"s effect on sodium excretion is due to enhancement of sodium reabsorption in the diluting segment of the distal nephron. Sodium 106-112 insulin Homo sapiens 14-21 1120786-13 1975 The effect of insulin on CH2O suggests that insulin"s effect on sodium excretion is due to enhancement of sodium reabsorption in the diluting segment of the distal nephron. Sodium 106-112 insulin Homo sapiens 44-51 234853-0 1975 Enhancement of the blood pressure activity of VAL5-and ILE5-angiotensin II by sodium and calcium ions. Sodium 78-84 angiotensinogen Homo sapiens 60-74 234666-10 1975 The cardiac attacks in these five patients all occurred during or shortly after procedures, such as sodium-depleting dialysis, renal artery surgery, or diazoxide administration, known to cause increase in plasma concentrations of renin and angiotensin II. Sodium 100-106 renin Homo sapiens 230-235 234666-10 1975 The cardiac attacks in these five patients all occurred during or shortly after procedures, such as sodium-depleting dialysis, renal artery surgery, or diazoxide administration, known to cause increase in plasma concentrations of renin and angiotensin II. Sodium 100-106 angiotensinogen Homo sapiens 240-254 1152349-7 1975 Most likely the increase of the plasma aldosterone, in spite of the fixed renin activity, is stimulated by the sodium depletion due to diuretics. Sodium 111-117 renin Homo sapiens 74-79 163889-1 1975 It is well established that active sodium-ion transport and water flow across isolated toad bladder are increased by antidiuretic hormone (ADH) and by cAMP. Sodium 35-41 arginine vasopressin Homo sapiens 117-143 163889-5 1975 Thus several agents (ADH, cAMP, theophylline, adenine, prostaglandin E1, and Mn Cl-2) caused a decrease in the amount of radioactive phosphate in the 49,000-dalton protein and also stimulated active sodium transport across the bladder. Sodium 199-205 arginine vasopressin Homo sapiens 21-24 182367-8 1975 An insulin-induced configurational change in the plasma membrane could simultaneously account for the effects of insulin on sodium and potassium permeability and the action on facilitated transport. Sodium 124-130 insulin Homo sapiens 3-10 182367-8 1975 An insulin-induced configurational change in the plasma membrane could simultaneously account for the effects of insulin on sodium and potassium permeability and the action on facilitated transport. Sodium 124-130 insulin Homo sapiens 113-120 234803-2 1975 Responses to angiotensin II were impaired by sodium deprivation but enhanced by sodium loading or bilateral nephrectomy. Sodium 45-51 angiotensinogen Rattus norvegicus 13-27 234803-2 1975 Responses to angiotensin II were impaired by sodium deprivation but enhanced by sodium loading or bilateral nephrectomy. Sodium 80-86 angiotensinogen Rattus norvegicus 13-27 4455565-6 1974 The volume of duodenal reflux occurring during insulin-stimulated secretion was estimated from the sodium output in normal controls, in preoperative patients with duodenal ulcer, and in patients following vagotomy with or without a drainage procedure. Sodium 99-105 insulin Homo sapiens 47-54 4852449-6 1974 These observations suggest that calcium transport across the brush border and basallateral membranes are identifiable components of the kinetics of (45)Ca uptake and release and that parathyroid hormone stimulates a sodium-dependent mechanism of calcium transport across the basal-lateral membranes. Sodium 216-222 parathyroid hormone Homo sapiens 183-202 4365595-2 1974 We have assessed the effect of decreased sodium intake on their responses to A II in man. Sodium 41-47 angiotensinogen Homo sapiens 77-81 4365595-9 1974 Sodium restriction reduced the pressor (P < 0.01) and the renal vascular response (P < 0.01), but potentiated the adrenal response to A II (P < 0.01). Sodium 0-6 angiotensinogen Homo sapiens 140-144 4365595-11 1974 Thus, sodium intake reciprocally influences vascular and adrenal responses to A II: salt restriction blunts the vascular response and potentiates the adrenal"s, a physiologically important influence in view of aldosterone"s role in sodium conservation. Sodium 6-12 angiotensinogen Homo sapiens 78-82 4365595-11 1974 Thus, sodium intake reciprocally influences vascular and adrenal responses to A II: salt restriction blunts the vascular response and potentiates the adrenal"s, a physiologically important influence in view of aldosterone"s role in sodium conservation. Sodium 232-238 angiotensinogen Homo sapiens 78-82 4377498-0 1974 Effect of a competitive antagonist (8-leu-angiotensin II) of angiotensin II on sodium and water transport in toad skin. Sodium 79-85 angiotensinogen Homo sapiens 42-56 4377498-0 1974 Effect of a competitive antagonist (8-leu-angiotensin II) of angiotensin II on sodium and water transport in toad skin. Sodium 79-85 angiotensinogen Homo sapiens 61-75 4428983-0 1974 [Effect of calcium and sodium in the production of renin in vitro: action of cycloheximide]. Sodium 23-29 renin Homo sapiens 51-56 4522176-0 1973 Renin suppression in hypertension in relation to body fluid volumes, patterns of sodium excretion and renal haemodynamics. Sodium 81-87 renin Homo sapiens 0-5 4756157-0 1973 [Effect of parathyroid hormone on urinary sodium and potassium excretion in hypothyroid children]. Sodium 42-48 parathyroid hormone Homo sapiens 11-30 4120488-0 1973 Abnormal relation between exchangeable sodium and the renin-angiotensin system in malignant hypertension and in hypertension with chronic renal failure. Sodium 39-45 renin Homo sapiens 54-59 4351809-5 1973 These and other results are compatible with the possibility that the regulation by vasopressin and cyclic AMP of sodium and/or water transport in toad bladder may be mediated through regulation of the phosphorylation of this specific protein. Sodium 113-119 arginine vasopressin Homo sapiens 83-94 4693691-0 1973 Vasopressin-related alterations of sodium reabsorption in the loop of Henle. Sodium 35-41 arginine vasopressin Homo sapiens 0-11 4345832-3 1972 Statistically significant correlations were found between plasma renin activity and plasma sodium concentration and between plasma renin activity and dietary sodium intake.Only one patient was found to have uncontrollable hypertension associated with a markedly raised plasma renin activity. Sodium 91-97 renin Homo sapiens 65-70 4345832-3 1972 Statistically significant correlations were found between plasma renin activity and plasma sodium concentration and between plasma renin activity and dietary sodium intake.Only one patient was found to have uncontrollable hypertension associated with a markedly raised plasma renin activity. Sodium 158-164 renin Homo sapiens 131-136 4345832-3 1972 Statistically significant correlations were found between plasma renin activity and plasma sodium concentration and between plasma renin activity and dietary sodium intake.Only one patient was found to have uncontrollable hypertension associated with a markedly raised plasma renin activity. Sodium 158-164 renin Homo sapiens 131-136 5083169-11 1972 It is concluded that the rise in PRC in these experiments is compatible with the theory that altered sodium transport at the macula densa was the stimulus for renin release. Sodium 101-107 renin Ovis aries 159-164 4341479-0 1972 Metabolism of angiotensin II in sodium depletion and hypertension in humans. Sodium 32-38 angiotensinogen Homo sapiens 14-28 4344726-6 1972 It therefore appears that ACTH and potassium stimulate steroidogenesis at an early step in the biosynthetic pathway through the activation of cyclic AMP, whereas the effect of angiotensins I and II involve another mechanism and decreased sodium concentration affects a later step in steroidogenesis. Sodium 238-244 proopiomelanocortin Homo sapiens 26-30 5048760-0 1972 [The effect of aldosterone and insulin on the transport of sodium across the cell membrane]. Sodium 59-65 insulin Homo sapiens 31-38 5032511-0 1972 Effects of change in posture and of sodium depletion on plasma levels of vasopressin and renin in normal human subjects. Sodium 36-42 arginine vasopressin Homo sapiens 73-84 5032511-0 1972 Effects of change in posture and of sodium depletion on plasma levels of vasopressin and renin in normal human subjects. Sodium 36-42 renin Homo sapiens 89-94 5032521-0 1972 The effect of bradykinin on proximal tubular sodium reabsorption in the dog: evidence for functional nephron heterogeneity. Sodium 45-51 kininogen 1 Canis lupus familiaris 14-24 4336938-7 1972 Administration of mineralocorticoid or ACTH consistently caused sodium retention. Sodium 64-70 proopiomelanocortin Homo sapiens 39-43 4337697-0 1972 Effect of angiotensin II on urinary magnesium, calcium, and sodium excretion in normal subjects. Sodium 60-66 angiotensinogen Homo sapiens 10-24 5009112-7 1972 Moreover, excretion and secretion of aldosterone and in many instances, plasma renin activity, appeared to be high with respect to sodium intake. Sodium 131-137 renin Homo sapiens 79-84 4631251-0 1972 Hormonal influences on transepithelial sodium transport: aldosterone vs. insulin. Sodium 39-45 insulin Homo sapiens 73-80 4340714-0 1972 [Activation of renin in the juxtaglomerular apparatus by tubular sodium in the macula densa segment]. Sodium 65-71 renin Homo sapiens 15-20 4108268-0 1971 Circulating angiotensin-II and aldosterone levels during dietary sodium restriction. Sodium 65-71 angiotensinogen Homo sapiens 12-26 5316353-0 1971 Effects of human growth hormone preparations on sodium transport in isolated frog skin. Sodium 48-54 growth hormone 1 Homo sapiens 17-31 5131851-0 1971 Tubule sodium reabsorption in vasopressin escape. Sodium 7-13 arginine vasopressin Homo sapiens 30-41 4328882-5 1971 Furthermore, changes in aldosterone secretory rate and levels of circulating renin produced by varying dietary sodium intake, did not alter sodium influx or fractional sodium outflux in either patients with Liddle"s syndrome or normal subjects. Sodium 111-117 renin Homo sapiens 77-82 5087392-0 1971 Effects of prolonged administration of vasopressin on plasma sodium and on renal excretion of electrolytes and water. Sodium 61-67 arginine vasopressin Homo sapiens 39-50 5087817-0 1971 Effects of hemorrhage and chronic sodium depletion on hepatic clearance of renin. Sodium 34-40 renin Homo sapiens 75-80 24173388-1 1971 Isolated sheets of epithelial cells as well as epithelial cells scraped from paired hemibladders mounted in chambers both showed significant increases in water, sodium and chloride contents after exposure to vasopressin (100 mU/ml), without any change in potassium content. Sodium 161-167 arginine vasopressin Homo sapiens 208-219 24173388-2 1971 In the isolated cells these changes were prevented by amiloride (10(-5) M), suggesting that the gain of sodium after vasopressin occurs across the mucosal membrane. Sodium 104-110 arginine vasopressin Homo sapiens 117-128 5575414-0 1971 Simultaneous measurement of the effect of vasopressin on sodium and water transport across toad bladder. Sodium 57-63 arginine vasopressin Homo sapiens 42-53 5142557-0 1971 Effect of sodium and osmotic concentration on renin release by renal cortical slices in vitro. Sodium 10-16 renin Homo sapiens 46-51 5107275-0 1971 [Influence of sodium concentration on the release of renin from kidney cortex slices and isolated glomeruli]. Sodium 14-20 renin Homo sapiens 53-58 5156048-0 1971 [Relation between sodium excretion and renin plasma level on physiologic and pathologic conditions]. Sodium 18-24 renin Homo sapiens 39-44 5479370-0 1970 The effect of vasopressin on the reabsorption of sodium, potassium and urea by the renal tubules in man. Sodium 49-55 arginine vasopressin Homo sapiens 14-25 5428805-0 1970 Changes of renin in individual glomeruli in response to variations of sodium intake in the rabbit. Sodium 70-76 LOW QUALITY PROTEIN: renin Oryctolagus cuniculus 11-16 4331448-0 1970 [Effect differences between angiotensin II and noradrenalin in reference to diuresis, sodium and potassium excretion in healthy persons and patients with kidney diseases]. Sodium 86-92 angiotensinogen Homo sapiens 28-42 5343354-3 1969 Vasopressin contractions are inhibited by replacement of sodium with mannitol or sucrose, elevation of potassium or magnesium concentrations, the presence of the metabolic inhibitors sodium azide and triethyl tin or tetrodotoxin in the bathing fluid. Sodium 57-63 arginine vasopressin Rattus norvegicus 0-11 5819296-0 1969 Effect of sodium depletion on renin activity of renal venous plasma in renovascular hypertension. Sodium 10-16 renin Homo sapiens 30-35 4389599-0 1969 [Action of sodium in liquid ammonia on the Buntesalt-A-chain of porcine insulin]. Sodium 11-17 insulin Homo sapiens 72-79 4303532-0 1969 Effect of high sodium intake on the response of the rat adrenal to angiotensin II. Sodium 15-21 angiotensinogen Rattus norvegicus 67-81 5699946-0 1968 Plasma renin activity in relation to serum sodium concentration and body fluid balance. Sodium 43-49 renin Homo sapiens 7-12 4304235-6 1968 The results are consistent with ADH causing an increase in permeability of the outer facing membranes to sodium ions.4. Sodium 105-111 arginine vasopressin Homo sapiens 32-35 4304235-12 1968 Separate explanations for the increase in sodium transport by ADH, theophylline and cyclic 3",5"-AMP are discussed. Sodium 42-48 arginine vasopressin Homo sapiens 62-65 5658591-4 1968 Application of vasopressin to the bladder serosa shortly after toxin resulted in only weak and transient stimulation of sodium transport; once maximal toxin activity had been established, exposure to the hormone was without effect. Sodium 120-126 arginine vasopressin Homo sapiens 15-26 5664238-7 1968 Vasopressin and aldosterone increased sodium transport from solutions of low Na concentration, but amphotericin B was ineffective until a level of about 40-60 mM was present.4. Sodium 38-44 arginine vasopressin Homo sapiens 0-11 5654401-0 1968 The site of the stimulatory action of vasopressin on sodium transport in toad bladder. Sodium 53-59 arginine vasopressin Homo sapiens 38-49 5654401-1 1968 Vasopressin increases the net transport of sodium across the isolated urinary bladder of the toad by increasing the mobility of sodium ion within the tissue. Sodium 43-49 arginine vasopressin Homo sapiens 0-11 5654401-1 1968 Vasopressin increases the net transport of sodium across the isolated urinary bladder of the toad by increasing the mobility of sodium ion within the tissue. Sodium 128-134 arginine vasopressin Homo sapiens 0-11 5648055-0 1968 Renin release: relation to renal sodium load and dissociation from hemodynamic changes. Sodium 33-39 renin Homo sapiens 0-5 5642688-0 1968 Plasma renin activity and aldosterone secretion in hypertensive patients during high and low sodium intake and administration of diuretic. Sodium 93-99 renin Homo sapiens 7-12 5651121-0 1968 Effect of nephrectomy and a low sodium diet on the increase in plasma renin levels produced by hemorrhage. Sodium 32-38 renin Homo sapiens 70-75 5639033-0 1968 Plasma renin in chronic experimental heart failure and during renal sodium "escape" from mineralocorticoids. Sodium 68-74 renin Homo sapiens 7-12 5748208-0 1968 [Influence of insulin and vasopressin on sodium distribution in tissues]. Sodium 41-47 insulin Homo sapiens 14-21 5748208-0 1968 [Influence of insulin and vasopressin on sodium distribution in tissues]. Sodium 41-47 arginine vasopressin Homo sapiens 26-37 4296172-0 1968 Hirano J, Masson GM: Effects of dietary sodium on hypertensive disease caused by renin. Sodium 40-46 renin Homo sapiens 81-86 5299948-0 1968 Somatotropin as the non-ACTH factor of anterior pituitary origin for the maintenance of enhanced aldosterone secretory responsiveness of dietary sodium restriction in chronically hypophysectomized rats. Sodium 145-151 growth hormone 1 Rattus norvegicus 0-12 6034759-5 1967 The evidence suggests that abolition of the ERG by ouabain is due principally to inhibition of the active transport of sodium: (a) Structurally modified glycosides which are considerably less potent inhibitors of alkali cation-activated ATPase activity in preparations of frog retinal outer segments are also poorer inhibitors of electrical activity in isolated retinas. Sodium 119-125 ETS transcription factor ERG Homo sapiens 44-47 6023776-5 1967 Concomitant measurements of endogenous creatinine clearance and the rates of excretion of sodium and potassium suggest that a fall in renal arterial perfusion resulting from upright posture induces increased release of renin and the subsequent secondary stimulation of aldosterone secretion. Sodium 90-96 renin Homo sapiens 219-224 4288511-0 1966 [Sodium-potassium quotient during ACTH administration--a simple function test of the adrenal cortex]. Sodium 1-7 proopiomelanocortin Homo sapiens 34-38 5843433-0 1965 Effect of insulin on short-circuit current and sodium transport across toad urinary bladder. Sodium 47-53 insulin Homo sapiens 10-17 5846793-0 1965 Action of aldosterone and vasopressin on the active transport of sodium by the isolated toad bladder. Sodium 65-71 arginine vasopressin Homo sapiens 26-37 5840797-5 1965 However, employing an indirect method for the estimation of sodium transport (oxygen consumption), it is possible to show that vasopressin exerts its usual effect on Q(oo2) when sodium is present in the bathing medium. Sodium 60-66 arginine vasopressin Homo sapiens 127-138 5840797-5 1965 However, employing an indirect method for the estimation of sodium transport (oxygen consumption), it is possible to show that vasopressin exerts its usual effect on Q(oo2) when sodium is present in the bathing medium. Sodium 178-184 arginine vasopressin Homo sapiens 127-138 14202192-0 1964 THE EFFECTS OF OSMOTIC DIURESIS AND VASOPRESSIN UPON THE DISTRIBUTION OF SODIUM, POTASSIUM AND UREA IN THE RAT KIDNEY. Sodium 73-79 arginine vasopressin Rattus norvegicus 36-47 14015990-0 1963 Influence of sodium loading and sodium depletion on plasma-renin in man. Sodium 13-19 renin Homo sapiens 59-64 14015990-0 1963 Influence of sodium loading and sodium depletion on plasma-renin in man. Sodium 32-38 renin Homo sapiens 59-64 14480554-0 1962 The effects of sodium, chloride, and calcium concentration on the response of melanophores to melanocyte-stimulating hormone (MSH). Sodium 15-21 proopiomelanocortin Homo sapiens 94-124 14480554-0 1962 The effects of sodium, chloride, and calcium concentration on the response of melanophores to melanocyte-stimulating hormone (MSH). Sodium 15-21 proopiomelanocortin Homo sapiens 126-129 33957085-1 2021 Increased glucagon level was hypothesized to participate in the ketoacidosis associated with sodium-glucose co-transporter 2 inhibitors (SGLT2i) treatment. Sodium 93-99 glucagon Homo sapiens 10-18 33168155-4 2021 Its pathogenesis is mainly related to the increase in plasma volume secondary to a sodium retaining actions of GH and IGF-1 in the kidney, but abnormalities in vessel architecture and reactivity participate. Sodium 83-89 growth hormone 1 Homo sapiens 111-113 33168155-4 2021 Its pathogenesis is mainly related to the increase in plasma volume secondary to a sodium retaining actions of GH and IGF-1 in the kidney, but abnormalities in vessel architecture and reactivity participate. Sodium 83-89 insulin like growth factor 1 Homo sapiens 118-123 33713776-0 2021 Aldosterone alleviates lipopolysaccharide-induced acute lung injury by regulating epithelial sodium channel through PI3K/Akt/SGK1 signaling pathway. Sodium 93-99 thymoma viral proto-oncogene 1 Mus musculus 121-124 33950864-6 2021 We found an inverse correlation between serum sodium and IL-6, whereas a direct correlation between serum sodium and PaO2/FiO2 ratio was observed. Sodium 46-52 interleukin 6 Homo sapiens 57-61 34037494-1 2021 The association of the cystic fibrosis transmembrane conductance regulator (CFTR) and epithelial sodium channel (ENaC) in the pathophysiology of cystic fibrosis (CF) is controversial. Sodium 97-103 CF transmembrane conductance regulator Homo sapiens 76-80 34018034-1 2021 Bulevirtide is a first-in-class entry inhibitor of the hepatitis B and hepatitis delta virus blocking the sodium/bile acid co-transporter NTCP, and was recently approved for the treatment of hepatitis D as a priority medicine (prime) in an accelerated assessment by the European Medicines Agency. Sodium 106-112 solute carrier family 10 member 1 Homo sapiens 138-142 34020858-1 2021 BACKGROUND: FGF12 (FHF1) gene encodes voltage-gated sodium channel (Nav)-binding protein fibroblast growth factor homologous factor 1, which could cause seizures by regulating voltage dependence of Nav fast inactivation and neuron excitability. Sodium 52-58 fibroblast growth factor 12 Homo sapiens 12-17 34020858-1 2021 BACKGROUND: FGF12 (FHF1) gene encodes voltage-gated sodium channel (Nav)-binding protein fibroblast growth factor homologous factor 1, which could cause seizures by regulating voltage dependence of Nav fast inactivation and neuron excitability. Sodium 52-58 fibroblast growth factor 12 Homo sapiens 19-23 34019877-0 2021 Real-Time Identification of Two Substrate-Binding Intermediates for the Light-Driven Sodium Pump Rhodopsin. Sodium 85-91 rhodopsin Homo sapiens 97-106 33949206-0 2021 Enhanced epithelial sodium channel activity in neonatal Scnn1b mouse lung attenuates high oxygen induced lung injury. Sodium 20-26 sodium channel, nonvoltage-gated 1 beta Mus musculus 56-62 33160031-8 2021 Considering all patients as a whole, copeptin correlated with systolic blood pressure (SBP; rho = -0.209, P = 0.027), eGFR rho = -0.271, P = 0.004), and serum sodium (rho = -0.208, P = 0.027), but not with ABI (rho = -0.068, P = 0.476). Sodium 159-165 arginine vasopressin Homo sapiens 37-45 33690157-7 2021 Eight children had homozygous mutations in the SCNN1A and SCNN1G genes encoding the epithelial sodium channel subunits alpha and gamma, respectively, including one novel mutation. Sodium 95-101 sodium channel epithelial 1 subunit alpha Homo sapiens 47-53 33882940-12 2021 In poor energetic situations increased proton production raises intracellular sodium via sodium-proton-exchanger subtype-1 (NHE1), the most important proton-extruder in skeletal muscle. Sodium 78-84 solute carrier family 9 member A1 Homo sapiens 124-128 33882940-12 2021 In poor energetic situations increased proton production raises intracellular sodium via sodium-proton-exchanger subtype-1 (NHE1), the most important proton-extruder in skeletal muscle. Sodium 89-95 solute carrier family 9 member A1 Homo sapiens 124-128 33889010-0 2021 Rosuvastatin Enhances Alveolar Fluid Clearance in Lipopolysaccharide-Induced Acute Lung Injury by Activating the Expression of Sodium Channel and Na,K-ATPase via the PI3K/AKT/Nedd4-2 Pathway. Sodium 127-133 AKT serine/threonine kinase 1 Rattus norvegicus 171-174 33855971-1 2021 Loss-of-function mutations of SCN1A encoding the pore-forming alpha subunit of the NaV1.1 neuronal sodium channel cause a severe developmental epileptic encephalopathy, Dravet syndrome (DS). Sodium 99-105 sodium channel, voltage-gated, type I, alpha Mus musculus 30-35 33855971-1 2021 Loss-of-function mutations of SCN1A encoding the pore-forming alpha subunit of the NaV1.1 neuronal sodium channel cause a severe developmental epileptic encephalopathy, Dravet syndrome (DS). Sodium 99-105 sodium channel, voltage-gated, type I, alpha Mus musculus 83-89 33873072-1 2021 Catalyzed by zDHHC-PAT enzymes and reversed by thioesterases, protein palmitoylation is the only post-translational modification recognized to regulate the sodium/calcium exchanger NCX1. Sodium 156-162 solute carrier family 8 member A1 Homo sapiens 181-185 33651884-0 2021 Nav1.3 and FGF14 are primary determinants of the TTX-sensitive sodium current in mouse adrenal chromaffin cells. Sodium 63-69 sodium channel, voltage-gated, type III, alpha Mus musculus 0-6 33651884-0 2021 Nav1.3 and FGF14 are primary determinants of the TTX-sensitive sodium current in mouse adrenal chromaffin cells. Sodium 63-69 fibroblast growth factor 14 Mus musculus 11-16 33916525-0 2021 DNA Methylation Patterns Correlate with the Expression of SCNN1A, SCNN1B, and SCNN1G (Epithelial Sodium Channel, ENaC) Genes. Sodium 97-103 sodium channel epithelial 1 subunit alpha Homo sapiens 58-64 33916525-1 2021 The interplay between the cystic fibrosis transmembrane conductance regulator (CFTR) and the epithelial sodium channel (ENaC) in respiratory epithelia has a crucial role in the pathogenesis of cystic fibrosis (CF). Sodium 104-110 CF transmembrane conductance regulator Homo sapiens 79-83 33641076-0 2021 Dexmedetomidine alleviates pulmonary edema through the epithelial sodium channel (ENaC) via the PI3K/Akt/Nedd4-2 pathway in LPS-induced acute lung injury. Sodium 66-72 AKT serine/threonine kinase 1 Homo sapiens 101-104 33796889-2 2022 Most is reabsorbed from the proximal tubule (> 60%) via a paracellular pathway composed of the tight junction proteins claudins-2 and -12, a process driven by sodium and consequently water reabsorption. Sodium 159-165 claudin 2 Homo sapiens 119-137 33607471-1 2021 Bartter Syndrome (BS) is a group of rare inherited autosome-recessive disease, which can be caused by the gene mutations of sodium-potassium-chloride cotransporter gene (SLC12A1). Sodium 124-130 solute carrier family 12 member 1 Homo sapiens 170-177 33733301-3 2022 The descriptions of two recently described salt-losing tubulopathies, transient antenatal Bartter syndrome and HELIX syndrome, which are caused by mutations in MAGED2 and CLDN10 genes, respectively, highlight the role of new players in the modulation of sodium reabsorption the thick ascending limb. Sodium 254-260 claudin 10 Homo sapiens 171-177 33688925-1 2021 The sodium/potassium-ATPase (NKA) is the enzyme that establishes gradients of sodium and potassium across the plasma membrane. Sodium 4-10 tachykinin precursor 1 Homo sapiens 29-32 33688925-1 2021 The sodium/potassium-ATPase (NKA) is the enzyme that establishes gradients of sodium and potassium across the plasma membrane. Sodium 78-84 tachykinin precursor 1 Homo sapiens 29-32 33730389-9 2021 In the peripheral nervous system, we revealed that the TLR4/NF-kappaB signaling pathway induced upregulation of voltage-gated sodium channel 1.7 (Nav1.7) in DRGs, triggering peripheral hyperalgesia in SMIR-induced CPSP. Sodium 126-132 toll-like receptor 4 Rattus norvegicus 55-59 33666288-7 2021 Finally, we detected that DmMANF also affects rhythms in glia themselves, since circadian oscillations in expression of the catalytic alpha subunit of the sodium pump in the lamina epithelial glia were abolished after DmMANF silencing. Sodium 155-161 Mesencephalic astrocyte-derived neurotrophic factor Drosophila melanogaster 26-32 33658209-0 2021 Cryo-EM structures of excitatory amino acid transporter 3 visualize coupled substrate, sodium, and proton binding and transport. Sodium 87-93 solute carrier family 1 member 1 Homo sapiens 22-57 33658209-2 2021 Here, we report cryo-EM structures of hEAAT3 in several functional states where the transporter is empty, bound to coupled sodium ions only, or fully loaded with three sodium ions, a proton, and the substrate aspartate. Sodium 123-129 solute carrier family 1 member 1 Homo sapiens 38-44 33658209-2 2021 Here, we report cryo-EM structures of hEAAT3 in several functional states where the transporter is empty, bound to coupled sodium ions only, or fully loaded with three sodium ions, a proton, and the substrate aspartate. Sodium 168-174 solute carrier family 1 member 1 Homo sapiens 38-44 33434105-6 2021 Such signaling may in turn adversely modulate transepithelial transport processes, especially those involving cystic fibrosis transmembrane conductance regulator (CFTR) and epithelial Na+ channel (ENaC), thereby shifting the delicate balance between anion secretion and sodium absorption that controls homeostasis of this fluid layer. Sodium 270-276 CF transmembrane conductance regulator Homo sapiens 110-161 33434105-6 2021 Such signaling may in turn adversely modulate transepithelial transport processes, especially those involving cystic fibrosis transmembrane conductance regulator (CFTR) and epithelial Na+ channel (ENaC), thereby shifting the delicate balance between anion secretion and sodium absorption that controls homeostasis of this fluid layer. Sodium 270-276 CF transmembrane conductance regulator Homo sapiens 163-167 33186624-12 2021 The results suggest that angiotensin II acts in the brain increasing the palatability of hypertonic sodium during the consummatory phase of sodium appetite. Sodium 100-106 angiotensinogen Rattus norvegicus 25-39 33186624-12 2021 The results suggest that angiotensin II acts in the brain increasing the palatability of hypertonic sodium during the consummatory phase of sodium appetite. Sodium 140-146 angiotensinogen Rattus norvegicus 25-39 32934369-0 2021 Acute infusion of angiotensin II regulates organic cation transporters function in the kidney: its impact on the renal dopaminergic system and sodium excretion. Sodium 143-149 angiotensinogen Rattus norvegicus 18-32 32934369-2 2021 Our aim was to study whether renal dopamine and ANG II can interact to modify renal sodium handling and then to elucidate the related mechanism. Sodium 84-90 angiotensinogen Rattus norvegicus 48-54 32934369-7 2021 ANG II decreased renal excretion of sodium in the presence of exogenous dopamine, increased Na+, K+-ATPase activity, and decreased the urinary dopamine concentration. Sodium 36-42 angiotensinogen Rattus norvegicus 0-6 32934369-8 2021 D-22 treatment exacerbated the ANG II-mediated decrease in renal excretion of sodium and dopamine urine excretion but did not modify ANG II stimulation of Na+, K+-ATPase activity. Sodium 78-84 angiotensinogen Rattus norvegicus 31-37 32934369-12 2021 This study demonstrates a relationship between ANG II and dopamine, where both agents counteract their effects on sodium excretion. Sodium 114-120 angiotensinogen Rattus norvegicus 47-53 33170350-0 2021 Syndecan-3 contributes to the regulation of the microenvironment at the node of Ranvier following end-to-side neurorrhaphy: sodium image analysis. Sodium 124-130 syndecan 3 Homo sapiens 0-10 33170350-8 2021 Our data showed that the re-clustering of sodium and Nav1.6 at nodal regions of the regenerating nerve corresponded to the distribution of SDC3 after ESN. Sodium 42-48 syndecan 3 Homo sapiens 139-143 33098824-8 2021 SiRNA transfection studies showed that PBA can be transported to NSC-34 cell lines through sodium-coupled MCT1. Sodium 91-97 modifier of curly tail 1 Mus musculus 106-110 33658720-1 2021 The human glycine transporter 1 (GlyT1) regulates glycine-mediated neuronal excitation and inhibition through the sodium- and chloride-dependent reuptake of glycine1-3. Sodium 114-120 solute carrier family 6 member 9 Homo sapiens 10-31 33658720-1 2021 The human glycine transporter 1 (GlyT1) regulates glycine-mediated neuronal excitation and inhibition through the sodium- and chloride-dependent reuptake of glycine1-3. Sodium 114-120 solute carrier family 6 member 9 Homo sapiens 33-38 33838996-11 2021 CONCLUSIONS: Sodium restriction significantly reduces SBP and DBP in patients with T2DM. Sodium 13-19 D-box binding PAR bZIP transcription factor Homo sapiens 62-65 33639159-1 2021 Voltage-gated sodium channels (Navs) are tightly regulated by multiple conserved auxiliary proteins, including the four fibroblast growth factor homologous factors (FGFs), which bind the Nav EF-hand like domain (EFL), and calmodulin (CaM), a multifunctional messenger protein that binds the NaV IQ motif. Sodium 14-20 calmodulin 1 Homo sapiens 222-232 33639159-1 2021 Voltage-gated sodium channels (Navs) are tightly regulated by multiple conserved auxiliary proteins, including the four fibroblast growth factor homologous factors (FGFs), which bind the Nav EF-hand like domain (EFL), and calmodulin (CaM), a multifunctional messenger protein that binds the NaV IQ motif. Sodium 14-20 calmodulin 1 Homo sapiens 234-237 33605160-13 2021 Further clinical investigation of novel and approved medications that target low renin physiology such as epithelial sodium channel inhibitors and mineralocorticoid receptor antagonists may be paramount in improving hypertension control in AAs. Sodium 117-123 renin Homo sapiens 81-86 33084880-2 2021 Uromodulin is almost exclusively expressed in the thick ascending limb of the loop of Henle (TAL) and its effect on BP appear to be mediated via the TAL sodium transporter, NKCC2. Sodium 153-159 solute carrier family 12 member 1 Homo sapiens 173-178 33597311-8 2021 During the second course of ifosamide, AVP infusion was commenced at the outset and tighter control of urine output and sodium levels was achieved. Sodium 120-126 arginine vasopressin Homo sapiens 39-42 33597311-12 2021 The use of a continuous AVP infusion and titrating with a sliding scale is more effective than oral desmopressin in regulating plasma sodium and fluid balance during hyperhydration therapy. Sodium 134-140 arginine vasopressin Homo sapiens 24-27 33597311-14 2021 Adjustment of the AVP infusion rate depends on urine output, fluid balance, plasma sodium levels and sensitivity/response of the child to titrated AVP doses. Sodium 83-89 arginine vasopressin Homo sapiens 18-21 33850915-4 2021 Inhibition of neprilysin increases bradykinin, natriuretic peptides and adrenomedullin levels counteract the neurohormal activation that leads to sodium retention, vasoconstriction, and cardiac remodeling. Sodium 146-152 membrane metalloendopeptidase Homo sapiens 14-24 33904662-0 2021 The role of NHE3 (Slc9a3) in oxalate and sodium transport by mouse intestine and regulation by cAMP. Sodium 41-47 solute carrier family 9 (sodium/hydrogen exchanger), member 3 Mus musculus 12-16 33842863-0 2021 Influence of sodium intake and change in sodium intake on plasma-renin in man. Sodium 13-19 renin Homo sapiens 65-70 33904662-0 2021 The role of NHE3 (Slc9a3) in oxalate and sodium transport by mouse intestine and regulation by cAMP. Sodium 41-47 solute carrier family 9 (sodium/hydrogen exchanger), member 3 Mus musculus 18-24 33668649-3 2021 The human sodium/iodide symporter (NIS) and the sodium/glucose transporter (SGLT1) are involved in diseases such as iodide transport defect or glucose-galactose malabsorption. Sodium 10-16 solute carrier family 5 member 1 Homo sapiens 76-81 33471524-8 2021 With respect to charge distribution, Glu192, together with the thrombin-specific sodium ion, helps in creating an electrostatic gradient across the S1 pocket. Sodium 81-87 coagulation factor II, thrombin Homo sapiens 63-71 33411695-2 2021 beta1 subunits modulate the cell-surface localization, gating, and kinetics of sodium channel pore-forming a subunits. Sodium 79-85 BCL2 related protein A1 Homo sapiens 0-5 33080499-3 2021 When employed as the anode of sodium-ion batteries, the Ge@C-CMK electrode exhibits stable capacity as well as long-term cycling stability (a stable capacity of 176 mAh g-1 at 1 A g-1 after 5000 cycles). Sodium 30-36 C-X-C motif chemokine ligand 9 Homo sapiens 61-64 33080499-5 2021 This demonstrates that the Ge@C-CMK electrode possesses promising application potential as an alternative anode in sodium and potassium ion storage applications. Sodium 115-121 C-X-C motif chemokine ligand 9 Homo sapiens 32-35 33571185-3 2021 In the nematode Caenorhabditis elegans, dominant mutations in the DEG/ENaC sodium channel subunit MEC-4 induce six mechanosensory (touch) neurons to undergo excitotoxic necrosis. Sodium 75-81 Degenerin mec-4 Caenorhabditis elegans 98-103 33842863-0 2021 Influence of sodium intake and change in sodium intake on plasma-renin in man. Sodium 41-47 renin Homo sapiens 65-70 33842863-1 2021 Background: Low sodium intake stimulates the production and activity of renin. Sodium 16-22 renin Homo sapiens 72-77 33842863-2 2021 The aim is to analyse the association between a large range of sodium intake and the plasma renin activity (PRA). Sodium 63-69 renin Homo sapiens 92-97 33416451-9 2021 Interestingly, we discover that mouse and human hearts expressed a shorter slc5a1 transcript, leading to SGLT1 protein lacking transmembrane domains and residues involved in glucose and sodium bindings. Sodium 186-192 solute carrier family 5 member 1 Homo sapiens 75-81 33633581-3 2021 In principal cell (PC) culture models FSS induces ERK, and ERK is implicated in the regulation of transepithelial sodium (Na) transport, as well as, proliferation. Sodium 114-120 mitogen-activated protein kinase 1 Mus musculus 59-62 33416451-9 2021 Interestingly, we discover that mouse and human hearts expressed a shorter slc5a1 transcript, leading to SGLT1 protein lacking transmembrane domains and residues involved in glucose and sodium bindings. Sodium 186-192 solute carrier family 5 member 1 Homo sapiens 105-110 33229341-7 2021 Dysregulated SLC1A1, a sodium-dependent glutamate carrier, actively recycled extracellular glutamate into cells, which enhanced the efficiency of cystine uptake via Xc- and GSH biosynthesis as measured by stable isotope-assisted metabolomics. Sodium 23-29 solute carrier family 1 member 1 Homo sapiens 13-19 33301562-4 2021 RESULTS: RYR1-p.R163C mouse muscles have chronically elevated intracellular calcium and sodium levels compared to wild-type muscles. Sodium 88-94 ryanodine receptor 1, skeletal muscle Mus musculus 9-13 33301562-9 2021 CONCLUSIONS: These data support previous findings that TRPC channels play an important role in causing the intracellular calcium and sodium dyshomeostasis associated with RYR1 variants that are pathogenic for malignant hyperthermia. Sodium 133-139 ryanodine receptor 1, skeletal muscle Mus musculus 171-175 33530911-4 2021 Studies on ANP"s physiological effects have demonstrated its activity on channels present in the apical membrane in the renal nephron, potentially inhibiting or decreasing sodium reabsorption. Sodium 172-178 natriuretic peptide A Homo sapiens 11-14 33216460-9 2021 Patients in the lower renin tertile had higher blood pressure and plasma sodium concentration (all P < 0.05). Sodium 73-79 renin Homo sapiens 22-27 33503881-7 2021 Presence of these substrates enables formation of SNAT6-caveolin complexes that aids in sodium dependent trafficking of SNAT6 off the plasma membrane. Sodium 88-94 solute carrier family 38 member 6 Homo sapiens 50-55 32956652-0 2021 The sodium/proton exchanger NHA2 regulates blood pressure through a WNK4-NCC dependent pathway in the kidney. Sodium 4-10 solute carrier family 12, member 3 Mus musculus 73-76 32956652-4 2021 Phosphorylation of the thiazide-sensitive sodium/chloride cotransporter NCC and its upstream activating kinase Ste20/SPS1-related proline/alanine rich kinase (SPAK), as well as the abundance of with no lysine kinase 4 (WNK4), were significantly reduced in the kidneys of NHA2 knock-out mice. Sodium 42-48 solute carrier family 12, member 3 Mus musculus 72-75 32956652-4 2021 Phosphorylation of the thiazide-sensitive sodium/chloride cotransporter NCC and its upstream activating kinase Ste20/SPS1-related proline/alanine rich kinase (SPAK), as well as the abundance of with no lysine kinase 4 (WNK4), were significantly reduced in the kidneys of NHA2 knock-out mice. Sodium 42-48 serine/threonine kinase 24 Mus musculus 111-116 32956652-4 2021 Phosphorylation of the thiazide-sensitive sodium/chloride cotransporter NCC and its upstream activating kinase Ste20/SPS1-related proline/alanine rich kinase (SPAK), as well as the abundance of with no lysine kinase 4 (WNK4), were significantly reduced in the kidneys of NHA2 knock-out mice. Sodium 42-48 selenophosphate synthetase 1 Mus musculus 117-121 33166587-2 2021 In normotensive rats, angiotensin II (ANG II)-induced sodium intake is blocked by the inactivation of p42/44 mitogen-activated protein kinase, also known as extracellular signal-regulated protein kinase1/2 (ERK1/2). Sodium 54-60 angiotensinogen Rattus norvegicus 22-36 33166587-2 2021 In normotensive rats, angiotensin II (ANG II)-induced sodium intake is blocked by the inactivation of p42/44 mitogen-activated protein kinase, also known as extracellular signal-regulated protein kinase1/2 (ERK1/2). Sodium 54-60 angiotensinogen Rattus norvegicus 38-44 33584198-1 2020 Dravet syndrome (DS) is an epileptic syndrome caused by mutations in the Scn1a gene encoding the alpha1 subunit of the sodium channel Nav1.1, which is associated with febrile seizures that progress to severe tonic-clonic seizures and associated comorbidities. Sodium 119-125 sodium channel, voltage-gated, type I, alpha Mus musculus 73-78 33524391-0 2021 Dietary sodium restriction alters muscle lipidomics that relates to insulin resistance in mice. Sodium 8-14 insulin Homo sapiens 68-75 33524391-2 2021 However, severe dietary sodium restriction promotes insulin resistance (IR) and dyslipidemia in animal models and humans. Sodium 24-30 insulin Homo sapiens 52-59 33511950-4 2022 Insulin-induced sympathetic activation, vasodilation, changes in vascular permeability and most importantly sodium retention play significant etiologic roles in the development of edema. Sodium 108-114 insulin Homo sapiens 0-7 33503881-7 2021 Presence of these substrates enables formation of SNAT6-caveolin complexes that aids in sodium dependent trafficking of SNAT6 off the plasma membrane. Sodium 88-94 solute carrier family 38 member 6 Homo sapiens 120-125 33552948-11 2020 Meanwhile, serum sodium was inversely correlated with cell counts of leukocytes, neutrophils, monocytes and C-reactive protein levels. Sodium 17-23 C-reactive protein Homo sapiens 108-126 33441779-2 2021 Since endothelial injury stimulates endothelial repair by enhancing CD34-positive cell production, the level of serum sodium may be inversely associated with that of circulating CD34-positive cells, thus indicating the degree of age-related endothelial injury. Sodium 118-124 CD34 molecule Homo sapiens 178-182 33532104-1 2021 Syndrome of inappropriate antidiuretic hormone (SIADH) is a disorder of fluid and sodium balance characterized by hypotonic hyponatremia, low plasma osmolality, and increased urine osmolality caused by excessive release of antidiuretic hormone (ADH). Sodium 82-88 arginine vasopressin Homo sapiens 26-46 33532104-1 2021 Syndrome of inappropriate antidiuretic hormone (SIADH) is a disorder of fluid and sodium balance characterized by hypotonic hyponatremia, low plasma osmolality, and increased urine osmolality caused by excessive release of antidiuretic hormone (ADH). Sodium 82-88 arginine vasopressin Homo sapiens 50-53 33460646-0 2021 Cryptic prokaryotic promoters explain instability of recombinant neuronal sodium channels in bacteria. Sodium 74-80 cripto, FRL-1, cryptic family 1 Homo sapiens 0-7 33478555-2 2021 Functional expression of the voltage-gated sodium channel NaV1.7 is under the control of SUMOylated collapsin response mediator protein 2 (CRMP2). Sodium 43-49 sodium channel, voltage-gated, type IX, alpha Mus musculus 58-64 33478555-2 2021 Functional expression of the voltage-gated sodium channel NaV1.7 is under the control of SUMOylated collapsin response mediator protein 2 (CRMP2). Sodium 43-49 dihydropyrimidinase-like 2 Mus musculus 100-137 33478555-2 2021 Functional expression of the voltage-gated sodium channel NaV1.7 is under the control of SUMOylated collapsin response mediator protein 2 (CRMP2). Sodium 43-49 dihydropyrimidinase-like 2 Mus musculus 139-144 33478555-8 2021 Finally, silencing these proteins in DRG neurons from female CRMP2K374A/K374A mice, restored the loss of sodium currents. Sodium 105-111 dihydropyrimidinase-like 2 Mus musculus 61-66 33478555-9 2021 Our study shows that the endocytic complex composed of Numb, Nedd4-2 and Eps15, is necessary for non-SUMOylated CRMP2-mediated internalization of sodium channels in vivo. Sodium 146-152 dihydropyrimidinase-like 2 Mus musculus 112-117 33441779-5 2021 Serum sodium concentration was positively associated with handgrip strength in non-hypertensive subjects [standardized parameter estimate (beta) = 0.29; p = 0.003], but not for hypertensive subjects (beta = 0.01; p = 0.878), while it was inversely associated with circulating CD34-positive cell levels in non-hypertensive subjects [simple correlation coefficient (r) = - 0.28; p = 0.002] but not for hypertensive subjects (r = - 0.07; p = 0.454). Sodium 6-12 CD34 molecule Homo sapiens 276-280 33441779-6 2021 For non-hypertensive elderly subjects, serum sodium concentration within the normal range is positively associated with handgrip strength and inversely associated with CD34-positive cells, thus partly indicating the degree of age-related endothelium injury. Sodium 45-51 CD34 molecule Homo sapiens 168-172 33436636-5 2021 We revealed that the intracellular domain of NRG1 interacts with the cytoplasmic loop 1 of Nav1.1, a sodium channel critical for the excitability of GABAergic interneurons, and inhibits Nav currents. Sodium 101-107 sodium channel, voltage-gated, type I, alpha Mus musculus 91-97 33489878-0 2020 Downregulation of miR-146b-3p Inhibits Proliferation and Migration and Modulates the Expression and Location of Sodium/Iodide Symporter in Dedifferentiated Thyroid Cancer by Potentially Targeting MUC20. Sodium 112-118 mucin 20, cell surface associated Homo sapiens 196-201 33436713-8 2021 The main independent risk factors associated with 72-h mortality among patients with AST levels >= 3000 U/L included higher serum values of alkaline phosphatase, creatine kinase, serum sodium, potassium, and phosphorus. Sodium 185-191 solute carrier family 17 member 5 Homo sapiens 85-88 33190558-10 2021 High-salt diet caused a rapid and sustained downregulation in mRNA encoding renal NHE3 (sodium-hydrogen-exchanger 3) and EnaC (epithelial sodium channel), although we did not observe a suppression in aldosterone until 7 days. Sodium 88-94 solute carrier family 9 (sodium/hydrogen exchanger), member 3 Mus musculus 82-86 33492304-9 2021 The mRNA and protein expression of sodium-dependent phosphorus transporter NPT-2b and Pit-1 on the membrane of the intestinal epithelial cells was detected by real-time polymerase chain reaction (PCR) and western blot analysis, respectively. Sodium 35-41 solute carrier family 34 (sodium phosphate), member 2 Mus musculus 75-81 33107589-13 2021 Our results help to explain why beta2 -m and RBP4 are more sensitive markers of PT dysfunction than albumin or alpha1 -m, and suggest that reduced PT sodium and water reabsorption in Fanconi syndrome may contribute to proteinuria. Sodium 150-156 glycoprotein hormone subunit alpha 2 Homo sapiens 32-37 32410367-9 2021 Claudin-3 and -6 may be associated with the transport of sodium through the bladder urothelium. Sodium 57-63 claudin 3 Rattus norvegicus 0-16 33250374-0 2021 Presynaptic congenital myasthenic syndrome due to three novel mutations in SLC5A7 encoding the sodium-dependant high-affinity choline transporter. Sodium 95-101 solute carrier family 5 member 7 Homo sapiens 75-81 33250374-1 2021 SLC5A7 encodes the presynaptic sodium-dependant high-affinity choline transporter 1 (CHT), which uptakes choline to the presynaptic nerve terminal following the breakdown of acetylcholine by the acetylcholinesterase within the synaptic cleft. Sodium 31-37 solute carrier family 5 member 7 Homo sapiens 0-6 33250374-1 2021 SLC5A7 encodes the presynaptic sodium-dependant high-affinity choline transporter 1 (CHT), which uptakes choline to the presynaptic nerve terminal following the breakdown of acetylcholine by the acetylcholinesterase within the synaptic cleft. Sodium 31-37 solute carrier family 5 member 7 Homo sapiens 48-83 33250374-1 2021 SLC5A7 encodes the presynaptic sodium-dependant high-affinity choline transporter 1 (CHT), which uptakes choline to the presynaptic nerve terminal following the breakdown of acetylcholine by the acetylcholinesterase within the synaptic cleft. Sodium 31-37 solute carrier family 5 member 7 Homo sapiens 85-88 33356004-1 2021 BACKGROUND: Furosemide inhibits the sodium potassium chloride cotransporter (NKCC2) in the thick ascending limb of the loop of Henle and increases urinary water and sodium excretion. Sodium 36-42 solute carrier family 12 member 1 Homo sapiens 77-82 33356004-1 2021 BACKGROUND: Furosemide inhibits the sodium potassium chloride cotransporter (NKCC2) in the thick ascending limb of the loop of Henle and increases urinary water and sodium excretion. Sodium 165-171 solute carrier family 12 member 1 Homo sapiens 77-82 33356011-2 2021 We tested the hypothesis that alpha1 -adrenergic blockade inhibits the increased BP response during and after 45-min stress in young normotensive Black adults, which may be mediated, in part, by dampened vasoconstriction and decreased renal sodium retention. Sodium 241-247 BCL2 related protein A1 Homo sapiens 30-36 33511145-3 2020 In the same patients, predialysis low serum sodium (sNa) has been associated with malnutrition and mortality. Sodium 44-50 snail family transcriptional repressor 1 Homo sapiens 52-55 33413413-12 2021 Sotagliflozin lowered diastolic [Ca2+] of CaT at baseline and in response to glucose influx, possibly related to a ~ 50% increase of sodium sodium-calcium exchanger (NCX) forward-mode activity. Sodium 133-139 solute carrier family 8 member A1 Rattus norvegicus 166-169 33413413-12 2021 Sotagliflozin lowered diastolic [Ca2+] of CaT at baseline and in response to glucose influx, possibly related to a ~ 50% increase of sodium sodium-calcium exchanger (NCX) forward-mode activity. Sodium 140-146 solute carrier family 8 member A1 Rattus norvegicus 166-169 33318128-1 2021 The sodium pump (Na+, K+-ATPase, NKA) is vital for animal cells, as it actively maintains Na+ and K+ electrochemical gradients across the cell membrane. Sodium 4-10 tachykinin precursor 1 Homo sapiens 33-36 33411788-1 2021 Dravet syndrome (DS) is a developmental and epileptic encephalopathy that results from mutations in the Nav1.1 sodium channel encoded by SCN1A. Sodium 111-117 sodium channel, voltage-gated, type I, alpha Mus musculus 104-110 33411788-1 2021 Dravet syndrome (DS) is a developmental and epileptic encephalopathy that results from mutations in the Nav1.1 sodium channel encoded by SCN1A. Sodium 111-117 sodium channel, voltage-gated, type I, alpha Mus musculus 137-142 33488393-3 2020 Our previous work identified adenoviral gene transfer of Hcn2 and SkM1, encoding a "funny current" and skeletal fast sodium current, respectively, as a potent combination to induce short-term biological pacing in dogs with atrioventricular block. Sodium 117-123 hyperpolarization activated cyclic nucleotide gated potassium and sodium channel 2 Canis lupus familiaris 57-61 33735863-14 2021 In addition, each increase in urinary sodium excretion by 2 SDs at year 1 increased prorenin and renin levels by 4 and 5% per year, respectively. Sodium 38-44 renin Homo sapiens 87-92 32980460-0 2021 Arsenic trioxide-increased MDCK cells proliferation requires activator protein 1-mediated increase of the sodium/proton exchanger 1 activity. Sodium 106-112 Jun proto-oncogene, AP-1 transcription factor subunit Canis lupus familiaris 61-80 33165026-12 2021 Treatment with mitochondrial damage-associated molecular patterns decreased the expression of epithelial sodium channel alpha, zonula occludens-1, and occludin via the formyl peptide receptor-1/p38 pathway in the primary rat alveolar epithelial type II cells. Sodium 105-111 formyl peptide receptor 1 Homo sapiens 168-193 32034761-3 2021 Actin binding proteins, including spectrin and alpha-actinin, serve as molecular linkages between the actin cytoskeleton and a diverse collection of receptors, including the NMDA receptor (NMDAR) and voltage gated sodium channels. Sodium 214-220 actinin alpha 1 Homo sapiens 47-60 33344518-2 2020 We previously demonstrated that sodium/glucose cotransporter 2 inhibitors (SGLT2i"s) have direct cardiac effects on ion homeostasis, possibly through inhibition of the cardiac sodium/hydrogen exchanger (NHE-1). Sodium 32-38 solute carrier family 9 (sodium/hydrogen exchanger), member 1 Mus musculus 203-208 33476169-10 2020 We conclude that the action potential conduction in the vagal motor fibers to the esophageal striated muscle in the mouse is mediated by TTX-sensitive voltage gated sodium channels including NaV1.7 and most probably NaV1.6. Sodium 165-171 sodium channel, voltage-gated, type IX, alpha Mus musculus 191-197 33615059-2 2021 However, there have been few reports regarding the importance of the change in serum sodium (SNa) concentration (DeltaSNa) during dialysis sessions. Sodium 85-91 snail family transcriptional repressor 1 Homo sapiens 93-96 33351140-11 2020 Higher plasma IL-6 and hsCRP levels correlated with increased muscle and skin sodium content in the overall study population. Sodium 78-84 interleukin 6 Homo sapiens 14-18 33419247-3 2020 There is substantial evidence that c-peptide counteracts the detrimental changes caused by hyperglycemia at the cellular level, such as decreased activation of endothelial nitric oxide synthase and sodium potassium ATPase, and increase in formation of pro-inflammatory molecules mediated by nuclear factor kappa-light-chain-enhancer of activated B cells: cytokines, chemokines, cell adhesion molecules, vascular endothelial growth factor, and transforming growth factor beta. Sodium 198-204 insulin Homo sapiens 35-44 33354677-9 2020 Rapid sodium correction rate (> 0.5 mmol/L/hr) was associated with an increased in-hospital mortality in both cohorts (Medical Information Mart for Intensive Care III: odds ratio, 1.08; 95% CI, 1.03-1.13 and electronic ICU: odds ratio, 1.10; 95% CI, 1.06-1.13). Sodium 6-12 septin 4 Homo sapiens 139-143 33344518-2 2020 We previously demonstrated that sodium/glucose cotransporter 2 inhibitors (SGLT2i"s) have direct cardiac effects on ion homeostasis, possibly through inhibition of the cardiac sodium/hydrogen exchanger (NHE-1). Sodium 176-182 solute carrier family 9 (sodium/hydrogen exchanger), member 1 Mus musculus 203-208 33362470-8 2020 Importantly, NGN2iSNs repetitively fire action potentials (APs) supported by voltage-gated sodium, potassium, and calcium conductances. Sodium 91-97 neurogenin 2 Rattus norvegicus 13-17 32529661-9 2020 Taken together, PCTR1 upregulates sodium channels" expression via activating the ALX/cAMP/P-Akt/Nedd4-2 pathway and increases Na, K-ATPase expression and activity to promote alveolar fluid clearance. Sodium 34-40 formyl peptide receptor 2-like Rattus norvegicus 81-84 33108349-0 2020 MIR448 antagomir reduces arrhythmic risk after myocardial infarction by upregulating the cardiac sodium channel. Sodium 97-103 microRNA 448 Homo sapiens 0-6 33108349-6 2020 miR-448 binding to this site suppressed SCN5A expression and sodium currents. Sodium 61-67 microRNA 448 Homo sapiens 0-7 32959887-0 2020 Discovery and characterization of ORM-11372, a unique and positively inotropic sodium-calcium exchanger/inhibitor. Sodium 79-85 orosomucoid 1 Homo sapiens 34-37 32815768-0 2020 Calmodulin binds to the N-terminal domain of the cardiac sodium channel Nav1.5. Sodium 57-63 calmodulin 1 Homo sapiens 0-10 32826430-11 2020 In exploratory analysis, the association of sodium levels and interleukin-6 levels (which has been linked to nonosmotic release of vasopressin) was assessed. Sodium 44-50 interleukin 6 Homo sapiens 62-75 32826430-11 2020 In exploratory analysis, the association of sodium levels and interleukin-6 levels (which has been linked to nonosmotic release of vasopressin) was assessed. Sodium 44-50 arginine vasopressin Homo sapiens 131-142 32826430-16 2020 Higher interleukin-6 levels correlated with lower sodium levels (p = 0.017). Sodium 50-56 interleukin 6 Homo sapiens 7-20 33055303-1 2020 Objective: Iodide transport across thyrocytes constitutes a critical step for thyroid hormone biosynthesis, mediated mainly by the basolateral sodium-iodide-symporter (NIS (SLC5A5)) and the apical anion exchanger pendrin (PDS (SLC26A4)). Sodium 143-149 solute carrier family 5 member 5 Homo sapiens 173-179 33124720-9 2020 SLC22A15 transport of several substrates was sodium-dependent and exhibited a higher Km for ergothioneine, carnitine, and carnosine compared to previously identified transporters for these ligands. Sodium 45-51 solute carrier family 22 member 15 Homo sapiens 0-8 33405317-0 2020 Role of free radical scavenging activity of vasoactive intestinal peptide in the attenuation of mitochondrial dysfunction to ameliorate dextran sulphate sodium-induced colitis in mice: Implications in ulcerative colitis. Sodium 153-159 vasoactive intestinal polypeptide Mus musculus 44-73 32750454-8 2020 Blocking epithelial sodium channel activity with Amiloride in Rrm2b-/- mice resulted in increased expression of its chaperone PCSK9 in the CCD, followed by elevated plasma levels and worsening hypercholesterolemia. Sodium 20-26 ribonucleotide reductase M2 B (TP53 inducible) Mus musculus 62-67 33329400-6 2020 We selected all hospitalized adult patients with RT-PCR-confirmed SARS-COV2 pneumonia and a registered admission serum sodium level (SNa). Sodium 119-125 snail family transcriptional repressor 1 Homo sapiens 133-136 33203750-10 2020 Our results suggest a novel mechanism by which the Na+-NQR system regulates antibiotic resistance via l-alanine metabolism in a cAMP/CRP complex-dependent manner.IMPORTANCE The Na+-NQR complex functions as a unique redox-driven sodium pump, generating membrane potential directly. Sodium 228-234 C-reactive protein Homo sapiens 133-136 32948286-3 2020 The voltage gated sodium channels contain a calmodulin (CaM)-binding IQ domain involved in channel slow inactivation, we here investigated the role of CaM regulation of Nav1.8 channel function, and showed that CaM enhanced slow inactivation of the Nav1.8 channel and hyperpolarized steady-state inactivation curve of sodium currents. Sodium 18-24 calmodulin 1 Homo sapiens 44-54 32948286-3 2020 The voltage gated sodium channels contain a calmodulin (CaM)-binding IQ domain involved in channel slow inactivation, we here investigated the role of CaM regulation of Nav1.8 channel function, and showed that CaM enhanced slow inactivation of the Nav1.8 channel and hyperpolarized steady-state inactivation curve of sodium currents. Sodium 18-24 calmodulin 1 Homo sapiens 56-59 32948286-3 2020 The voltage gated sodium channels contain a calmodulin (CaM)-binding IQ domain involved in channel slow inactivation, we here investigated the role of CaM regulation of Nav1.8 channel function, and showed that CaM enhanced slow inactivation of the Nav1.8 channel and hyperpolarized steady-state inactivation curve of sodium currents. Sodium 317-323 calmodulin 1 Homo sapiens 44-54 32948286-3 2020 The voltage gated sodium channels contain a calmodulin (CaM)-binding IQ domain involved in channel slow inactivation, we here investigated the role of CaM regulation of Nav1.8 channel function, and showed that CaM enhanced slow inactivation of the Nav1.8 channel and hyperpolarized steady-state inactivation curve of sodium currents. Sodium 317-323 calmodulin 1 Homo sapiens 56-59 33228183-4 2020 We observed that the upregulated expression of cardiac gene markers (NKX2-5, MYH6, TNNT2, and DES) and cardiac ion channel genes (sodium, calcium, the potassium) also the increased levels of Connexin 43 and Nkx2.5 proteins. Sodium 130-136 NK2 homeobox 5 Homo sapiens 69-75 33228183-4 2020 We observed that the upregulated expression of cardiac gene markers (NKX2-5, MYH6, TNNT2, and DES) and cardiac ion channel genes (sodium, calcium, the potassium) also the increased levels of Connexin 43 and Nkx2.5 proteins. Sodium 130-136 myosin heavy chain 6 Homo sapiens 77-81 33228183-4 2020 We observed that the upregulated expression of cardiac gene markers (NKX2-5, MYH6, TNNT2, and DES) and cardiac ion channel genes (sodium, calcium, the potassium) also the increased levels of Connexin 43 and Nkx2.5 proteins. Sodium 130-136 NK2 homeobox 5 Homo sapiens 207-213 33176139-4 2020 We show that leptin activates the sodium leak channel (NALCN), thereby depolarizing a subset of glutamatergic (VGluT2) LepRb NTS neurons expressing galanin. Sodium 34-40 galanin and GMAP prepropeptide Mus musculus 148-155 33165811-7 2021 Consistent with the previous results, sodium cantharidinate treatment decreased Bcl-2 and mitochondrial cytochrome-c protein expression, as well as phosphorylation of MDM2; meanwhile, it increased the levels of cleaved-caspase-3, cleaved-caspase-9, cleaved-PARP, Bax, and phosphorylated p53, thus inducing the apoptosis of pancreatic cancer cells. Sodium 38-44 BCL2 apoptosis regulator Homo sapiens 80-85 33165811-7 2021 Consistent with the previous results, sodium cantharidinate treatment decreased Bcl-2 and mitochondrial cytochrome-c protein expression, as well as phosphorylation of MDM2; meanwhile, it increased the levels of cleaved-caspase-3, cleaved-caspase-9, cleaved-PARP, Bax, and phosphorylated p53, thus inducing the apoptosis of pancreatic cancer cells. Sodium 38-44 cytochrome c, somatic Homo sapiens 104-116 33165811-7 2021 Consistent with the previous results, sodium cantharidinate treatment decreased Bcl-2 and mitochondrial cytochrome-c protein expression, as well as phosphorylation of MDM2; meanwhile, it increased the levels of cleaved-caspase-3, cleaved-caspase-9, cleaved-PARP, Bax, and phosphorylated p53, thus inducing the apoptosis of pancreatic cancer cells. Sodium 38-44 BCL2 associated X, apoptosis regulator Homo sapiens 263-266 33165811-7 2021 Consistent with the previous results, sodium cantharidinate treatment decreased Bcl-2 and mitochondrial cytochrome-c protein expression, as well as phosphorylation of MDM2; meanwhile, it increased the levels of cleaved-caspase-3, cleaved-caspase-9, cleaved-PARP, Bax, and phosphorylated p53, thus inducing the apoptosis of pancreatic cancer cells. Sodium 38-44 tumor protein p53 Homo sapiens 287-290 33328060-4 2020 Vasodilation also results in activation of the renin-angiotensin-aldosterone axis, which combined with changing tubular handling causes alterations in total body stores of electrolytes and total body water, resulting in a lower serum sodium concentration. Sodium 234-240 renin Homo sapiens 47-52 32979291-5 2020 Mouse models have suggested that Scn2a-, Scn3a-, and Scn8a-linked DEE variants are, in general, gain of function, resulting in increased persistent or resurgent sodium current (INa ) and pyramidal neuron hyperexcitability. Sodium 161-167 sodium channel, voltage-gated, type III, alpha Mus musculus 41-46 32394465-1 2020 Mutations in the SCN1A gene encoding the Nav1.1 sodium channel cause several forms of epilepsy, the most severe is Dravet syndrome (DS). Sodium 48-54 sodium channel, voltage-gated, type I, alpha Mus musculus 17-22 32394465-1 2020 Mutations in the SCN1A gene encoding the Nav1.1 sodium channel cause several forms of epilepsy, the most severe is Dravet syndrome (DS). Sodium 48-54 sodium channel, voltage-gated, type I, alpha Mus musculus 41-47 32934003-8 2020 Our results also suggest that SBMA and ALS share common axonal excitability changes; increased nodal persistent sodium and reduced potassium currents that may accelerate motor neuronal death and differently affect axons-innervating different muscles. Sodium 112-118 androgen receptor Homo sapiens 30-34 33254575-7 2020 ACE2 mediated dysregulation of sodium dependent glucose transporter (SGLT1 or SLC5A1) in the intestinal epithelium also links it to the pathogenesis of diabetes mellitus which can be a possible reason for the associated mortality in COVID-19 patients with diabetes. Sodium 31-37 solute carrier family 5 member 1 Homo sapiens 69-74 33254575-7 2020 ACE2 mediated dysregulation of sodium dependent glucose transporter (SGLT1 or SLC5A1) in the intestinal epithelium also links it to the pathogenesis of diabetes mellitus which can be a possible reason for the associated mortality in COVID-19 patients with diabetes. Sodium 31-37 solute carrier family 5 member 1 Homo sapiens 78-84 33185386-2 2020 Nav1.8 is an isoform of voltage-gated sodium channels and its expression regulation is closely related with PDN. Sodium 38-44 sodium voltage-gated channel alpha subunit 10 Rattus norvegicus 0-6 33350197-11 2020 We obtained 21 key targets, 154 signal pathways, and 382 biological processes in topological, GO, and KEGG enrichment analysis of the protein interaction network, and in the comprehensive analysis, it was found that Zuomua Decoction could reduce blood pressure by regulating renin angiotension aldosterone system, balancing the concentration of intracellular calcium and sodium ions and regulating vasoconstriction and relaxation. Sodium 371-377 renin Homo sapiens 275-280 33063475-9 2020 CONCLUSIONS: Elevation of ET-1 is related to clinical signs of peripheral congestion, low urine sodium excretion, and poor outcome in AHF. Sodium 96-102 endothelin 1 Homo sapiens 26-30 33167557-1 2020 BACKGROUND: Overcorrection of serum sodium (SNa) during therapy of hyponatremia can result in osmotic demyelination syndrome. Sodium 36-42 snail family transcriptional repressor 1 Homo sapiens 44-47 33105763-2 2020 By inhibiting sodium and glucose reabsorption from the proximal tubules, the improvement in insulin resistance and natriuresis improved the cardiovascular mortality in diabetes mellitus (DM) patients. Sodium 14-20 insulin Homo sapiens 92-99 33054868-10 2021 Among children higher sodium intakes were associated with higher intake of SSBs (4 studies, n=10,329, b=22, 16,26 g/d), no studies were retrieved for adults. Sodium 22-28 NADH:ubiquinone oxidoreductase subunit B9 Homo sapiens 102-106 33210088-9 2020 Subsequently, a vasopressin infusion was started with normalisation of diuresis and plasma sodium concentration by the end of surgery. Sodium 91-97 arginine vasopressin Homo sapiens 16-27 32963591-2 2020 Mutations in SLC34A3, the gene encoding the sodium-dependent cotransporter NPT2c, have previously been described as a cause of HHRH. Sodium 44-50 solute carrier family 34 member 3 Homo sapiens 13-20 33057157-2 2020 Additionally, [Na+]o modulates cardiomyocyte contractility via a sodium-calcium exchanger (NCX) mediated pathway. Sodium 65-71 solute carrier family 8 member A1 Rattus norvegicus 91-94 32840624-7 2020 The most significant locus was rs77958157 near cocaine- and amphetamine-regulated transcript prepropeptide (CARTPT) , a gene involved in eating behavior and appetite regulation (P = 2.3 x 10-8 with sodium-to-potassium ratio). Sodium 198-204 CART prepropeptide Homo sapiens 47-106 32840624-7 2020 The most significant locus was rs77958157 near cocaine- and amphetamine-regulated transcript prepropeptide (CARTPT) , a gene involved in eating behavior and appetite regulation (P = 2.3 x 10-8 with sodium-to-potassium ratio). Sodium 198-204 CART prepropeptide Homo sapiens 108-114 33020520-7 2020 Furthermore, inhibition of voltage-gated sodium channels mimicked the Cav1 loss-of-function phenotype. Sodium 41-47 caveolin 1 L homeolog Xenopus laevis 70-74 32799394-9 2020 These data emphasize a critical contribution of the NOX4-mediated pathway in maladaptive upregulation of ENaC-mediated sodium reabsorption in the distal nephron in the conditions of HS- and hyperglycemia-induced kidney injury. Sodium 119-125 sodium channel epithelial 1 subunit gamma Rattus norvegicus 105-109 32940654-0 2020 GRK4-Mediated Adiponectin Receptor-1 Phosphorylative Desensitization as a Novel Mechanism of Reduced Renal Sodium Excretion in Hypertension. Sodium 107-113 adiponectin receptor 1 Rattus norvegicus 14-36 31955161-12 2021 CONCLUSIONS: We thus have identified novel genes that might regulate vasopressin gene expression in the hypothalamus controlling the magnocellular neurons secretory response to body sodium depletion and consequently hypotonic stress. Sodium 182-188 arginine vasopressin Rattus norvegicus 69-80 33061491-9 2020 In multivariate linear-regression models (beta, CI), the day:night ratio of sodium excretion was significantly associated with arterial stiffness (cf-PWV -0.386, -0.559, -0.213, p <= 0.001) and with central hemodynamic parameters (cSBP -1.655, -2.800, -0.510; p <= 0.001; cDBP -1.319, -2.218, -0.420, p <= 0.001). Sodium 76-82 mitogen-activated protein kinase 14 Homo sapiens 231-238 32701602-7 2020 Individual subsets of activated T cells can secrete tumor necrosis factor-alpha (TNF-alpha), interleukin-17a (IL-17a), and interferon-gamma (IFN-gamma), each of which has augmented the elevation of blood pressure in hypertensive models by enhancing renal sodium transport. Sodium 255-261 interferon gamma Homo sapiens 141-150 33177919-3 2020 Activated corin cleaves pro-ANP to ANP, which regulates water-sodium balance and lowers blood pressure. Sodium 62-68 corin, serine peptidase Mus musculus 10-15 32891121-7 2020 Patients with lower serum sodium concentrations were older and had lower hemoglobin, calcium, phosphorus, and albumin levels. Sodium 26-32 albumin Homo sapiens 110-117 32940654-3 2020 Despite the established association between obesity/excess adiposity and hypertension, whether and how adiponectin, one of the adipokines, contributes to impaired sodium excretion in hypertension has not been previously investigated. Sodium 163-169 adiponectin, C1Q and collagen domain containing Homo sapiens 103-114 32940654-9 2020 Finally, we identified G protein-coupled receptor kinase 4 (GRK4) as a mediator of adiponectin receptor hyper-phosphorylation; mice transgenic for a hyperphosphorilating variant of GRK4 replicated the abnormal adiponectin function observed in SHRs, whereas down-regulation of GRK4 by renal-ultrasound-directed siRNA restored the adiponectin-mediated sodium excretion and reduced the blood pressure in SHRs. Sodium 350-356 G protein-coupled receptor kinase 4 Mus musculus 23-58 32940654-9 2020 Finally, we identified G protein-coupled receptor kinase 4 (GRK4) as a mediator of adiponectin receptor hyper-phosphorylation; mice transgenic for a hyperphosphorilating variant of GRK4 replicated the abnormal adiponectin function observed in SHRs, whereas down-regulation of GRK4 by renal-ultrasound-directed siRNA restored the adiponectin-mediated sodium excretion and reduced the blood pressure in SHRs. Sodium 350-356 G protein-coupled receptor kinase 4 Mus musculus 60-64 32940654-9 2020 Finally, we identified G protein-coupled receptor kinase 4 (GRK4) as a mediator of adiponectin receptor hyper-phosphorylation; mice transgenic for a hyperphosphorilating variant of GRK4 replicated the abnormal adiponectin function observed in SHRs, whereas down-regulation of GRK4 by renal-ultrasound-directed siRNA restored the adiponectin-mediated sodium excretion and reduced the blood pressure in SHRs. Sodium 350-356 G protein-coupled receptor kinase 4 Mus musculus 181-185 32940654-9 2020 Finally, we identified G protein-coupled receptor kinase 4 (GRK4) as a mediator of adiponectin receptor hyper-phosphorylation; mice transgenic for a hyperphosphorilating variant of GRK4 replicated the abnormal adiponectin function observed in SHRs, whereas down-regulation of GRK4 by renal-ultrasound-directed siRNA restored the adiponectin-mediated sodium excretion and reduced the blood pressure in SHRs. Sodium 350-356 G protein-coupled receptor kinase 4 Mus musculus 181-185 32940654-10 2020 We conclude that the stimulatory effect of adiponectin on sodium excretion is impaired in hypertension, which is ascribed to the increased renal GRK4 expression and activity. Sodium 58-64 G protein-coupled receptor kinase 4 Mus musculus 145-149 32940654-11 2020 Targeting GRK4 restores impaired adiponectin-mediated sodium excretion in hypertension, thus representing a novel strategy against hypertension. Sodium 54-60 G protein-coupled receptor kinase 4 Mus musculus 10-14 32788559-1 2020 BACKGROUND: Voltage-gated sodium channel Nav1.7 has been validated as a perspective target for selective inhibitors with analgesic and anti-itch activity. Sodium 26-32 sodium channel, voltage-gated, type IX, alpha Mus musculus 41-47 32788559-1 2020 BACKGROUND: Voltage-gated sodium channel Nav1.7 has been validated as a perspective target for selective inhibitors with analgesic and anti-itch activity. Sodium 26-32 itchy, E3 ubiquitin protein ligase Mus musculus 140-144 32788559-3 2020 The authors hypothesized that their approach would yield at least one new compound that inhibits sodium currents in vitro and exerts analgesic and anti-itch effects in mice. Sodium 97-103 itchy, E3 ubiquitin protein ligase Mus musculus 152-156 32903427-3 2020 While activation of the sodium-potassium-ATPase (NKA) in response to an elevation of extracellular K+ may decrease intracellular Na+, the cotransport of transmitters, such as glutamate, together with Na+ results in an increase in astrocytic Na+. Sodium 24-30 tachykinin precursor 1 Homo sapiens 49-52 32687659-3 2020 Persistently increased activity of G protein-coupled receptor kinase 4 (GRK4), caused by increased expression or genetic variants (eg, GRKgamma142V), impairs the ability of the kidney to excrete a sodium load, in part, by impairing renal dopamine D1 receptor function through persistent phosphorylation. Sodium 197-203 G protein-coupled receptor kinase 4 Mus musculus 35-70 32687659-3 2020 Persistently increased activity of G protein-coupled receptor kinase 4 (GRK4), caused by increased expression or genetic variants (eg, GRKgamma142V), impairs the ability of the kidney to excrete a sodium load, in part, by impairing renal dopamine D1 receptor function through persistent phosphorylation. Sodium 197-203 G protein-coupled receptor kinase 4 Mus musculus 72-76 32685251-3 2020 Close control and prompt substitution of serum sodium is required in neonates with advanced heart failure on high-dose vasopressin therapy. Sodium 47-53 arginine vasopressin Homo sapiens 119-130 32535224-1 2020 Rimeporide, a first-in-class sodium/proton exchanger Type 1 inhibitor (NHE-1 inhibitor) is repositioned by EspeRare for patients with Duchenne Muscular Dystrophy (DMD). Sodium 29-35 solute carrier family 9 member A1 Homo sapiens 71-76 32522618-4 2020 The construction of a pharmacophore model and the in silico molecular docking of EMB and CLX into the human voltage-gated sodium channel hNaV1.7 allowed establishing that these molecules are structurally similar to local anesthetics and other NaV channel blockers and can bind to the same site receptor in NaV channels; suggesting that both molecules are active components in T. roseus venom. Sodium 122-128 embigin Homo sapiens 81-84 32848094-1 2020 Dravet syndrome (DS) is an intractable developmental and epileptic encephalopathy caused largely by de novo variants in the SCN1A gene, resulting in haploinsufficiency of the voltage-gated sodium channel alpha subunit NaV1.1. Sodium 189-195 sodium channel, voltage-gated, type I, alpha Mus musculus 124-129 32922301-2 2020 TNF alpha reduces fluid absorption due to impairment of sodium and chloride transport required for building an osmotic gradient across epithelial cells, which in the airways maintains airway surface liquid helping to keep airways open and enabling bacterial clearance and aids water absorption from the alveolar spaces. Sodium 56-62 tumor necrosis factor Homo sapiens 0-9 32922301-6 2020 Confirmation of hypothesis and implications: The role of a reduction in the function of epithelial sodium and chloride transport could with regards to chloride transport be tested by analysis of chloride levels in exhaled breath condensate and levels correlated with TNF alpha concentrations. Sodium 99-105 tumor necrosis factor Homo sapiens 267-276 32790113-2 2020 Insulin treatment is associated with sodium and water retention, weight gain, and hypoglycaemia-all pathophysiological mechanisms related to HF decompensation. Sodium 37-43 insulin Homo sapiens 0-7 32673289-4 2020 Three new, inducible murine models were used to determine that HDAC1 and HDAC2 in the kidney epithelium are necessary for maintaining epithelial integrity and maintaining fluid-electrolyte balance during increased dietary sodium intake. Sodium 222-228 histone deacetylase 2 Mus musculus 73-78 32673289-5 2020 Moreover, single nucleus RNA sequencing determined that epithelial HDAC1 and HDAC2 are necessary for expression of many sodium or water transporters and channels. Sodium 120-126 histone deacetylase 2 Mus musculus 77-82 32631918-5 2020 Scnn1b-Tg mice overexpress the epithelial Na+ channel (ENaC) in their lungs, driving increased sodium absorption that causes lung pathology similar to CF. Sodium 95-101 sodium channel, nonvoltage-gated 1 beta Mus musculus 0-6 32665491-4 2020 RESULTS: RYR1-p.G2435R mouse muscle cells have chronically elevated intracellular resting calcium and sodium and rate of manganese quench (homozygous greater than heterozygous) compared with wild-type muscles. Sodium 102-108 ryanodine receptor 1, skeletal muscle Mus musculus 9-13 32665491-5 2020 After exposure to 1-oleoyl-2-acetyl-sn-glycerol, a TRPC3/6 activator, increases in intracellular resting calcium/sodium were significantly greater in RYR1-p.G2435R muscles (from 153 +- 11 nM/10 +- 0.5 mM to 304 +- 45 nM/14.2 +- 0.7 mM in heterozygotes P < 0.001] and from 251 +- 25 nM/13.9 +- 0.5 mM to 534 +- 64 nM/20.9 +- 1.5 mM in homozygotes [P < 0.001] compared with 123 +- 3 nM/8 +- 0.1 mM to 196 +- 27 nM/9.4 +- 0.7 mM in wild type). Sodium 113-119 transient receptor potential cation channel, subfamily C, member 3 Mus musculus 51-58 32665491-5 2020 After exposure to 1-oleoyl-2-acetyl-sn-glycerol, a TRPC3/6 activator, increases in intracellular resting calcium/sodium were significantly greater in RYR1-p.G2435R muscles (from 153 +- 11 nM/10 +- 0.5 mM to 304 +- 45 nM/14.2 +- 0.7 mM in heterozygotes P < 0.001] and from 251 +- 25 nM/13.9 +- 0.5 mM to 534 +- 64 nM/20.9 +- 1.5 mM in homozygotes [P < 0.001] compared with 123 +- 3 nM/8 +- 0.1 mM to 196 +- 27 nM/9.4 +- 0.7 mM in wild type). Sodium 113-119 ryanodine receptor 1, skeletal muscle Mus musculus 150-154 32624180-3 2020 We discovered a novel inhibitor, EOS789, that interacts with several sodium-dependent phosphate transporters (NaPi-IIb, PiT-1, and PiT-2) known to contribute to intestinal phosphate absorption. Sodium 69-75 POU class 1 homeobox 1 Rattus norvegicus 120-125 32606316-2 2020 The resulting defect in the cystic fibrosis transmembrane conductance regulator protein (CFTR) results in defective chloride and bicarbonate secretion, as well as dysregulation of epithelial sodium channels (ENaC). Sodium 191-197 CF transmembrane conductance regulator Homo sapiens 28-79 32606316-2 2020 The resulting defect in the cystic fibrosis transmembrane conductance regulator protein (CFTR) results in defective chloride and bicarbonate secretion, as well as dysregulation of epithelial sodium channels (ENaC). Sodium 191-197 CF transmembrane conductance regulator Homo sapiens 89-93 32573098-5 2020 Mechanistically, several calcium-handling proteins, including the sodium-calcium exchanger (NCX), contributed to ETC. Sodium 66-72 solute carrier family 8 member A1 Rattus norvegicus 92-95 32342987-4 2020 The mechanism of the intestinal glucose transport was elucidated throughout the gene expression of the intestinal glucose transporters, which included sodium dependent glucose transporter (SGLT1) and glucose transporter 2 (GLUT2), using quantitative real-time polymerase chain reaction (qRT-PCR). Sodium 151-157 solute carrier family 5 member 1 Homo sapiens 189-194 31828722-3 2020 The present results indicated that sodium fluoride (NaF) exposure to adult male golden hamsters severely impairs reproductive physiology as evident from markedly reduced sperm count/viability, testosterone level, androgen receptor (AR), testicular glucose transporter (GLUT-1), gap junction (connexin-43), and survival (Bcl-2) protein expression. Sodium 52-55 apoptosis regulator Bcl-2 Mesocricetus auratus 320-325 31828722-4 2020 NaF exposure markedly increased testicular oxidative load, inflammatory (NF-kB/COX-2), and apoptotic (caspase-3) protein expression. Sodium 0-3 cytochrome c oxidase subunit II Mesocricetus auratus 79-84 31756485-1 2020 As polysaccharide from Bletilla striata (BSP) was anticipated with mucoadhesive improvement in sodium alginate (SA) microspheres, BSP was mixed with SA to construct a composite microsphere to retain in the gastrointestinal tract for a long time. Sodium 95-101 integrin-binding sialoprotein Rattus norvegicus 41-44 33214341-0 2020 Potassium-dependent sodium/calcium exchanger 3 (Nckx3) depletion leads to abnormal motor function and social behavior in mice. Sodium 20-26 solute carrier family 24 (sodium/potassium/calcium exchanger), member 3 Mus musculus 48-53 32407847-9 2020 However, significant restoration of sodium, testosterone, and luteinizing hormone was apparent in CCl4 exposed rats received HES and/or TR. Sodium 36-42 C-C motif chemokine ligand 4 Rattus norvegicus 98-102 32848771-2 2020 The association between SCN10A/voltage-gated sodium channel 1.8 (NaV1.8) and cardiac conduction has been demonstrated; however, the exact role of SCN10A/NaV1.8 in the heart rate response to atropine remains unclear. Sodium 45-51 sodium channel, voltage-gated, type X, alpha Mus musculus 65-71 32770661-1 2020 Human studies have demonstrated that physiologically relevant changes in circulating glucagon-like peptide-1 (GLP-1) elicit a rapid increase in renal sodium excretion when combined with expansion of the extracellular fluid volume. Sodium 150-156 glucagon Homo sapiens 85-108 32770661-1 2020 Human studies have demonstrated that physiologically relevant changes in circulating glucagon-like peptide-1 (GLP-1) elicit a rapid increase in renal sodium excretion when combined with expansion of the extracellular fluid volume. Sodium 150-156 glucagon Homo sapiens 110-115 32770661-3 2020 This study was designed to investigate the hypothesis that the postprandial GLP-1 plasma concentration is sensitive to the sodium content in the meal. Sodium 123-129 glucagon Homo sapiens 76-81 32770661-11 2020 Sodium intake in addition to a glucose load selectively amplifies the postprandial GLP-1 plasma concentration. Sodium 0-6 glucagon Homo sapiens 83-88 32474115-8 2020 The protein expression of epithelial sodium channel (ENaC) was detected by Western blot. Sodium 37-43 sodium channel epithelial 1 subunit gamma Rattus norvegicus 53-57 32503841-9 2020 Despite these observations, palmitoylation-null beta1-p.C162A modulated sodium current and sorted to detergent-resistant membrane fractions normally. Sodium 72-78 BCL2 related protein A1 Homo sapiens 48-53 32532820-4 2020 Conversely, PTC cells in which MED16 had been further knocked down (MED16KD) exhibited enhanced cell migration, epithelial-mesenchymal transition (EMT), and RAI resistance, accompanied by decreased sodium/iodide symporter (NIS) levels. Sodium 198-204 mediator complex subunit 16 Homo sapiens 31-36 32683248-2 2020 Niacin is transported into the cells by the monocarboxylate transporters: sodium-dependent monocarboxylate transporter (SMCT1 and SMCT2) and monocarboxylate transporter (MCT1). Sodium 74-80 modifier of curly tail 1 Mus musculus 121-125 32418916-0 2020 Contribution of the neuronal sodium channel NaV1.8 to sodium- and calcium-dependent cellular proarrhythmia. Sodium 29-35 sodium channel, voltage-gated, type X, alpha Mus musculus 44-50 32909725-4 2020 These findings are consistent with abnormally increased renal sodium reabsorption, possibly caused by increased angiotensin II activity secondary to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-induced downregulation of angiotensin-converting enzyme 2 (ACE2) receptors. Sodium 62-68 angiotensinogen Homo sapiens 112-126 32194062-1 2020 Krokinobacter rhodopsin 2 (KR2) was discovered as the first light-driven sodium pumping rhodopsin (NaR) in 2013, which contains unique amino acid residues on C-helix (N112, D116, and Q123), referred to as an NDQ motif. Sodium 73-79 rhodopsin Homo sapiens 14-23 32645220-2 2020 FHF1 encodes a cytosolic protein that modulates neuronal sodium channel gating. Sodium 57-63 fibroblast growth factor 12 Homo sapiens 0-4 32437854-5 2020 Interactions with proteins such as N-methyl-D-aspartate receptors, syntaxin1A as well as voltage-gated calcium and sodium channels, suggest that CRMP2 may control both the electrical and chemical components of synaptic transmission. Sodium 115-121 dihydropyrimidinase like 2 Homo sapiens 145-150 31898359-8 2020 The expression of cardiomyocytes genes MYH6, TNNT2, DES together with ion channels genes of the heart (sodium, calcium, and potassium) decreased in p31/33 induced AF-MSCs. Sodium 103-109 ATPase H+ transporting V1 subunit E1 Homo sapiens 148-151 33040821-16 2020 Low-dose insulin combined with electrolyte supplementation is effective in the treatment of DKA in children, which can effectively control blood sugar, sodium, potassium level, and inflammatory factor concentration. Sodium 152-158 insulin Homo sapiens 9-16 32434409-7 2020 To explain these observations, we identified that TDAG51-/- VSMCs express reduced levels of the type III sodium-dependent Pi transporter, Pit-1, a solute transporter, a solute transporter, a solute transporter responsible for cellular Pi uptake. Sodium 105-111 pleckstrin homology like domain family A member 1 Homo sapiens 50-56 32311027-1 2020 CONTEXT: Hypophosphatemia and metabolic bone disease are associated with Hereditary Hypophosphatemic Rickets with Hypercalciuria (HHRH) due to biallelic mutations of SLC34A3 encoding the NPT2C sodium-phosphate cotransporter and Nephrolithiasis/osteoporosis, hypophosphatemic 1 (NPHLOP1) due to monoallelic mutations in SLC34A1 encoding the NPT2A sodium-phosphate cotransporter. Sodium 193-199 solute carrier family 34 member 3 Homo sapiens 166-173 32311027-1 2020 CONTEXT: Hypophosphatemia and metabolic bone disease are associated with Hereditary Hypophosphatemic Rickets with Hypercalciuria (HHRH) due to biallelic mutations of SLC34A3 encoding the NPT2C sodium-phosphate cotransporter and Nephrolithiasis/osteoporosis, hypophosphatemic 1 (NPHLOP1) due to monoallelic mutations in SLC34A1 encoding the NPT2A sodium-phosphate cotransporter. Sodium 346-352 solute carrier family 34 member 3 Homo sapiens 166-173 32360664-8 2020 Other cell-type specific processes altered in SOD1 mutant brainstem include those from motor neurons (axon regeneration, voltage-gated sodium and potassium channels underlying excitability, potassium ion transport), trigeminal sensory neurons (detection of temperature stimulus involved in sensory perception), and cellular response to toxic substances (uncharacterized cell populations). Sodium 135-141 superoxide dismutase 1, soluble Mus musculus 46-50 32545167-1 2020 NaV1.3 is a subtype of the voltage-gated sodium channel family. Sodium 41-47 sodium channel, voltage-gated, type III, alpha Mus musculus 0-6 32374170-0 2020 Core-Shell C@Sb Nanoparticles as a Nucleation Layer for High-Performance Sodium Metal Anodes. Sodium 73-85 chorionic somatomammotropin hormone 2 Homo sapiens 11-15 32374170-3 2020 Herein, we report that a nucleation buffer layer comprising elaborately-designed core-shell C@Sb nanoparticles (NPs) enables the homogenous electrochemical deposition of sodium metal for long-term cycling. Sodium 170-182 chorionic somatomammotropin hormone 2 Homo sapiens 92-96 32374170-4 2020 These C@Sb NPs can increase active sites for initial sodium nucleation through Sb-Na alloy cores, and keep these cores stable through carbon shells. Sodium 53-59 chorionic somatomammotropin hormone 2 Homo sapiens 6-10 32521252-1 2020 The transmembrane sodium-calcium (Na-Ca) exchanger 1 (NCX1) regulates cytoplasmic Ca levels by facilitating electrogenic exchange of Ca for Na. Sodium 18-24 solute carrier family 8 member A1 Homo sapiens 54-58 31833589-3 2020 A novel modified NaY zeolite (SMZ-La) with hexadecyl trimethyl ammonium bromide (HDTMA) and lanthanum (La) as modifying agents for NO3 - -N adsorption was investigated in this study. Sodium 17-20 NBL1, DAN family BMP antagonist Homo sapiens 131-134 32572427-4 2020 Serum 5-HT levels were detected with ELISA, and potassium/sodium hyperpolarization activated cyclic nucleotide-gated channel 2 (HCN2) and tryptophan hydroxylase 1 (TPH1) expression levels in colon epithelium of offspring were detected by Western blot and RT-qPCR. Sodium 58-64 tryptophan hydroxylase 1 Mus musculus 164-168 32571373-3 2020 We recently discovered that peripheral nerve injury-induced upregulation of an axonal guidance phosphoprotein collapsin response mediator protein 2 (CRMP2) and the N-type voltage-gated calcium (CaV2.2) as well as the NaV1.7 voltage-gated sodium channel, correlates with the development of neuropathic pain. Sodium 238-244 dihydropyrimidinase like 2 Homo sapiens 110-147 32571373-3 2020 We recently discovered that peripheral nerve injury-induced upregulation of an axonal guidance phosphoprotein collapsin response mediator protein 2 (CRMP2) and the N-type voltage-gated calcium (CaV2.2) as well as the NaV1.7 voltage-gated sodium channel, correlates with the development of neuropathic pain. Sodium 238-244 dihydropyrimidinase like 2 Homo sapiens 149-154 32368909-1 2020 Voltage-gated sodium channel NaV1.7 is a genetically validated target for pain. Sodium 14-20 sodium channel, voltage-gated, type IX, alpha Mus musculus 29-35 32418916-0 2020 Contribution of the neuronal sodium channel NaV1.8 to sodium- and calcium-dependent cellular proarrhythmia. Sodium 54-60 sodium channel, voltage-gated, type X, alpha Mus musculus 44-50 32045803-3 2020 By rationally controlling synthetic parameters, we find that optimum Cu0.3@Cu0.7CoOx@GO achieves a superior catalytic activity with a turnover frequency of 44.6 molH2 molM-1 min-1 in H2O and 98.2 molH2 molM-1 min-1 in 0.2 M NaOH, better than most of previously reported NM-free nanocatalysts. Sodium 224-228 CD59 molecule (CD59 blood group) Homo sapiens 174-179 32045803-3 2020 By rationally controlling synthetic parameters, we find that optimum Cu0.3@Cu0.7CoOx@GO achieves a superior catalytic activity with a turnover frequency of 44.6 molH2 molM-1 min-1 in H2O and 98.2 molH2 molM-1 min-1 in 0.2 M NaOH, better than most of previously reported NM-free nanocatalysts. Sodium 224-228 CD59 molecule (CD59 blood group) Homo sapiens 209-214 32129567-9 2020 Our research found that HIF-1alpha played a protective role in dextran sulphate sodium-induced colitis, which was partly due to its regulation of tight junction (TJ) protein expression. Sodium 80-86 hypoxia inducible factor 1 subunit alpha Homo sapiens 24-34 31797525-12 2020 Alizarin Red staining revealed enhanced mineralization in 50 muM NaF treated BMMSCs with increased expression of Runx2 and Osteocalcin, indicating their upregulated osteogenic differentiation. Sodium 65-68 RUNX family transcription factor 2 Rattus norvegicus 113-118 31797525-12 2020 Alizarin Red staining revealed enhanced mineralization in 50 muM NaF treated BMMSCs with increased expression of Runx2 and Osteocalcin, indicating their upregulated osteogenic differentiation. Sodium 65-68 bone gamma-carboxyglutamate protein Rattus norvegicus 123-134 31816431-4 2020 RESULTS: - Higher baseline copeptin correlated with higher HbA1c, lower 24-hour urine volume and sodium excretion, after correcting for age, sex, systolic blood pressure, and HbA1c. Sodium 97-103 arginine vasopressin Homo sapiens 27-35 32152499-2 2020 Hyperfiltration mainly occurs in response to signals passed from the tubule to the glomerulus: high levels of glucose in the glomerular filtrate drive increased reabsorption of glucose and sodium by the sodium-glucose cotransporters SGLT2 and SGLT1 in the proximal tubule. Sodium 189-195 solute carrier family 5 member 1 Homo sapiens 243-248 32066060-11 2020 Notably, NaAsO2 treatment diminished the interaction between SFPQ and miR92b-5p, accompanied by decreased binding between miR-92b-5p and 3"-UTR of DUOX2. Sodium 9-15 splicing factor proline and glutamine rich Homo sapiens 61-65 32066060-11 2020 Notably, NaAsO2 treatment diminished the interaction between SFPQ and miR92b-5p, accompanied by decreased binding between miR-92b-5p and 3"-UTR of DUOX2. Sodium 9-15 dual oxidase 2 Homo sapiens 147-152 32279611-1 2020 Background: To verify the hypothesis that the nature of trigeminal neuralgia (TN) is an ectopic impulse induced by sodium channel modulated by cytokines, we conducted an animal study using the infraorbital nerve chronic constriction injury (CCI) model in rats.Method: The expression of Nav1.3 or IL-6 in the infraorbital nerve (ION) and trigeminal ganglion (TG) were detected by western blot and immunocytochemistry after administration of antisense oligodeoxynucleotide sequence (AS), IL-6 or Anti-IL-6.Results: With intrathecal administration of AS or mismatch oligodeoxynucleotide sequence (MM) in the CCI rats, the Nav1.3-IR in ION and TG accounted for 2.2 +- 0.51% and 8.5 +- 3.1% in AS+CCI group vs. 6.9 +- 1.3% and 38.7 +- 4.8% in MM+CCI group (p < 0.05), respectively. Sodium 115-121 interleukin 6 Rattus norvegicus 296-300 32279611-1 2020 Background: To verify the hypothesis that the nature of trigeminal neuralgia (TN) is an ectopic impulse induced by sodium channel modulated by cytokines, we conducted an animal study using the infraorbital nerve chronic constriction injury (CCI) model in rats.Method: The expression of Nav1.3 or IL-6 in the infraorbital nerve (ION) and trigeminal ganglion (TG) were detected by western blot and immunocytochemistry after administration of antisense oligodeoxynucleotide sequence (AS), IL-6 or Anti-IL-6.Results: With intrathecal administration of AS or mismatch oligodeoxynucleotide sequence (MM) in the CCI rats, the Nav1.3-IR in ION and TG accounted for 2.2 +- 0.51% and 8.5 +- 3.1% in AS+CCI group vs. 6.9 +- 1.3% and 38.7 +- 4.8% in MM+CCI group (p < 0.05), respectively. Sodium 115-121 interleukin 6 Rattus norvegicus 486-490 32441256-5 2020 Mechanistically, PGE2 sensitizes dorsal root ganglia (DRG) neurons by modifying the voltage-gated sodium channel NaV1.8, evidenced by that genetically or pharmacologically inhibiting NaV1.8 in DRG neurons can substantially attenuate OA. Sodium 98-104 sodium channel, voltage-gated, type X, alpha Mus musculus 113-119 32565909-11 2020 In addition, the expression of sodium channel protein type 5 subunit alpha (SCN5A) and beta-2 adrenergic receptor (ADRB2) was downregulated, while muscarinic acetylcholine receptor M2 (CHRM2) was upregulated in the WXKL group (P < 0.05). Sodium 31-37 adrenoceptor beta 2 Sus scrofa 115-120 31972340-5 2020 Then, bovine mammary epithelial cells (BMECs) were isolated, and oxidative stress-related protein expression was measured, confirming that sodium butyrate (NaB) exerted antioxidant effects through GPR109A, NRF2 and H3K9/14 acetylation. Sodium 156-159 NFE2 like bZIP transcription factor 2 Bos taurus 206-210 32441256-5 2020 Mechanistically, PGE2 sensitizes dorsal root ganglia (DRG) neurons by modifying the voltage-gated sodium channel NaV1.8, evidenced by that genetically or pharmacologically inhibiting NaV1.8 in DRG neurons can substantially attenuate OA. Sodium 98-104 sodium channel, voltage-gated, type X, alpha Mus musculus 183-189 32390535-1 2020 Background Arginine vasopressin dependent antidiuresis plays a key role in water-sodium retention in heart failure. Sodium 81-87 arginine vasopressin Rattus norvegicus 20-31 32343134-3 2020 ET-1, a 21-amino acid residue peptide, plays fundamental roles in basal vascular tone, sodium balance, cell proliferation, and stress-responsive regulation. Sodium 87-93 endothelin 1 Homo sapiens 0-4 32385249-1 2020 The sodium channels Nav1.7, Nav1.8 and Nav1.9 are critical for pain perception in peripheral nociceptors. Sodium 4-10 sodium channel, voltage-gated, type IX, alpha Mus musculus 20-26 32392309-2 2020 Retinoschisin specifically interacts with the retinal sodium-potassium adenosine triphosphatase (Na/K-ATPase), a transmembrane ion pump. Sodium 54-60 retinoschisis (X-linked, juvenile) 1 (human) Mus musculus 0-13 32385249-1 2020 The sodium channels Nav1.7, Nav1.8 and Nav1.9 are critical for pain perception in peripheral nociceptors. Sodium 4-10 sodium channel, voltage-gated, type X, alpha Mus musculus 28-34 32385331-1 2020 Oral rehydration solutions (ORSs) is the key treatment of acute diarrhea in children, as it restores the electrolyte balance by stimulating the intestinal sodium/glucose transporter SGLT1 to induce fluid absorption. Sodium 155-161 solute carrier family 5 member 1 Homo sapiens 182-187 31916038-0 2020 Sodium absorption stimulator prostasin (PRSS8) has an anti-inflammatory effect via downregulation of TLR4 signaling in inflammatory bowel disease. Sodium 0-6 toll-like receptor 4 Mus musculus 101-105 32524056-3 2020 A favorable response to the sodium blocker phenytoin was reported in several cases, both in patients with an intragenic mutation and in patients with a duplication of FGF12. Sodium 28-34 fibroblast growth factor 12 Homo sapiens 167-172 32431610-5 2020 Recent cryo-electron microscopy structures of human KCNQ1 and hERG, along with the rat homolog of SCN5A and other mammalian sodium channels, provide atomic-level insight into the structure and function of these proteins that advance our understanding of their distinct functions in the cardiac action potential, as well as the molecular basis of LQTS. Sodium 124-130 ETS transcription factor ERG Homo sapiens 62-66 32058911-2 2020 Results showed that MEC-AGS yielded a higher proportion of CH4 than MEC (83.8 +- 0.4% vs 82.0 +- 1.0%, P < 0.05) with sodium acetate (NaAc) as the only carbon source. Sodium 137-141 C-C motif chemokine ligand 28 Homo sapiens 20-23 32172011-1 2020 Sodium-calcium exchanger (NCX) 1 and 3, have been demonstrated to play a relevant role in controlling the intracellular homeostasis of sodium and calcium ions in physiological and patho-physiological conditions. Sodium 135-141 solute carrier family 8 member A1 Homo sapiens 0-38 32259613-9 2020 The Low-sodium and High fiber diets had the greatest lowering effect on SBP and DBP in T2D patients. Sodium 8-14 D-box binding PAR bZIP transcription factor Homo sapiens 80-83 32259613-11 2020 The High-fiber and Low-sodium diets had the greatest lowering effect on SBP and DBP in T2D. Sodium 23-29 D-box binding PAR bZIP transcription factor Homo sapiens 80-83 32045596-1 2020 The voltage sodium channel 1.8 (NaV1.8) in the dorsal root ganglion (DRG) neurons contributes to the initiation and development of chronic inflammatory and neuropathic pain. Sodium 12-18 sodium voltage-gated channel alpha subunit 10 Rattus norvegicus 32-38 31420581-8 2020 QR showed that the consumption of sodium was positively associated with SBP (P10) and DBP (P10) in males, and positively associated with DBP (P80-P90) alone in females. Sodium 34-40 S100 calcium binding protein A10 Homo sapiens 77-80 31420581-8 2020 QR showed that the consumption of sodium was positively associated with SBP (P10) and DBP (P10) in males, and positively associated with DBP (P80-P90) alone in females. Sodium 34-40 S100 calcium binding protein A10 Homo sapiens 91-94 31420581-10 2020 Sodium to potassium ratio was positively associated with SBP (P10-P50, P80) and DBP (P70-P90) in males, and was positively associated with SBP(P10-P70, P90) in females. Sodium 0-6 S100 calcium binding protein A10 Homo sapiens 62-65 31635654-3 2020 A 98.4% photodegradation of 2,3-dichlorophenol (50 mg L-1) was attained in the presence of Bi2WO6/NaBiO3 (1:10) under the visible-light irradiation in 30 min. Sodium 98-104 L1 cell adhesion molecule Homo sapiens 54-57 30676433-6 2020 We recommend close monitoring of serum sodium levels and clinical status in patients with diabetes insipidus who have optic-hypothalamic gliomas and are started on treatment with MEK inhibitors. Sodium 39-45 mitogen-activated protein kinase kinase 7 Homo sapiens 179-182 32130622-1 2020 Mammalian Na+/H+ exchanger type I isoform (NHE1) is a ubiquitously expressed membrane protein that regulates intracellular pH (pHi) by removing one intracellular proton in exchange for one extracellular sodium ion. Sodium 203-209 solute carrier family 9 member A1 Homo sapiens 43-47 32227118-0 2020 An inducible intestinal epithelial cell-specific NHE3 knockout mouse model mimicking congenital sodium diarrhea. Sodium 96-102 solute carrier family 9 (sodium/hydrogen exchanger), member 3 Mus musculus 49-53 32426035-5 2020 In this model system and in the setting of furosemide-induced sodium excretion, alpha 2-AR activation inhibited adenylate cyclase, suppressed cAMP formation, and caused sodium retention. Sodium 169-175 glycoprotein hormone subunit alpha 2 Homo sapiens 80-87 32344597-0 2020 Does ENaC Work as Sodium Taste Receptor in Humans? Sodium 18-24 sodium channel epithelial 1 subunit gamma Rattus norvegicus 5-9 32344597-6 2020 In animal models, such as the mouse and the rat, the epithelial sodium channel (ENaC) has been proposed as a key protein for recognizing Na+ and for mediating preference responses to low-medium salt concentrations. Sodium 64-70 sodium channel epithelial 1 subunit gamma Rattus norvegicus 80-84 32018999-9 2020 The adsorption mechanism was ascribed to the inner-sphere surface complexation of Pb(II) by these groups and to the ion exchange between Pb(II) and Na(I). Sodium 148-153 submaxillary gland androgen regulated protein 3B Homo sapiens 82-88 31954305-8 2020 SNP/NaHS under stress increased activation of superoxide dismutase (SOD), peroxidase (POX), APX, glutathione reductase (GR), monodehydroascorbate reductase (MDHAR), dehydroascorbate reductase (DHAR), ascorbate (tAsA) and glutathione (GSH). Sodium 4-8 POD1 Triticum aestivum 92-95 32129084-5 2020 Based on the understanding that cAMP is a key regulator of epithelial sodium channel (ENaC), which is the limited step in sodium transport, we hypothesized that A2BAR signaling may affect AFC in acute lung injury (ALI) through regulating ENaC via cAMP, thus attenuating pulmonary edema. Sodium 70-76 sodium channel epithelial 1 subunit gamma Rattus norvegicus 86-90 32129084-5 2020 Based on the understanding that cAMP is a key regulator of epithelial sodium channel (ENaC), which is the limited step in sodium transport, we hypothesized that A2BAR signaling may affect AFC in acute lung injury (ALI) through regulating ENaC via cAMP, thus attenuating pulmonary edema. Sodium 122-128 sodium channel epithelial 1 subunit gamma Rattus norvegicus 86-90 31652395-10 2020 The CYP3A5*3/*3 genotype was associated with a higher serum sodium level in the patients with volume overload. Sodium 60-66 cytochrome P450 family 3 subfamily A member 5 Homo sapiens 4-10 31652395-13 2020 CYP3A5-deficient patients treated with tolvaptan had a higher serum sodium level. Sodium 68-74 cytochrome P450 family 3 subfamily A member 5 Homo sapiens 0-6 31911180-3 2020 Exposure of pancreatic tumor cells to [neratinib + sodium valproate] initially reduced the expression and phosphorylation of ERBB family receptors, c-MET and c-KIT. Sodium 51-57 MET proto-oncogene, receptor tyrosine kinase Homo sapiens 148-153 31911180-3 2020 Exposure of pancreatic tumor cells to [neratinib + sodium valproate] initially reduced the expression and phosphorylation of ERBB family receptors, c-MET and c-KIT. Sodium 51-57 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 158-163 31771816-5 2020 NaHS significantly increased the expressions of tight junction proteins (i.e., ZO-1, Occludin and claudin-1), and reduced apoptosis and secretion of pro-inflammatory cytokines (i.e., TNF-alpha, IL-6 and IL-1beta) in CS-exposed mouse lungs and CSE-incubated A549 cells, indicating H2S inhibits CS-induced inflammation, injury and apoptosis in alveolar epithelial cells. Sodium 0-4 tight junction protein 1 Mus musculus 79-83 31771816-5 2020 NaHS significantly increased the expressions of tight junction proteins (i.e., ZO-1, Occludin and claudin-1), and reduced apoptosis and secretion of pro-inflammatory cytokines (i.e., TNF-alpha, IL-6 and IL-1beta) in CS-exposed mouse lungs and CSE-incubated A549 cells, indicating H2S inhibits CS-induced inflammation, injury and apoptosis in alveolar epithelial cells. Sodium 0-4 occludin Mus musculus 85-93 31771816-5 2020 NaHS significantly increased the expressions of tight junction proteins (i.e., ZO-1, Occludin and claudin-1), and reduced apoptosis and secretion of pro-inflammatory cytokines (i.e., TNF-alpha, IL-6 and IL-1beta) in CS-exposed mouse lungs and CSE-incubated A549 cells, indicating H2S inhibits CS-induced inflammation, injury and apoptosis in alveolar epithelial cells. Sodium 0-4 tumor necrosis factor Mus musculus 183-192 31771816-5 2020 NaHS significantly increased the expressions of tight junction proteins (i.e., ZO-1, Occludin and claudin-1), and reduced apoptosis and secretion of pro-inflammatory cytokines (i.e., TNF-alpha, IL-6 and IL-1beta) in CS-exposed mouse lungs and CSE-incubated A549 cells, indicating H2S inhibits CS-induced inflammation, injury and apoptosis in alveolar epithelial cells. Sodium 0-4 interleukin 6 Mus musculus 194-198 31771816-5 2020 NaHS significantly increased the expressions of tight junction proteins (i.e., ZO-1, Occludin and claudin-1), and reduced apoptosis and secretion of pro-inflammatory cytokines (i.e., TNF-alpha, IL-6 and IL-1beta) in CS-exposed mouse lungs and CSE-incubated A549 cells, indicating H2S inhibits CS-induced inflammation, injury and apoptosis in alveolar epithelial cells. Sodium 0-4 interleukin 1 beta Mus musculus 203-211 31771816-7 2020 Moreover, NaHS inhibited CS-induced phosphorylation of ERK, JNK and p38 MAPK in vivo and in vitro, and treatment with their inhibitors reversed CSE-induced ZO-1 expression and inflammation in A549 cells. Sodium 10-14 tight junction protein 1 Mus musculus 156-160 31935586-2 2020 Ag nanoparticles were employed in freestanding and binder-free F-GNS electrode (the composite film electrode was labeled as FGA) as catalyst, which were shown to strongly facilitate the decomposition of NaF during charge process in sodium/carbon fluorides (Na/CFx) secondary batteries. Sodium 232-238 fibrinogen alpha chain Homo sapiens 124-127 31935586-2 2020 Ag nanoparticles were employed in freestanding and binder-free F-GNS electrode (the composite film electrode was labeled as FGA) as catalyst, which were shown to strongly facilitate the decomposition of NaF during charge process in sodium/carbon fluorides (Na/CFx) secondary batteries. Sodium 232-238 C-X-C motif chemokine ligand 8 Homo sapiens 203-206 30149743-5 2020 We measured serum sodium (SNa) levels at least once a week after the second week. Sodium 18-24 snail family transcriptional repressor 1 Homo sapiens 26-29 32004973-7 2020 The activation of the P2X7R can open the ion channels on the tumor cell membrane (sodium ion, calcium ion influx and potassium ion outflow), trigger rearrangement of the cytoskeleton and changes in membrane fluidity, allow small molecule substances to enter the cell, activate enzymes and kinases in related signaling pathways in cells (such as PKA, PKC, ERK1/2, AKT, and JNK), thereby affecting the development of tumor cells, and can also indirectly affect the growth, apoptosis and migration of tumor cells through tumor microenvironment. Sodium 82-88 purinergic receptor P2X 7 Homo sapiens 22-27 32423964-12 2020 Under these conditions, insulin still enhanced both glucose and sodium excretion. Sodium 64-70 insulin Homo sapiens 24-31 32423964-13 2020 CONCLUSIONS: Acute exogenous insulin infusion jointly stimulates renal glucose and sodium excretion, indicating that the effect may be mediated by SGLTs. Sodium 83-89 insulin Homo sapiens 29-36 31578830-3 2020 Here, we found that TXNIP expression induced by sodium butyrate (NaBu) was TRAF6-dependent. Sodium 65-69 thioredoxin interacting protein Homo sapiens 20-25 31578830-6 2020 NaBu reinforced the interaction of TRAF6/TXNIP as well as TXNIP" polyubiquitylation. Sodium 0-4 thioredoxin interacting protein Homo sapiens 41-46 31578830-6 2020 NaBu reinforced the interaction of TRAF6/TXNIP as well as TXNIP" polyubiquitylation. Sodium 0-4 thioredoxin interacting protein Homo sapiens 58-63 31578830-7 2020 Moreover, treated with NaBu, the A549 cells with TRAF6/TXNIP double knockdown showed an enhanced protein expression of E-cadherin comparing to cells with single gene or negative knockdown. Sodium 23-27 thioredoxin interacting protein Homo sapiens 55-60 31578830-7 2020 Moreover, treated with NaBu, the A549 cells with TRAF6/TXNIP double knockdown showed an enhanced protein expression of E-cadherin comparing to cells with single gene or negative knockdown. Sodium 23-27 cadherin 1 Homo sapiens 119-129 31578830-10 2020 Our results revealed TRAF6 regulated the expression and polyubiquitylation of TXNIP in a NaBu-dependent manner, alleviating tumorigenesis of TRAF6. Sodium 89-93 thioredoxin interacting protein Homo sapiens 78-83 32752588-0 2020 PI3K/Akt and ERK1/2 pathways are responsible for sodium butyrateinduced inhibition of neuronal apoptosis in rats with cerebral infarction. Sodium 49-55 AKT serine/threonine kinase 1 Rattus norvegicus 5-8 31420581-10 2020 Sodium to potassium ratio was positively associated with SBP (P10-P50, P80) and DBP (P70-P90) in males, and was positively associated with SBP(P10-P70, P90) in females. Sodium 0-6 S100 calcium binding protein A10 Homo sapiens 143-146 32391491-1 2020 In this work, by density functional theory (DFT) calculations, sp-sp2-hybridized boron-doped graphdiyne (BGDY) nanosheets have been investigated as an anode material for sodium storage. Sodium 170-176 Sp2 transcription factor Homo sapiens 66-69 32006563-10 2020 Co-Immunoprecipitation and immunoblotting were conducted to demonstrate that SAM/NaHS suppressed the assembly of CaMKII with the ASK1-MKK3-p38 signal module after cerebral I/R, which decreased the phosphorylation of p38. Sodium 81-85 mitogen-activated protein kinase 14 Homo sapiens 139-142 32006563-10 2020 Co-Immunoprecipitation and immunoblotting were conducted to demonstrate that SAM/NaHS suppressed the assembly of CaMKII with the ASK1-MKK3-p38 signal module after cerebral I/R, which decreased the phosphorylation of p38. Sodium 81-85 mitogen-activated protein kinase 14 Homo sapiens 216-219 32006563-12 2020 Taken together, the results suggested that SAM/NaHS could suppress cerebral I/R injury by downregulating p38 phosphorylation via decreasing the assembly of CaMKII with the ASK1-MKK3-p38 signal module. Sodium 47-51 mitogen-activated protein kinase 14 Homo sapiens 105-108 32006563-12 2020 Taken together, the results suggested that SAM/NaHS could suppress cerebral I/R injury by downregulating p38 phosphorylation via decreasing the assembly of CaMKII with the ASK1-MKK3-p38 signal module. Sodium 47-51 mitogen-activated protein kinase 14 Homo sapiens 182-185 32037087-9 2020 Treatment with NaHS also increased cell apoptosis by downregulating AKT/NF-kappaB signaling. Sodium 15-19 AKT serine/threonine kinase 1 Homo sapiens 68-71 32037087-9 2020 Treatment with NaHS also increased cell apoptosis by downregulating AKT/NF-kappaB signaling. Sodium 15-19 nuclear factor kappa B subunit 1 Homo sapiens 72-81 31918016-13 2020 CONCLUSIONS: NaFTV and QrLx treatment could decrease symptoms and inflammatory colitis, by decreasing of FICZ concentration and AhR signaling in colon, resulting in reducing the expression of IL-6, STAT3, and RORgammat, whereas increasing the expression of FOXP3, consequently reducing the proportion of Th17 cells and increasing the proportion of Treg cells, respectively. Sodium 13-18 aryl-hydrocarbon receptor Mus musculus 128-131 31918016-13 2020 CONCLUSIONS: NaFTV and QrLx treatment could decrease symptoms and inflammatory colitis, by decreasing of FICZ concentration and AhR signaling in colon, resulting in reducing the expression of IL-6, STAT3, and RORgammat, whereas increasing the expression of FOXP3, consequently reducing the proportion of Th17 cells and increasing the proportion of Treg cells, respectively. Sodium 13-18 interleukin 6 Mus musculus 192-196 31918016-13 2020 CONCLUSIONS: NaFTV and QrLx treatment could decrease symptoms and inflammatory colitis, by decreasing of FICZ concentration and AhR signaling in colon, resulting in reducing the expression of IL-6, STAT3, and RORgammat, whereas increasing the expression of FOXP3, consequently reducing the proportion of Th17 cells and increasing the proportion of Treg cells, respectively. Sodium 13-18 signal transducer and activator of transcription 3 Mus musculus 198-203 32252091-9 2020 Serum albumin showed a strong, negative correlation with soleus sodium concentrations in HD patients (r = -0.81, P < 0.01). Sodium 64-70 albumin Homo sapiens 0-13 31794131-0 2020 Rebuttal to Editorial: sodium retention by uPA in nephrotic syndrome? Sodium 23-29 plasminogen activator, urokinase Homo sapiens 43-46 31769840-3 2020 Glucose is absorbed via sodium (Na)-dependent glucose co-transport (SGLT1; SLC5A1) along the brush border membrane (BBM) of intestinal absorptive villus cells. Sodium 24-30 solute carrier family 5 member 1 Homo sapiens 68-73 31769840-3 2020 Glucose is absorbed via sodium (Na)-dependent glucose co-transport (SGLT1; SLC5A1) along the brush border membrane (BBM) of intestinal absorptive villus cells. Sodium 24-30 solute carrier family 5 member 1 Homo sapiens 75-81 32059997-1 2020 The inappropriate over-activation of the with-no-lysine kinase (WNK)-STE20/SPS1-related proline/alanine-rich kinase (SPAK)-sodium chloride cotransporter (NCC) phosphorylation cascade increases sodium reabsorption in distal kidney nephrons, resulting in salt-sensitive hypertension. Sodium 123-129 serine/threonine kinase 24 Mus musculus 69-74 31815915-0 2020 Dexpramipexole blocks Nav1.8 sodium channels and provides analgesia in multiple nociceptive and neuropathic pain models. Sodium 29-35 sodium channel, voltage-gated, type X, alpha Mus musculus 22-28 31815915-1 2020 Selective targeting of sodium channel subtypes Nav1.7, Nav1.8 and Nav1.9, preferentially expressed by peripheral nociceptors, represents a unique opportunity to develop analgesics devoid of central side effects. Sodium 23-29 sodium channel, voltage-gated, type IX, alpha Mus musculus 47-53 31815915-1 2020 Selective targeting of sodium channel subtypes Nav1.7, Nav1.8 and Nav1.9, preferentially expressed by peripheral nociceptors, represents a unique opportunity to develop analgesics devoid of central side effects. Sodium 23-29 sodium channel, voltage-gated, type X, alpha Mus musculus 55-61 32420151-12 2020 KEGG pathway analysis indicated that the common DEGs were particularly enriched in HIF-1 signaling pathway and aldosterone-regulated sodium reabsorption. Sodium 133-139 hypoxia inducible factor 1 subunit alpha Homo sapiens 83-88 32043994-4 2020 The microwave-assisted extraction in the presence of NaCl (10 g L-1) and NaOH (10 g L-1) was used for the isolation of arsenic species from the Lewatit FO 36 resin gel. Sodium 73-77 immunoglobulin kappa variable 1-16 Homo sapiens 84-87 31713651-8 2020 The fast H2S donor, NaHS, elicited a full and biphasic vasorelaxation response in mesenteric arteries (EC50 (1) 8.7 muM, EC50 (2) 0.6 mM), which was significantly inhibited in eNOS-/- vessels (P < 0.05), unaffected by endothelial removal, or blockers at any point in the NO via soluble guanylate cyclase and cGMP (NO-sGC-cGMP) vasorelaxation pathway. Sodium 20-24 latexin Homo sapiens 116-119 32059758-6 2020 We show a polymorph-dependent differential synaptic redistribution of alpha3-Na+/K+-ATPase, GluA2 subunit containing alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors, and GluN2B-subunit containing N-methyl-D-aspartate receptors, but not GluA1 subunit containing alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid and metabotropic glutamate receptor 5 receptors. Sodium 70-79 glutamate receptor, metabotropic 5 Mus musculus 341-374 32256376-1 2020 Canonical epithelial sodium channels (ENaCs) are heterotrimers formed by alpha, beta, and gamma ENaC subunits in vertebrates and belong to the Degenerin/ENaC family of proteins. Sodium 21-27 sodium channel, non voltage gated 1 gamma subunit S homeolog Xenopus laevis 90-100 32036698-9 2020 Additionally, model simulations highlight sodium handling in the kidney and renal sympathetic nerve activity sensitivity as key players in the increased resistance of females to angiotensin II-induced hypertension compared to males. Sodium 42-48 angiotensinogen Rattus norvegicus 178-192 32226389-6 2020 Such electrophysiological changes could be attributed to an increase in inward sodium current density and a decrease in funny current densities, which is consistent with the observed up- and downregulated SCN1B and HCN2/4 transcripts, respectively. Sodium 79-85 hyperpolarization activated cyclic nucleotide gated potassium and sodium channel 2 Homo sapiens 215-221 32178452-7 2020 The water secretion phase is triggered by an apical low volume-dependent factor opening the Cystic Fibrosis Transmembrane Regulator CFTR channel and secreting anions that are accompanied by paracellular sodium and water transport. Sodium 203-209 CF transmembrane conductance regulator Homo sapiens 132-136 32210813-7 2020 Consistent with a conserved structure-function amongst sodium-dependent neurotransmitter transporters, S1 residues A73, A77 (G100 in hSERT), N78, V148 (I150 in hSERT), N153, G320, F329 (Y331 in d DAT), N350, and G423 are conserved in DAT and SERT, indicating they likely play conserved functional roles. Sodium 55-61 solute carrier family 6 member 4 Homo sapiens 133-138 32210813-7 2020 Consistent with a conserved structure-function amongst sodium-dependent neurotransmitter transporters, S1 residues A73, A77 (G100 in hSERT), N78, V148 (I150 in hSERT), N153, G320, F329 (Y331 in d DAT), N350, and G423 are conserved in DAT and SERT, indicating they likely play conserved functional roles. Sodium 55-61 solute carrier family 6 member 4 Homo sapiens 160-165 31957111-5 2020 Furthermore, we found that NaB inhibited migration and induced AMPK/mTOR pathway-activated autophagy and reactive oxygen species (ROS) overproduction via the miR-139-5p/Bmi-1 axis. Sodium 27-30 mechanistic target of rapamycin kinase Homo sapiens 68-72 31935590-6 2020 Although palmitoylation does not regulate the normal forward or reverse ion transport modes of NCX1, NCX1 palmitoylation is required for its inactivation: sodium-dependent inactivation and inactivation by PIP2 depletion are significantly impaired for unpalmitoylatable NCX1. Sodium 155-161 solute carrier family 8 member A1 Homo sapiens 101-105 31935590-6 2020 Although palmitoylation does not regulate the normal forward or reverse ion transport modes of NCX1, NCX1 palmitoylation is required for its inactivation: sodium-dependent inactivation and inactivation by PIP2 depletion are significantly impaired for unpalmitoylatable NCX1. Sodium 155-161 solute carrier family 8 member A1 Homo sapiens 101-105 31925683-6 2020 The optimum catalyst dosage for both Mn-doped ZnS quantum dots capped by L-cysteine and Mn-doped ZnS on zeolite NaY was 0.017 g L-1 and for Mn-doped ZnS quantum dots capped by polyethylene glycol was 0.033 g L-1. Sodium 104-115 immunoglobulin kappa variable 1-16 Homo sapiens 128-131 31927508-0 2020 Accelerated liver recovery after acute CCl4 poisoning in rats treated with sodium phthalhydrazide. Sodium 75-97 C-C motif chemokine ligand 4 Rattus norvegicus 39-43 31830809-1 2020 Dravet Syndrome (DS) is a neurodevelopmental genetic disorder caused by mutations in the SCN1A gene encoding the subunit of the NaV1.1 voltage-gated sodium channel that controls neuronal action potential firing. Sodium 151-157 sodium channel, voltage-gated, type I, alpha Mus musculus 89-94 31830809-1 2020 Dravet Syndrome (DS) is a neurodevelopmental genetic disorder caused by mutations in the SCN1A gene encoding the subunit of the NaV1.1 voltage-gated sodium channel that controls neuronal action potential firing. Sodium 151-157 sodium channel, voltage-gated, type I, alpha Mus musculus 130-136 31922248-0 2020 A novel mutation in GPD1-L associated with early repolarization syndrome via modulation of cardiomyocyte fast sodium currents. Sodium 110-116 glycerol-3-phosphate dehydrogenase 1 like Homo sapiens 20-26 31901681-1 2020 As a solute carrier electrogenic transporter, the sodium/calcium exchanger (NCX1-3/SLC8A1-A3) links the trans-plasmalemmal gradients of sodium and calcium ions (Na+, Ca2+) to the membrane potential of astrocytes. Sodium 50-56 solute carrier family 8 member A1 Homo sapiens 76-82 31901681-1 2020 As a solute carrier electrogenic transporter, the sodium/calcium exchanger (NCX1-3/SLC8A1-A3) links the trans-plasmalemmal gradients of sodium and calcium ions (Na+, Ca2+) to the membrane potential of astrocytes. Sodium 136-142 solute carrier family 8 member A1 Homo sapiens 76-82 31868637-6 2020 With an initial OTC concentration of 44 muM, after 30 min the removal rates of chemical oxygen demand (COD) by Raw-GF and NaOH-GF were 59.18% and 83.75%, respectively. Sodium 122-126 latexin Homo sapiens 40-43 31756367-5 2020 We review the evidence for an important role of sodium-coupled glucose uptake through SGLT1 for carbohydrate sensing, of free-fatty acid receptors FFAR1/FFAR4 and the monoacyl-glycerol sensing receptor GPR119 for lipid detection, of the calcium-sensing receptor CASR and GPR142 for protein sensing, and additional modulation by neurotransmitters such as somatostatin and galanin. Sodium 48-54 solute carrier family 5 member 1 Homo sapiens 86-91 31756367-5 2020 We review the evidence for an important role of sodium-coupled glucose uptake through SGLT1 for carbohydrate sensing, of free-fatty acid receptors FFAR1/FFAR4 and the monoacyl-glycerol sensing receptor GPR119 for lipid detection, of the calcium-sensing receptor CASR and GPR142 for protein sensing, and additional modulation by neurotransmitters such as somatostatin and galanin. Sodium 48-54 calcium sensing receptor Homo sapiens 262-266 31887021-0 2020 Allosteric Communication to the Retinal Chromophore upon Ion Binding in a Light-driven Sodium Ion Pumping Rhodopsin. Sodium 87-93 rhodopsin Homo sapiens 106-115 32041305-9 2020 Regarding the interaction of NaDC with serum albumin (SA), albumin is determined in human serum samples as human serum albumin (HSA), which was collected from different volunteers of different ages and gender. Sodium 29-33 albumin Homo sapiens 39-52 32041305-9 2020 Regarding the interaction of NaDC with serum albumin (SA), albumin is determined in human serum samples as human serum albumin (HSA), which was collected from different volunteers of different ages and gender. Sodium 29-33 albumin Homo sapiens 113-126 31904729-0 2020 Sphingosine-1-phosphate signal transducer and activator of transcription 3 signaling pathway contributes to baicalein-mediated inhibition of dextran sulfate sodium-induced experimental colitis in mice. Sodium 157-163 signal transducer and activator of transcription 3 Homo sapiens 24-74 32016357-0 2020 All-trans retinoic acid reduces the transcriptional regulation of intestinal sodium-dependent phosphate co-transporter gene (Npt2b). Sodium 77-83 solute carrier family 34 (sodium phosphate), member 2 Mus musculus 125-130 32016357-1 2020 Inorganic phosphate (Pi) homeostasis is regulated by intestinal absorption via type II sodium-dependent co-transporter (Npt2b) and by renal reabsorption via Npt2a and Npt2c. Sodium 87-93 solute carrier family 34 (sodium phosphate), member 2 Mus musculus 120-125 32079768-3 2020 Compared with other ligands, AngII promotes more-substantial rearrangements not only at the bottom of the ligand-binding pocket but also in a key polar network in the receptor core, which forms a sodium-binding site in most GPCRs. Sodium 196-202 angiotensinogen Homo sapiens 29-34 31887021-1 2020 Krokinobacter rhodopsin 2 (KR2) serves as a light-driven sodium ion pump in the presence of sodium ion and works as a proton pump in the presence of larger monovalent cations such as potassium ion, rubidium ion, and cesium ion. Sodium 57-63 rhodopsin Homo sapiens 14-23 31887021-1 2020 Krokinobacter rhodopsin 2 (KR2) serves as a light-driven sodium ion pump in the presence of sodium ion and works as a proton pump in the presence of larger monovalent cations such as potassium ion, rubidium ion, and cesium ion. Sodium 92-98 rhodopsin Homo sapiens 14-23 31886722-2 2020 Our results have revealed a complex set of mechanisms consisting in 1) well-known PiT1/PiT2-mediated sodium-dependent Pi transport; 2) Slc20-unrelated sodium-dependent Pi transport that is sensitive to the stilbene derivatives 4,4"-diisothiocyanatostilbene-2,2"-disulphonic acid (DIDS) and (4-acetamido-4-isothiocyanostilbene-2,2-disulfonate) (SITS); 3) a sodium-independent Pi uptake system that is competitively inhibited by sulfate, bicarbonate, and arsenate and is weakly inhibited by DIDS, SITS, and phosphonoformate; and 4) an exit pathway from the cell that is partially chloride-dependent and unrelated to the known anion-exchangers expressed in VSMC. Sodium 101-107 POU class 1 homeobox 1 Rattus norvegicus 82-86 31944097-3 2020 Topologically, the 4-c Na(I) ion directs in situ assembly of 4-c SDCA linker and 6-c Co(II) ion, resulting in the formation of 4,4,6-c net with a topology named as smm3. Sodium 23-28 mitochondrially encoded cytochrome c oxidase II Homo sapiens 85-91 31952079-5 2020 Similar to ASIC1a, E18" residues create an energetic preference for sodium ions at the lower end of the pore in ASIC2a-containing channels. Sodium 68-74 acid sensing ion channel subunit 2 Homo sapiens 112-118 31626714-0 2020 Voltage-gated sodium channels beta3 subunit promotes tumorigenesis in hepatocellular carcinoma by facilitating p53 degradation. Sodium 14-20 tumor protein p53 Homo sapiens 111-114 31908015-3 2020 At day 2 after the induction of NS, the increased abundance of NHE3 and phosphorylated NCC in nephrotic mice compared with controls suggest that early sodium retention occurs mainly in the proximal and distal tubules. Sodium 151-157 solute carrier family 9 (sodium/hydrogen exchanger), member 3 Mus musculus 63-67 31649313-4 2020 Hyperinsulinemia caused by insulin resistance stimulates sodium reabsorption, enhances sodium retention, and increases circulating plasma volume. Sodium 57-63 insulin Homo sapiens 5-12 31649313-4 2020 Hyperinsulinemia caused by insulin resistance stimulates sodium reabsorption, enhances sodium retention, and increases circulating plasma volume. Sodium 87-93 insulin Homo sapiens 5-12 31794424-0 2020 Stomach gastrin is regulated by sodium via PPAR-alpha and dopamine D1 receptor. Sodium 32-38 dopamine receptor D1 Homo sapiens 58-78 31794424-1 2020 Gastrin, secreted by stomach G cells in response to ingested sodium, stimulates the renal cholecystokinin B receptor (CCKBR) to increase renal sodium excretion. Sodium 61-67 cholecystokinin B receptor Homo sapiens 90-116 31794424-1 2020 Gastrin, secreted by stomach G cells in response to ingested sodium, stimulates the renal cholecystokinin B receptor (CCKBR) to increase renal sodium excretion. Sodium 61-67 cholecystokinin B receptor Homo sapiens 118-123 31794424-1 2020 Gastrin, secreted by stomach G cells in response to ingested sodium, stimulates the renal cholecystokinin B receptor (CCKBR) to increase renal sodium excretion. Sodium 143-149 cholecystokinin B receptor Homo sapiens 90-116 31794424-1 2020 Gastrin, secreted by stomach G cells in response to ingested sodium, stimulates the renal cholecystokinin B receptor (CCKBR) to increase renal sodium excretion. Sodium 143-149 cholecystokinin B receptor Homo sapiens 118-123 31735358-0 2020 Insulin promotes sodium transport but suppresses gluconeogenesis via distinct cellular pathways in human and rat renal proximal tubules. Sodium 17-23 insulin Homo sapiens 0-7 31735358-1 2020 Insulin is known to promote sodium transport and regulate gluconeogenesis in renal proximal tubules. Sodium 28-34 insulin Homo sapiens 0-7 31735358-3 2020 To help define this, we examined the components of insulin signaling in sodium transport and gluconeogenesis in isolated human and rat proximal tubules, and also investigated the role of insulin in sodium handling and mTORC1 in insulin signaling in vivo. Sodium 72-78 insulin Homo sapiens 51-58 31735358-6 2020 Furthermore, insulin decreased sodium excretion, and this effect depended on phosphoinositide 3 kinase in vivo. Sodium 31-37 insulin Homo sapiens 13-20 31735358-11 2020 These results indicate that insulin-stimulated proximal tubule sodium transport is mediated via the Akt2/mTORC2 pathway, whereas insulin-suppressed proximal tubule gluconeogenesis is mediated via the IRS1/Akt2/mTORC1/2 pathway. Sodium 63-69 insulin Homo sapiens 28-35 31820315-11 2020 Furthermore, tumor necrosis factor-alpha and interleukin-1beta were upregulated upon NaAsO2 treatment, suggesting the induction of inflammation. Sodium 85-91 tumor necrosis factor Mus musculus 13-40 31820315-11 2020 Furthermore, tumor necrosis factor-alpha and interleukin-1beta were upregulated upon NaAsO2 treatment, suggesting the induction of inflammation. Sodium 85-91 interleukin 1 beta Mus musculus 45-62 31820315-12 2020 Moreover, NaAsO2 triggered apoptosis in the liver by upregulating Bax and caspase-3 and downregulating Bcl-2. Sodium 10-16 B cell leukemia/lymphoma 2 Mus musculus 103-108 32109341-1 2020 STK39 encodes a serine threonine kinase, SPAK, which is part of a multi-kinase network that determines renal Na+ reabsorption and blood pressure (BP) through regulation of sodium-chloride co-transporters in the kidney. Sodium 172-178 serine/threonine kinase 39 Homo sapiens 0-5 32109341-1 2020 STK39 encodes a serine threonine kinase, SPAK, which is part of a multi-kinase network that determines renal Na+ reabsorption and blood pressure (BP) through regulation of sodium-chloride co-transporters in the kidney. Sodium 172-178 serine/threonine kinase 39 Homo sapiens 41-45 31872845-3 2020 Hence, we evaluated the histopathological structure, the imbalance of the biochemical index of bone metabolism, and the expression levels of PI3K/AKT apoptosis signaling pathway-related genes in rats treated with sodium fluoride (NaF, F) and/or calcium carbonate (CaCO3) for 120 days. Sodium 230-233 AKT serine/threonine kinase 1 Rattus norvegicus 146-149 31992767-9 2020 We also found alterations in the properties of voltage-gated sodium channel currents in Jedi-1 null neurons. Sodium 61-67 platelet endothelial aggregation receptor 1 Mus musculus 88-94 32038177-3 2020 KCNT1 and KCNT2 respectively encode the KNa1.1 (Slack) and KNa1.2 (Slick) subunits of the sodium-dependent voltage-gated potassium channel KNa. Sodium 90-96 potassium sodium-activated channel subfamily T member 1 Homo sapiens 0-5 31974511-0 2020 Sodium-induced population shift drives activation of thrombin. Sodium 0-6 coagulation factor II, thrombin Homo sapiens 53-61 31799581-0 2020 Metal-free late-stage C(sp2)-H functionalization of N-aryl amines with various sodium salts. Sodium 79-85 Sp2 transcription factor Homo sapiens 22-27 31799581-1 2020 Metal-free consecutive C(sp2)-X (X = Cl, Br, S, N) bond formations of N-aryl amines (cyclic, fused, carbamate, and aminium radicals) were achieved under mild conditions using [bis(trifluoroacetoxy)iodo]benzene (PIFA) and simple nonharmful sodium salts. Sodium 239-245 Sp2 transcription factor Homo sapiens 23-28 31969611-7 2020 More importantly, voltage-dependent sodium and L-type calcium channel blockers and intracellular calcium signaling modulators remarkably suppressed rotenone-induced Nfl downregulation, whereas none of these agents modified NMDA-induced Nfl downregulation. Sodium 36-42 neurofilament light chain Rattus norvegicus 165-168 32038274-0 2019 High-Salt Loading Downregulates Nrf2 Expression in a Sodium-Dependent Manner in Renal Collecting Duct Cells. Sodium 53-59 nuclear factor, erythroid derived 2, like 2 Mus musculus 32-36 32038274-14 2019 Conclusion: High salt downregulated Nrf2 mainly via a sodium-dependent manner in kidney collecting duct cells, which might contribute to the excessive renal oxidative stress and CKD progression. Sodium 54-60 nuclear factor, erythroid derived 2, like 2 Mus musculus 36-40 31870150-8 2020 Furthermore, epidermal growth factor receptor (EGFR), but not the mitogen-activated protein kinase (MAPK) pathway, is vital during the NaB-induced pBD3 and pEP2C regulation process. Sodium 135-138 epidermal growth factor receptor Sus scrofa 13-45 31870150-8 2020 Furthermore, epidermal growth factor receptor (EGFR), but not the mitogen-activated protein kinase (MAPK) pathway, is vital during the NaB-induced pBD3 and pEP2C regulation process. Sodium 135-138 epidermal growth factor receptor Sus scrofa 47-51 31870150-10 2020 This study showed that NaB simultaneously induces pBD3 and pEP2C via TLR2 and EGFR in IPEC J2 cells without increasing the risk of a harmful inflammatory response. Sodium 23-26 epidermal growth factor receptor Sus scrofa 78-82 31594586-0 2020 A "signal-on" chemiluminescence biosensor for thrombin detection based on DNA functionalized magnetic sodium alginate hydrogel and metalloporphyrinic metal-organic framework nanosheets. Sodium 102-108 coagulation factor II, thrombin Homo sapiens 46-54 31594586-2 2020 The thrombin aptamer1-functionalized magnetic sodium alginate (Malg-Apt1) hydrogel was synthesized by physical interaction between sodium alginate and Ca2+, and it was used in the biosensor for separating and enriching thrombin. Sodium 46-52 coagulation factor II, thrombin Homo sapiens 219-227 31594586-2 2020 The thrombin aptamer1-functionalized magnetic sodium alginate (Malg-Apt1) hydrogel was synthesized by physical interaction between sodium alginate and Ca2+, and it was used in the biosensor for separating and enriching thrombin. Sodium 131-137 coagulation factor II, thrombin Homo sapiens 4-12 31594589-1 2020 Herein, a sodium hexametaphosphate ((NaPO3)6) modulated fluorescence responsive probe based on the integration of reduced graphene quantum dots (rGQDs) and chitosan (CS) via self-assembly/disassembly for label-free alkaline phosphatase assay was constructed. Sodium 36-44 alkaline phosphatase, placental Homo sapiens 215-235 31594589-4 2020 By introducing alkaline phosphatase (ALP) into the system, (NaPO3)6 can be hydrolyzed to give phosphate anions. Sodium 59-67 alkaline phosphatase, placental Homo sapiens 15-35 31594589-4 2020 By introducing alkaline phosphatase (ALP) into the system, (NaPO3)6 can be hydrolyzed to give phosphate anions. Sodium 59-67 alkaline phosphatase, placental Homo sapiens 37-40 31683218-9 2020 Overexpression of miR-15a caused apoptosis and necroptosis and its inhibition partially reversed apoptosis and necroptosis of LMH cells caused by NaHS stimulation and lncRNA3037 knockdown. Sodium 146-150 microRNA 15a Gallus gallus 18-25 31936426-8 2020 In addition, 0.1 M NaOH has the best desorption efficiency of As(V) adsorbed on CS-modified Dt, and the removal efficiency of As(V) was still higher than 90% when after six adsorption-desorption cycles. Sodium 19-23 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 62-67 31936426-8 2020 In addition, 0.1 M NaOH has the best desorption efficiency of As(V) adsorbed on CS-modified Dt, and the removal efficiency of As(V) was still higher than 90% when after six adsorption-desorption cycles. Sodium 19-23 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 126-131 31607539-2 2020 Here we tested whether catalytically dead Cas9 (dCas9)-mediated Scn1a gene activation can rescue Scn1a haploinsufficiency in a mouse DS model and restore physiological levels of its gene product, the Nav1.1 voltage-gated sodium channel. Sodium 221-227 sodium channel, voltage-gated, type I, alpha Mus musculus 64-69 31993308-3 2020 In this review, we focus on several solute carrier (SLC) transporters known to be involved in transporting clinically used radiopharmaceutical agents into cancer cells, including the sodium/iodine symporter (NIS), norepinephrine transporter (NET), glucose transporter 1 (GLUT1), and monocarboxylate transporters (MCTs). Sodium 183-189 solute carrier family 6 member 2 Homo sapiens 242-245 32477601-4 2020 In the kidneys of non-anesthetized rats, which received a water load of 2 ml per 100 g of body weight, three effects of vasopressin were revealed: 1) increased reabsorption of water and sodium, 2) increased excretion of potassium ions, and 3) increased excretion of sodium ions. Sodium 266-272 arginine vasopressin Rattus norvegicus 120-131 31913682-1 2020 Genes for the epithelial sodium channel (ENaC) subunits are expressed in a circadian manner, but whether this results in time of day differences in activity is not known. Sodium 25-31 sodium channel epithelial 1 subunit gamma Rattus norvegicus 41-45 31559686-0 2020 Sodium retention by uPA in nephrotic syndrome? Sodium 0-6 proline rich acidic protein 1 Homo sapiens 20-23 32477601-4 2020 In the kidneys of non-anesthetized rats, which received a water load of 2 ml per 100 g of body weight, three effects of vasopressin were revealed: 1) increased reabsorption of water and sodium, 2) increased excretion of potassium ions, and 3) increased excretion of sodium ions. Sodium 186-192 arginine vasopressin Rattus norvegicus 120-131 31594586-2 2020 The thrombin aptamer1-functionalized magnetic sodium alginate (Malg-Apt1) hydrogel was synthesized by physical interaction between sodium alginate and Ca2+, and it was used in the biosensor for separating and enriching thrombin. Sodium 46-52 coagulation factor II, thrombin Homo sapiens 4-12 32407275-9 2020 CONCLUSION: These results indicated that the sodium channel Nav1.7 in the DRG exerted an important function in paclitaxel-induced neuropathy, which was associated with ERK phosphorylation in neurons. Sodium 45-51 Eph receptor B1 Rattus norvegicus 168-171 31880072-2 2020 The mutant mice express L263V-mutated alpha1 subunits in voltage-gated NaV 1.1 sodium channels (Scn1aL263V ). Sodium 79-85 sodium channel, voltage-gated, type I, alpha Mus musculus 71-78 32452328-2 2020 This beta-secretase cleaves not only Amyloid precursor protein (APP) and its homologues but also small series of substrate including neuregulin and beta subunit of voltage gated sodium channel that play a very important role in the development and normal function of the brain. Sodium 178-184 amyloid beta precursor protein Homo sapiens 37-62 31914597-1 2020 The Slack (KCNT1) gene encodes sodium-activated potassium channels that are abundantly expressed in the central nervous system. Sodium 31-37 potassium sodium-activated channel subfamily T member 1 Homo sapiens 4-9 30963979-9 2020 The myriad effects due to mutation in phosphodiesterase 3A (PDE3A) lead to severe hypertension underlying sodium-independent autosomal dominant hypertension with brachydactyly. Sodium 106-112 phosphodiesterase 3A Homo sapiens 38-58 30963979-9 2020 The myriad effects due to mutation in phosphodiesterase 3A (PDE3A) lead to severe hypertension underlying sodium-independent autosomal dominant hypertension with brachydactyly. Sodium 106-112 phosphodiesterase 3A Homo sapiens 60-65 31237219-5 2020 RESULTS: Angiotensin II (ANG II), beside stimulating aldosterone, vasopressin and CRH-ACTH release, sodium and water retention, thirst, and sympathetic nerve activity, exerts its effects on the immune system via the Angiotensin Type 1 Receptor (AT 1R) that is located in the brain, pituitary adrenal gland, and kidney. Sodium 100-106 angiotensinogen Homo sapiens 9-23 31237219-5 2020 RESULTS: Angiotensin II (ANG II), beside stimulating aldosterone, vasopressin and CRH-ACTH release, sodium and water retention, thirst, and sympathetic nerve activity, exerts its effects on the immune system via the Angiotensin Type 1 Receptor (AT 1R) that is located in the brain, pituitary adrenal gland, and kidney. Sodium 100-106 angiotensinogen Homo sapiens 25-31 31885713-9 2020 Furthermore, NaHS inhibited the expression of NLRP3, ASC and cleaved caspase-1, and the production of IL-1beta and IL-18 in adipocytes treated with HG. Sodium 13-17 NLR family pyrin domain containing 3 Homo sapiens 46-51 31885713-9 2020 Furthermore, NaHS inhibited the expression of NLRP3, ASC and cleaved caspase-1, and the production of IL-1beta and IL-18 in adipocytes treated with HG. Sodium 13-17 PYD and CARD domain containing Homo sapiens 53-56 31885713-9 2020 Furthermore, NaHS inhibited the expression of NLRP3, ASC and cleaved caspase-1, and the production of IL-1beta and IL-18 in adipocytes treated with HG. Sodium 13-17 caspase 1 Homo sapiens 69-78 31885713-9 2020 Furthermore, NaHS inhibited the expression of NLRP3, ASC and cleaved caspase-1, and the production of IL-1beta and IL-18 in adipocytes treated with HG. Sodium 13-17 interleukin 1 beta Homo sapiens 102-110 31914597-1 2020 The Slack (KCNT1) gene encodes sodium-activated potassium channels that are abundantly expressed in the central nervous system. Sodium 31-37 potassium sodium-activated channel subfamily T member 1 Homo sapiens 11-16 31909644-8 2020 Treatment with Dex increased the SOD1, SOD2, GPx1, and GPx2 expression in H9C2 cells in OGD/R, while Na2SeO3 increased the GPx1-4 and TrxR1-3 mRNA levels. Sodium 101-108 glutathione peroxidase 1 Rattus norvegicus 123-127 31909644-11 2020 Na2SeO3 enhanced the inhibitory effect of Dex on phosphorylated (p)-p65, p65, and NLRP3 in OGD/R. Sodium 0-7 synaptotagmin 1 Rattus norvegicus 68-71 31909644-11 2020 Na2SeO3 enhanced the inhibitory effect of Dex on phosphorylated (p)-p65, p65, and NLRP3 in OGD/R. Sodium 0-7 synaptotagmin 1 Rattus norvegicus 73-76 31909644-11 2020 Na2SeO3 enhanced the inhibitory effect of Dex on phosphorylated (p)-p65, p65, and NLRP3 in OGD/R. Sodium 0-7 NLR family, pyrin domain containing 3 Rattus norvegicus 82-87 33416748-1 2020 High-sodium diets (e.g., fast-food intake, FF) may contribute to increased hyper-tension risk among low-income populations. Sodium 5-11 Fas activated serine/threonine kinase Homo sapiens 25-29 32838581-5 2020 RT-qPCR confirmed that the epithelial sodium channel (ENACalpha) gene is an ARPE-19 cell-specific GR target gene, whereas the FK506 binding protein 5 (FKBP5) gene was A549 cell-specific. Sodium 38-44 sodium channel epithelial 1 subunit alpha Homo sapiens 54-63 31902896-1 2020 The secondary structures of human serum albumin (HSA) and bovine serum albumin (BSA) were disrupted in the solution of sodium dodecyl sulfate (SDS), while being hardly damaged in the solution of the bile salt, sodium cholate (NaCho). Sodium 226-231 albumin Homo sapiens 34-47 31503134-9 2020 Plasma renin activity correlated negatively with sweat sodium (rs = -0.43, P = 0.012) and muscle sodium levels (rs = -0.42, P < 0.001). Sodium 55-61 renin Homo sapiens 7-12 31503134-9 2020 Plasma renin activity correlated negatively with sweat sodium (rs = -0.43, P = 0.012) and muscle sodium levels (rs = -0.42, P < 0.001). Sodium 97-103 renin Homo sapiens 7-12 31902896-1 2020 The secondary structures of human serum albumin (HSA) and bovine serum albumin (BSA) were disrupted in the solution of sodium dodecyl sulfate (SDS), while being hardly damaged in the solution of the bile salt, sodium cholate (NaCho). Sodium 226-231 albumin Homo sapiens 65-78 30715488-9 2020 While MgCO3 supplementation alone resulted in decreased calcification severity, it resulted in increased intestinal expression of the phosphate transporters type II sodium-dependent phosphate transporter 1 (Pit-1). Sodium 165-171 POU domain, class 1, transcription factor 1 Mus musculus 207-212 31993555-6 2020 Here we show that dapagliflozin-sensitive glucose- and insulin-dependent sodium uptake stimulates somatostatin secretion by elevating the cytoplasmic Na+ concentration ([Na+]i) and promoting intracellular Ca2+-induced Ca2+ release (CICR). Sodium 73-79 insulin Homo sapiens 55-62 31888677-1 2019 Clinical and preclinical studies have shown that patients with Diabetic Neuropathy Pain (DNP) present with increased tumor necrosis factor alpha (TNF-alpha) serum concentration, whereas studies with diabetic animals have shown that TNF-alpha induces an increase in NaV1.7 sodium channel expression. Sodium 272-278 tumor necrosis factor Homo sapiens 232-241 31704583-7 2020 Mechanistically, NaHS upregulated SIRT1 expression, but inhibited activation of TGF-beta1/Smad3 signaling in vivo and in vitro. Sodium 17-21 transforming growth factor beta 1 Homo sapiens 80-89 31783472-2 2020 This work employed zeolites NaA, NaX, and HZSM-5 with different pore sizes and Na(I) contents to selectively separate and recover Co(II)/Mn(II) from PTA wastewater and to understand the adsorption mechanism. Sodium 28-31 mitochondrially encoded cytochrome c oxidase II Homo sapiens 130-136 31783472-2 2020 This work employed zeolites NaA, NaX, and HZSM-5 with different pore sizes and Na(I) contents to selectively separate and recover Co(II)/Mn(II) from PTA wastewater and to understand the adsorption mechanism. Sodium 33-36 mitochondrially encoded cytochrome c oxidase II Homo sapiens 130-136 31783472-3 2020 It is found that only NaA can exclusively adsorb Co(II)/Mn(II) through ion-exchange without adsorbing any aromatic organic compound (AOC); oppositely, HZSM-5 shows the highest adsorption capacity for AOCs but almost no adsorption for Co(II)/Mn(II); and NaX exhibits moderate adsorption capacities for both Co(II)/Mn(II) and AOCs. Sodium 22-25 mitochondrially encoded cytochrome c oxidase II Homo sapiens 49-55 31783472-3 2020 It is found that only NaA can exclusively adsorb Co(II)/Mn(II) through ion-exchange without adsorbing any aromatic organic compound (AOC); oppositely, HZSM-5 shows the highest adsorption capacity for AOCs but almost no adsorption for Co(II)/Mn(II); and NaX exhibits moderate adsorption capacities for both Co(II)/Mn(II) and AOCs. Sodium 22-25 mitochondrially encoded cytochrome c oxidase II Homo sapiens 234-240 31783472-3 2020 It is found that only NaA can exclusively adsorb Co(II)/Mn(II) through ion-exchange without adsorbing any aromatic organic compound (AOC); oppositely, HZSM-5 shows the highest adsorption capacity for AOCs but almost no adsorption for Co(II)/Mn(II); and NaX exhibits moderate adsorption capacities for both Co(II)/Mn(II) and AOCs. Sodium 22-25 mitochondrially encoded cytochrome c oxidase II Homo sapiens 234-240 31783472-6 2020 Importantly, bench-scale experiments for simulating the industrial operation were carried out, and the results show that the adsorption capacity of the NaA particles for Co(II)/Mn(II) from the industrial PTA wastewater is 9.1/8.6 mg/g, respectively, without adsorbing any AOC. Sodium 152-155 mitochondrially encoded cytochrome c oxidase II Homo sapiens 170-176 31888677-6 2019 Our results show that TNF-alpha exposure increased the density of the total, TTXs and TTXr sodium current in DRG neurons. Sodium 91-97 tumor necrosis factor Rattus norvegicus 22-31 31888677-7 2019 Furthermore, TNF-alpha shifted the steady state activation and inactivation curves of the total and TTXs sodium current. Sodium 105-111 tumor necrosis factor Rattus norvegicus 13-22 31888677-9 2019 In conclusion, TNF-alpha sensitizes DRG neurons via augmentation of whole cell sodium current. Sodium 79-85 tumor necrosis factor Rattus norvegicus 15-24 31892216-1 2019 Humans with dilated cardiomyopathy (DCM) and heart failure (HF) develop low levels of corin, a multi-domain, cardiac-selective serine protease involved in natriuretic peptide cleavage and sodium and water regulation. Sodium 188-194 corin, serine peptidase Mus musculus 86-91 31902156-7 2019 Finally grafted GDNF-hNSPCs substantially reversed the increased expression of voltage-gated sodium channels and neuropeptide Y, and elevated expression of GABA in the injured spinal cord, which are involved in the attenuation of neuropathic pain after SCI. Sodium 93-99 glial cell derived neurotrophic factor Homo sapiens 16-20 31655649-4 2019 Three HMIs, including Cu(II), Co(II) and Hg(II), were selected as studied ions and reacted with chelating agent sodium diethyldithiocarbamatetrihydrate to form metallic coordination compounds. Sodium 112-151 mitochondrially encoded cytochrome c oxidase II Homo sapiens 30-36 31857666-4 2019 One of them is located in the Dmd gene encoding dystrophin, a protein important for the function and stabilization of voltage-gated calcium (Cav1.2) and sodium (Nav1.5) channels, respectively. Sodium 153-159 dystrophin, muscular dystrophy Mus musculus 30-33 31857666-4 2019 One of them is located in the Dmd gene encoding dystrophin, a protein important for the function and stabilization of voltage-gated calcium (Cav1.2) and sodium (Nav1.5) channels, respectively. Sodium 153-159 dystrophin, muscular dystrophy Mus musculus 48-58 31697467-0 2019 The Natural Flavonoid Naringenin Elicits Analgesia through Inhibition of NaV1.8 Voltage-Gated Sodium Channels. Sodium 94-100 sodium channel, voltage-gated, type X, alpha Mus musculus 73-79 31697467-3 2019 Computational studies predicted that (2R)-naringenin may act on voltage-gated ion channels, particularly the N-type calcium channel (CaV2.2) and the NaV1.7 sodium channel-both of which are key for pain signaling. Sodium 156-162 sodium channel, voltage-gated, type IX, alpha Mus musculus 149-155 31933626-6 2019 Using Western blot studies and high-resolution confocal microscopy in the prefrontal frontal cortex (PFC), our data indicate disrupted expression of different isoforms of the voltage-gated sodium channels (NaV) at the AIS, whereas other components of AIS such as ankyrin-G and fibroblast growth factor 14 (FGF14) and contactin-associated protein 1 (Caspr) in BTBR were comparable to those in wild-type control mice. Sodium 189-195 fibroblast growth factor 14 Mus musculus 277-304 31933626-6 2019 Using Western blot studies and high-resolution confocal microscopy in the prefrontal frontal cortex (PFC), our data indicate disrupted expression of different isoforms of the voltage-gated sodium channels (NaV) at the AIS, whereas other components of AIS such as ankyrin-G and fibroblast growth factor 14 (FGF14) and contactin-associated protein 1 (Caspr) in BTBR were comparable to those in wild-type control mice. Sodium 189-195 fibroblast growth factor 14 Mus musculus 306-311 30391505-2 2019 Although recent hSERT crystal structures represent a milestone for structure-function analyses of mammalian neurotransmitter:sodium symporters, they are all derived from thermostabilized but transport-deficient constructs. Sodium 125-131 solute carrier family 6 member 4 Homo sapiens 16-21 30790582-1 2019 GAT1 is a member of the neurotransmitter:sodium: symporter family and mediates transport of GABA together with sodium and chloride in an electrogenic process enabling efficient synaptic transmission. Sodium 41-47 solute carrier family 6 member 1 Homo sapiens 0-4 30790582-1 2019 GAT1 is a member of the neurotransmitter:sodium: symporter family and mediates transport of GABA together with sodium and chloride in an electrogenic process enabling efficient synaptic transmission. Sodium 111-117 solute carrier family 6 member 1 Homo sapiens 0-4 31825310-4 2019 TCAs activate both TPC1 and TPC2 in a voltage-dependent manner, referred to as Lysosomal Na+ channel Voltage-dependent Activators (LyNa-VAs). Sodium 131-135 two pore segment channel 1 Homo sapiens 19-23 32611999-0 2020 Synthesis and Structure-Activity Relationship of C-Phenyl D-Glucitol (TP0454614) Derivatives as Selective Sodium-Dependent Glucose Cotransporter 1 (SGLT1) Inhibitors. Sodium 106-112 solute carrier family 5 member 1 Homo sapiens 148-153 31920633-0 2019 Pharmacological Profile of the Sodium Current in Human Stem Cell-Derived Cardiomyocytes Compares to Heterologous Nav1.5+beta1 Model. Sodium 31-37 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 120-125 31811815-5 2019 In this study, we observed that interleukin-1beta (IL-1beta)-induced MMP-9 secretion in pericytes increased BBB permeability to sodium fluorescein (Na-F) by damaging the disruption of VE-cadherin, occludin, claudin-5, and zonula occludin-1 (ZO-1). Sodium 148-152 interleukin 1 beta Homo sapiens 32-49 31822662-5 2019 In these conditions, we show that there are elevated levels of PGE2 which activate sensory nerves, leading to sodium influx through Nav 1.8 channels. Sodium 110-116 sodium channel, voltage-gated, type X, alpha Mus musculus 132-139 31811815-5 2019 In this study, we observed that interleukin-1beta (IL-1beta)-induced MMP-9 secretion in pericytes increased BBB permeability to sodium fluorescein (Na-F) by damaging the disruption of VE-cadherin, occludin, claudin-5, and zonula occludin-1 (ZO-1). Sodium 148-152 interleukin 1 beta Homo sapiens 51-59 31811815-5 2019 In this study, we observed that interleukin-1beta (IL-1beta)-induced MMP-9 secretion in pericytes increased BBB permeability to sodium fluorescein (Na-F) by damaging the disruption of VE-cadherin, occludin, claudin-5, and zonula occludin-1 (ZO-1). Sodium 148-152 cadherin 5 Homo sapiens 184-195 31630621-8 2019 DC ACT kidneys showed augmented protein expression of gamma-epithelial sodium channel and NHE3 (sodium-hydrogen antiporter 3). Sodium 96-102 solute carrier family 9 (sodium/hydrogen exchanger), member 3 Mus musculus 90-94 31659119-0 2019 On the mechanism of the GIRK2 channel gating by phosphatidylinositol bisphosphate (PIP2), sodium, and the Gbetagamma dimer. Sodium 90-96 potassium inwardly rectifying channel subfamily J member 6 Homo sapiens 24-29 31817623-1 2019 A higher sodium intake is conceivably associated with insulin resistant conditions like obesity, but associations of non-alcoholic fatty liver disease (NAFLD) with a higher sodium intake determined by 24 hours (24 h) urine collections are still unclear. Sodium 9-15 insulin Homo sapiens 54-61 31817623-11 2019 Insulin resistance-related processes may contribute to the association of NAFLD with sodium intake. Sodium 85-91 insulin Homo sapiens 0-7 31676603-3 2019 Recently, it has been demonstrated that a major route of DHA entry in the retina is the delivery across the blood-retina barrier by the sodium-dependent lipid transporter, Mfsd2a. Sodium 136-142 major facilitator superfamily domain containing 2A Mus musculus 172-178 31703480-5 2019 After 150 d, the results showed a significant increase in testicular cytokines levels including of IL-17A, IL-6, IFN-gamma and TNF-alpha in NaF and EAO groups compared with control group. Sodium 140-143 interleukin 6 Mus musculus 107-111 31703480-5 2019 After 150 d, the results showed a significant increase in testicular cytokines levels including of IL-17A, IL-6, IFN-gamma and TNF-alpha in NaF and EAO groups compared with control group. Sodium 140-143 interferon gamma Mus musculus 113-122 31703480-5 2019 After 150 d, the results showed a significant increase in testicular cytokines levels including of IL-17A, IL-6, IFN-gamma and TNF-alpha in NaF and EAO groups compared with control group. Sodium 140-143 tumor necrosis factor Mus musculus 127-136 31703480-7 2019 In addition, findings showed that in NaF and EAO groups, macrophages and T cells both significantly secreted IL-17A, and the protein and mRNA levels of cytokines (IL-6 and TGF-beta) were significantly increased. Sodium 37-40 interleukin 6 Mus musculus 163-167 31791063-9 2019 Many solute carriers (SLC) that are potential prodrug targets were present on both cellular surfaces, whereas putative sodium-coupled neutral amino acid transporter 7 (SNAT7) and riboflavin transporter (RFT3) were enriched on the basolateral and sodium- and chloride-dependent neutral and basic amino acid transporter (ATB0+) on the apical membrane. Sodium 119-125 solute carrier family 38 member 7 Homo sapiens 168-173 31791063-9 2019 Many solute carriers (SLC) that are potential prodrug targets were present on both cellular surfaces, whereas putative sodium-coupled neutral amino acid transporter 7 (SNAT7) and riboflavin transporter (RFT3) were enriched on the basolateral and sodium- and chloride-dependent neutral and basic amino acid transporter (ATB0+) on the apical membrane. Sodium 246-252 solute carrier family 38 member 7 Homo sapiens 168-173 31657247-0 2019 Impact of Angiotensin II-mediated stimulation of sodium transporters in the nephron assessed by computational modelling. Sodium 49-55 angiotensinogen Rattus norvegicus 10-24 31588796-0 2019 Glucocorticoid receptor activation stimulates the sodium-chloride cotransporter and influences the diurnal rhythm of its phosphorylation. Sodium 50-56 nuclear receptor subfamily 3, group C, member 1 Mus musculus 0-23 31449800-8 2019 Comparative structure and sequence analyses of sodium-binding GPCRs indicate a key role for the conserved leucine residue in the second transmembrane helix (Leu2.46) in coupling sodium translocation to receptor activation. Sodium 47-53 deleted in lymphocytic leukemia 2 Homo sapiens 157-161 30739221-0 2019 The sodium pump alpha1 subunit regulates bufalin sensitivity of human glioblastoma cells through the p53 signaling pathway. Sodium 4-10 tumor protein p53 Homo sapiens 101-104 31025580-2 2019 CRMP2 regulation of the activity and trafficking of NaV1.7 voltage-gated sodium channels as well as the N-type (CaV2.2) voltage-gated calcium channel (VGCC) has been reported. Sodium 73-79 dihydropyrimidinase like 2 Homo sapiens 0-5 31709768-1 2019 OBJECTIVE: Patients with Early Infantile Epileptic Encephalopathy (EIEE) 52 have inherited, homozygous variants in the gene SCN1B, encoding the voltage-gated sodium channel (VGSC) beta1 and beta1B non-pore-forming subunits. Sodium 158-164 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 180-185 31709768-8 2019 Biochemical and electrophysiological analyses of the SCN1B variant expressed in heterologous cells showed cell surface expression of the mutant beta1 subunit, similar to wild-type (WT), but with loss of normal beta1-mediated modification of human Nav 1.1-generated sodium current, suggesting that SCN1B-p.Arg85Cys is a loss-of-function (LOF) variant. Sodium 265-271 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 144-149 31768591-2 2019 The pencil graphite electrode"s surface was directly modified from graphite to graphene with cyclic voltammetry method in a single step by performing potential cycling between - 0.9 and - 1.4 V in 0.2 mol L-1 NaOH modifying solution. Sodium 209-213 L1 cell adhesion molecule Homo sapiens 205-208 31776946-4 2019 The obtained data suggest that prolactin provides fine tuning of various sodium transporters in different parts of the nephron under pathological conditions. Sodium 73-79 prolactin Rattus norvegicus 31-40 31114845-3 2019 Among the most abundant circRNA, one stems from the sodium-calcium exchanger gene, Slc8a1, exon 2 locus. Sodium 52-58 solute carrier family 8 member A1 Homo sapiens 83-89 31680630-2 2019 CRMP2 achieves this control of nociceptive signaling by virtue of its ability to regulate voltage-gated calcium and sodium channels. Sodium 116-122 dihydropyrimidinase like 2 Homo sapiens 0-5 31284779-9 2019 The western blot analysing showed that the levels of apoptosis-associated Bcl-2 and Nrf2 were dramatically decreased following the sodium selenite treatment. Sodium 131-137 BCL2 apoptosis regulator Homo sapiens 74-79 31284779-9 2019 The western blot analysing showed that the levels of apoptosis-associated Bcl-2 and Nrf2 were dramatically decreased following the sodium selenite treatment. Sodium 131-137 NFE2 like bZIP transcription factor 2 Homo sapiens 84-88 31755034-9 2019 Low-sodium intake was associated with lower levels of Hb (P = .027), lower TNF-alpha (P = .011), and lower IL-10 (P = .029). Sodium 4-10 tumor necrosis factor Homo sapiens 75-84 31758544-2 2019 Recent evidence suggests that the ECS may be a promising target for the treatment of epilepsy, including epilepsy subtypes that arise from mutations in the voltage-gated sodium channel SCN1A. Sodium 170-176 sodium channel, voltage-gated, type I, alpha Mus musculus 185-190 31805638-0 2019 3"-O-Methylorobol Inhibits the Voltage-Gated Sodium Channel Nav1.7 with Anti-Itch Efficacy in A Histamine-Dependent Itch Mouse Model. Sodium 45-51 itchy, E3 ubiquitin protein ligase Mus musculus 77-81 31573044-7 2019 NaHS was indicated to inhibit EndMT and PAH progression by inhibiting the induction of the nuclear factor (NF)-kappaB-Snail pathway. Sodium 0-4 snail family transcriptional repressor 1 Homo sapiens 118-123 31573044-9 2019 In HPAECs, NaHS dose-dependently inhibited TGF-beta1-induced EndMT and the activation of the NF-kappaB-Snail pathway. Sodium 11-15 transforming growth factor beta 1 Homo sapiens 43-52 31573044-9 2019 In HPAECs, NaHS dose-dependently inhibited TGF-beta1-induced EndMT and the activation of the NF-kappaB-Snail pathway. Sodium 11-15 snail family transcriptional repressor 1 Homo sapiens 103-108 31805638-0 2019 3"-O-Methylorobol Inhibits the Voltage-Gated Sodium Channel Nav1.7 with Anti-Itch Efficacy in A Histamine-Dependent Itch Mouse Model. Sodium 45-51 itchy, E3 ubiquitin protein ligase Mus musculus 116-120 31872561-5 2019 In the presence of RyR mutations, frequent spontaneous calcium leaks from sarcoplasmic reticulum (SR) initiated calcium waves, which upon reaching the cell periphery produced delayed afterdepolarizations (DADs) via sodium-calcium exchanger (NCX) and T-type calcium (ICaT ) channel activation. Sodium 215-221 ryanodine receptor 1, skeletal muscle Mus musculus 19-22 31637558-6 2019 E. coli transformant containing the ORF1 showed resistance to 1 mM Na2TeO3. Sodium 67-74 hypothetical protein Escherichia coli 36-40 31728700-0 2019 beta1 and beta3 subunits amplify mechanosensitivity of the cardiac voltage-gated sodium channel Nav1.5. Sodium 81-87 BCL2 related protein A1 Homo sapiens 0-15 31728700-7 2019 beta3, on the other hand, almost doubles stress-induced speeding of time to sodium current transient peak (Deltatime to peak at - 30 mV: 0.19 ms without and 0.37 ms with beta3 co-expression). Sodium 76-82 T cell immune regulator 1, ATPase H+ transporting V0 subunit a3 Homo sapiens 0-5 31795454-8 2019 NaIO3-induced PTX3 expression was decreased in the presence of phosphoinositide 3 (PI3) kinase inhibitors, ERK inhibitors, and ROS scavengers. Sodium 0-5 pentraxin 3 Homo sapiens 14-18 31653700-1 2019 Endoplasmic reticulum protein of 29 kDa (ERp29) is a thioredoxin-homologous endoplasmic reticulum (ER) protein that regulates the biogenesis of cystic fibrosis transmembrane conductance regulator (CFTR) and the epithelial sodium channel (ENaC). Sodium 222-228 CF transmembrane conductance regulator Homo sapiens 144-195 31653700-1 2019 Endoplasmic reticulum protein of 29 kDa (ERp29) is a thioredoxin-homologous endoplasmic reticulum (ER) protein that regulates the biogenesis of cystic fibrosis transmembrane conductance regulator (CFTR) and the epithelial sodium channel (ENaC). Sodium 222-228 CF transmembrane conductance regulator Homo sapiens 197-201 31795454-6 2019 (3) Results: NaIO3 increased PTX3 expression, in a dose- and time-dependent manner, in H-RPE and ARPE-19 cells. Sodium 13-18 pentraxin 3 Homo sapiens 29-33 31795454-8 2019 NaIO3-induced PTX3 expression was decreased in the presence of phosphoinositide 3 (PI3) kinase inhibitors, ERK inhibitors, and ROS scavengers. Sodium 0-5 mitogen-activated protein kinase 1 Homo sapiens 107-110 31795454-7 2019 We found phosphorylated Akt, a downstream target of the PI3 kinase pathway, phosphor- mitogen-activated protein kinase kinase 1/2 (ERK), and intracellular reactive oxygen species (ROS) were predominantly induced by NaIO3. Sodium 215-220 AKT serine/threonine kinase 1 Homo sapiens 24-27 31795454-9 2019 Furthermore, NaIO3 enhanced mRNA expression of antioxidant enzymes such as glucose-6-phosphate dehydrogenase (G6PDH), catalase (CAT), and glutathione S-reductase (GSR) in the control shRNA expressing RPE cells, but not in hPTX3 shRNA expressing RPE cells. Sodium 13-18 catalase Homo sapiens 118-126 31795454-7 2019 We found phosphorylated Akt, a downstream target of the PI3 kinase pathway, phosphor- mitogen-activated protein kinase kinase 1/2 (ERK), and intracellular reactive oxygen species (ROS) were predominantly induced by NaIO3. Sodium 215-220 mitogen-activated protein kinase 1 Homo sapiens 131-134 31795454-9 2019 Furthermore, NaIO3 enhanced mRNA expression of antioxidant enzymes such as glucose-6-phosphate dehydrogenase (G6PDH), catalase (CAT), and glutathione S-reductase (GSR) in the control shRNA expressing RPE cells, but not in hPTX3 shRNA expressing RPE cells. Sodium 13-18 catalase Homo sapiens 128-131 31795454-9 2019 Furthermore, NaIO3 enhanced mRNA expression of antioxidant enzymes such as glucose-6-phosphate dehydrogenase (G6PDH), catalase (CAT), and glutathione S-reductase (GSR) in the control shRNA expressing RPE cells, but not in hPTX3 shRNA expressing RPE cells. Sodium 13-18 pentraxin 3 Homo sapiens 222-227 31609572-0 2019 Hierarchical Nanostructured NiS/MoS2/C Composite Hollow Spheres for High Performance Sodium-Ion Storage Performance. Sodium 85-91 solute carrier family 5 member 5 Homo sapiens 28-31 31852640-12 2019 Compared with those in BCNI group, the rats in BCNI+NaHS group had significantly decreased expressions of caspase-3 and Bax proteins (P < 0.05) with significantly enhanced Bcl-2 protein expression and an increased Bcl-2/Bax ratio (P < 0.05). Sodium 52-56 BCL2, apoptosis regulator Rattus norvegicus 175-180 31852640-12 2019 Compared with those in BCNI group, the rats in BCNI+NaHS group had significantly decreased expressions of caspase-3 and Bax proteins (P < 0.05) with significantly enhanced Bcl-2 protein expression and an increased Bcl-2/Bax ratio (P < 0.05). Sodium 52-56 BCL2, apoptosis regulator Rattus norvegicus 217-222 31621295-4 2019 These mass peaks were identified to be protonated and sodium adducts of LPC 16:0 by using tandem mass spectra (MS2 and MS3) of purely synthesized LPC 16:0 and extracted LPC 16:0 from a healthy control and a sepsis patient. Sodium 54-60 MS3 Homo sapiens 119-122 31723053-4 2019 10mIR caused renal injury with elevation of fractional excretion of sodium, although histological damage by oxidative stress was limited. Sodium 68-74 microRNA 615 Mus musculus 2-5 31853224-9 2019 The phosphorylation of IRE1alpha, PERK and eIF2alpha and the expression of nuclear ATF4, and GADD34 in L2 cells were all significantly reduced with NaHS. Sodium 148-152 activating transcription factor 4 Rattus norvegicus 83-87 31853224-10 2019 Nuclear NF-kappaB p65, MAPK p38, JNK, and ERK were all activated by cyclic strain, but inhibited by the ER stress inhibitor 4-PBA or NaHS. Sodium 133-137 nuclear factor kappa B subunit 1 Homo sapiens 8-17 31853224-10 2019 Nuclear NF-kappaB p65, MAPK p38, JNK, and ERK were all activated by cyclic strain, but inhibited by the ER stress inhibitor 4-PBA or NaHS. Sodium 133-137 synaptotagmin 1 Rattus norvegicus 18-21 31853224-10 2019 Nuclear NF-kappaB p65, MAPK p38, JNK, and ERK were all activated by cyclic strain, but inhibited by the ER stress inhibitor 4-PBA or NaHS. Sodium 133-137 Eph receptor B1 Rattus norvegicus 42-45 31490733-1 2019 Previously we have shown that increased expression of renal epithelial sodium channels (ENaC) may contribute to the renal sodium and water retention observed during chronic heart failure (CHF). Sodium 71-77 sodium channel epithelial 1 subunit gamma Rattus norvegicus 88-92 31490733-11 2019 These findings suggest a critical role for renal nerves in the enhanced expression of ENaC and AQP2 and subsequent pathophysiology of renal sodium and water retention associated with CHF. Sodium 140-146 sodium channel epithelial 1 subunit gamma Rattus norvegicus 86-90 30955077-13 2019 The increase in sodium excretion was correlated with the change in eGFR (r = 0.371; p = 0.015). Sodium 16-22 epidermal growth factor receptor Homo sapiens 67-71 31720603-3 2019 It is revealed that the SEI layer contains a large amount of NaF and O-As-O polymer which enables the stable cycling of sodium metal anodes. Sodium 120-126 C-X-C motif chemokine ligand 8 Homo sapiens 61-64 31365096-1 2019 CONTEXT: Although the physiology of sodium, water and arginine vasopressin (AVP), also known as antidiuretic hormone (ADH), has long been known, accumulating data suggest that this system operates as a more complex network than previously thought. Sodium 36-42 arginine vasopressin Homo sapiens 76-79 31365096-1 2019 CONTEXT: Although the physiology of sodium, water and arginine vasopressin (AVP), also known as antidiuretic hormone (ADH), has long been known, accumulating data suggest that this system operates as a more complex network than previously thought. Sodium 36-42 arginine vasopressin Homo sapiens 96-116 31365096-1 2019 CONTEXT: Although the physiology of sodium, water and arginine vasopressin (AVP), also known as antidiuretic hormone (ADH), has long been known, accumulating data suggest that this system operates as a more complex network than previously thought. Sodium 36-42 arginine vasopressin Homo sapiens 118-121 31715083-3 2019 A similar pathogenesis cascade is observed in all of these organs: loss of CFTR function leads to altered ion transport, consisting of decreased chloride and bicarbonate secretion via the CFTR channel and increased sodium absorption via epithelial sodium channel upregulation. Sodium 215-221 CF transmembrane conductance regulator Homo sapiens 75-79 31715083-3 2019 A similar pathogenesis cascade is observed in all of these organs: loss of CFTR function leads to altered ion transport, consisting of decreased chloride and bicarbonate secretion via the CFTR channel and increased sodium absorption via epithelial sodium channel upregulation. Sodium 248-254 CF transmembrane conductance regulator Homo sapiens 75-79 31715088-3 2019 CFTR primarily functions as a chloride channel that transports ions across the apical membrane of epithelial cells but has other functions, including bicarbonate secretion and inhibition of sodium transport. Sodium 190-196 CF transmembrane conductance regulator Homo sapiens 0-4 31655555-3 2019 The cause of Liddle syndrome is missense or frameshift mutations in SCNN1A, SCNN1B, or SCNN1G genes that encode epithelial sodium channel subunits. Sodium 123-129 sodium channel epithelial 1 subunit alpha Homo sapiens 68-74 31754387-1 2019 Lung epithelial sodium channel (ENaC) encoded by Scnn1 genes is essential for maintaining transepithelial salt and fluid homeostasis in the airway and the lung. Sodium 16-22 sodium channel epithelial 1 subunit alpha Homo sapiens 49-54 31618838-1 2019 This article describes the development of a French CEA in-house phased array Electro Magnetic Acoustic Transducer (EMAT) adapted to hot and opaque sodium environment for in-service inspection of Sodium Fast Reactors. Sodium 147-153 CEA cell adhesion molecule 3 Homo sapiens 51-54 31680980-2 2019 Ang II acts on Ang II type 1 receptors promoting sodium retention and vasoconstriction. Sodium 49-55 angiotensinogen Rattus norvegicus 0-6 31618838-1 2019 This article describes the development of a French CEA in-house phased array Electro Magnetic Acoustic Transducer (EMAT) adapted to hot and opaque sodium environment for in-service inspection of Sodium Fast Reactors. Sodium 195-201 CEA cell adhesion molecule 3 Homo sapiens 51-54 31680960-7 2019 Treatment of NaAsO2 resulted in increased cell proliferation and promotion of cell cycle progression from G1 to S/G2M phase, both of which could be attenuated by MK2206, a highly selective inhibitor of Akt. Sodium 13-19 AKT serine/threonine kinase 1 Homo sapiens 202-205 31601020-2 2019 In the kidney, HCN1, HCN2 and HCN3 are differentially expressed and contribute to the transport of sodium, potassium (K+) and ammonium into the nephrons. Sodium 99-105 hyperpolarization activated cyclic nucleotide gated potassium and sodium channel 2 Homo sapiens 21-25 31680960-10 2019 Our findings indicated that the phosphorylated activation of Akt played a role in the proliferation of HaCat cells upon long-term, low-dose NaAsO2 exposure through the phosphorylative regulation of its downstream cell cycle regulating factors of GSK-3beta/cyclin D1, p21 and p27, which could induce the promotion of cell cycle progression from G1 to S/G2M phase. Sodium 140-146 AKT serine/threonine kinase 1 Homo sapiens 61-64 31601786-1 2019 The sodium leak channel NALCN is a key player in establishing the resting membrane potential (RMP) in neurons and transduces changes in extracellular Ca2+ concentration ([Ca2+]e) into increased neuronal excitability as the downstream effector of calcium-sensing receptor (CaSR). Sodium 4-10 calcium sensing receptor Homo sapiens 246-270 31601786-1 2019 The sodium leak channel NALCN is a key player in establishing the resting membrane potential (RMP) in neurons and transduces changes in extracellular Ca2+ concentration ([Ca2+]e) into increased neuronal excitability as the downstream effector of calcium-sensing receptor (CaSR). Sodium 4-10 calcium sensing receptor Homo sapiens 272-276 31686980-11 2019 Immediately after the marathon race, we observed a negative correlation between IL-8 and daily EI, carbohydrate, fiber, fat, iron, calcium, potassium, and sodium intakes, and higher levels of IL-8 on runners with <3 g/kg/day of carbohydrate intake compared to runners with >5 g/kg/day. Sodium 155-161 C-X-C motif chemokine ligand 8 Homo sapiens 80-84 31578435-2 2019 In up to 90% of cases, it is caused by functional happloinsufficiency of the SCN1A gene, which encodes the alpha subunit of a voltage-dependent sodium channel (Nav1.1). Sodium 144-150 sodium channel, voltage-gated, type I, alpha Mus musculus 77-82 31578435-2 2019 In up to 90% of cases, it is caused by functional happloinsufficiency of the SCN1A gene, which encodes the alpha subunit of a voltage-dependent sodium channel (Nav1.1). Sodium 144-150 sodium channel, voltage-gated, type I, alpha Mus musculus 160-166 31339776-8 2019 Furthermore, plasma sodium levels were associated with log2 copeptin (males: st. beta=0.18, P<0.001; females: st. beta=0.17, P<0.001), log2 NT-proBNP (males: st. beta=0.07, P=0.008; females: st. beta=0.12, P<0.001) and log2 aldosterone (males: st. beta= -0.06, P=0.005; females: st. beta= -0.09, P<0.001). Sodium 20-26 arginine vasopressin Homo sapiens 60-68 31339776-9 2019 Copeptin and NT-proBNP showed interaction in their association with plasma sodium. Sodium 75-81 arginine vasopressin Homo sapiens 0-8 31339776-10 2019 Thus, our data support that [1] osmoregulation, as estimated from copeptin levels, is a main associate of plasma sodium, and moreover, [2] show a consistent association with volume markers, with higher NT-proBNP and lower aldosterone in subjects with higher plasma sodium. Sodium 113-119 arginine vasopressin Homo sapiens 66-74 31220425-0 2019 Interaction of central angiotensin II and aldosterone on sodium intake and blood pressure. Sodium 57-63 angiotensinogen Rattus norvegicus 23-37 30446179-8 2019 Alterations in metabolic pathways associated with the sensitivity of sodium, potassium, magnesium and calcium may lead to obesity, hypertension, and insulin resistance. Sodium 69-75 insulin Homo sapiens 149-156 31734652-15 2019 NaHS caused more limitation of inflammation than leptin and curcumin by affecting iNOS. Sodium 0-4 nitric oxide synthase 2 Rattus norvegicus 82-86 31299140-2 2019 A central component of the NMJ is the sodium-dependent high-affinity choline transporter 1 (CHT1), a solute carrier protein (gene symbol SLC5A7), responsible for the reuptake of choline into nerve termini has recently been implicated as one of several autosomal recessive causes of CMS. Sodium 38-44 solute carrier family 5 member 7 Homo sapiens 55-90 31299140-2 2019 A central component of the NMJ is the sodium-dependent high-affinity choline transporter 1 (CHT1), a solute carrier protein (gene symbol SLC5A7), responsible for the reuptake of choline into nerve termini has recently been implicated as one of several autosomal recessive causes of CMS. Sodium 38-44 solute carrier family 5 member 7 Homo sapiens 92-96 31299140-2 2019 A central component of the NMJ is the sodium-dependent high-affinity choline transporter 1 (CHT1), a solute carrier protein (gene symbol SLC5A7), responsible for the reuptake of choline into nerve termini has recently been implicated as one of several autosomal recessive causes of CMS. Sodium 38-44 solute carrier family 5 member 7 Homo sapiens 137-143 31626691-6 2019 Results: The study demonstrated that NaHS suppressed ERK 1/2 pathway activity similarly to PD98059 in retinas of experimental glaucoma rats, while PD98059 also similarly suppressed glial activation, NF-kappaB pathway, NADPH oxidase, and TNF-alpha production. Sodium 37-41 tumor necrosis factor Rattus norvegicus 237-246 31368174-6 2019 Detailed analysis of Nphs2 pod during early sodium retention, revealed increased expression of full-length ENaC subunits and alphaENaC cleavage product with concomitant increase in ENaC activity as tested by amiloride application, and augmented collecting duct Na+ /K+ -ATPase expression. Sodium 44-50 NPHS2 stomatin family member, podocin Homo sapiens 21-26 31368174-11 2019 In conclusion, characterizing the volume handling of Nphs2 pod revealed early sodium retention occurring independent to aberrantly filtered plasma proteases. Sodium 78-84 NPHS2 stomatin family member, podocin Homo sapiens 53-58 31311986-5 2019 FGF12 positively regulates the activity of voltage-gated sodium channels. Sodium 57-63 fibroblast growth factor 12 Homo sapiens 0-5 30407370-3 2019 Our objective was to evaluate the impact of renin angiotensin system activation, on hemodynamic deficiency and renal outcome in patient with septic shock and to assess whether urinary sodium could be a reliable test for high plasma renin concentration screening. Sodium 184-190 renin Homo sapiens 232-237 32514438-7 2020 Conclusion: The incidence of hyponatremia is not low during treatment with terlipressin; a higher baseline serum sodium level is a risk factor for hyponatremia during treatment with terlipressin, and the mechanism may be related to endogenous vasopressin preconditioning. Sodium 113-119 arginine vasopressin Homo sapiens 243-254 31546789-9 2019 Such integrated modulation of peripheral taste sensitivity by AngII may play an important role in sodium/calorie homeostasis. Sodium 98-104 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 62-67 31532390-0 2019 ENaC-mediated sodium influx exacerbates NLRP3-dependent inflammation in Cystic Fibrosis. Sodium 14-20 NLR family pyrin domain containing 3 Homo sapiens 40-45 31530276-6 2019 AVP (1 muM) treated PV cardiomyocytes had higher late sodium (Na+) and Na+/Ca2+ exchanger (NCX) currents than control PV cardiomyocytes. Sodium 54-60 arginine vasopressin Homo sapiens 0-3 31532390-6 2019 These data support a role for sodium in modulating NLRP3-inflammasome activation. Sodium 30-36 NLR family pyrin domain containing 3 Homo sapiens 51-56 31720149-3 2019 Hyponatremia, delineated as a serum sodium (sNa) concentration <135 mmol/l, is a frequently seen electrolyte disturbance in practice and the prevalence, clinical impact; the prognostic factor of low SNa in STEMI/heart failure patients vary widely. Sodium 36-42 snail family transcriptional repressor 1 Homo sapiens 44-47 31720149-3 2019 Hyponatremia, delineated as a serum sodium (sNa) concentration <135 mmol/l, is a frequently seen electrolyte disturbance in practice and the prevalence, clinical impact; the prognostic factor of low SNa in STEMI/heart failure patients vary widely. Sodium 36-42 snail family transcriptional repressor 1 Homo sapiens 199-202 31632551-0 2019 Pre-B-cell colony enhancing factor regulates the alveolar epithelial sodium-water transport system through the ERK and AKT pathways. Sodium 69-75 mitogen-activated protein kinase 1 Homo sapiens 111-114 31632551-0 2019 Pre-B-cell colony enhancing factor regulates the alveolar epithelial sodium-water transport system through the ERK and AKT pathways. Sodium 69-75 AKT serine/threonine kinase 1 Homo sapiens 119-122 31632551-12 2019 In conclusion, PBEF inhibited the sodium-water transport system by activation of ERK and suppression of AKT signaling. Sodium 34-40 mitogen-activated protein kinase 1 Homo sapiens 81-84 31632551-12 2019 In conclusion, PBEF inhibited the sodium-water transport system by activation of ERK and suppression of AKT signaling. Sodium 34-40 AKT serine/threonine kinase 1 Homo sapiens 104-107 31572187-8 2019 These data together indicate that the transgenerational disruption in spermatogenesis by NH4Cl and/or Na2S may be through ERalpha-related DNA methylation and histone methylation pathways. Sodium 102-106 estrogen receptor 1 Homo sapiens 122-129 31565882-1 2019 BACKGROUND: Striatin and caveolin-1 (cav-1) are scaffolding/regulating proteins that are associated with salt-sensitive high blood pressure and promote renal sodium and water reabsorption, respectively. Sodium 158-164 caveolin 1 Rattus norvegicus 25-35 31129252-2 2019 Angiotensin II and aldosterone are the two most powerful biologically active products of the RAAS, inducing all of the classical actions of the RAAS including vasoconstriction, sodium retention, tissue remodeling and pro-inflammatory and pro-fibrotic effects. Sodium 177-183 angiotensinogen Homo sapiens 0-14 31565882-1 2019 BACKGROUND: Striatin and caveolin-1 (cav-1) are scaffolding/regulating proteins that are associated with salt-sensitive high blood pressure and promote renal sodium and water reabsorption, respectively. Sodium 158-164 caveolin 1 Rattus norvegicus 37-42 31276916-3 2019 Here we show that by ketohexokinase - the primary enzyme of fructose - is involved in regulation of renal sodium reabsorption and blood pressure via activation of the sodium hydrogen exchanger in renal proximal tubular cells. Sodium 106-112 ketohexokinase Mus musculus 21-35 31352823-11 2019 These data indicate that Agt reabsorbed by proximal tubules via megalin in nephrotic syndrome is converted to Ang II, which may contribute to sodium retention and edema formation by activating NHE3 and Epithelial Na Channel. Sodium 142-148 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 25-28 31352823-11 2019 These data indicate that Agt reabsorbed by proximal tubules via megalin in nephrotic syndrome is converted to Ang II, which may contribute to sodium retention and edema formation by activating NHE3 and Epithelial Na Channel. Sodium 142-148 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 110-116 31276916-9 2019 In conclusion, fructose metabolism by ketohexokinase increases sodium hydrogen exchanger activity in renal proximal tubular cells via decreased intracellular cAMP level, resulting in increased renal sodium reabsorption and blood pressure in mice. Sodium 63-69 ketohexokinase Mus musculus 38-52 31347464-6 2019 Urine NAG index was significantly correlated with urinary fractional excretion of sodium (FENa; rho = 0.76, p < 0.001) and plasma creatinine (rho = 0.74, p = 0.001). Sodium 82-88 N-acetyl-alpha-glucosaminidase Homo sapiens 6-9 31171222-3 2019 In comparison to aqueous dispersions, non-spectral interferences caused by sodium lead to under-evaluation of arsenic and silver NPs diameter by about 7% and 15% at NaCl concentration of 450 mg L-1 and about 28% and 41% at NaCl concentration of 4500 mg L-1, respectively. Sodium 75-81 immunoglobulin kappa variable 1-16 Homo sapiens 194-197 31171222-3 2019 In comparison to aqueous dispersions, non-spectral interferences caused by sodium lead to under-evaluation of arsenic and silver NPs diameter by about 7% and 15% at NaCl concentration of 450 mg L-1 and about 28% and 41% at NaCl concentration of 4500 mg L-1, respectively. Sodium 75-81 immunoglobulin kappa variable 1-16 Homo sapiens 253-256 31171222-4 2019 As a consequence of lower transport efficiency, sodium non-spectral interferences also lead to about a 9% lower number of detected NPs for dispersions of both arsenic and silver NPs in 4500 mg L-1 NaCl. Sodium 48-54 immunoglobulin kappa variable 1-16 Homo sapiens 193-196 31455381-0 2019 Influence of androgenic blockade with flutamide on pain behaviour and expression of the genes that encode the NaV1.7 and NaV1.8 voltage-dependent sodium channels in a rat model of postoperative pain. Sodium 146-152 sodium voltage-gated channel alpha subunit 10 Rattus norvegicus 121-127 31300201-6 2019 A cross-sectional association between baseline sodium intake and hs-cTnT (but not NT-proBNP) was observed, driven predominantly by a strong positive relation at an intake range of 0.2 to 2.4 g/day. Sodium 47-53 troponin T2, cardiac type Homo sapiens 68-72 31768122-5 2019 Occurrence of salinity induction in expression of SlSOS2 and P5CS, encoding a sodium/hydrogen antiporter and an enzyme for proline biosynthesis, is limited specifically to the morning, whereas that of SlDREB2, which encodes a transcription factor involved in tomato responses to several abiotic stresses such as salinity and drought, is restricted specifically to the evening. Sodium 78-84 calcineurin B-like interacting protein kinase Solanum lycopersicum 50-56 31768122-5 2019 Occurrence of salinity induction in expression of SlSOS2 and P5CS, encoding a sodium/hydrogen antiporter and an enzyme for proline biosynthesis, is limited specifically to the morning, whereas that of SlDREB2, which encodes a transcription factor involved in tomato responses to several abiotic stresses such as salinity and drought, is restricted specifically to the evening. Sodium 78-84 delta-1-pyrroline-5-carboxylate synthase Solanum lycopersicum 61-65 31474871-0 2019 Lack of Renal Tubular Glucocorticoid Receptor Decreases the Thiazide-Sensitive Na+/Cl- Cotransporter NCC and Transiently Affects Sodium Handling. Sodium 129-135 nuclear receptor subfamily 3, group C, member 1 Mus musculus 22-45 31474871-4 2019 Following diet switch to low sodium, Nr3c1 Pax8/LC1 mice exhibit a transient but significant reduction in the activity of NCC and expression of NHE3 and NKCC2 accompanied by significant increased Spak activity. Sodium 29-35 nuclear receptor subfamily 3, group C, member 1 Mus musculus 37-42 31474871-4 2019 Following diet switch to low sodium, Nr3c1 Pax8/LC1 mice exhibit a transient but significant reduction in the activity of NCC and expression of NHE3 and NKCC2 accompanied by significant increased Spak activity. Sodium 29-35 microtubule-associated protein 1B Mus musculus 48-51 31474871-4 2019 Following diet switch to low sodium, Nr3c1 Pax8/LC1 mice exhibit a transient but significant reduction in the activity of NCC and expression of NHE3 and NKCC2 accompanied by significant increased Spak activity. Sodium 29-35 solute carrier family 9 (sodium/hydrogen exchanger), member 3 Mus musculus 144-148 31474871-4 2019 Following diet switch to low sodium, Nr3c1 Pax8/LC1 mice exhibit a transient but significant reduction in the activity of NCC and expression of NHE3 and NKCC2 accompanied by significant increased Spak activity. Sodium 29-35 solute carrier family 12, member 1 Mus musculus 153-158 31375088-9 2019 The majority of sodium and calcium but few chloride channels showed differential expression in the song system, among them SCN8A and CACNA1E in the direct motor pathway, and CACNG4 and RYR2 in the anterior forebrain pathway. Sodium 16-22 voltage-dependent R-type calcium channel subunit alpha-1E Taeniopygia guttata 133-140 31102435-0 2019 Insulin Resistance and Renal Sodium Handling Influence Arterial Stiffness in Hypertensive Patients with Prevailing Sodium Intake. Sodium 115-121 insulin Homo sapiens 0-7 31339707-6 2019 For example, Na0.9Mo2O4 forms during thermal treatment of the 50% sodium discharged Sc2(MoO4)3 while KMo4O6 and K2MoO4 form with thermal treatment of 100% potassium discharged Sc2(MoO4)3. Sodium 66-72 trans-2,3-enoyl-CoA reductase Homo sapiens 84-87 31375088-9 2019 The majority of sodium and calcium but few chloride channels showed differential expression in the song system, among them SCN8A and CACNA1E in the direct motor pathway, and CACNG4 and RYR2 in the anterior forebrain pathway. Sodium 16-22 voltage-dependent calcium channel gamma-4 subunit Taeniopygia guttata 174-180 31375088-9 2019 The majority of sodium and calcium but few chloride channels showed differential expression in the song system, among them SCN8A and CACNA1E in the direct motor pathway, and CACNG4 and RYR2 in the anterior forebrain pathway. Sodium 16-22 ryanodine receptor 2 Taeniopygia guttata 185-189 31271255-1 2019 AIMS: Insulin causes sodium retention and hypoglycaemia and its use is associated with worse outcomes in heart failure (HF) with reduced ejection fraction. Sodium 21-27 insulin Homo sapiens 6-13 31169994-10 2019 In mice lacking the active transcellular Pi transport component sodium-dependent Pi transporter NaPi-IIb, the paracellular pathway was not upregulated. Sodium 64-70 solute carrier family 34 (sodium phosphate), member 2 Mus musculus 96-104 31049746-1 2019 BACKGROUND: A wide range of interesting mathematical models has been derived to predict the effect of intravenous fluid therapy on the serum sodium concentration (most notably the Adrogue-Madias equation), but unfortunately, these models cannot be applied to patients with disorders characterized by aberrant antidiuretic hormone (ADH) release, such as the syndrome of inappropriate ADH secretion (SIADH). Sodium 141-147 arginine vasopressin Homo sapiens 309-329 31168066-1 2019 Over the past 25 years, successive cloning of SLC34A1, SLC34A2 and SLC34A3, which encode the sodium-dependent inorganic phosphate (Pi) cotransport proteins 2a-2c, has facilitated the identification of molecular mechanisms that underlie the regulation of renal and intestinal Pi transport. Sodium 93-99 solute carrier family 34 member 3 Homo sapiens 67-74 31365577-4 2019 Sodium storage capacity was decreased in Ext1+/-Ext2+/- mice as reflected by a 77% reduction in endothelial surface layer thickness and a lower skin sodium-to-glycosaminoglycan ratio. Sodium 0-6 exostosin glycosyltransferase 1 Mus musculus 41-45 31365577-4 2019 Sodium storage capacity was decreased in Ext1+/-Ext2+/- mice as reflected by a 77% reduction in endothelial surface layer thickness and a lower skin sodium-to-glycosaminoglycan ratio. Sodium 149-155 exostosin glycosyltransferase 1 Mus musculus 41-45 31340476-4 2019 Initial studies demonstrated that sodium caseinate induced a M2-like macrophage phenotype that was attributed to the kappa-casein subunit. Sodium 34-40 casein kappa Bos taurus 117-129 31327057-4 2019 Two of them considered a Cx26 hemichannel embedded on a POPC bilayer with one of the di-cations and a sodium-chlorine solution. Sodium 102-108 gap junction protein beta 2 Homo sapiens 25-29 31145900-3 2019 For example, NKCC2 resorbs chloride with sodium and potassium ions at the apical membrane of epithelial cells in the kidney, whereas KCC3 releases chloride with potassium ions at the basolateral membrane. Sodium 41-47 solute carrier family 12 member 1 Homo sapiens 13-18 31061086-13 2019 This study uncovers a hitherto uncharacterized consequence of rhodopsin mislocalization: the activation of the lysosomal pathway, which negatively regulates the amount of the sodium-potassium ATPase (NKAalpha) on the inner segment plasma membrane. Sodium 175-181 rhodopsin Homo sapiens 62-71 30885820-1 2019 Nav1.1 and Nav1.2 are the voltage-gated sodium channel alpha subunit1 and 2, encoded by the genes of SCN1A and SCN2A. Sodium 40-46 sodium voltage-gated channel alpha subunit 1 Rattus norvegicus 101-106 30855313-2 2019 Altered salt taste perception caused by angiotensin-converting enzyme (ACE) inhibitors commonly prescribed to patients with HF may increase sodium consumption. Sodium 140-146 angiotensin I converting enzyme Homo sapiens 40-69 30855313-2 2019 Altered salt taste perception caused by angiotensin-converting enzyme (ACE) inhibitors commonly prescribed to patients with HF may increase sodium consumption. Sodium 140-146 angiotensin I converting enzyme Homo sapiens 71-74 30855313-3 2019 We hypothesized sodium intake, indicated by dietary sodium density, would be significantly higher among patients with HF prescribed ACE inhibitors compared with those not prescribed the drug. Sodium 16-22 angiotensin I converting enzyme Homo sapiens 132-135 30855313-3 2019 We hypothesized sodium intake, indicated by dietary sodium density, would be significantly higher among patients with HF prescribed ACE inhibitors compared with those not prescribed the drug. Sodium 52-58 angiotensin I converting enzyme Homo sapiens 132-135 30855313-4 2019 OBJECTIVE: The aim of this study was to assess the association between prescribed ACE inhibitors and dietary sodium density in patients with HF. Sodium 109-115 angiotensin I converting enzyme Homo sapiens 82-85 30855313-9 2019 t Tests were conducted to compare sodium intake between groups, and linear regression was conducted to examine whether prescribed ACE inhibitors independently predicted sodium density controlling for age, gender, New York Heart Association class, prescribed diuretics, and beta-blockers. Sodium 169-175 angiotensin I converting enzyme Homo sapiens 130-133 30855313-11 2019 Compared with those not prescribed an ACE inhibitor, 13% more sodium per kilocalorie was consumed by patients prescribed an ACE inhibitor. Sodium 62-68 angiotensin I converting enzyme Homo sapiens 38-41 30855313-11 2019 Compared with those not prescribed an ACE inhibitor, 13% more sodium per kilocalorie was consumed by patients prescribed an ACE inhibitor. Sodium 62-68 angiotensin I converting enzyme Homo sapiens 124-127 30855313-12 2019 Prescribed ACE inhibitor independently predicted dietary sodium density (beta = 0.238, P = .009). Sodium 57-63 angiotensin I converting enzyme Homo sapiens 11-14 30855313-13 2019 CONCLUSIONS: Sodium intake was higher among patients prescribed ACE inhibitors. Sodium 13-19 angiotensin I converting enzyme Homo sapiens 64-67 31127034-3 2019 In this study, we discovered that the sodium-dependent lysophosphatidylcholine (LPC) transporter major facilitator superfamily domain containing 2A (MFSD2A) is upregulated on activated CD8+ T cells and is required for memory T cell maintenance. Sodium 38-44 major facilitator superfamily domain containing 2A Mus musculus 149-155 31042565-0 2019 Cardiotonic steroid ouabain stimulates steroidogenesis in Leydig cells via the alpha3 isoform of the sodium pump. Sodium 101-107 cholinergic receptor, nicotinic, alpha polypeptide 3 Mus musculus 79-85 30835273-7 2019 RESULTS: During GLP-1 infusion, urinary sodium and osmolar excretions increased significantly compared with vehicle. Sodium 40-46 glucagon Homo sapiens 16-21 31042565-3 2019 The murine Leydig cell line MLTC-1 expresses both the ubiquitous, relatively ouabain-insensitive alpha1 isoform of the sodium pump and the ouabain-sensitive alpha3 isoform that is normally found in neuronal cells. Sodium 119-125 brain protein 1 Mus musculus 97-103 30985903-3 2019 In this study, we tested whether supplementation with chenodeoxycholic acid (CDCA) sodium, a hydrophobic bile salt, could sensitize rats to liver injury caused by a BSEP-inhibiting drug. Sodium 83-89 ATP binding cassette subfamily B member 11 Rattus norvegicus 165-169 31055186-11 2019 A high VWF:Ag/ADAMTS13:AC ratio was associated with increased white blood cell counts, together with decreased serum albumin and sodium at Pre and 1 W. CONCLUSIONS: A high VWF:Ag/ADAMTS13:AC ratio in acute-KD persisted after primary treatment in non-responders, and unbalanced substrate-to-enzyme ratio appeared to associate with vascular endothelial damage. Sodium 129-135 von Willebrand factor Homo sapiens 172-175 31055186-11 2019 A high VWF:Ag/ADAMTS13:AC ratio was associated with increased white blood cell counts, together with decreased serum albumin and sodium at Pre and 1 W. CONCLUSIONS: A high VWF:Ag/ADAMTS13:AC ratio in acute-KD persisted after primary treatment in non-responders, and unbalanced substrate-to-enzyme ratio appeared to associate with vascular endothelial damage. Sodium 129-135 von Willebrand factor Homo sapiens 7-10 30765103-1 2019 Mutations in the SLC34A3 gene, encoding the sodium/phosphate cotransporter 2C (NPTIIc), induce decreased renal phosphate reabsorption, hypophosphatemia, decreased fibroblast growth factor 23 and parathyroid hormone, and increased 1,25-dihydroxyvitamin D (1,25[OH]2D) levels. Sodium 44-50 solute carrier family 34 member 3 Homo sapiens 17-24 31115276-2 2019 ITD is an uncommon cause of dyshormonogenetic congenital hypothyroidism that results from inactivating mutations in the sodium/iodide symporter (NIS)-coding SLC5A5 gene. Sodium 120-126 solute carrier family 5 member 5 Homo sapiens 157-163 31321958-3 2019 Interleukin-1beta inhibited sodium currents in mouse hippocampal neurons and verified that protein kinase C epsilon contributed to the effect of Interleukin-1beta exposure. Sodium 28-34 interleukin 1 beta Mus musculus 0-17 31261774-1 2019 Regardless of the cause, symptomatic heart failure (HF) with reduced ejection fraction (rEF) is characterized by pathological activation of the renin-angiotensin-aldosterone system (RAAS) with sodium retention and extracellular fluid expansion (edema). Sodium 193-199 renin Homo sapiens 144-149 31269062-10 2019 The treatment with V2R antagonist (V2A) in the presence and absence of OT induced diuresis, sodium and potassium outflow. Sodium 92-98 arginine vasopressin receptor 2 Rattus norvegicus 19-22 30936040-5 2019 Additionally, two-year-old mice have an accumulation of TRPA1 channels and sodium channels NaV1.8 and NaV1.9 in the L4 and L5 lumbar dorsal root ganglia consistent with changes in nociceptive signaling. Sodium 75-81 sodium channel, voltage-gated, type X, alpha Mus musculus 91-97 31030607-0 2019 The Dopamine D1 Receptor and Angiotensin II Type-2 Receptor are Required for Inhibition of Sodium Transport Through a Protein Phosphatase 2A Pathway. Sodium 91-97 dopamine receptor D1 Homo sapiens 4-24 31012036-2 2019 TRPC3 has been shown to function in the modulation of calcium and sodium entry, but whether TRPC3 plays a role in cellular abnormalities of ADPKD cells has not been defined. Sodium 66-72 transient receptor potential cation channel, subfamily C, member 3 Mus musculus 0-5 30905471-0 2019 The TNF-derived TIP peptide activates the epithelial sodium channel and ameliorates experimental nephrotoxic serum nephritis. Sodium 53-59 tumor necrosis factor Mus musculus 4-7 31015582-3 2019 Factors that contribute to increased sodium reabsorption in obesity include kidney compression by visceral, perirenal and renal sinus fat; increased renal sympathetic nerve activity (RSNA); increased levels of anti-natriuretic hormones, such as angiotensin II and aldosterone; and adipokines, particularly leptin. Sodium 37-43 angiotensinogen Homo sapiens 245-259 31150497-12 2019 CONCLUSIONS: Exercise induces a continuous rise of plasma copeptin levels in healthy male volunteers independently of sodium levels and fluid intake. Sodium 118-124 arginine vasopressin Homo sapiens 58-66 30765103-1 2019 Mutations in the SLC34A3 gene, encoding the sodium/phosphate cotransporter 2C (NPTIIc), induce decreased renal phosphate reabsorption, hypophosphatemia, decreased fibroblast growth factor 23 and parathyroid hormone, and increased 1,25-dihydroxyvitamin D (1,25[OH]2D) levels. Sodium 44-50 solute carrier family 34 member 3 Homo sapiens 79-85 30765103-1 2019 Mutations in the SLC34A3 gene, encoding the sodium/phosphate cotransporter 2C (NPTIIc), induce decreased renal phosphate reabsorption, hypophosphatemia, decreased fibroblast growth factor 23 and parathyroid hormone, and increased 1,25-dihydroxyvitamin D (1,25[OH]2D) levels. Sodium 44-50 parathyroid hormone Homo sapiens 195-214 31113930-0 2019 Estrogen negatively regulates the renal epithelial sodium channel (ENaC) by promoting Derlin-1 expression and AMPK activation. Sodium 51-57 protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus 110-114 30100257-1 2019 BACKGROUND: The epithelial sodium channel ENaC consists of three subunits encoded by Scnn1a, Scnn1b, and Scnn1g and increased sodium absorption through this channel is hypothesized to lead to mucus dehydration and accumulation in cystic fibrosis (CF) patients. Sodium 27-33 sodium channel epithelial 1 subunit alpha Homo sapiens 85-91 30804211-0 2019 Naja atra venom peptide reduces pain by selectively blocking the voltage-gated sodium channel Nav1.8. Sodium 79-85 sodium channel, voltage-gated, type X, alpha Mus musculus 94-100 30804211-1 2019 The voltage-gated sodium channel Nav1.8 is preferentially expressed in peripheral nociceptive neurons and contributes to inflammatory and neuropathic pain. Sodium 18-24 sodium channel, voltage-gated, type X, alpha Mus musculus 33-39 31019304-1 2019 The serotonin transporter (SERT) regulates neurotransmitter homeostasis through the sodium- and chloride-dependent recycling of serotonin into presynaptic neurons1-3. Sodium 84-90 solute carrier family 6 member 4 Homo sapiens 4-25 31019304-1 2019 The serotonin transporter (SERT) regulates neurotransmitter homeostasis through the sodium- and chloride-dependent recycling of serotonin into presynaptic neurons1-3. Sodium 84-90 solute carrier family 6 member 4 Homo sapiens 27-31 30058365-2 2019 NHE1 uses the energy of allowing an extracellular sodium down its gradient into cells to remove one intracellular proton. Sodium 50-56 solute carrier family 9 member A1 Homo sapiens 0-4 31074207-1 2019 In the mammalian small intestine, sodium is primarily absorbed by Na+ /H+ exchange (NHE3) and Na-glucose cotransport (SGLT1) in the brush border membrane (BBM) of villus cells. Sodium 34-40 solute carrier family 5 member 1 Homo sapiens 118-123 30583414-6 2019 Considering the process convenience and food safety of reducing sodium chloride with natural alkaline salt reagent in industrial pasta production, this could be a potential approach for sodium reduction. Sodium 64-70 solute carrier family 45 member 1 Homo sapiens 129-134 30975755-7 2019 We find that the antagonists shift CCR2 into several stable inactive conformations that are distinct from the crystal structure conformation and disrupt a continuous internal water and sodium ion pathway, preventing transitions to an active-like state. Sodium 185-191 C-C motif chemokine receptor 2 Homo sapiens 35-39 31032385-1 2019 The aim of this study was to assess the feasibility of rapid sodium MRI (23Na-MRI) for the imaging of peritoneal cancer deposits in high grade serous ovarian cancer (HGSOC) and to evaluate the relationship of 23Na-MRI with tumour cellularity. Sodium 61-67 cell cycle regulator of NHEJ Homo sapiens 73-81 31032385-9 2019 This study demonstrates that 23Na-MRI using 3D-cones can rapidly assess sodium concentration in peritoneal deposits of HGSOC and that TSC may serve as a biomarker of tumour cellularity. Sodium 72-78 cell cycle regulator of NHEJ Homo sapiens 29-37 30816701-6 2019 We discovered that sodium adduct ions, [M + H + Na]2+, allowed baseline SLIM SUPER IM resolution for all Abeta epimer sets assessed, while such baseline separations were unachievable for their [M + 2H]2+ doubly protonated ions. Sodium 19-25 amyloid beta precursor protein Homo sapiens 105-110 30771107-5 2019 Other than poor dissolution, cation adduction such as by sodium ions is also a major contributing factor to the mass-dependent loss in sensitivity in both ESI and DESI, leading to an increase in limits of detection for larger proteins. Sodium 57-63 desumoylating isopeptidase 2 Homo sapiens 163-167 30328093-9 2019 After multivariable adjustment, a 1 mmol/L increase in baseline serum sodium was associated with a 1.5 mL/min/1.73 m2 decline in eGFR during the study period (95% CI 0.9, 2.0). Sodium 70-76 CD59 molecule (CD59 blood group) Homo sapiens 106-111 30803087-1 2019 Angiotensin II (Ang II) acts on Ang II type 1 (AT1) receptors located in the organum vasculosum and subfornical organ (SFO) of the lamina terminalis as a main facilitatory mechanism of sodium appetite. Sodium 185-191 angiotensinogen Homo sapiens 0-23 29522854-6 2019 In addition, we found upregulation of neuronal inhibitory ligands and their cognate microglial receptors, while downregulation of Esr1 and Scn1a, encoding estrogen receptor alpha and voltage-gated sodium-channel Na(v)1.1, respectively, was observed. Sodium 197-203 sodium voltage-gated channel alpha subunit 1 Rattus norvegicus 139-144 30862903-0 2019 Postprandial Effects on ENaC-Mediated Sodium Absorption. Sodium 38-44 sodium channel epithelial 1 subunit gamma Rattus norvegicus 24-28 30663188-4 2019 We hypothesized that activation of TRPV1 by acid enabled QX-314, a membrane impermeable sodium channel blocker, to inhibit acid-induced activation of esophageal nociceptive C fiber neurons. Sodium 88-94 transient receptor potential cation channel subfamily V member 1 Cavia porcellus 35-40 30663188-11 2019 CONCLUSION AND INFERENCES: Our data demonstrated that activation of TRPV1 by acid enabled membrane impermeable sodium channel blocker QX-314 to inhibit acid-induced activation in esophageal nociceptive C fibers. Sodium 111-117 transient receptor potential cation channel subfamily V member 1 Cavia porcellus 68-73 31344212-1 2019 The renin-angiotensin-aldosterone system modulates volume, sodium and potassium homeostasis. Sodium 59-65 renin Homo sapiens 4-9 31344212-2 2019 In the setting of a high sodium diet, up to 30% of patients with hypertension have a low or suppressed renin and increased volume. Sodium 25-31 renin Homo sapiens 103-108 30790705-13 2019 Our results also suggest that vascular angiotensin II is the main mediator of high sodium-programmed endothelial dysfunction, promoting COX-2 expression and oxidative stress. Sodium 83-89 angiotensinogen Rattus norvegicus 39-53 30379098-0 2019 (Pro)renin receptor contributes to pregnancy-induced sodium-water retention in rats via activation of intrarenal RAAS and alpha-ENaC. Sodium 53-59 ATPase H+ transporting accessory protein 2 Rattus norvegicus 5-19 30566002-7 2019 In human renal proximal tubule cells, the transient expression of GPR37LI increased intracellular sodium, whereas the silencing of GPR37LI decreased intracellular sodium. Sodium 98-104 G protein-coupled receptor 37 Homo sapiens 66-71 30566002-7 2019 In human renal proximal tubule cells, the transient expression of GPR37LI increased intracellular sodium, whereas the silencing of GPR37LI decreased intracellular sodium. Sodium 163-169 G protein-coupled receptor 37 Homo sapiens 131-136 29976269-3 2019 The milk concentration of calcium (Ca), potassium (K), magnesium (Mg), sodium (Na) and phosphorus (P) in the present study was quantified from mid-IR spectroscopy on 12 223 test-day records from 1717 Holstein-Friesian cows. Sodium 71-77 Weaning weight-maternal milk Bos taurus 4-8 30661474-3 2019 Extremely low-sodium diets (<=500 mg/d) elicit activation of the renin-angiotensin-aldosterone system and stimulate sympathetic outflow. Sodium 14-20 renin Homo sapiens 68-73 30661474-10 2019 Reducing sodium to 1000 mg/d increased renin activity, angiotensin II, and aldosterone ( P<0.01 for all) but did not alter mean arterial pressure (78+-2 versus 77+-2 mm Hg, P=0.56), muscle sympathetic nerve activity (13.9+-1.3 versus 13.9+-0.8 bursts/min, P=0.98), or plasma/urine norepinephrine. Sodium 9-15 renin Homo sapiens 39-44 30661474-10 2019 Reducing sodium to 1000 mg/d increased renin activity, angiotensin II, and aldosterone ( P<0.01 for all) but did not alter mean arterial pressure (78+-2 versus 77+-2 mm Hg, P=0.56), muscle sympathetic nerve activity (13.9+-1.3 versus 13.9+-0.8 bursts/min, P=0.98), or plasma/urine norepinephrine. Sodium 9-15 angiotensinogen Homo sapiens 55-69 30661474-12 2019 These data suggest that reducing sodium from 2300 to 1000 mg/d stimulates the renin-angiotensin-aldosterone system, does not increase resting basal sympathetic outflow, and reduces sympathetic vascular transduction in normotensive adults. Sodium 33-39 renin Homo sapiens 78-83 30731085-1 2019 Cardiac sodium (Na+) potassium ATPase (NaK) pumps, neuronal sodium channels (INa), and sodium calcium (Ca2+) exchangers (NCX1) may co-localize to form a Na+ microdomain. Sodium 8-14 solute carrier family 8 member A1 Canis lupus familiaris 121-125 30604288-1 2019 Sodium-coupled monocarboxylate transporters SMCT1 (SLC5A8) and SMCT2 (SLC5A12) mediate the high- and low-affinity transport of lactate in the kidney, but their regulatory mechanism is still unknown. Sodium 0-6 solute carrier family 5 member 12 Homo sapiens 63-68 30604288-1 2019 Sodium-coupled monocarboxylate transporters SMCT1 (SLC5A8) and SMCT2 (SLC5A12) mediate the high- and low-affinity transport of lactate in the kidney, but their regulatory mechanism is still unknown. Sodium 0-6 solute carrier family 5 member 12 Homo sapiens 70-77 30839176-1 2019 Sodium transport in the thick ascending loop of Henle (TAL) is tightly regulated by numerous factors, especially angiotensin II (Ang II), a key end-product of the renin-angiotensin system (RAS). Sodium 0-6 angiotensinogen Homo sapiens 113-127 30839176-1 2019 Sodium transport in the thick ascending loop of Henle (TAL) is tightly regulated by numerous factors, especially angiotensin II (Ang II), a key end-product of the renin-angiotensin system (RAS). Sodium 0-6 angiotensinogen Homo sapiens 129-135 30617209-0 2019 Increased Resurgent Sodium Currents in Nav1.8 Contribute to Nociceptive Sensory Neuron Hyperexcitability Associated with Peripheral Neuropathies. Sodium 20-26 sodium channel, voltage-gated, type X, alpha Mus musculus 39-45 30617209-5 2019 We show that, in male DRG neurons, these mutations, which impair inactivation, significantly increase TTX-resistant resurgent sodium currents mediated by Nav1.8. Sodium 126-132 sodium channel, voltage-gated, type X, alpha Mus musculus 154-160 30724273-1 2019 The monovalent sodium ion (Na+) is a critical modulator of thrombin. Sodium 15-21 coagulation factor II, thrombin Homo sapiens 59-67 30718474-3 2019 Here, we are able to trigger the activity of the third sodium electrochemically via the formation of a disordered NaxV2(PO4)2F3 phase of tetragonal symmetry (I4/mmm space group). Sodium 55-61 PPP1R2C family member C Homo sapiens 158-176 30862903-2 2019 An abundance of research supports the ability of insulin to augment epithelial sodium channel (ENaC) transport. Sodium 79-85 sodium channel epithelial 1 subunit gamma Rattus norvegicus 95-99 30862903-3 2019 This study hypothesized that ENaC contributes to the increase in renal sodium reabsorption following a meal. Sodium 71-77 sodium channel epithelial 1 subunit gamma Rattus norvegicus 29-33 30862903-10 2019 These results demonstrate that insulin regulation of ENaC is a potential mechanism to preserve sodium and volume loss following a meal, and that this regulation is distinct from classical ENaC regulation by RAAS. Sodium 95-101 sodium channel epithelial 1 subunit gamma Rattus norvegicus 53-57 30788735-0 2019 Correlation between Urinary Excretion of Arginine-Vasopressin and Renal Reabsorption of Sodium and Water. Sodium 88-94 arginine vasopressin Rattus norvegicus 50-61 30353743-2 2019 Acute GLP-1RA administration increases urinary excretion of sodium and other electrolytes. Sodium 60-66 glucagon Homo sapiens 6-11 30788735-4 2019 It was found that urinary excretion of arginine-vasopressin directly correlated with reabsorption of solute-free water and renal sodium excretion. Sodium 129-135 arginine vasopressin Rattus norvegicus 48-59 30419292-4 2019 The majority of proximal tubule sodium reabsorption is directly or indirectly mediated by the sodium-hydrogen exchanger 3 (NHE3). Sodium 32-38 solute carrier family 9 (sodium/hydrogen exchanger), member 3 Mus musculus 94-121 30419292-4 2019 The majority of proximal tubule sodium reabsorption is directly or indirectly mediated by the sodium-hydrogen exchanger 3 (NHE3). Sodium 32-38 solute carrier family 9 (sodium/hydrogen exchanger), member 3 Mus musculus 123-127 30252533-7 2019 Instead, sodium-hydrogen exchanger type 3 levels in the proximal tubule were dramatically reduced in Epac1-/- and Epac2-/- mice. Sodium 9-15 Rap guanine nucleotide exchange factor (GEF) 3 Mus musculus 101-106 30252533-10 2019 Deletion of Epac1 and Epac2 decreases sodium-hydrogen exchanger type 3 expression in the proximal tubule, leading to polyuria and osmotic diuresis.-Cherezova, A., Tomilin, V., Buncha, V., Zaika, O., Ortiz, P. A., Mei, F., Cheng, X., Mamenko, M., Pochynyuk, O. Urinary concentrating defect in mice lacking Epac1 or Epac2. Sodium 38-44 Rap guanine nucleotide exchange factor (GEF) 3 Mus musculus 12-17 30055194-4 2019 In contrast to NET, DAT and SERT, OCT3 has higher capacity and lower affinity for substrates, is sodium-independent, and is multi-specific, with the capacity to transport norepinephrine, dopamine, serotonin and histamine. Sodium 97-103 solute carrier family 6 member 4 Homo sapiens 28-32 30559144-0 2019 Kir4.1/Kir5.1 Activity Is Essential for Dietary Sodium Intake-Induced Modulation of Na-Cl Cotransporter. Sodium 48-54 solute carrier family 12, member 3 Mus musculus 84-103 30559144-1 2019 BACKGROUND: Dietary sodium intake regulates the thiazide-sensitive Na-Cl cotransporter (NCC) in the distal convoluted tubule (DCT). Sodium 20-26 solute carrier family 12, member 3 Mus musculus 67-86 30559144-1 2019 BACKGROUND: Dietary sodium intake regulates the thiazide-sensitive Na-Cl cotransporter (NCC) in the distal convoluted tubule (DCT). Sodium 20-26 solute carrier family 12, member 3 Mus musculus 88-91 30559144-6 2019 Low sodium intake increased total and phosphorylated NCC expression and augmented hydrochlorothiazide-induced natriuresis; high sodium intake had opposite effects. Sodium 4-10 solute carrier family 12, member 3 Mus musculus 53-56 30559144-7 2019 Thus, elevated NCC activity induced by low sodium intake was associated with upregulation of Kir4.1/Kir5.1 activity in the DCT, whereas inhibition of NCC activity by high sodium intake was associated with diminished Kir4.1/Kir5.1 activity. Sodium 43-49 solute carrier family 12, member 3 Mus musculus 15-18 30559144-7 2019 Thus, elevated NCC activity induced by low sodium intake was associated with upregulation of Kir4.1/Kir5.1 activity in the DCT, whereas inhibition of NCC activity by high sodium intake was associated with diminished Kir4.1/Kir5.1 activity. Sodium 171-177 solute carrier family 12, member 3 Mus musculus 150-153 30559144-11 2019 CONCLUSIONS: Stimulation of Kir4.1/Kir5.1 by low intake of dietary sodium is essential for NCC upregulation, and inhibition of Kir4.1/Kir5.1 induced by high sodium intake is a key step for downregulation of NCC. Sodium 67-73 solute carrier family 12, member 3 Mus musculus 91-94 30559144-11 2019 CONCLUSIONS: Stimulation of Kir4.1/Kir5.1 by low intake of dietary sodium is essential for NCC upregulation, and inhibition of Kir4.1/Kir5.1 induced by high sodium intake is a key step for downregulation of NCC. Sodium 67-73 solute carrier family 12, member 3 Mus musculus 207-210 30508412-4 2019 The present results are the first to demonstrate that PKC/p38 MAPK signaling is involved in ANGII-induced water and sodium intake and oxytocin (OT) secretion in OVX rats. Sodium 116-122 angiotensinogen Rattus norvegicus 92-97 30740300-7 2019 The present case of isolated ACTH deficiency was characterized by a slowly progressive decline in the serum sodium level, which became manifest well before appearance of any clinical symptoms, suggesting that the serum sodium level may be used to predict progression to isolated ACTH deficiency.Thus, not only serum sodium levels need to be monitored in patients suspected of having isolated ACTH deficiency, but ACTH and cortisol levels need to be monitored in those exhibiting a decline in serum sodium levels. Sodium 108-114 proopiomelanocortin Homo sapiens 29-33 30740300-7 2019 The present case of isolated ACTH deficiency was characterized by a slowly progressive decline in the serum sodium level, which became manifest well before appearance of any clinical symptoms, suggesting that the serum sodium level may be used to predict progression to isolated ACTH deficiency.Thus, not only serum sodium levels need to be monitored in patients suspected of having isolated ACTH deficiency, but ACTH and cortisol levels need to be monitored in those exhibiting a decline in serum sodium levels. Sodium 219-225 proopiomelanocortin Homo sapiens 29-33 30740300-7 2019 The present case of isolated ACTH deficiency was characterized by a slowly progressive decline in the serum sodium level, which became manifest well before appearance of any clinical symptoms, suggesting that the serum sodium level may be used to predict progression to isolated ACTH deficiency.Thus, not only serum sodium levels need to be monitored in patients suspected of having isolated ACTH deficiency, but ACTH and cortisol levels need to be monitored in those exhibiting a decline in serum sodium levels. Sodium 219-225 proopiomelanocortin Homo sapiens 279-283 30740300-7 2019 The present case of isolated ACTH deficiency was characterized by a slowly progressive decline in the serum sodium level, which became manifest well before appearance of any clinical symptoms, suggesting that the serum sodium level may be used to predict progression to isolated ACTH deficiency.Thus, not only serum sodium levels need to be monitored in patients suspected of having isolated ACTH deficiency, but ACTH and cortisol levels need to be monitored in those exhibiting a decline in serum sodium levels. Sodium 219-225 proopiomelanocortin Homo sapiens 279-283 30740300-7 2019 The present case of isolated ACTH deficiency was characterized by a slowly progressive decline in the serum sodium level, which became manifest well before appearance of any clinical symptoms, suggesting that the serum sodium level may be used to predict progression to isolated ACTH deficiency.Thus, not only serum sodium levels need to be monitored in patients suspected of having isolated ACTH deficiency, but ACTH and cortisol levels need to be monitored in those exhibiting a decline in serum sodium levels. Sodium 219-225 proopiomelanocortin Homo sapiens 279-283 30740300-7 2019 The present case of isolated ACTH deficiency was characterized by a slowly progressive decline in the serum sodium level, which became manifest well before appearance of any clinical symptoms, suggesting that the serum sodium level may be used to predict progression to isolated ACTH deficiency.Thus, not only serum sodium levels need to be monitored in patients suspected of having isolated ACTH deficiency, but ACTH and cortisol levels need to be monitored in those exhibiting a decline in serum sodium levels. Sodium 219-225 proopiomelanocortin Homo sapiens 29-33 30740300-7 2019 The present case of isolated ACTH deficiency was characterized by a slowly progressive decline in the serum sodium level, which became manifest well before appearance of any clinical symptoms, suggesting that the serum sodium level may be used to predict progression to isolated ACTH deficiency.Thus, not only serum sodium levels need to be monitored in patients suspected of having isolated ACTH deficiency, but ACTH and cortisol levels need to be monitored in those exhibiting a decline in serum sodium levels. Sodium 219-225 proopiomelanocortin Homo sapiens 279-283 30740300-7 2019 The present case of isolated ACTH deficiency was characterized by a slowly progressive decline in the serum sodium level, which became manifest well before appearance of any clinical symptoms, suggesting that the serum sodium level may be used to predict progression to isolated ACTH deficiency.Thus, not only serum sodium levels need to be monitored in patients suspected of having isolated ACTH deficiency, but ACTH and cortisol levels need to be monitored in those exhibiting a decline in serum sodium levels. Sodium 219-225 proopiomelanocortin Homo sapiens 279-283 30740300-7 2019 The present case of isolated ACTH deficiency was characterized by a slowly progressive decline in the serum sodium level, which became manifest well before appearance of any clinical symptoms, suggesting that the serum sodium level may be used to predict progression to isolated ACTH deficiency.Thus, not only serum sodium levels need to be monitored in patients suspected of having isolated ACTH deficiency, but ACTH and cortisol levels need to be monitored in those exhibiting a decline in serum sodium levels. Sodium 219-225 proopiomelanocortin Homo sapiens 279-283 30740300-7 2019 The present case of isolated ACTH deficiency was characterized by a slowly progressive decline in the serum sodium level, which became manifest well before appearance of any clinical symptoms, suggesting that the serum sodium level may be used to predict progression to isolated ACTH deficiency.Thus, not only serum sodium levels need to be monitored in patients suspected of having isolated ACTH deficiency, but ACTH and cortisol levels need to be monitored in those exhibiting a decline in serum sodium levels. Sodium 219-225 proopiomelanocortin Homo sapiens 29-33 30740300-7 2019 The present case of isolated ACTH deficiency was characterized by a slowly progressive decline in the serum sodium level, which became manifest well before appearance of any clinical symptoms, suggesting that the serum sodium level may be used to predict progression to isolated ACTH deficiency.Thus, not only serum sodium levels need to be monitored in patients suspected of having isolated ACTH deficiency, but ACTH and cortisol levels need to be monitored in those exhibiting a decline in serum sodium levels. Sodium 219-225 proopiomelanocortin Homo sapiens 279-283 30740300-7 2019 The present case of isolated ACTH deficiency was characterized by a slowly progressive decline in the serum sodium level, which became manifest well before appearance of any clinical symptoms, suggesting that the serum sodium level may be used to predict progression to isolated ACTH deficiency.Thus, not only serum sodium levels need to be monitored in patients suspected of having isolated ACTH deficiency, but ACTH and cortisol levels need to be monitored in those exhibiting a decline in serum sodium levels. Sodium 219-225 proopiomelanocortin Homo sapiens 279-283 30740300-7 2019 The present case of isolated ACTH deficiency was characterized by a slowly progressive decline in the serum sodium level, which became manifest well before appearance of any clinical symptoms, suggesting that the serum sodium level may be used to predict progression to isolated ACTH deficiency.Thus, not only serum sodium levels need to be monitored in patients suspected of having isolated ACTH deficiency, but ACTH and cortisol levels need to be monitored in those exhibiting a decline in serum sodium levels. Sodium 219-225 proopiomelanocortin Homo sapiens 279-283 30544113-1 2019 BACKGROUND: Low serum sodium (SNa) is associated with an increased mortality in chronic hemodialysis (HD) patients. Sodium 22-28 snail family transcriptional repressor 1 Homo sapiens 30-33 30236706-0 2019 Cooking parameters affect the sodium content of prepared pasta. Sodium 30-36 solute carrier family 45 member 1 Homo sapiens 57-62 30236706-4 2019 Pasta cooked without salt had <5 mg sodium/140 g serving, and 247-490 mg/serving when cooked in salted water by the different variations. Sodium 39-45 solute carrier family 45 member 1 Homo sapiens 0-5 30236706-6 2019 There was a linear relationship between salt concentration in cooking water and sodium in cooked pasta; doubling the concentration increased sodium by 243 mg/serving (>10% of 2300 mg/day), relative to the reference method. Sodium 80-86 solute carrier family 45 member 1 Homo sapiens 97-102 30236706-8 2019 Results allow more accurate estimation of sodium intake from cooked pasta, since food composition tables that do not reflect variations in cooking parameters. Sodium 42-48 solute carrier family 45 member 1 Homo sapiens 68-73 29902069-7 2019 The associations between the plasma renin activity and blood-pressure outcomes were evident in adults with especially high urine sodium excretion. Sodium 129-135 renin Homo sapiens 36-41 30071192-1 2019 The mammalian Na+/H+ exchanger isoform 1 (NHE1) is an integral membrane protein that regulates intracellular pH (pHi) by removing a single intracellular proton in exchange for one extracellular sodium ion. Sodium 194-200 solute carrier family 9 member A1 Homo sapiens 14-40 30071192-1 2019 The mammalian Na+/H+ exchanger isoform 1 (NHE1) is an integral membrane protein that regulates intracellular pH (pHi) by removing a single intracellular proton in exchange for one extracellular sodium ion. Sodium 194-200 solute carrier family 9 member A1 Homo sapiens 42-46 30849550-11 2019 Priming of IECs with recombinant human IFN-lambda3 promoted cellular defense against C parvum infection and abrogated C parvum-induced loss of barrier function by decreasing paracellular permeability to sodium. Sodium 203-209 interferon lambda 3 Homo sapiens 39-50 29902069-8 2019 CONCLUSION: Low plasma renin activity was associated with the development of hypertension in the middle-aged Asian population, especially in peoples with high sodium intake. Sodium 159-165 renin Homo sapiens 23-28 31692426-6 2019 Also, IGF-1 stimulates vascular relaxation through regulation of sodium/potassiumadenosine- triphosphatase. Sodium 65-71 insulin like growth factor 1 Homo sapiens 6-11 30843458-7 2019 Clinicians should monitor serum sodium levels in such patients not only just after the initiation of ACE inhibitors but also upon the appearance of those factors. Sodium 32-38 angiotensin I converting enzyme Homo sapiens 101-104 32097945-6 2019 Disorders of vasopressin secretion and action result in disturbances of body fluids tonicity, which are clinically recognized as abnormalities in reduced plasma sodium concentration or hyponatremia. Sodium 161-167 arginine vasopressin Homo sapiens 13-24 30244375-1 2019 The expression cloning some 25 years ago of the first member of SLC34 solute carrier family, the renal sodium-coupled inorganic phosphate cotransporter (NaPi-IIa) from rat and human tissue, heralded a new era of research into renal phosphate handling by focussing on the carrier proteins that mediate phosphate transport. Sodium 103-109 solute carrier family 34 member 1 Rattus norvegicus 153-161 30343332-5 2019 Generation of a conditional NaPi-IIb knockout mouse has demonstrated that this protein is critical for the maintenance of skeletal integrity during periods of phosphate restriction and that under normal physiological conditions, the passive sodium-independent pathway is likely be the more dominant pathway for intestinal phosphate absorption. Sodium 241-247 solute carrier family 34 (sodium phosphate), member 2 Mus musculus 28-36 31061349-2 2019 The vasopressor effects of Ang II include direct contraction of myocardium and vascular smooth muscles (SMs) along with aldosterone-mediated sodium retention. Sodium 141-147 angiotensinogen Homo sapiens 27-33 30582047-3 2018 It was found that when the compound containing sodium, such as Na2CO3 or Na2SO4 was added into NaF saturated solution to product the common ion effect of Na+, most of the NaF can be crystallized without evaporating concentration, and the added Na2CO3 or Na2SO4 can be recovered by cooling crystallization. Sodium 47-53 C-X-C motif chemokine ligand 8 Homo sapiens 95-98 30582047-3 2018 It was found that when the compound containing sodium, such as Na2CO3 or Na2SO4 was added into NaF saturated solution to product the common ion effect of Na+, most of the NaF can be crystallized without evaporating concentration, and the added Na2CO3 or Na2SO4 can be recovered by cooling crystallization. Sodium 47-53 C-X-C motif chemokine ligand 8 Homo sapiens 171-174 30266221-4 2018 With a therapeutic window this narrow, clinicians would like to know how serum sodium (SNa) concentration will respond to their therapy. Sodium 79-85 snail family transcriptional repressor 1 Homo sapiens 87-90 30266221-5 2018 Based on isotopic measurements, Edelman showed SNa level to be a function of exchangeable sodium and potassium divided by total-body water. Sodium 90-96 snail family transcriptional repressor 1 Homo sapiens 47-50 30043185-10 2018 Zonulin concentrations correlated significantly with total calorie-, protein-, carbohydrate-, sodium- and vitamin B12 intake. Sodium 94-100 haptoglobin Homo sapiens 0-7 30323262-8 2018 During the low-sodium intervention, markers rs858009, rs2835904, and rs860795 in KCNJ6 were significantly associated with the systolic BP (SBP) response (P = 8.82 x 10-6, 3.32 x 10-6, and 2.39 x 10-4, respectively), whereas rs858009 and rs2835904 were significantly correlated with the mean arterial pressure (MAP) response (P = 1.64 x 10-4 and 2.72 x 10-4, respectively). Sodium 15-21 potassium inwardly rectifying channel subfamily J member 6 Homo sapiens 81-86 30323262-11 2018 Gene-based analyses consistently revealed that KCNJ6 was significantly associated with the BP response to the sodium interventions. Sodium 110-116 potassium inwardly rectifying channel subfamily J member 6 Homo sapiens 47-52 30323262-12 2018 These findings suggest that KCNJ6 may contribute to variation of BP responses to dietary sodium interventions. Sodium 89-95 potassium inwardly rectifying channel subfamily J member 6 Homo sapiens 28-33 30571237-0 2018 Role of Insulin-Mediated Antinatriuresis in Sodium Homeostasis and Hypertension. Sodium 44-50 insulin Homo sapiens 8-15 30361971-6 2018 In this study, we have focused our attention on determining how the presence of sodium ion binding and additionally its first hydration sphere, in hA2AAR could influence the ligand positioning accuracy during molecular docking simulations for most of the available resting and activated hA2A AR crystal structures, using DockBench as a comparative benchmarking tool and implementing a new correlation coefficient (EM). Sodium 80-86 G protein-coupled receptor 162 Homo sapiens 147-150 29865968-8 2018 The results showed an average sodium intake of 179 mmol (4.1 g) per day [higher in males at 186 mmol (4.3 g) vs. 173 mmol (4.0 g) for females], significantly above the current WHO recommendations, though only 8% regularly add salt to food. Sodium 30-36 erythrocyte membrane protein band 4.1 like 2 Homo sapiens 57-62 30540824-6 2018 For the prediction of 3-month and 6-month mortality, serum sodium (sNa) levels had the highest area under curve (AUC; 0.799 and 0.818, respectively) among all parameters, and ALBI score showed the best performance (AUC = 0.691 and 0.740, respectively) compared with other 5 noninvasive models. Sodium 59-65 snail family transcriptional repressor 1 Homo sapiens 67-70 29913320-0 2018 Assessing the role of the acid-sensing ion channel ASIC4b in sodium uptake by larval zebrafish. Sodium 61-67 acid-sensing (proton-gated) ion channel family member 4b Danio rerio 51-57 30118317-9 2018 Targeted inhibition of sodium absorption by the NHE3 inhibitor tenapanor produced improvements in gastrointestinal transit similar to those produced by linaclotide treatment, suggesting that inhibition of fluid absorption by linaclotide contributes to improved gastrointestinal transit in CF. Sodium 23-29 solute carrier family 9 (sodium/hydrogen exchanger), member 3 Mus musculus 48-52 30063108-6 2018 The correlation analysis showed that S100A12 was positively associated with the somatic cell count and the sodium and chloride concentrations of milk. Sodium 107-113 S100 calcium binding protein A12 Bos taurus 37-44 30405154-8 2018 Sodium levels correlated negatively with WBC (P = 0.037), CRP (P < 0.0001), and number of hospital days (P = 0.020). Sodium 0-6 C-reactive protein Homo sapiens 58-61 30118317-10 2018 Our results demonstrate that linaclotide improves gastrointestinal transit in CF mouse models by increasing luminal fluidity through inhibiting NHE3-mediated sodium absorption. Sodium 158-164 solute carrier family 9 (sodium/hydrogen exchanger), member 3 Mus musculus 144-148 30498610-1 2018 We present a case of small-cell lung cancer (SCLC) with syndrome of inappropriate antidiuretic hormone secretion (SIADH) in which serum sodium gradually normalized with the onset of hypertension, refractory hypokalemia, and chloride-resistant metabolic alkalosis due to ectopic adrenocorticotrophic hormone (ACTH) secretion (EAS). Sodium 136-142 proopiomelanocortin Homo sapiens 308-312 30766810-1 2018 Parathyroid hormone (PTH) is the main regulator of calcium, phosphate, magnesium, sodium, and potassium homeostasis. Sodium 82-88 parathyroid hormone Homo sapiens 0-19 30766810-1 2018 Parathyroid hormone (PTH) is the main regulator of calcium, phosphate, magnesium, sodium, and potassium homeostasis. Sodium 82-88 parathyroid hormone Homo sapiens 21-24 29571302-6 2018 Sodium remained as the charge of the fragment ions and, thus, was useful for their structural identification through MSn. Sodium 0-6 moesin Homo sapiens 117-120 29356783-5 2018 On multivariate regression, severity of hypoalbuminemia was associated with increasing waitlist mortality, even after correcting for model for end stage liver disease-sodium and HCC [albumin, 2.5 to 3.4 g/dL: hazard ratio (HR), 1.81; 95% confidence interval (CI), 1.62-2.01; P<0.001; <2.5 g/dL: HR, 2.46; 95% CI, 2.20-2.76; P<0.001]. Sodium 167-173 albumin Homo sapiens 44-51 30374221-14 2018 We found a significant inverse linear correlation between serum sodium and C-reactive protein, as well as serum sodium and procalcitonin. Sodium 64-70 C-reactive protein Homo sapiens 75-93 30289627-2 2018 Loss of CFTR function disrupts chloride, bicarbonate and regulation of sodium transport, producing a cascade of mucus obstruction, inflammation, pulmonary infection, and ultimately damage in numerous organs. Sodium 71-77 CF transmembrane conductance regulator Homo sapiens 8-12 30377822-5 2018 Macrophages expressing VEGF-C impact non-osmotic sodium storage in the skin that in turn regulates salt sensitivity. Sodium 49-55 vascular endothelial growth factor C Mus musculus 23-29 30984869-0 2018 CENTRAL DIABETES INSIPIDUS AND CHEMOTHERAPY: USE OF A CONTINUOUS ARGININE VASOPRESSIN INFUSION FOR FLUID AND SODIUM BALANCE. Sodium 109-115 arginine vasopressin Homo sapiens 74-85 30338975-3 2018 Here, a novel and stable sodium titanate/carbon-black phosphorus (NTO/C-BP) hybrids are first fabricated as a promising anode material for advanced sodium-ion batteries. Sodium 25-31 CREB binding protein Homo sapiens 70-74 30333031-1 2018 BACKGROUND: Sodium/hydrogen exchanger 1 (NHE1), encoded by the SLC9A1 gene (SoLute Carrier family 9A1) in humans, is the main H+ efflux mechanism in maintaining alkaline intracellular pH (pHi) and Warburg effects in glioma. Sodium 12-18 solute carrier family 9 member A1 Homo sapiens 41-45 30333031-1 2018 BACKGROUND: Sodium/hydrogen exchanger 1 (NHE1), encoded by the SLC9A1 gene (SoLute Carrier family 9A1) in humans, is the main H+ efflux mechanism in maintaining alkaline intracellular pH (pHi) and Warburg effects in glioma. Sodium 12-18 solute carrier family 9 member A1 Homo sapiens 63-69 30326586-0 2018 Dietary Sodium Restriction Reduces Arterial Stiffness, Vascular TGF-beta-Dependent Fibrosis and Marinobufagenin in Young Normotensive Rats. Sodium 8-14 transforming growth factor, beta 1 Rattus norvegicus 64-72 30405294-10 2018 Conclusions: Ang II contributes to sodium retention in retainers. Sodium 35-41 angiotensinogen Homo sapiens 13-19 29923768-5 2018 In rats receiving intrarenal vehicle or intrarenal SCR siRNA, systemic angiotensin II infusion increased sodium retention and BP on day 1, and BP remained elevated throughout the 5-day study. Sodium 105-111 angiotensinogen Rattus norvegicus 71-85 29923768-7 2018 However, intrarenal GR siRNA infusion prevented angiotensin II-mediated sodium retention on day 1, induced a continuously negative cumulative sodium balance compared with angiotensin II alone, and reduced BP chronically. Sodium 72-78 angiotensinogen Rattus norvegicus 48-62 29758100-4 2018 Most often, low-renin levels are expression of a physiological response to sodium-volume overload, but also a significant number of secondary hereditary or acquired conditions falls within this category. Sodium 75-81 renin Homo sapiens 16-21 29944390-8 2018 In contrast, the ANG II infusion significantly lowered oxytocin levels from 1,498.5 +- 94.7 vs. 1,151.7 +- 118.1 pg/ml ( P < 0.001) on the low-sodium diet and from 1,663.3 +- 213.9 vs. 1,095.2 +- 87.4 pg/ml ( P = 0.03) on the liberal-sodium diet. Sodium 146-152 angiotensinogen Homo sapiens 17-23 29944390-8 2018 In contrast, the ANG II infusion significantly lowered oxytocin levels from 1,498.5 +- 94.7 vs. 1,151.7 +- 118.1 pg/ml ( P < 0.001) on the low-sodium diet and from 1,663.3 +- 213.9 vs. 1,095.2 +- 87.4 pg/ml ( P = 0.03) on the liberal-sodium diet. Sodium 237-243 angiotensinogen Homo sapiens 17-23 30120881-1 2018 Na+ , K+ -ATPase (NKA) activity, which establishes the sodium and potassium gradient across the cell membrane and is instrumental in the propagation of the nerve impulses, is altered in a number of neurological and neuropsychiatric disorders, including autism spectrum disorders (ASD). Sodium 55-61 tachykinin precursor 1 Homo sapiens 0-16 30120881-1 2018 Na+ , K+ -ATPase (NKA) activity, which establishes the sodium and potassium gradient across the cell membrane and is instrumental in the propagation of the nerve impulses, is altered in a number of neurological and neuropsychiatric disorders, including autism spectrum disorders (ASD). Sodium 55-61 tachykinin precursor 1 Homo sapiens 18-21 29777899-8 2018 A homozygous mutation of the intron 9 splice acceptor site of SLC5A5 gene, encoding the sodium/iodine symporter (NIS), was found in the DNA of one of the affected dogs. Sodium 88-94 solute carrier family 5 member 5 Canis lupus familiaris 62-68 30367157-3 2018 Here, we show that the MR and other members of the mineralocorticoid signalling pathway including HSP90 and FKBP4, possess anti-viral activity against HSV-1 independent of their effect on sodium transport, as shown by sodium channel inhibitors. Sodium 218-224 FKBP prolyl isomerase 4 Homo sapiens 108-113 30018422-2 2018 NHE1 plays an important role in maintaining intracellular pH homeostasis by exchanging one intracellular proton for one extracellular sodium ion. Sodium 134-140 solute carrier family 9 member A1 Homo sapiens 0-4 30172469-3 2018 One of these syndromes is caused by the impairment of the presynaptic sodium-dependent high-affinity choline transporter 1, as a result of a mutation of the SCL5A7 gene associated with congenital myasthenic syndrome type 20 (MIM # 617143). Sodium 70-76 solute carrier family 5 member 7 Homo sapiens 87-122 30323912-0 2018 An association of urinary sodium-potassium ratio with insulin resistance among Korean adults. Sodium 26-32 insulin Homo sapiens 54-61 30323912-1 2018 BACKGROUND/OBJECTIVES: This study was conducted to investigate the effects of sodium-potassium ratio on insulin resistance and sensitivity in Korean adults. Sodium 78-84 insulin Homo sapiens 104-111 30323912-5 2018 The generalized linear model was applied to determine the association between urinary sodium-potassium ratio and insulin resistance. Sodium 86-92 insulin Homo sapiens 113-120 30323912-8 2018 CONCLUSION: The present study suggests that high sodium-potassium ratio is related to high insulin resistance and low insulin sensitivity. Sodium 49-55 insulin Homo sapiens 91-98 30323912-8 2018 CONCLUSION: The present study suggests that high sodium-potassium ratio is related to high insulin resistance and low insulin sensitivity. Sodium 49-55 insulin Homo sapiens 118-125 30323912-9 2018 Decreasing sodium intake and increasing potassium intake are important for maintaining insulin sensitivity. Sodium 11-17 insulin Homo sapiens 87-94 30142028-0 2018 Neuronal (pro)renin receptor regulates deoxycorticosterone-induced sodium intake. Sodium 67-73 ATPase, H+ transporting, lysosomal accessory protein 2 Mus musculus 0-28 30142028-3 2018 Here, we investigated the involvement of the (pro)renin receptor (PRR), a component of the brain renin-angiotensin system, in the regulation of sodium intake in a neuron-specific PRR knockout (PRRKO) mouse model generated previously in our laboratory. Sodium 144-150 ATPase, H+ transporting, lysosomal accessory protein 2 Mus musculus 50-64 30350402-0 2018 The renal and blood pressure response to low sodium diet in P2X4 receptor knockout mice. Sodium 45-51 purinergic receptor P2X, ligand-gated ion channel 4 Mus musculus 60-64 30350402-8 2018 However, when P2X4-/- mice were placed on a low sodium diet, BP normalized. Sodium 48-54 purinergic receptor P2X, ligand-gated ion channel 4 Mus musculus 14-18 30104343-1 2018 Dravet syndrome is a severe, childhood-onset epilepsy largely due to heterozygous loss-of-function mutation of the gene SCN1A, which encodes the type 1 neuronal voltage-gated sodium (Na+) channel alpha subunit Nav1.1. Sodium 175-181 sodium channel, voltage-gated, type I, alpha Mus musculus 120-125 30319546-1 2018 Objectives: To examine the prevalence of genetic alterations of thyroid-stimulating hormone receptor (TSHR) gene and sodium-iodine symporter (NIS) in a series of thyroid fine needle biopsy (FNB) specimens with indeterminate cytology, and to assess the correlation of the type of genetic changes with clinical features and follow-up results in the target thyroid nodule. Sodium 117-123 solute carrier family 5 member 5 Homo sapiens 142-145 29959186-6 2018 The results showed that EPO could promote interleukin (IL) 10 (IL-10) expression; inhibit tumor necrosis factor-alpha (TNF-alpha), IL-6, and inducible nitric oxide synthase (iNOS) expressions; reduce the fractional excretion of sodium (FENa) and plasma creatinine (CREA) and urea; and promote the recovery of water and salt handling and AQP2 expression in BUO-R rats, especially in the high dose of EPO-treated group rats. Sodium 228-234 nitric oxide synthase 2 Rattus norvegicus 174-178 30231858-2 2018 The direct effect of angiotensin II (ANGII) on the AT-1 receptor in the proximal tubules is partly responsible for the sodium retention. Sodium 119-125 angiotensinogen Rattus norvegicus 21-35 30231858-2 2018 The direct effect of angiotensin II (ANGII) on the AT-1 receptor in the proximal tubules is partly responsible for the sodium retention. Sodium 119-125 angiotensinogen Rattus norvegicus 37-42 29489063-0 2018 Plasma kallikrein activates the epithelial sodium channel in vitro but is not essential for volume retention in nephrotic mice. Sodium 43-49 kallikrein B, plasma 1 Mus musculus 0-17 29771704-4 2018 Postmortem vitreous humor sodium and chloride (PMVSC) was reported to be a useful biochemical test in diagnosing saltwater drowning when the immersion time is less than 1 hour (SWD1). Sodium 26-32 RB binding protein 5, histone lysine methyltransferase complex subunit Homo sapiens 177-181 29790390-0 2018 Collecting duct principal, but not intercalated, cell prorenin receptor regulates renal sodium and water excretion. Sodium 88-94 ATPase, H+ transporting, lysosomal accessory protein 2 Mus musculus 54-71 30354328-8 2018 Standard renin-angiotensin-aldosterone system phenotyping confirmed the expected response to sodium loading. Sodium 93-99 renin Homo sapiens 9-14 30354328-9 2018 Cycle threshold values for MR-regulated targets ( SCNN1A, SCNN1G, TSC22D3) changed after sodium loading, and MR-regulated targets ( SCNN1A, SCNN1G, SGK1, and TSC22D3) correlated significantly with serum aldosterone and inversely with urinary sodium excretion. Sodium 89-95 sodium channel epithelial 1 subunit alpha Homo sapiens 50-56 29664160-12 2018 This suggests that stress- and vasopressin-independent mechanisms are responsible for the association of low sodium levels with mortality. Sodium 109-115 arginine vasopressin Homo sapiens 31-42 30032030-2 2018 Physiologically, NTCP is responsible for the majority of sodium-dependent bile acids uptake by hepatocytes. Sodium 57-63 solute carrier family 10 member 1 Homo sapiens 17-21 29050460-5 2018 We analyzed 90-day and 1-year all-cause mortality (ACM) in relation to predialysis serum sodium (sNa). Sodium 89-95 snail family transcriptional repressor 1 Homo sapiens 97-100 30200235-0 2018 Cardiotonic Steroids and the Sodium Trade Balance: New Insights into Trade-Off Mechanisms Mediated by the Na+/K+-ATPase. Sodium 29-35 tachykinin precursor 1 Homo sapiens 106-119 30145856-2 2018 The main factor of ascites formation is renal sodium retention due to activation of the renin-angiotensin-aldosterone system and sympathetic nervous system by the reduced effective volume secondary to splanchnic arterial vasodilation. Sodium 46-52 renin Homo sapiens 88-93 30134847-14 2018 CONCLUSIONS: A transient intradialytic increase in plasma sodium did not affect indices of endothelial function or sympathetic activity compared with standard hemodialysis, but coincided with higher plasma vasopressin levels. Sodium 58-64 arginine vasopressin Homo sapiens 206-217 30134847-15 2018 The beneficial effect of higher intradialytic sodium levels on hemodynamic stability might be mediated by vasopressin. Sodium 46-52 arginine vasopressin Homo sapiens 106-117 30118514-2 2018 In this study we hypothesized that the renal PRR mediates high fat diet (HFD)-induced sodium retention and elevated systolic blood pressure (SBP) by enhancing expression of the epithelial sodium channel (alpha-ENaC). Sodium 86-92 ATPase, H+ transporting, lysosomal accessory protein 2 Mus musculus 45-48 30118514-11 2018 We conclude that obesity induced sodium retention and elevated SBP are mediated by the PRR-SGK-1- alpha-ENaC pathway independent of Ang II. Sodium 33-39 ATPase, H+ transporting, lysosomal accessory protein 2 Mus musculus 87-90 30154700-4 2018 However, cytosolic sodium and calcium are also allosteric regulators of the NCX, thus adding kinetic constraints on the NCX-mediated fluxes and providing for complexity of the system dynamics. Sodium 19-25 solute carrier family 8 member A1 Homo sapiens 76-79 30154700-4 2018 However, cytosolic sodium and calcium are also allosteric regulators of the NCX, thus adding kinetic constraints on the NCX-mediated fluxes and providing for complexity of the system dynamics. Sodium 19-25 solute carrier family 8 member A1 Homo sapiens 120-123 30154700-5 2018 Our modeling indicates that the calcium-dependent activation and also calcium-dependent escape from the sodium-mediated inactive state of the NCX in astrocytes can form a positive feedback loop and lead to regenerative calcium influx. Sodium 104-110 solute carrier family 8 member A1 Homo sapiens 142-145 30089272-5 2018 Mechanistically, PKD2L1 deficiency increased p300-mediated acetylation of histone 3 lysine 27 on the promoter of sodium/calcium exchange 1 (NCX1) by repressing AMP-activated protein kinase (AMPK) activity, resulting in NCX1 overexpression and mitochondrial Ca2+ overload. Sodium 113-119 solute carrier family 8 member A1 Homo sapiens 140-144 30627311-4 2018 Treatment with a vasopressin analogue, desamino-D-arginine vasopressin (DDAVP) and forced intake of water restored plasma osmolality and serum sodium levels to normal. Sodium 143-149 arginine vasopressin Homo sapiens 17-28 30627311-4 2018 Treatment with a vasopressin analogue, desamino-D-arginine vasopressin (DDAVP) and forced intake of water restored plasma osmolality and serum sodium levels to normal. Sodium 143-149 arginine vasopressin Homo sapiens 59-70 30029710-5 2018 Most of articles in this review reported that 2.6-3 g/day of dietary sodium is effective for decreased BNP, renin, and aldosterone (neurohormonal) plasma levels in patients with HF. Sodium 69-75 renin Homo sapiens 108-113 30205538-1 2018 Changes in serum sodium concentration ([Na+]serum) can permit evaluation of the treatment effect of vasopressin antagonists (vaptans) in patients with worsening heart failure (HF) or cirrhotic ascites; that is, they may act as a treatment stratification biomarker. Sodium 17-23 arginine vasopressin Homo sapiens 100-111 30042401-0 2018 FliL association with flagellar stator in the sodium-driven Vibrio motor characterized by the fluorescent microscopy. Sodium 46-52 FLII actin remodeling protein Homo sapiens 0-4 29727629-2 2018 BACKGROUND: The renin angiotensin system (RAS) and the renal dopaminergic system (RDS) act as autocrine and paracrine systems to regulate renal sodium management and inflammation and their alterations have been associated to hypertension and renal damage. Sodium 144-150 renin Homo sapiens 16-21 30038319-0 2018 Allosteric sodium binding cavity in GPR3: a novel player in modulation of Abeta production. Sodium 11-17 G protein-coupled receptor 3 Homo sapiens 36-40 29505789-6 2018 We examined the mechanisms underlying these effects, with poly I:C significantly reducing peak sodium current, an effect dependent on the MyD88-independent TRIF dependent pathway. Sodium 95-101 TIR domain containing adaptor molecule 1 Homo sapiens 156-160 30038319-7 2018 The latter, when mutated into alanine, completely abolished the constitutive and agonist-stimulated adenylate cyclase activity of GPR3 receptor by disrupting its sodium binding cavity. Sodium 162-168 G protein-coupled receptor 3 Homo sapiens 130-134 30038319-9 2018 Taken together, these results suggest an important role of the allosteric sodium binding site for GPR3 activity and open a possible avenue for the modulation of Abeta production in the Alzheimer"s Disease. Sodium 74-80 G protein-coupled receptor 3 Homo sapiens 98-102 28882065-10 2018 Approximately 9.7% of the variation in serum high-sensitive C-reactive protein in diabetic non-hypertensive patients could be explained by body mass index, and intake of sodium, iron and cholesterol. Sodium 170-176 C-reactive protein Homo sapiens 60-78 28882065-13 2018 There was a significant association between dietary factors include zinc, iron, sodium and cholesterol and serum high-sensitive C-reactive protein, while there was an inverse association between dietary calcium and serum high-sensitive C-reactive protein in diabetic hypertensive individuals. Sodium 80-86 C-reactive protein Homo sapiens 128-146 29978892-8 2018 ANP augments vascular permeability and reduces vascular contractility, renin and aldosterone secretion, sympathetic nerve activity, and renal tubular sodium transport. Sodium 150-156 natriuretic peptide A Homo sapiens 0-3 29655575-7 2018 Here, we tested if CRISPR/Cas9-mediated editing of the Nf1 gene, which leads to functional remodeling of peripheral nociceptors through effects on the tetrodotoxin-sensitive (TTX-S) Na+ voltage-gated sodium channel (NaV1.7) and CaV2.2, could be affected using CNRP1, a peptide designed to target the CRMP2-neurofibromin interface. Sodium 200-206 neurofibromin 1 Homo sapiens 55-58 29779889-3 2018 Importantly, alteration of fluid flow promotes proliferation of SEZ cells in an ENaC-dependent manner, eliciting sodium and calcium signals that regulate proliferation via calcium-release-activated channels and phosphorylation of ERK. Sodium 113-119 mitogen-activated protein kinase 1 Mus musculus 230-233 29735631-8 2018 Collectively, the data are the first to demonstrate a role for TNF produced by the kidney in the modulation of sodium homeostasis and blood pressure regulation. Sodium 111-117 tumor necrosis factor Mus musculus 63-66 29659026-0 2018 beta1 subunit stabilises sodium channel Nav1.7 against mechanical stress. Sodium 25-31 BCL2 related protein A1 Homo sapiens 0-5 29626530-11 2018 Since NHE3 promotes sodium absorption, and it was increased in HFD group, this finding could contribute to explain the hypertension observed in obesity. Sodium 20-26 solute carrier family 9 (sodium/hydrogen exchanger), member 3 Mus musculus 6-10 29592526-2 2018 The purpose of the study aimed to investigate whether melamine and cyanuric acid induced NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation in the kidney, which may contribute to abnormal water and sodium handling in a rat model. Sodium 230-236 NLR family, pyrin domain containing 3 Rattus norvegicus 141-146 30038578-9 2018 GR+/+ mice increased fractional sodium excretion and reduced renal vascular resistance during the high salt challenge, retaining neutral sodium balance. Sodium 32-38 nuclear receptor subfamily 3, group C, member 1 Mus musculus 0-2 30038578-9 2018 GR+/+ mice increased fractional sodium excretion and reduced renal vascular resistance during the high salt challenge, retaining neutral sodium balance. Sodium 137-143 nuclear receptor subfamily 3, group C, member 1 Mus musculus 0-2 30116758-6 2018 However, a positive correlation was detected between sodium intake and levels of CD4+CD25+Foxp3+ Treg cells in SLE and a negative association between CD4+CD69+Foxp3- Treg cells and sodium intake in RA. Sodium 53-59 CD4 molecule Homo sapiens 81-84 30116758-6 2018 However, a positive correlation was detected between sodium intake and levels of CD4+CD25+Foxp3+ Treg cells in SLE and a negative association between CD4+CD69+Foxp3- Treg cells and sodium intake in RA. Sodium 181-187 CD4 molecule Homo sapiens 150-153 29967479-6 2018 Remarkably, ETV1 induction in human induced pluripotent stem cell-derived cardiomyocytes increases rapid conduction gene expression and inward sodium currents, converting them towards a HPS phenotype. Sodium 143-149 ETS variant transcription factor 1 Homo sapiens 12-16 30063865-2 2018 CFTR is an ion channel regulating transport of chloride, bicarbonate, and water, and influencing sodium resorption. Sodium 97-103 CF transmembrane conductance regulator Homo sapiens 0-4 31949699-9 2018 Cells treated with NaHS for 24 h showed significant upregulation of p-JAK2, and p-STAT3 expression, as well as increased cell viability when compared to the control cells. Sodium 19-23 signal transducer and activator of transcription 3 Homo sapiens 82-87 29953167-15 2018 Vasopressin receptor antagonists probably increase the intermediate outcome of serum sodium concentration (21 studies, 2641 participants: MD 4.17 mmol/L, 95% CI 3.18 to 5.16), corresponding to two and a half as many people having a 5 to 6 mmol/L increase in sodium concentration compared with placebo at 4 to 180 days (moderate certainty evidence due to risk of attrition bias) (18 studies, 2014 participants: RR 2.49, 95% CI 1.95 to 3.18). Sodium 85-91 arginine vasopressin Homo sapiens 0-11 29953167-15 2018 Vasopressin receptor antagonists probably increase the intermediate outcome of serum sodium concentration (21 studies, 2641 participants: MD 4.17 mmol/L, 95% CI 3.18 to 5.16), corresponding to two and a half as many people having a 5 to 6 mmol/L increase in sodium concentration compared with placebo at 4 to 180 days (moderate certainty evidence due to risk of attrition bias) (18 studies, 2014 participants: RR 2.49, 95% CI 1.95 to 3.18). Sodium 258-264 arginine vasopressin Homo sapiens 0-11 29953167-19 2018 AUTHORS" CONCLUSIONS: In people with chronic hyponatraemia, vasopressin receptor antagonists modestly raise serum sodium concentration at the cost of a 3% increased risk of it being rapid. Sodium 114-120 arginine vasopressin Homo sapiens 60-71 29915394-1 2018 A new microbial rhodopsin class that actively transports sodium out of the cell upon illumination was described in 2013. Sodium 57-63 rhodopsin Homo sapiens 16-25 29875317-6 2018 In particular, we use a small molecule to show that selective NaV1.1 inhibition (a) decreases sodium currents in colon-innervating dorsal root ganglion neurons, (b) reduces colonic nociceptor mechanical responses, and (c) normalizes the enhanced visceromotor response to distension observed in 2 mouse models of irritable bowel syndrome. Sodium 94-100 sodium channel, voltage-gated, type I, alpha Mus musculus 62-68 29514831-6 2018 Viral gene transfer of Kir2.1Delta314-315 in adult rat ventricular myocytes and human induced pluripotent stem cell-derived cardiomyocytes reduced inward rectifier potassium current and inward sodium current, maximum diastolic potential and action potential depolarization rate, and increased action potential duration. Sodium 193-199 potassium inwardly-rectifying channel, subfamily J, member 2 Rattus norvegicus 23-29 29514831-10 2018 Silencing the AP1 Upsilon-adaptin subunit in human induced pluripotent stem cell-derived cardiomyocytes reduced inward rectifier potassium current, inward sodium current, and maximum diastolic potential and impaired rate-dependent action potential duration adaptation. Sodium 155-161 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 14-17 28592435-8 2018 The adrenal response to exogenous angiotensin II was significantly lower in men than in women on both sodium intakes. Sodium 102-108 angiotensinogen Homo sapiens 34-48 29996375-6 2018 Results: The expression of TNF-alpha in serum of 7th day [ (17.03+-0.82) ng/ml] and 14th day [ (15.74+-0.91) ng/ml] of sodium aescinate group were lower than the corresponding period of PQ groups", and the difference had statistical significance (P<0.05) . Sodium 119-125 tumor necrosis factor Rattus norvegicus 27-36 29996375-7 2018 The expression of TGF-beta(1) in serum of 7th day[ (225.93+-8.33) ng/ml], 14th day [ (216.62+-9.48) ng/ml] and 28th[ (181.41+-6.10) ng/ml] of sodium aescinate group were lower than the corresponding period of PQ groups", and the difference had statistical significance (P<0.05) . Sodium 142-148 transforming growth factor, beta 1 Rattus norvegicus 18-29 29726784-8 2018 DIND was associated with a combination of decreasing sodium levels and increasing copeptin concentrations.CONCLUSIONSIncreased AVP may be the unifying factor explaining the co-occurrence of hyponatremia and DIND. Sodium 53-59 arginine vasopressin Homo sapiens 127-130 29765330-1 2018 It is known that circulating angiotensin II (ANG-II) acts on the circumventricular organs (CVOs), which partially lack a normal blood-brain barrier, to stimulate pressor responses, vasopressin (AVP), and oxytocin (OT) secretion, as well as sodium and water intake. Sodium 240-246 angiotensinogen Rattus norvegicus 29-43 28814103-7 2018 A significant negative linear correlation was demonstrated between serum sodium and plasma renin activity ( P = 0.005) and direct renin concentration ( P = 0.015) and between estimated glomerular filtration rate and aldosterone measured using radioimmunoassay ( P = 0.02) and immunochemiluminometric assay ( P = 0.016). Sodium 73-79 renin Homo sapiens 91-96 28814103-8 2018 A significant negative linear correlation existed between urine sodium and plasma renin activity ( P = 0.04) and aldosterone measured using radioimmunoassay ( P = 0.045). Sodium 64-70 renin Homo sapiens 82-87 29488676-2 2018 As insulin causes sodium retention and hypoglycaemia, its use might be associated with worse outcomes. Sodium 18-24 insulin Homo sapiens 3-10 29493068-2 2018 These pathophysiological abnormalities may be related to the increased actions of specific adipocyte-derived signalling molecules (aldosterone, neprilysin and leptin) that work in concert with increased renal sympathetic nerve traffic and activated beta2 -adrenergic receptors to promote sodium retention, microvascular rarefaction, cardiac fibrosis and systemic inflammation. Sodium 288-294 membrane metalloendopeptidase Homo sapiens 144-154 28796300-3 2018 Studies show that apelin mRNA is highly expressed in the inner stripe of kidney outer medulla, which plays an important role in process of water and sodium balance. Sodium 149-155 apelin Homo sapiens 18-24 29700922-0 2018 The responses of the inflammatory marker, pentraxin 3, to dietary sodium and potassium interventions. Sodium 66-72 pentraxin 3 Homo sapiens 42-53 29700922-10 2018 We found a positive correlation between the ln-transformed concentrations of pentraxin-3 and 24-hour urinary sodium during low and high Na+ periods (r = .269, P = .012) and a negative relationship with 24 hours urinary potassium excretion during high-salt and high-salt plus potassium periods (r = -.246, P = .02). Sodium 109-115 pentraxin 3 Homo sapiens 77-88 29765330-1 2018 It is known that circulating angiotensin II (ANG-II) acts on the circumventricular organs (CVOs), which partially lack a normal blood-brain barrier, to stimulate pressor responses, vasopressin (AVP), and oxytocin (OT) secretion, as well as sodium and water intake. Sodium 240-246 angiotensinogen Rattus norvegicus 45-51 29765330-6 2018 Furthermore, previous FCt decreased AVP secretion and sodium intake induced by central ANG-II. Sodium 54-60 angiotensinogen Rattus norvegicus 87-93 29447844-2 2018 Angiotensin II (Ang II) is important in the generation of sodium appetite and may function as a neurotransmitter or modulator to affect the synaptic transmission and the excitability of neurons. Sodium 58-64 angiotensinogen Rattus norvegicus 0-14 28623618-6 2018 The hyperpolarizing effect of ET-1 appears to be orchestrated via modulation of membrane conductances, namely voltage-gated sodium current (I Na) and outward transient potassium current (I KT). Sodium 124-130 endothelin 1 Rattus norvegicus 30-34 29447844-2 2018 Angiotensin II (Ang II) is important in the generation of sodium appetite and may function as a neurotransmitter or modulator to affect the synaptic transmission and the excitability of neurons. Sodium 58-64 angiotensinogen Rattus norvegicus 16-22 29031006-6 2018 Glucagon-like peptide-1 (GLP-1) has been reported to increase glomerular filtration rate (GFR), renal blood flow, and the fractional excretion both of sodium and potassium, with renal GLP-1 receptors present in afferent arteriolar vascular smooth muscle cells, glomerular endothelial cells and macrophages, juxtaglomerular cells, and the proximal tubule, perhaps mediating the greater natriuresis seen after oral than intravenous sodium. Sodium 151-157 glucagon Homo sapiens 0-23 29573721-0 2018 Novel heparin mimetics reveal cooperativity between exosite 2 and sodium-binding site of thrombin. Sodium 66-72 coagulation factor II, thrombin Homo sapiens 89-97 29573721-8 2018 Label-free surface plasmon resonance was used to assess the role of sodium ion in LMWL binding to thrombin at a fixed ionic strength. Sodium 68-74 coagulation factor II, thrombin Homo sapiens 98-106 29573721-11 2018 Interestingly, LMWLs display preference for the sodium-bound form of thrombin, which supports the existence of an energetic coupling between exosite 2 and sodium-binding site of thrombin. Sodium 48-54 coagulation factor II, thrombin Homo sapiens 69-77 29573721-11 2018 Interestingly, LMWLs display preference for the sodium-bound form of thrombin, which supports the existence of an energetic coupling between exosite 2 and sodium-binding site of thrombin. Sodium 48-54 coagulation factor II, thrombin Homo sapiens 178-186 29573721-11 2018 Interestingly, LMWLs display preference for the sodium-bound form of thrombin, which supports the existence of an energetic coupling between exosite 2 and sodium-binding site of thrombin. Sodium 155-161 coagulation factor II, thrombin Homo sapiens 69-77 29573721-11 2018 Interestingly, LMWLs display preference for the sodium-bound form of thrombin, which supports the existence of an energetic coupling between exosite 2 and sodium-binding site of thrombin. Sodium 155-161 coagulation factor II, thrombin Homo sapiens 178-186 29642240-0 2018 Sodium bicarbonate cotransporter NBCe2 gene variants increase sodium and bicarbonate transport in human renal proximal tubule cells. Sodium 62-68 solute carrier family 4 member 5 Homo sapiens 33-38 29642240-5 2018 We hypothesized that SLC4A5 rs10177833 and rs7571842 increase NBCe2 expression and human renal proximal tubule cell (hRPTC) sodium transport and may be a cause of salt sensitivity of blood pressure. Sodium 124-130 solute carrier family 4 member 5 Homo sapiens 21-27 29642240-9 2018 Increasing intracellular sodium enhanced the apical location of NBCe2 in HV hRPTCs (4.24+-0.35% to 11.06+-1.72% (P<0.05, N = 3, 2-way ANOVA, Holm-Sidak test)) as determined by Total Internal Reflection Fluorescence Microscopy (TIRFM). Sodium 25-31 solute carrier family 4 member 5 Homo sapiens 64-69 29642240-10 2018 In hRPTCs isolated from kidney tissue, increasing intracellular sodium enhanced bicarbonate-dependent pH recovery rate and increased NBCe2 mRNA and protein expressions to a greater extent in HV than WT SLC4A5 (+38.00+-6.23% vs HV normal salt (P<0.01, N = 4, 2-way ANOVA, Holm-Sidak test)). Sodium 64-70 solute carrier family 4 member 5 Homo sapiens 133-138 29642240-10 2018 In hRPTCs isolated from kidney tissue, increasing intracellular sodium enhanced bicarbonate-dependent pH recovery rate and increased NBCe2 mRNA and protein expressions to a greater extent in HV than WT SLC4A5 (+38.00+-6.23% vs HV normal salt (P<0.01, N = 4, 2-way ANOVA, Holm-Sidak test)). Sodium 64-70 solute carrier family 4 member 5 Homo sapiens 202-208 29642240-15 2018 CONCLUSION: NBCe2 activity is stimulated by an increase in intracellular sodium and is hyper-responsive in hRPTCs carrying HV SLC4A5 rs7571842 through an aberrant HNF4A-mediated mechanism. Sodium 73-79 solute carrier family 4 member 5 Homo sapiens 12-17 29642240-15 2018 CONCLUSION: NBCe2 activity is stimulated by an increase in intracellular sodium and is hyper-responsive in hRPTCs carrying HV SLC4A5 rs7571842 through an aberrant HNF4A-mediated mechanism. Sodium 73-79 solute carrier family 4 member 5 Homo sapiens 126-132 29329985-0 2018 The scavenger activity of the human P2X7 receptor differs from P2X7 pore function by insensitivity to antagonists, genetic variation and sodium concentration: Relevance to inflammatory brain diseases. Sodium 137-143 purinergic receptor P2X 7 Homo sapiens 36-49 29329985-0 2018 The scavenger activity of the human P2X7 receptor differs from P2X7 pore function by insensitivity to antagonists, genetic variation and sodium concentration: Relevance to inflammatory brain diseases. Sodium 137-143 purinergic receptor P2X 7 Homo sapiens 36-40 29378857-3 2018 We hypothesized that APCs participate in renal sodium transport and, thus, development of high blood pressure in response to angiotensin II plus a high-salt diet. Sodium 47-53 angiotensinogen Homo sapiens 125-139 29395172-1 2018 OBJECTIVES: To define the incidence and risk factors of postoperative sodium alterations in pediatric patients undergoing transsphenoidal surgery (TSS) for adrenocorticotropic hormone and growth hormone secreting pituitary adenomas. Sodium 70-76 proopiomelanocortin Homo sapiens 156-183 29669139-13 2018 Clinical Trial: Sodium-Restricted Diet and Diuretic in the Treatment of Severe Sleep Apnea (DESALT), https://clinicaltrials.gov/ct2/show/NCT01945801 ClinicalTrials.gov number: NCT01945801. Sodium 16-22 solute carrier family 6 member 10, pseudogene Homo sapiens 128-131 29973322-16 2018 The mRNA levels of 5-HIAA and MAO-A increased in the gastric tissues, and IDO1, 5-HT1A and 5-HT3A mRNAs decreased in the sodium chromate group. Sodium 121-127 5-hydroxytryptamine (serotonin) receptor 1A Mus musculus 80-86 29543590-0 2018 Relationship between urinary sodium-creatinine ratios and insulin resistance in Korean children and adolescents with obesity. Sodium 29-35 insulin Homo sapiens 58-65 29543590-2 2018 This study aimed to use data from the 2010 Korea National Health and Nutrition Examination Survey (KNHANES) to investigate the association between sodium (Na) intake and insulin resistance in children and adolescents with obesity. Sodium 147-153 insulin Homo sapiens 170-177 29556787-6 2018 Thirdly, the cooperative action of Ang II acting on AT1R and AVP stimulating both V1aR and V2 receptors in the kidney is necessary for the appropriate regulation of renal blood flow and the efficient resorption of sodium and water. Sodium 214-220 angiotensinogen Homo sapiens 35-41 29556787-6 2018 Thirdly, the cooperative action of Ang II acting on AT1R and AVP stimulating both V1aR and V2 receptors in the kidney is necessary for the appropriate regulation of renal blood flow and the efficient resorption of sodium and water. Sodium 214-220 arginine vasopressin Homo sapiens 61-64 29636870-1 2018 To investigate whether the reverse mode of sodium/calcium exchanger subtype 1 (NCX1) plays an important role in the excitability of detrusor cells in rats with partial bladder outflow obstruction (PBOO), PBOO was maintained for 6 weeks in forty female Wistar rats. Sodium 43-49 solute carrier family 8 member A1 Rattus norvegicus 79-83 29405531-1 2018 The allosteric modulation of G-protein-coupled receptors (GPCRs) by sodium ions has received significant attention as crystal structures of several receptors show Na+ ions bound to the inactive conformations at the conserved Asp2.50 . Sodium 68-74 beta-secretase 1 Homo sapiens 225-229 29530008-9 2018 After initiation of insulin therapy, capillary glucose normalized, and serum sodium rose from 133 on admission to 144 mmol/l during the hospital stay. Sodium 77-83 insulin Homo sapiens 20-27 29182730-7 2018 RESULTS: In the process of acute sodium loading, after adjusting for age and 24-hour urinary sodium concentration, SNPs in CYP11B2, PRKG1, SLC8A1 genes were significantly associated with systolic BP (SBP) rising in the additive and recessive model; SNPs in CYP4A11, PRKG1, SLC8A1, and ADRB2 genes were significantly associated with diastolic BP (DBP) rising. Sodium 33-39 solute carrier family 8 member A1 Homo sapiens 139-145 29182730-7 2018 RESULTS: In the process of acute sodium loading, after adjusting for age and 24-hour urinary sodium concentration, SNPs in CYP11B2, PRKG1, SLC8A1 genes were significantly associated with systolic BP (SBP) rising in the additive and recessive model; SNPs in CYP4A11, PRKG1, SLC8A1, and ADRB2 genes were significantly associated with diastolic BP (DBP) rising. Sodium 33-39 solute carrier family 8 member A1 Homo sapiens 273-279 29182730-7 2018 RESULTS: In the process of acute sodium loading, after adjusting for age and 24-hour urinary sodium concentration, SNPs in CYP11B2, PRKG1, SLC8A1 genes were significantly associated with systolic BP (SBP) rising in the additive and recessive model; SNPs in CYP4A11, PRKG1, SLC8A1, and ADRB2 genes were significantly associated with diastolic BP (DBP) rising. Sodium 93-99 solute carrier family 8 member A1 Homo sapiens 139-145 29182730-11 2018 CONCLUSION: SLC8A1 gene may contribute to BP change in the process of acute sodium loading in a Han Chinese population. Sodium 76-82 solute carrier family 8 member A1 Homo sapiens 12-18 29329358-10 2018 CONCLUSIONS: The results suggest that in AngII-dependent hypertension, Ang1-7 deficit contributes to sodium and fluid retention and thereby to BP elevation; a correction by Ang1-7 infusion seems mediated by AT1 and not Mas receptors. Sodium 101-107 angiotensinogen Rattus norvegicus 41-46 29512852-7 2018 These purinergic receptor subtypes are permeable to sodium vs. calcium in varying amounts and this could play an important role in the release of vasopressin vs. oxytocin during bursting activity. Sodium 52-58 arginine vasopressin Homo sapiens 146-157 29450421-3 2018 The decomposition of FEC provides a NaF-containing solid electrolyte interphase with homogenous morphology and high modulus, leading to stable sodium deposition and high Coulombic efficiency (88% over 50 cycles) of the sodium metal anode. Sodium 143-149 C-X-C motif chemokine ligand 8 Homo sapiens 36-39 29450421-3 2018 The decomposition of FEC provides a NaF-containing solid electrolyte interphase with homogenous morphology and high modulus, leading to stable sodium deposition and high Coulombic efficiency (88% over 50 cycles) of the sodium metal anode. Sodium 219-231 C-X-C motif chemokine ligand 8 Homo sapiens 36-39 29187749-4 2018 Hypoproteinemia, a common finding in patients receiving PN, induces an overestimation of serum sodium (SNa) levels, when using indirect electrolyte methodology. Sodium 95-101 snail family transcriptional repressor 1 Homo sapiens 103-106 29237740-5 2018 Here, we report that collecting duct-specific deletion of an epithelial transcription factor, grainyhead-like 2 (GRHL2), in mice led to reduced expression of tight junction-associated barrier components, reduced collecting duct transepithelial resistance, and defective renal medullary accumulation of sodium and other osmolytes. Sodium 302-308 grainyhead like transcription factor 2 Mus musculus 94-111 29237740-5 2018 Here, we report that collecting duct-specific deletion of an epithelial transcription factor, grainyhead-like 2 (GRHL2), in mice led to reduced expression of tight junction-associated barrier components, reduced collecting duct transepithelial resistance, and defective renal medullary accumulation of sodium and other osmolytes. Sodium 302-308 grainyhead like transcription factor 2 Mus musculus 113-118 29237740-6 2018 In vitro, Grhl2-deficient collecting duct cells displayed increased paracellular flux of sodium, chloride, and urea. Sodium 89-95 grainyhead like transcription factor 2 Mus musculus 10-15 29251736-0 2018 PGE2 EP1 receptor inhibits vasopressin-dependent water reabsorption and sodium transport in mouse collecting duct. Sodium 72-78 prostaglandin E receptor 1 (subtype EP1) Mus musculus 5-8 29251736-2 2018 This study examined the contribution of PGE2 EP1 receptors to sodium and water homeostasis. Sodium 62-68 prostaglandin E receptor 1 (subtype EP1) Mus musculus 45-48 29251736-11 2018 Taken together, the data suggest that EP1 regulates renal aquaporins and sodium transporters, attenuates AVP-water transport and inhibits sodium transport in the mouse collecting duct, which is mediated by both ENaC and pendrin-dependent pathways. Sodium 73-79 prostaglandin E receptor 1 (subtype EP1) Mus musculus 38-41 29309055-1 2018 Most G-protein-coupled receptors (GPCRs) are stabilized in common in the inactive state by the formation of the sodium ion-centered water cluster with the conserved Asp2.50 inside the seven-transmembrane domain. Sodium 112-118 beta-secretase 1 Homo sapiens 165-169 29360682-13 2018 CONCLUSION: Considering that the renin-angiotensin pathway plays a central role in blood pressure and plasma sodium concentration, and our observation that ACE and PTPRD expression increased over the spectrum of childhood development, this finding could potentially impact the dosing of an entire class of drugs known as ACE-inhibitors in pediatric patients. Sodium 109-115 renin Homo sapiens 33-38 29360682-13 2018 CONCLUSION: Considering that the renin-angiotensin pathway plays a central role in blood pressure and plasma sodium concentration, and our observation that ACE and PTPRD expression increased over the spectrum of childhood development, this finding could potentially impact the dosing of an entire class of drugs known as ACE-inhibitors in pediatric patients. Sodium 109-115 angiotensin I converting enzyme Homo sapiens 156-159 29433578-2 2018 Identifying the contribution of intravascular volume and serum renin in maintaining BP levels could help tailor more effective hypertension treatment, whether acting on the control of intravascular volume or sodium balance, or acting on the effects of the renin-angiotensin-aldosterone system (RAAS) on the kidney. Sodium 208-214 renin Homo sapiens 63-68 29433578-11 2018 Thus, identifying the contribution of intravascular volume and serum renin in maintaining BP levels could help tailor more effective hypertension treatment, whether by acting on the control of intravascular volume or sodium balance, or by acting on the effects of the RAAS on the kidney. Sodium 217-223 renin Homo sapiens 69-74 29467657-0 2018 Effects of Sodium and Amino Acid Substrate Availability upon the Expression and Stability of the SNAT2 (SLC38A2) Amino Acid Transporter. Sodium 11-17 solute carrier family 38 member 7 Homo sapiens 113-135 29180450-11 2018 Our results suggest that knocking out mitochondrial VDAC3 increases ROS, alters renal sodium transport, and leads to hypertension. Sodium 86-92 voltage-dependent anion channel 3 Mus musculus 52-57 29079359-10 2018 In multivariate models, race time, serum sodium, creatinine and cortisol were significant predictors of copeptin levels. Sodium 41-47 arginine vasopressin Homo sapiens 104-112 29305116-3 2018 Plasmin activates the epithelial sodium channel in the collecting ducts potentially causing impaired sodium excretion, suppression of the renin-angiotensin-aldosterone system, and hypertension in PE. Sodium 33-39 renin Homo sapiens 138-143 29712960-1 2018 We aim to evaluate the association of systolic and diastolic blood pressure (SBP and DBP) with estimated urinary sodium (Na) and potassium(K) excretions, and their gram-to-gram Na/K ratio across various salt-diet regions during 2005-2009 in China. Sodium 113-119 D-box binding PAR bZIP transcription factor Homo sapiens 85-88 29357474-2 2018 The present study tested the hypothesis that increases in pOsm and serum sodium (sNa+) concentration would exaggerate muscle sympathetic nerve activity (MSNA) and blood pressure (BP) responses to handgrip (HG) exercise and postexercise ischemia (PEI). Sodium 73-79 snail family transcriptional repressor 1 Homo sapiens 81-84 29031006-6 2018 Glucagon-like peptide-1 (GLP-1) has been reported to increase glomerular filtration rate (GFR), renal blood flow, and the fractional excretion both of sodium and potassium, with renal GLP-1 receptors present in afferent arteriolar vascular smooth muscle cells, glomerular endothelial cells and macrophages, juxtaglomerular cells, and the proximal tubule, perhaps mediating the greater natriuresis seen after oral than intravenous sodium. Sodium 151-157 glucagon Homo sapiens 25-30 29031006-6 2018 Glucagon-like peptide-1 (GLP-1) has been reported to increase glomerular filtration rate (GFR), renal blood flow, and the fractional excretion both of sodium and potassium, with renal GLP-1 receptors present in afferent arteriolar vascular smooth muscle cells, glomerular endothelial cells and macrophages, juxtaglomerular cells, and the proximal tubule, perhaps mediating the greater natriuresis seen after oral than intravenous sodium. Sodium 430-436 glucagon Homo sapiens 0-23 29031006-6 2018 Glucagon-like peptide-1 (GLP-1) has been reported to increase glomerular filtration rate (GFR), renal blood flow, and the fractional excretion both of sodium and potassium, with renal GLP-1 receptors present in afferent arteriolar vascular smooth muscle cells, glomerular endothelial cells and macrophages, juxtaglomerular cells, and the proximal tubule, perhaps mediating the greater natriuresis seen after oral than intravenous sodium. Sodium 430-436 glucagon Homo sapiens 25-30 29303781-0 2018 Association of sodium intake with insulin resistance in Korean children and adolescents: the Korea National Health and Nutrition Examination Survey 2010. Sodium 15-21 insulin Homo sapiens 34-41 29303781-1 2018 BACKGROUND: This study aimed to evaluate the relationship between sodium intake and insulin resistance indices. Sodium 66-72 insulin Homo sapiens 84-91 29303781-9 2018 CONCLUSIONS: Our results suggest that sodium intake, as estimated by the urinary sodium to urinary creatinine ratio, may be independently associated with insulin resistance in children and adolescents. Sodium 38-44 insulin Homo sapiens 154-161 29303781-9 2018 CONCLUSIONS: Our results suggest that sodium intake, as estimated by the urinary sodium to urinary creatinine ratio, may be independently associated with insulin resistance in children and adolescents. Sodium 81-87 insulin Homo sapiens 154-161 29143051-0 2018 An open holey structure enhanced rate capability in a NaTi2(PO4)3/C nanocomposite and provided ultralong-life sodium-ion storage. Sodium 110-116 proopiomelanocortin Homo sapiens 54-67 29299574-0 2018 Structural evolution and stability of Sc2(WO4)3 after discharge in a sodium-based electrochemical cell. Sodium 69-75 trans-2,3-enoyl-CoA reductase Homo sapiens 38-41 29178675-1 2018 PURPOSE: Claudin-4 has been reported to function as a paracellular sodium barrier and is one of the 3 major claudins expressed in lung alveolar epithelial cells. Sodium 67-73 claudin 4 Homo sapiens 9-18 29316438-3 2018 (2017) provide evidence that a transmembrane flux of sodium ions drives PTCH1 activity and that cholesterol regulates Smoothened via its transmembrane domain. Sodium 53-59 patched 1 Homo sapiens 72-77 30081699-4 2018 Using a rational design strategy, we identified a heptamer peptide harboring CRMP2"s SUMO motif that disrupted the CRMP2-Ubc9 interaction, inhibited CRMP2 SUMOylation, inhibited NaV1.7 membrane trafficking, and specifically inhibited NaV1.7 sodium influx in sensory neurons. Sodium 241-247 dihydropyrimidinase like 2 Homo sapiens 77-82 29359681-0 2018 Involvement of NLRP3 inflammasome in the impacts of sodium and potassium on insulin resistance in normotensive Asians. Sodium 52-58 NLR family pyrin domain containing 3 Homo sapiens 15-20 29359681-0 2018 Involvement of NLRP3 inflammasome in the impacts of sodium and potassium on insulin resistance in normotensive Asians. Sodium 52-58 insulin Homo sapiens 76-83 30081699-4 2018 Using a rational design strategy, we identified a heptamer peptide harboring CRMP2"s SUMO motif that disrupted the CRMP2-Ubc9 interaction, inhibited CRMP2 SUMOylation, inhibited NaV1.7 membrane trafficking, and specifically inhibited NaV1.7 sodium influx in sensory neurons. Sodium 241-247 dihydropyrimidinase like 2 Homo sapiens 115-120 30081699-4 2018 Using a rational design strategy, we identified a heptamer peptide harboring CRMP2"s SUMO motif that disrupted the CRMP2-Ubc9 interaction, inhibited CRMP2 SUMOylation, inhibited NaV1.7 membrane trafficking, and specifically inhibited NaV1.7 sodium influx in sensory neurons. Sodium 241-247 dihydropyrimidinase like 2 Homo sapiens 115-120 29045337-5 2018 RECENT FINDINGS: A variety of investigative approaches have demonstrated that angiotensin II signaling via AT1a receptors, specifically in the renal proximal tubule, is a major regulator of BP and sodium homeostasis. Sodium 197-203 angiotensinogen Homo sapiens 78-92 29246686-2 2018 Our preclinical studies demonstrate an important role for renal endothelin-1 (ET-1) in regulating sodium excretion. Sodium 98-104 endothelin 1 Homo sapiens 64-76 28930524-2 2018 Hyperinsulinemia may increase cardiovascular (CV) risk through its promotion of hypertension, which is possibly a result of chronic enhancement of sympathetic nervous system activity, stimulation of the renin-angiotensin-aldosterone system leading to increased renal tubular sodium reabsorption, modulating cation transport, or inducing vascular smooth muscle cell hypertrophy. Sodium 275-281 renin Homo sapiens 203-208 29246686-2 2018 Our preclinical studies demonstrate an important role for renal endothelin-1 (ET-1) in regulating sodium excretion. Sodium 98-104 endothelin 1 Homo sapiens 78-82 29246686-4 2018 We hypothesize that reduced renal ET-1 accounts for derangements in sodium handling under stress, a link never explored in a large human cohort. Sodium 68-74 endothelin 1 Homo sapiens 34-38 29246686-12 2018 Thus, loss of ET-1-dependent natriuresis may account for sodium retention during stress and may predispose retainers to renal diseases such as hypertension and kidney disease. Sodium 57-63 endothelin 1 Homo sapiens 14-18 30099444-15 2018 CONCLUSION: We found that in patients with CKD, urinary sodium and potassium excretion is closely correlated to renal handling of uric acid, which was pronounced in hypertensive patients with low eGFR. Sodium 56-62 epidermal growth factor receptor Homo sapiens 196-200 29956586-2 2018 The pore-forming alpha-subunits (sodium channel alpha subunits) of the voltage-sensitive channels (i.e., Nav1.1-1.9) and the nonvoltage-dependent channel (i.e., Nax) share a common structural motif and selectivity for sodium ions. Sodium 33-39 sodium channel, voltage-gated, type I, alpha Mus musculus 105-111 30387376-5 2018 We demonstrate that NPY2R+ nociceptors, CHRNA3+ "silent" nociceptors and polymodal C-fibre nociceptors express different combinations of sodium channel alpha- and beta-subunits and accordingly exhibit functionally different sodium currents. Sodium 137-143 cholinergic receptor, nicotinic, alpha polypeptide 3 Mus musculus 40-46 29439274-1 2018 AIM: The sodium-sparing effect of insulin leads to increase in total sodium pool of the body which is a chronic stimulus for atrial natriuretic peptide (ANP). Sodium 9-15 insulin Homo sapiens 34-41 29439274-1 2018 AIM: The sodium-sparing effect of insulin leads to increase in total sodium pool of the body which is a chronic stimulus for atrial natriuretic peptide (ANP). Sodium 9-15 natriuretic peptide A Homo sapiens 125-151 29439274-1 2018 AIM: The sodium-sparing effect of insulin leads to increase in total sodium pool of the body which is a chronic stimulus for atrial natriuretic peptide (ANP). Sodium 9-15 natriuretic peptide A Homo sapiens 153-156 29439274-1 2018 AIM: The sodium-sparing effect of insulin leads to increase in total sodium pool of the body which is a chronic stimulus for atrial natriuretic peptide (ANP). Sodium 69-75 insulin Homo sapiens 34-41 29439274-1 2018 AIM: The sodium-sparing effect of insulin leads to increase in total sodium pool of the body which is a chronic stimulus for atrial natriuretic peptide (ANP). Sodium 69-75 natriuretic peptide A Homo sapiens 125-151 29439274-1 2018 AIM: The sodium-sparing effect of insulin leads to increase in total sodium pool of the body which is a chronic stimulus for atrial natriuretic peptide (ANP). Sodium 69-75 natriuretic peptide A Homo sapiens 153-156 29059065-1 2017 BACKGROUND: Elevation in postmortem vitreous humor sodium and chloride (PMVSC) in salt water drowning (SWD) when the immersion time is less than 1 hour (SWD1) is hypothesized to result from electrolyte changes in blood from salt water inhalation/ingestion during drowning. Sodium 51-57 RB binding protein 5, histone lysine methyltransferase complex subunit Homo sapiens 153-157 28708422-10 2017 Our data suggest a potential role for delta-ENaC in controlling sodium reabsorption in the airways, and advance the plausibility of ENaC as a therapeutic target in CF. Sodium 64-70 sodium channel epithelial 1 subunit delta Homo sapiens 38-48 28814438-0 2017 Collecting duct prorenin receptor knockout reduces renal function, increases sodium excretion, and mitigates renal responses in ANG II-induced hypertensive mice. Sodium 77-83 ATPase, H+ transporting, lysosomal accessory protein 2 Mus musculus 16-33 28987817-5 2018 We found that Lu AE98134 facilitated the sodium current mediated by NaV1.1 expressed in HEK cells by shifting its activation to more negative values, decreasing its inactivation kinetics and promoting a persistent inward current. Sodium 41-47 sodium channel, voltage-gated, type I, alpha Mus musculus 68-74 29106511-4 2017 The sodium acetate tolerance was dependent on the extrusion of intracellular sodium ions by the plasma membrane-localized sodium pumps Ena1, Ena2, and Ena5 (Ena1/2/5) and two known upstream regulators: the Rim101 pH signaling pathway and the Hog1 mitogen-activated protein kinase. Sodium 4-10 mitogen-activated protein kinase HOG1 Saccharomyces cerevisiae S288C 242-246 29084882-6 2017 Conversely, low-sodium diet unexpectedly induced an exaggerated aldosterone response, which seemed to result from an increase in adrenal renin and angiotensin type 1 receptor expression. Sodium 16-22 ATPase, H+ transporting, lysosomal accessory protein 2 Mus musculus 137-174 29087023-3 2017 Rank correlation analysis revealed that interleukin 6 expression exhibited significant positive correlations with urinary sodium (R = .13) and sodium to potassium ratio (R = .13). Sodium 122-128 interleukin 6 Homo sapiens 40-53 29087023-3 2017 Rank correlation analysis revealed that interleukin 6 expression exhibited significant positive correlations with urinary sodium (R = .13) and sodium to potassium ratio (R = .13). Sodium 143-149 interleukin 6 Homo sapiens 40-53 28912346-5 2017 Interestingly, Cyp4a14(-/-) male mice treated with 20-SOLA displayed increased urinary sodium excretion that was paralleled by the reduction of blood pressure suggestive of an antinatriuretic activity of endogenous 20-HETE in the hypertensive mice. Sodium 87-93 cytochrome P450, family 4, subfamily a, polypeptide 14 Mus musculus 15-22 28943585-2 2017 The vasopressin V2-receptor antagonist tolvaptan is used to treat cirrhotic patients with ascites and increases the serum sodium (Na) level. Sodium 122-128 arginine vasopressin receptor 2 Homo sapiens 4-27 28961453-1 2017 INTRODUCTION: Antithrombin resistance (ATR) prothrombinemia is an inherited thrombophilic disorder caused by missense mutations in prothrombin gene (F2) at Arg596 of the sodium-binding region. Sodium 170-176 coagulation factor II, thrombin Homo sapiens 44-55 28150887-1 2017 The maintenance of a low intracellular sodium concentration by the Na+ /K+ -ATPase (NKA) is critical for brain function. Sodium 39-45 tachykinin precursor 1 Homo sapiens 67-82 28150887-1 2017 The maintenance of a low intracellular sodium concentration by the Na+ /K+ -ATPase (NKA) is critical for brain function. Sodium 39-45 tachykinin precursor 1 Homo sapiens 84-87 28150887-2 2017 In both neurons and glial cells, NKA activity is required to counteract changes in the sodium gradient due to opening of voltage- and ligand-gated channels and/or activation of sodium-dependent secondary active transporters. Sodium 87-93 tachykinin precursor 1 Homo sapiens 33-36 28961453-11 2017 CONCLUSIONS: Mutation of prothrombin at the sodium-binding site caused ATR-phenotypes. Sodium 44-50 coagulation factor II, thrombin Homo sapiens 25-36 29124052-9 2017 Sweat chloride/sweat sodium and sweat sodium-sweat chloride indexes showed association with sex, reason for ST indication, and CFTR mutations. Sodium 38-44 CF transmembrane conductance regulator Homo sapiens 127-131 29079724-3 2017 Gene silencing experiments targeting alpha1D reduced the migration and the basal cytosolic Ca2+ concentration of HCT116 colon cancer cell line and modified the cytosolic Ca2+ oscillations induced by the sodium/calcium exchanger NCX1/3 working in its reverse mode. Sodium 203-209 solute carrier family 8 member A1 Homo sapiens 228-234 29069584-2 2017 We describe a pathway by which sodium enters dendritic cells (DCs) through amiloride-sensitive channels including the alpha and gamma subunits of the epithelial sodium channel and the sodium hydrogen exchanger 1. Sodium 31-37 solute carrier family 9 (sodium/hydrogen exchanger), member 1 Mus musculus 184-211 29069584-5 2017 DCs activated by excess sodium produce increased interleukin-1beta (IL-1beta) and promote T cell production of cytokines IL-17A and interferon gamma (IFN-gamma). Sodium 24-30 interleukin 1 beta Mus musculus 49-66 29069584-5 2017 DCs activated by excess sodium produce increased interleukin-1beta (IL-1beta) and promote T cell production of cytokines IL-17A and interferon gamma (IFN-gamma). Sodium 24-30 interleukin 1 beta Mus musculus 68-76 29069584-5 2017 DCs activated by excess sodium produce increased interleukin-1beta (IL-1beta) and promote T cell production of cytokines IL-17A and interferon gamma (IFN-gamma). Sodium 24-30 interferon gamma Mus musculus 132-159 29047375-4 2017 We enrolled 56 adult patients with a serum sodium (SNa) concentration of <=125 mEq/L who were treated in an intensive care unit by nephrologists using a locally developed, fixed treatment algorithm between February 2012 and April 2014. Sodium 43-49 snail family transcriptional repressor 1 Homo sapiens 51-54 29066763-7 2017 UII raises BP transiently when sodium intake and renal function are normal, but progressively in salt-loaded uninephrectomized rats. Sodium 31-37 urotensin 2 Rattus norvegicus 0-3 29038209-2 2017 Activation of the sodium-hydrogen exchanger in the heart and vasculature (NHE1 isoform) and the kidneys (NHE3 isoform) may serve as a common mechanism that links both disorders and may underlie their interplay. Sodium 18-24 solute carrier family 9 member A1 Homo sapiens 74-78 28649750-1 2017 Vasopressin (AVP) plays a major role in the regulation of water and sodium homeostasis by its antidiuretic action on the kidney, mediated by V2 receptors. Sodium 68-74 arginine vasopressin Homo sapiens 0-11 28602864-7 2017 Thus, the potassium/sodium/calcium exchanger of NCKX3 KO mice proceeded normally in this study. Sodium 20-26 solute carrier family 24 (sodium/potassium/calcium exchanger), member 3 Mus musculus 48-53 29221188-1 2017 Angiotensinogen (AGT) is involved in the production of angiotensin II which is the main mediator of action of the rennin-angiotensin system (RAS), whereas the RAS mediates the regulation of sodium homeostasis, blood pressure, and inflammation. Sodium 190-196 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 0-15 29221188-1 2017 Angiotensinogen (AGT) is involved in the production of angiotensin II which is the main mediator of action of the rennin-angiotensin system (RAS), whereas the RAS mediates the regulation of sodium homeostasis, blood pressure, and inflammation. Sodium 190-196 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 17-20 28446807-9 2017 Urine sodium concentration was significantly lower in the nesf/NUCB2-Tg mice, although the serum sodium concentration and urine sodium excretion were not different between the genotypes. Sodium 6-12 nucleobindin 2 Mus musculus 63-68 28772209-1 2017 Renin-angiotensin-aldosterone system (RAAS) is a vital system of human body, as it maintains plasma sodium concentration, arterial blood pressure and extracellular volume. Sodium 100-106 renin Homo sapiens 0-5 28823028-3 2017 Milliseconds after the pore opens, sodium influx is terminated by inactivation processes mediated by regulatory proteins including calmodulin (CaM). Sodium 35-41 calmodulin 1 Homo sapiens 131-141 28384411-1 2017 The renin-angiotensin system (RAS) generates, maintains, and makes worse hypertension and cardiovascular diseases (CVDs) through its biologically active component angiotensin II (Ang II), that causes vasoconstriction, sodium retention, and structural alterations of the heart and the arteries. Sodium 218-224 angiotensinogen Homo sapiens 163-177 28384411-1 2017 The renin-angiotensin system (RAS) generates, maintains, and makes worse hypertension and cardiovascular diseases (CVDs) through its biologically active component angiotensin II (Ang II), that causes vasoconstriction, sodium retention, and structural alterations of the heart and the arteries. Sodium 218-224 angiotensinogen Homo sapiens 179-185 28727929-6 2017 Due to muscular intracellular acidosis, the intracellular sodium overload in DMD and BMD was also due to sodium influx through the sodium-hydrogen exchanger NHE-1. Sodium 58-64 solute carrier family 9 member A1 Homo sapiens 157-162 28727929-6 2017 Due to muscular intracellular acidosis, the intracellular sodium overload in DMD and BMD was also due to sodium influx through the sodium-hydrogen exchanger NHE-1. Sodium 105-111 solute carrier family 9 member A1 Homo sapiens 157-162 31966371-2 2017 Mutations of SCN2A, the gene encoding the aII subunit of the voltage-gated sodium channel (Nav1.2), have been detected in some EOEE patients. Sodium 75-81 NLR family pyrin domain containing 3 Homo sapiens 42-45 28674042-1 2017 Mice lacking distal tubular expression of CLDN10, the gene encoding the tight junction protein Claudin-10, show enhanced paracellular magnesium and calcium permeability and reduced sodium permeability in the thick ascending limb (TAL), leading to a urine concentrating defect. Sodium 181-187 claudin 10 Homo sapiens 42-48 28674042-1 2017 Mice lacking distal tubular expression of CLDN10, the gene encoding the tight junction protein Claudin-10, show enhanced paracellular magnesium and calcium permeability and reduced sodium permeability in the thick ascending limb (TAL), leading to a urine concentrating defect. Sodium 181-187 claudin 10 Homo sapiens 95-105 29081083-4 2017 Concentrated sodium solutions with various anions caused feeding suppression dependent on Ir76b. Sodium 13-19 Ionotropic receptor 76b Drosophila melanogaster 90-95 28963831-2 2017 Inhibition of neprilysin by inhibiting the breakdown of natriuretic peptides, increases their bioavailability resulting in an increase in diuresis and sodium excretion and, in addition to exerting an inhibition of the renin-angiotensin-aldosterone (RAAS) system. Sodium 151-157 membrane metalloendopeptidase Homo sapiens 14-24 28743496-2 2017 Activation of WNK-OSR1/SPAK-NaCl cotransporter (NCC) cascade increases sodium reabsorption in the kidney, leading to pseudohypoaldosteronism type II (PHA II) characterized by salt-sensitive hypertension and hyperkalemia. Sodium 71-77 odd-skipped related transcription factor 1 Mus musculus 14-22 28649750-1 2017 Vasopressin (AVP) plays a major role in the regulation of water and sodium homeostasis by its antidiuretic action on the kidney, mediated by V2 receptors. Sodium 68-74 arginine vasopressin Homo sapiens 13-16 28849814-2 2017 Depending upon the binding of sodium ions, thrombin presents significantly different enzymatic activities. Sodium 30-36 coagulation factor II, thrombin Homo sapiens 43-51 28849814-3 2017 In the environment with sodium ions, thrombin is highly active in cleaving the coagulated substrates and this is referred to as the "fast" form; in the environment without sodium ions, thrombin turns catalytically less active and is in the "slow" form. Sodium 24-30 coagulation factor II, thrombin Homo sapiens 37-45 28849814-3 2017 In the environment with sodium ions, thrombin is highly active in cleaving the coagulated substrates and this is referred to as the "fast" form; in the environment without sodium ions, thrombin turns catalytically less active and is in the "slow" form. Sodium 24-30 coagulation factor II, thrombin Homo sapiens 185-193 28849814-3 2017 In the environment with sodium ions, thrombin is highly active in cleaving the coagulated substrates and this is referred to as the "fast" form; in the environment without sodium ions, thrombin turns catalytically less active and is in the "slow" form. Sodium 172-178 coagulation factor II, thrombin Homo sapiens 37-45 28849814-3 2017 In the environment with sodium ions, thrombin is highly active in cleaving the coagulated substrates and this is referred to as the "fast" form; in the environment without sodium ions, thrombin turns catalytically less active and is in the "slow" form. Sodium 172-178 coagulation factor II, thrombin Homo sapiens 185-193 28849814-10 2017 Our study of thrombin in the presence of sodium/potassium ions suggests Na+-mediated generalized allostery is the mechanism of thrombin"s functional switch between the "fast" and "slow" forms. Sodium 41-47 coagulation factor II, thrombin Homo sapiens 13-21 28849814-10 2017 Our study of thrombin in the presence of sodium/potassium ions suggests Na+-mediated generalized allostery is the mechanism of thrombin"s functional switch between the "fast" and "slow" forms. Sodium 41-47 coagulation factor II, thrombin Homo sapiens 127-135 29955681-10 2017 Consumption of "pasta mixed dishes" was associated with a 5% increase in both potassium and sodium intakes (~150 and 190 mg/d, respectively). Sodium 92-98 solute carrier family 45 member 1 Homo sapiens 16-21 29955681-13 2017 These pasta patterns contribute in different ways to diet quality and intakes of fiber, sodium, and potassium. Sodium 88-94 solute carrier family 45 member 1 Homo sapiens 6-11 28614116-3 2017 This review outlines our current understanding of PTH"s effects on renal tubular calcium transport, focusing on the more recent discoveries beyond its direct regulation of epithelial Ca channel transient receptor potential vanilloid 5 (TRPV5) and looking at its interaction with sodium transport and the hormones fibroblast growth factor 23 (FGF23) and klotho. Sodium 279-285 parathyroid hormone Homo sapiens 50-53 28739252-3 2017 The aim of this study was to assess the influence of valproic acid (200 muM) on TTX-resistant sodium currents in mPFC pyramidal neurons. Sodium 94-100 latexin Homo sapiens 72-75 28905546-4 2017 The low renin hypertension phenotype seems to be caused by an increase in sodium retention at renal level. Sodium 74-80 renin Homo sapiens 8-13 28833693-10 2017 An application of TGF-beta1 itself attenuated generation of action potentials, inhibited sodium current and potentiated potassium currents. Sodium 89-95 transforming growth factor, beta 1 Rattus norvegicus 18-27 28479338-10 2017 Blockade of GLT-1 caused significant reduction in whole-cell sodium currents and changes in CSD wave spatiotemporal characteristics as well, slowing it or even "trapping" its propagation. Sodium 61-67 solute carrier family 1 member 2 Rattus norvegicus 12-17 29028089-8 2017 RESULTS: Serum sodium was negatively correlated with the plasma levels of ANP (r=-0.171, p=0.017) and AVP (r = -0.244, p=0.001) in all SCLC patients. Sodium 15-21 natriuretic peptide A Homo sapiens 74-77 29028089-9 2017 In the brain metastatic subgroup, there was also a negative correlation between serum sodium and ANP (r=-0.399, p=0.004), while there was no correlation between serum sodium and AVP (r=-0.232, p=0.101). Sodium 86-92 natriuretic peptide A Homo sapiens 97-100 28970664-1 2017 A 4-year-old girl admitted with altered mental status, new-onset diabetes mellitus, and diabetic ketoacidosis (DKA) had a rapid rise in serum sodium from 158 mEq/L (corrected sodium 165 mEq/L) at the admission to 204 mEq/L within 18 hours of admission despite standard fluid and insulin therapy recommended for the treatment of DKA. Sodium 142-148 insulin Homo sapiens 279-286 28637815-8 2017 This effect was likely mediated by the transient sodium current, as TNF-alpha increased the magnitude of the current and lowered its threshold of activation. Sodium 49-55 tumor necrosis factor Rattus norvegicus 68-77 28836382-0 2017 Sodium appetite elicited by low-sodium diet is dependent on p44/42 mitogen-activated protein kinase (extracellular signal-regulated kinase 1/2) activation in the brain. Sodium 0-6 mitogen-activated protein kinase 3 Homo sapiens 101-142 28836382-0 2017 Sodium appetite elicited by low-sodium diet is dependent on p44/42 mitogen-activated protein kinase (extracellular signal-regulated kinase 1/2) activation in the brain. Sodium 32-38 mitogen-activated protein kinase 3 Homo sapiens 101-142 28836382-1 2017 Sodium appetite is regulated by several signalling molecules, among which angiotensin II (Ang II) serves as a key driver of robust salt intake by binding to Ang II type 1 receptors (AT1R) in several regions in the brain. Sodium 0-6 angiotensinogen Homo sapiens 74-88 28836382-1 2017 Sodium appetite is regulated by several signalling molecules, among which angiotensin II (Ang II) serves as a key driver of robust salt intake by binding to Ang II type 1 receptors (AT1R) in several regions in the brain. Sodium 0-6 angiotensinogen Homo sapiens 90-96 28836382-2 2017 The activation of these receptors recruits the mitogen-activated protein kinase (MAPK) pathway, which has previously been linked to Ang II-induced increases in sodium appetite. Sodium 160-166 angiotensinogen Homo sapiens 132-138 28836382-4 2017 An increase in extracellular signal-regulated kinase (ERK) phosphorylation in the laminae terminalis and mediobasal hypothalamus was observed after low-sodium diet consumption. Sodium 152-158 mitogen-activated protein kinase 1 Homo sapiens 15-52 28836382-4 2017 An increase in extracellular signal-regulated kinase (ERK) phosphorylation in the laminae terminalis and mediobasal hypothalamus was observed after low-sodium diet consumption. Sodium 152-158 mitogen-activated protein kinase 1 Homo sapiens 54-57 28836382-7 2017 This result indicates that low-sodium diet consumption activates the MAPK pathway via Ang II/AT1R signalling on the laminae terminalis. Sodium 31-37 angiotensinogen Homo sapiens 86-92 28836382-11 2017 injection of Ang II increased ERK phosphorylation on the laminae terminalis and mediobasal hypothalamus; this increase achieved a response magnitude similar to those observed in both the normal and low-sodium diet groups. Sodium 202-208 angiotensinogen Homo sapiens 13-19 28625546-1 2017 Angiotensin II (ANG II) is a typical facilitatory stimulus for sodium appetite. Sodium 63-69 angiotensinogen Rattus norvegicus 0-14 28625546-1 2017 Angiotensin II (ANG II) is a typical facilitatory stimulus for sodium appetite. Sodium 63-69 angiotensinogen Rattus norvegicus 16-22 28867800-6 2017 P-CTX-1-induced CGRP release from skin is dependent on extracellular calcium and sodium, but independent from the activation of various thermosensory transient receptor potential (TRP) ion channels. Sodium 81-87 calcitonin/calcitonin-related polypeptide, alpha Mus musculus 16-20 28336391-8 2017 RESULTS: Unadjusted and adjusted multivariate analyses indicate that there was a significant positive association between dietary protein and sodium intake and serum hs-CRP concentrations. Sodium 142-148 C-reactive protein Homo sapiens 169-172 28336391-11 2017 CONCLUSION: We have found a significant positive association between the dietary intake of fat, protein, cholesterol and sodium and hs-CRP level, and an inverse correlation between dietary carbohydrate and fiber and serum hs-CRP in a large representative Iranian population. Sodium 121-127 C-reactive protein Homo sapiens 135-138 28614116-5 2017 In addition, PTH alters sodium transport that indirectly leads to enhanced TRPV5 activity. Sodium 24-30 parathyroid hormone Homo sapiens 13-16 28807015-6 2017 RESULTS: In women (n = 12), Cav1.2alpha (primary subunit of the L-type calcium channel protein 1) and NCX1 (sodium-calcium exchange protein) levels were higher at the base than apex of the epicardium (40 +- 14 and 81 +- 30%, respectively, P < 0.05), but not in men (n = 6) or postmenopausal women (n = 6). Sodium 108-114 solute carrier family 8 member A1 Homo sapiens 102-106 28566337-7 2017 When participants in the clinical study were maintained on a high sodium balance, renin activity progressively declined with older age, whereas serum and urinary aldosterone did not significantly decline. Sodium 66-72 renin Homo sapiens 82-87 28003189-3 2017 The epithelial sodium channel (ENaC) is a trimeric ion channel expressed in the distal nephron that plays a critical role in the regulation of sodium reabsorption in both normal and pathological conditions. Sodium 15-21 sodium channel epithelial 1 subunit gamma Rattus norvegicus 31-35 28385297-1 2017 The sodium/proton exchanger isoform 3 (NHE3) is expressed in the intestine and the kidney, where it facilitates sodium (re)absorption and proton secretion. Sodium 4-10 solute carrier family 9 (sodium/hydrogen exchanger), member 3 Mus musculus 39-43 28385297-6 2017 Ten days of low or high sodium chloride diet did not affect plasma sodium in control mice; however, NHE3loxloxCre mice were susceptible to low sodium chloride (about -4 mM) or high sodium chloride intake (about +2 mM) versus baseline, effects without differences in plasma aldosterone between groups. Sodium 24-30 solute carrier family 9 (sodium/hydrogen exchanger), member 3 Mus musculus 100-104 28385297-11 2017 Thus, renal NHE3 is required to maintain blood pressure and steady-state plasma sodium levels when dietary sodium chloride intake is modified. Sodium 80-86 solute carrier family 9 (sodium/hydrogen exchanger), member 3 Mus musculus 12-16 28559392-1 2017 Genome-wide analysis of renal sodium-transporting system has identified specific variations of Mendelian hypertensive disorders, including HSD11B2 gene variants in apparent mineralocorticoid excess. Sodium 30-36 hydroxysteroid 11-beta dehydrogenase 2 Mus musculus 139-146 28248529-6 2017 The main cardiovascular and autonomic responses to a change in plasma sodium concentration are: i) changes in arterial blood pressure and heart rate; ii) changes in sympathetic activity to the renal system in order to ensure adequate renal sodium excretion/absorption, and iii) the secretion of compounds involved in sodium ion homeostasis (ANP, Ang-II, and ADH, for example). Sodium 70-76 natriuretic peptide A Homo sapiens 341-344 27517720-7 2017 Administration of TGF-beta1 significantly shifted current-voltage relation of sodium current toward more positive membrane potential without change to maximal current amplitude. Sodium 78-84 transforming growth factor beta 1 Homo sapiens 18-27 28507171-9 2017 Big ET-1 increased the fractional excretion of sodium (from 0.5 to 1.0%). Sodium 47-53 endothelin 1 Homo sapiens 4-8 28507171-12 2017 Sodium and water excretion increased in the absence of significant hemodynamic perturbation, supporting a direct action of ET-1 on the renal tubule. Sodium 0-6 endothelin 1 Homo sapiens 123-127 28507171-13 2017 Our data also suggest that sodium reabsorption is stimulated by ET-1 in the thick ascending limb and suppressed in the distal renal tubule. Sodium 27-33 endothelin 1 Homo sapiens 64-68 28417649-1 2017 Sodium retention in cirrhosis is associated with changes in the renin-angiotensin-aldosterone system (RAAS), the sympathetic nervous system (SNS), and the glomerular filtration rate (GFR). Sodium 0-6 renin Homo sapiens 64-69 28473457-9 2017 AMG8379 is a potent and selective NaV1.7 inhibitor that blocks sodium current in heterologous cells as well as DRG neurons, inhibits action potential firing in peripheral nerve fibers, and exhibits pharmacodynamic effects in translatable models of both itch and pain. Sodium 63-69 sodium channel, voltage-gated, type IX, alpha Mus musculus 34-40 28383808-2 2017 In light of its high capacity and fast charging-discharging performance, Sc2 C exhibits significant potential as an anode material for lithium- and sodium-ion batteries. Sodium 148-154 trans-2,3-enoyl-CoA reductase Homo sapiens 73-76 28383808-4 2017 The metallic character of pristine and adsorbed Sc2 C ensures desirable electric conductivity, which indicates the advantages of 2D Sc2 C for lithium- and sodium-ion batteries. Sodium 155-161 trans-2,3-enoyl-CoA reductase Homo sapiens 48-51 28383808-8 2017 Herein, our results suggest that Sc2 C could be a promising anode candidate for both lithium-ion and sodium-ion batteries. Sodium 101-107 trans-2,3-enoyl-CoA reductase Homo sapiens 33-36 28778258-2 2017 Regardless of its source, high sodium intake can both lead to hypertension and reduce the efficacy of renin-angiotensin-aldosterone system inhibitors, which are currently guideline-recommended treatments for hypertension, chronic kidney disease, and heart failure. Sodium 31-37 renin Homo sapiens 102-107 28591637-4 2017 We confirm and extend these findings by demonstrating that glucagon pathway blockade selectively increases expression of the sodium-coupled neutral amino acid transporter Slc38a5 in a subset of highly proliferative alpha cells and that Slc38a5 controls the pancreatic response to glucagon pathway blockade; most notably, mice deficient in Slc38a5 exhibit markedly decreased alpha cell hyperplasia to glucagon pathway blockade-induced hyperaminoacidemia. Sodium 125-131 solute carrier family 38, member 7 Mus musculus 148-170 28254494-8 2017 Angiotensin II-induced blood pressure rise was blunted (~50%) in the low-sodium fed rats while cardiac hypertrophy and fibrosis were prevented. Sodium 73-79 angiotensinogen Rattus norvegicus 0-14 28160049-11 2017 The low pH prevailing at this site and the acidic pH preference of PRCP suggest a role of this enzyme in regulating AngII degradation in the collecting tubule where this peptide increases sodium reabsorption and therfore BP. Sodium 188-194 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 116-121 28626572-3 2017 The endogeneous hormone ANP signals via the natriuretic peptide receptor A (NPR-A) through raising intracellular cGMP concentrations, and is involved in blood pressure regulation and sodium homeostasis, as well as lipid metabolism and pancreatic function. Sodium 183-189 natriuretic peptide receptor 1 Homo sapiens 76-81 28501983-4 2017 Evolutionarily, sodium retention mechanisms in the context of low dietary sodium provided a survival advantage and are highly conserved, exemplified by the renin-angiotensin system. Sodium 16-22 renin Homo sapiens 156-161 28501983-7 2017 From these perspectives, several mechanisms can be envisioned whereby a low-sodium diet could potentially cause harm, including the renin-angiotensin system and the sympathetic nervous system. Sodium 76-82 renin Homo sapiens 132-137 28302554-1 2017 BACKGROUND: The renin-angiotensin system (RAS) plays an important role in regulating blood pressure and controlling sodium levels in the blood. Sodium 116-122 renin Homo sapiens 16-21 28492364-5 2017 Mechanistically, TCR stimulation induced rapid sodium influx in Napahyh/hyh CD4 T cells, which reduced intracellular ATP, [ATP]i. Depletion of [ATP]i inhibited mTORC2 dependent NFkappaB activation in Napahyh/hyh cells but ablation of Orai1 restored it. Sodium 47-53 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 177-185 28503166-9 2017 Phenytoin at a concentration of 25 microg/mL also decreased AVP mRNA levels in Lu-165 cells under the sodium challenge with added sodium at 10 mEq/L, but not at 20 mEq/L. Sodium 102-108 arginine vasopressin Homo sapiens 60-63 28490576-2 2017 Moreover, because neutrophil activity is highly dependent on intracellular pH (pHi), we propose a direct mechanistic link between complement activation and neutrophil pHi In this article, we demonstrate that in vitro exposure of human neutrophils to C5a significantly increased pHi by selective activation of the sodium/hydrogen exchanger. Sodium 313-319 complement C5a receptor 1 Homo sapiens 250-253 28503166-9 2017 Phenytoin at a concentration of 25 microg/mL also decreased AVP mRNA levels in Lu-165 cells under the sodium challenge with added sodium at 10 mEq/L, but not at 20 mEq/L. Sodium 130-136 arginine vasopressin Homo sapiens 60-63 28503166-12 2017 These results suggest that Lu-165 cells are sensitive to phenytoin and sodium to control of AVP release and its gene expression. Sodium 71-77 arginine vasopressin Homo sapiens 92-95 28205210-0 2017 Urinary sodium and calcium excretion: via endothelin-1 do they part? Sodium 8-14 endothelin 1 Homo sapiens 42-54 28391629-20 2017 AUTHORS" CONCLUSIONS: Sodium reduction from an average high usual sodium intake level (201 mmol/day) to an average level of 66 mmol/day, which is below the recommended upper level of 100 mmol/day (5.8 g salt), resulted in a decrease in SBP/DBP of 1/0 mmHg in white participants with normotension and a decrease in SBP/DBP of 5.5/2.9 mmHg in white participants with hypertension. Sodium 22-28 D-box binding PAR bZIP transcription factor Homo sapiens 240-243 28420122-3 2017 Gastrin, which is produced by the G-cells of the stomach and duodenum, can increase renal sodium excretion and regulate blood pressure by acting on the cholecystokinin B receptor. Sodium 90-96 cholecystokinin B receptor Homo sapiens 152-178 28242754-2 2017 This mutation introduces abnormal sodium permeability to TREK-1. Sodium 34-40 potassium two pore domain channel subfamily K member 2 Homo sapiens 57-63 28242754-4 2017 Increased sodium permeability and stretch-sensitivity of mutant TREK-1 channels may trigger arrhythmias in areas of the heart with high physical strain such as the RVOT We present a pharmacological strategy to rescue the selectivity defect of the TREK-1 pore. Sodium 10-16 potassium two pore domain channel subfamily K member 2 Homo sapiens 247-253 28251313-3 2017 By contrast, VEGF-C-expressing macrophages in the skin can facilitate the removal of excess interstitial stores of sodium by stimulating lymphangiogenesis. Sodium 115-121 vascular endothelial growth factor C Homo sapiens 13-19 28490751-8 2017 Additionally, chronically GS967-treated Scn1a +/- mice exhibited normalized pyramidal neuron sodium current density and reduced hippocampal NaV1.6 protein levels, whereas lamotrigine treatment had no effect on either pyramidal neuron sodium current or hippocampal NaV1.6 levels. Sodium 93-99 sodium channel, voltage-gated, type I, alpha Mus musculus 40-45 28298088-4 2017 Moreover, the potential signals of the IS-TGT for sodium and potassium ions, which are usually included in biological environments, were evaluated. Sodium 50-56 queuine tRNA-ribosyltransferase catalytic subunit 1 Homo sapiens 42-45 28082350-5 2017 Endogenous ANGII production induced by dietary sodium restriction was higher in SCTR-/- than in C57BL/6N [wild-type (WT)] mice, but CYP11B2 and aldosterone synthesis were not elevated. Sodium 47-53 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 11-16 28082350-5 2017 Endogenous ANGII production induced by dietary sodium restriction was higher in SCTR-/- than in C57BL/6N [wild-type (WT)] mice, but CYP11B2 and aldosterone synthesis were not elevated. Sodium 47-53 secretin receptor Mus musculus 80-84 28082350-6 2017 Reduced accumulation of cholesteryl ester-the precursor of aldosterone-was observed in adrenal glands of SCTR-/- mice that were fed a low-sodium diet. Sodium 138-144 secretin receptor Mus musculus 105-109 28082350-9 2017 In summary, the SCT/SCTR axis is involved in aldosterone precursor uptake, and the knockout of SCTR results in defective aldosterone biosynthesis/release and altered sensitivity of ENaCs to amiloride.-Bai, J., Chow, B. K. C. Secretin is involved in sodium conservation through the renin-angiotensin-aldosterone system. Sodium 249-255 secretin receptor Mus musculus 20-24 28082350-9 2017 In summary, the SCT/SCTR axis is involved in aldosterone precursor uptake, and the knockout of SCTR results in defective aldosterone biosynthesis/release and altered sensitivity of ENaCs to amiloride.-Bai, J., Chow, B. K. C. Secretin is involved in sodium conservation through the renin-angiotensin-aldosterone system. Sodium 249-255 secretin receptor Mus musculus 95-99 27677909-6 2017 RESULTS: Patients treated with vasopressin in addition to other vasoactive drugs had significantly higher sodium changes compared to those treated with other vasoactive drugs (-4.7 +- 6 vs -0.1 +- 2.4 mmol/L, respectively, p value 0.001). Sodium 106-112 arginine vasopressin Homo sapiens 31-42 27677909-10 2017 Serum sodium should be monitored closely when vasopressin is being used in the SAH population. Sodium 6-12 arginine vasopressin Homo sapiens 46-57 27677909-11 2017 Further studies are needed to confirm the effect of exogenous vasopressin on serum sodium levels in SAH populations. Sodium 83-89 arginine vasopressin Homo sapiens 62-73 28213519-1 2017 The GABA transporter GAT-1 mediates electrogenic transport of its substrate together with sodium and chloride. Sodium 90-96 solute carrier family 6 member 1 Homo sapiens 21-26 28273873-6 2017 CSK rs1378942 and CSK-MIR4513 rs3784789 were significantly modified by urinary sodium-potassium excretion ratio. Sodium 79-85 microRNA 4513 Homo sapiens 22-29 28273873-8 2017 The present study results indicated that the mutant alleles of CSK rs1378942 and CSK-MIR4513 rs3784789 had the strongest protective effects against hypertension in the middle group of 24 h estimated urinary sodium-potassium excretion ratio. Sodium 207-213 microRNA 4513 Homo sapiens 85-92 28391629-20 2017 AUTHORS" CONCLUSIONS: Sodium reduction from an average high usual sodium intake level (201 mmol/day) to an average level of 66 mmol/day, which is below the recommended upper level of 100 mmol/day (5.8 g salt), resulted in a decrease in SBP/DBP of 1/0 mmHg in white participants with normotension and a decrease in SBP/DBP of 5.5/2.9 mmHg in white participants with hypertension. Sodium 22-28 D-box binding PAR bZIP transcription factor Homo sapiens 318-321 28199631-5 2017 Most importantly, we show that, in BY4741 background, the lack of Ist2 results in the accumulation of higher amounts of sodium when the cells are exposed to the presence of this cation, demonstrating the importance of Ist2 for the maintenance of low intracellular levels of toxic sodium. Sodium 120-126 Ist2p Saccharomyces cerevisiae S288C 66-70 28199631-0 2017 Lack of cortical endoplasmic reticulum protein Ist2 alters sodium accumulation in Saccharomyces cerevisiae cells. Sodium 59-65 Ist2p Saccharomyces cerevisiae S288C 47-51 28199631-5 2017 Most importantly, we show that, in BY4741 background, the lack of Ist2 results in the accumulation of higher amounts of sodium when the cells are exposed to the presence of this cation, demonstrating the importance of Ist2 for the maintenance of low intracellular levels of toxic sodium. Sodium 120-126 Ist2p Saccharomyces cerevisiae S288C 218-222 28199631-5 2017 Most importantly, we show that, in BY4741 background, the lack of Ist2 results in the accumulation of higher amounts of sodium when the cells are exposed to the presence of this cation, demonstrating the importance of Ist2 for the maintenance of low intracellular levels of toxic sodium. Sodium 280-286 Ist2p Saccharomyces cerevisiae S288C 66-70 28199631-6 2017 As the function and localisation of alkali-metal-cation exporters is not affected in ist2Delta cells, IST2 deletion results in an increased non-specific uptake of sodium to cells. Sodium 163-169 Ist2p Saccharomyces cerevisiae S288C 102-106 28428931-5 2017 Angiotensin II is probably the most important stimulator of sodium reabsorption. Sodium 60-66 angiotensinogen Homo sapiens 0-14 28428931-9 2017 Insulin stimulates the proximal tubule sodium transport, which is IRS2-dependent. Sodium 39-45 insulin Homo sapiens 0-7 27090529-2 2017 Determination of sodium sieving is used as a parameter for AQP1 function analysis, while coupled water removal is essential for adequate sodium and water balance and thus blood pressure control. Sodium 17-23 aquaporin 1 (Colton blood group) Homo sapiens 59-63 28289374-3 2017 High affinity choline uptake (HACU) into acetylcholine (ACh)-synthesizing neurons is critically mediated by the sodium- and pH-dependent high-affinity choline transporter (CHT, encoded by the SLC5A7 gene). Sodium 112-118 solute carrier family 5 member 7 Homo sapiens 151-170 28289374-3 2017 High affinity choline uptake (HACU) into acetylcholine (ACh)-synthesizing neurons is critically mediated by the sodium- and pH-dependent high-affinity choline transporter (CHT, encoded by the SLC5A7 gene). Sodium 112-118 solute carrier family 5 member 7 Homo sapiens 172-175 28289374-3 2017 High affinity choline uptake (HACU) into acetylcholine (ACh)-synthesizing neurons is critically mediated by the sodium- and pH-dependent high-affinity choline transporter (CHT, encoded by the SLC5A7 gene). Sodium 112-118 solute carrier family 5 member 7 Homo sapiens 192-198 27359349-3 2017 This study analyses whether the diffusive transport of sodium and water occurs through a common pore of the claudin-2 channel. Sodium 55-61 claudin 2 Canis lupus familiaris 108-117 28162808-6 2017 FGF13 increased Nav1.7 sodium currents and maintained the membrane localization of Nav1.7 during noxious heat stimulation, enabling the sustained firing of action potentials. Sodium 23-29 sodium channel, voltage-gated, type IX, alpha Mus musculus 16-22 28212604-3 2017 Claudin-2 forms gated paracellular channels and allows sodium ions and other small positively charged ions to cross between adjacent cells. Sodium 55-61 claudin 2 Homo sapiens 0-9 28117294-3 2017 The sodium dependent iodide transport activity of the thyroid gland is mainly attributed to the functional expression of the Na+/I- Symporter (NIS) localized at the basolateral membrane of thyrocytes. Sodium 4-10 solute carrier family 5 member 5 Homo sapiens 125-141 28117294-3 2017 The sodium dependent iodide transport activity of the thyroid gland is mainly attributed to the functional expression of the Na+/I- Symporter (NIS) localized at the basolateral membrane of thyrocytes. Sodium 4-10 solute carrier family 5 member 5 Homo sapiens 143-146 27981497-14 2017 In addition, canagliflozin decreased plasma ANP and NT-proBNP levels and increased plasma renin activity, which may be a compensatory mechanism for sodium retention, leading to subsequent urine output recovery. Sodium 148-154 renin Homo sapiens 90-95 28179232-4 2017 AMPKalpha1 knockout (KO) mice exhibit normal renal sodium handling and a moderate antidiuretic state. Sodium 51-57 protein kinase, AMP-activated, alpha 1 catalytic subunit Mus musculus 0-10 28233236-11 2017 Leptin, together with insulin, will induce activation of sympathetic nervous system with consequences at renal, vascular, and cardiac levels, driving to sodium retention, hypertension, and left ventricular hypertrophy. Sodium 153-159 insulin Homo sapiens 22-29 27841780-2 2017 Blacks have a greater propensity to salt sensitivity and suppressed plasma renin suggesting a predisposition to sodium retention. Sodium 112-118 renin Homo sapiens 75-80 27918529-0 2017 HSD2 neurons in the hindbrain drive sodium appetite. Sodium 36-42 hydroxysteroid 11-beta dehydrogenase 2 Mus musculus 0-4 27918529-2 2017 Here we show that chemogenetic activation of aldosterone-sensitive neurons that express 11beta-hydroxysteroid dehydrogenase type 2 (HSD2) in the nucleus of the solitary tract is sufficient to drive consumption of sodium-containing solutions in mice, independently of thirst or hunger. Sodium 213-219 hydroxysteroid 11-beta dehydrogenase 2 Mus musculus 88-130 27918529-2 2017 Here we show that chemogenetic activation of aldosterone-sensitive neurons that express 11beta-hydroxysteroid dehydrogenase type 2 (HSD2) in the nucleus of the solitary tract is sufficient to drive consumption of sodium-containing solutions in mice, independently of thirst or hunger. Sodium 213-219 hydroxysteroid 11-beta dehydrogenase 2 Mus musculus 132-136 27918529-3 2017 These HSD2-positive neurons are necessary for full expression of sodium appetite and have distinct downstream targets that are activated during sodium depletion. Sodium 65-71 hydroxysteroid 11-beta dehydrogenase 2 Mus musculus 6-10 27918529-3 2017 These HSD2-positive neurons are necessary for full expression of sodium appetite and have distinct downstream targets that are activated during sodium depletion. Sodium 144-150 hydroxysteroid 11-beta dehydrogenase 2 Mus musculus 6-10 27780818-1 2017 Gastrin is a peptide hormone that is involved in the regulation of sodium balance and blood pressure. Sodium 67-73 gastrin Mus musculus 0-7 27959641-5 2017 Every additional gram of sodium intake at baseline was associated with an increase in DBP z score of 0.04 (p < 0.05) between baseline and follow-up. Sodium 25-31 D-box binding PAR bZIP transcription factor Homo sapiens 86-89 28361424-4 2017 Parallel influence of prolactin on the clearance of bicarbonates and sodium ions was observed. Sodium 69-75 prolactin Rattus norvegicus 22-31 28130379-6 2017 Changes in sodium levels in patients with ultrafiltration were negatively correlated to those in serum creatinine and plasma renin activity. Sodium 11-17 renin Homo sapiens 125-130 27629265-2 2017 Increased Angiotensin II (AngII) leads to sympathoexcitation, oxidative stress, and alterations in sodium and water balance. Sodium 99-105 angiotensinogen Rattus norvegicus 10-24 27629265-2 2017 Increased Angiotensin II (AngII) leads to sympathoexcitation, oxidative stress, and alterations in sodium and water balance. Sodium 99-105 angiotensinogen Rattus norvegicus 26-31 27882774-5 2017 Urinary sodium excretion to plasma copeptin (copeptin/UNa Secretion) ratio was significantly lower in Syndrome of Inappropriate Antidiuretic Hormone (SIADH) Secretion patients than in patients with hyponatremia of other origin. Sodium 8-14 arginine vasopressin Homo sapiens 35-43 27882774-5 2017 Urinary sodium excretion to plasma copeptin (copeptin/UNa Secretion) ratio was significantly lower in Syndrome of Inappropriate Antidiuretic Hormone (SIADH) Secretion patients than in patients with hyponatremia of other origin. Sodium 8-14 arginine vasopressin Homo sapiens 45-53 28127476-15 2017 A protocol using dilute vasopressin bolus can be an alternative for managing acute, central DI postoperatively, particularly in setting of hypovolemic shock resulting in a consistent control of serum sodium. Sodium 200-206 arginine vasopressin Homo sapiens 24-35 28484659-3 2017 She was found to have a known mutation in the SCNN1A gene and subsequently required treatment with sodium supplementation. Sodium 99-105 sodium channel epithelial 1 subunit alpha Homo sapiens 46-52 28957796-0 2017 Wild-Type P53 Induces Sodium/Iodide Symporter Expression Allowing Radioiodide Therapy in Anaplastic Thyroid Cancer. Sodium 22-28 tumor protein p53 Homo sapiens 10-13 28573057-5 2017 Patient"s serum sodium (SNa) decreased from 138 to 133 and 125 mEq/L within 24 and 48 hours of cisplatin therapy, respectively. Sodium 16-22 snail family transcriptional repressor 1 Homo sapiens 24-27 29055942-7 2017 With EAAT3, the NAG-induced current was sodium-dependent and saturable (Km 409 microM). Sodium 40-46 solute carrier family 1 member 1 Homo sapiens 5-10 29055942-7 2017 With EAAT3, the NAG-induced current was sodium-dependent and saturable (Km 409 microM). Sodium 40-46 N-acetyl-alpha-glucosaminidase Homo sapiens 16-19 29050005-8 2017 Inverse correlation between the serum GLP-1 level and 24-h urinary sodium excretion was also found among different dietary interventions in SS subjects. Sodium 67-73 glucagon Homo sapiens 38-43 29276908-0 2017 [Correlations of IL-18 and IL-6 with sodium consumption in patients with arterial hypertension and diabetes mellitus]. Sodium 37-43 interleukin 6 Homo sapiens 27-31 29276908-1 2017 AIM: To determine correlations of AH-associated interleukins (IL-18, IL-6) with sodium consumption in AH patients with and without DM. Sodium 80-86 interleukin 6 Homo sapiens 69-73 27151921-9 2017 In conclusion, NDCBE is necessary for maintaining sodium balance and intravascular volume during salt depletion or NCC inactivation in mice. Sodium 50-56 solute carrier family 4 (anion exchanger), member 8 Mus musculus 15-20 28684123-10 2017 On the other hand, higher aspirin doses have been reported to exert a negative impact on blood pressure due to inhibition of cyclooxygenase-2 activity, which reduces renal blood flow, glomerular filtration rate and sodium and water excretion. Sodium 215-221 prostaglandin-endoperoxide synthase 2 Homo sapiens 125-141 29131070-4 2017 A common pathway between oxidative stress and hypertension induced by CNIs may be identified in the involvement of the activation of RhoA/Rho kinase pathway, key for the induction of hypertension and cardiovascular-renal remodeling, of the oxidative stress mediated increased nitric oxide (NO) metabolism and increased renal sodium retention via increased activity of thiazide-sensitive sodium chloride cotransporter (NCC) in the distal tubule. Sodium 325-331 ras homolog family member A Homo sapiens 133-137 29131070-6 2017 Based on the available data, we have provided support to the activation of RhoA/Rho kinase pathway as an important effector in the pathophysiology of CNIs induced post-transplant hypertension via activation of oxidative stress and sodium retention. Sodium 231-237 ras homolog family member A Homo sapiens 75-79 27742514-5 2017 We reviewed the clinical histories, intensive care unit treatment, medication administration records, and laboratory values of these patients, and we found recurrent elevated serum sodium and urine output and decreased urine specific gravity after discontinuation of AVP. Sodium 181-187 arginine vasopressin Homo sapiens 267-270 27878608-9 2017 In the distal tubules, claudin-4 and -8 form paracellular chloride pathway to facilitate electrogenic sodium reabsorption. Sodium 102-108 claudin 4 Homo sapiens 23-39 28066414-0 2016 TGF-beta Affects the Differentiation of Human GM-CSF+ CD4+ T Cells in an Activation- and Sodium-Dependent Manner. Sodium 89-95 transforming growth factor beta 1 Homo sapiens 0-8 28066414-0 2016 TGF-beta Affects the Differentiation of Human GM-CSF+ CD4+ T Cells in an Activation- and Sodium-Dependent Manner. Sodium 89-95 CD4 molecule Homo sapiens 54-57 28008944-6 2016 JNK and CDK5 inhibitor attenuated increases in Nav1.6 sodium currents induced by overexpression of APP. Sodium 54-60 mitogen-activated protein kinase 8 Homo sapiens 0-3 27966362-1 2016 Na+/K+-ATPase (NKA) is an essential cation pump protein responsible for the maintenance of the sodium and potassium gradients across the plasma membrane. Sodium 95-101 tachykinin precursor 1 Homo sapiens 0-13 27966362-1 2016 Na+/K+-ATPase (NKA) is an essential cation pump protein responsible for the maintenance of the sodium and potassium gradients across the plasma membrane. Sodium 95-101 tachykinin precursor 1 Homo sapiens 15-18 28066414-8 2016 Importantly, under low sodium conditions in the medium or upon stimulation with plate-bound instead of bead-bound anti-CD3 and anti-CD28 antibodies, the effects of TGF-beta on GM-CSF, but not on FOXP3, were reversed. Sodium 23-29 transforming growth factor beta 1 Homo sapiens 164-172 27934887-7 2016 In addition, sodium intake induced by sodium depletion or low-sodium diet fell within 30 min after injection into the NTS of the MR antagonist spironolactone, while G15 had no effect. Sodium 13-19 nuclear receptor subfamily 3, group C, member 2 Rattus norvegicus 129-131 27934887-7 2016 In addition, sodium intake induced by sodium depletion or low-sodium diet fell within 30 min after injection into the NTS of the MR antagonist spironolactone, while G15 had no effect. Sodium 38-44 nuclear receptor subfamily 3, group C, member 2 Rattus norvegicus 129-131 27934887-7 2016 In addition, sodium intake induced by sodium depletion or low-sodium diet fell within 30 min after injection into the NTS of the MR antagonist spironolactone, while G15 had no effect. Sodium 38-44 nuclear receptor subfamily 3, group C, member 2 Rattus norvegicus 129-131 27627464-4 2016 The functional interplay between TRPV1, MCU and NCLX, in controlling the cytosolic and mitochondrial calcium and sodium transients and subsequently the nociceptive excitability, is poorly understood. Sodium 113-119 mitochondrial calcium uniporter Homo sapiens 40-43 27627464-3 2016 A mitochondrial Ca2+ uniporter - MCU, controls mitochondrial Ca2+ entry while a sodium/calcium transporter - NCLX shapes calcium and sodium transients by mediating sodium entry into and removing calcium from the mitochondria. Sodium 80-86 mitochondrial calcium uniporter Homo sapiens 33-36 27627464-6 2016 We show that the propagation of the TRPV1-induced cytosolic calcium and sodium fluxes into mitochondria is dependent on coordinated activity of NCLX and MCU. Sodium 72-78 mitochondrial calcium uniporter Homo sapiens 153-156 27627464-3 2016 A mitochondrial Ca2+ uniporter - MCU, controls mitochondrial Ca2+ entry while a sodium/calcium transporter - NCLX shapes calcium and sodium transients by mediating sodium entry into and removing calcium from the mitochondria. Sodium 133-139 mitochondrial calcium uniporter Homo sapiens 33-36 27631841-11 2016 Sodium levels were found correlated with copeptin levels; yet, an even stronger correlation was found between copeptin levels and APACHE II score (r = 0.52; P<.001). Sodium 0-6 arginine vasopressin Homo sapiens 41-49 27879314-6 2016 Three single nucleotide polymorphisms in solute carrier family 8, member 1 (SLC8A1), a sodium/calcium exchanger encoding NCX1, were validated in an independent Japanese genome-wide association study data set (meta-analysis P=0.0001). Sodium 87-93 solute carrier family 8 member A1 Homo sapiens 41-74 27879314-6 2016 Three single nucleotide polymorphisms in solute carrier family 8, member 1 (SLC8A1), a sodium/calcium exchanger encoding NCX1, were validated in an independent Japanese genome-wide association study data set (meta-analysis P=0.0001). Sodium 87-93 solute carrier family 8 member A1 Homo sapiens 76-82 27879314-6 2016 Three single nucleotide polymorphisms in solute carrier family 8, member 1 (SLC8A1), a sodium/calcium exchanger encoding NCX1, were validated in an independent Japanese genome-wide association study data set (meta-analysis P=0.0001). Sodium 87-93 solute carrier family 8 member A1 Homo sapiens 121-125 27748389-9 2016 Renal sodium transport is preserved in insulin resistance and contributes to the salt-sensitivity of blood pressure in hyperinsulinaemia. Sodium 6-12 insulin Homo sapiens 39-46 27529686-6 2016 Nav 1.7 suppression resulted in reduced voltage-gated sodium currents, decreased NHE1 expression, increased extracellular pH and decreased intracellular pH, and ultimately, reduced invasion and proliferation rates of GC cells and growth of GC xenografts in nude mice. Sodium 54-60 sodium channel, voltage-gated, type IX, alpha Mus musculus 0-7 27865823-4 2016 Various hormones and peptides secreted from gut such as gastrin, glucocorticoids, Glucagon-like peptide-1 impact on kidney function and BP especially influencing sodium absorption from gut. Sodium 162-168 glucagon Homo sapiens 82-105 27775552-7 2016 Loss of Etv1 resulted in a complete disruption of the normal sodium current heterogeneity that exists between atrial, VCS, and ventricular myocytes. Sodium 61-67 ETS variant transcription factor 1 Homo sapiens 8-12 27849613-0 2016 Endogenous central amygdala mu-opioid receptor signaling promotes sodium appetite in mice. Sodium 66-72 opioid receptor, mu 1 Mus musculus 28-46 27849613-3 2016 Using selective pharmacological antagonists of opioid receptor subtypes, we reveal that endogenous mu-opioid receptor (MOR) signaling strongly drives sodium appetite in sodium-depleted mice, whereas a role for kappa (KOR) and delta (DOR) opioid receptor signaling was not detected, at least in sodium-depleted mice. Sodium 150-156 opioid receptor, mu 1 Mus musculus 99-117 27849613-3 2016 Using selective pharmacological antagonists of opioid receptor subtypes, we reveal that endogenous mu-opioid receptor (MOR) signaling strongly drives sodium appetite in sodium-depleted mice, whereas a role for kappa (KOR) and delta (DOR) opioid receptor signaling was not detected, at least in sodium-depleted mice. Sodium 150-156 opioid receptor, mu 1 Mus musculus 119-122 27849613-3 2016 Using selective pharmacological antagonists of opioid receptor subtypes, we reveal that endogenous mu-opioid receptor (MOR) signaling strongly drives sodium appetite in sodium-depleted mice, whereas a role for kappa (KOR) and delta (DOR) opioid receptor signaling was not detected, at least in sodium-depleted mice. Sodium 169-175 opioid receptor, mu 1 Mus musculus 99-117 27849613-3 2016 Using selective pharmacological antagonists of opioid receptor subtypes, we reveal that endogenous mu-opioid receptor (MOR) signaling strongly drives sodium appetite in sodium-depleted mice, whereas a role for kappa (KOR) and delta (DOR) opioid receptor signaling was not detected, at least in sodium-depleted mice. Sodium 169-175 opioid receptor, mu 1 Mus musculus 119-122 27638195-0 2016 Thyrotropin and Insulin-Like Growth Factor 1 Receptor Crosstalk Upregulates Sodium-Iodide Symporter Expression in Primary Cultures of Human Thyrocytes. Sodium 76-82 insulin like growth factor 1 Homo sapiens 16-44 27849613-3 2016 Using selective pharmacological antagonists of opioid receptor subtypes, we reveal that endogenous mu-opioid receptor (MOR) signaling strongly drives sodium appetite in sodium-depleted mice, whereas a role for kappa (KOR) and delta (DOR) opioid receptor signaling was not detected, at least in sodium-depleted mice. Sodium 169-175 opioid receptor, mu 1 Mus musculus 99-117 27849613-3 2016 Using selective pharmacological antagonists of opioid receptor subtypes, we reveal that endogenous mu-opioid receptor (MOR) signaling strongly drives sodium appetite in sodium-depleted mice, whereas a role for kappa (KOR) and delta (DOR) opioid receptor signaling was not detected, at least in sodium-depleted mice. Sodium 169-175 opioid receptor, mu 1 Mus musculus 119-122 27849613-5 2016 The CeA was subsequently targeted with bilateral infusions of the MOR antagonist naloxonazine, which significantly reduced sodium appetite in mice. Sodium 123-129 opioid receptor, mu 1 Mus musculus 66-69 27806966-6 2016 Here we present evidence of the same blunting in Scn10a-/- compared to wild-type ventricular myocytes, supporting the conclusion that Nav1.8 contributes to late sodium current at slow rates. Sodium 161-167 sodium channel, voltage-gated, type X, alpha Mus musculus 134-140 27510906-9 2016 Moreover, these findings support the notion that NHE3 dephosphorylation at serine 552 may represent a key event in the regulation of renal proximal tubule sodium handling by ANG II in the presence of natriuretic hormones that promote cAMP accumulation and transporter phosphorylation. Sodium 155-161 angiotensinogen Rattus norvegicus 174-180 27836073-2 2016 It was hypothesized that primary renal sodium retention blunted the reactivity of the renin-angiotensin-aldosterone system to changes in salt intake in preeclampsia (PE). Sodium 39-45 renin Homo sapiens 86-91 27582096-2 2016 Endothelin-1 (ET-1) regulates sodium balance by promoting natriuresis through the endothelin B receptor (ETB) in response to increased salt in the diet, but the effect that the time of day has on this natriuretic response is not known. Sodium 30-36 endothelin 1 Rattus norvegicus 0-12 27582096-2 2016 Endothelin-1 (ET-1) regulates sodium balance by promoting natriuresis through the endothelin B receptor (ETB) in response to increased salt in the diet, but the effect that the time of day has on this natriuretic response is not known. Sodium 30-36 endothelin 1 Rattus norvegicus 14-18 27517656-7 2016 CONCLUSIONS: Administration of perindopril arginine 10, 14, or 20mg to mildly sodium-depleted healthy volunteers is associated with a dose-dependent inhibition of in vivo ACE activity with significant between-dose differences. Sodium 78-84 angiotensin I converting enzyme Homo sapiens 171-174 27822054-12 2016 Local inhibition of the renin-angiotensin-aldosterone system secondary to increased delivery of sodium to the juxtaglomerular apparatus during SGLT2 inhibition has also been postulated. Sodium 96-102 renin Homo sapiens 24-29 27530546-2 2016 Dysmyelination in these mice is associated with an ectopic expression of the sensory neuron specific sodium channel isoform NaV1.8 on motor axons. Sodium 101-107 sodium channel, voltage-gated, type X, alpha Mus musculus 124-130 27627089-4 2016 The changes of the total water volume (CTV) and ABB may be presented at the same time in the values of the difference and ratio between serum concentrations of natrium and chlorides (SNa+ - SCl-; SNa+/SCl-). Sodium 160-167 snail family transcriptional repressor 1 Homo sapiens 183-186 27627089-4 2016 The changes of the total water volume (CTV) and ABB may be presented at the same time in the values of the difference and ratio between serum concentrations of natrium and chlorides (SNa+ - SCl-; SNa+/SCl-). Sodium 160-167 snail family transcriptional repressor 1 Homo sapiens 196-199 27428770-12 2016 Milder phenotypes of PA, where PRA is not as suppressed, are most susceptible to dietary sodium influences on renin and ARR. Sodium 89-95 renin Homo sapiens 110-115 27784314-9 2016 For the subset of 169 patients with CF and two CFTR mutations Class I, II and/or III, in comparative analysis, there was a positive association with: (i) sweat chloride/sodium ratio (p < 0.001), (ii) sweat chloride values (p = 0.047), (iii) subject"s age at the time of the ST grouped by numerical order (p = 0.001). Sodium 169-175 CF transmembrane conductance regulator Homo sapiens 47-51 27600292-8 2016 Our study indicates that this "ghrelin-Sirt1 system" may participate in regulating sodium reabsorption in the distal nephron. Sodium 83-89 sirtuin 1 Rattus norvegicus 39-44 27569547-3 2016 Whole-exome sequencing and Sanger sequencing in six unrelated families identified compound heterozygous and homozygous mutations in SLC5A7 encoding the presynaptic sodium-dependent high-affinity choline transporter 1 (CHT), which is known to be mutated in one dominant form of distal motor neuronopathy (DHMN7A). Sodium 164-170 solute carrier family 5 member 7 Homo sapiens 132-138 27569547-3 2016 Whole-exome sequencing and Sanger sequencing in six unrelated families identified compound heterozygous and homozygous mutations in SLC5A7 encoding the presynaptic sodium-dependent high-affinity choline transporter 1 (CHT), which is known to be mutated in one dominant form of distal motor neuronopathy (DHMN7A). Sodium 164-170 solute carrier family 5 member 7 Homo sapiens 218-221 27422117-4 2016 Further, p53 strongly favors G-quadruplexes folded in potassium over those formed in sodium, thus indicating the telomeric G-quadruplex conformational selectivity of p53. Sodium 85-91 tumor protein p53 Homo sapiens 9-12 27422117-4 2016 Further, p53 strongly favors G-quadruplexes folded in potassium over those formed in sodium, thus indicating the telomeric G-quadruplex conformational selectivity of p53. Sodium 85-91 tumor protein p53 Homo sapiens 166-169 27343265-8 2016 These results suggest that corin-mediated pro-ANP activation may occur in renal segments and that locally produced ANP may act in an autocrine manner to regulate sodium and water reabsorption in situ Our results also point to the proximal convoluted tubules as a major site for local ANP action. Sodium 162-168 natriuretic peptide A Homo sapiens 115-118 27636896-1 2016 The NHE1 isoform of the mammalian Na+/H+ exchanger is a ubiquitous plasma membrane protein that regulates intracellular pH in mammalian cells by removing one intracellular proton in exchange for one extracellular sodium. Sodium 213-219 solute carrier family 9 member A1 Homo sapiens 4-8 27637026-1 2016 BACKGROUND: Tissue Angiotensin II (Ang-II), produced through local non ACE-dependent pathways, stimulates liver fibrogenesis, renal vasoconstriction and sodium retention. Sodium 153-159 angiotensinogen Homo sapiens 19-33 27637026-1 2016 BACKGROUND: Tissue Angiotensin II (Ang-II), produced through local non ACE-dependent pathways, stimulates liver fibrogenesis, renal vasoconstriction and sodium retention. Sodium 153-159 angiotensinogen Homo sapiens 35-41 27628629-0 2016 The Renal Sodium Bicarbonate Cotransporter NBCe2: Is It a Major Contributor to Sodium and pH Homeostasis? Sodium 10-16 solute carrier family 4 member 5 Homo sapiens 43-48 27628629-3 2016 Subsequently, NBCe2 was found in diverse locations where it plays a role in regulating sodium and bicarbonate transport, influencing intracellular, extracellular, interstitial, and ultimately plasma pH (Boron et al. Sodium 87-93 solute carrier family 4 member 5 Homo sapiens 14-19 27628629-10 2016 While much is known about the two electrogenic sodium bicarbonate cotransporters, NBCe1 and NBCe2, in the regulation of sodium homeostasis and pH balance in the rodent kidney, little is known about their roles in human renal physiology. Sodium 47-53 solute carrier family 4 member 5 Homo sapiens 92-97 27628629-11 2016 NBCe2 is located in the proximal tubule Golgi apparatus under basal conditions and then disperses throughout the cell, but particularly into the apical membrane microvilli, during various maneuvers that increase intracellular sodium. Sodium 226-232 solute carrier family 4 member 5 Homo sapiens 0-5 26872488-2 2016 Herein, we demonstrated in cultured cells and in vivo that increased levels of extracellular Pi activated the AKT/mammalian target of rapamycin complex 1 (mTORC1) pathway by suppressing membrane-bound phosphatase and tensin homolog (PTEN) levels in a manner requiring the sodium-dependent Pi transporter PiT-1. Sodium 272-278 AKT serine/threonine kinase 1 Homo sapiens 110-113 27188842-8 2016 We review evidence from experiments conducted in vivo and in cultured cells that indicates aldosterone and vasopressin, the two major hormones regulating sodium reabsorption by CD, generate a coordinated stimulation of apical ENaC and basolateral Na(+),K(+)-ATPase. Sodium 154-160 arginine vasopressin Homo sapiens 107-118 27188842-9 2016 Moreover, we discuss evidence suggesting that variations in sodium entry per se induce a coordinated change in Na(+),K(+)-ATPase activity through the signaling of protein kinases such as protein kinase A and p38 mitogen-activated protein kinase. Sodium 60-66 mitogen-activated protein kinase 14 Homo sapiens 208-211 27343265-8 2016 These results suggest that corin-mediated pro-ANP activation may occur in renal segments and that locally produced ANP may act in an autocrine manner to regulate sodium and water reabsorption in situ Our results also point to the proximal convoluted tubules as a major site for local ANP action. Sodium 162-168 natriuretic peptide A Homo sapiens 115-118 27068441-2 2016 Mouse models suggest that OSR1 mainly activates NKCC2-mediated sodium transport along the thick ascending limb, while SPAK mainly activates NCC along the distal convoluted tubule, but the kinases may compensate for each other. Sodium 63-69 odd-skipped related transcription factor 1 Mus musculus 26-30 27011258-0 2016 Genetic variants in adiponectin and blood pressure responses to dietary sodium or potassium interventions: a family-based association study. Sodium 72-78 adiponectin, C1Q and collagen domain containing Homo sapiens 20-31 27011258-2 2016 The aim of this study was to assess the association of common genetic variants of the adiponectin gene with BP responses to controlled dietary sodium or potassium interventions. Sodium 143-149 adiponectin, C1Q and collagen domain containing Homo sapiens 86-97 27011258-10 2016 Our study indicated that the genetic polymorphisms in the adiponectin gene are significantly associated with BP responses to dietary sodium and potassium intake. Sodium 133-139 adiponectin, C1Q and collagen domain containing Homo sapiens 58-69 27068441-2 2016 Mouse models suggest that OSR1 mainly activates NKCC2-mediated sodium transport along the thick ascending limb, while SPAK mainly activates NCC along the distal convoluted tubule, but the kinases may compensate for each other. Sodium 63-69 solute carrier family 12, member 1 Mus musculus 48-53 27068441-13 2016 The distal convoluted tubule has been proposed to sense plasma [K(+) ], with NCC activation serving as the primary effector pathway that modulates K(+) secretion, by metering sodium delivery to the collecting duct. Sodium 175-181 solute carrier family 12, member 3 Mus musculus 77-80 26152401-4 2016 The WNK-OSR1/SPAK-SLC12a signaling cascade is present in the kidneys and vascular smooth muscle cells (VSMCs) and regulates salt sensitivity physiologically, i.e. urinary sodium excretion and arterial tone by various hormonal and dietary factors. Sodium 171-177 odd-skipped related transcription factor 1 Homo sapiens 8-12 26152401-4 2016 The WNK-OSR1/SPAK-SLC12a signaling cascade is present in the kidneys and vascular smooth muscle cells (VSMCs) and regulates salt sensitivity physiologically, i.e. urinary sodium excretion and arterial tone by various hormonal and dietary factors. Sodium 171-177 serine/threonine kinase 39 Homo sapiens 13-17 28149313-4 2016 Digoxin increases the intracellular sodium concentration by inhibition of Na+/K+-ATPase that affects Na+/Ca2+ exchanger (NCX), which raises intracellular calcium and thus attenuates heart failure. Sodium 36-42 solute carrier family 8 member A1 Rattus norvegicus 101-119 27163523-0 2016 Effects of interleukin-1 beta injections into the subfornical organ and median preoptic nucleus on sodium appetite, blood pressure and body temperature of sodium-depleted rats. Sodium 99-105 interleukin 1 beta Rattus norvegicus 11-29 27163523-4 2016 IL-1beta injections into the SFO and MnPO at the doses of 0.2, 0.4, 0.8 and 1.6ng/0.2mul promoted a dose-dependent inhibition of salt intake in sodium-depleted rats. Sodium 144-150 interleukin 1 beta Rattus norvegicus 0-8 27163523-10 2016 Further studies are required to clarify the mechanisms involved in fever, blood pressure increase and inhibition of sodium appetite induced by injections of IL-1beta into the SFO and MnPO in sodium-depleted rats. Sodium 116-122 interleukin 1 beta Rattus norvegicus 157-165 27163523-10 2016 Further studies are required to clarify the mechanisms involved in fever, blood pressure increase and inhibition of sodium appetite induced by injections of IL-1beta into the SFO and MnPO in sodium-depleted rats. Sodium 191-197 interleukin 1 beta Rattus norvegicus 157-165 27583358-12 2016 Diets with frequent pizza and pasta consumption were high in energy, saturated fatty acids, trans-fatty acids, sodium and low in other antioxidants. Sodium 111-117 solute carrier family 45 member 1 Homo sapiens 30-35 27335124-5 2016 Sodium permeation in alpha-SNAP-deficient cells cannot be corrected by tethering multiple Stim1 domains to Orai1 C-terminal tail, demonstrating that alpha-SNAP regulates functional assembly and calcium selectivity of Orai1 multimers independently of Stim1 levels. Sodium 0-6 stromal interaction molecule 1 Mus musculus 90-95 27335124-5 2016 Sodium permeation in alpha-SNAP-deficient cells cannot be corrected by tethering multiple Stim1 domains to Orai1 C-terminal tail, demonstrating that alpha-SNAP regulates functional assembly and calcium selectivity of Orai1 multimers independently of Stim1 levels. Sodium 0-6 stromal interaction molecule 1 Mus musculus 250-255 27323774-3 2016 METHODS AND RESULTS: In rats, Ang II infusion increased both sodium (Na(+)) retention and BP on day 1, and BP remained elevated throughout the 7-day infusion period. Sodium 61-67 angiotensinogen Rattus norvegicus 30-36 26582410-6 2016 SLC4A4 marker rs4254735 was significantly associated with diastolic BP (DBP) response to low-sodium intervention (P=5.05 x 10(-4)), with mean (95% confidence interval (CI)) response of -2.91 (-3.21, -2.61) and -0.40 (-1.84, 1.05) mmHg for genotype AA and AG, respectively. Sodium 93-99 solute carrier family 4 member 4 Homo sapiens 0-6 26582410-7 2016 In addition, BP responses to high-sodium intervention significantly increased with the number of minor C alleles of SLC4A4 marker rs10022637. Sodium 34-40 solute carrier family 4 member 4 Homo sapiens 116-122 26582410-9 2016 In brief, the present study indicated that common variants in the SLC4A4 gene might contribute to the variation of BP responses to dietary sodium intake in Han Chinese population. Sodium 139-145 solute carrier family 4 member 4 Homo sapiens 66-72 26282188-10 2016 Runners with the CFTR-7T/7T genotype exhibited increased sweat sodium concentrations during a marathon. Sodium 63-69 CF transmembrane conductance regulator Homo sapiens 17-21 27610358-9 2016 Forty percent of patients (17/42) with a serum sodium (SNa) less than 140 mEq/L experienced a fall in SNa with 12.5% of all patients (7/56) developing hospital-acquired or aggravated hyponatremia (126-134 mEq/L) with fall in SNa between 2 and 10 mEq/L. Sodium 47-53 snail family transcriptional repressor 1 Homo sapiens 55-58 27610358-9 2016 Forty percent of patients (17/42) with a serum sodium (SNa) less than 140 mEq/L experienced a fall in SNa with 12.5% of all patients (7/56) developing hospital-acquired or aggravated hyponatremia (126-134 mEq/L) with fall in SNa between 2 and 10 mEq/L. Sodium 47-53 snail family transcriptional repressor 1 Homo sapiens 102-105 27610358-9 2016 Forty percent of patients (17/42) with a serum sodium (SNa) less than 140 mEq/L experienced a fall in SNa with 12.5% of all patients (7/56) developing hospital-acquired or aggravated hyponatremia (126-134 mEq/L) with fall in SNa between 2 and 10 mEq/L. Sodium 47-53 snail family transcriptional repressor 1 Homo sapiens 102-105 26821241-5 2016 Loss-of beta-III spectrin function appears to underpin cerebellar dysfunction and degeneration in both diseases resulting in thinner dendrites, excessive dendritic protrusion with loss of planarity, reduced resurgent sodium currents and abnormal glutamatergic neurotransmission. Sodium 217-223 spectrin beta, non-erythrocytic 2 Homo sapiens 8-25 26701978-2 2016 The very high plasma aldosterone levels detected under hypovolemic or hyperkalemic challenge can lead to increased or decreased sodium reabsorption, respectively, through the Na(+)/Cl(-) cotransporter (NCC). Sodium 128-134 solute carrier family 12, member 3 Mus musculus 175-200 27266988-8 2016 In multivariable regression analysis, sodium excretion remained significantly correlated with phosphate excretion after adjustment for age, gender, BMI, and eGFR in all observational cohorts. Sodium 38-44 epidermal growth factor receptor Homo sapiens 157-161 27355970-2 2016 In contrast to this straightforward deprotonation of the amidine units, the reaction of 1 with the bis(trimethylsilyl)amides of sodium or potassium unexpectedly leads to a beta-metalation and an immediate deamidation reaction yielding [(thf)2 Na{Dipp-N=C(tBu)-N(H)}] (4 a) or [(thf)2 K{Dipp-N=C(tBu)-N(H)}] (4 b), respectively, as well as 2-vinylpyridine in both cases. Sodium 128-134 nudix hydrolase 3 Homo sapiens 246-250 27355970-2 2016 In contrast to this straightforward deprotonation of the amidine units, the reaction of 1 with the bis(trimethylsilyl)amides of sodium or potassium unexpectedly leads to a beta-metalation and an immediate deamidation reaction yielding [(thf)2 Na{Dipp-N=C(tBu)-N(H)}] (4 a) or [(thf)2 K{Dipp-N=C(tBu)-N(H)}] (4 b), respectively, as well as 2-vinylpyridine in both cases. Sodium 128-134 nudix hydrolase 3 Homo sapiens 286-290 27111173-0 2016 Effect of sodium intake on renin level: Analysis of general population and meta-analysis of randomized controlled trials. Sodium 10-16 renin Homo sapiens 27-32 27111173-1 2016 BACKGROUND: We evaluated the association between sodium intake and plasma renin levels in the cross sectional study and meta-analysis of randomized controlled trials, whether there is a persistent elevation of plasma renin by longer-term sodium intake restriction. Sodium 49-55 renin Homo sapiens 74-79 27111173-8 2016 In the meta-analysis, the standard mean difference (SMD) of renin level by sodium intake reduction was 1.26 (95% CI: 1.08 to 1.44, Z=12.80, P<0.001, I(2)=87%). Sodium 75-81 renin Homo sapiens 60-65 28149313-4 2016 Digoxin increases the intracellular sodium concentration by inhibition of Na+/K+-ATPase that affects Na+/Ca2+ exchanger (NCX), which raises intracellular calcium and thus attenuates heart failure. Sodium 36-42 solute carrier family 8 member A1 Rattus norvegicus 121-124 27197160-5 2016 The most robust and frequent inductions were of the sodium-driven bicarbonate transporters SLC4A4 and SLC4A9, which rely upon both HIF1alpha and HIF2alpha activity for their expression. Sodium 52-58 solute carrier family 4 member 4 Homo sapiens 91-97 27197160-5 2016 The most robust and frequent inductions were of the sodium-driven bicarbonate transporters SLC4A4 and SLC4A9, which rely upon both HIF1alpha and HIF2alpha activity for their expression. Sodium 52-58 hypoxia inducible factor 1 subunit alpha Homo sapiens 131-140 27677137-0 2016 Loss of Adiponectin-Induced Renal Sodium Excretion in Hypertension. Sodium 34-40 adiponectin, C1Q and collagen domain containing Homo sapiens 8-19 26223346-1 2016 A recent study from the United Kingdom indicates an association between pre hemodialysis (HD) serum sodium (SNa(+)) and systolic and diastolic blood pressure (SBP and DBP) in chronic HD patients. Sodium 100-106 snail family transcriptional repressor 1 Homo sapiens 108-111 27477809-11 2016 Importantly, sodium selenite treatment retarded the growth of the transplanted SGC7901 cells in nude mice, with the induction of SBP1 expression, which was associated with the decrease of Nrf2 expression and the inactivation of the Wnt/beta-catenin signaling pathway. Sodium 13-19 vesicle (multivesicular body) trafficking 1 Mus musculus 129-133 27477809-11 2016 Importantly, sodium selenite treatment retarded the growth of the transplanted SGC7901 cells in nude mice, with the induction of SBP1 expression, which was associated with the decrease of Nrf2 expression and the inactivation of the Wnt/beta-catenin signaling pathway. Sodium 13-19 nuclear factor, erythroid derived 2, like 2 Mus musculus 188-192 26223346-1 2016 A recent study from the United Kingdom indicates an association between pre hemodialysis (HD) serum sodium (SNa(+)) and systolic and diastolic blood pressure (SBP and DBP) in chronic HD patients. Sodium 100-106 D-box binding PAR bZIP transcription factor Homo sapiens 167-170 25744274-2 2016 Both vitamin D receptor activator (VDRA) treatment and dietary sodium restriction potentiate the efficacy of renin-angiotensin-aldosterone-system (RAAS) blockade to reduce albuminuria. Sodium 63-69 renin Homo sapiens 109-114 27038931-0 2016 Stromal Cell-Derived Factor 1 Increases Tetrodotoxin-Resistant Sodium Currents Nav1.8 and Nav1.9 in Rat Dorsal Root Ganglion Neurons via Different Mechanisms. Sodium 63-69 sodium voltage-gated channel alpha subunit 10 Rattus norvegicus 79-85 27038933-8 2016 The swelling induced by the P2Y1 receptor antagonist was mediated by induction of oxidative-nitrosative stress, mitochondrial dysfunction, production of inflammatory lipid mediators, and a sodium influx from the extracellular space. Sodium 189-195 purinergic receptor P2Y1 Rattus norvegicus 28-32 27038933-12 2016 In the normal retina, ATP release and autocrine P2Y1 receptor activation serve to inhibit the induction of oxidative-nitrosative stress, mitochondrial dysfunction, and production of inflammatory lipid mediators, which otherwise will induce a sodium influx and cytotoxic Muller cell swelling under anisoosmotic conditions. Sodium 242-248 purinergic receptor P2Y1 Rattus norvegicus 48-52 27424689-8 2016 The renin-angiotensin-aldosterone system of VLBW infants seems to be able, even immediately after birth, to respond to variations of plasma sodium concentrations; measurement of UAE constitutes an interesting method to determine aldosterone production in VLBW infants. Sodium 140-146 renin Homo sapiens 4-9 27037930-2 2016 The main reason for this abnormality is related to the fact that these patients have portal hypertension and this leads to systemic vasodilation that in turn activates sodium-retaining and water-retaining systems such as the renin-angiotensin-aldosterone system and arginine vasopressin (AVP). Sodium 168-174 arginine vasopressin Homo sapiens 275-286 26803690-0 2016 Effects of Dietary Sodium Restriction in Kidney Transplant Recipients Treated With Renin-Angiotensin-Aldosterone System Blockade: A Randomized Clinical Trial. Sodium 19-25 renin Homo sapiens 83-88 26803690-1 2016 BACKGROUND: In patients with chronic kidney disease receiving renin-angiotensin-aldosterone system (RAAS) blockade, dietary sodium restriction is an often-used treatment strategy to reduce blood pressure (BP) and albuminuria. Sodium 124-130 renin Homo sapiens 62-67 26908285-1 2016 Overall binding affinity of sodium or indazolium cis/trans-[MCl4(1H-indazole)(NO)] (M = Ru, Os) complexes towards human serum albumin (HSA) and high molecular mass components of the blood serum was monitored by ultrafiltration. Sodium 28-34 albumin Homo sapiens 120-133 27125438-6 2016 CONCLUSIONS: A significant relationship between plasmatic sodium levels and C-reactive protein was found, apart from of the underlying disease. Sodium 58-64 C-reactive protein Homo sapiens 76-94 27274855-6 2016 Treatment of diabetes insipidus (DI) with replacement antidiuretic hormone (ADH) was complicated by extreme difficulties in achieving a satisfactory sodium and water balance. Sodium 149-155 arginine vasopressin Homo sapiens 54-80 27493921-10 2016 However, the changes in serum vitamin D, and PTH levels across tertiles of urinary sodium were not significant. Sodium 83-89 parathyroid hormone Homo sapiens 45-48 27193532-4 2016 Serum sodium levels were correlated negatively with ESR (p =0.001) and positively with serum albumin levels (p < 0.0001) and C3 (p = 0.008) in children with SLE and those levels were correlated negatively with serum interleukin-6 levels (p = 0.003) in adults with SLE. Sodium 6-12 interleukin 6 Homo sapiens 219-232 27058411-10 2016 The alphaENaC mRNA levels and sodium transport were increased in SOCS-1 overexpressing MLE-12 cells exposed to IL-1beta. Sodium 30-36 interleukin 1 beta Mus musculus 111-119 26786162-4 2016 Nav1.5 N-terminal domain, by itself (the 132 aa peptide) (Nter), exerts a "chaperone-like" effect that increases sodium (I(Na)) and inward rectifier potassium (I(K1)) currents by enhancing the expression of Nav1.5, Kir2.1, and Kir2.2 channels as demonstrated in Chinese hamster ovary (CHO) cells and in rat cardiomyocytes. Sodium 113-119 potassium inwardly rectifying channel subfamily J member 12 Homo sapiens 227-233 26951941-4 2016 We showed that the inhibitory effect of E2 on ANGII-induced water and sodium intake requires the ERK1/2 and JNK signaling pathways. Sodium 70-76 angiotensinogen Rattus norvegicus 46-51 26951941-8 2016 Taken together, these results demonstrate that E2 modulates ANGII-induced water and sodium intake and AVP secretion by affecting the ERK1/2 and JNK pathways in the lamina terminalis and ERK1/2 signaling in the hypothalamic nuclei (PVN and SON) in OVX rats. Sodium 84-90 angiotensinogen Rattus norvegicus 60-65 27008858-3 2016 Mfsd2a is a newly described sodium-dependent lysophosphatidylcholine (LPC) symporter expressed at the blood-brain barrier that transports LPCs containing DHA and other long-chain fatty acids. Sodium 28-34 major facilitator superfamily domain containing 2A Mus musculus 0-6 27101299-4 2016 On the contrary, insulin is an antilipolytic hormone that increases sodium retention, suggesting a possible functional link with NP. Sodium 68-74 insulin Homo sapiens 17-24 27037930-2 2016 The main reason for this abnormality is related to the fact that these patients have portal hypertension and this leads to systemic vasodilation that in turn activates sodium-retaining and water-retaining systems such as the renin-angiotensin-aldosterone system and arginine vasopressin (AVP). Sodium 168-174 arginine vasopressin Homo sapiens 288-291 27045029-8 2016 Agtr1a(-/-) mice had decreased mesenteric artery expression of the calcium-activated potassium channel Kcnmb1, which may enhance myogenic tone and together with sodium retention, exacerbate BP responses to aldosterone/salt in Agtr1a(-/-) mice. Sodium 161-167 angiotensin II receptor, type 1a Mus musculus 0-6 27028729-3 2016 An N,O-dual doped carbon (denoted as NOC) network is designed and synthesized, which is greatly favorable for sodium storage. Sodium 110-116 nocturnin Homo sapiens 37-40 26945070-0 2016 Structural Insights into the Transport Mechanism of the Human Sodium-dependent Lysophosphatidylcholine Transporter MFSD2A. Sodium 62-68 major facilitator superfamily domain containing 2A Homo sapiens 115-121 27028729-5 2016 The NOC composite with 3D well-defined porosity and N,O-dual doped induces active sites, contributing to the enhanced sodium storage. Sodium 118-124 nocturnin Homo sapiens 4-7 27143858-1 2016 A low sodium diet enhances the hemodynamic effect of renin-angiotensin system blockers. Sodium 6-12 renin Homo sapiens 53-58 27143858-2 2016 It was suggested that the substrates of P-glycoprotein or cytochrome P450 3A4 were reduced on a high sodium diet. Sodium 101-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-77 27143858-3 2016 This study aimed to investigate the influence of high sodium diet on the pharmacokinetics and pharmacodynamics of fimasartan, which is a substrate of cytochrome P450 3A4 but not P-glycoprotein. Sodium 54-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-169 27053360-0 2016 Sodium Intake Regulates Glucose Homeostasis through the PPARdelta/Adiponectin-Mediated SGLT2 Pathway. Sodium 0-6 peroxisome proliferator activator receptor delta Mus musculus 56-65 27053360-4 2016 Here, we report that high sodium intake remarkably increased natriuresis in wild-type mice, but this effect was blunted in adipose-specific PPARdelta knockout mice and diabetic mice. Sodium 26-32 peroxisome proliferator activator receptor delta Mus musculus 140-149 27053360-5 2016 PPARdelta activation in perirenal fat by agonist or high sodium intake inhibited renal sodium-glucose cotransporter 2 (SGLT2) function, which is mediated by increased production of adipose adiponectin. Sodium 57-63 peroxisome proliferator activator receptor delta Mus musculus 0-9 27053360-8 2016 Our findings provide insights into the distinctive role of the PPARdelta/adiponectin/SGLT2 pathway in the regulation of sodium and glucose homeostasis. Sodium 120-126 peroxisome proliferator activator receptor delta Mus musculus 63-72 26951843-6 2016 When offered saline to drink, Hsd11b2.BKO mice consumed 3 times more sodium than controls and became hypertensive. Sodium 69-75 hydroxysteroid 11-beta dehydrogenase 2 Mus musculus 30-37 26951843-12 2016 Our data suggest that 11betaHSD2-positive neurons integrate salt appetite and the blood pressure response to dietary sodium through a mineralocorticoid receptor-dependent pathway. Sodium 117-123 hydroxysteroid 11-beta dehydrogenase 2 Mus musculus 22-32 26862153-3 2016 Using a split-root system to simulate a non-uniform root zone salinity in Gossypium hirsutum L., we showed that the up-regulated expression of sodium efflux-related genes (SOS1, SOS2, PMA1, and PMA2) and water uptake-related genes (PIP1 and PIP2) was possibly involved in the elevated Na(+) efflux and water use in the the roots in the non-saline side. Sodium 143-149 CBL-interacting serine/threonine-protein kinase 24-like Gossypium hirsutum 178-182 27049939-1 2016 The serotonin transporter (SERT) terminates serotonergic signalling through the sodium- and chloride-dependent reuptake of neurotransmitter into presynaptic neurons. Sodium 80-86 solute carrier family 6 member 4 Homo sapiens 4-25 27049939-1 2016 The serotonin transporter (SERT) terminates serotonergic signalling through the sodium- and chloride-dependent reuptake of neurotransmitter into presynaptic neurons. Sodium 80-86 solute carrier family 6 member 4 Homo sapiens 27-31 26819275-1 2016 Severe myoclonic epilepsy of infancy (SMEI) is associated with loss of function of the SCN1A gene encoding the NaV1.1 sodium channel isoform. Sodium 118-124 sodium channel, voltage-gated, type I, alpha Mus musculus 87-92 26819275-1 2016 Severe myoclonic epilepsy of infancy (SMEI) is associated with loss of function of the SCN1A gene encoding the NaV1.1 sodium channel isoform. Sodium 118-124 sodium channel, voltage-gated, type I, alpha Mus musculus 111-117 26854262-6 2016 It is proposed that gastrin produced by G-cells via its receptor, cholecystokinin B receptor, interacts with renal D1 -like dopamine receptors to increase renal sodium excretion. Sodium 161-167 cholecystokinin B receptor Homo sapiens 66-92 26854262-12 2016 Gastrin, via its receptor, the cholecystokinin type B receptor (CCKBR), is natriuretic in mammals, including humans, by inhibition of renal sodium transport. Sodium 140-146 cholecystokinin B receptor Homo sapiens 31-62 26854262-12 2016 Gastrin, via its receptor, the cholecystokinin type B receptor (CCKBR), is natriuretic in mammals, including humans, by inhibition of renal sodium transport. Sodium 140-146 cholecystokinin B receptor Homo sapiens 64-69 27372528-8 2016 Mixed-effects multivariable linear regression models assessed the association of SBP and DBP with sodium intake. Sodium 98-104 D-box binding PAR bZIP transcription factor Homo sapiens 89-92 26786906-3 2016 The simultaneous separation and sensitive detection of sodium (Na(+)), potassium (K(+)), ammonium (NH4 (+)), chloride (Cl(-)) and nitrate (NO3 (-)) in a single run was achieved by using 98% 1.5 mM MgSO4 and 2% acetonitrile eluent with a mixed-bed ion-exchange separation column without suppressor column system. Sodium 55-61 NBL1, DAN family BMP antagonist Homo sapiens 139-142 26791475-0 2016 Role of Vasopressin in the Regulation of Renal Sodium Excretion: Interaction with Glucagon-Like Peptide-1. Sodium 47-53 arginine vasopressin Rattus norvegicus 8-19 26791475-7 2016 It was hypothesised that the basis for the fast elimination of excess sodium following an oral NaCl load could be the involvement of GLP-1 in osmoregulation combined with vasopressin. Sodium 70-76 arginine vasopressin Rattus norvegicus 171-182 26791475-9 2016 It was also shown that vasopressin at doses of 1-10 mug/kg and the selective V1a agonist (1 mug/kg) induced an increase in sodium fractional excretion to 10 +- 2% and 8 +- 2%, respectively. Sodium 123-129 arginine vasopressin Rattus norvegicus 23-34 26791475-11 2016 These data suggest that GLP-1 combined with vasopressin could be involved in the regulation of sodium balance in the hyperosmolar state as a result of NaCl loading. Sodium 95-101 arginine vasopressin Rattus norvegicus 44-55 26791475-12 2016 Vasopressin regulates the reabsorption of a significant portion of filtered sodium in the distal segment of the nephron and modulates the natriuretic effect of GLP-1. Sodium 76-82 arginine vasopressin Rattus norvegicus 0-11 27124037-0 2016 Association of Urinary Sodium Excretion With Insulin Resistance in Korean Adolescents: Results From the Korea National Health and Nutrition Examination Survey 2009-2010. Sodium 23-29 insulin Homo sapiens 45-52 27124037-2 2016 Reports have suggested an association of sodium intake with insulin resistance (IR) and type 2 diabetes mellitus in adults. Sodium 41-47 insulin Homo sapiens 60-67 27028743-0 2016 alpha1-Syntrophin Variant Identified in Drug-Induced Long QT Syndrome Increases Late Sodium Current. Sodium 85-91 syntrophin alpha 1 Homo sapiens 0-17 27028743-3 2016 We tested whether a novel SNTA1 (alpha1-syntrophin) variant (p.E409Q) found in a patient with diLQTS increases late sodium current (INa-L), thereby providing a disease mechanism. Sodium 116-122 syntrophin alpha 1 Homo sapiens 26-31 27028743-3 2016 We tested whether a novel SNTA1 (alpha1-syntrophin) variant (p.E409Q) found in a patient with diLQTS increases late sodium current (INa-L), thereby providing a disease mechanism. Sodium 116-122 syntrophin alpha 1 Homo sapiens 33-50 26963391-8 2016 The increase in UO in NCC KO mice was associated with a significant increase in sodium excretion (from 0.25 mmol/24 hrs at baseline to 0.35 mmol/24 hrs after amiloride injection, p<0.05, n = 4). Sodium 80-86 solute carrier family 12, member 3 Mus musculus 22-25 26843409-2 2016 The impact of sodium, potassium, choline, guanidinium, and 1-ethyl-3-methylimidazolium chloride on the fibrillation kinetics of insulin in an acid-denaturing solvent environment is studied by fluorescence spectroscopy using thioflavin T as a fibril-specific stain. Sodium 14-20 insulin Homo sapiens 128-135 27156761-7 2016 The copeptin to urinary sodium ratio differentiates accurately between volume-depleted and normovolemic disorders. Sodium 24-30 arginine vasopressin Homo sapiens 4-12 26224401-5 2016 RESULTS: SNP rs5063 in the NPPA gene and SNP rs2077386 in the NPPC gene exhibited significant associations with BP response to low-sodium dietary intervention under recessive genetic model. Sodium 131-137 natriuretic peptide A Homo sapiens 27-31 26730722-5 2016 In particular, rats treated with both mineralocorticoid and AngII preferentially worked for access to sodium versus water compared with rats given only one of these hormones. Sodium 102-108 angiotensinogen Rattus norvegicus 60-65 25586061-2 2016 Furthermore, GLAST and GLT-1 are sodium-dependent Glu transporters (GluTs) that rely on sodium and potassium gradients generated principally by Na(+), K(+)-ATPase to generate ion gradients that drive Glu uptake. Sodium 33-39 solute carrier family 1 member 3 Homo sapiens 13-18 25586061-2 2016 Furthermore, GLAST and GLT-1 are sodium-dependent Glu transporters (GluTs) that rely on sodium and potassium gradients generated principally by Na(+), K(+)-ATPase to generate ion gradients that drive Glu uptake. Sodium 33-39 solute carrier family 1 member 2 Homo sapiens 23-28 26661654-2 2016 Luminal ANG II has been shown to stimulate sodium transport in the proximal tubule and distal nephron. Sodium 43-49 angiotensinogen Rattus norvegicus 8-14 26678829-8 2016 In loss-of-function experiments, microinjection of glucocorticoid receptor (gr) morpholino (MO) suppressed sodium content, ncc expression, and the density of ncc-expressing cells, but injection of mr MO had no such effects. Sodium 107-113 nuclear receptor subfamily 3, group C, member 1 (glucocorticoid receptor) Danio rerio 51-74 26747232-8 2016 Interestingly, the toxin also inhibited sodium current on all the mammalian channels tested, with the higher current inhibition on Nav1.3 (38.43 +- 8.04%, IC50 = 1.5 muM). Sodium 40-46 latexin Homo sapiens 166-169 26686590-4 2016 Similarly, natriuretic peptide (ANP) regulates blood pressure through a variety of mechanisms affecting the sodium concentration and the amount of extracellular fluid. Sodium 108-114 natriuretic peptide A Homo sapiens 32-35 26869812-3 2016 We hypothesized that chronic ingestion of resveratrol would reduce angiotensin II (Ang II)-induced increases in blood pressure by decreasing oxidative stress and by also decreasing sodium reabsorption through a nitric oxide-dependent mechanism. Sodium 181-187 angiotensinogen Rattus norvegicus 67-81 26540173-11 2016 CONCLUSIONS: In the largest series to date, age, GFR, number of metastatic sites, and baseline sodium level were found to be independent risk factors for TrTD in mRCC patients receiving VEGF-targeted therapy. Sodium 95-101 vascular endothelial growth factor A Homo sapiens 186-190 26608659-9 2016 These data demonstrate that increased levels of NE prevent dietary sodium-evoked suppression of the NCC, via an ANG II-independent mechanism, to stimulate the development of salt-sensitive hypertension. Sodium 67-73 angiotensinogen Rattus norvegicus 112-118 26751218-1 2016 Renal dopamine D1-like receptors (D1R and D5R) and the gastrin receptor (CCKBR) are involved in the maintenance of sodium homeostasis. Sodium 115-121 gastrin Mus musculus 55-62 26259627-3 2016 In this study, we report the results of a first-of-a-kind clinical trial studying late sodium (mexiletine and lidocaine) and calcium (diltiazem) current blocking drugs to counteract the effects of hERG potassium channel blocking drugs (dofetilide and moxifloxacin). Sodium 87-93 ETS transcription factor ERG Homo sapiens 197-201 26667412-4 2016 Signaling through dopamine D1 receptor and angiotensin II type I receptor (AT1R) reciprocally modulates renal sodium excretion and blood pressure. Sodium 110-116 dopamine receptor D1 Homo sapiens 18-38 26667412-4 2016 Signaling through dopamine D1 receptor and angiotensin II type I receptor (AT1R) reciprocally modulates renal sodium excretion and blood pressure. Sodium 110-116 angiotensinogen Homo sapiens 43-57 26871780-0 2016 Low Response of Renin-Angiotensin System to Sodium Intake Intervention in Chinese Hypertensive Patients. Sodium 44-50 renin Homo sapiens 16-21 26871780-2 2016 However, the influence of short-term sodium intake intervention in the response of renin-angiotensin system (RAS) on hypertensive patients is still unclear. Sodium 37-43 renin Homo sapiens 83-88 26820468-12 2016 These data suggest GV sPLA2 is involved in the maintenance of tubular cell function and integrity, promoting sodium retention through increased cortical (Na+ + K+)-ATPase expression and activity. Sodium 109-115 phospholipase A2, group V Mus musculus 22-27 26475588-4 2016 The classic RAS comprises the ACE-ANG II-AT1R axis that promotes vasoconstriction; water intake; sodium retention; and increased oxidative stress, fibrosis, cellular growth, and inflammation. Sodium 97-103 angiotensin I converting enzyme Homo sapiens 30-33 26760974-6 2016 During a 1-hour 3.86% mini-peritoneal equilibration test (mini-PET), AQP1fl/fl; Cdh5-Cre+ mice exhibited strongly decreased indices for AQP1-related transcellular water transport (43.0% in net ultrafiltration, 93.0% in sodium sieving and 57.9% in free water transport) compared to controls. Sodium 219-225 cadherin 5 Mus musculus 80-84 26869812-3 2016 We hypothesized that chronic ingestion of resveratrol would reduce angiotensin II (Ang II)-induced increases in blood pressure by decreasing oxidative stress and by also decreasing sodium reabsorption through a nitric oxide-dependent mechanism. Sodium 181-187 angiotensinogen Rattus norvegicus 83-89 26839871-1 2016 It is well known that high sodium intake is closely associated with the risk of cardiovascular disease, but the effect of low sodium intake on insulin resistance is not clear. Sodium 126-132 insulin Homo sapiens 143-150 26684962-2 2016 In this work, eight highly active sodium and potassium phenolates as highly isoselective catalysts for the ROP of rac-lactide are reported. Sodium 34-40 AKT serine/threonine kinase 1 Homo sapiens 114-117 26440927-4 2016 Sensitivity to high Na(+) concentrations of the erv14 mutant associated to the intracellular mislocalization of Nha1p-GFP, together with a lower Na(+) efflux, indicate the involvement of this mutual association to accomplish the survival of the yeast cell upon sodium stress. Sodium 261-267 Nha1p Saccharomyces cerevisiae S288C 112-117 27247938-7 2016 Insulin signaling via IRS2 continues to stimulate sodium reabsorption in the proximal tubule and causes sodium retention, edema, and hypertension. Sodium 50-56 insulin Homo sapiens 0-7 27247938-7 2016 Insulin signaling via IRS2 continues to stimulate sodium reabsorption in the proximal tubule and causes sodium retention, edema, and hypertension. Sodium 104-110 insulin Homo sapiens 0-7 26434759-1 2016 BACKGROUND: High serum sodium (sNa) concentrations may be associated with hypertension, which deteriorates kidney function. Sodium 23-29 snail family transcriptional repressor 1 Homo sapiens 31-34 26839871-2 2016 In this article, we summarize findings from previous studies focusing on the association between low sodium intake and insulin resistance. Sodium 101-107 insulin Homo sapiens 119-126 27349000-2 2016 A specific mutation G460T of the alpha-adducin gene (ADD1) is associated with high renal tubular sodium reabsorption. Sodium 97-103 adducin 1 Homo sapiens 33-46 27349000-2 2016 A specific mutation G460T of the alpha-adducin gene (ADD1) is associated with high renal tubular sodium reabsorption. Sodium 97-103 adducin 1 Homo sapiens 53-57 26714441-4 2016 In this study, we investigated whether sodium-dependent high-affinity gamma-aminobutyric acid (GABA) and glutamate uptake by isolated nerve terminals of the human neocortex could be modulated by ATP acting via slow-desensitizing P2X7 receptor (P2X7R). Sodium 39-45 purinergic receptor P2X 7 Homo sapiens 229-242 26632535-2 2016 Serum sodium (sNa) cut-off, however, is not defined in HFpEF. Sodium 6-12 snail family transcriptional repressor 1 Homo sapiens 14-17 26728597-0 2016 Regulation of SCN3B/scn3b by Interleukin 2 (IL-2): IL-2 modulates SCN3B/scn3b transcript expression and increases sodium current in myocardial cells. Sodium 114-120 interleukin 2 Homo sapiens 29-42 26728597-0 2016 Regulation of SCN3B/scn3b by Interleukin 2 (IL-2): IL-2 modulates SCN3B/scn3b transcript expression and increases sodium current in myocardial cells. Sodium 114-120 interleukin 2 Homo sapiens 44-48 26728597-0 2016 Regulation of SCN3B/scn3b by Interleukin 2 (IL-2): IL-2 modulates SCN3B/scn3b transcript expression and increases sodium current in myocardial cells. Sodium 114-120 interleukin 2 Homo sapiens 51-55 26728597-4 2016 Western blot assays and electrophysiological studies were performed to demonstrate the effect of IL-2 on the translation of SCN3B/scn3b and sodium currents. Sodium 140-146 interleukin 2 Homo sapiens 97-101 26728597-7 2016 The result of electrophysiological studies showed that sodium current density increased significantly in cells which treated by IL-2 and the effect of IL-2 on sodium currents was independent of SCN3B (1.4 folds, p = 0.023). Sodium 55-61 interleukin 2 Homo sapiens 128-132 26728597-7 2016 The result of electrophysiological studies showed that sodium current density increased significantly in cells which treated by IL-2 and the effect of IL-2 on sodium currents was independent of SCN3B (1.4 folds, p = 0.023). Sodium 55-61 interleukin 2 Homo sapiens 151-155 26728597-7 2016 The result of electrophysiological studies showed that sodium current density increased significantly in cells which treated by IL-2 and the effect of IL-2 on sodium currents was independent of SCN3B (1.4 folds, p = 0.023). Sodium 159-165 interleukin 2 Homo sapiens 128-132 26728597-7 2016 The result of electrophysiological studies showed that sodium current density increased significantly in cells which treated by IL-2 and the effect of IL-2 on sodium currents was independent of SCN3B (1.4 folds, p = 0.023). Sodium 159-165 interleukin 2 Homo sapiens 151-155 26728597-10 2016 CONCLUSIONS: The present study suggested that IL-2, may play role in the arrhythmia by regulating the expression of SCN3B and sodium current density. Sodium 126-132 interleukin 2 Homo sapiens 46-50 26714441-4 2016 In this study, we investigated whether sodium-dependent high-affinity gamma-aminobutyric acid (GABA) and glutamate uptake by isolated nerve terminals of the human neocortex could be modulated by ATP acting via slow-desensitizing P2X7 receptor (P2X7R). Sodium 39-45 purinergic receptor P2X 7 Homo sapiens 244-249 28097020-12 2016 We first demonstrate that renal UII system can play important roles in the regulation of blood pressure in Dahl SR rats which can be highly correlated to its effect on renal tubular sodium absorption. Sodium 182-188 urotensin 2 Rattus norvegicus 32-35 26403564-0 2016 Vasopressin 1a receptor partial agonism increases sodium excretion and reduces portal hypertension and ascites in cirrhotic rats. Sodium 50-56 arginine vasopressin Rattus norvegicus 0-11 26530729-7 2016 The high sodium level upregulated the expression of PCNA and the phosphorylation levels of JNK, ERK1/2 and p38 MAPK. Sodium 9-15 mitogen-activated protein kinase 8 Homo sapiens 91-94 26530729-7 2016 The high sodium level upregulated the expression of PCNA and the phosphorylation levels of JNK, ERK1/2 and p38 MAPK. Sodium 9-15 mitogen-activated protein kinase 3 Homo sapiens 96-102 26530729-11 2016 On the whole, our findings demonstrate that a relatively high sodium level per se directly promotes the proliferation of VSMCs through the JNK/ERK1/2/PCNA pathway. Sodium 62-68 mitogen-activated protein kinase 8 Homo sapiens 139-142 26530729-11 2016 On the whole, our findings demonstrate that a relatively high sodium level per se directly promotes the proliferation of VSMCs through the JNK/ERK1/2/PCNA pathway. Sodium 62-68 mitogen-activated protein kinase 3 Homo sapiens 143-149 25977313-1 2016 The renin-angiotensin-aldosterone (RAAS) and renal dopaminergic systems interact to maintain sodium balance. Sodium 93-99 renin Homo sapiens 4-9 27431273-0 2016 A high sodium intake reduces antiproteinuric response to renin-angiotensin-aldosterone system blockade in kidney transplant recipients. Sodium 7-13 renin Homo sapiens 57-62 26671983-2 2016 The purinergic ionotropic P2X7 receptor (P2X7R) is an atypical P2X subtype that gates calcium and sodium ions. Sodium 98-104 purinergic receptor P2X 7 Homo sapiens 26-39 26671983-2 2016 The purinergic ionotropic P2X7 receptor (P2X7R) is an atypical P2X subtype that gates calcium and sodium ions. Sodium 98-104 purinergic receptor P2X 7 Homo sapiens 41-46 26656402-2 2016 The objective of this article was to study the relationship between predialysis serum sodium (sNa) and mortality in an HD population. Sodium 86-92 snail family transcriptional repressor 1 Homo sapiens 94-97 26756638-6 2015 Proximal and distal tubular sodium transport and fluid and electrolyte homeostasis are also significantly influenced by renal CYP and LO levels. Sodium 28-34 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 126-129 26859849-2 2016 In this segment, while transport is increased by ADH via cAMP, sodium reabsorption results from Ang II-induced superoxide (O2(-)) production. Sodium 63-69 angiotensinogen Rattus norvegicus 96-102 26365358-4 2015 We show that IL-13 impairs ENaC-dependent sodium transport by activating the JAK1/2-STAT6 signalling pathway. Sodium 42-48 interleukin 13 Mus musculus 13-18 26365358-8 2015 In the present study, we investigated whether IL-13 also acts as a potent modulator of epithelial sodium transport via ENaC, and the signalling components involved. Sodium 98-104 interleukin 13 Mus musculus 46-51 26365358-11 2015 We show that IL-13, in both the cell model and in native intestinal tissue, impaired epithelial sodium absorption via ENaC (JNa ) as a result of decreased transcription levels of beta- and gamma-ENaC subunits and SGK1, a post-translational regulator of ENaC activity, due to impaired promoter activity. Sodium 96-102 interleukin 13 Mus musculus 13-18 26450935-2 2015 Both vitamin D and sodium intake interact with the renin-angiotensin-aldosterone system. Sodium 19-25 renin Homo sapiens 51-56 26420482-7 2015 We further observed that the mutation N111(3.35)A in the putative sodium-binding site affects binding of the endogenous peptide agonist angiotensin II but not the beta-arrestin-biased peptide TRV120027. Sodium 66-72 angiotensinogen Homo sapiens 136-150 26447209-7 2015 Following an acute short-term increase in intracellular sodium, NBCe2 expression was increased at the apical membrane in cultured slices of human kidney and polarized, immortalized RPTCs. Sodium 56-62 solute carrier family 4 member 5 Homo sapiens 64-69 26447209-10 2015 Therefore, future studies will examine the role of NBCe2 in mediating increased renal sodium transport in humans whose blood pressures are elevated by an increase in sodium intake. Sodium 86-92 solute carrier family 4 member 5 Homo sapiens 51-56 25319728-6 2015 DAI monosulfates were transported by the carriers NTCP and SOAT in a sodium-dependent manner, while OAT4-HEK293 cells revealed a partly sodium-dependent transport for these compounds. Sodium 69-75 solute carrier family 10 member 1 Homo sapiens 50-54 25319728-6 2015 DAI monosulfates were transported by the carriers NTCP and SOAT in a sodium-dependent manner, while OAT4-HEK293 cells revealed a partly sodium-dependent transport for these compounds. Sodium 136-142 solute carrier family 22 member 11 Homo sapiens 100-104 26523501-4 2015 In a mouse model of dextran-sulfate-sodium-induced typhlitis and colitis, development of intestinal pathology was associated with increases in neutrophils and CD11b(+) myeloid cells and a decrease in CD45R(+) B cells, similar to those observed in old Terc(-/-) mice. Sodium 36-42 telomerase RNA component Homo sapiens 251-255 25855778-0 2015 Vascular Type 1A Angiotensin II Receptors Control BP by Regulating Renal Blood Flow and Urinary Sodium Excretion. Sodium 96-102 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 17-31 25918036-9 2015 These findings indicate that FGF1 expression in the kidney is at least under partial genetic control and that renal expression of several FGF1 partner genes involved in the natriuretic peptide catabolism pathway, renin-angiotensin cascade, and sodium handling network may explain the association between FGF1 and BP. Sodium 244-250 fibroblast growth factor 1 Homo sapiens 138-142 25918036-9 2015 These findings indicate that FGF1 expression in the kidney is at least under partial genetic control and that renal expression of several FGF1 partner genes involved in the natriuretic peptide catabolism pathway, renin-angiotensin cascade, and sodium handling network may explain the association between FGF1 and BP. Sodium 244-250 fibroblast growth factor 1 Homo sapiens 138-142 26445872-0 2015 Corticotropin-releasing factor increases Purkinje neuron excitability by modulating sodium, potassium, and Ih currents. Sodium 84-90 corticotropin releasing hormone Rattus norvegicus 0-30 28124939-1 2016 During the past 50 years the molecular mechanisms of renal reabsorption of sodium and water have been described and molecules specifically interfering with these mechanisms have been developed (diuretics, vasopressin receptor antagonists). Sodium 75-81 arginine vasopressin Homo sapiens 205-216 28124939-3 2016 Vaptans (vasopressin antagonists, vasopressin V2-receptor inhibitors) reduce reabsorption of water in the distal nephron, they increase free water excretion and normalize serum concentrations of sodium in normovolemic and hypervolemic conditions associated with hyponatremia. Sodium 195-201 arginine vasopressin Homo sapiens 9-20 28124939-3 2016 Vaptans (vasopressin antagonists, vasopressin V2-receptor inhibitors) reduce reabsorption of water in the distal nephron, they increase free water excretion and normalize serum concentrations of sodium in normovolemic and hypervolemic conditions associated with hyponatremia. Sodium 195-201 arginine vasopressin receptor 2 Homo sapiens 34-57 26571018-9 2015 Even after adjustment for confounding factors including body fat and hypertension, the association between higher estimated 24-h urinary sodium excretion and NAFLD remained significant (Odds ratios (OR) 1.39, 95% confidence interval (CI) 1.26-1.55, in HSI; OR 1.75, CI 1.39-2.20, in FLI, both P < 0.001). Sodium 137-143 olfactory receptor family 14 subfamily K member 1 Homo sapiens 186-207 26299338-8 2015 RESULTS: Repeated amphetamine exposure (a) prevented the increase in sodium intake and Fos-IR cells in caudate-putamen and accumbens nucleus induced by ANG II i.c.v. Sodium 69-75 angiotensinogen Rattus norvegicus 152-158 26486596-11 2015 Urine sodium was associated with low and normal angiotensin II levels (P value 0.007). Sodium 6-12 angiotensinogen Homo sapiens 48-62 26472483-2 2015 Comparison of the recently solved high-resolution structures of the sodium-translocating bacterial rhodopsin and various Na(+)-binding GPCRs revealed striking similarity of their sodium-binding sites. Sodium 68-74 rhodopsin Homo sapiens 99-108 26116142-6 2015 After adjustment for gestational age, urinary angiotensinogen level correlated with urinary fractional excretion of sodium and urinary levels of cystatin-C and alpha1-microglobulin. Sodium 116-122 angiotensinogen Homo sapiens 46-61 26801661-4 2015 Meanwhile, at the molecular level, PCB congeners may activate phosphorylation of Akt, p-Akt, and forkhead box O3a (FoxO3a) protein resulting in inhibition of the natrium/iodide symporter. Sodium 162-169 pyruvate carboxylase Homo sapiens 35-38 26801661-4 2015 Meanwhile, at the molecular level, PCB congeners may activate phosphorylation of Akt, p-Akt, and forkhead box O3a (FoxO3a) protein resulting in inhibition of the natrium/iodide symporter. Sodium 162-169 AKT serine/threonine kinase 1 Homo sapiens 81-84 26801661-4 2015 Meanwhile, at the molecular level, PCB congeners may activate phosphorylation of Akt, p-Akt, and forkhead box O3a (FoxO3a) protein resulting in inhibition of the natrium/iodide symporter. Sodium 162-169 AKT serine/threonine kinase 1 Homo sapiens 88-91 26801661-4 2015 Meanwhile, at the molecular level, PCB congeners may activate phosphorylation of Akt, p-Akt, and forkhead box O3a (FoxO3a) protein resulting in inhibition of the natrium/iodide symporter. Sodium 162-169 forkhead box O3 Homo sapiens 97-113 26801661-4 2015 Meanwhile, at the molecular level, PCB congeners may activate phosphorylation of Akt, p-Akt, and forkhead box O3a (FoxO3a) protein resulting in inhibition of the natrium/iodide symporter. Sodium 162-169 forkhead box O3 Homo sapiens 115-121 26552350-3 2015 MATERIALS AND METHODS: We created conditional deletion of CREB in mice with low-sodium diet, specifically in renin cells of the kidney. Sodium 80-86 cAMP responsive element binding protein 1 Mus musculus 58-62 26552350-3 2015 MATERIALS AND METHODS: We created conditional deletion of CREB in mice with low-sodium diet, specifically in renin cells of the kidney. Sodium 80-86 renin Homo sapiens 109-114 26552350-6 2015 RESULTS: With low-sodium diet, renin was expressed along the whole wall of the afferent glomerular arterioles in wild-type mice, while there was no increase or even decrease in renin expression in CREB-specific deletion mice; RNA level of renin in cultured cells decreased by 50% with single knock-down of CREB, CBP, or p300, and decreased 70% with triple knock-down of CREB, CBP, and p300. Sodium 18-24 renin Homo sapiens 31-36 26363965-8 2015 A myotonia-like symptom without myotonic discharge may present as an early neurological sign of SBMA, which possibly reflects a sodium channel dysfunction in skeletal muscles. Sodium 128-134 androgen receptor Homo sapiens 96-100 25771952-0 2015 Extracellular sodium and potassium levels modulate cardiac conduction in mice heterozygous null for the Connexin43 gene. Sodium 14-20 gap junction protein, alpha 1 Mus musculus 104-114 26445434-5 2015 We find that under compression, tumor cells actively efflux sodium to decrease their intracellular tonicity, and that this is reversible by blockade of sodium channel NHE1. Sodium 60-66 solute carrier family 9 member A1 Homo sapiens 167-171 26209011-6 2015 With Western blot assays and electrophysiological studies, we demonstrated that miR-192-5p significantly reduced expression of SCN5A and Nav1.5 as well as peak sodium current density INa generated by Nav1.5. Sodium 160-166 microRNA 192 Homo sapiens 80-87 26277316-3 2015 Camel chymosin was also used as a coagulant to help reduce bitterness development (a common defect in low-sodium cheeses). Sodium 106-112 chymosin Camelus bactrianus 6-14 26471758-14 2015 Our data also suggest that the relationship between renal handling of sodium and urinary renin is sexually dimorphic. Sodium 70-76 renin Homo sapiens 89-94 26421717-0 2015 Calmodulin Interacts with the Sodium/Calcium Exchanger NCX1 to Regulate Activity. Sodium 30-36 calmodulin 1 Homo sapiens 0-10 26421717-0 2015 Calmodulin Interacts with the Sodium/Calcium Exchanger NCX1 to Regulate Activity. Sodium 30-36 solute carrier family 8 member A1 Homo sapiens 55-59 26311597-5 2015 Although currently available vasopressin (V2 receptors) antagonists have been shown to increase serum sodium concentrations and improve ascites control, their role in the treatment of hyponatremia in liver disease patients remains questionable because of adverse effect profiles, high cost, and poor data on long-term mortality benefits. Sodium 102-108 arginine vasopressin Homo sapiens 29-40 26378152-8 2015 Inward sodium current density was significantly decreased in MHC-Cre LKB1(fl/fl) neonatal atrial myocytes. Sodium 7-13 serine/threonine kinase 11 Mus musculus 69-73 26382850-0 2015 EGF-induced sodium influx regulates EGFR trafficking through HDAC6 and tubulin acetylation. Sodium 12-18 epidermal growth factor receptor Homo sapiens 36-40 26382850-0 2015 EGF-induced sodium influx regulates EGFR trafficking through HDAC6 and tubulin acetylation. Sodium 12-18 histone deacetylase 6 Homo sapiens 61-66 26382850-5 2015 RESULTS: EGF-induced sodium influx regulates EGFR trafficking through increased microtubule acetylation. Sodium 21-27 epidermal growth factor receptor Homo sapiens 45-49 26382850-6 2015 Increased sodium influx induced either by sodium ionophores or Na,K-ATPase blockade mimicked the EGF-induced effects on EGFR trafficking through histone deacetylase (HDAC) 6 inactivation and accumulation of acetylated tubulin. Sodium 10-16 epidermal growth factor receptor Homo sapiens 120-124 26382850-7 2015 In turn, blocking sodium influx reduced tubulin acetylation and EGF-induced EGFR turnover. Sodium 18-24 epidermal growth factor receptor Homo sapiens 76-80 26382850-8 2015 Knockdown of HDAC6 reversed the effect of sodium influx indicating that HDAC6 is necessary to modulate sodium-dependent tubulin acetylation. Sodium 42-48 histone deacetylase 6 Homo sapiens 13-18 26382850-8 2015 Knockdown of HDAC6 reversed the effect of sodium influx indicating that HDAC6 is necessary to modulate sodium-dependent tubulin acetylation. Sodium 42-48 histone deacetylase 6 Homo sapiens 72-77 26382850-8 2015 Knockdown of HDAC6 reversed the effect of sodium influx indicating that HDAC6 is necessary to modulate sodium-dependent tubulin acetylation. Sodium 103-109 histone deacetylase 6 Homo sapiens 13-18 26382850-8 2015 Knockdown of HDAC6 reversed the effect of sodium influx indicating that HDAC6 is necessary to modulate sodium-dependent tubulin acetylation. Sodium 103-109 histone deacetylase 6 Homo sapiens 72-77 26382850-9 2015 CONCLUSIONS: These studies provide a novel regulatory mechanism to attenuate EGFR signaling in which EGF modulates EGFR trafficking through intracellular sodium-mediated HDAC6 inactivation and tubulin acetylation. Sodium 154-160 epidermal growth factor receptor Homo sapiens 77-81 26382850-9 2015 CONCLUSIONS: These studies provide a novel regulatory mechanism to attenuate EGFR signaling in which EGF modulates EGFR trafficking through intracellular sodium-mediated HDAC6 inactivation and tubulin acetylation. Sodium 154-160 epidermal growth factor receptor Homo sapiens 115-119 26382850-9 2015 CONCLUSIONS: These studies provide a novel regulatory mechanism to attenuate EGFR signaling in which EGF modulates EGFR trafficking through intracellular sodium-mediated HDAC6 inactivation and tubulin acetylation. Sodium 154-160 histone deacetylase 6 Homo sapiens 170-175 26241673-4 2015 Corin is a TTSP and acts as the pro-atrial natriuretic peptide convertase that is essential for sodium homeostasis and normal blood pressure. Sodium 96-102 corin, serine peptidase Mus musculus 0-5 26074089-1 2015 Atrial natriuretic peptide (ANP) is a cardiac hormone that regulates salt-water balance and blood pressure by promoting renal sodium and water excretion and stimulating vasodilation. Sodium 126-132 natriuretic peptide A Homo sapiens 0-26 26074089-1 2015 Atrial natriuretic peptide (ANP) is a cardiac hormone that regulates salt-water balance and blood pressure by promoting renal sodium and water excretion and stimulating vasodilation. Sodium 126-132 natriuretic peptide A Homo sapiens 28-31 26240299-9 2015 The effect of sodium restriction was higher in the cohorts including patients on concomitant renin-angiotensin-aldosterone system-blocking therapy, in the studies with intervention lasting at least 2 weeks, and among participants with evidence of kidney damage. Sodium 14-20 renin Homo sapiens 93-98 26240299-12 2015 CONCLUSIONS: This meta-analysis indicates that sodium intake reduction markedly reduces albumin excretion, more so during concomitant renin-angiotensin-aldosterone system-blocking therapy and among patients with kidney damage. Sodium 47-53 renin Homo sapiens 134-139 26041443-0 2015 Vasopressin regulation of sodium transport in the distal nephron and collecting duct. Sodium 26-32 arginine vasopressin Homo sapiens 0-11 26125647-2 2015 SGLT1 mediates almost all sodium-dependent glucose uptake in the small intestine, while in the kidney SGLT2, and to a lesser extent SGLT1, account for more than 90% and nearly 3%, respectively, of glucose reabsorption from the glomerular ultrafiltrate. Sodium 26-32 solute carrier family 5 member 1 Homo sapiens 0-5 26169051-0 2015 Critical Role of Striatin in Blood Pressure and Vascular Responses to Dietary Sodium Intake. Sodium 78-84 striatin Homo sapiens 17-25 26169051-9 2015 Thus, striatin deficiency is associated with salt sensitivity of blood pressure, enhanced vasoconstriction, and decreased vascular relaxation, suggesting a critical role for striatin, through modulation of endothelial NO-cGMP, in regulation of vascular function and BP during changes in sodium intake. Sodium 287-293 striatin Homo sapiens 6-14 26169051-9 2015 Thus, striatin deficiency is associated with salt sensitivity of blood pressure, enhanced vasoconstriction, and decreased vascular relaxation, suggesting a critical role for striatin, through modulation of endothelial NO-cGMP, in regulation of vascular function and BP during changes in sodium intake. Sodium 287-293 striatin Homo sapiens 174-182 26426658-8 2015 Body fat percentage, body fat mass, and insulin level were positively related to sodium excretion (P <= 0.001), and HOMA-IR was significantly associated with sodium excretion (P < 0.05). Sodium 81-87 insulin Homo sapiens 40-47 26426658-10 2015 Sodium intake is significantly associated with all components of MS, body fat, and insulin resistance. Sodium 0-6 insulin Homo sapiens 83-90 26259032-15 2015 Our results indicate that PCSK6 is the long-sought corin activator and is important for sodium homeostasis and normal blood pressure. Sodium 88-94 corin, serine peptidase Homo sapiens 51-56 25735476-7 2015 Serum VEGF levels and the extent of nerve edema partly correlated with nerve conduction slowing, as well as persistent sodium currents and inward rectification. Sodium 119-125 vascular endothelial growth factor A Homo sapiens 6-10 26041443-4 2015 The antinatriuretic effects of AVP are mediated by the regulation of sodium transport throughout the distal nephron, from the thick ascending limb through to the collecting duct, which in turn partially facilitates osmotic movement of water. Sodium 69-75 arginine vasopressin Homo sapiens 31-34 25987608-2 2015 The increased intrarenal angiotensin II (Ang II) elicits renal vasoconstriction and enhanced tubular sodium reabsorption in proximal and distal nephron segments. Sodium 101-107 angiotensinogen Homo sapiens 25-39 25987608-2 2015 The increased intrarenal angiotensin II (Ang II) elicits renal vasoconstriction and enhanced tubular sodium reabsorption in proximal and distal nephron segments. Sodium 101-107 angiotensinogen Homo sapiens 41-47 25987608-4 2015 The increased AGT formation and secretion into the proximal tubular lumen leads to local formation of Ang II, which stimulates proximal transporters such as the sodium/hydrogen exchanger. Sodium 161-167 angiotensinogen Homo sapiens 14-17 25987608-4 2015 The increased AGT formation and secretion into the proximal tubular lumen leads to local formation of Ang II, which stimulates proximal transporters such as the sodium/hydrogen exchanger. Sodium 161-167 angiotensinogen Homo sapiens 102-108 25987608-6 2015 There is also increased Ang II concentration in distal nephron with stimulation of distal sodium transport. Sodium 90-96 angiotensinogen Homo sapiens 24-30 25827427-0 2015 Effect of angiotensin II on voltage-gated sodium currents in aortic baroreceptor neurons and arterial baroreflex sensitivity in heart failure rats. Sodium 42-48 angiotensinogen Rattus norvegicus 10-24 25293433-7 2015 RESULTS: Sixty percent of participants who had estimated sodium intake above recommendation (>100 mmol/day or 6 g salt/day) also had higher diastolic blood pressure, mean arterial pressure (MAP), urinary albumin-to-creatinine ratio, high-sensitive C-reactive protein and uric acid and used a greater number of anti-hypertensive drugs. Sodium 57-63 C-reactive protein Homo sapiens 251-269 25701775-1 2015 BACKGROUND: The human cardiac action potential in atrial and ventricular cells is initiated by a fast-activating, fast-inactivating sodium current generated by the SCN5A/Nav1.5 channel in association with its beta1/SCN1B subunit. Sodium 132-138 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 209-214 26142600-10 2015 T&A led to normalization of ADH and BNP, probably through a calcium- and sodium-dependent mechanism. Sodium 77-83 arginine vasopressin Homo sapiens 32-35 26005865-0 2015 A partially inactivating mutation in the sodium-dependent lysophosphatidylcholine transporter MFSD2A causes a non-lethal microcephaly syndrome. Sodium 41-47 major facilitator superfamily domain containing 2A Homo sapiens 94-100 26005865-1 2015 The major pathway by which the brain obtains essential omega-3 fatty acids from the circulation is through a sodium-dependent lysophosphatidylcholine (LPC) transporter (MFSD2A), expressed in the endothelium of the blood-brain barrier. Sodium 109-115 major facilitator superfamily domain containing 2A Homo sapiens 169-175 25669316-7 2015 Systolic and diastolic BP (SBP and DBP, respectively) significantly increased from the lower to the higher tertile of sodium from snacks and with increasing frequency of salty snacks consumption. Sodium 118-124 D-box binding PAR bZIP transcription factor Homo sapiens 35-38 25669316-9 2015 In the 400 individuals, the average total sodium intake was 3.1 g/day and was significantly higher in individuals belonging to the highest quartile of SBP and DBP. Sodium 42-48 D-box binding PAR bZIP transcription factor Homo sapiens 159-162 25933494-9 2015 CONCLUSIONS: In this study, NF1 patients consumed an unhealthy diet that was rich in fats and sodium and lacking in fiber, vitamins, and minerals. Sodium 94-100 neurofibromin 1 Homo sapiens 28-31 25866180-0 2015 Stimulatory effect of insulin on renal proximal tubule sodium transport is preserved in type 2 diabetes with nephropathy. Sodium 55-61 insulin Homo sapiens 22-29 26009231-4 2015 Insulin, for example, induces sodium retention and thiazolidinediones increase the risk of heart failure. Sodium 30-36 insulin Homo sapiens 0-7 25992604-2 2015 Microsomal epoxide hydrolase (mEH) is a bifunctional protein that plays a central role in the metabolism of numerous xenobiotics as well as mediating the sodium-dependent transport of bile acids into hepatocytes. Sodium 154-160 epoxide hydrolase 1, microsomal Mus musculus 30-33 25651559-7 2015 In the medullary collecting duct, ANP reduces sodium reabsorption by inhibiting the cyclic nucleotide-gated cation channels, the epithelial sodium channel, and the heteromeric channel transient receptor potential-vanilloid 4 and -polycystin 2 and diminishes vasopressin-induced water reabsorption. Sodium 46-52 natriuretic peptide A Homo sapiens 34-37 25651559-8 2015 Long-term ANP treatment may lead to NPR-A desensitization and ANP resistance, resulting in augmented sodium and water reabsorption. Sodium 101-107 natriuretic peptide A Homo sapiens 10-13 25651559-9 2015 In mice, corin deficiency impairs sodium excretion and causes salt-sensitive hypertension. Sodium 34-40 corin, serine peptidase Mus musculus 9-14 25740157-4 2015 We were surprised to find that simultaneous loss of Tmod1 and CP49, which disrupts cytoskeletal networks in lens fiber cells, results in increased gap junction coupling resistance, hydrostatic pressure, and sodium concentration. Sodium 207-213 beaded filament structural protein 2, phakinin Mus musculus 62-66 25908470-6 2015 The additional autocrine and paracrine activities of adipose tissue contribute to inappropriate activation of the renin-angiotensin-aldosterone system and the sympathetic nervous system that promote kidney microvascular remodeling, stiffness, and sodium (Na(+)) retention that in turn promote HTN and in the CKD patient, resistance. Sodium 247-253 renin Homo sapiens 114-119 25500109-15 2015 CONCLUSIONS: Important lifestyle- and diet-related factors associated with copeptin concentration are current smoking, alcohol use, protein and potassium intake, and particularly fluid and sodium intake. Sodium 189-195 arginine vasopressin Homo sapiens 75-83 25736793-1 2015 PURPOSE: As part of a large scale systematic screen to determine the effects of gene knockout mutations in mice, a retinal phenotype was found in mice lacking the Slc9a8 gene, encoding the sodium/hydrogen ion exchange protein NHE8. Sodium 189-195 solute carrier family 9 (sodium/hydrogen exchanger), member 8 Mus musculus 163-169 25736793-1 2015 PURPOSE: As part of a large scale systematic screen to determine the effects of gene knockout mutations in mice, a retinal phenotype was found in mice lacking the Slc9a8 gene, encoding the sodium/hydrogen ion exchange protein NHE8. Sodium 189-195 solute carrier family 9 (sodium/hydrogen exchanger), member 8 Mus musculus 226-230 26524901-8 2015 An increased sodium concentration inside the brain activates epithelial sodium channels and the renin-angiotensin-aldosterone system in the brain. Sodium 13-19 renin Homo sapiens 96-101 26121854-7 2015 NF-kappaB blockers PDTC and sodium ferulateresisted the effects of H2O2 on A549 cells, that decreased the mRNA and protein expression of NALP3 and the mRNA expression of NF-kappaB (P65), reduced the degeneration of IkappaBalpha and the secretion of IL-1beta (P<0. Sodium 28-34 nuclear factor kappa B subunit 1 Homo sapiens 0-9 26121854-7 2015 NF-kappaB blockers PDTC and sodium ferulateresisted the effects of H2O2 on A549 cells, that decreased the mRNA and protein expression of NALP3 and the mRNA expression of NF-kappaB (P65), reduced the degeneration of IkappaBalpha and the secretion of IL-1beta (P<0. Sodium 28-34 NLR family pyrin domain containing 3 Homo sapiens 137-142 26121854-7 2015 NF-kappaB blockers PDTC and sodium ferulateresisted the effects of H2O2 on A549 cells, that decreased the mRNA and protein expression of NALP3 and the mRNA expression of NF-kappaB (P65), reduced the degeneration of IkappaBalpha and the secretion of IL-1beta (P<0. Sodium 28-34 nuclear factor kappa B subunit 1 Homo sapiens 170-179 26121854-7 2015 NF-kappaB blockers PDTC and sodium ferulateresisted the effects of H2O2 on A549 cells, that decreased the mRNA and protein expression of NALP3 and the mRNA expression of NF-kappaB (P65), reduced the degeneration of IkappaBalpha and the secretion of IL-1beta (P<0. Sodium 28-34 NFKB inhibitor alpha Homo sapiens 215-227 26121854-7 2015 NF-kappaB blockers PDTC and sodium ferulateresisted the effects of H2O2 on A549 cells, that decreased the mRNA and protein expression of NALP3 and the mRNA expression of NF-kappaB (P65), reduced the degeneration of IkappaBalpha and the secretion of IL-1beta (P<0. Sodium 28-34 interleukin 1 beta Homo sapiens 249-257 26090330-3 2015 Increasing intake of salt leads to abnormal transport of sodium ions at the cellular level with activation of the sympathetic nervous system and renin-angiotensin-aldosterone system. Sodium 57-63 renin Homo sapiens 145-150 25866180-6 2015 These results revealed that insulin can stimulate PT sodium transport even in type 2 diabetes with overt nephropathy. Sodium 53-59 insulin Homo sapiens 28-35 25866180-7 2015 In addition to hypoglycemia, insulin-induced renal sodium retention might also play a role in increased cardiovascular risk associated with intensive glycemic control in type 2 diabetic patients with nephropathy. Sodium 51-57 insulin Homo sapiens 29-36 25587116-9 2015 Here, we show for the first time that PRL activates sodium and chloride transport in renal epithelial cells via ENaC and ClC4. Sodium 52-58 prolactin Homo sapiens 38-41 25681793-1 2015 Angiotensin II (AngII) is an octapeptide hormone that plays a central role in regulation of sodium balance, plasma volume, and blood pressure. Sodium 92-98 angiotensinogen Homo sapiens 0-14 25681793-1 2015 Angiotensin II (AngII) is an octapeptide hormone that plays a central role in regulation of sodium balance, plasma volume, and blood pressure. Sodium 92-98 angiotensinogen Homo sapiens 16-21 25734516-2 2015 Although both populations express similar endogenous conductances, we have discovered that AVPV/PeN Kiss1 neurons express a subthreshold, persistent sodium current (INaP) that dramatically alters their firing activity. Sodium 149-155 proprotein convertase subtilisin/kexin type 1 inhibitor Mus musculus 96-99 25861425-6 2015 A reduction of 28 mmol sodium excretion decreased SBP/DBP to 135.5 (+- 13.0)/82.5 (+- 12.8) (P < 0.001). Sodium 23-29 D-box binding PAR bZIP transcription factor Homo sapiens 54-57 25858030-2 2015 The sympathetic control of renal sodium tubular reabsorption is dependent on activation of the intrarenal renin-angiotensin system and activation of the angiotensin II type 1 (AT1 ) receptor by angiotensin II. Sodium 33-39 angiotensinogen Homo sapiens 153-167 25858030-6 2015 In this short review, the crosstalk between intrarenal angiotensin II and renal nerve activity and its effect on sodium reabsorption is addressed. Sodium 113-119 angiotensinogen Homo sapiens 55-69 25858030-11 2015 Pharmacological blockade of the AT1 receptor with losartan prior to RNS abolished both the functional and the molecular responses, suggesting that intrarenal Ang II acting via the AT1 receptor is a major factor for NHE3-mediated sodium and water reabsorption induced by RNS. Sodium 229-235 angiotensinogen Homo sapiens 158-164 25354240-2 2015 To test whether the stimulatory effect of insulin on renal proximal tubule sodium transport is preserved in insulin resistance, we compared the effects of insulin on abdominal adipocytes and proximal tubules in rats and humans. Sodium 75-81 insulin Homo sapiens 42-49 25134060-5 2015 Some of these genes encode proteins expressed in the kidney that are needed to excrete a sodium load, for example, dopamine receptors and their regulators, G protein-coupled receptor kinase 4 (GRK4). Sodium 89-95 G protein-coupled receptor kinase 4 Homo sapiens 193-197 25805925-3 2015 Portal hypertension and the associated systemic vasodilation lead to activation of the sodium-retaining neurohumoral mechanisms which include the renin-angiotensin-aldosterone system, sympathetic nervous system and antidiuretic hormone (ADH). Sodium 87-93 renin Homo sapiens 146-151 25760855-1 2015 The SLC9A1 gene, the Na+/H+ exchanger isoform 1 is the principal plasma membrane Na+/H+ exchanger of mammalian cells and functions by exchanging one intracellular proton for one extracellular sodium. Sodium 192-198 solute carrier family 9 member A1 Homo sapiens 4-10 25704353-4 2015 Calcineurin inhibitors, the most commonly used class of immunosuppressives, cause endothelial dysfunction, increase vascular tone, and sodium retention via the renin-angiotensin-aldosterone system resulting in systemic hypertension. Sodium 135-141 renin Homo sapiens 160-165 25530107-4 2015 Thus, we hypothesized that compared to high dialysate sodium, low dialysate sodium concentration would lower endothelin 1 levels, increase NO release, and reduce BP. Sodium 76-82 endothelin 1 Homo sapiens 109-121 25530107-9 2015 MEASUREMENTS: Mixed linear regression was used to compare the effect of dialysate sodium (low vs high) and randomization arm (low-then-high vs high-then-low) on intradialytic changes in endothelin 1, NO2(-), and BP values. Sodium 82-88 endothelin 1 Homo sapiens 186-198 25601932-8 2015 Our results suggest that during Ang-II hypertension both IFN-gamma and IL-17A production interfere with the pressure natriuretic decrease in proximal tubule sodium transport and that IFN-gamma production is necessary to activate distal sodium reabsorption. Sodium 157-163 interferon gamma Mus musculus 57-66 25601932-8 2015 Our results suggest that during Ang-II hypertension both IFN-gamma and IL-17A production interfere with the pressure natriuretic decrease in proximal tubule sodium transport and that IFN-gamma production is necessary to activate distal sodium reabsorption. Sodium 236-242 interferon gamma Mus musculus 183-192 25858030-0 2015 Crosstalk between the renal sympathetic nerve and intrarenal angiotensin II modulates proximal tubular sodium reabsorption. Sodium 103-109 angiotensinogen Homo sapiens 61-75 25767287-5 2015 Cytokines released from these cells, including interleukin-17, interferon-gamma, tumor necrosis factoralpha, and interleukin-6 promote both renal and vascular dysfunction and damage, leading to enhanced sodium retention and increased systemic vascular resistance. Sodium 203-209 interferon gamma Homo sapiens 63-126 25767289-2 2015 Increasing sodium intake is associated with increasing blood pressure, whereas low sodium intake results in increased renin and aldosterone levels. Sodium 83-89 renin Homo sapiens 118-123 25768006-9 2015 The obesity risk increased 7.06, 16.8, and 46.09-fold more in boys with GRK4 A486V, ACE, and SLC12A3 mutants as sodium intake increased. Sodium 112-118 angiotensin I converting enzyme Homo sapiens 84-87 25477470-0 2015 STE20/SPS1-related proline/alanine-rich kinase (SPAK) is critical for sodium reabsorption in isolated, perfused thick ascending limb. Sodium 70-76 serine/threonine kinase 24 Mus musculus 0-5 25477470-0 2015 STE20/SPS1-related proline/alanine-rich kinase (SPAK) is critical for sodium reabsorption in isolated, perfused thick ascending limb. Sodium 70-76 selenophosphate synthetase 1 Mus musculus 6-10 24978482-12 2015 SNP-diet interactions were not significant, although HRs suggested interaction between SNPs in ACE and sodium intake. Sodium 103-109 angiotensin I converting enzyme Homo sapiens 95-98 24496589-6 2015 Interestingly, studies using NaPi-IIb knockout mice with adenine-induced CKD show only partial attenuation of hyperphosphatemia, suggesting that an additional sodium-independent pathway is involved in phosphate absorption. Sodium 159-165 solute carrier family 34 (sodium phosphate), member 2 Mus musculus 29-37 25646622-9 2015 Conversely, the sodium/BA-cotransporter function of NTCP seemed not to be required for HDV infection since infection was similar in the presence or absence of a sodium gradient across the plasma membrane. Sodium 16-22 solute carrier family 10 member 1 Homo sapiens 52-56 24958786-1 2015 BACKGROUND: In cross-sectional studies, the aldosterone-to-renin ratio (ARR) has been reported to be associated with hypertension under conditions of higher sodium intake. Sodium 157-163 renin Homo sapiens 59-64 25371970-5 2015 We identified that sodium flux in keratinocytes is mediated by epithelial sodium channels (ENaCs) and causes increased secretion of proinflammatory cytokines, which activate fibroblast via the cyclooxygenase 2 (COX-2)/prostaglandin E2 (PGE2) pathway. Sodium 19-25 prostaglandin-endoperoxide synthase 2 Homo sapiens 193-209 25371970-5 2015 We identified that sodium flux in keratinocytes is mediated by epithelial sodium channels (ENaCs) and causes increased secretion of proinflammatory cytokines, which activate fibroblast via the cyclooxygenase 2 (COX-2)/prostaglandin E2 (PGE2) pathway. Sodium 19-25 prostaglandin-endoperoxide synthase 2 Homo sapiens 211-216 25371970-9 2015 Other experiments demonstrate that the activation of COX-2 in response to increased sodium flux is mediated through the PIK3/Akt pathway. Sodium 84-90 prostaglandin-endoperoxide synthase 2 Homo sapiens 53-58 25371970-9 2015 Other experiments demonstrate that the activation of COX-2 in response to increased sodium flux is mediated through the PIK3/Akt pathway. Sodium 84-90 AKT serine/threonine kinase 1 Homo sapiens 125-128 25456501-2 2015 Mutations of the ANK2 gene in the rare condition Ankyrin-B syndrome result in loss of function of the ankyrin-B protein which in turn leads to abnormal regulation of intracellular sodium and calcium and a predisposition to cardiac arrhythmia including torsades de pointes. Sodium 180-186 ankyrin 2 Homo sapiens 17-21 25012180-9 2015 Notably, membrane staining of beta1 was reduced throughout collecting ducts of AE1-null mouse kidney, where increased fractional excretion of sodium has been reported. Sodium 142-148 solute carrier family 4 (anion exchanger), member 1 Mus musculus 79-82 25456501-2 2015 Mutations of the ANK2 gene in the rare condition Ankyrin-B syndrome result in loss of function of the ankyrin-B protein which in turn leads to abnormal regulation of intracellular sodium and calcium and a predisposition to cardiac arrhythmia including torsades de pointes. Sodium 180-186 ankyrin 2 Homo sapiens 49-58 25456501-2 2015 Mutations of the ANK2 gene in the rare condition Ankyrin-B syndrome result in loss of function of the ankyrin-B protein which in turn leads to abnormal regulation of intracellular sodium and calcium and a predisposition to cardiac arrhythmia including torsades de pointes. Sodium 180-186 ankyrin 2 Homo sapiens 102-111 25615643-1 2015 PURPOSE: The aim of this study was to design a method of radionuclide for imaging and therapy of nasopharyngeal carcinoma (NPC) using the transferred human sodium/iodide symporter (hNIS) gene. Sodium 156-163 solute carrier family 5 member 5 Homo sapiens 181-185 25100048-8 2015 After HD, patients with low VEGF-C levels had significantly higher skin sodium content compared with patients with high VEGF-C levels (low VEGF-C: 2.3 ng/ml and skin sodium: 24.3 mmol/l; high VEGF-C: 4.1 ng/ml and skin sodium: 18.2 mmol/l). Sodium 72-78 vascular endothelial growth factor C Homo sapiens 28-34 25100048-10 2015 Age and VEGF-C-related local tissue-specific clearance mechanisms may determine the efficacy of tissue sodium removal with HD. Sodium 103-109 vascular endothelial growth factor C Homo sapiens 8-14 25603341-5 2015 Pre-treatment with phosphatase inhibitor sodium or thovanadate halted dephosphorylation of AKT and GSK3beta, and blocked ophiobolin O-induced G1 phase arrest. Sodium 41-47 AKT serine/threonine kinase 1 Homo sapiens 91-94 25355965-0 2015 The role of slow and persistent TTX-resistant sodium currents in acute tumor necrosis factor-alpha-mediated increase in nociceptors excitability. Sodium 46-52 tumor necrosis factor Rattus norvegicus 71-98 25552692-6 2015 Hence, this review summarizes what is known about the effect of PI3K and its downstream effectors, including Akt, on sodium, potassium, and calcium currents in cardiac myocytes. Sodium 117-123 AKT serine/threonine kinase 1 Homo sapiens 109-112 25252899-2 2015 This study was designed to assess the usefulness of copeptin measurement in children with community-acquired pneumonia (CAP) and copeptin"s relation with disease severity and sodium equilibrium. Sodium 175-181 arginine vasopressin Homo sapiens 52-60 25252899-2 2015 This study was designed to assess the usefulness of copeptin measurement in children with community-acquired pneumonia (CAP) and copeptin"s relation with disease severity and sodium equilibrium. Sodium 175-181 arginine vasopressin Homo sapiens 129-137 25252899-8 2015 Yet there was only a weak reverse correlation between the sodium and the copeptin concentrations (Spearmann"s rank coefficient = -0.19). Sodium 58-64 arginine vasopressin Homo sapiens 73-81 25377091-1 2015 Sodium/hydrogen exchanger (NHE) 8 is expressed at the apical membrane of the epithelial cells and plays important roles in neutral sodium absorption in the gastrointestinal tract and the kidney. Sodium 131-137 solute carrier family 9 (sodium/hydrogen exchanger), member 8 Mus musculus 0-33 26491696-2 2015 In proximal tubules, Akt mediates insulin signaling via insulin receptor substrate 2 (IRS2) and stimulates sodium-bicarbonate cotransporter (NBCe1), resulting in increased sodium reabsorption. Sodium 107-113 AKT serine/threonine kinase 1 Homo sapiens 21-24 26491696-3 2015 In insulin resistance, the IRS2 in kidney cortex is exceptionally preserved and may mediate the stimulatory effect of insulin on NBCe1 to cause hypertension in diabetes via sodium retention. Sodium 173-179 insulin Homo sapiens 118-125 25649809-4 2015 Various mutant combinations produced different influences on calcium-dependent membrane-binding behavior and on the sodium-dependent dissociation of membrane-bound Anx4. Sodium 116-122 annexin A4 Homo sapiens 164-168 26112332-10 2015 Expression of antisense miR-22 significantly attenuated the levels of liver fibrosis, portal hypertension and sodium retention caused by CCl4, possibly through upregulation of BMP7. Sodium 110-116 microRNA 22 Homo sapiens 24-30 26028241-5 2015 It is thought that the renin-angiotensin system may play an important role in determining how much sodium the body expels or retains after salt intake is suddenly reduced or augmented. Sodium 99-105 renin Homo sapiens 23-28 24510463-4 2015 On the other hand, lowering sodium intake too much, as recommended to avoid the development of hypertension, particularly in sodium-sensitive people, might lead to insulin resistance and thereby might risk increasing fasting as well as postprandial blood glucose concentrations. Sodium 28-34 insulin Homo sapiens 164-171 24510463-4 2015 On the other hand, lowering sodium intake too much, as recommended to avoid the development of hypertension, particularly in sodium-sensitive people, might lead to insulin resistance and thereby might risk increasing fasting as well as postprandial blood glucose concentrations. Sodium 125-131 insulin Homo sapiens 164-171 26045274-6 2015 NTCP is responsible for most sodium-dependent bile salt uptake in liver. Sodium 29-35 solute carrier family 10 member 1 Homo sapiens 0-4 26552299-0 2015 Thrombin modulates persistent sodium current in CA1 pyramidal neurons of young and adult rat hippocampus. Sodium 30-36 coagulation factor II Rattus norvegicus 0-8 25506941-2 2014 Four activating CaSR mutations cause additional renal wasting of sodium, chloride and other salts, a condition called Bartter syndrome (BS) type 5. Sodium 65-71 calcium sensing receptor Homo sapiens 16-20 25347235-3 2015 The primary exposure was pre-operative hyponatremia, defined as a serum sodium (SNa) <133 mmol/L. Sodium 72-78 snail family transcriptional repressor 1 Homo sapiens 80-83 25347235-6 2015 RESULTS: Of 366 LTx, 69 (18.9%) had pre-operative hyponatremia, 6 (8.7%) of whom had a rapid rise in serum sodium (SNa). Sodium 107-113 snail family transcriptional repressor 1 Homo sapiens 115-118 25895625-8 2015 Although the precise mechanism responsible for the subsequently renal morphological and functional response in Sk offspring is incompletely known, the current data suggest that changes in renal function are conducive to excess sodium tubule reabsorption that is associated with enhanced TGF-beta1, fibronectin and collagen deposition, intrinsically related to fibrotic process, might potentiate the programming of adult hypertension. Sodium 227-233 transforming growth factor, beta 1 Rattus norvegicus 287-296 26024055-5 2015 Based largely on rodent studies, low-sodium diets have been associated with changes in glycemic control, energy metabolism, cardiovascular disease risk, cholesterol concentrations, inflammation, and functioning of the renin-angiotensin-aldosterone system. Sodium 37-43 renin Homo sapiens 218-223 25503076-2 2014 Nav1.8, a tetrodotoxin-resistant (TTX-R) sodium channel, contributes most of the sodium current underlying the action potential upstroke and accounts for most of the current in later spikes in a train. Sodium 41-47 sodium voltage-gated channel alpha subunit 10 Rattus norvegicus 0-6 25378098-2 2014 Reaction is initiated by an electron impacting a helium nanodroplet containing sodium atoms and SF6 molecules, leading to preferential production of energetically favorable structures based on the unit cell of crystalline NaF. Sodium 79-85 C-X-C motif chemokine ligand 8 Homo sapiens 222-225 25162926-1 2014 The NHE1 isoform of the mammalian Na(+)/H(+) exchanger is a ubiquitous plasma membrane protein that regulates intracellular pH in cells by removing one intracellular proton in exchange for one extracellular sodium. Sodium 207-213 solute carrier family 9 member A1 Homo sapiens 4-8 25350536-1 2014 Na(+)/H(+) exchanger isoform 1 (NHE1) is the principal plasma membrane Na(+)/H(+) exchanger of mammalian cells and functions by exchanging one intracellular proton for one extracellular sodium ion. Sodium 186-192 solute carrier family 9 member A1 Homo sapiens 0-30 25350536-1 2014 Na(+)/H(+) exchanger isoform 1 (NHE1) is the principal plasma membrane Na(+)/H(+) exchanger of mammalian cells and functions by exchanging one intracellular proton for one extracellular sodium ion. Sodium 186-192 solute carrier family 9 member A1 Homo sapiens 32-36 25398584-4 2014 A retrospective chart review was performed on the first 100 inpatients with serum sodium (sNa) <=128 mmol/L during hospitalisation. Sodium 82-88 snail family transcriptional repressor 1 Homo sapiens 90-93 25411946-5 2014 A significant trend towards lower levels of plasmatic sodium, paralleling the increase of C--reactive protein, was showed. Sodium 54-60 C-reactive protein Homo sapiens 90-109 25411946-6 2014 CONCLUSION: A significant relationship between plasmatic sodium levels and C--reactive protein was found, apart from the underlying disease. Sodium 57-63 C-reactive protein Homo sapiens 75-94 25398734-3 2014 The role that modified sodium or potassium intake plays in influencing the renin-angiotensin system, arterial stiffness, and endothelial dysfunction remains of interest in current research. Sodium 23-29 renin Homo sapiens 75-80 25398084-9 2014 At 12-months, participants in the intervention group who possessed a risk version of the ACE gene, and were advised to limit their sodium intake, significantly reduced their sodium intake (mg/day) compared to the control group (-287.3 +- 114.1 vs. 129.8 +- 118.2, p = 0.008). Sodium 131-137 angiotensin I converting enzyme Homo sapiens 89-92 25398084-9 2014 At 12-months, participants in the intervention group who possessed a risk version of the ACE gene, and were advised to limit their sodium intake, significantly reduced their sodium intake (mg/day) compared to the control group (-287.3 +- 114.1 vs. 129.8 +- 118.2, p = 0.008). Sodium 174-180 angiotensin I converting enzyme Homo sapiens 89-92 25374825-4 2014 AngII generally stimulates sodium reabsorption by triggering sodium and fluid retention in almost all segments of renal tubules. Sodium 27-33 angiotensinogen Homo sapiens 0-5 25374825-4 2014 AngII generally stimulates sodium reabsorption by triggering sodium and fluid retention in almost all segments of renal tubules. Sodium 61-67 angiotensinogen Homo sapiens 0-5 25374805-5 2014 Increased levels of antidiuretic hormone can result in hyponatremia, defined as a plasma sodium level < 136 mmol/L, which causes cells to draw in excess water and swell. Sodium 89-95 arginine vasopressin Homo sapiens 20-40 25368024-2 2015 We tested the hypothesis that striatin would in turn affect mineralocorticoid receptor function and consequently sodium, water, and blood pressure homeostasis in an animal model. Sodium 113-119 striatin, calmodulin binding protein Mus musculus 30-38 25368024-4 2015 Compared with wild type, striatin heterozygote exhibited a significant increase in blood pressure when sodium intake was increased from restricted (0.03%) to liberal (1.6%) sodium. Sodium 103-109 striatin, calmodulin binding protein Mus musculus 25-33 25368024-4 2015 Compared with wild type, striatin heterozygote exhibited a significant increase in blood pressure when sodium intake was increased from restricted (0.03%) to liberal (1.6%) sodium. Sodium 173-179 striatin, calmodulin binding protein Mus musculus 25-33 25368024-5 2015 Furthermore, renal expression of mineralocorticoid receptor and its genomic downstream targets serum/glucocorticoid-regulated kinase 1, and epithelial sodium channel was increased in striatin heterozygote versus wild-type mice on liberal sodium intake while the pAkt/Akt ratio, readout of mineralocorticoid receptor"s rapid, nongenomic pathway, was reduced. Sodium 151-157 striatin, calmodulin binding protein Mus musculus 183-191 25495276-1 2015 The objective of this study was to test the association of the rs1049305 (G > C) variant within the 3"-untranslated region of the aquaporin 1 gene, AQP1, with changes in body weight, post-race serum sodium concentration and performance in Ironman triathletes. Sodium 202-208 aquaporin 1 (Colton blood group) Homo sapiens 133-144 25495276-1 2015 The objective of this study was to test the association of the rs1049305 (G > C) variant within the 3"-untranslated region of the aquaporin 1 gene, AQP1, with changes in body weight, post-race serum sodium concentration and performance in Ironman triathletes. Sodium 202-208 aquaporin 1 (Colton blood group) Homo sapiens 151-155 26304834-1 2015 The sodium-hydrogen exchanger isoform-1 [NHE1] is a ubiquitously expressed plasma membrane protein that plays a central role in intracellular pH and cell volume homeostasis by catalyzing an electroneutral exchange of extracellular sodium and intracellular hydrogen. Sodium 4-10 solute carrier family 9 member A1 Homo sapiens 41-45 25657495-6 2015 RESULTS: Apart from sodium (2.40%, 3.83%), chloride (2.52% and 2.51%) for both L1 and L2 respectively, and glucose (4.82%), cholesterol (4.86%) for L2, CVs for all other parameters (both L1 and L2) were >5%. Sodium 20-26 L1 cell adhesion molecule Homo sapiens 79-88 25279988-2 2015 Epithelial Na(+) channel (ENaC) is responsible for sodium reabsorption in the aldosterone-sensitive distal nephron. Sodium 51-57 sodium channel epithelial 1 subunit gamma Rattus norvegicus 0-24 25279988-2 2015 Epithelial Na(+) channel (ENaC) is responsible for sodium reabsorption in the aldosterone-sensitive distal nephron. Sodium 51-57 sodium channel epithelial 1 subunit gamma Rattus norvegicus 26-30 25817868-0 2015 Control of ENaC-mediated sodium reabsorption in the distal nephron by Bradykinin. Sodium 25-31 kininogen 1 Homo sapiens 70-80 25817868-2 2015 Apart from being a vasodilator, BK also increases urinary sodium excretion to reduce systemic blood pressure. Sodium 58-64 kininogen 1 Homo sapiens 32-34 25817868-3 2015 It is becoming appreciated that BK modulates function of the epithelial Na(+) channel in the distal part of the renal nephron to affect tubular sodium reabsorption. Sodium 144-150 kininogen 1 Homo sapiens 32-34 25468964-0 2014 Sodium recognition by the Na+/Ca2+ exchanger in the outward-facing conformation. Sodium 0-6 solute carrier family 8 member A1 Homo sapiens 26-44 25336645-1 2014 Cardiac sodium (Na(+))-calcium (Ca(2+)) exchanger 1 (NCX1) is central to the maintenance of normal Ca(2+) homeostasis and contraction. Sodium 8-14 solute carrier family 8 member A1 Homo sapiens 53-57 25339171-1 2014 The sodium- and chloride-coupled GABA transporter GAT-1 is a member of the neurotransmitter:sodium:symporters, which are crucial for synaptic transmission. Sodium 4-10 solute carrier family 6 member 1 Homo sapiens 50-55 25554067-5 2014 Increased distal sodium delivery may also act to suppress the intrarenal renin-angiotensin-aldosterone system, although systemic activity may be modestly increased due to osmotic diuresis. Sodium 17-23 renin Homo sapiens 73-78 25240195-5 2014 Our results suggest that PKC can increase sodium resurgent currents through phosphorylation of a conserved Serine residue located in the domain III-IV linker of sodium channels. Sodium 42-48 proline rich transmembrane protein 2 Homo sapiens 25-28 25164821-1 2014 The Ste20-related kinase SPAK regulates sodium, potassium, and chloride transport in a variety of tissues. Sodium 40-46 serine/threonine kinase 39 Homo sapiens 25-29 25143384-1 2014 GAT-1 is a sodium- and chloride-coupled GABA transporter and a member of the neurotransmitter:sodium:symporters, which are crucial for synaptic transmission. Sodium 11-17 solute carrier family 6 member 1 Homo sapiens 0-5 25106430-2 2014 Claudin 4 has been reported to function as a paracellular sodium barrier and is one of three major claudins expressed in lung alveolar epithelial cells (AEC). Sodium 58-64 claudin 4 Mus musculus 0-9 25354428-3 2014 NHE1 is the major isoform found in the myocardium where it plays an important role in the regulation of intracellular pH by exchanging one intracellular proton for one extracellular sodium. Sodium 182-188 solute carrier family 9 member A1 Homo sapiens 0-4 25164814-0 2014 Role of Rho GDP dissociation inhibitor alpha in control of epithelial sodium channel (ENaC)-mediated sodium reabsorption. Sodium 70-76 sodium channel epithelial 1 subunit gamma Rattus norvegicus 86-90 25164814-1 2014 The epithelial sodium channel (ENaC) is expressed in the aldosterone-sensitive distal nephron where it performs sodium reabsorption from the lumen. Sodium 15-21 sodium channel epithelial 1 subunit gamma Rattus norvegicus 31-35 25164814-6 2014 Knockdown of RhoGDIalpha in cultured cortical collecting duct principal cells increased ENaC subunits expression and ENaC-mediated sodium reabsorption. Sodium 131-137 sodium channel epithelial 1 subunit gamma Rattus norvegicus 117-121 25029426-0 2014 Dietary sodium restriction decreases insulin secretion without affecting insulin sensitivity in humans. Sodium 8-14 insulin Homo sapiens 37-44 25029426-8 2014 MAIN OUTCOME MEASURES: Change in acute insulin secretory response assessed during hyperglycemic clamps while in sodium balance during a low-sodium vs high-sodium diet during aldosterone vs vehicle. Sodium 140-146 insulin Homo sapiens 39-46 25029426-8 2014 MAIN OUTCOME MEASURES: Change in acute insulin secretory response assessed during hyperglycemic clamps while in sodium balance during a low-sodium vs high-sodium diet during aldosterone vs vehicle. Sodium 140-146 insulin Homo sapiens 39-46 25029426-9 2014 RESULTS: A low-sodium diet increased endogenous aldosterone and plasma renin activity, and acute glucose-stimulated insulin (-16.0 +- 5.6%; P = .007) and C-peptide responses (-21.8 +- 8.4%; P = .014) were decreased, whereas the insulin sensitivity index was unchanged (-1.0 +- 10.7%; P = .98). Sodium 15-21 renin Homo sapiens 71-76 25029426-9 2014 RESULTS: A low-sodium diet increased endogenous aldosterone and plasma renin activity, and acute glucose-stimulated insulin (-16.0 +- 5.6%; P = .007) and C-peptide responses (-21.8 +- 8.4%; P = .014) were decreased, whereas the insulin sensitivity index was unchanged (-1.0 +- 10.7%; P = .98). Sodium 15-21 insulin Homo sapiens 154-163 25029426-9 2014 RESULTS: A low-sodium diet increased endogenous aldosterone and plasma renin activity, and acute glucose-stimulated insulin (-16.0 +- 5.6%; P = .007) and C-peptide responses (-21.8 +- 8.4%; P = .014) were decreased, whereas the insulin sensitivity index was unchanged (-1.0 +- 10.7%; P = .98). Sodium 15-21 insulin Homo sapiens 228-235 25029426-12 2014 CONCLUSIONS: Low dietary sodium intake reduces insulin secretion in humans, independent of insulin sensitivity. Sodium 25-31 insulin Homo sapiens 47-54 25274824-10 2014 Additionally, our data further suggest the presence of a sodium leak in EAAT2. Sodium 57-63 solute carrier family 1 member 2 Rattus norvegicus 72-77 25371524-0 2014 Dynamics of sodium retention in preascitic cirrhotic rats assessed through parathyroid hormone injection. Sodium 12-18 parathyroid hormone Rattus norvegicus 75-94 25371524-6 2014 S.c. administration of PTH normalized urine and sodium excretion in cirrhotic rats and also increased renal plasma flow, PGE2 urinary excretion, and free-water clearance. Sodium 48-54 parathyroid hormone Rattus norvegicus 23-26 25371524-9 2014 PTH returns these biomolecular changes, along with sodium and urine excretions, to normality, suggesting that exaggerated sodium reabsorption occurs primarily in the Henle"s loop in preascitic cirrhosis. Sodium 122-128 parathyroid hormone Rattus norvegicus 0-3 24990699-4 2014 Such as, apelin/APJ system may be concerned in hyperfunction of the sympathetic nervous system, renin-angiotensin-aldosterone system, endothelial injury, excessive endothelin, sodium retention, vascular remodeling, insulin resistance elicit hypertension, as well as in hypertension-induced organ damaged. Sodium 176-182 apelin Homo sapiens 9-15 24442122-10 2014 Furthermore, sodium excretion was lowered in cGKII-KO mice during volume load. Sodium 13-19 protein kinase, cGMP-dependent, type II Mus musculus 45-50 25109219-7 2014 RESULTS: The patients with higher quartile (higher serum sodium) had a trend of lower age, peritoneal dialysis (PD) duration, co-morbidity index, D/P Cr and white blood cell counts and higher renal Kt/Vurea (Kt/V) and serum albumin level. Sodium 57-63 albumin Homo sapiens 224-231 26989732-8 2014 Sodium selenite treatment of the diabetic rats resulted in significant increases in GPX activity in the kidneys and livers, and CAT activity in the sera and livers. Sodium 0-6 catalase Rattus norvegicus 128-131 25109219-8 2014 Stepwise multiple linear regression analysis showed that serum sodium level was positively associated with albumin, residual renal Kt/V and negatively associated with age and PD duration in CPD patients. Sodium 63-69 albumin Homo sapiens 107-114 25269146-0 2014 FGF14 modulates resurgent sodium current in mouse cerebellar Purkinje neurons. Sodium 26-32 fibroblast growth factor 14 Mus musculus 0-5 24886881-0 2014 Artemisinin protects against dextran sulfate-sodium-induced inflammatory bowel disease, which is associated with activation of the pregnane X receptor. Sodium 45-51 nuclear receptor subfamily 1 group I member 2 Homo sapiens 131-150 25317016-6 2014 During the 16-week follow-up period, an increase in urinary sodium excretion predicted an increase in urinary angiotensinogen excretion. Sodium 60-66 angiotensinogen Homo sapiens 110-125 25317016-0 2014 Urinary sodium excretion has positive correlation with activation of urinary renin angiotensin system and reactive oxygen species in hypertensive chronic kidney disease. Sodium 8-14 renin Homo sapiens 77-82 23223089-1 2014 INTRODUCTION: A low-sodium diet (LSD) was shown to increase both angiotensin II (AngII) and aldosterone levels, and to accelerate atherosclerosis in apolipoprotein E-deficient (E0) mice. Sodium 20-26 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 65-79 23223089-1 2014 INTRODUCTION: A low-sodium diet (LSD) was shown to increase both angiotensin II (AngII) and aldosterone levels, and to accelerate atherosclerosis in apolipoprotein E-deficient (E0) mice. Sodium 20-26 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 81-86 24951051-5 2014 ZnT-1 facilitates zinc efflux in a sodium-independent, pH-driven and calcium-sensitive manner. Sodium 35-41 solute carrier family 30 member 1 Homo sapiens 0-5 25009258-1 2014 Angiotensin II (AngII) and aldosterone cooperate centrally to produce a robust sodium appetite. Sodium 79-85 angiotensinogen Rattus norvegicus 0-14 24934256-4 2014 The mechanism leading to impaired degranulation involves altered ion homeostasis caused by defective CFTR function with increased cytosolic levels of chloride and sodium, yet decreased magnesium measured in CF neutrophils. Sodium 163-169 CF transmembrane conductance regulator Homo sapiens 101-105 24840884-1 2014 PURPOSE OF REVIEW: The purpose of this review is to describe the renin-angiotensin-aldosterone system and its regulatory control of sodium, potassium, chloride, hydrogen ion, and water homeostasis through its effects on the expression and activity of distal renal tubular cotransporter proteins and to discuss the gene mutations encoding these structures that disturb the function of this system. Sodium 132-138 renin Homo sapiens 65-70 25254266-6 2014 A 1 muM LOD for sodium and a 1.6 muM LOD for potassium ions were revealed for the detector. Sodium 16-22 latexin Homo sapiens 4-7 24890824-0 2014 Transient receptor potential vanilloid 1 activation by dietary capsaicin promotes urinary sodium excretion by inhibiting epithelial sodium channel alpha subunit-mediated sodium reabsorption. Sodium 90-96 transient receptor potential cation channel, subfamily V, member 1 Mus musculus 0-40 24890824-5 2014 Here, we report that TRPV1 activation by dietary capsaicin increased urinary sodium excretion through reducing sodium reabsorption in wild-type (WT) mice on a HS diet but not in TRPV1(-/-) mice. Sodium 77-83 transient receptor potential cation channel, subfamily V, member 1 Mus musculus 21-26 24890824-5 2014 Here, we report that TRPV1 activation by dietary capsaicin increased urinary sodium excretion through reducing sodium reabsorption in wild-type (WT) mice on a HS diet but not in TRPV1(-/-) mice. Sodium 111-117 transient receptor potential cation channel, subfamily V, member 1 Mus musculus 21-26 24890824-12 2014 It concludes that TRPV1 activation in the cortical collecting ducts by capsaicin increases urinary sodium excretion and avoids HS diet-induced hypertension through antagonizing alphaENaC-mediated urinary sodium reabsorption. Sodium 99-105 transient receptor potential cation channel, subfamily V, member 1 Mus musculus 18-23 24890824-12 2014 It concludes that TRPV1 activation in the cortical collecting ducts by capsaicin increases urinary sodium excretion and avoids HS diet-induced hypertension through antagonizing alphaENaC-mediated urinary sodium reabsorption. Sodium 204-210 transient receptor potential cation channel, subfamily V, member 1 Mus musculus 18-23 25043186-1 2014 Homeostatic control of extracellular fluid osmolality in rats requires a parallel excitation of vasopressin (VP) and oxytocin (OT) neurosecretory neurons by osmoreceptor afferents to regulate the amount of water and sodium in the urine under normal conditions. Sodium 216-222 arginine vasopressin Rattus norvegicus 96-107 25043186-1 2014 Homeostatic control of extracellular fluid osmolality in rats requires a parallel excitation of vasopressin (VP) and oxytocin (OT) neurosecretory neurons by osmoreceptor afferents to regulate the amount of water and sodium in the urine under normal conditions. Sodium 216-222 arginine vasopressin Rattus norvegicus 109-111 24740791-7 2014 ANG II induced threefold increases in phosphorylated MAP kinases ERK1/2 and a onefold increase in phosphorylated sodium and hydrogen exchanger 3 (NHE3) proteins, which were also blocked by losartan and megalin-siRNA. Sodium 113-119 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 0-6 24603075-0 2014 beta-III spectrin underpins ankyrin R function in Purkinje cell dendritic trees: protein complex critical for sodium channel activity is impaired by SCA5-associated mutations. Sodium 110-116 spectrin beta, non-erythrocytic 2 Homo sapiens 0-17 24603075-0 2014 beta-III spectrin underpins ankyrin R function in Purkinje cell dendritic trees: protein complex critical for sodium channel activity is impaired by SCA5-associated mutations. Sodium 110-116 spectrin beta, non-erythrocytic 2 Homo sapiens 149-153 24603075-7 2014 Moreover, a wild-type beta-III spectrin/ankyrin-R complex increases sodium channel levels and activity in cell culture, whereas mutant beta-III spectrin complexes fail to enhance sodium currents. Sodium 68-74 spectrin beta, non-erythrocytic 2 Homo sapiens 22-39 25009258-1 2014 Angiotensin II (AngII) and aldosterone cooperate centrally to produce a robust sodium appetite. Sodium 79-85 angiotensinogen Rattus norvegicus 16-21 25009258-3 2014 Male rats pretreated with both deoxycorticosterone (DOC; a synthetic precursor of aldosterone) and central AngII exhibited a marked sodium intake, as classically described. Sodium 132-138 angiotensinogen Rattus norvegicus 107-112 25009258-4 2014 Disruption of inositol trisphosphate signaling, but not extracellular-regulated receptor kinase 1 and 2 signaling, prevented the cooperativity of DOC and AngII on sodium intake. Sodium 163-169 angiotensinogen Rattus norvegicus 154-159 25009258-9 2014 In addition, when action potentials in the PVN were inhibited with intraparenchymal lidocaine, AngII-induced sodium ingestion was exaggerated. Sodium 109-115 angiotensinogen Rattus norvegicus 95-100 24573382-0 2014 Rubbing salt into wounded endothelium: sodium potentiates proatherogenic effects of TNF-alpha under non-uniform shear stress. Sodium 39-45 tumor necrosis factor Homo sapiens 84-93 24944035-1 2014 The renin-angiotensin system has powerful effects in control of the blood pressure and sodium homeostasis. Sodium 87-93 renin Homo sapiens 4-9 25024004-5 2014 Essentially, T-lymphocytes determine an increase in angiotensin ii production which raises sodium and water retention. Sodium 91-97 angiotensinogen Homo sapiens 52-66 24840297-1 2014 PURPOSE OF REVIEW: Sodium balance is primarily regulated through the renin-angiotensin-aldosterone system. Sodium 19-25 renin Homo sapiens 69-74 24840297-2 2014 Extracellular fluid (ECF) sodium concentrations ([Na]) reflect the overall body sodium content, but are also influenced by the osmoregulatory system, which is regulated by the posterior pituitary hormone arginine vasopressin (AVP). Sodium 26-32 arginine vasopressin Homo sapiens 213-224 24777977-7 2014 Using an isoform selective inhibitor and an adenovirus expressing dominant negative protein kinase C-alpha revealed that protein kinase C-alpha in the subfornical organ was necessary to mediate elevated fluid and sodium intake in sRA mice. Sodium 213-219 protein kinase C, alpha Mus musculus 84-106 24777977-7 2014 Using an isoform selective inhibitor and an adenovirus expressing dominant negative protein kinase C-alpha revealed that protein kinase C-alpha in the subfornical organ was necessary to mediate elevated fluid and sodium intake in sRA mice. Sodium 213-219 protein kinase C, alpha Mus musculus 121-143 24511122-2 2014 Notably, in rats, mice, and rabbits, the regulation of PT sodium transport by Ang II is biphasic: transport is stimulated by picomolar to nanomolar concentrations of Ang II but inhibited by nanomolar to micromolar concentrations of Ang II. Sodium 58-64 angiotensinogen Homo sapiens 78-84 24511122-2 2014 Notably, in rats, mice, and rabbits, the regulation of PT sodium transport by Ang II is biphasic: transport is stimulated by picomolar to nanomolar concentrations of Ang II but inhibited by nanomolar to micromolar concentrations of Ang II. Sodium 58-64 angiotensinogen Homo sapiens 166-172 24511122-2 2014 Notably, in rats, mice, and rabbits, the regulation of PT sodium transport by Ang II is biphasic: transport is stimulated by picomolar to nanomolar concentrations of Ang II but inhibited by nanomolar to micromolar concentrations of Ang II. Sodium 58-64 angiotensinogen Homo sapiens 166-172 25697321-1 2014 INTRODUCTION: Cystic fibrosis (CF) is an autosomal recessive disease caused by a mutation in the CFTR gene, resulting in an alteration of a protein involved in sodium and chloride transport in the apical plasma membrane of epithelial cells in respiratory and intestinal tracts. Sodium 160-166 CF transmembrane conductance regulator Homo sapiens 97-101 24970686-11 2014 CONCLUSIONS: In response to hypertonic saline, u-NKCC2 increased, suggesting an increased sodium reabsorption via NKCC2 in patients with CKD. Sodium 90-96 solute carrier family 12 member 1 Homo sapiens 49-54 24970686-11 2014 CONCLUSIONS: In response to hypertonic saline, u-NKCC2 increased, suggesting an increased sodium reabsorption via NKCC2 in patients with CKD. Sodium 90-96 solute carrier family 12 member 1 Homo sapiens 114-119 24923603-2 2014 CASE PRESENTATION: We describe the case of a 63-year-old Korean male with inappropriate antidiuretic hormone syndrome due to an ectopic antidiuretic hormone-producing advanced gastric adenocarcinoma manifested with overt serum hypo-osmolar hyponatremia and high urinary sodium concentrations. Sodium 270-276 arginine vasopressin Homo sapiens 88-108 24891603-4 2014 The sodium/hydrogen exchanger 1 (NHE-1) is linked to the cytoskeleton by ezrin/radixin/moesin family proteins and is known to regulate invadopodium-mediated matrix degradation. Sodium 4-10 solute carrier family 9 member A1 Homo sapiens 33-38 24888603-0 2014 Physiological sodium concentrations enhance the iodide affinity of the Na+/I- symporter. Sodium 14-20 solute carrier family 5 member 5 Homo sapiens 71-87 28510183-5 2014 Many studies have also demonstrated that CFTR also regulates channel pore opening and the transport of sodium, chloride and potassium. Sodium 103-109 CF transmembrane conductance regulator Homo sapiens 41-45 24671621-9 2014 Our findings suggest that hair mineral concentrations, such as calcium, magnesium, zinc, sodium, and potassium concentrations, may play a role in the development of insulin resistance. Sodium 89-95 insulin Homo sapiens 165-172 24590923-1 2014 The aim of this study was to assess whether endogenous Ang II and oxidative stress produced by acute hypertonic sodium overload may regulate the expression of aquaporin-1 (AQP-1) and aquaporin-2 (AQP-2) in the kidney. Sodium 112-118 angiotensinogen Rattus norvegicus 55-61 24891603-4 2014 The sodium/hydrogen exchanger 1 (NHE-1) is linked to the cytoskeleton by ezrin/radixin/moesin family proteins and is known to regulate invadopodium-mediated matrix degradation. Sodium 4-10 moesin Homo sapiens 87-93 25161687-1 2014 BACKGROUND: To study the relationship between cortisol, insulin, and thyroid hormone levels with 24-h urinary sodium (Na) excretion levels in essential hypertensive patients. Sodium 110-116 insulin Homo sapiens 56-63 24622156-10 2014 CONCLUSIONS: This study demonstrated the different responses of renin and aldosterone in SS and SR subjects based on dietary sodium intake whether or not they had hypertension. Sodium 125-131 renin Homo sapiens 64-69 24622156-0 2014 The unique response of renin and aldosterone to dietary sodium intervention in sodium sensitivity. Sodium 56-62 renin Homo sapiens 23-28 24622156-0 2014 The unique response of renin and aldosterone to dietary sodium intervention in sodium sensitivity. Sodium 79-85 renin Homo sapiens 23-28 24622156-2 2014 The renin-angiotensin-aldosterone system plays a critical role in sodium handling and hypertension. Sodium 66-72 renin Homo sapiens 4-9 24622156-3 2014 We identified the specific responses of renin and aldosterone based on dietary sodium intake and revealed the relationship between these hormonal changes and dietary sodium intake in patients with SS. Sodium 79-85 renin Homo sapiens 40-45 24828044-7 2014 Unexpectedly, cell-based studies indicate that Mfsd2a transports DHA in the form of lysophosphatidylcholine (LPC), but not unesterified fatty acid, in a sodium-dependent manner. Sodium 153-159 major facilitator superfamily domain containing 2A Mus musculus 47-53 23594269-0 2014 High sodium intake is associated with increased glucocorticoid production, insulin resistance and metabolic syndrome. Sodium 5-11 insulin Homo sapiens 75-82 23594269-1 2014 OBJECTIVE: High sodium (HS) diet is associated with hypertension (HT) and insulin resistance (IR). Sodium 16-22 insulin Homo sapiens 74-81 23594269-6 2014 RESULTS: Urinary sodium was correlated with UFC (r = +0 45, P < 0 001), cortisol THM (r = +0 41, P < 0 001) and inversely with adiponectin, HDL and aldosterone, after adjusting by age, gender and BMI. Sodium 17-23 adiponectin, C1Q and collagen domain containing Homo sapiens 133-144 23594269-7 2014 Subjects with high, compared with adequate sodium intake (50-149 mEq/day) had higher UFC (P < 0 001), THM (P < 0 001), HOMA-IR (P = 0 04), HT (81% vs 50%, P < 0 001), MetS (69% vs 41%, P < 0 001) and lower adiponectin (P = 0 003). Sodium 43-49 adiponectin, C1Q and collagen domain containing Homo sapiens 218-229 24509840-3 2014 Alternative translation initiation produces a shorter, N terminus truncated form of TREK1 with a much reduced open probability and a proposed increased permeability to sodium compared with the longer form. Sodium 168-174 potassium two pore domain channel subfamily K member 2 Homo sapiens 84-89 24583165-10 2014 RESULTS: There was an association of CFTR class mutation and sodium/chloride concentration in the sweat test (sodium: p=0.040; chloride: p=0.016), onset of digestive symptoms (p=0.012), lung function parameter (SpO2 - p=0.016), Bhalla score (p=0.021), age at diagnosis (p=0.008) and CF-related diabetes (p=0.029). Sodium 61-67 CF transmembrane conductance regulator Homo sapiens 37-41 24583165-10 2014 RESULTS: There was an association of CFTR class mutation and sodium/chloride concentration in the sweat test (sodium: p=0.040; chloride: p=0.016), onset of digestive symptoms (p=0.012), lung function parameter (SpO2 - p=0.016), Bhalla score (p=0.021), age at diagnosis (p=0.008) and CF-related diabetes (p=0.029). Sodium 110-116 CF transmembrane conductance regulator Homo sapiens 37-41 24408226-11 2014 The findings suggest that appropriate AVP secretion in response to an increase in serum osmolality caused by renal sodium retention is necessary for excess extracellular fluid accumulation in NS. Sodium 115-121 arginine vasopressin Homo sapiens 38-41 24581676-1 2014 In a meta-analysis that investigated the effects of dietary sodium restriction in diabetes nephropathy, although blood pressure fell, there were significant increases in plasma renin and aldosterone levels. Sodium 60-66 renin Homo sapiens 177-182 24602802-8 2014 Under normonatremic conditions, delta-opioid receptors may be necessary to modulate sodium intake, a response that could be mediated by angiotensin II. Sodium 84-90 angiotensinogen Rattus norvegicus 136-150 24610784-5 2014 Sodium is reabsorbed in this segment through the actions of the NaCl co-transporter (NCC), which is regulated by the with-no-lysine kinases (WNKs). Sodium 0-6 solute carrier family 12, member 3 Mus musculus 64-83 24610784-5 2014 Sodium is reabsorbed in this segment through the actions of the NaCl co-transporter (NCC), which is regulated by the with-no-lysine kinases (WNKs). Sodium 0-6 solute carrier family 12, member 3 Mus musculus 85-88 24610784-6 2014 The goal of this study was to test if Per1 regulates sodium transport in the DCT through modulation of NCC and the WNK kinases, WNK1 and WNK4. Sodium 53-59 solute carrier family 12, member 3 Mus musculus 103-106 24608976-0 2014 A novel tescalcin-sodium/hydrogen exchange axis underlying sorafenib resistance in FLT3-ITD+ AML. Sodium 18-24 fms related receptor tyrosine kinase 3 Homo sapiens 83-87 24500283-1 2014 Loss of cystic fibrosis transmembrane conductance regulator (CFTR) function reduces chloride secretion and increases sodium uptake, but it is not clear why CFTR mutation also results in progressive lung inflammation and infection. Sodium 117-123 CF transmembrane conductance regulator Homo sapiens 8-59 24500283-1 2014 Loss of cystic fibrosis transmembrane conductance regulator (CFTR) function reduces chloride secretion and increases sodium uptake, but it is not clear why CFTR mutation also results in progressive lung inflammation and infection. Sodium 117-123 CF transmembrane conductance regulator Homo sapiens 61-65 24477233-1 2014 The sodium-coupled glucose transporter-1 (SGLT1)-based oral rehydration solution (ORS) used in the management of acute diarrhea does not substantially reduce stool output, despite the fact that glucose stimulates the absorption of sodium and water. Sodium 4-10 solute carrier family 5 member 1 Homo sapiens 42-47 24955166-0 2014 Cardiac ablation of Rheb1 reduces sodium currents in infant mice. Sodium 34-40 RHEB pseudogene 1 Homo sapiens 20-25 24620851-7 2014 The distance between the sodium ions and micelle also depends on the number of waters binding to sodium ions in the presence of surfactant head groups, which depends on both the sodium ion and water models, and for the same sodium model increases as the water model is changed in the order: TIP4P, SPC/E, SPC, and TIP3P. Sodium 25-31 proline rich protein gene cluster Homo sapiens 298-301 24620851-7 2014 The distance between the sodium ions and micelle also depends on the number of waters binding to sodium ions in the presence of surfactant head groups, which depends on both the sodium ion and water models, and for the same sodium model increases as the water model is changed in the order: TIP4P, SPC/E, SPC, and TIP3P. Sodium 25-31 proline rich protein gene cluster Homo sapiens 305-308 24620851-7 2014 The distance between the sodium ions and micelle also depends on the number of waters binding to sodium ions in the presence of surfactant head groups, which depends on both the sodium ion and water models, and for the same sodium model increases as the water model is changed in the order: TIP4P, SPC/E, SPC, and TIP3P. Sodium 97-103 proline rich protein gene cluster Homo sapiens 298-301 24620851-7 2014 The distance between the sodium ions and micelle also depends on the number of waters binding to sodium ions in the presence of surfactant head groups, which depends on both the sodium ion and water models, and for the same sodium model increases as the water model is changed in the order: TIP4P, SPC/E, SPC, and TIP3P. Sodium 97-103 proline rich protein gene cluster Homo sapiens 305-308 24620851-7 2014 The distance between the sodium ions and micelle also depends on the number of waters binding to sodium ions in the presence of surfactant head groups, which depends on both the sodium ion and water models, and for the same sodium model increases as the water model is changed in the order: TIP4P, SPC/E, SPC, and TIP3P. Sodium 97-103 proline rich protein gene cluster Homo sapiens 298-301 24620851-7 2014 The distance between the sodium ions and micelle also depends on the number of waters binding to sodium ions in the presence of surfactant head groups, which depends on both the sodium ion and water models, and for the same sodium model increases as the water model is changed in the order: TIP4P, SPC/E, SPC, and TIP3P. Sodium 97-103 proline rich protein gene cluster Homo sapiens 305-308 24620851-7 2014 The distance between the sodium ions and micelle also depends on the number of waters binding to sodium ions in the presence of surfactant head groups, which depends on both the sodium ion and water models, and for the same sodium model increases as the water model is changed in the order: TIP4P, SPC/E, SPC, and TIP3P. Sodium 97-103 proline rich protein gene cluster Homo sapiens 298-301 24620851-7 2014 The distance between the sodium ions and micelle also depends on the number of waters binding to sodium ions in the presence of surfactant head groups, which depends on both the sodium ion and water models, and for the same sodium model increases as the water model is changed in the order: TIP4P, SPC/E, SPC, and TIP3P. Sodium 97-103 proline rich protein gene cluster Homo sapiens 305-308 24722141-0 2014 Functional analysis of a missense mutation in the serine protease inhibitor SPINT2 associated with congenital sodium diarrhea. Sodium 110-116 serine peptidase inhibitor, Kunitz type, 2 L homeolog Xenopus laevis 76-82 24722141-3 2014 A Y163C mutation in the SPINT2 gene encoding the serine protease inhibitor Hepatocyte Growth Factor Inhibitor HAI-2 is associated with a congenital sodium diarrhea. Sodium 148-154 serine peptidase inhibitor, Kunitz type, 2 L homeolog Xenopus laevis 24-30 24549959-13 2014 Thus, the hyperexcitability of MRGPRA3+ and MRGPRD+ neurons, brought about in part by enhanced sodium currents, may contribute to the spontaneous itch- and pain-related behaviours accompanying contact hypersensitivity and/or other inflammatory diseases in humans. Sodium 95-101 itchy E3 ubiquitin protein ligase Homo sapiens 146-150 24730007-9 2014 Thiazides and angiotensin-converting enzyme inhibitors were the only medications associated with low postoperative sodium values. Sodium 115-121 angiotensin I converting enzyme Homo sapiens 14-43 24423979-3 2014 The main purpose of this review was to analyze how GH and IGF-1 regulate renal development, glomerular functions, and tubular handling of sodium, calcium, phosphate, and glucose. Sodium 138-144 insulin like growth factor 1 Homo sapiens 58-63 24623760-5 2014 We also show that CREB3L1 mRNA levels correlate with AVP transcription level in SONs and PVNs following sodium depletion, and as a consequence of diurnal rhythm in the suprachiasmatic nucleus. Sodium 104-110 arginine vasopressin Rattus norvegicus 53-56 24424051-0 2014 The acute inhibitory effect of iodide excess on sodium/iodide symporter expression and activity involves the PI3K/Akt signaling pathway. Sodium 48-54 AKT serine/threonine kinase 1 Rattus norvegicus 114-117 24308971-3 2014 We now offer and describe a novel mechanism by which D3R decreases sodium transport in the long term by inhibiting the deubiquitinylating activity of ubiquitin-specific peptidase 48 (USP48), thereby promoting Na(+)-H(+) exchanger (NHE)-3 degradation. Sodium 67-73 solute carrier family 9 (sodium/hydrogen exchanger), member 3 Mus musculus 209-237 24760523-0 2014 Rapid elevation of sodium transport through insulin is mediated by AKT in alveolar cells. Sodium 19-25 AKT serine/threonine kinase 1 Rattus norvegicus 67-70 24324041-11 2014 Collectively, we demonstrate that UMOD regulates sodium uptake in the thick ascending limb of the loop of Henle by modulating the effect of tumor necrosis factor-alpha on NKCC2A expression, making UMOD an important determinant of blood pressure control. Sodium 49-55 tumor necrosis factor Mus musculus 140-167 24829986-12 2014 Furthermore, we were able to attenuate sodium intake behavior of sodium appetite by application of antagonists of dopamine receptor-1 (DRD1) both systemically as well as by microinjection into the lateral hypothalamus. Sodium 39-45 dopamine receptor D1 Homo sapiens 135-139 24374853-6 2014 Both the transgenic lines (Bt and chitinase) showed significant decrease in the amounts of sodium in comparison to the non-transgenic counterpart plants. Sodium 91-97 endochitinase 2 Gossypium hirsutum 34-43 23863802-3 2014 Increased CYP3A5 activity could cause sodium and water retention by affecting the metabolism of cortisol in the kidneys. Sodium 38-44 cytochrome P450 family 3 subfamily A member 5 Homo sapiens 10-16 23897018-5 2014 Individuals with CF develop hypovolemic hyponatremia by sodium loss via sweat through a defective chloride ion transport channel, the CF transmembrane conductance regulator (CFTR). Sodium 56-62 CF transmembrane conductance regulator Homo sapiens 134-172 23897018-5 2014 Individuals with CF develop hypovolemic hyponatremia by sodium loss via sweat through a defective chloride ion transport channel, the CF transmembrane conductance regulator (CFTR). Sodium 56-62 CF transmembrane conductance regulator Homo sapiens 174-178 23897018-6 2014 Elevated sweat sodium concentrations in CF single heterozygotes suggest that athletes developing EAH may be CFTR carriers. Sodium 15-21 CF transmembrane conductance regulator Homo sapiens 108-112 24390325-1 2014 UNLABELLED: The liver bile acids transporter sodium taurocholate cotransporting polypeptide (NTCP) is responsible for the majority of sodium-dependent bile salts uptake by hepatocytes. Sodium 45-51 solute carrier family 10 member 1 Homo sapiens 93-97 24390325-5 2014 Mutations of NTCP residues critical for bile salts binding severely impair viral infection by HDV and HBV; to a lesser extent, the residues important for sodium binding also inhibit viral infection. Sodium 154-160 solute carrier family 10 member 1 Homo sapiens 13-17 24488738-9 2014 Multiple linear regressions revealed that dietary sodium intake was independently associated with body weight (beta = 0.23), BMI (beta = 0.23), waist circumference (beta = 0.23), percent body fat (beta = 0.17), fat mass (beta = 0.23), subcutaneous abdominal adipose tissue (beta = 0.25), leptin (beta = 0.20), and tumor necrosis factor-alpha (beta = 0.61; all Ps < .05). Sodium 50-56 tumor necrosis factor Homo sapiens 314-341 24744909-2 2014 Previous studies have demonstrated that this salt-sensitive component is due to increased activity of the sympathetic nervous system, suggesting an interaction of plasma AngII with sodium-sensitive regions of the brain. Sodium 181-187 angiotensinogen Rattus norvegicus 170-175 24401989-5 2014 Angiotensin II, mineralocorticoids, and extracellular osmotic changes act on forebrain areas to facilitate sodium appetite and thirst. Sodium 107-113 angiotensinogen Rattus norvegicus 0-14 24218433-1 2014 G-protein-coupled receptor kinase 4 (GRK4) gene variants, via impairment of renal dopamine receptor and enhancement of renin-angiotensin system functions, cause sodium retention and increase blood pressure. Sodium 161-167 G protein-coupled receptor kinase 4 Mus musculus 0-35 24218433-1 2014 G-protein-coupled receptor kinase 4 (GRK4) gene variants, via impairment of renal dopamine receptor and enhancement of renin-angiotensin system functions, cause sodium retention and increase blood pressure. Sodium 161-167 G protein-coupled receptor kinase 4 Mus musculus 37-41 24179170-0 2014 Sodium transport is modulated by p38 kinase-dependent cross-talk between ENaC and Na,K-ATPase in collecting duct principal cells. Sodium 0-6 sodium channel epithelial 1 subunit gamma Rattus norvegicus 73-77 23900806-0 2014 Increased dietary sodium induces COX2 expression by activating NFkappaB in renal medullary interstitial cells. Sodium 18-24 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 63-71 23900806-8 2014 These data therefore suggest that renal medullary interstitial cell NFkappaB plays an important role in mediating renal medullary COX2 expression and promoting renal PGE2 synthesis in response to increased dietary sodium. Sodium 214-220 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 68-76 24321189-0 2014 Enhanced angiotensin-converting enzyme activity and systemic reactivity to angiotensin II in normotensive rats exposed to a high-sodium diet. Sodium 129-135 angiotensinogen Rattus norvegicus 75-89 24324142-3 2014 TGF-beta applied to the alveolar airspaces of live rabbits or isolated rabbit lungs blocked sodium transport and caused fluid retention, which--together with patch-clamp and flow cytometry studies--identified ENaC as the target of TGF-beta. Sodium 92-98 transforming growth factor beta 1 Homo sapiens 0-8 24409169-5 2014 The classic RAS can be defined as the ACE-Ang II-AT1R axis that promotes vasoconstriction, sodium retention, and other mechanisms to maintain blood pressure, as well as increased oxidative stress, fibrosis, cellular growth, and inflammation in pathological conditions. Sodium 91-97 angiotensin I converting enzyme Homo sapiens 38-41 24829986-12 2014 Furthermore, we were able to attenuate sodium intake behavior of sodium appetite by application of antagonists of dopamine receptor-1 (DRD1) both systemically as well as by microinjection into the lateral hypothalamus. Sodium 65-71 dopamine receptor D1 Homo sapiens 135-139 24511399-8 2014 The following case report analyzes the role of vasopressin antagonists in the treatment of hyponatremia and the need for daily dosing of tolvaptan and the monitoring of serum sodium levels to avoid rapid overcorrection which can result in osmotic demyelination syndrome (ODS). Sodium 175-181 arginine vasopressin Homo sapiens 47-58 24743480-7 2014 However, 2 days after discontinuation of intravenous hANP, CHF recurred and serum sodium decreased to 128 mEq/l. Sodium 82-88 natriuretic peptide A Homo sapiens 53-57 24714077-5 2014 Neutrophils acidified by an ammonium prepulse showed an EIPA-resistant recovery of pHi that was inhibited by the blocker of the anionic transporters SITS or the Na(+)/HCO3(-) cotransporter (NBC) selective inhibitor S0859, and abolished when sodium was removed from the extracellular medium. Sodium 241-247 solute carrier family 4 member 4 Homo sapiens 161-188 24603133-0 2014 PPARgamma-induced stimulation of amiloride-sensitive sodium current in renal collecting duct principal cells is serum and insulin dependent. Sodium 53-59 peroxisome proliferator activated receptor gamma Homo sapiens 0-9 24603133-0 2014 PPARgamma-induced stimulation of amiloride-sensitive sodium current in renal collecting duct principal cells is serum and insulin dependent. Sodium 53-59 insulin Homo sapiens 122-129 25043079-0 2014 Effects of mildly increasing dialysis sodium removal on renin and sympathetic system in hemodialysis patients. Sodium 38-44 renin Homo sapiens 56-61 25043079-1 2014 BACKGROUND: It has been argued that the benefits of reducing sodium loading may be offset by increased activation of the renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system. Sodium 61-67 renin Homo sapiens 121-126 23688012-4 2014 Augmented EGFR signaling contributes to abnormalities of vascular tone and renal sodium handling as well as vascular remodeling and myocardial hypertrophy through various intracellular mechanisms, in particular extracellular signal-regulated kinases (ERK) and phosphoinositide 3-kinase (PI3K). Sodium 81-87 epidermal growth factor receptor Homo sapiens 10-14 23688012-7 2014 Stimulation of EGFR and ErbB2 downstream signaling pathways such as ERK and PI3K in the vascular wall and the kidney may contribute to the increase in vascular tone, enhanced tubular sodium reabsorption as well as vascular and renal lesions in hyperleptinemic obese subjects. Sodium 183-189 epidermal growth factor receptor Homo sapiens 15-19 23688012-7 2014 Stimulation of EGFR and ErbB2 downstream signaling pathways such as ERK and PI3K in the vascular wall and the kidney may contribute to the increase in vascular tone, enhanced tubular sodium reabsorption as well as vascular and renal lesions in hyperleptinemic obese subjects. Sodium 183-189 erb-b2 receptor tyrosine kinase 2 Homo sapiens 24-29 23815567-3 2014 Multiple pathogenic mechanisms have been proposed, including insulin-induced sodium and water retention. Sodium 77-83 insulin Homo sapiens 61-68 24026042-0 2014 High sodium augments angiotensin II-induced vascular smooth muscle cell proliferation through the ERK 1/2-dependent pathway. Sodium 5-11 angiotensinogen Rattus norvegicus 21-35 24026042-2 2014 This study examined the effects of high-sodium level on Ang II-induced cell proliferation in rat vascular smooth muscle cells (VSMCs). Sodium 40-46 angiotensinogen Rattus norvegicus 56-62 24026042-7 2014 Ang II (100 nmol l(-1)) significantly increased ERK 1/2 phosphorylation and cell proliferation in the both medium containing standard sodium and high sodium. Sodium 134-140 angiotensinogen Rattus norvegicus 0-6 24258619-3 2014 FXYD (FXYD domain-containing protein) 2, the gamma-subunit of NKA, is the first identified and the most abundant member of FXYD family, affecting the sodium/potassium affinity of NKA in the kidney. Sodium 150-156 tachykinin precursor 1 Homo sapiens 62-65 24026042-7 2014 Ang II (100 nmol l(-1)) significantly increased ERK 1/2 phosphorylation and cell proliferation in the both medium containing standard sodium and high sodium. Sodium 150-156 angiotensinogen Rattus norvegicus 0-6 24026042-8 2014 High-sodium level augmented Ang II-induced ERK 1/2 phosphorylation and cell proliferation compared with standard sodium. Sodium 5-11 angiotensinogen Rattus norvegicus 28-34 24026042-8 2014 High-sodium level augmented Ang II-induced ERK 1/2 phosphorylation and cell proliferation compared with standard sodium. Sodium 113-119 angiotensinogen Rattus norvegicus 28-34 24026042-13 2014 Ang II increased intracellular pH via NHE-1 activation, and high-sodium level augmented the pH increase induced by Ang II. Sodium 65-71 angiotensinogen Rattus norvegicus 115-121 24026042-14 2014 These data suggest that high-sodium level directly augments Ang II-induced VSMC proliferation through NHE-1- and ERK 1/2-dependent pathways and may offer new insights into the mechanisms of vascular remodeling by high-sodium/Ang II. Sodium 29-35 angiotensinogen Rattus norvegicus 60-66 24026042-14 2014 These data suggest that high-sodium level directly augments Ang II-induced VSMC proliferation through NHE-1- and ERK 1/2-dependent pathways and may offer new insights into the mechanisms of vascular remodeling by high-sodium/Ang II. Sodium 29-35 angiotensinogen Rattus norvegicus 225-231 24026042-14 2014 These data suggest that high-sodium level directly augments Ang II-induced VSMC proliferation through NHE-1- and ERK 1/2-dependent pathways and may offer new insights into the mechanisms of vascular remodeling by high-sodium/Ang II. Sodium 218-224 angiotensinogen Rattus norvegicus 60-66 25117718-4 2014 On the other hand, in hypertensive patients there is experimental evidence indicating that a very low sodium diet (<50 mEq/day) generates a pro-inflammatory phenotype characterized by an increase in Procalcitonin and TNF-alpha and a reduction in an anti-inflammatory cytokine like Adiponectin. Sodium 102-108 tumor necrosis factor Homo sapiens 220-229 25117718-4 2014 On the other hand, in hypertensive patients there is experimental evidence indicating that a very low sodium diet (<50 mEq/day) generates a pro-inflammatory phenotype characterized by an increase in Procalcitonin and TNF-alpha and a reduction in an anti-inflammatory cytokine like Adiponectin. Sodium 102-108 adiponectin, C1Q and collagen domain containing Homo sapiens 284-295 24258619-3 2014 FXYD (FXYD domain-containing protein) 2, the gamma-subunit of NKA, is the first identified and the most abundant member of FXYD family, affecting the sodium/potassium affinity of NKA in the kidney. Sodium 150-156 tachykinin precursor 1 Homo sapiens 179-182 23690164-10 2013 CONCLUSIONS: Deletion of GSTM1 was associated with low USE and modulated the interaction between sodium intake and blood pressure in Brazilian subjects. Sodium 97-103 glutathione S-transferase mu 1 Homo sapiens 25-30 24736260-6 2014 In cystic fibrosis, salt and fluid absorption is prevented by the loss of CFTR and ENaC is not appropriately regulated, resulting in increased fluid and sodium resorption from the airways and formation of a contracted viscous surface liquid layer. Sodium 153-159 CF transmembrane conductance regulator Homo sapiens 74-78 24481877-1 2014 The amiloride-sensitive epithelial sodium channel (ENaC) is a major contributor to intracellular sodium homeostasis. Sodium 35-41 sodium channel epithelial 1 subunit gamma Rattus norvegicus 51-55 24310820-5 2014 For example, the recent discoveries that NCC is activated by angiotensin II but inhibited by dietary potassium shed light on how the kidney handles sodium during hypovolemia (high angiotensin II) and hyperkalemia. Sodium 148-154 angiotensinogen Homo sapiens 180-194 24310820-6 2014 The additive effect of angiotensin II and aldosterone maximizes sodium reabsorption during hypovolemia, whereas the inhibitory effect of potassium on NCC increases delivery of sodium to the potassium-secreting portion of the nephron. Sodium 64-70 angiotensinogen Homo sapiens 23-37 24416046-4 2013 Serum sodium levels in hyponatremia are inversely correlated with the percentage of neutrophils, C-reactive protein, and N-terminal-pro brain type natriuretic peptide. Sodium 6-12 C-reactive protein Homo sapiens 97-115 25019012-1 2013 Various models of experimental hypertension and clinical examples of increased renin formation from a stenotic kidney or a juxtaglomerular cell tumor have shown that increased circulating angiotensin II (Ang II) stimulates the intrarenal/intratubular renin-angiotensin system (RAS) that elicits renal vasoconstriction, enhanced tubular sodium reabsorption, and progressive development of hypertension and renal injury. Sodium 336-342 renin Homo sapiens 79-84 25019012-1 2013 Various models of experimental hypertension and clinical examples of increased renin formation from a stenotic kidney or a juxtaglomerular cell tumor have shown that increased circulating angiotensin II (Ang II) stimulates the intrarenal/intratubular renin-angiotensin system (RAS) that elicits renal vasoconstriction, enhanced tubular sodium reabsorption, and progressive development of hypertension and renal injury. Sodium 336-342 angiotensinogen Homo sapiens 188-202 25019012-1 2013 Various models of experimental hypertension and clinical examples of increased renin formation from a stenotic kidney or a juxtaglomerular cell tumor have shown that increased circulating angiotensin II (Ang II) stimulates the intrarenal/intratubular renin-angiotensin system (RAS) that elicits renal vasoconstriction, enhanced tubular sodium reabsorption, and progressive development of hypertension and renal injury. Sodium 336-342 angiotensinogen Homo sapiens 204-210 25019012-1 2013 Various models of experimental hypertension and clinical examples of increased renin formation from a stenotic kidney or a juxtaglomerular cell tumor have shown that increased circulating angiotensin II (Ang II) stimulates the intrarenal/intratubular renin-angiotensin system (RAS) that elicits renal vasoconstriction, enhanced tubular sodium reabsorption, and progressive development of hypertension and renal injury. Sodium 336-342 renin Homo sapiens 251-256 25019012-7 2013 The augmented intratubular Ang II concentrations together with elevated renal interstitial Ang II concentrations contribute to sustained stimulation of sodium reabsorption, vasoconstriction, development of hypertension, and progressive renal injury and fibrosis. Sodium 152-158 angiotensinogen Homo sapiens 27-33 25019012-7 2013 The augmented intratubular Ang II concentrations together with elevated renal interstitial Ang II concentrations contribute to sustained stimulation of sodium reabsorption, vasoconstriction, development of hypertension, and progressive renal injury and fibrosis. Sodium 152-158 angiotensinogen Homo sapiens 91-97 24070585-3 2013 LPS (10 and 100 ng/ml) caused a dose- and time-dependent accumulation of intracellular sodium [(Na(+))i] in BV-2 cells. Sodium 87-93 toll-like receptor 4 Mus musculus 0-3 24048572-7 2013 In calcium-deficient medium, high-pH treatment induced motility loss, consistent with influx of sodium through open CatSper channels in the absence of environmental calcium. Sodium 96-102 cation channel, sperm associated 1 Mus musculus 116-123 24283218-0 2013 Inhibition of tetrodotoxin-resistant sodium current in dorsal root ganglia neurons mediated by D1/D5 dopamine receptors. Sodium 37-43 dopamine receptor D5 Homo sapiens 95-119 24283218-10 2013 CONCLUSIONS: We conclude that activation of D1/D5 dopamine receptors inhibits TTX-R sodium current in unmyelinated nociceptive neurons and dampens their intrinsic excitability by reducing the number of action potentials in response to stimulus. Sodium 84-90 dopamine receptor D5 Homo sapiens 44-68 24049115-9 2013 Hence, some of the same circulating hormones controlling ENaC expression in kidney, such as angiotensin II and atrial natriuretic peptide, may coordinate ENaC expression in sensory CVO neurons and could potentially orchestrate sodium appetite, osmoregulation, and vasomotor sympathetic drive. Sodium 227-233 angiotensinogen Homo sapiens 92-106 24117259-7 2013 Therefore, the in vivo application of a selective iNOS inhibitor partially improved the acute UUO-induced distal nephron acidification defect, while post-treatment but not pre-treatment with aminoguanidine ameliorated decrements of glomerular filtration, sodium reabsorption, and urine-concentrating ability. Sodium 255-261 nitric oxide synthase 2 Rattus norvegicus 50-54 23714182-1 2013 Microsomal epoxide hydrolase (mEH) is a bifunctional protein that plays a central role in the metabolism of numerous xenobiotics as well as mediating the sodium-dependent transport of bile acids into hepatocytes where they are involved in cholesterol excretion and metabolism, lipid digestion and regulating numerous signaling pathways. Sodium 154-160 epoxide hydrolase 1, microsomal Mus musculus 30-33 24046327-7 2013 VIP increased delayed rectifier K+ current and L-type calcium current but decreased the transient outward K+ current and sodium current. Sodium 121-127 vasoactive intestinal peptide Canis lupus familiaris 0-3 23911204-5 2013 To evidence that role of TNFalpha, we carried out a simulation of the sodium and potassium currents and action potential (AP) of isolated muscle fibre. Sodium 70-76 tumor necrosis factor Rattus norvegicus 25-33 23136031-0 2013 The dual blockade of the renin-angiotensin system in hemodialysis patients requires decreased dialysate sodium concentration. Sodium 104-110 renin Homo sapiens 25-30 23136031-1 2013 PURPOSE: The study evaluated whether the dual blockade of the renin-angiotensin system may influence the sodium balance in hemodialysis. Sodium 105-111 renin Homo sapiens 62-67 23136031-9 2013 CONCLUSIONS: The dual blockade of the renin-angiotensin system affects sodium balance, increasing the sodium gradient, thus elevating thirst sensation and enhancing interdialytic weight gain. Sodium 71-77 renin Homo sapiens 38-43 24077057-5 2013 Expression of the short Sin3B variant strongly reduced native sodium current and Na(v)-channel gating charge in the neuronal cell line N1E-115, without affecting the voltage-dependence of activation. Sodium 62-68 SIN3 transcription regulator family member B Homo sapiens 24-29 23935101-1 2013 The vasopressin type 2 receptor (V2R) is a critical G protein-coupled receptor (GPCR) for vertebrate physiology, including the balance of water and sodium ions. Sodium 148-154 arginine vasopressin receptor 2 Homo sapiens 4-36 30546768-6 2013 It is known that the long-term usage of loop diuretics causes tolerance because it promotes sodium re-absorption through the proximal renal tubules by activating the renin-angiotensin-aldosterone system. Sodium 92-98 renin Homo sapiens 166-171 24052075-1 2013 Thyroid iodide accumulation via the sodium/iodide symporter (NIS; SLC5A5) has been the basis for the longtime use of radio-iodide in the diagnosis and treatment of thyroid cancers. Sodium 36-42 solute carrier family 5 member 5 Homo sapiens 61-64 24052075-1 2013 Thyroid iodide accumulation via the sodium/iodide symporter (NIS; SLC5A5) has been the basis for the longtime use of radio-iodide in the diagnosis and treatment of thyroid cancers. Sodium 36-42 solute carrier family 5 member 5 Homo sapiens 66-72 23958258-7 2013 However, in the primary study, there was significant (Pint <= 0.045) interaction between 3 SNPs (rs6668352, rs198388, and rs198389) at the NPPA-NPPB locus and urinary sodium excretion in relation to ABI, and the rs6668352 polymorphism had the strongest association (Pint = 0.018). Sodium 170-176 natriuretic peptide A Homo sapiens 142-146 23958258-10 2013 CONCLUSION: The minor alleles of 3 SNPs at the NPPA-NPPB locus are associated with a lower risk of PAD, especially in the subjects of high sodium intake. Sodium 139-145 natriuretic peptide A Homo sapiens 47-51 24851297-5 2013 However, concerns have been raised that a low sodium intake may adversely affect certain risk factors, including blood lipids and insulin resistance, and thus potentially increase risk of heart disease and stroke. Sodium 46-52 insulin Homo sapiens 130-137 23835093-6 2013 V1a agonist (Phe(2)-Ile(3)-Orn(8)-vasopressin) reproduced the renal effects of dAVT on sodium and potassium excretion but not on water reabsorption. Sodium 87-93 arginine vasopressin Rattus norvegicus 34-45 23897888-4 2013 Cells lacking IST1 (increased sodium tolerance 1), an endosomal sorting complex required for transport (ESCRT) component to which spastin binds, also had increased endosomal tubulation. Sodium 30-36 IST1 factor associated with ESCRT-III Danio rerio 14-18 24689065-8 2014 The administration of tempol together with the sodium overload increased the natriuresis further and prevented the elevation of blood pressure and the increased expression of ANP, TGF-beta1, and HIF-1alpha compared to their control. Sodium 47-53 transforming growth factor, beta 1 Rattus norvegicus 180-189 25472577-6 2014 RESULTS: At baseline, the independent predictors of lower plasma sodium were C-reactive protein (CRP; OR 0.96; 95% CI 0.91-0.99) and body mass index (OR 0.89; 95% CI 0.78-0.99). Sodium 65-71 C-reactive protein Homo sapiens 77-95 25472577-6 2014 RESULTS: At baseline, the independent predictors of lower plasma sodium were C-reactive protein (CRP; OR 0.96; 95% CI 0.91-0.99) and body mass index (OR 0.89; 95% CI 0.78-0.99). Sodium 65-71 C-reactive protein Homo sapiens 97-100 25472577-7 2014 An inverse correlation between plasma sodium and CRP was observed (r = -0.32; p = 0.01). Sodium 38-44 C-reactive protein Homo sapiens 49-52 25472577-9 2014 During follow-up, patients with lower sodium at baseline showed persistently lower sodium values (p = 0.04), higher CRP (p = 0.05), lower serum albumin (p < 0.01) and higher erythropoietin-stimulating agent resistance index (p = 0.05). Sodium 38-44 C-reactive protein Homo sapiens 116-119 24583585-6 2014 According as administration of acetic Ringer"s solution and insulin injection, the laboratory data 14 hours after admission showed glucose 235 mg/dl, serum osmolality 290 mOsm/l and serum sodium 131 mEq/l. Sodium 188-194 insulin Homo sapiens 60-67 25125726-11 2014 Current evidence indicates that production of cytokines including tumor necrosis factor alpha, interleukin 17, and interleukin 6 contribute to hypertension, likely by promoting vasoconstriction, production of reactive oxygen species, and sodium reabsorption in the kidney. Sodium 238-244 tumor necrosis factor Mus musculus 66-93 25125726-11 2014 Current evidence indicates that production of cytokines including tumor necrosis factor alpha, interleukin 17, and interleukin 6 contribute to hypertension, likely by promoting vasoconstriction, production of reactive oxygen species, and sodium reabsorption in the kidney. Sodium 238-244 interleukin 6 Mus musculus 115-128 24354674-4 2013 This study aimed to clarify the relationship between serum sodium level (sNa) and infection risk in ESRD patients. Sodium 59-65 snail family transcriptional repressor 1 Homo sapiens 73-76 24103391-0 2013 GABAergic excitation of vasopressin neurons: possible mechanism underlying sodium-dependent hypertension. Sodium 75-81 arginine vasopressin Rattus norvegicus 24-35 24092518-5 2013 In addition, 50 muM sodium metasilicate decreased interleukin-6 production, and the degree of suppression was comparable to that of 10 muM TBHQ treatment. Sodium 20-26 interleukin 6 Mus musculus 50-63 24092518-6 2013 LPS-induced messenger RNA (mRNA) expression of tumor necrosis factor-alpha and inducible nitric oxide synthase was significantly decreased by 1, 5, 10, and 50 muM sodium metasilicate. Sodium 163-169 tumor necrosis factor Mus musculus 47-74 24092518-6 2013 LPS-induced messenger RNA (mRNA) expression of tumor necrosis factor-alpha and inducible nitric oxide synthase was significantly decreased by 1, 5, 10, and 50 muM sodium metasilicate. Sodium 163-169 nitric oxide synthase 2, inducible Mus musculus 79-110 24191006-4 2013 A biophysical method has been used to measure sodium dissociation constants (Kd) of wild-type and mutant human sodium glucose cotransport (hSGLT1) proteins to identify the Na(+) binding sites in hSGLT1. Sodium 46-52 solute carrier family 5 member 1 Homo sapiens 139-145 24191006-4 2013 A biophysical method has been used to measure sodium dissociation constants (Kd) of wild-type and mutant human sodium glucose cotransport (hSGLT1) proteins to identify the Na(+) binding sites in hSGLT1. Sodium 46-52 solute carrier family 5 member 1 Homo sapiens 195-201 24054177-4 2013 Low sodium diets may adversely affect insulin resistance, serum lipids, and neurohormonal pathways, leading to increases in the incidence of new cardiometabolic disease, the severity of existing cardiometabolic disease, and greater cardiovascular and all-cause mortality. Sodium 4-10 insulin Homo sapiens 38-45 23996477-0 2013 Quantitative assessment of the contribution of sodium-dependent taurocholate co-transporting polypeptide (NTCP) to the hepatic uptake of rosuvastatin, pitavastatin and fluvastatin. Sodium 47-53 solute carrier family 10 member 1 Homo sapiens 106-110 23996477-3 2013 The present study revisited the interaction of statin drugs, including pitavastatin, fluvastatin and rosuvastatin, with the sodium-dependent taurocholate co-transporting polypeptide (NTCP) using gene transfected cell models. Sodium 124-130 solute carrier family 10 member 1 Homo sapiens 183-187 24019399-10 2013 These data suggest that there is a synergism between CCKBR and D1-like receptors to increase sodium excretion. Sodium 93-99 cholecystokinin B receptor Rattus norvegicus 53-58 23562556-0 2013 Cloning and functional characterization of the mouse sodium-dependent organic anion transporter Soat (Slc10a6). Sodium 53-59 solute carrier family 10 (sodium/bile acid cotransporter family), member 6 Mus musculus 96-100 23562556-0 2013 Cloning and functional characterization of the mouse sodium-dependent organic anion transporter Soat (Slc10a6). Sodium 53-59 solute carrier family 10 (sodium/bile acid cotransporter family), member 6 Mus musculus 102-109 23562556-6 2013 Stably transfected mSoat-HEK293 cells revealed sodium-dependent transport for dehydroepiandrosterone sulfate (DHEAS), estrone-3-sulfate, and pregnenolone sulfate (PREGS) with apparent Km values of 60.3muM, 2.1muM, and 2.5muM, respectively. Sodium 47-53 latexin Homo sapiens 201-204 23946287-1 2013 Both sodium reabsorption in the thick ascending limb of the loop of Henle (TAL) and macula densa salt sensing crucially depend on the function of the Na/K/2Cl cotransporter NKCC2. Sodium 5-11 talipes Mus musculus 75-78 23946287-1 2013 Both sodium reabsorption in the thick ascending limb of the loop of Henle (TAL) and macula densa salt sensing crucially depend on the function of the Na/K/2Cl cotransporter NKCC2. Sodium 5-11 solute carrier family 12, member 1 Mus musculus 173-178 23841645-2 2013 We hypothesized that NOS1- and/or NOS2-derived NO blunts T1D-induced activation of sodium transport in the mTAL. Sodium 83-89 nitric oxide synthase 2 Rattus norvegicus 34-38 23841645-13 2013 Inhibition of NADPH oxidase to preserve NO bioavailability reveals an inhibitory impact of NOS1- and NOS2-derived NO on sodium transport in the mTAL. Sodium 120-126 nitric oxide synthase 2 Rattus norvegicus 101-105 23986260-5 2013 GlyT2 function is strictly coupled to the sodium electrochemical gradient actively generated by the Na+/K+-ATPase (NKA). Sodium 42-48 tachykinin precursor 1 Homo sapiens 100-113 23986260-5 2013 GlyT2 function is strictly coupled to the sodium electrochemical gradient actively generated by the Na+/K+-ATPase (NKA). Sodium 42-48 tachykinin precursor 1 Homo sapiens 115-118 23836888-12 2013 Diminution of sodium currents, largely NaV1.7, was recapitulated in sensory neurons expressing CRMP2-K374A. Sodium 14-20 dihydropyrimidinase like 2 Homo sapiens 95-100 23678047-1 2013 The mammalian Na+/H+ exchanger isoform 1 (NHE1) is a ubiquitous plasma membrane protein that regulates intracellular pH by removing a proton in exchange for extracellular sodium. Sodium 171-177 solute carrier family 9 member A1 Homo sapiens 14-40 23678047-1 2013 The mammalian Na+/H+ exchanger isoform 1 (NHE1) is a ubiquitous plasma membrane protein that regulates intracellular pH by removing a proton in exchange for extracellular sodium. Sodium 171-177 solute carrier family 9 member A1 Homo sapiens 42-46 23768927-4 2013 We demonstrate that allografted mHCN4-transfected rMSCs survived in the host heart for >4 weeks; that they expressed If, which is generated by the mHCN4 channel, with a similar amplitude but greater negative activation compared with parallel cells cultured in vitro; that they did not express optical action potentials or depolarization-activated inward sodium or calcium currents; and that they exhibited a low incidence of gap-junctional coupling with host cardiomyocytes. Sodium 357-363 hyperpolarization-activated, cyclic nucleotide-gated K+ 4 Mus musculus 32-37 23832211-1 2013 NBCe1-A membrane-embedded macromolecules that cotransport sodium and bicarbonate ions across the bilayer serve to maintain acid-base homeostasis throughout the body. Sodium 58-64 solute carrier family 4 member 4 Homo sapiens 0-7 23637204-8 2013 Collectively, these results suggest that EGF-ErbB signaling pathways could be major determinants in the progress of renal lesions, including its effects on the regulation of sodium reabsorption in collecting ducts. Sodium 174-180 epidermal growth factor receptor Homo sapiens 45-49 23706055-9 2013 The mean serum sodium level (SNa) at baseline was 155 +- 7.1 mEq/L, and after multiple boluses of 14.6% HTS, S(Na) at 12 hours was 154 +- 7.1 mEq/L. Sodium 15-21 snail family transcriptional repressor 1 Homo sapiens 29-32 23414830-10 2013 Correspondence analyses were consistent with PFA and also showed that lower feeding levels were related to reduced milk stability, high plasma lactose, high sodium in milk, low milk lactose (another parameter used to assess TJ permeability) and higher cortisol levels, indicating the stress to which animals were submitted. Sodium 157-163 Weaning weight-maternal milk Bos taurus 167-171 23912284-2 2013 OBJECTIVES: To assess variations in serum sodium (sNa) following the intravenous administration of isotonic maintenance fluids (0.9% NaCl/5% dextrose) compared to hypotonic maintenance fluids (0.45% NaCl/5% dextrose). Sodium 42-48 snail family transcriptional repressor 1 Homo sapiens 50-53 23980733-1 2013 The high intake of dietary sodium (Na(+)) has been associated with obesity and insulin resistance, sparking the hypothesis that the consumption of salty foods affects food intake (FI) and postprandial blood glucose (BG) response. Sodium 27-33 insulin Homo sapiens 79-86 23744888-5 2013 Sodium depletion and captopril led to activation and differentiation of these cells into renin-expressing cells in the adult kidney. Sodium 0-6 renin Homo sapiens 89-94 23361943-6 2013 Using sodium-dependent and sodium-free conditions, we demonstrate that the inhibition of GLUT2 was greater than SGLT1. Sodium 27-33 solute carrier family 5 member 1 Homo sapiens 112-117 23480725-7 2013 Glucose or phlorizin, a sodium-dependent GLT (SGLT) inhibitor, reduced the absorption rates of gastrodin from perfused rat intestines. Sodium 24-30 solute carrier family 1 member 2 Rattus norvegicus 41-44 23608658-0 2013 Effect of contrasted sodium diets on the pharmacokinetics and pharmacodynamic effects of renin-angiotensin system blockers. Sodium 21-27 renin Homo sapiens 89-94 23608658-1 2013 Dietary sodium, the main determinant of the pharmacodynamic response to renin-angiotensin system blockade, influences the pharmacokinetics of various cardiovascular drugs. Sodium 8-14 renin Homo sapiens 72-77 23486205-4 2013 Here we show that acute exposure of primary wild-type spinal cord cultures to conditioned medium derived from astrocytes expressing mutant SOD1 (ACM-hSOD1(G93A)) increases persistent sodium inward currents (PC(Na)), repetitive firing, and intracellular calcium transients, leading to specific motoneuron death days later. Sodium 183-189 superoxide dismutase 1 Homo sapiens 139-143 23486205-4 2013 Here we show that acute exposure of primary wild-type spinal cord cultures to conditioned medium derived from astrocytes expressing mutant SOD1 (ACM-hSOD1(G93A)) increases persistent sodium inward currents (PC(Na)), repetitive firing, and intracellular calcium transients, leading to specific motoneuron death days later. Sodium 183-189 superoxide dismutase 1 Homo sapiens 149-154 23874689-0 2013 Delphinidin-3-glucoside protects against oxidized low-density lipoprotein-induced mitochondrial dysfunction in vascular endothelial cells via the sodium-dependent glucose transporter SGLT1. Sodium 146-152 solute carrier family 5 member 1 Homo sapiens 183-188 23874689-5 2013 Furthermore, in vitro and in vivo data showed that Dp was transported into endothelial cells in a temperature, concentration, and time-dependent manner via the sodium-dependent glucose transporter (SGLT1). Sodium 160-166 solute carrier family 5 member 1 Homo sapiens 198-203 23913386-1 2013 The renin-angiotensin-aldosterone system plays a key role in regulating blood pressure by maintaining vascular tone and the water/sodium balance. Sodium 130-136 renin Homo sapiens 4-9 23739961-8 2013 Using RNA interference, we observed that loss of Pum2 leads to increased sodium current (I(Na)) and action potential firing, mimicking the response by these neurons to being deprived of synaptic depolarization. Sodium 73-79 pumilio RNA binding family member 2 Homo sapiens 49-53 23548411-0 2013 Renin-angiotensin system blockers may create more risk than reward for sodium-depleted cardiovascular patients with high plasma renin levels. Sodium 71-77 renin Homo sapiens 0-5 23548411-0 2013 Renin-angiotensin system blockers may create more risk than reward for sodium-depleted cardiovascular patients with high plasma renin levels. Sodium 71-77 renin Homo sapiens 128-133 23548411-5 2013 RESULTS: We showed (i) that PRA levels are usually medium to low in treated cardiovascular patients, but are sometimes abnormally high, (ii) that excessive sodium depletion can induce such high PRA levels, (iii) that the higher PRA patients exhibited evidence of sodium depletion: lower blood pressures, more frequent natriuretic drug usage, lower N-terminal pro b-type natriuretic peptide (NT-proBNP), and higher blood urea nitrogen and uric acid levels, with similar usage of renin-angiotensin blocking drugs. Sodium 156-162 renin Homo sapiens 478-483 23486012-7 2013 Glucose increased AQP11 protein expression in wild-type kidney and upregulation of AQP11 expression by glucose in vitro was prevented by phlorizin, an inhibitor of sodium-dependent glucose transport across PT. Sodium 164-170 aquaporin 11 Mus musculus 83-88 23443727-7 2013 Conversely, the VWF rs2239153 C variant was associated with increased salt sensitivity, conferring larger DBP and MAP reductions during low-sodium intervention (P = 1.22x10(-4) and 4.44x10(-5), respectively). Sodium 140-146 von Willebrand factor Homo sapiens 16-19 23590941-2 2013 Among them, the Slo1 and C. elegans SLO-2 channels are gated by calcium (Ca ( 2+) ), while mammalian Slo2 channels are activated by both sodium (Na (+) ) and chloride (Cl (-) ). Sodium 137-143 Ion_trans_2 domain-containing protein Caenorhabditis elegans 36-41 23370527-0 2013 Role of the EGF receptor in PPARgamma-mediated sodium and water transport in human proximal tubule cells. Sodium 47-53 epidermal growth factor receptor Homo sapiens 12-24 23370527-0 2013 Role of the EGF receptor in PPARgamma-mediated sodium and water transport in human proximal tubule cells. Sodium 47-53 peroxisome proliferator activated receptor gamma Homo sapiens 28-37 23370527-1 2013 AIM/HYPOTHESIS: This study aimed to determine the interaction between the EGF receptor (EGFR) and peroxisome proliferator-activated receptor gamma (PPARgamma) and the role of EGFR in sodium and water transport in the proximal tubule. Sodium 183-189 epidermal growth factor receptor Homo sapiens 175-179 23370527-14 2013 CONCLUSIONS/INTERPRETATION: Our data suggest that EGFR activation mediates PPARgamma-induced sodium and water reabsorption via upregulation of NHE3 and AQP1 channels in the proximal tubule. Sodium 93-99 epidermal growth factor receptor Homo sapiens 50-54 23370527-14 2013 CONCLUSIONS/INTERPRETATION: Our data suggest that EGFR activation mediates PPARgamma-induced sodium and water reabsorption via upregulation of NHE3 and AQP1 channels in the proximal tubule. Sodium 93-99 peroxisome proliferator activated receptor gamma Homo sapiens 75-84 23418736-2 2013 Once internalized, it is metabolized by glutamine synthetase to glutamine and released to the synaptic space through sodium-dependent neutral amino acid carriers of the N System (SNAT3/slc38a3/SN1, SNAT5/slc38a5/SN2). Sodium 117-123 glutamate-ammonia ligase Homo sapiens 40-60 23532834-3 2013 The subject of this study was a search for vasopressin and vasotocin analogues with selective effects on renal water, sodium and potassium excretion. Sodium 118-124 arginine vasopressin Rattus norvegicus 43-54 23352982-7 2013 The equations generated here and the DBP product could help producers achieve acceptable purge while reducing sodium use. Sodium 110-116 D-box binding PAR bZIP transcription factor Homo sapiens 37-40 23270855-1 2013 Opioid mechanisms are involved in the control of water and NaCl intake and opioid receptors (ORs) are present in the central nucleus of the amygdala (CeA), a site of important facilitatory mechanisms related to the control of sodium appetite. Sodium 226-232 carcinoembryonic antigen gene family 4 Rattus norvegicus 150-153 23463656-9 2013 CONCLUSION: The results indicate that although GLP-1 markedly reduces proximal tubule sodium reabsorption, the acute effects on GFR and RPF are very limited in healthy humans. Sodium 86-92 glucagon Homo sapiens 47-52 23344470-6 2013 These beneficial effects of sodium depletion were associated with a decrease in renal inflammation (macrophage infiltration, IL-6, TNF-alpha) and oxidative stress (NADPH oxidase activity), and a prevention of histologic changes in retroperitoneal fat induced by high fructose. Sodium 28-34 interleukin 6 Rattus norvegicus 125-129 23344470-6 2013 These beneficial effects of sodium depletion were associated with a decrease in renal inflammation (macrophage infiltration, IL-6, TNF-alpha) and oxidative stress (NADPH oxidase activity), and a prevention of histologic changes in retroperitoneal fat induced by high fructose. Sodium 28-34 tumor necrosis factor Rattus norvegicus 131-140 26105897-14 2013 Angiotensin II promotes sodium retention at the proximal tubule independently of aldosterone. Sodium 24-30 angiotensinogen Homo sapiens 0-14 23522043-3 2013 In C. elegans, the loss of either NLF-1 or NCA leads to a reduced sodium leak current, and a hyperpolarized resting membrane potential in premotor interneurons. Sodium 66-72 NCA Localization Factor Caenorhabditis elegans 34-39 23418736-2 2013 Once internalized, it is metabolized by glutamine synthetase to glutamine and released to the synaptic space through sodium-dependent neutral amino acid carriers of the N System (SNAT3/slc38a3/SN1, SNAT5/slc38a5/SN2). Sodium 117-123 solute carrier family 38 member 3 Homo sapiens 179-184 23418736-2 2013 Once internalized, it is metabolized by glutamine synthetase to glutamine and released to the synaptic space through sodium-dependent neutral amino acid carriers of the N System (SNAT3/slc38a3/SN1, SNAT5/slc38a5/SN2). Sodium 117-123 solute carrier family 38 member 3 Homo sapiens 185-192 23418736-2 2013 Once internalized, it is metabolized by glutamine synthetase to glutamine and released to the synaptic space through sodium-dependent neutral amino acid carriers of the N System (SNAT3/slc38a3/SN1, SNAT5/slc38a5/SN2). Sodium 117-123 solute carrier family 38 member 3 Homo sapiens 193-196 23418736-2 2013 Once internalized, it is metabolized by glutamine synthetase to glutamine and released to the synaptic space through sodium-dependent neutral amino acid carriers of the N System (SNAT3/slc38a3/SN1, SNAT5/slc38a5/SN2). Sodium 117-123 solute carrier family 38 member 5 Homo sapiens 198-203 23418736-2 2013 Once internalized, it is metabolized by glutamine synthetase to glutamine and released to the synaptic space through sodium-dependent neutral amino acid carriers of the N System (SNAT3/slc38a3/SN1, SNAT5/slc38a5/SN2). Sodium 117-123 solute carrier family 38 member 5 Homo sapiens 204-211 23454174-5 2013 Nociceptin has been implicated in many physiological functions including, nociception, locomotion, stressed-induced analgesia, learning and memory, neurotransmitter and hormone release, renal function, neuronal differentiation, sexual and reproductive behavior, uterine contraction, feeding, anxiety, gastrointestinal motility, cardiovascular function, micturition, cough, hypoxic-ischemic brain injury, diuresis and sodium balance, temperature regulation, vestibular function, and mucosal transport. Sodium 417-423 prepronociceptin Homo sapiens 0-10 23595759-2 2013 BACE1, which is elevated in AD patients and APP transgenic mice, also cleaves the beta2-subunit of voltage-gated sodium channels (Navbeta2). Sodium 113-119 beta-secretase 1 Homo sapiens 0-5 23427083-8 2013 Twenty-four hour urinary sodium excretion was decreased by day 7 with proximal tubule-dominant transfer of AT(1a)R/GFP alone (P < 0.01) or with AT(1a)R/GFP and ECFP/ANG II cotransfer (P < 0.01). Sodium 25-31 angiotensin II receptor, type 1a Mus musculus 107-112 23427083-8 2013 Twenty-four hour urinary sodium excretion was decreased by day 7 with proximal tubule-dominant transfer of AT(1a)R/GFP alone (P < 0.01) or with AT(1a)R/GFP and ECFP/ANG II cotransfer (P < 0.01). Sodium 25-31 angiotensin II receptor, type 1a Mus musculus 147-152 23427083-8 2013 Twenty-four hour urinary sodium excretion was decreased by day 7 with proximal tubule-dominant transfer of AT(1a)R/GFP alone (P < 0.01) or with AT(1a)R/GFP and ECFP/ANG II cotransfer (P < 0.01). Sodium 25-31 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 168-174 23575826-2 2013 Here, we show that Angiotensin II (AngII), a major mediator of body fluid and sodium homeostasis, modulates salty and sweet taste sensitivities, and that this modulation critically influences ingestive behaviors in mice. Sodium 78-84 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 19-33 23575826-2 2013 Here, we show that Angiotensin II (AngII), a major mediator of body fluid and sodium homeostasis, modulates salty and sweet taste sensitivities, and that this modulation critically influences ingestive behaviors in mice. Sodium 78-84 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 35-40 23575826-9 2013 The specific reduction of amiloride-sensitive salt taste sensitivity by AngII may contribute to increased sodium intake. Sodium 106-112 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 72-77 23575826-11 2013 The linkage between salty and sweet preferences via AngII signaling may optimize sodium and calorie intakes. Sodium 81-87 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 52-57 23467203-9 2013 Urine AGT and angiotensin II (Ang II) excretion were higher in KL and K mice than in L or wild-type mice on a normal-sodium diet and increased with high sodium intake. Sodium 153-159 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 6-9 23467203-9 2013 Urine AGT and angiotensin II (Ang II) excretion were higher in KL and K mice than in L or wild-type mice on a normal-sodium diet and increased with high sodium intake. Sodium 153-159 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 30-36 23467203-10 2013 During high sodium intake, urine AGT and Ang II were higher in all transgenic mice vs wild-type mice. Sodium 12-18 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 33-36 23467203-10 2013 During high sodium intake, urine AGT and Ang II were higher in all transgenic mice vs wild-type mice. Sodium 12-18 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 41-47 23467203-12 2013 Systemic AGT may stimulate endogenous renal AGT synthesis during high sodium intake, leading to hypertension in L mice. Sodium 70-76 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 9-12 23467203-12 2013 Systemic AGT may stimulate endogenous renal AGT synthesis during high sodium intake, leading to hypertension in L mice. Sodium 70-76 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 44-47 23270855-9 2013 Thus stimulating mu-ORs in the CeA increases hypertonic sodium intake, whereas antagonizing these sites inhibits hypertonic sodium intake. Sodium 56-62 carcinoembryonic antigen gene family 4 Rattus norvegicus 31-34 23270855-10 2013 Together, our results implicate mu-ORs in the CeA in a positive regulation of sodium intake. Sodium 78-84 carcinoembryonic antigen gene family 4 Rattus norvegicus 46-49 23254305-7 2013 RESULTS: During high sodium the hemopexin activity was lower; 1.6 x 10 (0.6 x 10 - 4.7 x 10) versus 2.8 x 10 (1.1 x 10 - 5.1 x 10) arbitrary units (P < 0.01) and the pressor response to 3 ng ang II/kg per minute larger than during low sodium (17.6 +- 6.5 versus 14.6 +- 6.9 mmHg, P < 0.01). Sodium 21-27 hemopexin Homo sapiens 32-41 23254305-7 2013 RESULTS: During high sodium the hemopexin activity was lower; 1.6 x 10 (0.6 x 10 - 4.7 x 10) versus 2.8 x 10 (1.1 x 10 - 5.1 x 10) arbitrary units (P < 0.01) and the pressor response to 3 ng ang II/kg per minute larger than during low sodium (17.6 +- 6.5 versus 14.6 +- 6.9 mmHg, P < 0.01). Sodium 238-244 hemopexin Homo sapiens 32-41 23254305-8 2013 Hemopexin activity negatively correlated with the pressor response to ang II during either type of sodium intake (high sodium: r = 0.42, P < 0.05; low sodium: r = 0.35, P < 0.05). Sodium 99-105 hemopexin Homo sapiens 0-9 23254305-8 2013 Hemopexin activity negatively correlated with the pressor response to ang II during either type of sodium intake (high sodium: r = 0.42, P < 0.05; low sodium: r = 0.35, P < 0.05). Sodium 119-125 hemopexin Homo sapiens 0-9 23254305-8 2013 Hemopexin activity negatively correlated with the pressor response to ang II during either type of sodium intake (high sodium: r = 0.42, P < 0.05; low sodium: r = 0.35, P < 0.05). Sodium 119-125 hemopexin Homo sapiens 0-9 23002791-6 2013 A low-sodium diet increased kidney renin and liver angiotensinogen mRNA levels but not lung angiotensin-converting enzyme mRNA expression. Sodium 6-12 renin Rattus norvegicus 35-40 23283344-5 2013 Exposure to QX-314 and capsaicin induces in small DRG neurons a robust sodium current block within 30 s. In sciatic nerves, application of extracellular QX-314 with capsaicin persistently reduces C-fiber but not A-fiber compound action potentials and this effect does not occur in TRPV1(-/-) mice. Sodium 71-77 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 281-286 23397215-3 2013 The characteristic low-renin, salt-sensitive hypertension of blacks is consistent with the kidney reabsorbing additional sodium (Na), which leads to an expanded plasma volume that drives the BP. Sodium 121-127 renin Homo sapiens 23-28 24216674-2 2013 AIM: To evaluate the potential role of intradialytic sodium gradient (NaG) on blood pressure values and IDHyper during HD. Sodium 53-59 sodium voltage-gated channel alpha subunit 7 Homo sapiens 70-73 22372527-8 2013 Furthermore, ET(A) receptors may have a favourable effect on sodium excretion and reducing renal damage in females. Sodium 62-68 endothelin receptor type A Homo sapiens 13-18 23238424-4 2013 We found that embryonic motoneurons with a genetic loss of the low-threshold sodium channel NaV1.9 show fewer fluctuations in intracellular calcium in axonal compartments and growth cones than wild-type littermates. Sodium 77-83 sodium voltage-gated channel alpha subunit 11 Homo sapiens 92-98 23059770-0 2013 Common variation in with no-lysine kinase 1 (WNK1) and blood pressure responses to dietary sodium or potassium interventions- family-based association study. Sodium 91-97 WNK lysine deficient protein kinase 1 Homo sapiens 45-49 23059770-7 2013 CONCLUSIONS: The WNK1 gene might be mechanistically involved in the variation in BP response to dietary sodium and potassium intake among individuals, and might contribute to the variation of this complex phenotype. Sodium 104-110 WNK lysine deficient protein kinase 1 Homo sapiens 17-21 23257389-6 2013 Whole-cell patch clamp recordings of the transfected cells revealed that the sodium currents were significantly reduced by the SCN3B mutation. Sodium 77-83 sodium voltage-gated channel beta subunit 3 Homo sapiens 127-132 23257389-7 2013 CONCLUSIONS: The Val110Ile mutation of SCN3B is a relatively common cause of SCN5A-negative BrS in Japan, which has a reduced sodium current because of the loss of cell surface expression of Nav1.5. Sodium 126-132 sodium voltage-gated channel beta subunit 3 Homo sapiens 39-44 23104093-6 2013 The insulin receptor has also been shown to perform an important role in the distal regions of the renal tubules, regulating sodium excretion and blood pressure control here. Sodium 125-131 insulin receptor Homo sapiens 4-20 23615125-0 2013 The effect of sodium restricted diet on plasma visfatin levels in hypertensive patients with visceral obesity. Sodium 14-20 nicotinamide phosphoribosyltransferase Homo sapiens 47-55 23615125-2 2013 The aim of the present study was the assessment of the effect of dietary sodium restriction with RAA system activation on visfatin level in hypertensive and normotensive patients with visceral obesity. Sodium 73-79 nicotinamide phosphoribosyltransferase Homo sapiens 122-130 24281140-2 2013 Lack of JAK3 triggers inflammatory bowel disease, which in turn has been shown to affect intestinal activity of the epithelial Na(+) channel ENaC and thus colonic sodium absorption. Sodium 163-169 Janus kinase 3 Mus musculus 8-12 23383067-4 2013 NALCN channels with alternative calcium, (EEEE) and sodium, (EKEE or EEKE) -selective pores are conserved in simple bilaterally symmetrical animals like flatworms to non-chordate deuterostomes. Sodium 52-58 sodium leak channel, non-selective Homo sapiens 0-5 23108657-2 2012 The sodium-proton-exchanger subtype 3 (NHE3) is an important mediator of sodium absorption in the gut. Sodium 4-10 solute carrier family 9 member A3 Rattus norvegicus 39-43 23108657-5 2012 In spontaneously hypertensive rats-lean, inhibition of intestinal NHE3 by SAR increased feces sodium excretion and reduced urinary sodium excretion, whereas absolute sodium balance and serum sodium concentration were not changed. Sodium 94-100 solute carrier family 9 member A3 Rattus norvegicus 66-70 23108657-5 2012 In spontaneously hypertensive rats-lean, inhibition of intestinal NHE3 by SAR increased feces sodium excretion and reduced urinary sodium excretion, whereas absolute sodium balance and serum sodium concentration were not changed. Sodium 131-137 solute carrier family 9 member A3 Rattus norvegicus 66-70 23108657-5 2012 In spontaneously hypertensive rats-lean, inhibition of intestinal NHE3 by SAR increased feces sodium excretion and reduced urinary sodium excretion, whereas absolute sodium balance and serum sodium concentration were not changed. Sodium 131-137 solute carrier family 9 member A3 Rattus norvegicus 66-70 23108657-5 2012 In spontaneously hypertensive rats-lean, inhibition of intestinal NHE3 by SAR increased feces sodium excretion and reduced urinary sodium excretion, whereas absolute sodium balance and serum sodium concentration were not changed. Sodium 131-137 solute carrier family 9 member A3 Rattus norvegicus 66-70 22885233-1 2012 The present study investigated the effects of a microinjection of GABA(A) receptor agonist (muscimol) and antagonist (bicuculline) into the central nucleus of the amygdala (CeA) in sodium-depleted rats. Sodium 181-187 carcinoembryonic antigen gene family 4 Rattus norvegicus 173-176 22885233-5 2012 The inhibitory effect of muscimol (0.20 nmol) on the sodium and water intake could be blocked by pretreatment with bicuculline intra-CeA microinjection (0.4 nmol). Sodium 53-59 carcinoembryonic antigen gene family 4 Rattus norvegicus 133-136 22798424-0 2012 Identification of SPLUNC1"s ENaC-inhibitory domain yields novel strategies to treat sodium hyperabsorption in cystic fibrosis airways. Sodium 84-90 BPI fold containing family A member 1 Homo sapiens 18-25 23442378-3 2013 NALCN"s most distinctive feature is that that it possesses a highly adaptable pore with a calcium-like EEEE selectivity filter in radially symmetrical animals and a more sodium-like EEKE or EKEE selectivity filter in bilaterally symmetrical animals including vertebrates. Sodium 170-176 sodium leak channel, non-selective Homo sapiens 0-5 23442378-4 2013 Two lineages of animals evolved alternative calcium-like EEEE and sodium-like EEKE / EKEE pores, spliced to regulate NALCN functions in differing cellular environments, such as muscle (heart and skeletal) and secretory tissue (brain and glands), respectively. Sodium 66-72 sodium leak channel, non-selective Homo sapiens 117-122 23442378-8 2013 We propose that NALCN serves as a variable sensor that responds to calcium or sodium ion flux, depending on whether the total cellular current density is generated more from calcium-selective or sodium-selective channels. Sodium 78-84 sodium leak channel, non-selective Homo sapiens 16-21 22987869-8 2012 Adjusted odds ratios comparing risk for pre-HBP/HPB among subjects in the highest versus lowest sodium intake quartile were 2.0 (95% CI: 0.95-4.1, P = .062) overall and 3.5 (95% CI: 1.3-9.2, P = .013) among those overweight/obese. Sodium 96-102 heme binding protein 1 Homo sapiens 44-47 22398203-13 2013 A marked increase in COX-2 indicates that it may be an important factor in reducing renal handling of sodium and water in response to PUUO. Sodium 102-108 cytochrome c oxidase II, mitochondrial Rattus norvegicus 21-26 23360655-0 2013 Effect of overexpressing nhaA and nhaR on sodium tolerance and lactate production in Escherichia coli. Sodium 42-48 Na(+):H(+) antiporter NhaA Escherichia coli str. K-12 substr. MG1655 25-29 23451068-4 2013 Sodium-dependent fructose uptake disappeared in renal brush border membrane vesicles from SGLT5-deficient mice, and the increased urinary fructose in SGLT5-deficient mice indicated that SGLT5 was the major fructose reabsorption transporter in the kidney. Sodium 0-6 solute carrier family 5 (sodium/glucose cotransporter), member 10 Mus musculus 90-95 23382806-8 2013 These sodium current increases were unaffected by acyclovir pre-treatment but were abolished by exposure to Tetrodotoxin (TTX) which blocks the TTX-sensitive fast Nav 1.6 and Nav 1.7 channels but not the TTX-resistant slow Nav 1.8 channel. Sodium 6-12 neuron navigator 1 Homo sapiens 163-168 23015756-4 2012 Here we assess comprehensively the ESCRT-III interactions of the MIT-domain family member MITD1 and identify strong interactions with charged multivesicular body protein 1B (CHMP1B), CHMP2A, and increased sodium tolerance-1 (IST1). Sodium 205-211 microtubule interacting and trafficking domain containing 1 Homo sapiens 90-95 23015756-4 2012 Here we assess comprehensively the ESCRT-III interactions of the MIT-domain family member MITD1 and identify strong interactions with charged multivesicular body protein 1B (CHMP1B), CHMP2A, and increased sodium tolerance-1 (IST1). Sodium 205-211 IST1 factor associated with ESCRT-III Homo sapiens 225-229 22885233-8 2012 These results suggest that GABA(A) receptors within the CeA may be involved in mediating the sodium intake in the sodium-depleted rat, and the cNTS, iNTS and LPBN were probably involved in this mechanism. Sodium 93-99 carcinoembryonic antigen gene family 4 Rattus norvegicus 56-59 23720263-4 2012 The classic RAS can be defined as the ACE-Ang II-AT1R axis that promotes vasoconstriction, water intake, sodium retention, and other mechanisms to maintain blood pressure, as well as increase oxidative stress, fibrosis, cellular growth, and inflammation in pathological conditions. Sodium 105-111 angiogenin Homo sapiens 42-45 23720263-4 2012 The classic RAS can be defined as the ACE-Ang II-AT1R axis that promotes vasoconstriction, water intake, sodium retention, and other mechanisms to maintain blood pressure, as well as increase oxidative stress, fibrosis, cellular growth, and inflammation in pathological conditions. Sodium 105-111 angiotensin II receptor type 1 Homo sapiens 49-53 22575762-5 2012 Cells cotransduced with Tbx5, Mef2c, Myocd expressed cardiac contractile proteins, had cardiac-like potassium and sodium currents and action potentials could be elicited. Sodium 114-120 T-box 5 Mus musculus 24-28 22708976-1 2012 We evaluated whether changes in expression and activity of the three sodium/calcium exchanger isoforms, NCX1, NCX2, and NCX3 occurred in PC12 cells when the extracellular-signal-regulated kinases 1/2 (ERK1/2), c-Jun N-terminal kinases (JNK), and p38 mitogen-activated protein kinases (MAPKs) were silenced, pharmacologically blocked, or activated with nerve growth factor (NGF). Sodium 69-75 mitogen activated protein kinase 3 Rattus norvegicus 201-207 22987869-9 2012 Sodium intake and weight status appeared to have synergistic effects on risk for pre-HBP/HPB (relative excess risk for interaction = 0.29 (95% CI: 0.01-0.90, P < .05). Sodium 0-6 heme binding protein 1 Homo sapiens 85-88 22987869-10 2012 CONCLUSIONS: Sodium intake is positively associated with SBP and risk for pre-HBP/HPB among US children and adolescents, and this association may be stronger among those who are overweight/obese. Sodium 13-19 heme binding protein 1 Homo sapiens 78-81 22594923-4 2012 The chloride-oxalate exchanger slc26a6 (also known as CFEX or PAT-1), located in the renal proximal tubule, was originally thought to have an important role in sodium homeostasis and thereby blood pressure control, but it has recently been shown to have a key function in oxalate balance by mediating oxalate secretion in the gut. Sodium 160-166 solute carrier family 26, member 6 Mus musculus 31-38 22594923-4 2012 The chloride-oxalate exchanger slc26a6 (also known as CFEX or PAT-1), located in the renal proximal tubule, was originally thought to have an important role in sodium homeostasis and thereby blood pressure control, but it has recently been shown to have a key function in oxalate balance by mediating oxalate secretion in the gut. Sodium 160-166 solute carrier family 26, member 6 Mus musculus 54-58 22594923-4 2012 The chloride-oxalate exchanger slc26a6 (also known as CFEX or PAT-1), located in the renal proximal tubule, was originally thought to have an important role in sodium homeostasis and thereby blood pressure control, but it has recently been shown to have a key function in oxalate balance by mediating oxalate secretion in the gut. Sodium 160-166 solute carrier family 26, member 6 Mus musculus 62-67 22674027-6 2012 In rats on normal-salt chow, the stimulation of renal medullary ET(B) receptor by ET(B) receptor agonist sarafotoxin 6c (S6c) causes an increase in water (3.6 +- 0.4 from baseline vs. 10.5 +- 1.3 mul/min following S6c infusion; P < 0.05) and sodium excretion (0.38 +- 0.06 vs. 1.23 +- 0.17 mumol/min; P < 0.05). Sodium 245-251 endothelin receptor type B Rattus norvegicus 64-69 22674027-6 2012 In rats on normal-salt chow, the stimulation of renal medullary ET(B) receptor by ET(B) receptor agonist sarafotoxin 6c (S6c) causes an increase in water (3.6 +- 0.4 from baseline vs. 10.5 +- 1.3 mul/min following S6c infusion; P < 0.05) and sodium excretion (0.38 +- 0.06 vs. 1.23 +- 0.17 mumol/min; P < 0.05). Sodium 245-251 endothelin receptor type B Rattus norvegicus 82-87 22674027-9 2012 Receptor binding assays determined that the sodium-depleted diet resulted in a similar level of ET(B) receptor binding in renal inner medulla compared with rats on a normal-salt diet. Sodium 44-50 endothelin receptor type B Rattus norvegicus 96-101 22674027-11 2012 We conclude that endogenous ANG II attenuates renal medullary ET(B) receptor function to conserve sodium during salt deprivation independently of receptor expression. Sodium 98-104 endothelin receptor type B Rattus norvegicus 62-67 22791335-0 2012 Kidney-specific WNK1 inhibits sodium reabsorption in the cortical thick ascending limb. Sodium 30-36 WNK lysine deficient protein kinase 1 Mus musculus 16-20 22732308-2 2012 Detection of pheromones or other emitted signaling molecules occurs in the dendritic microvilli of vomeronasal sensory neurons, where the binding of molecules to vomeronasal receptors leads to the influx of sodium and calcium ions mainly through the transient receptor potential canonical 2 (TRPC2) channel. Sodium 207-213 transient receptor potential cation channel, subfamily C, member 2 Mus musculus 250-290 22732308-2 2012 Detection of pheromones or other emitted signaling molecules occurs in the dendritic microvilli of vomeronasal sensory neurons, where the binding of molecules to vomeronasal receptors leads to the influx of sodium and calcium ions mainly through the transient receptor potential canonical 2 (TRPC2) channel. Sodium 207-213 transient receptor potential cation channel, subfamily C, member 2 Mus musculus 292-297 22418981-6 2012 Cox regression modeling found that higher baseline dietary sodium and the ratio of sodium to calorie or potassium were each independently associated with greater all-cause mortality. Sodium 59-65 cytochrome c oxidase subunit 8A Homo sapiens 0-3 22418981-6 2012 Cox regression modeling found that higher baseline dietary sodium and the ratio of sodium to calorie or potassium were each independently associated with greater all-cause mortality. Sodium 83-89 cytochrome c oxidase subunit 8A Homo sapiens 0-3 22671585-8 2012 In kidney proximal tubules, claudin-2, claudin-10, and claudin-17 allow for paracellular reabsorption of sodium, chloride, and water. Sodium 105-111 claudin 17 Homo sapiens 55-65 21167014-4 2012 Preclinical studies with the GLP-1R agonists GLP-1, exenatide, or liraglutide provided evidence that GLP-1R stimulation favorably affects endothelial function, sodium excretion, recovery from ischemic injury, and myocardial function in animals. Sodium 160-166 glucagon like peptide 1 receptor Homo sapiens 101-107 22504846-10 2012 CONCLUSIONS: These results indicate that the renal AT(2) receptor, via nitric oxide/cGMP/Sp1 pathway, regulates AT(1 )receptor expression and function, which may be important in the regulation of sodium excretion and blood pressure. Sodium 196-202 angiotensin II receptor, type 2 Mus musculus 51-65 22366186-1 2012 Regulation of intracellular pH (pHi) and protection against cytosolic acidification is primarily a function of the ubiquitous plasma membrane Na+/H+exchanger-1 (NHE1), which uses a highly conserved process to transfer cytosolic hydrogen ions (H+) across plasma membranes in exchange for extracellular sodium ions (Na+). Sodium 301-307 glucose-6-phosphate isomerase Homo sapiens 32-35 22358497-8 2012 These results indicate that ERbeta regulates the expression of NHE3 in the proximal colon of pregnant mice through estrogen action, suggesting the involvement of increased sodium absorption by up-regulated NHE3 in constipation during pregnancy. Sodium 172-178 estrogen receptor 2 (beta) Mus musculus 28-34 21603903-11 2012 The sodium restriction group achieved significantly more reduction in SBP (-11.1 mmHg vs. -5.0 mmHg, P = 0.022), DBP (-9.4 mmHg vs. -2.1 mmHg, P = 0.009), and urine protein excretion [-465 (-855 to -340) mg/day vs. -150 (-570 to 40) mg/day, P = 0.024]. Sodium 4-10 selenium binding protein 1 Homo sapiens 70-73 21603903-12 2012 A positive correlation was observed between the change of 24-h UNa and the change of SBP (r = 0.450, P = 0.047) in the sodium restriction group. Sodium 119-125 selenium binding protein 1 Homo sapiens 85-88 22082831-10 2012 We reason that the loss of sodium-sparing bicarbonate reabsorption by SLC4A5 initiates a regulatory cascade consisting of compensatory bicarbonate reabsorption via other sodium-bicarbonate transporters (e.g. SLC4A7) at the expense of an increased sodium uptake. Sodium 170-176 solute carrier family 4 member 7 Homo sapiens 208-214 22212718-5 2012 SGLT-5 mediates sodium-dependent [(14)C]-alpha-methyl-D-glucose (AMG) transport that can be inhibited by mannose, fructose, glucose, and galactose. Sodium 16-22 amelogenin X-linked Homo sapiens 65-68 22158645-7 2012 In addition, AT(2)R stimulation significantly increased sodium and water excretion to a similar extent in males and females (P(Group)=0.05 and 0.005). Sodium 56-62 angiotensin II receptor, type 2 Rattus norvegicus 13-19 22383044-1 2012 The present work was initiated to investigate regulation of the taurine transporter TauT by reactive oxygen species (ROS) and the tonicity-responsive enhancer binding protein (TonEBP) in NIH3T3 mouse fibroblasts during acute and long-term (4 h) exposure to low-sodium/hypo-osmotic stress. Sodium 261-267 solute carrier family 6 (neurotransmitter transporter, taurine), member 6 Mus musculus 84-88 21968275-6 2012 Indeed, recent evidence indicates that MBG, via interaction with alpha1 isoforms of the sodium pump, can activate various intracellular signaling pathways at physiological concentrations too low to notably inhibit pump activity. Sodium 88-94 ATPase H+ transporting V0 subunit a1 Homo sapiens 65-71 21466573-0 2012 Proteinuric diseases with sodium retention: Is plasmin the link? Sodium 26-32 plasminogen Homo sapiens 47-54 22080858-5 2012 In contrast, COX-2 influences on sodium excretion were contingent on the prevailing RAS activity. Sodium 33-39 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 13-18 22927777-7 2012 Frequency of MIF -173 CC genotype was significantly higher in patients (p<0.05), and sodium levels were higher in patients with MIF -173 CC genotype. Sodium 88-94 macrophage migration inhibitory factor Homo sapiens 131-134 22496969-5 2012 Univariate regressions showed that changes in urinary sodium/potassium ratio (beta = 1.99) and plasma renin activity (beta = -15.78) and percent change in plasma nitrite after hyperemia were associated with SBP changes at week one (all P < 0.05). Sodium 54-60 selenium binding protein 1 Homo sapiens 207-210 22037285-0 2011 L-pGlu-(2-propyl)-L-His-L-ProNH2 attenuates 4-aminopyridine-induced epileptiform activity and sodium current: a possible action of new thyrotropin-releasing hormone analog for its anticonvulsant potential. Sodium 94-100 thyrotropin releasing hormone Homo sapiens 135-164 22105349-4 2011 We provide evidence that cortactin-cofilin binding is regulated by local pH changes at invadopodia that are mediated by the sodium-hydrogen exchanger NHE1. Sodium 124-130 cofilin 1 Homo sapiens 35-42 22071811-6 2011 MAIN RESULTS: A total of 167 studies were included in this 2011 update.The effect of sodium reduction in normotensive Caucasians was SBP -1.27 mmHg (95% CI: -1.88, -0.66; p=0.0001), DBP -0.05 mmHg (95% CI: -0.51, 0.42; p=0.85). Sodium 85-91 high mobility group box 1 Homo sapiens 133-139 22071811-7 2011 The effect of sodium reduction in normotensive Blacks was SBP -4.02 mmHg (95% CI:-7.37, -0.68; p=0.002), DBP -2.01 mmHg (95% CI:-4.37, 0.35; p=0.09). Sodium 14-20 selenium binding protein 1 Homo sapiens 58-61 22071811-8 2011 The effect of sodium reduction in normotensive Asians was SBP -1.27 mmHg (95% CI: -3.07, 0.54; p=0.17), DBP -1.68 mmHg (95% CI:-3.29, -0.06; p=0.04). Sodium 14-20 selenium binding protein 1 Homo sapiens 58-61 22071811-9 2011 The effect of sodium reduction in hypertensive Caucasians was SBP -5.48 mmHg (95% CI: -6.53, -4.43; p<0.00001), DBP -2.75 mmHg (95% CI: -3.34, -2.17; p<0.00001). Sodium 14-20 selenium binding protein 1 Homo sapiens 62-65 22071811-10 2011 The effect of sodium reduction in hypertensive Blacks was SBP -6.44 mmHg (95% CI:-8.85, -4.03; p=0.00001), DBP -2.40 mmHg (95% CI:-4.68, -0.12; p=0.04). Sodium 14-20 selenium binding protein 1 Homo sapiens 58-61 21865262-5 2011 Human NaDC3 was stably expressed as proven by immunochemical methods and by sodium-dependent uptake of succinate (K(0.5) for sodium activation, 44.6 mM; Hill coefficient, 2.1; K(m) for succinate, 18 muM). Sodium 125-131 solute carrier family 13 member 3 Homo sapiens 6-11 21956643-1 2011 Ghrelin, a peptide hormone from the stomach, has been recently discovered to reduce sodium excretion from the kidney. Sodium 84-90 ghrelin Mus musculus 0-7 21956643-9 2011 The location in the straight parts of the distal tubules accords with observations that ghrelin promotes sodium retention. Sodium 105-111 ghrelin Mus musculus 88-95 21784787-5 2011 We found that ghrelin attenuated saline intake stimulated by angiotensin II, by water deprivation followed by partial rehydration and by dietary sodium deficiency. Sodium 145-151 ghrelin and obestatin prepropeptide Rattus norvegicus 14-21 21796099-5 2011 Electrophysiological recordings in Xenopus oocytes injected with HCN2 cRNA found that potassium was transported better than ammonium, each of which was transported significantly better than sodium, criteria that are compatible with a role for HCN2 in ammonium transport. Sodium 190-196 hyperpolarization activated cyclic nucleotide gated potassium and sodium channel 2 Rattus norvegicus 65-69 21814178-2 2011 As the Na/H exchanger-3 (NHE3) mediates the bulk of apical sodium transport and a significant fraction of oxygen consumption in the proximal tubule, we examined mechanisms by which ischemia-reperfusion affects the expression of NHE3. Sodium 59-65 solute carrier family 9 member A3 Rattus norvegicus 7-23 21814178-2 2011 As the Na/H exchanger-3 (NHE3) mediates the bulk of apical sodium transport and a significant fraction of oxygen consumption in the proximal tubule, we examined mechanisms by which ischemia-reperfusion affects the expression of NHE3. Sodium 59-65 solute carrier family 9 member A3 Rattus norvegicus 25-29 21670672-8 2011 SUMMARY: The discovery of serine protease-mediated activation of renal ENaC in physiological and pathophysiological conditions opens the way for new understanding of the pathogenesis of proteinuric sodium retention, which may involve plasmin and present several potential new drug targets. Sodium 198-204 plasminogen Homo sapiens 234-241 21633357-6 2011 The intrarenal infusion of PD128907 (1 mug kg(-1) min(-1)) that increased sodium excretion also increased the co-immunoprecipitations of D(3)/Galpha(12) and D(3)/Galpha(13) in renal BBMs; their co-immunoprecipitation was confirmed in RPT cells. Sodium 74-80 G protein subunit alpha 12 Rattus norvegicus 142-152 21633357-8 2011 We conclude that a D(3) receptor interaction with Galpha(12)/Galpha(13) that increases sodium excretion may have a role in the regulation of blood pressure. Sodium 87-93 G protein subunit alpha 12 Rattus norvegicus 50-60 21697807-10 2011 Thus, PKCalpha and PKCbetaII, GSK3alpha and GSK3beta, and cAMP-dependent signaling pathways may have important roles in regulating proximal tubular sodium and fluid transport in Ang II-induced hypertensive rats. Sodium 148-154 glycogen synthase kinase 3 alpha Rattus norvegicus 30-39 21697807-10 2011 Thus, PKCalpha and PKCbetaII, GSK3alpha and GSK3beta, and cAMP-dependent signaling pathways may have important roles in regulating proximal tubular sodium and fluid transport in Ang II-induced hypertensive rats. Sodium 148-154 glycogen synthase kinase 3 beta Rattus norvegicus 44-52 21866161-5 2011 The BASS2 protein is localized at the chloroplast envelope membrane, and is highly abundant in C(4) plants that have the sodium-dependent pyruvate transporter. Sodium 121-127 Sodium Bile acid symporter family Arabidopsis thaliana 4-9 21866161-6 2011 Recombinant BASS2 shows sodium-dependent pyruvate uptake activity. Sodium 24-30 Sodium Bile acid symporter family Arabidopsis thaliana 12-17 21866161-7 2011 Sodium influx is balanced by a sodium:proton antiporter (NHD1), which was mimicked in recombinant Escherichia coli cells expressing both BASS2 and NHD1. Sodium 0-6 Sodium Bile acid symporter family Arabidopsis thaliana 137-142 21866161-7 2011 Sodium influx is balanced by a sodium:proton antiporter (NHD1), which was mimicked in recombinant Escherichia coli cells expressing both BASS2 and NHD1. Sodium 31-37 Sodium Bile acid symporter family Arabidopsis thaliana 137-142 21866161-10 2011 Orthologues of BASS2 can be detected in all the genomes of land plants that have been characterized so far, thus indicating the widespread importance of sodium-coupled pyruvate import into plastids. Sodium 153-159 Sodium Bile acid symporter family Arabidopsis thaliana 15-20 21642665-0 2011 Combined immunotherapy with low-dose IL-2 plus IFN-alpha for metastatic renal cell carcinoma: survival benefit for selected patients with lung metastasis and serum sodium level. Sodium 164-170 interferon alpha 2 Homo sapiens 47-56 21636648-2 2011 Sodium-driven and proton-driven motors have the stator proteins PomA and PomB or MotA and MotB, respectively, which interact with each other in their transmembrane (TM) regions to form an ion channel. Sodium 0-6 FRAS1 related extracellular matrix 1 Homo sapiens 81-85 21746918-3 2011 Genome-wide microarrays in sodium-deficient mice or after ACTH infusion showed up-regulation of hypothalamic genes, including dopamine- and cAMP-regulated neuronal phosphoprotein 32 kDa (DARPP-32), dopamine receptors-1 and -2, alpha-2C- adrenoceptor, and striatally enriched protein tyrosine phosphatase (STEP). Sodium 27-33 pro-opiomelanocortin-alpha Mus musculus 58-62 21389090-10 2011 The downregulation of NHE3 and NCC may contribute to the BP-attenuating effect of dietary potassium associated with increased urinary sodium excretion. Sodium 134-140 solute carrier family 9 member A3 Rattus norvegicus 22-26 21389090-10 2011 The downregulation of NHE3 and NCC may contribute to the BP-attenuating effect of dietary potassium associated with increased urinary sodium excretion. Sodium 134-140 solute carrier family 12 member 3 Rattus norvegicus 31-34 21396420-4 2011 This process is sodium-dependent and it is not prevented by glutamate receptor antagonists such as MK-801, DNQX or AIDA nor mimicked by glutamatergic agonists like kainate, NMDA or trans-ACPD. Sodium 16-22 homer scaffold protein 2 Homo sapiens 187-191 21358416-12 2011 It explains why Ang II acts at levels far below K(D), why AT1R blockers are effective in hypertension even when [Ang II] is low, and why the constrictor action of Ang II appears so much suppressed by sodium depletion. Sodium 200-206 angiotensin II receptor type 1 Homo sapiens 58-62 21189402-12 2011 In conclusion, the AT2R modulates pressure-natriuresis, allowing the same level of sodium to be excreted at a lower pressure in both genders. Sodium 83-89 angiotensin II receptor, type 2 Rattus norvegicus 19-23 20927043-8 2011 Angiotensin II inhibited ROMK channels in the cortical collecting duct of rats on a low sodium diet, an effect blocked by protein tyrosine kinase inhibition. Sodium 88-94 potassium inwardly rectifying channel subfamily J member 1 Homo sapiens 25-29 21143427-4 2011 The absorption of salt (sodium and chloride) in the small intestine is predominantly mediated via the chloride/base exchangers DRA (Down Regulated in Adenoma) (SLC26A3) and PAT1 (Putative Anion Transporter 1) (SLC26A6), and the Na(+) /H(+) exchanger NHE3 (Sodium Hydrogen Exchanger3) (SLC9A3). Sodium 24-30 solute carrier family 26, member 6 Mus musculus 173-177 21143427-4 2011 The absorption of salt (sodium and chloride) in the small intestine is predominantly mediated via the chloride/base exchangers DRA (Down Regulated in Adenoma) (SLC26A3) and PAT1 (Putative Anion Transporter 1) (SLC26A6), and the Na(+) /H(+) exchanger NHE3 (Sodium Hydrogen Exchanger3) (SLC9A3). Sodium 24-30 solute carrier family 26, member 6 Mus musculus 179-207 20943769-2 2011 Renal dopamine D1 (D1R) and angiotensin II AT1 (AT1R) receptors maintain sodium homeostasis and BP. Sodium 73-79 angiotensin II receptor, type 1a Rattus norvegicus 48-52 21997255-7 2011 RESULTS: Significant correlations were found between HAp erosion and the concentration of phosphorus in unstimulated saliva (r = 0.40, p = 0.03) and between HAp erosion and the concentration of sodium (r = -0.40, p = 0.03), chloride (r = -0.47, p = 0.01), phosphorus (r = 0.45, p = 0.01) and flow (r = -0.39, p = 0.04) of stimulated saliva. Sodium 194-200 reticulon 3 Homo sapiens 157-160 21997255-8 2011 Multivariate analysis revealed a significant role in the HAp erosion for sodium, urea, total protein, albumin, pH and flow of unstimulated saliva and for sodium, potassium, urea, and phosphorus of stimulated saliva. Sodium 73-79 reticulon 3 Homo sapiens 57-60 22016812-10 2011 Furthermore, increasing sodium intake was associated with elevated medullary 20-HETE (5.6+-.8 in NS vs. 14.3+-3.7 pg/mg in HS), an effect that was completely abolished by renal medullary ET-B receptor blockade (4.9+-.8 for NS and 4.5+-.6 pg/mg for HS). Sodium 24-30 endothelin receptor type B Rattus norvegicus 187-191 21113090-1 2010 A method for quantifying the tissue sodium concentration (TSC) in the rat brain from 23Na-MR images was developed. Sodium 36-42 solute carrier family 12 member 3 Rattus norvegicus 58-61 20807796-2 2010 We assessed the role of AT1 and AT2 receptors, NAD(P)H oxidase and protein kinase C (PKC) in Ang II-induced sodium and water excretion and their capacity to stimulate antioxidant enzymes in the rat hypothalamus, a brain structure known to express a high density of AngII receptors. Sodium 108-114 angiotensin II receptor, type 1a Rattus norvegicus 24-27 20807796-2 2010 We assessed the role of AT1 and AT2 receptors, NAD(P)H oxidase and protein kinase C (PKC) in Ang II-induced sodium and water excretion and their capacity to stimulate antioxidant enzymes in the rat hypothalamus, a brain structure known to express a high density of AngII receptors. Sodium 108-114 angiotensin II receptor, type 2 Rattus norvegicus 32-35 21105923-0 2010 Type-B response regulators ARR1 and ARR12 regulate expression of AtHKT1;1 and accumulation of sodium in Arabidopsis shoots. Sodium 94-100 response regulator 12 Arabidopsis thaliana 36-41 21168641-8 2010 The Cox regression for survival time showed that patients with low serum sodium values (group B) had: Child-Pugh scores with 1.13% plus risk of death for each point; cold ischemia time with 1.001% less risk of death for each minute; glycemia with 0.6% for each mg/dL; 0.66% use of cell-saver; plus a risk of death for each 100 mL plus 1.02% risk of death for each year of donor age. Sodium 73-79 cytochrome c oxidase subunit 8A Homo sapiens 4-7 20849418-4 2010 In this study, we investigated the interaction between calpain 7 and a newly reported ESCRT-III family member, increased sodium tolerance-1 (IST1), which possesses two different types of MIT-interacting motifs (MIM1 and MIM2). Sodium 121-127 calpain 7 Homo sapiens 55-64 20849418-4 2010 In this study, we investigated the interaction between calpain 7 and a newly reported ESCRT-III family member, increased sodium tolerance-1 (IST1), which possesses two different types of MIT-interacting motifs (MIM1 and MIM2). Sodium 121-127 IST1 factor associated with ESCRT-III Homo sapiens 141-145 21433378-0 2010 Discovery of a small molecule inhibitor of ROMK and Kir7.1 The specific aim of this project is to identify small molecule inhibitors of Renal Outer Medullary Potassium Channel (ROMK, Kir1.1, KCNJ1), a potassium channel located in the renal tubule, where it critically regulates sodium and potassium balance. Sodium 278-284 potassium inwardly rectifying channel subfamily J member 1 Homo sapiens 43-47 21433378-0 2010 Discovery of a small molecule inhibitor of ROMK and Kir7.1 The specific aim of this project is to identify small molecule inhibitors of Renal Outer Medullary Potassium Channel (ROMK, Kir1.1, KCNJ1), a potassium channel located in the renal tubule, where it critically regulates sodium and potassium balance. Sodium 278-284 potassium inwardly rectifying channel subfamily J member 1 Homo sapiens 177-181 21433378-0 2010 Discovery of a small molecule inhibitor of ROMK and Kir7.1 The specific aim of this project is to identify small molecule inhibitors of Renal Outer Medullary Potassium Channel (ROMK, Kir1.1, KCNJ1), a potassium channel located in the renal tubule, where it critically regulates sodium and potassium balance. Sodium 278-284 potassium inwardly rectifying channel subfamily J member 1 Homo sapiens 183-189 21433378-0 2010 Discovery of a small molecule inhibitor of ROMK and Kir7.1 The specific aim of this project is to identify small molecule inhibitors of Renal Outer Medullary Potassium Channel (ROMK, Kir1.1, KCNJ1), a potassium channel located in the renal tubule, where it critically regulates sodium and potassium balance. Sodium 278-284 potassium inwardly rectifying channel subfamily J member 1 Homo sapiens 191-196 21433391-0 2010 Discovery of a small molecule inhibitor of ROMK with unprecedented selectivity The specific aim of this project is to identify small molecule inhibitors of Renal Outer Medullary Potassium Channel (ROMK, Kir1.1, KCNJ1), a potassium channel located in the renal tubule, where it critically regulates sodium and potassium balance. Sodium 298-304 potassium inwardly rectifying channel subfamily J member 1 Homo sapiens 43-47 21433391-0 2010 Discovery of a small molecule inhibitor of ROMK with unprecedented selectivity The specific aim of this project is to identify small molecule inhibitors of Renal Outer Medullary Potassium Channel (ROMK, Kir1.1, KCNJ1), a potassium channel located in the renal tubule, where it critically regulates sodium and potassium balance. Sodium 298-304 potassium inwardly rectifying channel subfamily J member 1 Homo sapiens 197-201 21433391-0 2010 Discovery of a small molecule inhibitor of ROMK with unprecedented selectivity The specific aim of this project is to identify small molecule inhibitors of Renal Outer Medullary Potassium Channel (ROMK, Kir1.1, KCNJ1), a potassium channel located in the renal tubule, where it critically regulates sodium and potassium balance. Sodium 298-304 potassium inwardly rectifying channel subfamily J member 1 Homo sapiens 203-209 21433391-0 2010 Discovery of a small molecule inhibitor of ROMK with unprecedented selectivity The specific aim of this project is to identify small molecule inhibitors of Renal Outer Medullary Potassium Channel (ROMK, Kir1.1, KCNJ1), a potassium channel located in the renal tubule, where it critically regulates sodium and potassium balance. Sodium 298-304 potassium inwardly rectifying channel subfamily J member 1 Homo sapiens 211-216 20921400-4 2010 By inactivating KS-WNK1 in mice, we show here that this isoform is an important regulator of sodium transport. Sodium 93-99 WNK lysine deficient protein kinase 1 Mus musculus 19-23 20921400-5 2010 KS-WNK1(-/-) mice display an increased activity of the Na-Cl cotransporter NCC, expressed specifically in the distal convoluted tubule, where it participates in the fine tuning of sodium reabsorption. Sodium 180-186 WNK lysine deficient protein kinase 1 Mus musculus 3-7 20932306-0 2010 Effect of neutrophil elastase and its inhibitor EPI-hNE4 on transepithelial sodium transport across normal and cystic fibrosis human nasal epithelial cells. Sodium 76-82 elastase, neutrophil expressed Homo sapiens 10-29 22891322-0 2012 Deletion of claudin-10 (Cldn10) in the thick ascending limb impairs paracellular sodium permeability and leads to hypermagnesemia and nephrocalcinosis. Sodium 81-87 claudin 10 Mus musculus 12-22 22891322-0 2012 Deletion of claudin-10 (Cldn10) in the thick ascending limb impairs paracellular sodium permeability and leads to hypermagnesemia and nephrocalcinosis. Sodium 81-87 claudin 10 Mus musculus 24-30 22891322-6 2012 We show that claudin-10 determines paracellular sodium permeability, and that its loss leads to hypermagnesemia and nephrocalcinosis. Sodium 48-54 claudin 10 Mus musculus 13-23 22891322-7 2012 In isolated perfused TAL tubules of claudin-10-deficient mice, paracellular permeability of sodium is decreased, and the relative permeability of calcium and magnesium is increased. Sodium 92-98 claudin 10 Mus musculus 36-46 23331097-4 2013 We hypothesized that NOS1 splice variant expression and NO production in the inner medullary collecting duct (IMCD) are regulated differently in mice and rats by high dietary sodium. Sodium 175-181 nitric oxide synthase 1, neuronal Mus musculus 21-25 23129822-2 2013 However, it is not clear whether a low-sodium diet has beneficial effects on the development of interstitial fibrosis because it activates the renin-angiotensin-aldosterone system. Sodium 39-45 renin Rattus norvegicus 143-148 23129822-7 2013 In the acute experiment, the increases in expression of osteopontin, MCP-1, alpha-SMA, TGF-beta and collagen III were significantly reduced by dietary sodium restriction. Sodium 151-157 secreted phosphoprotein 1 Rattus norvegicus 56-67 22587908-7 2012 KEY FINDINGS: A high-sodium diet downregulated AQP-1 and AQP-2 expression levels in the proximal tubule and collecting duct, respectively. Sodium 21-27 aquaporin 1 Rattus norvegicus 47-52 20616716-1 2010 PURPOSE OF REVIEW: We integrate recent evidence that demonstrates the importance of the gastric (HKalpha1) and nongastric (HKalpha2)-containing hydrogen potassium adenosine triphosphatases (H,K-ATPases) on physiological function and their role in potassium (K), sodium (Na), and acid-base balance. Sodium 262-268 ATPase, H+/K+ transporting, nongastric, alpha polypeptide Mus musculus 123-131 22592638-1 2012 High sodium intake is known to regulate the renal renin-angiotensin system (RAS) and is a risk factor for the pathogenesis of obesity-related hypertension. Sodium 5-11 renin Rattus norvegicus 50-55 23195681-0 2013 Kidney-specific WNK1 regulates sodium reabsorption and potassium secretion in mouse cortical collecting duct. Sodium 31-37 WNK lysine deficient protein kinase 1 Mus musculus 16-20 20711351-4 2010 Remarkably, the presence of a sodium ion at this allosteric site induces a conformational change of the rotamer toggle switch Trp6.48 which locks in a conformation identical to the one found in the partially inactive state of the crystallized human beta(2) adrenergic receptor. Sodium 30-36 transient receptor potential cation channel subfamily C member 6 Homo sapiens 126-130 23255591-6 2013 Plasma renin and angiotensin (1-7) were highest in the rats on the low-sodium diet and depressed in the rats on a high-sodium diet. Sodium 71-77 renin Rattus norvegicus 7-12 23255591-6 2013 Plasma renin and angiotensin (1-7) were highest in the rats on the low-sodium diet and depressed in the rats on a high-sodium diet. Sodium 119-125 renin Rattus norvegicus 7-12 22913624-0 2013 Endogenous angiotensin II-induced p44/42 mitogen-activated protein kinase activation mediates sodium appetite but not thirst or neurohypophysial secretion in male rats. Sodium 94-100 mitogen activated protein kinase 3 Rattus norvegicus 34-37 22913624-3 2013 In the brain, AngII binds to the angiotensin type 1 receptor (AT1R) to stimulate thirst, sodium appetite and both arginine vasopressin (AVP) and oxytocin (OT) secretion. Sodium 89-95 angiotensin II receptor, type 1a Rattus norvegicus 33-60 20333436-0 2010 Potassium and sodium transport in non-animal cells: the Trk/Ktr/HKT transporter family. Sodium 14-20 neurotrophic receptor tyrosine kinase 1 Homo sapiens 56-59 22913624-3 2013 In the brain, AngII binds to the angiotensin type 1 receptor (AT1R) to stimulate thirst, sodium appetite and both arginine vasopressin (AVP) and oxytocin (OT) secretion. Sodium 89-95 angiotensin II receptor, type 1a Rattus norvegicus 62-66 22913624-10 2013 Taken together, these results indicate that p44/42 MAPK is required for AngII-induced sodium appetite but not thirst or neurohypophysial secretion. Sodium 86-92 mitogen activated protein kinase 3 Rattus norvegicus 44-47 22913624-11 2013 This result may allow for the discovery of more specific downstream targets of p44/42 MAPK to curb sodium appetite, known to exacerbate hypertension, at the same time as leaving thirst and neurohypophysial hormone secretion undisturbed. Sodium 99-105 mitogen activated protein kinase 3 Rattus norvegicus 79-82 20728215-3 2010 Using a neuronal cell model (differentiated human IMR32 neuroblastoma cells), we demonstrate a central role for sodium entry via TRPC3/6 channels in receptor-mediated increases in intracellular calcium. Sodium 112-118 transient receptor potential cation channel subfamily C member 3 Homo sapiens 129-134 20505684-4 2010 These diverse spectrums of diseases compose a novel channelopathy, TRPV4-pathy, which could further include polygenic traits such as serum sodium concentration and a chronic obstructive pulmonary disease. Sodium 139-145 transient receptor potential cation channel subfamily V member 4 Homo sapiens 67-72 20459109-3 2010 At saturating concentrations, KIIIA incompletely blocks the sodium current of Na(V)1.2, leaving a 5% residual current (rI(Na)). Sodium 60-66 sodium voltage-gated channel alpha subunit 2 Rattus norvegicus 78-86 22833716-1 2012 The Scn7a gene encodes for the specific sodium channel Na(X), which is considered a primary determinant of sodium sensing in the brain. Sodium 40-46 sodium voltage-gated channel alpha subunit 7 Rattus norvegicus 4-9 22609249-2 2012 Classically, it binds to its intracellular mineralocorticoid receptor to induce expression of proteins influencing the reabsorption of sodium and water in the distal nephron. Sodium 135-141 nuclear receptor subfamily 3 group C member 2 Homo sapiens 43-69 22753890-4 2012 TRPML3 can be activated or rather de-inhibited by exposing it first to sodium-free extracellular solution and subsequently to high extracellular sodium. Sodium 71-77 mucolipin TRP cation channel 3 Homo sapiens 0-6 22753890-4 2012 TRPML3 can be activated or rather de-inhibited by exposing it first to sodium-free extracellular solution and subsequently to high extracellular sodium. Sodium 145-151 mucolipin TRP cation channel 3 Homo sapiens 0-6 22753890-6 2012 Furthermore, it was found that TRPML3 is constitutively active in low or no sodium-containing extracellular solution. Sodium 76-82 mucolipin TRP cation channel 3 Homo sapiens 31-37 22753890-8 2012 Here, we present mutagenesis data generated based on the hypothesis that negatively charged amino acids in the extracellular loops of TRPML3 may interfere with the observed sodium inhibition. Sodium 173-179 mucolipin TRP cation channel 3 Homo sapiens 134-140 22753890-9 2012 We systematically mutated negatively charged amino acids in the first and second extracellular loops and found that mutating Glu-361 in the second loop has a significant impact on the sodium-mediated block of TRPML3. Sodium 184-190 mucolipin TRP cation channel 3 Homo sapiens 209-215 22753890-10 2012 We further demonstrate that the TRPML3-related cation channel TRPML2 is also activated by lowering the extracellular sodium concentration as well as by a subset of small chemical compounds that were previously identified as activators of TRPML3, thus confirming the functional activity of TRPML2 at the plasma membrane and suggesting similar gating mechanisms for both TRPML channels. Sodium 117-123 mucolipin TRP cation channel 3 Homo sapiens 32-38 22753890-10 2012 We further demonstrate that the TRPML3-related cation channel TRPML2 is also activated by lowering the extracellular sodium concentration as well as by a subset of small chemical compounds that were previously identified as activators of TRPML3, thus confirming the functional activity of TRPML2 at the plasma membrane and suggesting similar gating mechanisms for both TRPML channels. Sodium 117-123 mucolipin TRP cation channel 2 Homo sapiens 62-68 22753890-10 2012 We further demonstrate that the TRPML3-related cation channel TRPML2 is also activated by lowering the extracellular sodium concentration as well as by a subset of small chemical compounds that were previously identified as activators of TRPML3, thus confirming the functional activity of TRPML2 at the plasma membrane and suggesting similar gating mechanisms for both TRPML channels. Sodium 117-123 mucolipin TRP cation channel 3 Homo sapiens 238-244 22753890-10 2012 We further demonstrate that the TRPML3-related cation channel TRPML2 is also activated by lowering the extracellular sodium concentration as well as by a subset of small chemical compounds that were previously identified as activators of TRPML3, thus confirming the functional activity of TRPML2 at the plasma membrane and suggesting similar gating mechanisms for both TRPML channels. Sodium 117-123 mucolipin TRP cation channel 2 Homo sapiens 289-295 21630263-8 2012 Functional activity of Na(V) 1.6 channels in the plasma membrane of CaC cells was confirmed by whole-cell patch-clamp experiments using Cn2, a Na(V) 1.6-specific toxin, which blocked ~30% of the total sodium current. Sodium 201-207 neuron navigator 1 Homo sapiens 23-30 22129970-4 2012 Expression of a dominant negative (DN) form of Rab11a or Rab11b significantly reduced the basal and cAMP-stimulated ENaC-dependent sodium (Na(+)) transport. Sodium 131-137 RAB11B, member RAS oncogene family Mus musculus 57-63 19617399-0 2010 AMPK agonists ameliorate sodium and fluid transport and inflammation in cystic fibrosis airway epithelial cells. Sodium 25-31 protein kinase AMP-activated catalytic subunit alpha 2 Homo sapiens 0-4 19617399-7 2010 These findings suggest that novel therapies to activate AMPK in the CF airway may be beneficial by blunting excessive sodium and ASL absorption and by reducing excessive airway inflammation, which are major contributors to CF lung disease. Sodium 118-124 protein kinase AMP-activated catalytic subunit alpha 2 Homo sapiens 56-60 20517693-10 2010 Our data evidenced an increase in Na(V)1.5 channels and the involvement of beta subunits in the regulation of sodium current and fiber excitability. Sodium 110-116 sodium voltage-gated channel alpha subunit 5 Rattus norvegicus 34-42 20014428-2 2010 Extracellular sodium depletion or coincubation with the OATP/Oatp inhibitors rifampicin and digoxin revealed that about 35% of active CGamF accumulation was mediated by Ntcp/NTCP in rat and human hepatocytes, while the contribution of this sodium-dependent transporter reached 50-60% in dog and pig hepatocytes. Sodium 14-20 solute carrier family 10 member 1 Rattus norvegicus 169-173 20014428-2 2010 Extracellular sodium depletion or coincubation with the OATP/Oatp inhibitors rifampicin and digoxin revealed that about 35% of active CGamF accumulation was mediated by Ntcp/NTCP in rat and human hepatocytes, while the contribution of this sodium-dependent transporter reached 50-60% in dog and pig hepatocytes. Sodium 240-246 solute carrier family 10 member 1 Rattus norvegicus 169-173 20204400-0 2010 Biophysical characterisation of the persistent sodium current of the Nav1.6 neuronal sodium channel: a single-channel analysis. Sodium 47-53 neuron navigator 1 Homo sapiens 69-73 20349193-3 2010 The present experiments explored whether AMPK participates in the regulation of tubuloglomerular feedback (TGF) and renal tubular sodium handling. Sodium 130-136 protein kinase AMP-activated catalytic subunit alpha 1 Rattus norvegicus 41-45 20088904-6 2010 To understand the mechanism of enhanced salt and drought resistance of the AtABCG36 overexpressing plants, we measured sodium contents and found that AtABCG36 overexpressing plants were lower in sodium content than the wild-type. Sodium 119-125 ABC-2 and Plant PDR ABC-type transporter family protein Arabidopsis thaliana 75-83 20088904-6 2010 To understand the mechanism of enhanced salt and drought resistance of the AtABCG36 overexpressing plants, we measured sodium contents and found that AtABCG36 overexpressing plants were lower in sodium content than the wild-type. Sodium 195-201 ABC-2 and Plant PDR ABC-type transporter family protein Arabidopsis thaliana 75-83 20088904-6 2010 To understand the mechanism of enhanced salt and drought resistance of the AtABCG36 overexpressing plants, we measured sodium contents and found that AtABCG36 overexpressing plants were lower in sodium content than the wild-type. Sodium 195-201 ABC-2 and Plant PDR ABC-type transporter family protein Arabidopsis thaliana 150-158 20088904-7 2010 Our data suggest that AtABCG36 contributes to drought and salt resistance in Arabidopsis by a mechanism that includes reduction of sodium content in plants. Sodium 131-137 ABC-2 and Plant PDR ABC-type transporter family protein Arabidopsis thaliana 22-30 20104189-9 2010 At the tubular level, Ang II significantly reduced urinary volume (-84%) and urinary sodium excretion (-65%) (P < 0.01). Sodium 85-91 angiogenin Homo sapiens 22-25 22538947-3 2012 Recent studies have provided strong evidence that the sodium-phosphate cotransporter NaPi-IIb is responsible for sodium-dependent phosphate absorption by the small intestine, and this protein might link changes in dietary phosphate to altered renal phosphate excretion in order to maintain the phosphate balance. Sodium 54-60 solute carrier family 34 member 2 Homo sapiens 85-93 22082831-10 2012 We reason that the loss of sodium-sparing bicarbonate reabsorption by SLC4A5 initiates a regulatory cascade consisting of compensatory bicarbonate reabsorption via other sodium-bicarbonate transporters (e.g. SLC4A7) at the expense of an increased sodium uptake. Sodium 27-33 solute carrier family 4 member 7 Homo sapiens 208-214 22180603-0 2012 Connexin43 regulates sodium current; ankyrin-G modulates gap junctions: the intercalated disc exchanger. Sodium 21-27 gap junction protein alpha 1 Homo sapiens 0-10 22025386-8 2012 Spread of sodium to neighboring cells was disturbed on pharmacological inhibition of gap junctions, reduced in animals at P4 and virtually omitted in Cx30/Cx43 double-deficient mice. Sodium 10-16 gap junction protein, beta 6 Mus musculus 150-154 22025386-10 2012 Cx30/Cx43-mediated sodium diffusion between astrocytes could represent a signal indicating increased metabolic needs, independent of concomitant calcium signaling. Sodium 19-25 gap junction protein, beta 6 Mus musculus 0-4 22068710-6 2012 The effect of sodium reduction in: (i) Normotensives: Caucasians: systolic BP (SBP) -1.27 mm Hg (95% confidence interval (CI): -1.88, -0.66; P = 0.0001), diastolic BP (DBP) -0.05 mm Hg (95% CI: -0.51, 0.42; P = 0.85). Sodium 14-20 high mobility group box 1 Homo sapiens 66-86 23077628-7 2012 The reduction in sodium excretion was associated with up-regulations in the renal gene expression of NHE3 and Na(+)/K(+) ATPase alpha and beta subunits in the kidney cortex of the uni-x compared to the sham animals (P<0.05). Sodium 17-23 sodium/hydrogen exchanger 3 Ovis aries 101-105 22384007-13 2012 On multivariate analysis, BNP reduction correlated with sodium levels and weight reduction (R = 0.8, p<0.001). Sodium 56-62 natriuretic peptide B Homo sapiens 26-29 22384007-15 2012 BNP levels were significantly reduced due to negative water and sodium balance. Sodium 64-70 natriuretic peptide B Homo sapiens 0-3 21204798-6 2011 Currently, four genes are identified to be involved in myotonia: the muscle voltage-gated sodium and chloride channel genes SCN4A and CLCN1, the myotonic dystrophy protein kinase (DMPK) gene, and the CCHC-type zinc finger, nucleic acid binding protein gene CNBP. Sodium 90-96 CCHC-type zinc finger nucleic acid binding protein Homo sapiens 257-261 21855134-5 2011 KS1 and its poly(2-hydroxyethyl methacrylate)-co-poly(acrylamide) (PHEMA-co-PAM) thin films show high selectivity for K(+) over competing sodium ions (Na(+)) at physiological concentrations. Sodium 138-144 zinc finger protein 382 Homo sapiens 0-3 21753145-2 2011 Given the close relationship between renal sodium handling and blood pressure regulation, we hypothesized that modulating the action of ANG II specifically in the renal proximal tubules would alter the chronic level of blood pressure. Sodium 43-49 angiogenin, ribonuclease, RNase A family, 5 Mus musculus 136-139 21873888-12 2011 Studies are needed to determine whether CYP4A11 T8590C genotype predicts responses to medications that affect sodium homeostasis in hypertensive individuals. Sodium 110-116 cytochrome P450 family 4 subfamily A member 11 Homo sapiens 40-47 19909794-1 2010 The lateral parabrachial nucleus (LPBN) and the central nucleus of the amygdala (CeA) are important areas for the control of sodium appetite. Sodium 125-131 carcinoembryonic antigen gene family 4 Rattus norvegicus 81-84 19925636-1 2010 The mineralocorticoid receptor (MR) and its ligand aldosterone regulate renal sodium reabsorption and blood pressure and much knowledge has been accumulated in MR physiopathology, cellular and molecular targets. Sodium 78-84 nuclear receptor subfamily 3 group C member 2 Homo sapiens 4-30 19925636-1 2010 The mineralocorticoid receptor (MR) and its ligand aldosterone regulate renal sodium reabsorption and blood pressure and much knowledge has been accumulated in MR physiopathology, cellular and molecular targets. Sodium 78-84 nuclear receptor subfamily 3 group C member 2 Homo sapiens 32-34 20006571-11 2010 These results provide evidence for an endogenous TTX-sensitive sodium current in HEK293 cells that is associated primarily with the expression of the Na(v)1.7 sodium channel isoform. Sodium 63-69 immunoglobulin lambda variable 2-23 Homo sapiens 150-158 22028644-2 2011 Events in the development of reperfusion injury begin with the restoration of a proton gradient upon reperfusion, which then allows the sodium-proton exchanger (NHE) to increase flux, removing protons from the intracellular space while importing sodium. Sodium 136-142 solute carrier family 9 member C1 Homo sapiens 161-164 22028644-7 2011 In our simulations, when NHE inhibition is applied at the onset of reperfusion, increasing the degree of inhibition increases the peak sodium and calcium concentrations, as well as reducing intracellular pH recovery. Sodium 135-141 solute carrier family 9 member C1 Homo sapiens 25-28 22028644-10 2011 While NHE inhibition does indeed reduce sodium influx through that exchanger, the resulting prolongation of intracellular acidosis paradoxically increases sodium overload, largely mediated by impaired NaK function. Sodium 40-46 solute carrier family 9 member C1 Homo sapiens 6-9 21529330-11 2011 It is obligatory that future clinical studies on the effects of MR blockade on end-organ damage take into account the sodium status. Sodium 118-124 nuclear receptor subfamily 3 group C member 2 Homo sapiens 64-66 20078935-7 2009 RESULTS: Sodium selenite induced evident downregulation of COX IV protein in NB4 cells, while its mRNA level was almost unchanged. Sodium 9-15 cytochrome c oxidase subunit 4I1 Homo sapiens 59-65 19770404-7 2009 COX-2-derived prostaglandins in the renal medulla promote sodium excretion, and dopamine stimulates medullary prostaglandin production. Sodium 58-64 cytochrome c oxidase II, mitochondrial Mus musculus 0-5 21613418-10 2011 These results suggest that high sodium intake increases HCO(3)(-) absorptive capacity in the MTAL through 1) an adaptive increase in basolateral NHE1 activity that results secondarily in an increase in apical NHE3 activity; and 2) an adaptive increase in NHE3 activity, independent of NHE1 activity. Sodium 32-38 solute carrier family 9 member A3 Rattus norvegicus 209-213 21613418-10 2011 These results suggest that high sodium intake increases HCO(3)(-) absorptive capacity in the MTAL through 1) an adaptive increase in basolateral NHE1 activity that results secondarily in an increase in apical NHE3 activity; and 2) an adaptive increase in NHE3 activity, independent of NHE1 activity. Sodium 32-38 solute carrier family 9 member A3 Rattus norvegicus 255-259 21537151-12 2011 CONCLUSIONS: In salt-loaded rats, testosterone seems to activate the renin-angiotensin system, resulting in sodium retention, higher BP and renal injury. Sodium 108-114 renin Rattus norvegicus 69-74 21199648-3 2011 Recent work in rodents has also identified important effects of MSH"s, particularly gamma-MSH, on sodium metabolism and blood pressure regulation. Sodium 98-104 pro-opiomelanocortin-alpha Mus musculus 84-93 21199648-4 2011 Normal rats and mice respond to a high sodium diet with an increase in the plasma concentration of gamma-MSH, and remain normotensive, while those with genetic or pharmacologic gamma-MSH deficiency become hypertensive on a high sodium diet. Sodium 39-45 pro-opiomelanocortin-alpha Mus musculus 99-108 21199648-6 2011 Mice lacking the gamma-MSH receptor (the melanocortin 3 receptor, Mc3r) also become hypertensive on a high sodium diet but remain so when administered gamma-MSH, and infusions of physiologic levels of the peptide stimulate urinary sodium excretion in normal rats and mice, but not in mice with deletion of Mc3r. Sodium 107-113 pro-opiomelanocortin-alpha Mus musculus 17-26 21199648-6 2011 Mice lacking the gamma-MSH receptor (the melanocortin 3 receptor, Mc3r) also become hypertensive on a high sodium diet but remain so when administered gamma-MSH, and infusions of physiologic levels of the peptide stimulate urinary sodium excretion in normal rats and mice, but not in mice with deletion of Mc3r. Sodium 231-237 pro-opiomelanocortin-alpha Mus musculus 17-26 21573014-9 2011 We further focused on two genetic loci, SLC24A3 and SLC8A1 (plasma membrane sodium/calcium exchange proteins, NCKX3 and NCX1, respectively) with a functional relationship with the previous gene and associated to variations in systolic blood pressure (the imputed rs3790261, p = 4.55E-06; and rs434082, p = 4.7E-03). Sodium 76-82 solute carrier family 24 member 3 Homo sapiens 40-47 21464391-6 2011 Knockdown of Rac1 in native principal cells decreased ENaC-mediated sodium reabsorption and the number of channels at the apical plasma membrane. Sodium 68-74 Rac family small GTPase 1 Rattus norvegicus 13-17 19770404-9 2009 In DOCA/HS-treated COMT(-/-) mice, the COX-2 inhibitor SC-58236 reduced urinary sodium and prostaglandin E(2) excretion and increased systolic blood pressure (153+/-2 mm Hg). Sodium 80-86 cytochrome c oxidase II, mitochondrial Mus musculus 39-44 19635986-2 2009 Here we have investigated the effect of chronic ACTH infusion on renal sodium handling in adult male C57BL/6J mice using selective antagonists to dissect mineralocorticoid and glucocorticoid receptor-mediated pathways. Sodium 71-77 pro-opiomelanocortin-alpha Mus musculus 48-52 19635986-4 2009 ACTH caused an increase in blood pressure and a reduction in fractional sodium excretion associated with enhanced activity of the epithelial sodium channel. Sodium 72-78 pro-opiomelanocortin-alpha Mus musculus 0-4 19635986-6 2009 Dietary sodium depletion also prevented ACTH-induced hypertension. Sodium 8-14 pro-opiomelanocortin-alpha Mus musculus 40-44 19635986-9 2009 In summary, ACTH excess promotes renal sodium reabsorption, contributing to the increased blood pressure; both glucocorticoid and mineralocorticoid receptor pathways are involved. Sodium 39-45 pro-opiomelanocortin-alpha Mus musculus 12-16 19424768-4 2009 The resurgent sodium current that underlies the repeated firing of Purkinje cells is reduced in Scn8a mutant and knockout mice. Sodium 14-20 sodium channel, voltage-gated, type VIII, alpha Mus musculus 96-101 19477942-11 2009 Elucidation of regulatory mechanisms governing MR expression should lead to new strategies for the management of sodium waste in preterms and neonates. Sodium 113-119 nuclear receptor subfamily 3 group C member 2 Homo sapiens 47-49 21335042-1 2011 Gamma-Melanocyte Stimulating Hormone (Gamma-MSH) regulates sodium (Na(+)) balance and blood pressure through activation of the melanocortin receptor 3 (MC3-R). Sodium 59-65 pro-opiomelanocortin-alpha Mus musculus 0-36 21335042-1 2011 Gamma-Melanocyte Stimulating Hormone (Gamma-MSH) regulates sodium (Na(+)) balance and blood pressure through activation of the melanocortin receptor 3 (MC3-R). Sodium 59-65 pro-opiomelanocortin-alpha Mus musculus 38-47 21281609-5 2011 Co-injection of NKB suppressed the ANGII-induced sodium preference but did not affect the ANGII-induced water intake. Sodium 49-55 tachykinin precursor 3 Rattus norvegicus 16-19 21281609-10 2011 It is likely that the opposing effects of these two peptides on sodium preference can be explained by their differential actions in the CeA and BSTvl, both of which are inhibited by NKB and activated by ANGII. Sodium 64-70 tachykinin precursor 3 Rattus norvegicus 182-185 21440872-11 2011 CONCLUSIONS: Our data show that the combination of high diuretic dose and HSS infusion plus light restriction in dietary sodium intake determine a more rapid and significant hemodynamic stabilization through the improvement of echo-PCWP, BNP levels, and BIA parameters than the group treated without HSS. Sodium 121-127 natriuretic peptide B Homo sapiens 238-241 19460859-5 2009 This suggests that the up-regulation of the neuronal sodium current density by T(3) is not a direct effect but involves bFGF release and satellite cells. Sodium 53-59 fibroblast growth factor 2 Rattus norvegicus 120-124 19474389-10 2009 In conclusion, activation of ETB-R and ETA-R contributes to the enhanced and suppressed interaction between ERSNA and ARNA in conditions of HNa and LNa diet, respectively, suggesting a role for ET in the renal control of ERSNA that is dependent on dietary sodium. Sodium 256-262 endothelin receptor type B Rattus norvegicus 29-34 21328529-7 2011 These results suggest that Hynobius ENaCalpha plays an important role in the regulation of sodium transport in the external gills and pronephros of aquatic larvae, and in the skin and mesonephros of terrestrial adult. Sodium 91-97 sodium channel epithelial 1 subunit alpha Rattus norvegicus 36-45 19474389-10 2009 In conclusion, activation of ETB-R and ETA-R contributes to the enhanced and suppressed interaction between ERSNA and ARNA in conditions of HNa and LNa diet, respectively, suggesting a role for ET in the renal control of ERSNA that is dependent on dietary sodium. Sodium 256-262 endothelin receptor type A Rattus norvegicus 39-44 19429645-2 2009 Recent data in mice with genetic disruption of the gamma-melanocyte-stimulating hormone (gamma-MSH) system suggest that this system plays a role in the pathophysiological relationship between hypertension and altered glucose metabolism during ingestion of a high-sodium diet (8% NaCl, HSD). Sodium 263-269 pro-opiomelanocortin-alpha Mus musculus 51-87 19429645-2 2009 Recent data in mice with genetic disruption of the gamma-melanocyte-stimulating hormone (gamma-MSH) system suggest that this system plays a role in the pathophysiological relationship between hypertension and altered glucose metabolism during ingestion of a high-sodium diet (8% NaCl, HSD). Sodium 263-269 pro-opiomelanocortin-alpha Mus musculus 89-98 19502394-5 2009 Mutational analysis demonstrated that both MotX and MotY are critical for flagellar rotation of S. oneidensis MR-1 for both sodium- and proton-dependent stator systems but do not affect assembly of the flagellar filament. Sodium 124-130 sel1 repeat family protein Shewanella oneidensis MR-1 43-47 21282559-2 2011 Ang II activates renal Na(+)/H(+) exchanger 3 (NHE3) to increase sodium reabsorption, but the mechanisms are still elusive. Sodium 65-71 solute carrier family 9 member A3 Rattus norvegicus 23-45 21282559-2 2011 Ang II activates renal Na(+)/H(+) exchanger 3 (NHE3) to increase sodium reabsorption, but the mechanisms are still elusive. Sodium 65-71 solute carrier family 9 member A3 Rattus norvegicus 47-51 21282559-3 2011 In addition, the upregulation of AT(1)R during oxidative stress could promote sodium retention and lead to an increase in blood pressure. Sodium 78-84 angiotensin II receptor, type 1a Rattus norvegicus 33-39 21233144-2 2011 We previously showed that the acid-sensing ion channel 1 which, when activated under the acidotic tissue conditions found in inflammatory lesions opens to allow influx of sodium and calcium ions, contributes to axonal injury in experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis. Sodium 171-177 acid-sensing (proton-gated) ion channel 1 Mus musculus 30-56 19351654-0 2009 A C-terminal mutation of ATP1A3 underscores the crucial role of sodium affinity in the pathophysiology of rapid-onset dystonia-parkinsonism. Sodium 64-70 ATPase Na+/K+ transporting subunit alpha 3 Homo sapiens 25-31 19380724-1 2009 Hormonal control of transepithelial sodium (Na(+)) transport utilizes phosphatidylinositide 3"-kinase (PI3K) and Raf-MAPK/ERK kinase (MEK)-ERK-dependent signaling pathways, which impact numerous cell functions. Sodium 36-42 zinc fingers and homeoboxes 2 Homo sapiens 113-116 19388054-1 2009 Prostasin or human channel-activating protease 1 has been reported to play a critical role in the regulation of extracellular sodium ion transport via its activation of the epithelial cell sodium channel. Sodium 126-132 serine protease 8 Homo sapiens 0-9 19388054-1 2009 Prostasin or human channel-activating protease 1 has been reported to play a critical role in the regulation of extracellular sodium ion transport via its activation of the epithelial cell sodium channel. Sodium 126-132 serine protease 8 Homo sapiens 19-48 19471871-13 2009 The maximal sodium current decreased significantly in UT-B null mice (-8.80 +/- 0.92) nA vs that in wild-type mice ((-5.98 +/- 1.07) nA, P<0.05). Sodium 12-18 solute carrier family 14 (urea transporter), member 1 Mus musculus 54-58 19284629-12 2009 SCN2A, SCN3A and SCN9A gene products likely account for the tetrodotoxin-sensitive sodium currents in taste receptor cells. Sodium 83-89 sodium channel, voltage-gated, type II, alpha Mus musculus 0-5 19261867-2 2009 Sequencing of the positional candidate gene Scn8a encoding the sodium channel Na(v)1.6 identified a T>C transition in exon 1 resulting in the amino acid substitution p.S21P near the N terminus of the channel. Sodium 63-69 sodium channel, voltage-gated, type VIII, alpha Mus musculus 44-49 18795320-0 2009 Sodium-dependent activity of aquaporin-1 in rat glioma cells: a new mechanism of cell volume regulation. Sodium 0-6 aquaporin 1 Rattus norvegicus 29-40 21075848-1 2011 We tested whether ATP release through Connexin 30 (Cx30) is part of a local purinergic regulatory system intrinsic to the aldosterone-sensitive distal nephron (ASDN) important for proper control of sodium excretion; if changes in sodium intake influence ATP release via Cx30; and if this allows a normal ENaC response to changes in systemic sodium levels. Sodium 198-204 gap junction protein, beta 6 Mus musculus 38-49 21075848-1 2011 We tested whether ATP release through Connexin 30 (Cx30) is part of a local purinergic regulatory system intrinsic to the aldosterone-sensitive distal nephron (ASDN) important for proper control of sodium excretion; if changes in sodium intake influence ATP release via Cx30; and if this allows a normal ENaC response to changes in systemic sodium levels. Sodium 198-204 gap junction protein, beta 6 Mus musculus 51-55 21075848-3 2011 Urinary ATP levels in wild-type mice increase with sodium intake, being lower and less dependent on sodium intake in Cx30(-/-) mice. Sodium 100-106 gap junction protein, beta 6 Mus musculus 117-121 21075848-4 2011 Loss of inhibitory ATP regulation causes ENaC activity to be greater in Cx30(-/-) versus wild-type mice, particularly with high sodium intake. Sodium 128-134 gap junction protein, beta 6 Mus musculus 72-76 21075848-6 2011 Thus, loss of paracrine ATP feedback regulation of ENaC in Cx30(-/-) mice disrupts normal responses to changes in sodium intake. Sodium 114-120 gap junction protein, beta 6 Mus musculus 59-63 21075848-7 2011 Consequently, ENaC is hyperactive in Cx30(-/-) mice lowering sodium excretion particularly during increases in sodium intake. Sodium 61-67 gap junction protein, beta 6 Mus musculus 37-41 21075848-8 2011 Clamping mineralocorticoids high in Cx30(-/-) mice fed a high sodium diet causes a marked decline in renal sodium excretion. Sodium 62-68 gap junction protein, beta 6 Mus musculus 36-40 21075848-8 2011 Clamping mineralocorticoids high in Cx30(-/-) mice fed a high sodium diet causes a marked decline in renal sodium excretion. Sodium 107-113 gap junction protein, beta 6 Mus musculus 36-40 20955768-10 2011 We found that this toxin not only affects the inactivation of INaT but also increases the peak amplitude of the persistent sodium current (INaP). Sodium 123-129 NFKB inhibitor zeta Homo sapiens 139-143 21893993-11 2011 In a high-sodium diet, increased activation of ET(B)-R facilitates the interaction between RSNA and ARNA resulting in suppression of RSNA, via activation of the renorenal reflexes, to limit sodium retention. Sodium 10-16 endothelin receptor type B Rattus norvegicus 47-54 21893993-11 2011 In a high-sodium diet, increased activation of ET(B)-R facilitates the interaction between RSNA and ARNA resulting in suppression of RSNA, via activation of the renorenal reflexes, to limit sodium retention. Sodium 190-196 endothelin receptor type B Rattus norvegicus 47-54 21076398-2 2011 Cardiac glycosides increase the intracellular sodium concentration, which appears to inhibit the ATPase activity of the RNA sensor RIG-I, an essential and early component in the IFNbeta activation pathway. Sodium 46-52 interferon beta 1 Homo sapiens 178-185 21311141-8 2011 The prognosis of SCLC with hyponatremia is very poor, especially in those who can not regain normal values of serum sodium after the treatment. Sodium 116-122 SCLC1 Homo sapiens 17-21 20638418-6 2010 In contrast, increases in extracellular sodium levels induced by the sodium channel modulator, veratridine, enhanced 5-HT(1A) responsiveness for water intake and reduced the diuretic effects induced by 8-OH-DPAT. Sodium 40-46 5-hydroxytryptamine receptor 1A Rattus norvegicus 117-124 20638418-7 2010 These trials demonstrated that the responsiveness of the 5-HT(1A) receptor system in the LSA can be enhanced or depressed as a consequence of an induced rise in extracellular sodium. Sodium 175-181 5-hydroxytryptamine receptor 1A Rattus norvegicus 57-64 21105923-6 2010 Expression of the gene encoding Arabidopsis high-affinity K(+) transporter 1;1 (AtHKT1;1), a gene responsible for removing sodium ions from the root xylem, was repressed by cytokinin treatment, but showed significantly elevated expression in the cytokinin response double mutant arr1-3 arr12-1. Sodium 123-129 response regulator 12 Arabidopsis thaliana 286-291 21105923-7 2010 Our data suggest that cytokinin, acting through the transcription factors ARR1 and ARR12, regulates sodium accumulation in the shoots by controlling the expression of AtHKT1;1 in the roots. Sodium 100-106 response regulator 12 Arabidopsis thaliana 83-88 20668099-10 2010 These results demonstrate an augmented COX-2-mediated vasodilation that is not contingent on ANG II, in contrast to COX-2-mediated augmented sodium excretion, where ANG II activity is requisite. Sodium 141-147 cytochrome c oxidase II, mitochondrial Rattus norvegicus 116-121 20668099-12 2010 These results reflect COX-2 continual regulation of MBF and adaptive opposition to ANG II prohypertensinogenic effects on renal plasma flow, cortical blood flow, glomerular filtration rate, and absolute and fractional sodium excretion. Sodium 218-224 cytochrome c oxidase II, mitochondrial Rattus norvegicus 22-27 20659170-4 2010 We found for the first time that in the absence of Arl1p, Kha1p increases potassium, sodium and lithium tolerance, and can thus be categorized as an antiporter with broad substrate specificity. Sodium 85-91 Kha1p Saccharomyces cerevisiae S288C 58-63 20719964-5 2010 Using yeast two-hybrid and in vitro surface plasmon resonance assays, we demonstrate that the spartin MIT domain binds with micromolar affinity to the endosomal sorting complex required for transport (ESCRT)-III protein increased sodium tolerance (Ist)1 but not to ESCRT-III proteins charged multivesicular body proteins 1-7. Sodium 230-236 spartin Homo sapiens 94-101 20719964-5 2010 Using yeast two-hybrid and in vitro surface plasmon resonance assays, we demonstrate that the spartin MIT domain binds with micromolar affinity to the endosomal sorting complex required for transport (ESCRT)-III protein increased sodium tolerance (Ist)1 but not to ESCRT-III proteins charged multivesicular body proteins 1-7. Sodium 230-236 IST1 factor associated with ESCRT-III Homo sapiens 248-253 20718741-4 2010 EXPERIMENTAL APPROACH: Sodium current was investigated using patch clamp technique on wild-type and DeltaKPQ-mutated hNav1.5 channels transfected in HEK293 cells. Sodium 23-29 neuron navigator 1 Homo sapiens 117-122 20707915-3 2010 Previous research indicates that the FURIN gene may play a pivotal role in the renin-angiotensin system and maintaining the sodium-electrolyte balance. Sodium 124-130 furin, paired basic amino acid cleaving enzyme Homo sapiens 37-42 19025979-1 2009 Organic cation transporter 3 (OCT3) is a high-capacity, low-affinity transporter that mediates bidirectional, sodium-independent transport of dopamine, norepinephrine, epinephrine, serotonin, and histamine. Sodium 110-116 solute carrier family 22 member 3 Rattus norvegicus 0-28 20691059-2 2010 TRPV 1 ion channels respond with activation of calcium and sodium fluxes to pH, thermal, chemical, osmotic, mechanical and other stimuli abundant in inflamed joints. Sodium 59-65 transient receptor potential cation channel subfamily V member 1 Homo sapiens 0-6 20534868-2 2010 Recent studies have provided strong evidence that the sodium-phosphate cotransporter NaPi-IIb is responsible for sodium-dependent phosphate absorption by the small intestine, and it might be that this protein can link changes in dietary phosphate to altered renal phosphate excretion to maintain phosphate balance. Sodium 54-60 solute carrier family 34 member 2 Homo sapiens 85-93 20827336-8 2010 These findings suggest that decreased nNOS plays a role in the development of sodium retention in the nephrotic syndrome. Sodium 78-84 nitric oxide synthase 1 Homo sapiens 38-42 20827336-9 2010 Recovery of nNOS and increased renal ET(B)R synthesis may promote sodium excretion in later stages of the nephrotic syndrome (on day 14). Sodium 66-72 nitric oxide synthase 1 Homo sapiens 12-16 23106642-7 2013 Apelin (1 nM) increased sodium currents, ultra-rapid potassium currents and the reverse mode of sodium-calcium exchanger currents, but decreased late sodium currents and L-type calcium currents and did not change transient outward currents or inward rectifier potassium currents in LA myocytes. Sodium 24-30 APLN Oryctolagus cuniculus 0-6 23106642-7 2013 Apelin (1 nM) increased sodium currents, ultra-rapid potassium currents and the reverse mode of sodium-calcium exchanger currents, but decreased late sodium currents and L-type calcium currents and did not change transient outward currents or inward rectifier potassium currents in LA myocytes. Sodium 96-102 APLN Oryctolagus cuniculus 0-6 19025979-1 2009 Organic cation transporter 3 (OCT3) is a high-capacity, low-affinity transporter that mediates bidirectional, sodium-independent transport of dopamine, norepinephrine, epinephrine, serotonin, and histamine. Sodium 110-116 solute carrier family 22 member 3 Rattus norvegicus 30-34 19133747-1 2009 BACKGROUND: Several plasma membrane transporters have been shown to mediate the cellular influx and/or efflux of iodothyronines, including the sodium-independent organic anion co-transporting polypeptide 1 (OATP1), the sodium taurocholate co-transporting polypeptide (NTCP), the L-type amino acid transporter 1 (LAT1) and 2 (LAT2), and the monocarboxylate transporter 8 (MCT8). Sodium 143-149 solute carrier organic anion transporter family, member 1a1 Mus musculus 207-212 23184379-1 2013 Water and sodium retention precedes the development of high blood pressure (BP) and explains a compensatory rise in B-type natriuretic peptide (BNP) concentrations. Sodium 10-16 natriuretic peptide B Homo sapiens 116-142 23184379-1 2013 Water and sodium retention precedes the development of high blood pressure (BP) and explains a compensatory rise in B-type natriuretic peptide (BNP) concentrations. Sodium 10-16 natriuretic peptide B Homo sapiens 144-147 19133747-1 2009 BACKGROUND: Several plasma membrane transporters have been shown to mediate the cellular influx and/or efflux of iodothyronines, including the sodium-independent organic anion co-transporting polypeptide 1 (OATP1), the sodium taurocholate co-transporting polypeptide (NTCP), the L-type amino acid transporter 1 (LAT1) and 2 (LAT2), and the monocarboxylate transporter 8 (MCT8). Sodium 143-149 solute carrier family 16 (monocarboxylic acid transporters), member 2 Mus musculus 340-369 19032932-1 2009 To characterize the function of the sodium/inositol symporter SMIT2 in skeletal muscle, human SMIT2 cDNA was transfected into L6 myoblasts using pcDNA3.1 expression vector. Sodium 36-42 solute carrier family 5 member 11 Homo sapiens 62-67 23546343-3 2013 This study aims to identify the mean Serum Sodium (S.Na+) level and its duration among inpatients with SAH and to identify the relationship between hyponatremia and the outcome status of patients undergoing surgery for SAH. Sodium 43-49 acyl-CoA synthetase medium chain family member 3 Homo sapiens 103-106 19239183-2 2009 It is mainly transported by a sodium and chloride ion dependent taurine transporter (TauT), which is expressed in a variety of tissues, such as brain, retina, and placenta, but in bone the transporter has not yet been identified. Sodium 30-36 solute carrier family 6 (neurotransmitter transporter, taurine), member 6 Mus musculus 64-83 19239183-2 2009 It is mainly transported by a sodium and chloride ion dependent taurine transporter (TauT), which is expressed in a variety of tissues, such as brain, retina, and placenta, but in bone the transporter has not yet been identified. Sodium 30-36 solute carrier family 6 (neurotransmitter transporter, taurine), member 6 Mus musculus 85-89 19063706-1 2009 BACKGROUND: Na(+)/H(+) exchangers (NHE"s) are membrane proteins that regulate ion fluxes, they extrude one intracellular proton in exchange for one extracellular sodium thereby regulating intracellular pH. Sodium 162-168 solute carrier family 9 member C1 Homo sapiens 35-38 19053540-6 2008 The effect of the addition of the radical scavenger, formate, on the 310 nm photolysis of these solutions was also investigated and found to increase phi by a factor of 2 or more for both sodium and calcium nitrate solutions. Sodium 188-194 glucose-6-phosphate isomerase Homo sapiens 150-153 24247155-8 2013 CONCLUSION: hNaDC3 present at the basolateral membrane of proximal tubule cells mediates sodium-dependent GSH uptake. Sodium 89-95 solute carrier family 13 member 3 Homo sapiens 12-18 23026072-3 2012 Recent studies show that SCN7A/Nax channel serves as a sodium-level sensor of the body fluid that controls the Na-intake behavior by changing the excitability of neurons. Sodium 55-61 sodium voltage-gated channel alpha subunit 7 Homo sapiens 25-30 23108657-10 2012 Reduction of intestinal sodium absorption by selective NHE3 inhibition in the gut reduces high blood pressure and increases feces water excretion. Sodium 24-30 solute carrier family 9 member A3 Rattus norvegicus 55-59 22966159-8 2012 pS124-NCC levels also increased in abundance in rats after stimulation of the renin-angiotensin-aldosterone system by dietary low sodium intake. Sodium 130-136 renin Rattus norvegicus 78-83 22989884-3 2012 Once activated by WNK1, OSR1 and SPAK phosphorylate and stimulate the sodium, potassium, two chloride co-transporters, NKCC1 and NKCC2, and also affect other related ion co-transporters. Sodium 70-76 WNK lysine deficient protein kinase 1 Homo sapiens 18-22 22989884-3 2012 Once activated by WNK1, OSR1 and SPAK phosphorylate and stimulate the sodium, potassium, two chloride co-transporters, NKCC1 and NKCC2, and also affect other related ion co-transporters. Sodium 70-76 oxidative stress responsive kinase 1 Homo sapiens 24-28 22922412-3 2012 The mineralocorticoid receptor (MR), acting in the kidney, is known to regulate blood pressure through aldosterone binding and stimulation of sodium retention. Sodium 142-148 nuclear receptor subfamily 3 group C member 2 Homo sapiens 4-30 22922412-3 2012 The mineralocorticoid receptor (MR), acting in the kidney, is known to regulate blood pressure through aldosterone binding and stimulation of sodium retention. Sodium 142-148 nuclear receptor subfamily 3 group C member 2 Homo sapiens 32-34 22670598-2 2012 This suggests that cortisol--by activation of the mineralocorticoid receptor--may contribute to the abnormal sodium retention evident in cirrhosis. Sodium 109-115 nuclear receptor subfamily 3 group C member 2 Homo sapiens 50-76 22674025-6 2012 This agent was assessed in vitro, in vivo, and ex vivo to detect and quantify increases in plasma and kidney renin activity in sodium-sensitive inbred C57BL/6 mice maintained on a low dietary sodium and diuretic regimen. Sodium 127-133 renin Rattus norvegicus 109-114 22592638-3 2012 We hypothesized that high sodium intake differentially regulates and shifts a balance between opposing components of the renal RAS, namely, angiotensin-converting enzyme (ACE)-ANG II-type 1 ANG II receptor (AT(1)R) vs. AT(2)-ACE2-angiotensinogen (Ang) (1-7)-Mas receptor (MasR), in obesity. Sodium 26-32 angiotensin II receptor, type 1a Rattus norvegicus 207-213 18780819-7 2008 Here we studied the interaction of TREX1 with the monovalent cations lithium and sodium. Sodium 81-87 three prime repair exonuclease 1 Homo sapiens 35-40 22668657-7 2012 Magnesium deficiency by interfering with ATPase functions causes increased intracellular calcium and sodium and decreases intracellular potassium concentration. Sodium 101-107 dynein axonemal heavy chain 8 Homo sapiens 41-47 22474336-10 2012 Mutation of the Map1b binding site of Na(v)1.6 prevented generation of sodium current in transfected cells. Sodium 71-77 sodium channel, voltage-gated, type VIII, alpha Mus musculus 38-46 18678869-9 2008 PAR2 effects are mediated in part by a phospholipase C/protein kinase C/ERK1,2 cascade, which increases Na,K-ATPase maximal activity and the paracellular sodium permeability, and by a different phospholipase C-dependent, staurosporine-sensitive cascade that controls the sodium affinity of Na,K-ATPase. Sodium 154-160 mitogen activated protein kinase 3 Rattus norvegicus 72-78 18701624-1 2008 Sodium excretion is bidirectionally regulated by dopamine, acting on D1-like receptors (D1R) and angiotensin II, acting on AT1 receptors (AT1R). Sodium 0-6 angiotensin II receptor, type 1a Rattus norvegicus 123-136 18701624-1 2008 Sodium excretion is bidirectionally regulated by dopamine, acting on D1-like receptors (D1R) and angiotensin II, acting on AT1 receptors (AT1R). Sodium 0-6 angiotensin II receptor, type 1a Rattus norvegicus 138-142 18701624-7 2008 Results indicate that AT1R and D1R function as a unit of opposites, which should provide a highly versatile and sensitive system for short-term regulation of sodium excretion. Sodium 158-164 angiotensin II receptor, type 1a Rattus norvegicus 22-26 18986218-1 2008 INTRODUCTION: We conducted a molecular imaging and gene therapy method in alpha-fetoprotein (AFP)-producing hepatocellular carcinoma (HCC) by tumor-specific expression of the human sodium/iodide symporter (hNIS) using an AFP promoter. Sodium 181-187 HCC Homo sapiens 134-137 18562324-9 2008 We conclude that SLC5A8 is instrumental in preventing lactaturia and loss of sodium-dependent uptake of lactate in the colon but does not have any apparent role in the prevention of tumor formation and growth. Sodium 77-83 solute carrier family 5 (iodide transporter), member 8 Mus musculus 17-23 18695394-3 2008 Mutations of WNK1 and WNK4 in humans cause hypertension and hyperkalemia at least partly by altering renal sodium and potassium transport. Sodium 107-113 WNK lysine deficient protein kinase 1 Homo sapiens 13-17 22521760-0 2012 Maternal high-sodium intake alters the responsiveness of the renin-angiotensin system in adult offspring. Sodium 14-20 renin Rattus norvegicus 61-66 22521760-1 2012 AIMS: The goal of the current study was to evaluate the impact of maternal sodium intake during gestation on the systemic and renal renin-angiotensin-aldosterone-system (RAAS) of the adult offspring. Sodium 75-81 renin Rattus norvegicus 132-137 22436606-9 2012 Sodium intake correlated with change in plasma BNP between admission and fifth day (r=0.46; p<0.0001). Sodium 0-6 natriuretic peptide B Homo sapiens 47-50 18621678-3 2008 Only L263V and Q1489K generated quantifiable sodium currents when coexpressed in tsA201 cells with the human beta(1) and beta(2) accessory subunits. Sodium 45-51 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 121-128 18426992-8 2008 Upregulation of distal tubular renin helps to explain how sustained intrarenal angiotensin II formation occurs even during juxtaglomerular renin suppression, thus allowing maintained effects on tubular sodium reabsorption that contribute to the hypertension. Sodium 202-208 renin Rattus norvegicus 31-36 18347756-2 2008 However, the expression of LAT2 correlates negatively with plasma aldosterone levels after high sodium intake (Pinho et al., Am J Physiol Ren Physiol 292:F1452-F1463, 2007). Sodium 96-102 linker for activation of T cells family, member 2 Rattus norvegicus 27-31 18177483-13 2008 We conclude that noradrenaline-induced increases in the expression of NHE-3, NBC-1, BSC-1 and aquaporin-2 are likely to play an important role in the regulation of salt and water transport by noradrenaline in the kidney and may explain, at least in part, the altered renal sodium and water handling associated with overactivation of the sympathetic system. Sodium 273-279 solute carrier family 9 member A3 Rattus norvegicus 70-75 18413471-1 2008 BACKGROUND: Sodium channel alpha 1 subunit gene, SCN1A, is the gene encoding the neuronal voltage-gated sodium channel alpha 1 subunit (Na(v)1.1) and is mutated in different forms of epilepsy. Sodium 12-18 sodium voltage-gated channel alpha subunit 1 Homo sapiens 49-54 18413471-1 2008 BACKGROUND: Sodium channel alpha 1 subunit gene, SCN1A, is the gene encoding the neuronal voltage-gated sodium channel alpha 1 subunit (Na(v)1.1) and is mutated in different forms of epilepsy. Sodium 104-110 sodium voltage-gated channel alpha subunit 1 Homo sapiens 49-54 18277144-9 2008 SUMMARY: Mutations of WNK1 and WNK4 cause hypertension at least partly by increasing renal sodium retention. Sodium 91-97 WNK lysine deficient protein kinase 1 Homo sapiens 22-26 18310457-10 2008 These data and the fact that renal DDC inversely correlated with renal sodium reabsorption suggest that renal and intestinal gender dimorphism in DDC could be related to sex-related differences in sodium balance observed between males and females. Sodium 71-77 dopa decarboxylase Mus musculus 146-149 18310457-10 2008 These data and the fact that renal DDC inversely correlated with renal sodium reabsorption suggest that renal and intestinal gender dimorphism in DDC could be related to sex-related differences in sodium balance observed between males and females. Sodium 197-203 dopa decarboxylase Mus musculus 35-38 18310457-10 2008 These data and the fact that renal DDC inversely correlated with renal sodium reabsorption suggest that renal and intestinal gender dimorphism in DDC could be related to sex-related differences in sodium balance observed between males and females. Sodium 197-203 dopa decarboxylase Mus musculus 146-149 18329285-6 2008 In conclusion, activation of TRPV1 in the isolated kidney decreases renal PP and increases GFR and water/sodium excretion possibly via simultaneous activation of CGRP and SP receptors upon their enhanced release, suggesting that TRPV1 plays a key role in modulating renal hemodynamics and excretory function. Sodium 105-111 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 29-34 18329285-6 2008 In conclusion, activation of TRPV1 in the isolated kidney decreases renal PP and increases GFR and water/sodium excretion possibly via simultaneous activation of CGRP and SP receptors upon their enhanced release, suggesting that TRPV1 plays a key role in modulating renal hemodynamics and excretory function. Sodium 105-111 calcitonin-related polypeptide alpha Rattus norvegicus 162-166 18329285-6 2008 In conclusion, activation of TRPV1 in the isolated kidney decreases renal PP and increases GFR and water/sodium excretion possibly via simultaneous activation of CGRP and SP receptors upon their enhanced release, suggesting that TRPV1 plays a key role in modulating renal hemodynamics and excretory function. Sodium 105-111 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 229-234 18086951-3 2008 In the current study we determined the effects of overexpression of AT(2)R in the RVLM on sodium and water excretion and on blood pressure in conscious rats. Sodium 90-96 angiotensin II receptor, type 2 Rattus norvegicus 68-74 22389472-1 2012 OCTN2 is a bifunctional transporter that reabsorbs filtered carnitine in a sodium-dependent manner and secretes organic cations into urine as a proton antiport mechanism. Sodium 75-81 solute carrier family 22 member 5 Homo sapiens 0-5 18172057-1 2008 Renal sodium transport is increased by the angiotensin type 1 receptor (AT(1)R), which is counterregulated by dopamine via unknown mechanisms involving either the dopamine type 1 (D(1)R) or dopamine type 5 receptor (D(5)R) that belong to the D(1)-like receptor family of dopamine receptors. Sodium 6-12 angiotensin II receptor type 1 Homo sapiens 72-78 22193384-1 2012 Signaling through both angiotensin AT1 receptors (AT1R) and dopamine D1 receptors (D1R) modulates renal sodium excretion and arterial BP. Sodium 104-110 angiotensin II receptor type 1 Homo sapiens 35-48 22193384-1 2012 Signaling through both angiotensin AT1 receptors (AT1R) and dopamine D1 receptors (D1R) modulates renal sodium excretion and arterial BP. Sodium 104-110 angiotensin II receptor type 1 Homo sapiens 50-54 22303032-6 2012 COMT low-activity genotypes (Met/Met and Val/Met) were also significantly associated with reductions in plasma osmolality (p = 0.028) and in plasma sodium (p = 0.003). Sodium 148-154 catechol-O-methyltransferase Homo sapiens 0-4 22303032-7 2012 On conservative Bonferroni correction for two independent genes, the CYP2D6 and COMT plasma sodium findings remain significant. Sodium 92-98 catechol-O-methyltransferase Homo sapiens 80-84 21678490-3 2012 In this study, accurate quantification of tissue sodium concentration (TSC) was achieved in (23) Na images with voxel sizes of 1.2 muL acquired in 10 min. Sodium 49-55 solute carrier family 12 member 3 Rattus norvegicus 71-74 22383044-5 2012 Swelling-induced ROS production in NIH3T3 fibroblasts is generated by NOX4 and by increasing total ROS, by either exogenous application of H(2)O(2) or overexpressing NOX4, we demonstrate that TonEBP activity and taurine influx are regulated negatively by ROS under hypo-osmotic, low-sodium conditions, whereas the TauT mRNA level is unaffected. Sodium 283-289 NADPH oxidase 4 Mus musculus 166-170 22031782-2 2012 We therefore hypothesized that Na(+)/H(+) exchanger isoform 3 (NHE3), the major apical transcellular pathway for sodium reabsorption in the proximal tubule, is upregulated in an experimental model of HF. Sodium 113-119 solute carrier family 9 member A3 Rattus norvegicus 31-61 22031782-2 2012 We therefore hypothesized that Na(+)/H(+) exchanger isoform 3 (NHE3), the major apical transcellular pathway for sodium reabsorption in the proximal tubule, is upregulated in an experimental model of HF. Sodium 113-119 solute carrier family 9 member A3 Rattus norvegicus 63-67 22031782-6 2012 By means of stationary in vivo microperfusion and pH-dependent sodium uptake, we demonstrated that NHE3 transport activity was significantly higher in the proximal tubule of HF compared with sham rats. Sodium 63-69 solute carrier family 9 member A3 Rattus norvegicus 99-103 22031782-10 2012 Enhanced NHE3-mediated sodium reabsorption in the proximal tubule may contribute to extracellular volume expansion and edema, the hallmark feature of HF. Sodium 23-29 solute carrier family 9 member A3 Rattus norvegicus 9-13 17989136-9 2008 The dietary function line for plasma ANG II concentration increases from theoretical zero at a daily sodium intake of 17 mmol Na/kg (intercept) with a slope of 16 pM increase per decade of decrease in dietary sodium intake. Sodium 101-107 angiogenin Homo sapiens 37-40 17989136-9 2008 The dietary function line for plasma ANG II concentration increases from theoretical zero at a daily sodium intake of 17 mmol Na/kg (intercept) with a slope of 16 pM increase per decade of decrease in dietary sodium intake. Sodium 209-215 angiogenin Homo sapiens 37-40 17984664-5 2007 Capsaicin, a selective TRPV1 receptor agonist, or CGRP dose-dependently decreased MAP in normal or high-sodium-treated rats, with a greater effect in the latter. Sodium 104-110 calcitonin-related polypeptide alpha Rattus norvegicus 50-54 22477766-1 2012 BACKGROUND: The organic anion transporting polypeptides (OATP)/SLCO family represents an important class of hepatic drug uptake transporters that mediate the sodium independent transport of a diverse range of amphipathic organic compounds, including the protease inhibitors. Sodium 158-164 solute carrier organic anion transporter family member 1A2 Homo sapiens 16-55 22477766-1 2012 BACKGROUND: The organic anion transporting polypeptides (OATP)/SLCO family represents an important class of hepatic drug uptake transporters that mediate the sodium independent transport of a diverse range of amphipathic organic compounds, including the protease inhibitors. Sodium 158-164 solute carrier organic anion transporter family member 1A2 Homo sapiens 57-61 23056253-0 2012 Lack of the sodium-driven chloride bicarbonate exchanger NCBE impairs visual function in the mouse retina. Sodium 12-18 solute carrier family 4, sodium bicarbonate cotransporter-like, member 10 Mus musculus 57-61 23056253-2 2012 The sodium-driven chloride bicarbonate exchanger NCBE (Slc4a10), a member of the SLC4 family of bicarbonate transporters, uses the transmembrane gradient of sodium to drive cellular net uptake of bicarbonate and to extrude chloride, thereby modulating both intracellular pH (pH(i)) and chloride concentration ([Cl(-)](i)) in neurons. Sodium 4-10 solute carrier family 4, sodium bicarbonate cotransporter-like, member 10 Mus musculus 49-53 23056253-2 2012 The sodium-driven chloride bicarbonate exchanger NCBE (Slc4a10), a member of the SLC4 family of bicarbonate transporters, uses the transmembrane gradient of sodium to drive cellular net uptake of bicarbonate and to extrude chloride, thereby modulating both intracellular pH (pH(i)) and chloride concentration ([Cl(-)](i)) in neurons. Sodium 4-10 solute carrier family 4, sodium bicarbonate cotransporter-like, member 10 Mus musculus 55-62 23056253-2 2012 The sodium-driven chloride bicarbonate exchanger NCBE (Slc4a10), a member of the SLC4 family of bicarbonate transporters, uses the transmembrane gradient of sodium to drive cellular net uptake of bicarbonate and to extrude chloride, thereby modulating both intracellular pH (pH(i)) and chloride concentration ([Cl(-)](i)) in neurons. Sodium 157-163 solute carrier family 4, sodium bicarbonate cotransporter-like, member 10 Mus musculus 49-53 23056253-2 2012 The sodium-driven chloride bicarbonate exchanger NCBE (Slc4a10), a member of the SLC4 family of bicarbonate transporters, uses the transmembrane gradient of sodium to drive cellular net uptake of bicarbonate and to extrude chloride, thereby modulating both intracellular pH (pH(i)) and chloride concentration ([Cl(-)](i)) in neurons. Sodium 157-163 solute carrier family 4, sodium bicarbonate cotransporter-like, member 10 Mus musculus 55-62 21865264-11 2011 The greater availability of renin and AGT in the urine reflects the capability for intratubular ANG II formation which stimulates sodium reabsorption in distal nephron segments. Sodium 130-136 renin Rattus norvegicus 28-33 21865262-5 2011 Human NaDC3 was stably expressed as proven by immunochemical methods and by sodium-dependent uptake of succinate (K(0.5) for sodium activation, 44.6 mM; Hill coefficient, 2.1; K(m) for succinate, 18 muM). Sodium 76-82 solute carrier family 13 member 3 Homo sapiens 6-11 21865292-6 2011 Among these genes are two genes, Slc12a3 and kidney-specific Wnk1 (KS-Wnk1), that are known to be involved in sodium transport in the distal nephrons and could potentially be involved in the mechanism of CI-induced nephrotoxicity. Sodium 110-116 solute carrier family 12 member 3 Rattus norvegicus 33-40 21746791-2 2011 We tested the hypothesis that sodium intake regulates the type 1 angiotensin II receptor (AT(1)R), mineralocorticoid receptor (MR), and associated signaling pathways in heart tissue from healthy rodents. Sodium 30-36 angiotensin II receptor, type 1a Rattus norvegicus 58-88 21746791-2 2011 We tested the hypothesis that sodium intake regulates the type 1 angiotensin II receptor (AT(1)R), mineralocorticoid receptor (MR), and associated signaling pathways in heart tissue from healthy rodents. Sodium 30-36 angiotensin II receptor, type 1a Rattus norvegicus 90-96 21746791-7 2011 Decreased sodium intake was also associated with decreased cardiac levels of CAV-1 and CAV-3, decreased immunoprecipitation of AT(1)R-CAV-3 and MR-CAV-3 complexes, but increased immunoprecipitation of AT(1)R/MR complexes. Sodium 10-16 angiotensin II receptor, type 1a Rattus norvegicus 127-133 21746791-7 2011 Decreased sodium intake was also associated with decreased cardiac levels of CAV-1 and CAV-3, decreased immunoprecipitation of AT(1)R-CAV-3 and MR-CAV-3 complexes, but increased immunoprecipitation of AT(1)R/MR complexes. Sodium 10-16 angiotensin II receptor, type 1a Rattus norvegicus 201-207 17984664-6 2007 Baseline and NADA-induced increases in plasma CGRP levels were higher in high-sodium than normal-treated rats. Sodium 78-84 calcitonin-related polypeptide alpha Rattus norvegicus 46-50 17984664-7 2007 TRPV1 protein expression in mesenteric arteries was higher in high-sodium than normal-treated rats. Sodium 67-73 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 0-5 17984664-8 2007 In vitro, NADA caused a greater CGRP release from mesenteric arteries of high-sodium than normal-treated rats, which was blocked by capsazepine. Sodium 78-84 calcitonin-related polypeptide alpha Rattus norvegicus 32-36 17984664-11 2007 High sodium upregulates mesenteric TRPV1 expression, and increases NADA-induced CGRP release in vitro and in vivo. Sodium 5-11 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 35-40 17984664-11 2007 High sodium upregulates mesenteric TRPV1 expression, and increases NADA-induced CGRP release in vitro and in vivo. Sodium 5-11 calcitonin-related polypeptide alpha Rattus norvegicus 80-84 17947306-10 2007 In conclusion, these data suggest that while ATP1A3-isoforms regulate sodium and potassium homeostasis in subicular interneurones, ATP1A1-isoforms assume this function in pyramidal cells. Sodium 70-76 ATPase, Na+/K+ transporting, alpha 3 polypeptide Mus musculus 45-51 17996119-12 2007 MUC7 12-mer peptide (at 25 microM) also exerted killing activity in the presence of NaCl, (up to 25 mM for C. albicans and up to 150 mM for E. coli, a physiological concentration of sodium in the oral cavity and serum, respectively) and retained candidacidal activity in the presence of KCl (up to 40 mM). Sodium 182-188 mucin 7, secreted Homo sapiens 0-4 17928448-6 2007 Nonlinear loss of sodium current in Purkinje neurons from heterozygous and homozygous mutant animals suggested partial compensatory upregulation of Na(V)1.6 channel activity. Sodium 18-24 sodium channel, voltage-gated, type VIII, alpha Mus musculus 148-156 17845533-9 2007 These results indicate that sodium-independent transport of bile salts may be mediated by Oatp2 and 4 during biliary obstruction, because its expression remains unaffected and may compensate for loss of Oatp1 expression and function in cholestatic hepatocytes. Sodium 28-34 solute carrier organic anion transporter family, member 1a4 Rattus norvegicus 90-101 18219991-0 2007 [Effect of temperature and monensin on the level of intracellular sodium and pH in perfused RIF-1 cultured cells]. Sodium 66-72 replication timing regulatory factor 1 Homo sapiens 92-97 21917814-5 2011 This E(GABA) shift was associated with increased expression of Na(+)-K(+)-2Cl(-) cotransporter 1 (NKCC1) in MNCs and was blocked by the NKCC inhibitor bumetanide as well as by decreasing NKCC activity through a reduction of extracellular sodium. Sodium 238-244 solute carrier family 12 member 2 Rattus norvegicus 63-96 21917814-5 2011 This E(GABA) shift was associated with increased expression of Na(+)-K(+)-2Cl(-) cotransporter 1 (NKCC1) in MNCs and was blocked by the NKCC inhibitor bumetanide as well as by decreasing NKCC activity through a reduction of extracellular sodium. Sodium 238-244 solute carrier family 12 member 2 Rattus norvegicus 98-103 17438306-9 2007 Hypertensive groups displayed reduced plasma renin concentrations during high sodium conditions and hypertrophic kidneys and hearts with various degrees of histopathologic changes. Sodium 78-84 renin Rattus norvegicus 45-50 17517754-6 2007 However, the bovine lactating mammary gland also expresses GLUT3, GLUT4, GLUT5, GLUT8, GLUT12, and sodium-dependent SGLT1 and SGLT2 at different levels. Sodium 99-105 solute carrier family 5 member 1 Bos taurus 116-121 17371845-4 2007 Recent in vitro studies indicate that COMMD1 has multiple functions, including sodium transport and NF-kappaB signaling. Sodium 79-85 COMM domain containing 1 Mus musculus 38-44 17498579-9 2007 B-type natriuretic peptide quartile remained highly predictive of mortality even after adjustment for age, gender, systolic blood pressure, blood urea nitrogen, creatinine, sodium, pulse, and dyspnea at rest, Q4 versus Q1 (adjusted odds ratio 2.23 [95% confidence interval 1.91 to 2.62, p < 0.0001]). Sodium 173-179 natriuretic peptide B Homo sapiens 0-26 17218026-4 2007 Therefore, the aim of this study was to investigate the participation of serotonergic 5-HT(1A) receptors in the PVN on the sodium intake induced by sodium depletion followed by 24 h of deprivation (injection of the diuretic furosemide plus 24 h of sodium-deficient diet). Sodium 123-129 5-hydroxytryptamine receptor 1A Rattus norvegicus 86-93 17329572-1 2007 Gitelman syndrome (GS) is a recessive salt-losing tubulopathy that is caused by mutations in the SLC12A3 gene that encodes the sodium-chloride co-transporter (NCC). Sodium 127-133 solute carrier family 12 member 3 Homo sapiens 97-104 17344426-7 2007 With the use of Hek293 cells, Xenopus oocytes, and mpkCCD(c14) cells as expression systems, it was shown that Usp2-45 deubiquitylates ENaC and stimulates ENaC-mediated sodium transport, an effect that is not additive to that of Sgk1. Sodium 168-174 ubiquitin specific peptidase 2 Mus musculus 110-114 17512581-5 2007 Aldosterone is produced by the enzyme aldosterone synthase and competes with cortisol and progesterone for the mineralocorticoid receptor, thus affecting sodium reabsorption and maternal volume expansion. Sodium 154-160 nuclear receptor subfamily 3 group C member 2 Homo sapiens 111-137 21653632-1 2011 Renal magnesium (Mg(2+)) and sodium (Na(+)) loss are well-known side effects of cyclosporine (CsA) treatment in humans, but the underlying mechanisms still remain unclear. Sodium 29-35 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 94-97 21653632-4 2011 In the DCT, the final adjustment of renal sodium excretion is regulated by the thiazide-sensitive Na(+)-Cl(-) cotransporter (NCC), which is activated by the renin-angiotensin-aldosterone system (RAAS). Sodium 42-48 solute carrier family 12 member 3 Rattus norvegicus 79-123 21653632-4 2011 In the DCT, the final adjustment of renal sodium excretion is regulated by the thiazide-sensitive Na(+)-Cl(-) cotransporter (NCC), which is activated by the renin-angiotensin-aldosterone system (RAAS). Sodium 42-48 solute carrier family 12 member 3 Rattus norvegicus 125-128 21653632-13 2011 Furthermore, CsA downregulates the NCC in the DCT, associated with an inactivation of the RAAS, resulting in renal sodium loss. Sodium 115-121 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 13-16 21653632-13 2011 Furthermore, CsA downregulates the NCC in the DCT, associated with an inactivation of the RAAS, resulting in renal sodium loss. Sodium 115-121 solute carrier family 12 member 3 Rattus norvegicus 35-38 21849545-6 2011 Moreover, furosemide and bumetanide, two inhibitors of sodium-coupled and/or potassium-coupled chloride movement strongly modified the phase shift, suggesting an involvement of two neuronal cotransporters, NKCC1 (Na-K-Cl) and KCC2 (K-Cl) in the genesis of the optical signal. Sodium 55-61 solute carrier family 12, member 2 Mus musculus 206-211 21937806-0 2011 [Nerve growth factor increases sodium current via interferon regulatory factor-1 pathway in rat pheochromocytoma cells]. Sodium 31-37 interferon regulatory factor 1 Rattus norvegicus 50-80 21937806-1 2011 OBJECTIVE: To explore the effect of nerve growth factor(NGF) and interferon regulatory factor-1(IRF-1) on sodium current change of sensory neuron in rat pheochromocytoma cells. Sodium 106-112 nerve growth factor Rattus norvegicus 36-60 21937806-1 2011 OBJECTIVE: To explore the effect of nerve growth factor(NGF) and interferon regulatory factor-1(IRF-1) on sodium current change of sensory neuron in rat pheochromocytoma cells. Sodium 106-112 interferon regulatory factor 1 Rattus norvegicus 65-95 21937806-1 2011 OBJECTIVE: To explore the effect of nerve growth factor(NGF) and interferon regulatory factor-1(IRF-1) on sodium current change of sensory neuron in rat pheochromocytoma cells. Sodium 106-112 interferon regulatory factor 1 Rattus norvegicus 96-101 21937806-4 2011 RESULTS: Low concentration of NGF improved the sodium current, which was concentration dependent. Sodium 47-53 nerve growth factor Rattus norvegicus 30-33 21937806-8 2011 CONCLUSION: NGF can improve the sodium current in PC-12 cells concentration-dependently, and the improvement is regulated by IRF-1. Sodium 32-38 nerve growth factor Rattus norvegicus 12-15 21864785-6 2011 NGF enlarged TTX-sensitive sodium currents of PC12 cells, which associated with cell volume, membrane surface area, surface roughness of the membrane, and neurite outgrowth. Sodium 27-33 nerve growth factor Rattus norvegicus 0-3 21494136-3 2011 Interestingly, all the conditions centre on the regulation of sodium transport through its epithelial channel, either directly or through mediators that act via the mineralocorticoid receptor. Sodium 62-68 nuclear receptor subfamily 3 group C member 2 Homo sapiens 165-191 17511264-2 2007 Mutation of TSC is known to be responsible for Gitelman"s syndrome, an autosomal recessive renal tubular disorder characterized by low blood pressure due to renal sodium wasting, hypokalemia, metabolic alkalosis, hypomagnesemia and normocalcemic hypocaliuria. Sodium 163-169 solute carrier family 12 member 3 Homo sapiens 12-15 21467193-1 2011 Sodium wasting during the neonatal period is the consequence of a physiological aldosterone resistance, related to a low renal mineralocorticoid receptor (MR) expression at birth, both in humans and mice. Sodium 0-6 nuclear receptor subfamily 3 group C member 2 Homo sapiens 127-153 21467193-1 2011 Sodium wasting during the neonatal period is the consequence of a physiological aldosterone resistance, related to a low renal mineralocorticoid receptor (MR) expression at birth, both in humans and mice. Sodium 0-6 nuclear receptor subfamily 3 group C member 2 Homo sapiens 155-157 21413028-8 2011 Sodium-dependent pHi recovery from weak acid loading was inhibited by amiloride with the Ki consistent with NHEs. Sodium 0-6 glucose-6-phosphate isomerase Homo sapiens 17-20 21527392-2 2011 Dravet"s severe myoclonic epilepsy in infancy is especially interesting as it is associated with fever-provoked seizures and mutations in the alpha subunit of the sodium channel (SCN1A) in about one-third of the cases. Sodium 163-169 sodium voltage-gated channel alpha subunit 1 Homo sapiens 179-184 21321244-2 2011 The potassium-dependent sodium/calcium exchangers NCKX3 (gene SLC24A3) and NCX1 (gene SLC8A1) play a critical role in the transport of intracellular calcium across the cell membrane in exchange for extracellular sodium ions. Sodium 24-30 solute carrier family 24 member 3 Homo sapiens 50-55 21321244-2 2011 The potassium-dependent sodium/calcium exchangers NCKX3 (gene SLC24A3) and NCX1 (gene SLC8A1) play a critical role in the transport of intracellular calcium across the cell membrane in exchange for extracellular sodium ions. Sodium 24-30 solute carrier family 24 member 3 Homo sapiens 62-69 21321244-2 2011 The potassium-dependent sodium/calcium exchangers NCKX3 (gene SLC24A3) and NCX1 (gene SLC8A1) play a critical role in the transport of intracellular calcium across the cell membrane in exchange for extracellular sodium ions. Sodium 212-218 solute carrier family 24 member 3 Homo sapiens 50-55 21321244-2 2011 The potassium-dependent sodium/calcium exchangers NCKX3 (gene SLC24A3) and NCX1 (gene SLC8A1) play a critical role in the transport of intracellular calcium across the cell membrane in exchange for extracellular sodium ions. Sodium 212-218 solute carrier family 24 member 3 Homo sapiens 62-69 21531337-0 2011 Thiazolidinediones enhance sodium-coupled bicarbonate absorption from renal proximal tubules via PPARgamma-dependent nongenomic signaling. Sodium 27-33 peroxisome proliferator activated receptor gamma Mus musculus 97-106 21215314-1 2011 Sodium glucose co-transporter 2 (SGLT2) is a renal type III integral membrane protein that co-transports sodium and glucose from filtrate to epithelium in the proximal tubule. Sodium 105-111 solute carrier family 5 member 2 Rattus norvegicus 0-31 21215314-1 2011 Sodium glucose co-transporter 2 (SGLT2) is a renal type III integral membrane protein that co-transports sodium and glucose from filtrate to epithelium in the proximal tubule. Sodium 105-111 solute carrier family 5 member 2 Rattus norvegicus 33-38 17405690-12 2007 Renal cadmium reduces CYP4A11 and PPARs, which may be related to hypertension, sodium retention, glucose intolerance, dyslipidemia, and zinc deficiency. Sodium 79-85 cytochrome P450 family 4 subfamily A member 11 Homo sapiens 22-29 21177381-0 2011 Genetic analysis of mouse strains with variable serum sodium concentrations identifies the Nalcn sodium channel as a novel player in osmoregulation. Sodium 54-60 sodium leak channel, non-selective Mus musculus 91-96 21177381-6 2011 We identified a total of five loci associated with the serum sodium concentration of which the locus on chromosome 14, containing only one known gene (Nalcn), showed the strongest correlation. Sodium 61-67 sodium leak channel, non-selective Mus musculus 151-156 21177381-8 2011 The association of Nalcn with sodium levels was confirmed by analysis of heterozygous Nalcn knockout mice, which displayed hypernatremia compared with wild-type littermates. Sodium 30-36 sodium leak channel, non-selective Mus musculus 19-24 21177381-9 2011 Our study demonstrates that Nalcn associates with serum sodium concentrations in mice and indicates that Nalcn is an important novel player in osmoregulation. Sodium 56-62 sodium leak channel, non-selective Mus musculus 28-33 21051419-12 2011 The three mutations in SCN3B were investigated electrophysiologically and all led to loss of function in the sodium current, supporting the hypothesis that decreased sodium current enhances AF susceptibility. Sodium 109-115 sodium voltage-gated channel beta subunit 3 Homo sapiens 23-28 21051419-12 2011 The three mutations in SCN3B were investigated electrophysiologically and all led to loss of function in the sodium current, supporting the hypothesis that decreased sodium current enhances AF susceptibility. Sodium 166-172 sodium voltage-gated channel beta subunit 3 Homo sapiens 23-28 17487823-2 2007 Increased circulating and local tissue Ang II is one of the most important factors contributing to the development of sodium and fluid retention, hypertension and target organ damage. Sodium 118-124 angiogenin Homo sapiens 39-42 17068158-12 2007 Urinary sodium excretion increased 128 +/- 18 microeq/min with BNP 3-32 and 338 +/- 40* microeq/min with BNP 1-32. Sodium 8-14 natriuretic peptide B Homo sapiens 63-66 17068158-12 2007 Urinary sodium excretion increased 128 +/- 18 microeq/min with BNP 3-32 and 338 +/- 40* microeq/min with BNP 1-32. Sodium 8-14 natriuretic peptide B Homo sapiens 105-108 17211457-4 2007 Pre-adipocyte differentiation, expression of genes for adipogenesis (aP2), fatty acid oxidation (ACO) and sodium reabsorption (ENaCgamma and Na+, K+-ATPase); haemodilution parameters and serum electrolytes were measured to delineate the role of muraglitazar in causing weight gain vis a vis rosiglitazone. Sodium 106-112 sodium channel, nonvoltage-gated 1 gamma Mus musculus 127-136 21220707-0 2011 Intrarenal ghrelin infusion stimulates distal nephron-dependent sodium reabsorption in normal rats. Sodium 64-70 ghrelin and obestatin prepropeptide Rattus norvegicus 11-18 21224236-8 2011 Electrical activity in L-cells was due to large voltage gated sodium currents, inhibition of which by tetrodotoxin reduced both basal and glutamine-stimulated GLP-1 secretion. Sodium 62-68 glucagon Mus musculus 159-164 20732924-7 2011 RESULTS: The results of the current study confirmed that the stimulation of renal MR and CR elicited a renorenal reflex response, and that the renal pelvic administration of SP and CGRP increased ipsilateral ARNA and contralateral urinary sodium excretion with no changes in arterial pressure. Sodium 239-245 calcitonin-related polypeptide alpha Rattus norvegicus 181-185 21691967-0 2011 Angiotensin AT2 receptors: control of renal sodium excretion and blood pressure. Sodium 44-50 angiotensin II receptor type 2 Homo sapiens 12-15 20932251-2 2011 Such a desensitization process is triggered by the activation of the transient receptor potential vanilloid subtype 1 receptor channels (TRPV1) that open their cationic pores, permeable to sodium, potassium and calcium (Ca(2+)) ions. Sodium 189-195 transient receptor potential cation channel subfamily V member 1 Homo sapiens 137-142 20937801-2 2010 Dipeptide transport by AtPTR1 and AtPTR5 was found to be electrogenic and dependent on protons but not sodium. Sodium 103-109 peptide transporter 5 Arabidopsis thaliana 34-40 20926631-1 2010 Serum and glucocorticoid-regulated kinase 2 (sgk2) is 80% identical to the kinase domain of sgk1, an important mediator of mineralocorticoid-regulated sodium (Na(+)) transport in the distal nephron of the kidney. Sodium 151-157 serum/glucocorticoid regulated kinase 2 Homo sapiens 0-43 20926631-1 2010 Serum and glucocorticoid-regulated kinase 2 (sgk2) is 80% identical to the kinase domain of sgk1, an important mediator of mineralocorticoid-regulated sodium (Na(+)) transport in the distal nephron of the kidney. Sodium 151-157 serum/glucocorticoid regulated kinase 2 Homo sapiens 45-49 17223989-9 2007 CONCLUSIONS: MC2R mutations should be considered in children who have primary adrenal failure with apparent mild disturbances in renin-sodium homeostasis. Sodium 135-141 melanocortin 2 receptor Homo sapiens 13-17 17143069-2 2007 Recent observations have uncovered major functions for these peptides, particularly gamma-MSH, in cardiovascular regulation and sodium metabolism. Sodium 128-134 pro-opiomelanocortin-alpha Mus musculus 84-93 17460376-3 2007 In a series of experiments, we evaluated the contribution of the dopamine D(3) receptor to the renal sodium excretion and arterial blood pressure behavior in conscious as well as anesthetized dopamine D(3) receptor knockout (-/-) mice. Sodium 101-107 dopamine receptor D3 Mus musculus 65-87 17050776-0 2007 Ca2+-calmodulin and janus kinase 2 are required for activation of sodium-proton exchange by the Gi-coupled 5-hydroxytryptamine 1a receptor. Sodium 66-72 Janus kinase 2 Homo sapiens 20-34 19909806-5 2010 In AME, compromised 11betaHSD2 enzyme activity results in activation of the MR by cortisol, causing sodium retention, hypokalaemia, and salt-dependent hypertension. Sodium 100-106 nuclear receptor subfamily 3 group C member 2 Homo sapiens 76-78 20651700-0 2010 Neuronal nitric oxide synthase supports Renin release during sodium restriction through inhibition of phosphodiesterase 3. Sodium 61-67 nitric oxide synthase 1, neuronal Mus musculus 0-30 20651700-10 2010 CONCLUSIONS: The present study provides in vivo evidence supporting the view that NO, selectively derived from nNOS, mediates renin release during sodium restriction by inhibiting PDE3, which would increase renin release by elevating cAMP levels in the JG cells. Sodium 147-153 nitric oxide synthase 1, neuronal Mus musculus 111-115 20820615-0 2010 Sodium and potassium compounds of [(eta(6)-benzenecarboxylate)Cr(CO)(3)] and [(eta(6)-1,4-benzenedicarboxylate)Cr(CO)(3)]. Sodium 0-6 endothelin receptor type A Homo sapiens 36-39 20820615-0 2010 Sodium and potassium compounds of [(eta(6)-benzenecarboxylate)Cr(CO)(3)] and [(eta(6)-1,4-benzenedicarboxylate)Cr(CO)(3)]. Sodium 0-6 endothelin receptor type A Homo sapiens 79-82 20845974-1 2010 Sodium-coupled transport of citric acid cycle intermediates, such as succinate and citrate, is mediated by the NaDC1 transporter located on the apical membrane of kidney proximal tubule and small intestine cells. Sodium 0-6 solute carrier family 13 member 2 Homo sapiens 111-116 20845974-2 2010 Our previous study showed that transmembrane helix (TM) 11 of NaDC1 is important for sodium and lithium binding, as well as for determining citrate affinity [Kahn and Pajor (1999) Biochemistry 38, 6151]. Sodium 85-91 solute carrier family 13 member 2 Homo sapiens 62-67 20845974-7 2010 Although NaDC1 is inhibited by low concentrations of lithium in the presence of sodium, the I554C mutant was stimulated by lithium with a K(0.5) of 4.8 mM. Sodium 80-86 solute carrier family 13 member 2 Homo sapiens 9-14 20630932-2 2010 The Na(+)/H(+) exchanger isoform 3 (NHE3) represents the major route for sodium entry across the apical membrane of renal PT cells. Sodium 73-79 solute carrier family 9 member A3 Rattus norvegicus 36-40 20630932-9 2010 The molecular mechanisms of this adaptation possibly include an increase of P-NHE3/total and a redistribution of the NHE3-DPPIV complex from the body to the base of the PT microvilli, both predicted to decrease sodium reabsorption. Sodium 211-217 solute carrier family 9 member A3 Rattus norvegicus 117-121 20630932-9 2010 The molecular mechanisms of this adaptation possibly include an increase of P-NHE3/total and a redistribution of the NHE3-DPPIV complex from the body to the base of the PT microvilli, both predicted to decrease sodium reabsorption. Sodium 211-217 dipeptidylpeptidase 4 Rattus norvegicus 122-127 20668101-2 2010 However, the role of oxidative stress, especially superoxide radicals in renal sodium handling in response to AT1 and AT2 receptors, is not known. Sodium 79-85 angiotensin II receptor, type 1a Rattus norvegicus 110-113 20668101-2 2010 However, the role of oxidative stress, especially superoxide radicals in renal sodium handling in response to AT1 and AT2 receptors, is not known. Sodium 79-85 angiotensin II receptor, type 2 Rattus norvegicus 118-121 20535627-8 2010 Aldosterone and transforming growth factor-beta1 reciprocally regulate expression of prostasin, PN-1, and ENaC in renal epithelial cell, resulting in sodium retention or natriuresis, respectively. Sodium 150-156 serine protease 8 Homo sapiens 85-94 17940347-1 2007 BACKGROUND/AIMS: The renal sodium glucose cotransporter (SGLT2) and the water channel aquaporin-2 (AQP2) play a critical role in tubular sodium and water reabsorption and in the regulation of extracellular fluid volume both in physiologic and pathophysiologic conditions. Sodium 27-33 solute carrier family 5 member 2 Rattus norvegicus 57-62 18409348-6 2007 The first model hemodialysis (HD1) was performed with constant dialysate sodium concentration (140 mmol/L), the second (HD2) with linear and the third (HD3) with expotential decrease of dialysate sodium concentration (from 144 to 136 mmol/L). Sodium 196-202 histone deacetylase 3 Homo sapiens 152-155 20664544-14 2010 The underlying pathophysiological mechanism may be inappropriately high levels of aldosterone and up-regulation of SGK1-dependent renal sodium transport by ENaCalpha, leading to net increased sodium retention. Sodium 136-142 serum/glucocorticoid regulated kinase 1 Rattus norvegicus 115-119 20664544-14 2010 The underlying pathophysiological mechanism may be inappropriately high levels of aldosterone and up-regulation of SGK1-dependent renal sodium transport by ENaCalpha, leading to net increased sodium retention. Sodium 136-142 sodium channel epithelial 1 subunit alpha Rattus norvegicus 156-165 20664544-14 2010 The underlying pathophysiological mechanism may be inappropriately high levels of aldosterone and up-regulation of SGK1-dependent renal sodium transport by ENaCalpha, leading to net increased sodium retention. Sodium 192-198 serum/glucocorticoid regulated kinase 1 Rattus norvegicus 115-119 20664544-14 2010 The underlying pathophysiological mechanism may be inappropriately high levels of aldosterone and up-regulation of SGK1-dependent renal sodium transport by ENaCalpha, leading to net increased sodium retention. Sodium 192-198 sodium channel epithelial 1 subunit alpha Rattus norvegicus 156-165 20838240-4 2010 Therefore, we investigated the expression patterns of KCC2 and its functional opponent, the chloride influx-mediating sodium-potassium chloride cotransporter 1 (NKCC1), in the superoxide dismutase 1 (SOD1-G93A) mouse model of ALS. Sodium 118-124 solute carrier family 12, member 2 Mus musculus 161-166 21160910-1 2010 BACKGROUND: Sodium/hydrogen exchanger-1 (NHE-1) contributes to maintaining intracellular pH (pHi). Sodium 12-18 glucose-6-phosphate isomerase Homo sapiens 93-96 17969373-2 2007 The effect of angiotensin II is mediated via the angiotensin type I receptor (AT1 ) resulting in vasoconstriction, sodium retention and myocyte growth changes. Sodium 115-121 angiotensin II receptor type 1 Homo sapiens 78-81 17184504-2 2006 Recent studies suggest that leptin, a peptide hormone secreted by white adipose tissue, is involved in the pathogenesis of arterial hypertension, in part by regulating renal sodium handling. Sodium 174-180 leptin Rattus norvegicus 28-34 17075030-2 2006 In AS-null mice (AS(-/-)), but not in wild-type, low salt significantly decreased plasma sodium and increased potassium. Sodium 89-95 cytochrome P450, family 11, subfamily b, polypeptide 2 Mus musculus 17-19 16933033-6 2006 Incubation of cells with 6-deoxy-6-fluoro-ascorbic (F-ASA), i.e. a probe specific for the sodium-dependent Vitamin C uptake (SVCT2), revealed a 10-fold uptake suppression into mouse 17EM15 relative to human HLE-B3 and JAR choriocarcinoma cells (a control), that could be overcome by overexpressing hSVCT2 using two different promoter constructs. Sodium 90-96 solute carrier family 23 (nucleobase transporters), member 2 Mus musculus 125-130 20738386-2 2010 The SCN7A gene encodes an atypical sodium channel (Na(x) ), which is involved in osmoregulation via a sensing mechanism for the extracellular sodium concentration. Sodium 35-41 sodium voltage-gated channel alpha subunit 7 Homo sapiens 4-9 20429018-10 2010 Such lowering of phosphate content by pho4 mutations reversed the high calcium and sodium content of pho80 mutants and prevented the iron starvation response. Sodium 83-89 Pho80p Saccharomyces cerevisiae S288C 101-106 20530479-5 2010 We report here that p38 activation in hippocampal neurons from wild-type mice, but not from Scn8a(medtg) mice that lack Na(v)1.6, reduces tetrodotoxin-S sodium currents, suggesting isoform-specific modulation of Na(v)1.6 by p38 in these neurons. Sodium 153-159 mitogen-activated protein kinase 14 Mus musculus 20-23 20421346-1 2010 The human concentrative nucleoside transporter-3 C602R (hCNT3C602R), a recently identified human concentrative nucleoside transporter-3 (hCNT3) variant, has been shown to interact with natural nucleosides with apparent K(m) values similar to those of the wild-type transporter, although binding of one of the two sodium ions required for nucleoside translocation is impaired, resulting in decreased V(max) values (Mol Pharmacol 73:379-386, 2008). Sodium 313-319 solute carrier family 28 member 3 Homo sapiens 56-61 16933033-6 2006 Incubation of cells with 6-deoxy-6-fluoro-ascorbic (F-ASA), i.e. a probe specific for the sodium-dependent Vitamin C uptake (SVCT2), revealed a 10-fold uptake suppression into mouse 17EM15 relative to human HLE-B3 and JAR choriocarcinoma cells (a control), that could be overcome by overexpressing hSVCT2 using two different promoter constructs. Sodium 90-96 solute carrier family 23 member 2 Homo sapiens 298-304 16949774-2 2006 Consequently, DRSP, when combined with 17beta-estradiol (E2) as hormone replacement therapy (HRT), offsets E2-related water and sodium retention by blocking the mineralocorticoid receptor. Sodium 128-134 nuclear receptor subfamily 3 group C member 2 Homo sapiens 161-187 20144658-2 2010 Increasing evidence shows that 5-HT(1A) and OT neurons inhibit sodium urinary excretion. Sodium 63-69 5-hydroxytryptamine receptor 1A Rattus norvegicus 31-38 20144658-3 2010 The aim of this study was to investigate the part played by serotonergic (5-HT(1A)) and oxytocinergic receptors in the LSA in the sodium intake induced in rats by sodium depletion followed by 24h deprivation. Sodium 130-136 5-hydroxytryptamine receptor 1A Rattus norvegicus 74-81 20144658-6 2010 Pretreatment of the LSA with the 5-HT(1A) antagonist pMPPF partially reduced the inhibitory effect of 5-HT and totally reversed the effects of 8-OH-DPAT on 1.8% NaCl intake induced by sodium depletion. Sodium 184-190 5-hydroxytryptamine receptor 1A Rattus norvegicus 33-40 20144658-8 2010 These results show that 5-HT(1A) serotonergic receptors in the LSA, including some that interact with the oxytocinergic system, modulate sodium intake induced by sodium loss in rats. Sodium 137-143 5-hydroxytryptamine receptor 1A Rattus norvegicus 24-31 20144658-8 2010 These results show that 5-HT(1A) serotonergic receptors in the LSA, including some that interact with the oxytocinergic system, modulate sodium intake induced by sodium loss in rats. Sodium 162-168 5-hydroxytryptamine receptor 1A Rattus norvegicus 24-31 20519529-0 2010 The RCK2 domain uses a coordination site present in Kir channels to confer sodium sensitivity to Slo2.2 channels. Sodium 75-81 killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 4 Homo sapiens 52-55 20486282-8 2010 X chromosome renin-binding protein gene markers rs1557501 and rs2269372 were associated with SBP response to low sodium in men (P=0.00004 and 0.0001, respectively). Sodium 113-119 selenium binding protein 1 Homo sapiens 93-96 20222869-1 2010 TNF-alpha has recently been implicated in diabetic nephropathy, which is usually accompanied by higher sodium retention. Sodium 103-109 tumor necrosis factor Sus scrofa 0-9 16945433-0 2006 The neuroprotective effects of PACAP in monosodium glutamate-induced retinal lesion involve inhibition of proapoptotic signaling pathways. Sodium 40-50 adenylate cyclase activating polypeptide 1 Homo sapiens 31-36 17060380-0 2006 Mutant caveolin-3 induces persistent late sodium current and is associated with long-QT syndrome. Sodium 42-48 caveolin 3 Homo sapiens 7-17 17060380-7 2006 With the recent observation that the LQT3-associated, SCN5A-encoded cardiac sodium channel localizes in caveolae, which are known membrane microdomains whose major component in the striated muscle is caveolin-3, we hypothesized that mutations in caveolin-3 may represent a novel pathogenetic mechanism for LQTS. Sodium 76-82 caveolin 3 Homo sapiens 200-210 20398257-11 2010 The sodium absorption from endolymph mediated by ENaC in SCCD is regulated by signal pathways that include the kinases PKC and PI3-K. Sodium 4-10 protein kinase C delta Homo sapiens 119-122 19923365-4 2010 Results show that increased aldosterone serum concentrations in IUGR fetuses were associated with higher mRNA adrenal levels of angiotensin II receptor type 1 (AT(1)R) and cytochrome P450 aldosterone synthase in response to decreased serum sodium content. Sodium 240-246 angiotensin II receptor, type 1a Rattus norvegicus 128-166 20036246-8 2010 The effects of apelin on I(Na) amplitude were linked to activation of protein kinase C. Apelin also increased I(Na) "window" current by up to 600% suggesting that changes in intracellular sodium may contribute to the apelin inotropic effects. Sodium 188-194 apelin Canis lupus familiaris 217-223 20461205-2 2010 To investigate the relationship between dietary factors or anthropometric indexes and hypertension risk, we examined the association of systolic and diastolic blood pressure (SBP and DBP) with sodium, calcium, and potassium intakes and anthropometric indexes in 19~49-year-olds using data from Korean National Health and Nutrition Examination Survey (KNHANES) III. Sodium 193-199 selenium binding protein 1 Homo sapiens 175-178 20028335-3 2010 We screened a collection of Glc7 regulatory subunit mutants for altered tolerance to diverse cations (sodium, lithium and calcium) and alkaline pH. Sodium 102-108 type 1 serine/threonine-protein phosphatase catalytic subunit GLC7 Saccharomyces cerevisiae S288C 28-32 19940265-2 2010 Both traditional nonsteroidal antiinflammatory drugs (NSAIDs) that inhibit COX-1 and COX-2 and NSAIDs designed to be selective for inhibition of COX-2 cause sodium retention and elevate blood pressure. Sodium 157-163 cytochrome c oxidase II, mitochondrial Mus musculus 145-150 19589774-1 2010 BACKGROUND: Dravet syndrome is a severe infantile epileptic encephalopathy caused in approximately 80% of cases by mutations in the voltage gated sodium channel subunit gene SCN1A. Sodium 146-152 sodium voltage-gated channel alpha subunit 1 Homo sapiens 174-179 21099296-2 2010 In the present paper, we summarize and discuss our recent findings on a four domain cation channel named NALCN which has been previously described as mediating a TTX-resistant leak sodium current in neurons. Sodium 181-187 sodium leak channel, non-selective Mus musculus 105-110 17060380-7 2006 With the recent observation that the LQT3-associated, SCN5A-encoded cardiac sodium channel localizes in caveolae, which are known membrane microdomains whose major component in the striated muscle is caveolin-3, we hypothesized that mutations in caveolin-3 may represent a novel pathogenetic mechanism for LQTS. Sodium 76-82 caveolin 3 Homo sapiens 246-256 17060380-9 2006 CAV3 mutations were engineered by site-directed mutagenesis and the molecular phenotype determined by transient heterologous expression into cell lines that stably express the cardiac sodium channel hNa(v)1.5. Sodium 184-190 caveolin 3 Homo sapiens 0-4 17060380-11 2006 Electrophysiological analysis of sodium current in HEK293 cells stably expressing hNa(v)1.5 and transiently transfected with wild-type and mutant caveolin-3 demonstrated that mutant caveolin-3 results in a 2- to 3-fold increase in late sodium current compared with wild-type caveolin-3. Sodium 33-39 caveolin 3 Homo sapiens 146-156 17060380-11 2006 Electrophysiological analysis of sodium current in HEK293 cells stably expressing hNa(v)1.5 and transiently transfected with wild-type and mutant caveolin-3 demonstrated that mutant caveolin-3 results in a 2- to 3-fold increase in late sodium current compared with wild-type caveolin-3. Sodium 33-39 caveolin 3 Homo sapiens 182-192 17060380-11 2006 Electrophysiological analysis of sodium current in HEK293 cells stably expressing hNa(v)1.5 and transiently transfected with wild-type and mutant caveolin-3 demonstrated that mutant caveolin-3 results in a 2- to 3-fold increase in late sodium current compared with wild-type caveolin-3. Sodium 33-39 caveolin 3 Homo sapiens 182-192 17060380-11 2006 Electrophysiological analysis of sodium current in HEK293 cells stably expressing hNa(v)1.5 and transiently transfected with wild-type and mutant caveolin-3 demonstrated that mutant caveolin-3 results in a 2- to 3-fold increase in late sodium current compared with wild-type caveolin-3. Sodium 236-242 caveolin 3 Homo sapiens 146-156 17060380-11 2006 Electrophysiological analysis of sodium current in HEK293 cells stably expressing hNa(v)1.5 and transiently transfected with wild-type and mutant caveolin-3 demonstrated that mutant caveolin-3 results in a 2- to 3-fold increase in late sodium current compared with wild-type caveolin-3. Sodium 236-242 caveolin 3 Homo sapiens 182-192 17060380-11 2006 Electrophysiological analysis of sodium current in HEK293 cells stably expressing hNa(v)1.5 and transiently transfected with wild-type and mutant caveolin-3 demonstrated that mutant caveolin-3 results in a 2- to 3-fold increase in late sodium current compared with wild-type caveolin-3. Sodium 236-242 caveolin 3 Homo sapiens 182-192 17060380-13 2006 CONCLUSIONS: The present study reports the first CAV3 mutations in subjects with LQTS, and we provide functional data demonstrating a gain-of-function increase in late sodium current. Sodium 168-174 caveolin 3 Homo sapiens 49-53 16720863-0 2006 Disinhibitory pathways for control of sodium transport: regulation of ENaC by SGK1 and GILZ. Sodium 38-44 TSC22 domain family member 3 Homo sapiens 87-91 19854228-4 2010 Because obesity is associated with chronically elevated leptin, we examined if long-term hyperleptinemia impairs acute effects of leptin on sodium excretion and NO production in the absence of obesity. Sodium 140-146 leptin Rattus norvegicus 94-100 19854228-7 2010 Leptin increased fractional sodium excretion and decreased Na(+),K(+)-ATPase activity in the renal medulla. Sodium 28-34 leptin Rattus norvegicus 0-6 19733634-4 2009 In contrast, AT1, ACE mRNA in PVN, SON and OVLT decreased significantly in dietary sodium depleted rats, while AT2 mRNA expression did not change in the examined areas. Sodium 83-89 angiotensin II receptor, type 1a Rattus norvegicus 13-16 19733634-5 2009 These results suggest that many brain areas are activated by increased levels of plasma and/or brain ANG II and ALD, which underlies the elevated preference for hypertonic salt solution after prolonged exposure to low sodium diet, and that the regional AT1 and ACE mRNA are down-regulated after dietary sodium deprivation, which may be mediated by increased ANG II in plasma and/or brain tissue. Sodium 303-309 angiotensin II receptor, type 1a Rattus norvegicus 253-256 16720863-2 2006 The principal hormonal regulator of ENaC, aldosterone, acts through the mineralocorticoid receptor to modulate ENaC-mediated sodium transport, and considerable attention has focused on defining the components of the early phase of this response. Sodium 125-131 nuclear receptor subfamily 3 group C member 2 Homo sapiens 72-98 16825309-7 2006 LIL-6 males and IL-6 females showed decreased urinary flow rate and urinary sodium and potassium excretion. Sodium 76-82 Serum phospholipid level QTL 2 Rattus norvegicus 0-5 16921370-8 2006 Our results indicate that reduced sodium currents in GABAergic inhibitory interneurons in Scn1a+/- heterozygotes may cause the hyperexcitability that leads to epilepsy in patients with SMEI. Sodium 34-40 sodium voltage-gated channel alpha subunit 1 Homo sapiens 90-95 16741038-0 2006 Endothelin B receptor antagonism in the rat renal medulla reduces urine flow rate and sodium excretion. Sodium 86-92 endothelin receptor type B Rattus norvegicus 0-21 16741038-9 2006 These data suggest that: (i) intramedullary blockade of ETB receptor produces antidiuresis and antinatriuresis independently of hemodynamic changes, and (ii) the immediate response to intramedullary blockade of ETB receptor is the reduction of water excretion followed by the reduction of sodium excretion. Sodium 289-295 endothelin receptor type B Rattus norvegicus 56-59 16741038-9 2006 These data suggest that: (i) intramedullary blockade of ETB receptor produces antidiuresis and antinatriuresis independently of hemodynamic changes, and (ii) the immediate response to intramedullary blockade of ETB receptor is the reduction of water excretion followed by the reduction of sodium excretion. Sodium 289-295 endothelin receptor type B Rattus norvegicus 211-214 16541393-1 2006 De novo mutations in the SCN1A gene, encoding the alpha1-subunit of the neuronal voltage-gated sodium channel Nav1.1, are the most frequent genetic cause of Severe Myoclonic Epilepsy of Infancy known so far. Sodium 95-101 sodium voltage-gated channel alpha subunit 1 Homo sapiens 25-30 16541393-1 2006 De novo mutations in the SCN1A gene, encoding the alpha1-subunit of the neuronal voltage-gated sodium channel Nav1.1, are the most frequent genetic cause of Severe Myoclonic Epilepsy of Infancy known so far. Sodium 95-101 sodium voltage-gated channel alpha subunit 1 Homo sapiens 110-116 16195498-11 2006 These data show that MC3-R is expressed in rat IMCD cells in a manner modulated by dietary sodium intake. Sodium 91-97 melanocortin 3 receptor Rattus norvegicus 21-26 16195498-12 2006 Because MC3-R is the receptor with which gamma-MSH interacts, our findings suggest the existence of a sodium-regulating system, activated in response to a HSD, which increases urinary sodium excretion to balance the high-sodium intake. Sodium 102-108 melanocortin 3 receptor Rattus norvegicus 8-13 16195498-12 2006 Because MC3-R is the receptor with which gamma-MSH interacts, our findings suggest the existence of a sodium-regulating system, activated in response to a HSD, which increases urinary sodium excretion to balance the high-sodium intake. Sodium 184-190 melanocortin 3 receptor Rattus norvegicus 8-13 16195498-12 2006 Because MC3-R is the receptor with which gamma-MSH interacts, our findings suggest the existence of a sodium-regulating system, activated in response to a HSD, which increases urinary sodium excretion to balance the high-sodium intake. Sodium 184-190 melanocortin 3 receptor Rattus norvegicus 8-13 16352596-4 2006 We have shown that yeast cells can better adapt to the presence of sodium than lithium because of their ability to reduce pAp accumulation by activating HAL2 expression in a Gcn4p-dependent response, a regulatory loop that is likely to be conserved in different yeast species. Sodium 67-73 amino acid starvation-responsive transcription factor GCN4 Saccharomyces cerevisiae S288C 174-179 16352596-5 2006 We have thus identified a new role for the transcriptional activity of Gcn4p in maintaining an active mRNA degradation pathway under conditions of sodium stress. Sodium 147-153 amino acid starvation-responsive transcription factor GCN4 Saccharomyces cerevisiae S288C 71-76 16340664-9 2006 Mice with collecting duct-specific endothelin A receptor knockout have normal blood pressure and sodium excretion, but have reduced vasopressin responsiveness. Sodium 97-103 endothelin receptor type A Mus musculus 35-56 16287032-5 2006 A series of [M - nH + (n - 1)Na](-) peaks were observed for VII and VIII, showing in the latter case that the carboxylate groups may also form adducts with sodium ions. Sodium 156-162 cytochrome c oxidase subunit 8A Homo sapiens 68-72 19706730-1 2009 The renal outer medullary potassium channel (ROMK) is expressed in the kidney tubule and critically regulates sodium and potassium balance. Sodium 110-116 potassium inwardly rectifying channel subfamily J member 1 Homo sapiens 45-49 19662022-2 2009 Stimulation of ETB receptors in the kidney increases sodium excretion, in part, by decreasing sodium transport in the medullary thick ascending limb of Henle and in collecting duct. Sodium 53-59 endothelin receptor type B Rattus norvegicus 15-18 19662022-2 2009 Stimulation of ETB receptors in the kidney increases sodium excretion, in part, by decreasing sodium transport in the medullary thick ascending limb of Henle and in collecting duct. Sodium 94-100 endothelin receptor type B Rattus norvegicus 15-18 15942053-0 2005 Defective PTH regulation of sodium-dependent phosphate transport in NHERF-1-/- renal proximal tubule cells and wild-type cells adapted to low-phosphate media. Sodium 28-34 parathyroid hormone Mus musculus 10-13 15942053-1 2005 The present experiments using primary cultures from renal proximal tubule cells examine two aspects of the regulation of sodium-dependent phosphate transport and membrane sodium-dependent phosphate transporter (Npt2a) expression by parathyroid hormone (PTH). Sodium 121-127 parathyroid hormone Mus musculus 253-256 15942053-2 2005 Sodium-dependent phosphate transport in proximal tubule cells from wild-type mice grown in normal-phosphate media averaged 4.4 +/- 0.5 nmol.mg protein(-1).10 min(-1) and was inhibited by 30.5 +/- 8.6% by PTH (10(-7) M). Sodium 0-6 parathyroid hormone Mus musculus 204-207 16014321-7 2005 Finally, animals that are defective in HLH-17 via RNAi display egg-laying defects, while those carrying null mutations in hlh-17 do not develop beyond the L2 stage and are less attracted to potassium and sodium ions. Sodium 204-210 Helix-loop-helix protein 17 Caenorhabditis elegans 122-128 16061183-1 2005 Mineralocorticoid receptor (MR) controls sodium homeostasis and blood pressure through hormone binding and coactivator recruitment. Sodium 41-47 nuclear receptor subfamily 3 group C member 2 Homo sapiens 0-26 16061183-1 2005 Mineralocorticoid receptor (MR) controls sodium homeostasis and blood pressure through hormone binding and coactivator recruitment. Sodium 41-47 nuclear receptor subfamily 3 group C member 2 Homo sapiens 28-30 16014064-5 2005 In this condition, sodium transport is mainly due to convection, allowing the estimate of ultrafiltration of small pores and then of free water transport (total UF - UFSP). Sodium 19-25 UFM1 specific peptidase 1 (inactive) Homo sapiens 166-170 16121315-2 2005 Plasma BNP is elevated in cardiac ventricular dysfunction and plays a key role in protecting the body from volume overload by maintaining renal function and sodium balance. Sodium 157-163 natriuretic peptide B Homo sapiens 7-10 15774465-1 2005 The Na+/dicarboxylate co-transporter, NaDC-1, from the kidney and small intestine, transports three sodium ions together with one divalent anion substrate, such as succinate2-. Sodium 100-106 solute carrier family 13 member 2 Homo sapiens 38-44 15634742-0 2005 A role for ERK1/2 in EGF- and ATP-dependent regulation of amiloride-sensitive sodium absorption. Sodium 78-84 mitogen-activated protein kinase 3 Mus musculus 11-17 15634742-8 2005 The results of these studies demonstrate that acute inhibition of amiloride-sensitive sodium transport by extracelluar ATP and EGF involves ERK1/2 activation and suggests a role for MAP kinase signaling as a negative regulator of electrogenic sodium absorption in epithelia. Sodium 86-92 mitogen-activated protein kinase 3 Mus musculus 140-146 16036793-5 2005 Attempts to model the deficit using inhibitors of calcium transport across endoplasmic reticulum, mitochondrial, or plasma membrane indicated that blockade of the plasma membrane sodium/calcium exchanger was best able to reproduce the deficits seen during exposure to CSF(tox). Sodium 179-185 thymocyte selection associated high mobility group box Homo sapiens 272-275 15659399-6 2005 Like LAT3, the amino acid transport activity induced by LAT4 is sodium-, chloride- and pH-independent, is not trans-stimulated, and shows two kinetic components. Sodium 64-70 solute carrier family 43 member 1 Homo sapiens 5-9 19570553-1 2009 Melanocortin 3 receptor (MC3-R) has high affinity and specificity to gamma melanocyte-stimulating hormone (gammaMSH), a natriuretic peptide involved in regulation of blood pressure (BP) and sodium excretion. Sodium 190-196 melanocortin 3 receptor Rattus norvegicus 0-23 19570553-1 2009 Melanocortin 3 receptor (MC3-R) has high affinity and specificity to gamma melanocyte-stimulating hormone (gammaMSH), a natriuretic peptide involved in regulation of blood pressure (BP) and sodium excretion. Sodium 190-196 melanocortin 3 receptor Rattus norvegicus 25-30 19570553-2 2009 Recent studies showing increased MC3-R expression and elevated plasma gammaMSH in normal rats fed a high-salt diet support the role of this system in sodium homeostasis. Sodium 150-156 melanocortin 3 receptor Rattus norvegicus 33-38 19661460-0 2009 Loss of plakophilin-2 expression leads to decreased sodium current and slower conduction velocity in cultured cardiac myocytes. Sodium 52-58 plakophilin 2 Homo sapiens 8-21 19574959-4 2009 RESULTS: We identified a significant association between a rare ADD1 variant rs17833172 and SBP, DBP, and MAP responses to high sodium (P values <0.0001) and DBP response to low sodium (P value = 0.002). Sodium 128-134 selenium binding protein 1 Homo sapiens 92-95 19574959-4 2009 RESULTS: We identified a significant association between a rare ADD1 variant rs17833172 and SBP, DBP, and MAP responses to high sodium (P values <0.0001) and DBP response to low sodium (P value = 0.002). Sodium 181-187 selenium binding protein 1 Homo sapiens 92-95 15659399-6 2005 Like LAT3, the amino acid transport activity induced by LAT4 is sodium-, chloride- and pH-independent, is not trans-stimulated, and shows two kinetic components. Sodium 64-70 solute carrier family 43 member 2 Homo sapiens 56-60 15743391-2 2005 METHODS: Mice and rats, with indwelling femoral arterial and venous catheters, were chronically administered angiotensin II or pharmacological inhibitors of the renin-angiotensin system as sodium intake was altered. Sodium 189-195 renin Rattus norvegicus 161-166 15743391-3 2005 RESULTS: Increasing sodium intake led to suppression of circulating renin, angiotensin II, and aldosterone in rats and mice in the absence of alterations in arterial blood pressure. Sodium 20-26 renin Rattus norvegicus 68-73 15732056-3 2005 When rendered sodium hungry by ivc renin or by sodium depletion, these sucklings prefer urine and NH4Cl to NaCl, dilute urine, or an NaCl and KCl mineral mix equimolar to urine; however, by 18 days of age, urine and NH4Cl are no longer preferred to NaCl. Sodium 14-20 renin Rattus norvegicus 35-40 15664175-0 2005 Open-channel block by the cytoplasmic tail of sodium channel beta4 as a mechanism for resurgent sodium current. Sodium 46-52 tubulin beta 3 class III Homo sapiens 61-66 19666518-4 2009 We show that this polymorphism is significantly associated with serum sodium concentration and with hyponatremia (serum sodium concentration < or =135 mEq/L) in 2 non-Hispanic Caucasian male populations; in addition, mean serum sodium concentration is lower among subjects with the TRPV4(P19S) allele relative to the wild-type allele. Sodium 70-76 transient receptor potential cation channel subfamily V member 4 Homo sapiens 285-290 19666518-4 2009 We show that this polymorphism is significantly associated with serum sodium concentration and with hyponatremia (serum sodium concentration < or =135 mEq/L) in 2 non-Hispanic Caucasian male populations; in addition, mean serum sodium concentration is lower among subjects with the TRPV4(P19S) allele relative to the wild-type allele. Sodium 120-126 transient receptor potential cation channel subfamily V member 4 Homo sapiens 285-290 19666518-4 2009 We show that this polymorphism is significantly associated with serum sodium concentration and with hyponatremia (serum sodium concentration < or =135 mEq/L) in 2 non-Hispanic Caucasian male populations; in addition, mean serum sodium concentration is lower among subjects with the TRPV4(P19S) allele relative to the wild-type allele. Sodium 120-126 transient receptor potential cation channel subfamily V member 4 Homo sapiens 285-290 19575010-6 2009 Taken together, our data show the molecular basis of a muscarinic-activated inward sodium current that is independent of G-protein activation, and provide new insights into the properties of NALCN channels. Sodium 83-89 sodium leak channel, non-selective Homo sapiens 191-196 19359143-1 2009 The clinical features of severe myoclonic epilepsy of infancy (SMEI) resemble those of mitochondrial diseases, although most patients have the sodium channel (SCN1A) mutation. Sodium 143-149 sodium voltage-gated channel alpha subunit 1 Homo sapiens 159-164 19578709-6 2009 Ang-(1-7) has been reported to induce either natriuresis/diuresis or sodium and water retention, via modulation of sodium transporters in the proximal tubule and loop of Henle, and collecting duct water transport. Sodium 69-75 angiogenin, ribonuclease, RNase A family, 5 Mus musculus 0-8 19297450-8 2009 In contrast, PI-103, an inhibitor of class IA PI 3-kinase, inhibited insulin-stimulated sodium transport but did not significantly reduce insulin-stimulated H2O2 production. Sodium 88-94 peptidase inhibitor 3 Homo sapiens 46-50 19386989-11 2009 However, urinary sodium excretion increased less with BNP 8-32 than with BNP 1-32 (+171 +/- 24 vs. +433 +/- 43 muEq/min; P = 0.008), as did urinary potassium excretion, urine flow, and renal blood flow. Sodium 17-23 natriuretic peptide B Homo sapiens 54-57 19386989-11 2009 However, urinary sodium excretion increased less with BNP 8-32 than with BNP 1-32 (+171 +/- 24 vs. +433 +/- 43 muEq/min; P = 0.008), as did urinary potassium excretion, urine flow, and renal blood flow. Sodium 17-23 natriuretic peptide B Homo sapiens 73-76 15770929-6 2005 Nephrol Dial Transplant 2002; 17 (Suppl 1):17-18] suggested a technique to assess sodium-associated water transport based on sodium removal (Na+R) divided by the plasma Na+ concentration during a "fast-fast" (60 minute) peritoneal equilibration test (PET) for 3.86% glucose, yielding an estimate of the UF passing through the small pores (UFSP). Sodium 82-88 UFM1 specific peptidase 1 (inactive) Homo sapiens 339-343 15770929-15 2005 RESULTS: Estimating the UFSP from the sodium-associated water transport according to the method by La Milia et al. Sodium 38-44 UFM1 specific peptidase 1 (inactive) Homo sapiens 24-28 15456767-2 2004 The MEK1/2-ERK1/2 pathway controls many different ion transports both in proximal and distal nephron, raising the question of whether this pathway is involved in the basal and/or hormone-dependent transepithelial sodium reabsorption in the principal cell of the cortical collecting duct (CCD), a process mediated by the apical epithelial sodium channel and the basolateral sodium pump (Na,K-ATPase). Sodium 213-219 mitogen-activated protein kinase kinase 1 Mus musculus 4-10 15456767-6 2004 Basal and aldosterone- or vasopressin-stimulated sodium transport was down-regulated by the MEK1/2 inhibitor PD98059, in parallel with a decrease in pERK1/2 in vitro. Sodium 49-55 mitogen-activated protein kinase kinase 1 Mus musculus 92-98 15456767-10 2004 Our data demonstrate that the ERK1/2 pathway controls Na,K-ATPase activity and transepithelial sodium transport in the principal cell and indicate that basal constitutive activity of the ERK1/2 pathway is a critical component of this control. Sodium 95-101 mitogen-activated protein kinase 3 Mus musculus 30-36 15456767-10 2004 Our data demonstrate that the ERK1/2 pathway controls Na,K-ATPase activity and transepithelial sodium transport in the principal cell and indicate that basal constitutive activity of the ERK1/2 pathway is a critical component of this control. Sodium 95-101 mitogen-activated protein kinase 3 Mus musculus 187-193 15607623-11 2004 There was a significant effect of the final sodium level by diet on the change in SBP over time (P = .04 for three-way interaction among diet, time of visit, and sodium). Sodium 44-50 selenium binding protein 1 Homo sapiens 82-85 15838321-11 2004 Furthermore, downregulation of ETB in the collecting duct, only in rats with decompensated CHF, could contribute to sodium retention in that subgroup. Sodium 116-122 endothelin receptor type B Rattus norvegicus 31-34 15500134-2 2004 All classic physiological effects of AII, such as vasoconstriction, aldosterone and vasopressin release, sodium and water retention and sympathetic facilitation, are mediated by the AT1 receptor. Sodium 105-111 angiotensin II receptor type 1 Homo sapiens 182-185 15619959-5 2004 The data demonstrate that Scn8a is required for the complex spiking of cerebellar Purkinje cells and for persistent sodium current in several classes of neurons, including some with pacemaker roles. Sodium 116-122 sodium channel, voltage-gated, type VIII, alpha Mus musculus 26-31 15316768-2 2004 Sodium-dependent vitamin C transport is mediated by two transporters, SVCT 1 and SVCT 2, encoded by SLC23A1 and SLC23A2. Sodium 0-6 solute carrier family 23 member 2 Homo sapiens 81-87 19513789-3 2009 The mouse model Scn2a(Q54) has an epilepsy phenotype due to a mutation in Scn2a that results in elevated persistent sodium current. Sodium 116-122 sodium channel, voltage-gated, type II, alpha Mus musculus 16-21 19513789-3 2009 The mouse model Scn2a(Q54) has an epilepsy phenotype due to a mutation in Scn2a that results in elevated persistent sodium current. Sodium 116-122 sodium channel, voltage-gated, type II, alpha Mus musculus 74-79 19261867-0 2009 The ataxia3 mutation in the N-terminal cytoplasmic domain of sodium channel Na(v)1.6 disrupts intracellular trafficking. Sodium 61-67 sodium channel, voltage-gated, type VIII, alpha Mus musculus 4-11 15316768-2 2004 Sodium-dependent vitamin C transport is mediated by two transporters, SVCT 1 and SVCT 2, encoded by SLC23A1 and SLC23A2. Sodium 0-6 solute carrier family 23 member 2 Homo sapiens 112-119 15238568-8 2004 In subjects with sodium excretion >190 mmol/d, these associations with the CYP11B2 and AT1R polymorphisms were nonsignificant or in the opposite direction, respectively. Sodium 17-23 angiotensin II receptor type 1 Homo sapiens 90-94 15238568-9 2004 Thus, CYP11B2 C-344T and AT1R A1166C polymorphisms affect the autonomic modulation of heart rate, but these genetic effects depend on sodium excretion. Sodium 134-140 angiotensin II receptor type 1 Homo sapiens 25-29 15201549-3 2004 Our previous studies indicated that hypertension-prone rat strains have greater renal XOR activity than their normotensive counterparts, and that dietary sodium modifies renal XOR activity. Sodium 154-160 xanthine dehydrogenase Rattus norvegicus 176-179 15224206-6 2004 Decreased renin-angiotensin system activity might reduce aldosterone secretion, which in turn could result in (successively) urinary sodium loss, extracellular fluid volume contraction and reductions in glomerular filtration and renal plasma flow. Sodium 133-139 renin Rattus norvegicus 10-15 15499185-5 2004 We propose that sodium-dependent affinity for carnitine is dependent on sodium recognition by these critical amino acids in hOCTN2, whereas carnitine transport by OCTN2 requires functional linkage between TMD1-7 and TMD11. Sodium 72-78 solute carrier family 22 member 5 Homo sapiens 124-130 19119262-0 2009 Association of SLC34A2 variation and sodium-lithium countertransport activity in humans and baboons. Sodium 37-43 solute carrier family 34 member 2 Homo sapiens 15-22 19075092-7 2009 The increase in the urine sodium excretion rate was blocked by coinfusion of PD-123319, a selective AT(2)R antagonist. Sodium 26-32 angiotensin II receptor, type 2 Rattus norvegicus 100-106 18753604-4 2009 This study determined the effects of the estrous cycle, pregnancy, progesterone (P4), and interferon tau (IFNT) on expression of both facilitative (SLC2A1, SLC2A3, and SLC2A4) and sodium-dependent (SLC5A1 and SLC5A11) glucose transporters in ovine uterine endometria from Days 10 to 16 of the estrous cycle and Days 10 to 20 of pregnancy, as well as in conceptuses from Days 10 to 20 of pregnancy. Sodium 180-186 solute carrier family 5 member 11 Homo sapiens 209-216 19133984-1 2009 Although a persistent component of the sodium current (INaP) was described in cardiac tissue about three decades ago, its physiological role and potential as a therapeutic target was not immediately apparent. Sodium 39-45 NFKB inhibitor zeta Homo sapiens 55-59 18515971-3 2009 METHODS/RESULTS: A10 cells concentrated ascorbate against a gradient in a sodium-dependent manner, most likely on the sodium-dependent vitamin C transporter type 2 (SVCT2) ascorbate transporter, which was present in immunoblots of cell extracts. Sodium 74-80 solute carrier family 23 member 2 Homo sapiens 118-163 18515971-3 2009 METHODS/RESULTS: A10 cells concentrated ascorbate against a gradient in a sodium-dependent manner, most likely on the sodium-dependent vitamin C transporter type 2 (SVCT2) ascorbate transporter, which was present in immunoblots of cell extracts. Sodium 74-80 solute carrier family 23 member 2 Homo sapiens 165-170 15499185-5 2004 We propose that sodium-dependent affinity for carnitine is dependent on sodium recognition by these critical amino acids in hOCTN2, whereas carnitine transport by OCTN2 requires functional linkage between TMD1-7 and TMD11. Sodium 72-78 solute carrier family 22 member 5 Homo sapiens 125-130 15181098-3 2004 This study"s aim was to define the effects of GLP-1 on water and sodium excretion in both healthy and obese men. Sodium 65-71 glucagon like peptide 1 receptor Homo sapiens 46-51 15181098-4 2004 Fifteen healthy subjects and 16 obese men (mean body mass index, 36 kg/m2) were examined in a double-blind, placebo-controlled, crossover study to demonstrate the effects of a 3-h infusion of GLP-1 on urinary sodium excretion, urinary output, and the glomerular filtration rate after an i.v. Sodium 209-215 glucagon like peptide 1 receptor Homo sapiens 192-197 15181098-6 2004 Infusion of GLP-1 evoked a dose-dependent increase in urinary sodium excretion in healthy subjects (from 74 +/- 8 to 143 +/- 18 mmol/180 min, P = 0.0013). Sodium 62-68 glucagon like peptide 1 receptor Homo sapiens 12-17 15181098-8 2004 Intravenous infusions of GLP-1 enhance sodium excretion, reduce H+ secretion, and reduce glomerular hyperfiltration in obese men. Sodium 39-45 glucagon like peptide 1 receptor Homo sapiens 25-30 15150284-1 2004 Beta2-Adrenergic agonists stimulate alveolar epithelial sodium (Na(+)) transport and lung fluid clearance. Sodium 56-62 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 0-5 15075188-13 2004 The decreased abundance of NHE3, BSC-1, TSC, and Na-K-ATPase may play a compensatory role to promote sodium excretion. Sodium 101-107 solute carrier family 9 member A3 Rattus norvegicus 27-31 15075188-13 2004 The decreased abundance of NHE3, BSC-1, TSC, and Na-K-ATPase may play a compensatory role to promote sodium excretion. Sodium 101-107 solute carrier family 12 member 3 Rattus norvegicus 40-43 15205554-2 2004 Urinary tumor necrosis factor (TNF) excretion is increased during diabetes and serves as an important mediator of pathological changes during the initial stages of diabetic nephropathy, including sodium retention and renal hypertrophy. Sodium 196-202 tumor necrosis factor-like Rattus norvegicus 8-29 15205554-2 2004 Urinary tumor necrosis factor (TNF) excretion is increased during diabetes and serves as an important mediator of pathological changes during the initial stages of diabetic nephropathy, including sodium retention and renal hypertrophy. Sodium 196-202 tumor necrosis factor-like Rattus norvegicus 31-34 15086906-0 2004 Tumor necrosis factor induces sodium retention in diabetic rats through sequential effects on distal tubule cells. Sodium 30-36 tumor necrosis factor-like Rattus norvegicus 0-21 15086906-1 2004 BACKGROUND: Tumor necrosis factor (TNF) contributes to sodium retention during diabetes. Sodium 55-61 tumor necrosis factor-like Rattus norvegicus 12-33 15086906-1 2004 BACKGROUND: Tumor necrosis factor (TNF) contributes to sodium retention during diabetes. Sodium 55-61 tumor necrosis factor-like Rattus norvegicus 35-38 15086906-2 2004 TNF selectively stimulates sodium uptake in distal tubule cells isolated from diabetic rats, but not in cells from control rats. Sodium 27-33 tumor necrosis factor-like Rattus norvegicus 0-3 15086906-4 2004 METHODS: We examined acute TNF-stimulated sodium uptake in distal tubule cells chronically cultured with exogenous TNF and in distal tubule cells freshly isolated from diabetic rats treated with a specific TNF inhibitor. Sodium 42-48 tumor necrosis factor-like Rattus norvegicus 27-30 15086906-5 2004 We also tested the sodium transport and intracellular signaling pathway underlying TNF-induced sodium transport with pharmacologic inhibitors. Sodium 19-25 tumor necrosis factor-like Rattus norvegicus 83-86 15086906-5 2004 We also tested the sodium transport and intracellular signaling pathway underlying TNF-induced sodium transport with pharmacologic inhibitors. Sodium 95-101 tumor necrosis factor-like Rattus norvegicus 83-86 15086906-8 2004 In sensitized distal tubule cells, TNF-stimulated sodium uptake was blocked by amiloride and PD098059, inhibitors of epithelial sodium channels and extracellular signal-related protein kinase (ERK) activation, respectively. Sodium 50-56 tumor necrosis factor-like Rattus norvegicus 35-38 15086906-9 2004 CONCLUSION: TNF alters distal tubule sodium transport during diabetes through consecutive chronic and acute effects. Sodium 37-43 tumor necrosis factor-like Rattus norvegicus 12-15 15086906-11 2004 These findings are consistent with a sequential mechanism by which chronic and acute TNF actions at the distal tubule cellular level contribute to whole animal sodium retention during diabetes. Sodium 160-166 tumor necrosis factor-like Rattus norvegicus 85-88 15080790-1 2004 OBJECTIVE: Aldosterone binds the mineralocorticoid receptor (MR) and is involved in the regulation of ionic transport, mainly sodium retention. Sodium 126-132 nuclear receptor subfamily 3 group C member 2 Homo sapiens 33-59 15080790-1 2004 OBJECTIVE: Aldosterone binds the mineralocorticoid receptor (MR) and is involved in the regulation of ionic transport, mainly sodium retention. Sodium 126-132 nuclear receptor subfamily 3 group C member 2 Homo sapiens 61-63 14998720-5 2004 Either replacement of sodium ion with calcium ion or depolymerization of the Na-SP molecule to M(r) approximately 14,700 maintained the inhibitory activity, however, removal of sodium ion or desulfation markedly reduced the activity. Sodium 177-183 nuclear autoantigenic sperm protein Bos taurus 77-82 19495699-6 2009 We have shown that alterations of the renin-angiotensin-aldosterone system, by manipulating sodium intake in the rats, reduced the pregnancy-induced remodeling of uterine arteries. Sodium 92-98 renin Rattus norvegicus 38-43 18838565-2 2008 The objective of the present study was to extend our findings and to define the chronic actions of an advanced oral conjugated hBNP (hBNP-054) administered for 6 days on sodium excretion and blood pressure. Sodium 170-176 natriuretic peptide B Homo sapiens 127-131 18838565-2 2008 The objective of the present study was to extend our findings and to define the chronic actions of an advanced oral conjugated hBNP (hBNP-054) administered for 6 days on sodium excretion and blood pressure. Sodium 170-176 natriuretic peptide B Homo sapiens 133-137 18838565-12 2008 In the chronic study in normal dogs, oral hBNP-054 effectively reduced MAP for 6 days and induced a significant increase in 24-hour sodium excretion. Sodium 132-138 natriuretic peptide B Homo sapiens 42-46 18614617-12 2008 These data suggest that oxidative stress leads to AT1 receptor upregulation, which in turn causes overstimulation of sodium transporters and subsequently contributes to sodium retention and hypertension. Sodium 117-123 angiotensin II receptor, type 1a Rattus norvegicus 50-53 14998720-7 2004 The present data suggest that Na-SP is a potent inhibitor of arterial smooth muscle cell proliferation, and the inhibitory effect requires a certain minimum sequence of polysaccharide structure whose molecular conformation is maintained by sodium ion bound to sulfate group. Sodium 240-246 nuclear autoantigenic sperm protein Bos taurus 30-35 15136973-2 2004 administration of renin (R) decreases urinary volume and increases urinary sodium excretion. Sodium 75-81 renin Rattus norvegicus 18-23 14665638-0 2004 Tyrosine residues affecting sodium stimulation of carnitine transport in the OCTN2 carnitine/organic cation transporter. Sodium 28-34 solute carrier family 22 member 5 Homo sapiens 77-82 18403445-1 2008 This study tests the hypothesis that dysfunction of transient receptor potential vanilloid type 1 (TRPV1) channels occurs and contributes to the decrease in the glomerular filtration rate (GFR) and sodium/water excretion in Dahl salt-sensitive hypertensive rats. Sodium 198-204 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 52-97 18403445-1 2008 This study tests the hypothesis that dysfunction of transient receptor potential vanilloid type 1 (TRPV1) channels occurs and contributes to the decrease in the glomerular filtration rate (GFR) and sodium/water excretion in Dahl salt-sensitive hypertensive rats. Sodium 198-204 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 99-104 18591455-2 2008 In previous studies, variants in the genes for alpha-adducin (ADD1), WNK1, and NEDD4L, which all regulate renal sodium absorption, have been associated with increased BP. Sodium 112-118 WNK lysine deficient protein kinase 1 Homo sapiens 69-73 18591455-9 2008 Physiological interaction between the ADD1 and WNK1-NEDD4L pathways influences the effects of variants in these genes on sodium-related BP regulation. Sodium 121-127 WNK lysine deficient protein kinase 1 Homo sapiens 47-51 18591455-10 2008 Relatively common alleles in the ADD1, WNK1, and NEDD4L genes when present in combination may have significant effects on renal sodium handling, BP, and antihypertensive response to thiazides. Sodium 128-134 WNK lysine deficient protein kinase 1 Homo sapiens 39-43 18342948-7 2008 This review summarizes the data on sodium channel mutations and epilepsy and builds a case for the hypothesis that most Nav1.1 mutations have their ultimate epileptogenic effects by reducing Nav1.1-mediated whole cell sodium currents in GABAergic neurons, resulting in widespread loss of brain inhibition, an ideal background for the genesis of epileptic seizures. Sodium 35-41 sodium voltage-gated channel alpha subunit 1 Homo sapiens 120-126 18342948-7 2008 This review summarizes the data on sodium channel mutations and epilepsy and builds a case for the hypothesis that most Nav1.1 mutations have their ultimate epileptogenic effects by reducing Nav1.1-mediated whole cell sodium currents in GABAergic neurons, resulting in widespread loss of brain inhibition, an ideal background for the genesis of epileptic seizures. Sodium 35-41 sodium voltage-gated channel alpha subunit 1 Homo sapiens 191-197 14665638-6 2004 This was associated with an increase in the concentration of sodium required to half-maximally stimulate carnitine transport to 57.8 +/- 7.4 mM (p<0.01 versus normal OCTN2). Sodium 61-67 solute carrier family 22 member 5 Homo sapiens 169-174 14665638-10 2004 These natural mutations identify tyrosine residues possibly involved in coupling the sodium electrochemical gradient to transmembrane solute transfer in the sodium-dependent co-transporter OCTN2. Sodium 85-91 solute carrier family 22 member 5 Homo sapiens 189-194 14665638-10 2004 These natural mutations identify tyrosine residues possibly involved in coupling the sodium electrochemical gradient to transmembrane solute transfer in the sodium-dependent co-transporter OCTN2. Sodium 157-163 solute carrier family 22 member 5 Homo sapiens 189-194 14973256-5 2004 All calretinin-positive cells had sodium currents, although so did some calretinin-negative cells. Sodium 34-40 calbindin 2 Mus musculus 4-14 14558883-1 2004 Treatment with PTH (parathyroid hormone) or a high-P(i) diet causes internalization of the type IIa sodium-dependent phosphate (Na/P(i) IIa) co-transporter from the apical membrane and its degradation in the lysosome. Sodium 100-106 solute carrier family 34 member 1 Homo sapiens 128-139 15011249-0 2004 Effects of temperature on intracellular sodium, pH and cellular energy status in RIF-1 tumor cells. Sodium 40-46 replication timing regulatory factor 1 Homo sapiens 81-86 14742879-1 2004 In Arabidopsis thaliana, the calcium binding protein Salt Overly Sensitive3 (SOS3) interacts with and activates the protein kinase SOS2, which in turn activates the plasma membrane Na(+)/H(+) antiporter SOS1 to bring about sodium ion homeostasis and salt tolerance. Sodium 223-229 Calcium-binding EF-hand family protein Arabidopsis thaliana 77-81 18398380-11 2008 The TRPV1-induced sodium and water excretion appears to be mediated by increases in glomerular filtration rate and distal tubular delivery of sodium but not by suppression of renal proximal and distal tubular reabsorption, suggesting a key role of segmental regulation of renal function by TRPV1-positive primary sensory nerves in the maintenance of sodium and water homeostasis. Sodium 18-24 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 4-9 18398380-11 2008 The TRPV1-induced sodium and water excretion appears to be mediated by increases in glomerular filtration rate and distal tubular delivery of sodium but not by suppression of renal proximal and distal tubular reabsorption, suggesting a key role of segmental regulation of renal function by TRPV1-positive primary sensory nerves in the maintenance of sodium and water homeostasis. Sodium 18-24 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 290-295 18398380-11 2008 The TRPV1-induced sodium and water excretion appears to be mediated by increases in glomerular filtration rate and distal tubular delivery of sodium but not by suppression of renal proximal and distal tubular reabsorption, suggesting a key role of segmental regulation of renal function by TRPV1-positive primary sensory nerves in the maintenance of sodium and water homeostasis. Sodium 142-148 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 4-9 18398380-11 2008 The TRPV1-induced sodium and water excretion appears to be mediated by increases in glomerular filtration rate and distal tubular delivery of sodium but not by suppression of renal proximal and distal tubular reabsorption, suggesting a key role of segmental regulation of renal function by TRPV1-positive primary sensory nerves in the maintenance of sodium and water homeostasis. Sodium 142-148 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 4-9 14974053-7 2004 MAIN RESULTS: In 57 trials of mainly Caucasians with normal blood pressure, low sodium intake reduced SBP by -1.27 mm Hg (CI: -1.76; -0.77)(p<0.0001) and DBP by -0.54 mm Hg (CI: -0.94; -0.14) (p = 0.009) as compared to high sodium intake. Sodium 80-86 selenium binding protein 1 Homo sapiens 102-105 14974053-8 2004 In 58 trials of mainly Caucasians with elevated blood pressure, low sodium intake reduced SBP by -4.18 mm Hg (CI: -5.08; - 3.27) (p < 0.0001) and DBP by -1.98 mm Hg (CI: -2.46; -1.32) (p < 0.0001) as compared to high sodium intake. Sodium 68-74 selenium binding protein 1 Homo sapiens 90-93 14974053-11 2004 In 8 trials of blacks with normal or elevated blood pressure, low sodium intake reduced SBP by -6.44 mm Hg (CI: -9.13; -3.74) (p < 0.0001) and DBP by -1.98 mm Hg (CI: -4.75; 0.78) (p = 0.16) as compared to high sodium intake. Sodium 66-72 selenium binding protein 1 Homo sapiens 88-91 15273422-8 2004 Regardless of these increases, the intrarenal COX-2 inhibition caused comparable decreases in glomerular filtration rate, in absolute and fractional sodium excretion, as well as in urinary PGE2 excretion in TGR and HanSD rats kept on the LS diet. Sodium 149-155 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 46-51 18468451-12 2008 However, later reduction in AQP-2 and alpha-ENaC may represent an attempt to re-establish sodium and water balance. Sodium 90-96 sodium channel epithelial 1 subunit alpha Rattus norvegicus 38-48 12971909-1 2004 The relative roles of the three sodium-dependent transport systems: A, ASC and N in the uptake of [3H]Gln, and the compatibility of the uptake characteristics with the expression of mRNAs coding for the Gln transporting molecules, were examined in primary cultures of astrocytes and neurons derived from mouse cerebellum, a glutaminergic system-enriched structure, and in cerebral cortex. Sodium 32-38 steroid sulfatase Mus musculus 71-74 12930837-7 2003 The inhibitory effect of TGF-beta1 on sodium uptake and alphaENaC expression in ATII cells was mediated by activation of the MAPK, ERK1/2. Sodium 38-44 mitogen activated protein kinase 3 Rattus norvegicus 125-129 12930837-7 2003 The inhibitory effect of TGF-beta1 on sodium uptake and alphaENaC expression in ATII cells was mediated by activation of the MAPK, ERK1/2. Sodium 38-44 mitogen activated protein kinase 3 Rattus norvegicus 131-137 12930837-10 2003 This reduction in sodium and fluid transport is attributable in large part to a reduction in apical membrane alphaENaC expression mediated through an ERK1/2-dependent inhibition of the alphaENaC promoter activity. Sodium 18-24 mitogen activated protein kinase 3 Rattus norvegicus 150-156 12871209-2 2003 The activity of TAUT in the HepG2 cells was evaluated by means of a sodium- and chloride-dependent high-affinity transport system, the characteristics of which were similar to those of the beta amino-acid-specific taurine transport system described previously for various tissues [Uchida, Kwon, Yamauchi, Preston, Marumo and Handler (1992) Proc. Sodium 68-74 solute carrier family 6 member 6 Homo sapiens 16-20 18230619-0 2008 Novel gating and sensitizing mechanism of capsaicin receptor (TRPV1): tonic inhibitory regulation of extracellular sodium through the external protonation sites on TRPV1. Sodium 115-121 transient receptor potential cation channel subfamily V member 1 Homo sapiens 42-60 18230619-0 2008 Novel gating and sensitizing mechanism of capsaicin receptor (TRPV1): tonic inhibitory regulation of extracellular sodium through the external protonation sites on TRPV1. Sodium 115-121 transient receptor potential cation channel subfamily V member 1 Homo sapiens 62-67 18230619-0 2008 Novel gating and sensitizing mechanism of capsaicin receptor (TRPV1): tonic inhibitory regulation of extracellular sodium through the external protonation sites on TRPV1. Sodium 115-121 transient receptor potential cation channel subfamily V member 1 Homo sapiens 164-169 18294862-0 2008 Angiotensin AT2 receptors: control of renal sodium excretion and blood pressure. Sodium 44-50 angiotensin II receptor type 2 Homo sapiens 12-15 18242854-1 2008 Mutations in the sodium channel genes SCN1A and SCN2A have been identified in monogenic childhood epilepsies, but SCN3A has not previously been investigated as a candidate gene for epilepsy. Sodium 17-23 sodium voltage-gated channel alpha subunit 1 Homo sapiens 38-43 14561698-0 2003 A novel role for uroguanylin in the regulation of sodium balance. Sodium 50-56 guanylate cyclase activator 2b (retina) Mus musculus 17-28 14561698-1 2003 Uroguanylin is a peptide hormone that regulates sodium excretion by the kidney when excess NaCl is consumed. Sodium 48-54 guanylate cyclase activator 2b (retina) Mus musculus 0-11 14561698-2 2003 A new study demonstrates that mice deficient in uroguanylin have blunted urinary sodium excretion responses to oral sodium loads in addition to elevated blood pressure (see related article beginning on page 1244). Sodium 81-87 guanylate cyclase activator 2b (retina) Mus musculus 48-59 14561698-2 2003 A new study demonstrates that mice deficient in uroguanylin have blunted urinary sodium excretion responses to oral sodium loads in addition to elevated blood pressure (see related article beginning on page 1244). Sodium 116-122 guanylate cyclase activator 2b (retina) Mus musculus 48-59 14561698-3 2003 A physiological role for uroguanylin is discussed, linking the intestine and kidney in an endocrine axis for the maintenance of sodium balance. Sodium 128-134 guanylate cyclase activator 2b (retina) Mus musculus 25-36 14561709-2 2003 To explore the in vivo role of uroguanylin in the regulation of sodium excretion, we created gene-targeted mice in which uroguanylin gene expression had been ablated. Sodium 64-70 guanylate cyclase activator 2b (retina) Mus musculus 31-42 14508195-1 2003 BACKGROUND: The prevailing sodium intake and renin-angiotensin system status influence the blood pressure response to an angiotensin II type 1 (AT1) receptor antagonist or an angiotensin I converting enzyme inhibitor, which is known to be reinforced by a low sodium intake or administration of a diuretic. Sodium 27-33 angiotensin II receptor type 1 Homo sapiens 121-157 14508195-1 2003 BACKGROUND: The prevailing sodium intake and renin-angiotensin system status influence the blood pressure response to an angiotensin II type 1 (AT1) receptor antagonist or an angiotensin I converting enzyme inhibitor, which is known to be reinforced by a low sodium intake or administration of a diuretic. Sodium 259-265 angiotensin II receptor type 1 Homo sapiens 121-157 14519796-9 2003 Reducing sodium from the high to the low level significantly decreased serum OC 0.6 microg/L in subjects that consumed the DASH diet, fasting serum PTH 2.66 ng/L in control subjects and urinary calcium 0.5 mmol/24 h in both groups. Sodium 9-15 parathyroid hormone 2 Homo sapiens 148-153 14504318-1 2003 BACKGROUND: Mutations in SCN1A, the gene encoding the alpha1 subunit of the sodium channel, have been found in severe myoclonic epilepsy of infancy (SMEI) and generalized epilepsy with febrile seizures plus (GEFS+). Sodium 76-82 sodium voltage-gated channel alpha subunit 1 Homo sapiens 25-30 12924627-0 2003 Sodium load increases renal angiotensin type 1 receptors and decreases bradykinin type 2 receptors. Sodium 0-6 angiotensin II receptor, type 1a Rattus norvegicus 28-46 12924627-2 2003 We hypothesized that an altered balance between renal angiotensin type 1 (AT1) receptors and bradykinin type 2 (B2) receptors might contribute to an increase in blood pressure during periods of high-sodium intake. Sodium 199-205 angiotensin II receptor, type 1a Rattus norvegicus 54-72 12924627-2 2003 We hypothesized that an altered balance between renal angiotensin type 1 (AT1) receptors and bradykinin type 2 (B2) receptors might contribute to an increase in blood pressure during periods of high-sodium intake. Sodium 199-205 angiotensin II receptor, type 1a Rattus norvegicus 74-77 12784736-3 2003 Excessive activation of Na+/H+ exchanger (NHE) and Na+ channels may contribute to Na+ influx into the ischemic myocardium, resulting in sodium overload under ischemic conditions. Sodium 136-142 solute carrier family 9 member C1 Homo sapiens 24-40 12784736-3 2003 Excessive activation of Na+/H+ exchanger (NHE) and Na+ channels may contribute to Na+ influx into the ischemic myocardium, resulting in sodium overload under ischemic conditions. Sodium 136-142 solute carrier family 9 member C1 Homo sapiens 42-45 12511427-1 2003 Activation of the renin-angiotensin system in the brain is considered important in the arousal and expression of sodium appetite. Sodium 113-119 renin Rattus norvegicus 18-23 12460120-9 2003 Other mechanisms known to interact with ENaC and affect sodium transport include channel-activating protease 1 (CAP-1), a membrane-anchored protein, and the cystic fibrosis transmembrane regulator. Sodium 56-62 serine protease 8 Homo sapiens 81-110 12460120-9 2003 Other mechanisms known to interact with ENaC and affect sodium transport include channel-activating protease 1 (CAP-1), a membrane-anchored protein, and the cystic fibrosis transmembrane regulator. Sodium 56-62 serine protease 8 Homo sapiens 112-117 12576306-6 2003 Sodium currents were recorded in gastric sensory neurons from nodose and dorsal root ganglia cultured for 24 h in the presence of NGF or a neutralizing NGF antibody, respectively. Sodium 0-6 nerve growth factor Rattus norvegicus 130-133 12576306-6 2003 Sodium currents were recorded in gastric sensory neurons from nodose and dorsal root ganglia cultured for 24 h in the presence of NGF or a neutralizing NGF antibody, respectively. Sodium 0-6 nerve growth factor Rattus norvegicus 152-155 12556366-2 2003 In this study, we investigated whether the abundance and subcellular localization of pendrin are regulated in response to experimental metabolic acidosis and alkalosis with maintained water and sodium intake. Sodium 194-200 solute carrier family 26 member 4 Rattus norvegicus 85-92 12566275-4 2003 Mutations of the neuronal voltage-gated sodium channel alpha subunit type 1 gene (SCN1A) were recently reported in SMEI patients. Sodium 40-46 sodium voltage-gated channel alpha subunit 1 Homo sapiens 82-87 12631271-0 2003 Transport of taurocholate by mutants of negatively charged amino acids, cysteines, and threonines of the rat liver sodium-dependent taurocholate cotransporting polypeptide Ntcp. Sodium 115-121 solute carrier family 10 member 1 Rattus norvegicus 172-176 12631271-9 2003 In conclusion, loop amino acids are required for sodium-dependent substrate translocation by the Ntcp. Sodium 49-55 solute carrier family 10 member 1 Rattus norvegicus 97-101 12623980-12 2003 Thus, it is possible that increased apical Na+/H+ exchange caused by increasing the sodium concentration in the lumen of the macula densa activates macula densa nNOS. Sodium 84-90 nitric oxide synthase, brain Oryctolagus cuniculus 161-165 12538613-5 2003 Here we show that cortisone and 11-dehydrocorticosterone, the main cortisol and corticosterone metabolites produced in the distal nephron, where sodium reabsorption stimulated by aldosterone takes place, bind with high affinity to MR(L810). Sodium 145-151 nuclear receptor subfamily 3 group C member 2 Homo sapiens 231-233 12636174-1 2003 PURPOSE: The sodium-dependent, purine-selective nucleoside transporter, SPNT, has a unique steady-state expression pattern in renal epithelial cells. Sodium 13-19 solute carrier family 28 member 2 Rattus norvegicus 72-76 12388406-0 2003 Urinary tumor necrosis factor contributes to sodium retention and renal hypertrophy during diabetes. Sodium 45-51 tumor necrosis factor-like Rattus norvegicus 8-29 18247577-1 2008 Sodium-dependent vitamin C transporters, SVCT1 and SVCT2, are the only two known proteins for the uptake of ascorbate, the active form of vitamin C. Sodium 0-6 solute carrier family 23 member 2 Homo sapiens 51-56 18056581-2 2007 For FHM, three genes have been identified encoding subunits of a calcium channel (CACNA1A), a sodium-potassium pump (ATP1A2), and a sodium channel (SCN1A). Sodium 132-138 sodium voltage-gated channel alpha subunit 1 Homo sapiens 148-153 17956270-4 2007 Sodium inhibits the activity of CyaB1, CyaB2 and mammalian PDE2A in vitro through modulation of GAF domain function. Sodium 0-6 phosphodiesterase 2A Homo sapiens 59-64 17942579-0 2007 Altered sodium intake affects plasma concentrations of BNP but not proBNP in healthy individuals and patients with compensated heart failure. Sodium 8-14 natriuretic peptide B Homo sapiens 55-58 17942579-5 2007 In healthy individuals, the plasma BNP concentration increased significantly on high sodium intake with a ratio (high sodium/low sodium) of 2.00 (1.32-3.03, P = 0.004). Sodium 85-91 natriuretic peptide B Homo sapiens 35-38 17942579-5 2007 In healthy individuals, the plasma BNP concentration increased significantly on high sodium intake with a ratio (high sodium/low sodium) of 2.00 (1.32-3.03, P = 0.004). Sodium 118-124 natriuretic peptide B Homo sapiens 35-38 17942579-5 2007 In healthy individuals, the plasma BNP concentration increased significantly on high sodium intake with a ratio (high sodium/low sodium) of 2.00 (1.32-3.03, P = 0.004). Sodium 118-124 natriuretic peptide B Homo sapiens 35-38 17942579-9 2007 CONCLUSION: Sodium intake has a considerable effect on plasma BNP and therefore contributes to the intra-individual variability. Sodium 12-18 natriuretic peptide B Homo sapiens 62-65 17942579-10 2007 We suggest dietary sodium intake to be standardized at least 3 days prior to blood sampling for the determination of plasma BNP. Sodium 19-25 natriuretic peptide B Homo sapiens 124-127 17686957-7 2007 Finally, we discuss a potential role for regulation of insulin receptor signaling in the kidney in contributing to sodium balance and blood pressure. Sodium 115-121 insulin receptor Homo sapiens 55-71 17885550-1 2007 BACKGROUND: The thiazide-sensitive Na-Cl cotransporter (TSC) is involved in the fine regulation of sodium excretion by the kidney, and an increase in its activity causes salt-sensitive hypertension and hypercalciuria. Sodium 99-105 solute carrier family 12 member 3 Homo sapiens 16-54 17885550-1 2007 BACKGROUND: The thiazide-sensitive Na-Cl cotransporter (TSC) is involved in the fine regulation of sodium excretion by the kidney, and an increase in its activity causes salt-sensitive hypertension and hypercalciuria. Sodium 99-105 solute carrier family 12 member 3 Homo sapiens 56-59 17885550-8 2007 CONCLUSIONS: Our results show that the substitution of arginine for cysteine at position 919 of TSC increases Na transport function, and provide support for the hypothesis that mutations in renal tubular sodium transporters may contribute to the development of primary hypertension, a polygenic disorder, by increasing renal sodium reabsorption. Sodium 204-210 solute carrier family 12 member 3 Homo sapiens 96-99 17786049-1 2007 COMMD1 is a protein which is associated with multiple cellular pathways, including NFkappaB signaling, copper homeostasis and sodium transport. Sodium 126-132 COMM domain containing 1 Mus musculus 0-6 17632091-2 2007 Similar with cultured rat trigeminal ganglion (TG) neurons, the amplitude of tetrodotoxin-resistant (TTX-R) sodium current was reduced 85% by 1 muM capsaicin in capsaicin sensitive neurons, while only 6% was blocked in capsaicin insensitive neurons of TRPV1(+/+) mice. Sodium 108-114 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 252-257 17346947-5 2007 In addition, the highly Ca(2+)-selective channel, TRPV5, contributes to several acquired mineral (dys)regulation, such as diabetes mellitus (DM), acid-base disorders, diuretics, immunosuppressant agents, and vitamin D analogues-associated Ca(2+) imbalance whereas TRPV4 may function as an osmoreceptor in kidney and participate in the regulation of sodium and water balance. Sodium 349-355 transient receptor potential cation channel subfamily V member 5 Homo sapiens 50-55 17346947-5 2007 In addition, the highly Ca(2+)-selective channel, TRPV5, contributes to several acquired mineral (dys)regulation, such as diabetes mellitus (DM), acid-base disorders, diuretics, immunosuppressant agents, and vitamin D analogues-associated Ca(2+) imbalance whereas TRPV4 may function as an osmoreceptor in kidney and participate in the regulation of sodium and water balance. Sodium 349-355 transient receptor potential cation channel subfamily V member 4 Homo sapiens 264-269 17576410-2 2007 The voltage-gated sodium channel (Na(v)1) beta2-subunit (beta2), a type I membrane protein that covalently binds to Na(v)1 alpha-subunits, is a substrate for BACE1 and gamma-secretase. Sodium 18-24 neuron navigator 1 Homo sapiens 34-40 17576410-2 2007 The voltage-gated sodium channel (Na(v)1) beta2-subunit (beta2), a type I membrane protein that covalently binds to Na(v)1 alpha-subunits, is a substrate for BACE1 and gamma-secretase. Sodium 18-24 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 42-55 17506936-1 2007 AIM: To study the effects of haloperidol on sodium currents (I(Na)) in guinea pig ventricular myocytes. Sodium 44-50 alpha-internexin Cavia porcellus 61-66 17535874-0 2007 Liver-derived IGF-I regulates kidney size, sodium reabsorption, and renal IGF-II expression. Sodium 43-49 insulin-like growth factor 1 Mus musculus 14-19 17535874-6 2007 The 24-h urine excretion of sodium and potassium was increased in the LI-IGF-I(-/-) mice. Sodium 28-34 insulin-like growth factor 1 Mus musculus 73-78 17535874-9 2007 In conclusion, deficiency of circulating liver-derived IGF-I in mice results, despite an increase in GH secretion, in a global symmetrical decrease in kidney size, increased urinary sodium and potassium excretion, and a clear down regulation of renal IGF-II expression. Sodium 182-188 insulin-like growth factor 1 Mus musculus 55-60 17218026-9 2007 5-HT(1A) antagonists partially reduced the inhibitory effect of 5-HT on NaCl 1.8% intake induced by sodium depletion. Sodium 100-106 5-hydroxytryptamine receptor 1A Rattus norvegicus 0-7 17218026-11 2007 The results show that 5-HT(1A) serotonergic mechanisms in the PVN modulate sodium intake induced by sodium loss. Sodium 75-81 5-hydroxytryptamine receptor 1A Rattus norvegicus 22-29 17218026-11 2007 The results show that 5-HT(1A) serotonergic mechanisms in the PVN modulate sodium intake induced by sodium loss. Sodium 100-106 5-hydroxytryptamine receptor 1A Rattus norvegicus 22-29 17215321-1 2007 It has been suggested that the sodium/calcium exchanger NCX1 may have a more important physiological role in embryonic and neonatal hearts than in adult hearts. Sodium 31-37 solute carrier family 8 member A1 Gallus gallus 56-60 12691376-1 2003 Sodium-hydrogen ion exchange (NHE) is one of the principal mechanisms of restoring intracellular pH following ischemia and reperfusion. Sodium 0-6 solute carrier family 9 member C1 Homo sapiens 30-33 17464433-7 2007 AT-2 receptors modulate these intake responses depending on sodium in the diet, and diuretic-induced dehydration during pregnancy produces a higher salt intake in the offspring. Sodium 60-66 angiotensin II receptor, type 2 Rattus norvegicus 0-4 14580937-0 2003 Reduced sodium appetite and increased oxytocin gene expression in mutant mice lacking beta-endorphin. Sodium 8-14 pro-opiomelanocortin-alpha Mus musculus 86-100 17276074-5 2007 This was further investigated 48h after injecting Xenopus laevis oocytes with the mRNA of rat sodium/taurocholate (TC)-cotransporting polypeptide (Ntcp), rat apical sodium-dependent bile salt transporter (Asbt), or the human isoforms OATP-C/1B1 and OATP8/1B3 of organic anion-transporting polypeptides, when maximal functional expression was detected. Sodium 94-101 solute carrier family 10 member 1 Rattus norvegicus 147-151 17276074-7 2007 In the cases of Ntcp- and Asbt-mediated [(3)H]-TC uptake, these were sodium-dependent and were inhibited by BAPA-6>BAPA-8>BAPA-3 and BAPA-8>BAPA-6>BAPA-3, respectively. Sodium 69-75 solute carrier family 10 member 1 Rattus norvegicus 16-20 17275750-0 2007 Novel mechanism for sudden infant death syndrome: persistent late sodium current secondary to mutations in caveolin-3. Sodium 66-72 caveolin 3 Homo sapiens 107-117 17275750-9 2007 Voltage clamp studies showed that all three CAV3 mutations caused a significant fivefold increase in late sodium current compared with controls. Sodium 106-112 caveolin 3 Homo sapiens 44-48 17294067-4 2007 Sequence analysis indicated that the disease segregates with a novel mutation in the alpha subunit of the voltage-gated sodium channel (SCN9A or Na(v)1.7). Sodium 120-126 immunoglobulin lambda variable 2-23 Homo sapiens 145-153 17145499-3 2006 Functional analysis in vitro of three of these mutant Na(v)1.7 channels revealed a reduction in fast inactivation, leading to persistent sodium current. Sodium 137-143 immunoglobulin lambda variable 2-23 Homo sapiens 54-62 17125365-7 2006 2004, 126, 11377-11386) is able to accurately describe the adsorption properties of linear alkanes in the sodium form of FAU-type zeolites. Sodium 106-112 FAU ubiquitin like and ribosomal protein S30 fusion Homo sapiens 121-124 16705152-1 2006 Sodium-dependent phosphate transport in NHERF-1(-/-) proximal tubule cells does not increase when grown in a low phosphate media and is resistant to the normal inhibitory effects of parathyroid hormone (PTH). Sodium 0-6 parathyroid hormone Mus musculus 203-206 16720863-6 2006 Interestingly, both SGK1 and GILZ appear to negatively regulate tonic inhibition of ENaC and thus use disinhibition to propagate the rapid effects of aldosterone to increase sodium reabsorption in tight epithelia. Sodium 174-180 TSC22 domain family member 3 Homo sapiens 29-33 17054696-2 2006 METHODS: We performed mutation analyses of the sodium-channel gene SCN1A in two Japanese brothers with clinical features of SMEI and their parents, who had no history of febrile and epileptic seizures. Sodium 47-53 sodium voltage-gated channel alpha subunit 1 Homo sapiens 67-72 14580937-2 2003 In addition, previous studies support the existence of a functional interaction between opioid peptides and oxytocinergic pathways, and suggest that beta-endorphin neurons would modulate the activity of central oxytocinergic pathways, its pituitary secretion and sodium appetite. Sodium 263-269 pro-opiomelanocortin-alpha Mus musculus 149-163 14580937-4 2003 Our results show that beta-endorphin knockout (KO) and heterozygous (HT) mutant mice consume approximately a 50% less 2% NaCl solution compared with wild type mice (WT), after furosemide and low sodium diet treatment. Sodium 195-201 pro-opiomelanocortin-alpha Mus musculus 22-36 14580937-5 2003 These data suggest that beta-endorphin may facilitate induced sodium appetite, giving new evidence about the role of beta-endorphin on sodium appetite behavior. Sodium 62-68 pro-opiomelanocortin-alpha Mus musculus 24-38 14580937-9 2003 Taken together, our data suggest that the reduced sodium ingestion observed in beta-endorphin deficient mice could be due to a higher expression of the OT gene. Sodium 50-56 pro-opiomelanocortin-alpha Mus musculus 79-93 14580937-10 2003 This conclusion would support the hypothesis that OT inhibits sodium intake and provides new evidence about beta-endorphin modulation of OT synthesis and sodium appetite. Sodium 154-160 pro-opiomelanocortin-alpha Mus musculus 108-122 14622907-8 2003 Voltage-clamp recordings from the bipolar neurons indicated that chronic treatment with TGFalpha markedly decreased the current densities of slow delayed rectifier (IK) and transient voltage-gated potassium currents, whereas the treatment had no effect on voltage-gated sodium current and fast delayed rectifier potassium current densities. Sodium 270-276 transforming growth factor alpha Homo sapiens 88-96 17000989-1 2006 We examined cases of severe myoclonic epilepsy of infancy (SMEI) for exon deletions or duplications within the sodium channel SCN1A gene by multiplex ligation-dependent probe amplification. Sodium 111-117 sodium voltage-gated channel alpha subunit 1 Homo sapiens 126-131 16914123-0 2006 Effects of ApC, a sea anemone toxin, on sodium currents of mammalian neurons. Sodium 40-46 APC regulator of WNT signaling pathway Homo sapiens 11-14 16914123-1 2006 We have characterized the actions of ApC, a sea anemone polypeptide toxin isolated from Anthopleura elegantissima, on neuronal sodium currents (I(Na)) using current and voltage-clamp techniques. Sodium 127-133 APC regulator of WNT signaling pathway Homo sapiens 37-40 12372821-1 2002 Alveolar hypoxia may impair sodium-dependent alveolar fluid transport and induce pulmonary edema in rat and human lung, an effect that can be prevented by the inhalation of beta(2)-agonists. Sodium 28-34 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 173-179 12372821-2 2002 To investigate the mechanism of beta(2)-agonist-mediated stimulation of sodium transport under conditions of moderate hypoxia, we examined the effect of terbutaline on epithelial sodium channel (ENaC) expression and activity in cultured rat alveolar epithelial type II cells exposed to 3% O(2) for 24 h. Hypoxia reduced transepithelial sodium current and amiloride-sensitive sodium channel activity without decreasing ENaC subunit mRNA or protein levels. Sodium 72-78 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 32-38 12460920-3 2002 Here we show that with VHL gene transduction SY-SH5Y cells stably expressing the VHL protein had neurite-like processes with varicosities, showed the distinct expression of the neuronal markers neuropeptide Y and neurofilament 200, acquired regulated neurosecretion competence in response to depolarizing and cholinergic stimuli, and had large voltage-gated fast sodium currents and delayed rectifier potassium (Kv) currents compatible with those of functional neurons. Sodium 363-369 von Hippel-Lindau tumor suppressor Homo sapiens 23-26 12460920-3 2002 Here we show that with VHL gene transduction SY-SH5Y cells stably expressing the VHL protein had neurite-like processes with varicosities, showed the distinct expression of the neuronal markers neuropeptide Y and neurofilament 200, acquired regulated neurosecretion competence in response to depolarizing and cholinergic stimuli, and had large voltage-gated fast sodium currents and delayed rectifier potassium (Kv) currents compatible with those of functional neurons. Sodium 363-369 von Hippel-Lindau tumor suppressor Homo sapiens 81-84 12388591-11 2002 Instead, in many cases the orexin A-induced current reversed in calcium-free medium at a value (-23 mV) consistent with the activation of a mixed cation channel (with relative permeabilities for sodium and potassium of 0.43 and 1, respectively). Sodium 195-201 hypocretin Mus musculus 27-35 16622683-7 2006 Inward currents were also recorded from egl-19 (n582) which has a loss of function mutation in the pharyngeal L-type calcium channel and these were also markedly reduced in zero external sodium. Sodium 187-193 Voltage-dependent L-type calcium channel subunit alpha Caenorhabditis elegans 40-46 16390332-1 2006 The molecular mechanisms involved in the Ang-(1-7) [angiotensin-(1-7)] effect on sodium renal excretion remain to be determined. Sodium 81-87 angiopoietin 1 Homo sapiens 41-49 16339392-8 2006 The attenuation of sodium retention by clofibrate treatment is linked to decreased expression of NHE-3 in renal cortex. Sodium 19-25 solute carrier family 9 member A3 Rattus norvegicus 97-102 16496131-3 2006 OBJECTIVES: The aim of this study was to analyze the distinct effects of sodium-(Na-) and magnesium-valproate (Mg-VPA) in pyramidal neurons of the medial prefrontal cortex (mPFC) and their interactions with gamma-aminobutyric acid (GABA) and excitatory amino acid responses. Sodium 73-80 complement factor properdin Mus musculus 173-177 16673263-5 2006 It cleaves fibrinogen, factors XI (FXI) and FXIII, cofactors V and VIII, and the thrombin receptors; uses thrombomodulin to activate protein C and thrombin-activatable-fibrinolysis inhibitor; is inhibited by heparin cofactor II and antithrombin III with the help of acidic carbohydrates; and its activity/specificity is modulated by sodium ions. Sodium 333-339 coagulation factor XI Homo sapiens 35-38 12187101-11 2002 Furthermore, intrarenal COX isoforms may play differential roles, with COX-1 participating in modulation of renal hemodynamics, and COX-2 contributing to sodium excretion and Ang II formation. Sodium 154-160 cytochrome c oxidase subunit II Canis lupus familiaris 132-137 16430863-1 2006 Severe Myoclonic Epilepsy in Infancy (SMEI) is an intractable epileptic syndrome with onset in the first year of life and is commonly caused by de novo mutations in the SCN1A gene, encoding the alpha1-subunit of the neuronal voltage-gated sodium channel. Sodium 239-245 sodium voltage-gated channel alpha subunit 1 Homo sapiens 169-174 16601568-2 2006 RESULTS: AT1-receptor activation by angiotensin II is not only involved in the regulation of blood pressure, water and sodium homeostasis, and control of other neurohumoral systems, but also leads to excessive production of reactive oxygen species and to hypertrophy, proliferation, migration, and apoptosis of vascular cells. Sodium 119-125 angiotensin II receptor type 1 Homo sapiens 9-12 16352596-0 2006 Sodium-induced GCN4 expression controls the accumulation of the 5" to 3" RNA degradation inhibitor, 3"-phosphoadenosine 5"-phosphate. Sodium 0-6 amino acid starvation-responsive transcription factor GCN4 Saccharomyces cerevisiae S288C 15-19 16182313-3 2006 The renal aromatic l-amino acid decarboxylase (AADC) activity, the enzyme responsible for the synthesis of renal dopamine, was evaluated during negligible proteinuria accompanied with enhanced sodium retention (day 7), increased proteinuria accompanied with greatest sodium retention (day 14) as well as during increased proteinuria accompanied with negative sodium balance (day 21). Sodium 193-199 dopa decarboxylase Rattus norvegicus 10-45 16182313-3 2006 The renal aromatic l-amino acid decarboxylase (AADC) activity, the enzyme responsible for the synthesis of renal dopamine, was evaluated during negligible proteinuria accompanied with enhanced sodium retention (day 7), increased proteinuria accompanied with greatest sodium retention (day 14) as well as during increased proteinuria accompanied with negative sodium balance (day 21). Sodium 193-199 dopa decarboxylase Rattus norvegicus 47-51 16182313-3 2006 The renal aromatic l-amino acid decarboxylase (AADC) activity, the enzyme responsible for the synthesis of renal dopamine, was evaluated during negligible proteinuria accompanied with enhanced sodium retention (day 7), increased proteinuria accompanied with greatest sodium retention (day 14) as well as during increased proteinuria accompanied with negative sodium balance (day 21). Sodium 267-273 dopa decarboxylase Rattus norvegicus 47-51 16182313-3 2006 The renal aromatic l-amino acid decarboxylase (AADC) activity, the enzyme responsible for the synthesis of renal dopamine, was evaluated during negligible proteinuria accompanied with enhanced sodium retention (day 7), increased proteinuria accompanied with greatest sodium retention (day 14) as well as during increased proteinuria accompanied with negative sodium balance (day 21). Sodium 267-273 dopa decarboxylase Rattus norvegicus 47-51 16357110-2 2006 There are two sodium-dependent membrane transporters encoded by SLC23A1 and SLC23A2, which have key roles in human vitamin C metabolism and which control dietary uptake, reabsorption, and tissue distribution of vitamin C. Sodium 14-20 solute carrier family 23 member 2 Homo sapiens 76-83 12126985-2 2002 Intragastric sodium load increased plasma sodium concentration and osmolality by 5% and reduced plasma renin activity by half compared to rats that received intragastric load of water. Sodium 13-19 renin Rattus norvegicus 103-108 16229907-10 2005 The rates of creatinine (Cr), sodium (Na), and protein excretions of the animals infused leptin were significantly increased. Sodium 30-36 leptin Rattus norvegicus 89-95 12015312-1 2002 Inappropriate activation of the mineralocorticoid receptor (MR) results in renal sodium retention and potassium loss in patients with liver cirrhosis. Sodium 81-87 nuclear receptor subfamily 3 group C member 2 Homo sapiens 32-58 12412405-1 2002 A sodium-proton exchanger (NHE) is a membrane transport system taking part in intracellular sodium homeostasis. Sodium 2-8 solute carrier family 9 member C1 Homo sapiens 27-30 12146504-3 2002 Herein, physiological changes in the endogenous level of activity of the renin-angiotensin system were produced by alterations in the dietary sodium intake. Sodium 142-148 renin Rattus norvegicus 73-78 12146504-4 2002 Microinjection of the angiotensin II AT1 receptor antagonists losartan or candesartan into the rostral ventrolateral medulla produced the bradycardic, depressor and renal sympathoinhibitory responses which were greater in low sodium diet rats with stimulated activity of the renin-angiotensin system than in high sodium diet rats with suppressed activity of the renin-angiotensin system activity. Sodium 226-232 angiotensin II receptor, type 1a Rattus norvegicus 37-40 12146504-4 2002 Microinjection of the angiotensin II AT1 receptor antagonists losartan or candesartan into the rostral ventrolateral medulla produced the bradycardic, depressor and renal sympathoinhibitory responses which were greater in low sodium diet rats with stimulated activity of the renin-angiotensin system than in high sodium diet rats with suppressed activity of the renin-angiotensin system activity. Sodium 313-319 angiotensin II receptor, type 1a Rattus norvegicus 37-40 12052438-11 2002 In addition, the ratio of urinary sodium excretion to dietary sodium intake was significantly lower in the FAT group than in the CHO group. Sodium 34-40 FAT atypical cadherin 1 Rattus norvegicus 107-110 16320974-7 2005 CONCLUSIONS: Angiotensin II type 1 receptor blockade with a therapeutic dosage of candesartan maintains significant control of blood pressure and may improve QOL-scores, especially when combined with a reducing sodium diet. Sodium 211-217 angiotensin II receptor type 1 Homo sapiens 13-43 16172412-7 2005 Polymorphisms in genes regulating renal sodium transport, in particular WNK1, predict interindividual differences in antihypertensive responses to hydrochlorothiazide. Sodium 40-46 WNK lysine deficient protein kinase 1 Homo sapiens 72-76 16172423-1 2005 The dopaminergic and renin-angiotensin systems regulate blood pressure, in part, by affecting sodium transport in renal proximal tubules (RPTs). Sodium 94-100 renin Rattus norvegicus 21-26 16172430-7 2005 Prostasin was detectable in all subjects regardless of gender, dietary sodium intake, and spironolactone treatment. Sodium 71-77 serine protease 8 Homo sapiens 0-9 16172430-12 2005 In addition to a "basal" aliquot of prostasin, constitutively released in human urine regardless of sodium balance and aldosterone activation, there exists a second "aldosterone-responsive" aliquot modulated by Na+ intake and potentially suitable as candidate marker of ENaC activation. Sodium 100-106 serine protease 8 Homo sapiens 36-45 15970509-5 2005 The pharmacological selectivity and safety of PST 2238 suggests that the compound may be effective for the treatment of those forms of hypertension in which renal sodium handling alterations and cardiovascular complications are associated with increased production of EO. Sodium 163-169 sulfotransferase family 1A member 1 Homo sapiens 46-49 15802372-2 2005 In recent years, evidence has been provided for an important role of MR not only in the regulation of sodium and water homeostasis but also in cardiovascular function, neuronal fate, and adipocyte differentiation. Sodium 102-108 nuclear receptor subfamily 3 group C member 2 Homo sapiens 69-71 12052438-11 2002 In addition, the ratio of urinary sodium excretion to dietary sodium intake was significantly lower in the FAT group than in the CHO group. Sodium 62-68 FAT atypical cadherin 1 Rattus norvegicus 107-110 12134182-0 2002 Endogenous sodium-potassium ATPase inhibition related biochemical cascade in trisomy 21 and Huntington"s disease: neural regulation of genomic function. Sodium 11-17 dynein axonemal heavy chain 8 Homo sapiens 28-34 12094292-1 2002 Sodium spirulan (Na-SP) is a sulfated polysaccharide isolated from the blue-green alga Spirulina platensis, which consists of two types of disaccharide repeating units, O-hexuronosyl-rhamnose (aldobiuronic acid) and O-rhamnosyl-3-O-methylrhamnose (acofriose) with sulfate groups, other minor saccharides and sodium ion. Sodium 308-314 nuclear autoantigenic sperm protein Bos taurus 17-22 15956070-0 2005 Sodium retention in rats with liver cirrhosis is associated with increased renal abundance of NaCl cotransporter (NCC). Sodium 0-6 solute carrier family 12 member 3 Rattus norvegicus 94-112 15956070-0 2005 Sodium retention in rats with liver cirrhosis is associated with increased renal abundance of NaCl cotransporter (NCC). Sodium 0-6 solute carrier family 12 member 3 Rattus norvegicus 114-117 15913657-12 2005 Leptin decreased absolute and fractional sodium excretion by 44.5% and 44.7%, respectively. Sodium 41-47 leptin Rattus norvegicus 0-6 12119799-4 2002 The DASH-Sodium trial demonstrates significant increases in SBP and DBP, with sodium intake greater than 65 mmol/d (= 3.7 g NaCl--see equivalencies in Appendix A) and with the usual American diet (versus the DASH diet). Sodium 9-15 selenium binding protein 1 Homo sapiens 60-63 11834730-1 2002 SAT1-3 comprise members of the recently cloned family of System A transporters that mediate the sodium-coupled uptake of short chain neutral amino acids, and their activity is regulated extensively by stimuli such as insulin, growth factors, and amino acid availability. Sodium 96-102 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-4 11893620-4 2002 Combined volume expansion and L-arginine infusion tended to increase arterial blood pressure and increased GFR by 31%, whereas peak sodium excretion was enhanced to 335 +/- 23 micromol/min at plasma ANG II levels of 3.0 +/- 1.1 pg/ml; urine flow and osmolar clearance were increased at constant free water clearance. Sodium 132-138 angiogenin Homo sapiens 199-202 16261999-1 2005 The content of calcium (Ca) and magnesium (Mg) in sweat during exercise is considerably higher during a relatively low intake of sodium (Na) of 100 mmol/d than with an intake of 170 mmol/d. Sodium 129-135 SMU1 DNA replication regulator and spliceosomal factor Homo sapiens 30-31 16261999-1 2005 The content of calcium (Ca) and magnesium (Mg) in sweat during exercise is considerably higher during a relatively low intake of sodium (Na) of 100 mmol/d than with an intake of 170 mmol/d. Sodium 129-135 SMU1 DNA replication regulator and spliceosomal factor Homo sapiens 56-57 16054936-0 2005 Mutation in the neuronal voltage-gated sodium channel SCN1A in familial hemiplegic migraine. Sodium 39-45 sodium voltage-gated channel alpha subunit 1 Homo sapiens 54-59 16054936-6 2005 Sequencing of candidate genes in this region revealed a heterozygous missense mutation (Gln1489Lys) in the neuronal voltage-gated sodium channel gene SCN1A, mutations of which have been associated with epilepsy. Sodium 130-136 sodium voltage-gated channel alpha subunit 1 Homo sapiens 150-155 16054936-10 2005 INTERPRETATION: Dysfunction of the neuronal sodium channel SCN1A can cause familial hemiplegic migraine. Sodium 44-50 sodium voltage-gated channel alpha subunit 1 Homo sapiens 59-64 15987778-1 2005 The renal outer-medullary K+ channel (ROMK; Kir1.1) mediates K+ secretion in the renal mammalian nephron that is critical to both sodium and potassium homeostasis. Sodium 130-136 potassium inwardly rectifying channel subfamily J member 1 Homo sapiens 4-36 15987778-1 2005 The renal outer-medullary K+ channel (ROMK; Kir1.1) mediates K+ secretion in the renal mammalian nephron that is critical to both sodium and potassium homeostasis. Sodium 130-136 potassium inwardly rectifying channel subfamily J member 1 Homo sapiens 38-42 15987778-1 2005 The renal outer-medullary K+ channel (ROMK; Kir1.1) mediates K+ secretion in the renal mammalian nephron that is critical to both sodium and potassium homeostasis. Sodium 130-136 potassium inwardly rectifying channel subfamily J member 1 Homo sapiens 44-50 11932310-18 2002 This together with unchanged or decreased atrial natriuretic peptides and BNP may prevent pressure-induced escape of sodium. Sodium 117-123 natriuretic peptide B Homo sapiens 74-77 11901224-6 2002 Uptake of both Bamets by Ntcp-transfected CHO cells was stimulated by extracellular sodium. Sodium 84-90 solute carrier family 10 member 1 Rattus norvegicus 25-29 11832422-9 2002 Sodium uptake was lower in oocytes injected with both antisense grp58 cRNA and sense NCC compared with sense NCC oocytes. Sodium 0-6 solute carrier family 12 member 3 Rattus norvegicus 85-88 11821059-0 2002 Evidence for cardiac sodium-calcium exchanger association with caveolin-3. Sodium 21-27 caveolin 3 Homo sapiens 63-73 11913598-9 2002 Change in urinary sodium-to-creatinine ratios of 3 consecutive pooled overnight 8-hour urine collections correlated with changes in 24-hour ambulatory SBP (r = 0.294, P<.001) and DBP (r = 0.193, P<.05); however, change in total urinary sodium content was uncorrelated. Sodium 18-24 selenium binding protein 1 Homo sapiens 151-154 11913598-9 2002 Change in urinary sodium-to-creatinine ratios of 3 consecutive pooled overnight 8-hour urine collections correlated with changes in 24-hour ambulatory SBP (r = 0.294, P<.001) and DBP (r = 0.193, P<.05); however, change in total urinary sodium content was uncorrelated. Sodium 242-248 selenium binding protein 1 Homo sapiens 151-154 11787028-7 2002 X-ray diffraction revealed the presence of mica and diopside as major crystalline phases in the sodium-free composition. Sodium 96-102 MHC class I polypeptide-related sequence A Homo sapiens 43-47 15799965-5 2005 RNAi of mps-2, mps-3, or both, enhance the taste of the animal for sodium without altering the susceptibility to other attractants. Sodium 67-73 MiRP K channel accessory Subunit Caenorhabditis elegans 8-13 15799965-5 2005 RNAi of mps-2, mps-3, or both, enhance the taste of the animal for sodium without altering the susceptibility to other attractants. Sodium 67-73 MiRP K channel accessory Subunit Caenorhabditis elegans 15-20 11787028-9 2002 The microstructure of the sodium-free glass-ceramic was characterized by the presence of hexagonal mica crystals and prismatic diopside crystals. Sodium 26-32 MHC class I polypeptide-related sequence A Homo sapiens 99-103 11752091-0 2002 Simultaneous intracellular calcium and sodium flux imaging in human vanilloid receptor 1 (VR1)-transfected human embryonic kidney cells: a method to resolve ionic dependence of VR1-mediated cell death. Sodium 39-45 transient receptor potential cation channel subfamily V member 1 Homo sapiens 90-93 11752091-2 2002 Activation of VR1 leads to increases in intracellular concentrations of calcium and sodium. Sodium 84-90 transient receptor potential cation channel subfamily V member 1 Homo sapiens 14-17 11738055-1 2001 OBJECTIVE: Although it is believed that sodium-driven acid-base transport plays a central role in the development of the reperfusion injury that follows cardiac ischemia, research to date has demonstrated only a role for Na(+)/H(+) exchange (NHE). Sodium 40-46 solute carrier family 9 member C1 Homo sapiens 242-245 11722471-1 2001 Defects of both sodium-hydrogen exchange (NHE) and sodium-lithium countertransport (SLC) have been described in subjects at increased risk of coronary heart disease (CHD). Sodium 16-22 solute carrier family 9 member C1 Homo sapiens 42-45 11602666-1 2001 Rat oatp1 (Slc21a1) and oatp2 (Slc21a5) transport many structurally unrelated endogenous and exogenous compounds across the sinusoidal membrane of hepatocytes in a sodium-independent manner. Sodium 164-170 solute carrier organic anion transporter family, member 1a4 Rattus norvegicus 24-29 11602666-1 2001 Rat oatp1 (Slc21a1) and oatp2 (Slc21a5) transport many structurally unrelated endogenous and exogenous compounds across the sinusoidal membrane of hepatocytes in a sodium-independent manner. Sodium 164-170 solute carrier organic anion transporter family, member 1a4 Rattus norvegicus 31-38 11507017-5 2001 Despite the elevated plasma renin concentration, plasma ANG II in mice on low-sodium level averaged 14 +/- 3 pg/ml and was significantly suppressed to 6 +/- 1 pg/ml by high-sodium intake (n = 7). Sodium 78-84 angiogenin, ribonuclease, RNase A family, 5 Mus musculus 56-59 11507017-5 2001 Despite the elevated plasma renin concentration, plasma ANG II in mice on low-sodium level averaged 14 +/- 3 pg/ml and was significantly suppressed to 6 +/- 1 pg/ml by high-sodium intake (n = 7). Sodium 173-179 angiogenin, ribonuclease, RNase A family, 5 Mus musculus 56-59 11544140-7 2001 In order to obtain information about the mechanism involved in the sodium transport diminution provoked by alloxan, in this study the function of Na+-K+ ATPase enzyme on transepithelial sodium transport altered by alloxan is explored. Sodium 67-73 dynein axonemal heavy chain 8 Homo sapiens 153-159 11544140-7 2001 In order to obtain information about the mechanism involved in the sodium transport diminution provoked by alloxan, in this study the function of Na+-K+ ATPase enzyme on transepithelial sodium transport altered by alloxan is explored. Sodium 186-192 dynein axonemal heavy chain 8 Homo sapiens 153-159 11399753-1 2001 The Na(+)/dicarboxylate co-transporter, NaDC-1, couples the transport of sodium and Krebs cycle intermediates, such as succinate and citrate. Sodium 73-79 solute carrier family 13 member 2 Homo sapiens 40-46 11487728-12 2001 In summary, these studies describe the expression cloning of CNT2 from a rat BBB library and show that the pattern of sodium dependency and NBTI insensitivity of the cloned CNT2 are identical to patterns of adenosine transport across the BBB in vivo. Sodium 118-124 solute carrier family 28 member 2 Rattus norvegicus 61-65 11493618-10 2001 Results suggest a sodium-specific inhibitory effect on up-regulation of beta2-integrins of fMLP-stimulated PMNLs, which is unlikely to be caused by alterations of fMLP receptor binding, decrease in cytosolic calcium, attenuation of calcium or protein kinase C-dependent pathways, suppression of p38- or p44/42 MAP kinase-dependent pathways, or cellular ability to increase or decrease volumes. Sodium 18-24 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 72-77 11473661-9 2001 RESULTS: In the Cox model, comorbidity, total sodium and fluid removals, hypertensive status, serum creatinine, and RRF were independent factors affecting survival. Sodium 46-52 cytochrome c oxidase subunit 8A Homo sapiens 16-19 15811336-0 2005 Nav1.6 channels generate resurgent sodium currents in spinal sensory neurons. Sodium 35-41 neuron navigator 1 Mus musculus 0-4 15709964-1 2005 The sodium/hydrogen exchange (NHE) gene family plays an integral role in neutral sodium absorption in the mammalian intestine. Sodium 4-10 solute carrier family 9 member C1 Homo sapiens 30-33 15709964-1 2005 The sodium/hydrogen exchange (NHE) gene family plays an integral role in neutral sodium absorption in the mammalian intestine. Sodium 81-87 solute carrier family 9 member C1 Homo sapiens 30-33 15759054-0 2005 Effect of nonsteroidal anti-inflammatory drugs with varying extent of COX-2-COX-1 selectivity on urinary sodium and potassium excretion in the rat. Sodium 105-111 prostaglandin-endoperoxide synthase 1 Rattus norvegicus 76-81 15246975-0 2004 Prostasin, a membrane-anchored serine peptidase, regulates sodium currents in JME/CF15 cells, a cystic fibrosis airway epithelial cell line. Sodium 59-65 serine protease 8 Homo sapiens 0-9 15651314-2 2004 Mutations of voltage-gated sodium channel genes SCN1A and SCN2A have been reported in epilepsies with a variety of phenotypes including generalized epilepsy with febrile seizures plus (GEFS +), severe myoclonic epilepsy in infancy (SMEI), intractable childhood epilepsy with generalized tonic-clonic seizures (ICEGTC), and benign familial neonatal-infantile seizures (BFNIS). Sodium 27-33 sodium voltage-gated channel alpha subunit 1 Homo sapiens 48-53 15492316-6 2004 In men, in the population- and family-based analyses, the allelic effects of the AGTR2 polymorphism on LVM index differed (P=0.01) according to sodium excretion. Sodium 144-150 angiotensin II receptor type 2 Homo sapiens 81-86 15492316-9 2004 The ACE D/I polymorphism, together with the ACE genotype-by-sodium interaction term, significantly and independently improved the models relating LVM index to the AGTR2 polymorphism and the AGTR2 genotype-by-sodium interaction. Sodium 60-66 angiotensin II receptor type 2 Homo sapiens 163-168 15492316-9 2004 The ACE D/I polymorphism, together with the ACE genotype-by-sodium interaction term, significantly and independently improved the models relating LVM index to the AGTR2 polymorphism and the AGTR2 genotype-by-sodium interaction. Sodium 60-66 angiotensin II receptor type 2 Homo sapiens 190-195 15492316-9 2004 The ACE D/I polymorphism, together with the ACE genotype-by-sodium interaction term, significantly and independently improved the models relating LVM index to the AGTR2 polymorphism and the AGTR2 genotype-by-sodium interaction. Sodium 208-214 angiotensin II receptor type 2 Homo sapiens 190-195 15314032-0 2004 Inhibition of cyclooxygenase-2 in the rat renal medulla leads to sodium-sensitive hypertension. Sodium 65-71 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 14-30 15385606-1 2004 Although the physiological basis of erythermalgia, an autosomal dominant painful neuropathy characterized by redness of the skin and intermittent burning sensation of extremities, is not known, two mutations of Na(v)1.7, a sodium channel that produces a tetrodotoxin-sensitive, fast-inactivating current that is preferentially expressed in dorsal root ganglia (DRG) and sympathetic ganglia neurons, have recently been identified in patients with primary erythermalgia. Sodium 223-229 immunoglobulin lambda variable 2-23 Homo sapiens 211-219 15371515-6 2004 Direct GLP-1 agonist actions on membrane potential were abolished by choline substitution for extracellular Na+, and dependent on intracellular GDP, suggesting that they were mediated by sodium-dependent conductances in a G-protein-dependent manner. Sodium 187-193 glucagon Mus musculus 7-12 11455025-0 2001 Modeling and mutational analysis of a putative sodium-binding pocket on the dopamine D2 receptor. Sodium 47-53 dopamine receptor D2 Homo sapiens 76-96 11474229-9 2001 Its expression in the kidney tubules, the major site of sulphation in the kidney, suggests that CDO in the kidney may play a role in both xenobiotic metabolism and sodium and water homeostasis. Sodium 164-170 cysteine dioxygenase type 1 Rattus norvegicus 96-99 11499660-19 2001 administration of HgCl2 with and without in vivo fixation, accompanied by a significant decrease in aquaporin-mediated water transport, estimated as the sieving of sodium (p < 0.001). Sodium 164-170 lens fiber major intrinsic protein Oryctolagus cuniculus 100-109 11322861-1 2001 The Na-H exchanger (NHE) represents a family of transporters which regulate intracellular pH by removing protons in exchange for sodium influx in an electroneutral 1:1 stoichiometric relationship. Sodium 129-135 solute carrier family 9 member C1 Homo sapiens 4-18 15359088-7 2004 Adding the variables sodium ([Na(+)]) and fibrinogen ([Fibr]) concentration the coefficient of correlation further improved to r(2) = 0.928 and the relation became: eta = -0.6844 + 0.038 R + 0.038 [Na(+)] + 0.514 [Fibr]. Sodium 21-27 endothelin receptor type A Homo sapiens 165-168 11322861-1 2001 The Na-H exchanger (NHE) represents a family of transporters which regulate intracellular pH by removing protons in exchange for sodium influx in an electroneutral 1:1 stoichiometric relationship. Sodium 129-135 solute carrier family 9 member C1 Homo sapiens 20-23 11250940-9 2001 The early onset of SGK induction in kidney and colon and the correlation with urinary changes in terms of both time course and dose response suggest that SGK plays an important role in mediating the effects of aldosterone on sodium homeostasis in vivo. Sodium 225-231 serum/glucocorticoid regulated kinase 1 Rattus norvegicus 19-22 11250940-9 2001 The early onset of SGK induction in kidney and colon and the correlation with urinary changes in terms of both time course and dose response suggest that SGK plays an important role in mediating the effects of aldosterone on sodium homeostasis in vivo. Sodium 225-231 serum/glucocorticoid regulated kinase 1 Rattus norvegicus 154-157 11496924-7 2001 The Scn8a mutations provide insight into the mode of inheritance, effect on neuronal sodium currents, and role of modifier genes in sodium channel disease, highlighting the ways in which mouse models of human mutations can be used in the future to understand the pathophysiology of human disease. Sodium 85-91 sodium channel, voltage-gated, type VIII, alpha Mus musculus 4-9 11196466-0 2000 Regulation of MAPK activity in response to dietary sodium in the rat adrenal gland. Sodium 51-57 mitogen activated protein kinase 3 Rattus norvegicus 14-18 11196466-2 2000 MAPK (p42/p44) is involved in cell proliferation, and is also activated by AII, but its role in the adrenal response to dietary sodium is unclear. Sodium 128-134 mitogen activated protein kinase 3 Rattus norvegicus 0-4 11196466-4 2000 In adrenals from animals on a sodium deplete diet, total ligand binding to both ATR subtypes decreased in the zona glomerulosa (ZG). Sodium 30-36 angiotensin II receptor, type 2 Rattus norvegicus 80-83 11196466-8 2000 In adrenals from sodium-loaded animals, type 2 ATR (AT2R) binding was reduced in the ZG, while type 1 ATR (AT1R) increased in the IZ. Sodium 17-23 angiotensin II receptor, type 2 Rattus norvegicus 47-50 11196466-8 2000 In adrenals from sodium-loaded animals, type 2 ATR (AT2R) binding was reduced in the ZG, while type 1 ATR (AT1R) increased in the IZ. Sodium 17-23 angiotensin II receptor, type 2 Rattus norvegicus 52-56 11196466-8 2000 In adrenals from sodium-loaded animals, type 2 ATR (AT2R) binding was reduced in the ZG, while type 1 ATR (AT1R) increased in the IZ. Sodium 17-23 angiotensin II receptor, type 2 Rattus norvegicus 102-105 11196466-8 2000 In adrenals from sodium-loaded animals, type 2 ATR (AT2R) binding was reduced in the ZG, while type 1 ATR (AT1R) increased in the IZ. Sodium 17-23 angiotensin II receptor, type 2 Rattus norvegicus 107-111 10998198-9 2000 OK cells exhibited endogenous sodium-dependent sulfate transport; significantly increased sodium/sulfate co-transport was also observed in OK cells that were preincubated with GH, IGF-1, and PG/EST, although not with EST alone. Sodium 90-96 insulin like growth factor 1 Canis lupus familiaris 180-185 11787472-1 2000 Gastric sodium loading results in an increase in the portal venous concentration of vasoactive intestinal peptide (VIP) and down-regulation of both the intrahepatic and circulating renin-angiotensin systems. Sodium 8-14 renin Rattus norvegicus 181-186 11787472-10 2000 These changes are similar to those reported after gastric sodium loading, and we suggest, therefore, that the increase in portal venous VIP that occurs after gastric sodium is the means by which the gastric sodium sensor signals the liver to effect these changes in the renin-angiotensin system. Sodium 58-64 renin Rattus norvegicus 270-275 11787472-10 2000 These changes are similar to those reported after gastric sodium loading, and we suggest, therefore, that the increase in portal venous VIP that occurs after gastric sodium is the means by which the gastric sodium sensor signals the liver to effect these changes in the renin-angiotensin system. Sodium 166-172 renin Rattus norvegicus 270-275 11787472-10 2000 These changes are similar to those reported after gastric sodium loading, and we suggest, therefore, that the increase in portal venous VIP that occurs after gastric sodium is the means by which the gastric sodium sensor signals the liver to effect these changes in the renin-angiotensin system. Sodium 166-172 renin Rattus norvegicus 270-275 11016794-9 2000 (c) In the Japanese sample, multiple linear regression analyses (using a stepwise procedure) showed that SBP had a significant positive association with BMI and sodium excretion, and a significant negative association with magnesium excretion, while DBP had a significant positive association with BMI and a significant negative association with the 3MH to creatinine ratio (3MH/Cre). Sodium 161-167 selenium binding protein 1 Homo sapiens 105-108 15265699-4 2004 Because sodium/hydrogen (Na(+)/H(+)) exchangers (NHEs) are known to regulate intracellular pH, melanocytes were treated with NHE inhibitors to determine what effect this inhibition might have on tyrosinase activity. Sodium 8-14 solute carrier family 9 member C1 Homo sapiens 49-52 11016794-10 2000 In the Chinese sample, both SBP and DBP showed a significant positive association with BMI and sodium, and a significant negative association with 3MH/Cre. Sodium 95-101 selenium binding protein 1 Homo sapiens 28-31 11108153-3 2000 The present experiment was designed to determine (1) whether expression of the type 1 Ang II (AT1) receptor in the MTAL is regulated by altered sodium intake, and (2) the specific pathway(s) mediating sodium-induced AT1 expression in the MTAL. Sodium 144-150 angiotensin II receptor, type 1a Rattus norvegicus 94-97 11108153-3 2000 The present experiment was designed to determine (1) whether expression of the type 1 Ang II (AT1) receptor in the MTAL is regulated by altered sodium intake, and (2) the specific pathway(s) mediating sodium-induced AT1 expression in the MTAL. Sodium 201-207 angiotensin II receptor, type 1a Rattus norvegicus 94-97 15521360-3 2004 Under normal conditions, D1-like receptors (D1 and D5) inhibit sodium transport in the kidney and the intestine. Sodium 63-69 leiomodin 1 Homo sapiens 44-53 11108153-3 2000 The present experiment was designed to determine (1) whether expression of the type 1 Ang II (AT1) receptor in the MTAL is regulated by altered sodium intake, and (2) the specific pathway(s) mediating sodium-induced AT1 expression in the MTAL. Sodium 201-207 angiotensin II receptor, type 1a Rattus norvegicus 216-219 11108153-5 2000 Northern blot analysis and radioligand binding showed that in rats fed a normal sodium diet the rank of order for both AT1 mRNA expression and receptor density was outer medulla > cortex > inner medulla. Sodium 80-86 angiotensin II receptor, type 1a Rattus norvegicus 119-122 11108153-6 2000 Sodium restriction significantly increased both AT1 mRNA expression and receptor density in the outer medulla. Sodium 0-6 angiotensin II receptor, type 1a Rattus norvegicus 48-51 15229341-5 2004 RESULTS: In the control group (n = 8), an intravenous bolus of leptin, 400 microg/kg body weight, increased urinary sodium excretion 4- to 6-fold. Sodium 116-122 leptin Rattus norvegicus 63-69 11108153-8 2000 Losartan treatment (3 mg/kg/per day by oral gavage for 2 weeks) prevented low sodium-induced upregulation of the AT1 receptor in the outer medulla, but it had no effect on AT1 expression in the outer medulla of rats fed a normal sodium diet. Sodium 78-84 angiotensin II receptor, type 1a Rattus norvegicus 113-116 15229341-7 2004 Acute sodium nitroprusside infusion to Sprague-Dawley rats chronically treated with L-NAME (n = 8) was associated with partial restoration of the sodium excretory response to leptin administration. Sodium 6-12 leptin Rattus norvegicus 175-181 11108153-10 2000 Low sodium intake significantly increased AT1 mRNA level by 184% and AT1 receptor density by 58% in MTALs. Sodium 4-10 angiotensin II receptor, type 1a Rattus norvegicus 42-45 11108153-10 2000 Low sodium intake significantly increased AT1 mRNA level by 184% and AT1 receptor density by 58% in MTALs. Sodium 4-10 angiotensin II receptor, type 1a Rattus norvegicus 69-72 11108153-13 2000 We conclude that (1) sodium restriction but not sodium loading increases AT1 receptor expression in the MTAL, (2) low sodium-induced upregulation of the AT1 receptor in the MTAL is Ang II-dependent, and (3) Ang II-induced upregulation of the AT1 receptor in the MTAL is mediated, at least in part, by cytochrome P450 pathways. Sodium 21-27 angiotensin II receptor, type 1a Rattus norvegicus 73-76 15007040-2 2004 The serum and glucocorticoid inducible kinase (Sgk) is thought to participate in the regulation of sodium handling in distal tubular segments. Sodium 99-105 serum/glucocorticoid regulated kinase 1 Rattus norvegicus 4-45 15007040-2 2004 The serum and glucocorticoid inducible kinase (Sgk) is thought to participate in the regulation of sodium handling in distal tubular segments. Sodium 99-105 serum/glucocorticoid regulated kinase 1 Rattus norvegicus 47-50 11108153-13 2000 We conclude that (1) sodium restriction but not sodium loading increases AT1 receptor expression in the MTAL, (2) low sodium-induced upregulation of the AT1 receptor in the MTAL is Ang II-dependent, and (3) Ang II-induced upregulation of the AT1 receptor in the MTAL is mediated, at least in part, by cytochrome P450 pathways. Sodium 21-27 angiotensin II receptor, type 1a Rattus norvegicus 153-156 11108153-13 2000 We conclude that (1) sodium restriction but not sodium loading increases AT1 receptor expression in the MTAL, (2) low sodium-induced upregulation of the AT1 receptor in the MTAL is Ang II-dependent, and (3) Ang II-induced upregulation of the AT1 receptor in the MTAL is mediated, at least in part, by cytochrome P450 pathways. Sodium 21-27 angiotensin II receptor, type 1a Rattus norvegicus 153-156 14993604-9 2004 Human OATP4C1 transports cardiac glycosides (digoxin, K(m) = 7.8 microM and ouabain, K(m) = 0.38 microM), thyroid hormone (triiodothyronine, K(m) = 5.9 microM and thyroxine), cAMP, and methotrexate in a sodium-independent manner. Sodium 203-209 solute carrier organic anion transporter family member 4C1 Homo sapiens 6-13 10954003-10 2000 CONCLUSIONS: One component of the chronic stimulation of PRA by dietary sodium restriction via the macula densa pathway appears to involve the induction of COX-2. Sodium 72-78 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 156-161 12928314-10 2003 These results identify a marked and highly segment-specific downregulation of beta-ENaC and gamma-ENaC in the cortical and outer medullary collecting duct, chief sites for collecting duct sodium reabsorption, in rats with a lithium-induced increase in fractional excretion of sodium. Sodium 188-194 sodium channel epithelial 1 subunit beta Rattus norvegicus 78-87 12928314-10 2003 These results identify a marked and highly segment-specific downregulation of beta-ENaC and gamma-ENaC in the cortical and outer medullary collecting duct, chief sites for collecting duct sodium reabsorption, in rats with a lithium-induced increase in fractional excretion of sodium. Sodium 276-282 sodium channel epithelial 1 subunit beta Rattus norvegicus 78-87 10783384-8 2000 The E452K mutation is the first natural mutation in a mammalian cotransporter affecting sodium-coupled solute transfer and identifies a novel domain of the OCTN2 cotransporter involved in transmembrane sodium/solute transfer. Sodium 88-94 solute carrier family 22 member 5 Homo sapiens 156-161 10869292-5 2000 In contrast, sodium-independent taurocholate uptake mediated by the organic anion transporting polypeptides, Oatp1 and Oatp2, was already substantially inhibited by 10 micromol/L rifamycin SV. Sodium 13-19 solute carrier organic anion transporter family, member 1a4 Rattus norvegicus 119-124 10912764-10 2000 Renal augmentation of ANG II, hypertension, and suppressed sodium excretion are blocked by AT1 receptor blockers. Sodium 59-65 angiotensin II receptor, type 1a Rattus norvegicus 91-94 10912764-16 2000 The augmented intrarenal ANG II coupled with sustained levels of AT1 receptors contribute to the continued ANG II dependent suppression of renal function and sodium excretion thereby maintaining the hypertension. Sodium 158-164 angiotensin II receptor, type 1a Rattus norvegicus 65-68 10860927-1 2000 We have demonstrated previously that a planar conformation of the molecular frame is required for steroids to acquire optimal sodium-retaining activity and binding properties to the mineralocorticoid receptor (MR). Sodium 126-132 nuclear receptor subfamily 3 group C member 2 Homo sapiens 182-208 10860927-1 2000 We have demonstrated previously that a planar conformation of the molecular frame is required for steroids to acquire optimal sodium-retaining activity and binding properties to the mineralocorticoid receptor (MR). Sodium 126-132 nuclear receptor subfamily 3 group C member 2 Homo sapiens 210-212 10841345-6 2000 Furthermore, we propose that the observed sodium-dependent ascorbate transport in cultured astrocytes may be due to artificial upregulation of SVCT2 during cell culturing. Sodium 42-48 solute carrier family 23 member 2 Homo sapiens 143-148 10818067-8 2000 The results suggest that increased angiotensin II, in response to sodium restriction and valsartan infusion, stimulates AT(2)R, which mediates a BK and NO cascade. Sodium 66-72 angiotensin II receptor, type 2 Rattus norvegicus 120-126 10770262-7 2000 The results showed that (1) Sodium was positively, and 3MH negatively associated with systolic and diastolic BP (SBP, DBP) in both the total sample and in those who were not administered anti-hypertensive drugs; these associations were all significant (p< 0.05), and remained so after adjustment for age, sex, body mass index [BMI, weight (kg)/height (m2)], alcohol intake and potassium excretion. Sodium 28-34 selenium binding protein 1 Homo sapiens 113-116 10770262-9 2000 In general, subjects who had higher sodium and lower 3MH levels had higher mean SBP and DBP. Sodium 36-42 selenium binding protein 1 Homo sapiens 80-83 10726708-2 2000 Inhibition by xenobiotics such as liquorice or mutations in the HSD11 B2 gene, as occur in the rare monogenic hypertensive syndrome of apparent mineralocorticoid excess (AME), result in a compromised 11 betaHSD2 enzyme activity, which in turn leads to overstimulation of the MR by cortisol, sodium retention, hypokalaemia, low plasma renin and aldosterone concentrations, and hypertension. Sodium 291-297 nuclear receptor subfamily 3 group C member 2 Homo sapiens 275-277 10726717-12 2000 Reductions in sodium intake, insulin levels and sympathetic tone combined with possible improvements in arterial compliance induce persistent 24 h reductions in SBP and pulse BP. Sodium 14-20 selenium binding protein 1 Homo sapiens 161-164 14689370-1 2003 In the kidney, neutral endopeptidase (NEP) is implicated in the metabolism of several peptides involved in blood pressure and sodium homeostasis control, such as the atrial natriuretic peptide, bradykinin and angiotensin I. Sodium 126-132 membrane metallo endopeptidase Mus musculus 15-36 14689370-1 2003 In the kidney, neutral endopeptidase (NEP) is implicated in the metabolism of several peptides involved in blood pressure and sodium homeostasis control, such as the atrial natriuretic peptide, bradykinin and angiotensin I. Sodium 126-132 membrane metallo endopeptidase Mus musculus 38-41 12842829-6 2003 Ntcp mediated high affinity, sodium-dependent transport of [35S]sulfobromophthalein with a Km similar to that of oatp1-mediated transport of [35S]sulfobromophthalein (Km = 3.7 vs. 3.3 muM, respectively). Sodium 29-35 solute carrier family 10 member 1 Rattus norvegicus 0-4 12869368-9 2003 ANG II decreased sodium excretion by 70%, potassium excretion by 50%, and urine flow by 80%, whereas urine osmolality increased. Sodium 17-23 angiogenin Homo sapiens 0-3 12869368-13 2003 It is concluded that 1) ANG III and ANG IV are cleared much faster from plasma than ANG II, 2) ANG II causes hypofiltration, urinary concentration, and sodium and potassium retention at constant plasma concentrations of vasopressin and atrial natriuretic peptide, and 3) a very small increase in the concentration of ANG III, undetectable by usual techniques, may increase aldosterone secretion substantially. Sodium 152-158 angiogenin Homo sapiens 36-39 12869368-13 2003 It is concluded that 1) ANG III and ANG IV are cleared much faster from plasma than ANG II, 2) ANG II causes hypofiltration, urinary concentration, and sodium and potassium retention at constant plasma concentrations of vasopressin and atrial natriuretic peptide, and 3) a very small increase in the concentration of ANG III, undetectable by usual techniques, may increase aldosterone secretion substantially. Sodium 152-158 angiogenin Homo sapiens 36-39 12869368-13 2003 It is concluded that 1) ANG III and ANG IV are cleared much faster from plasma than ANG II, 2) ANG II causes hypofiltration, urinary concentration, and sodium and potassium retention at constant plasma concentrations of vasopressin and atrial natriuretic peptide, and 3) a very small increase in the concentration of ANG III, undetectable by usual techniques, may increase aldosterone secretion substantially. Sodium 152-158 angiogenin Homo sapiens 36-39 12869368-13 2003 It is concluded that 1) ANG III and ANG IV are cleared much faster from plasma than ANG II, 2) ANG II causes hypofiltration, urinary concentration, and sodium and potassium retention at constant plasma concentrations of vasopressin and atrial natriuretic peptide, and 3) a very small increase in the concentration of ANG III, undetectable by usual techniques, may increase aldosterone secretion substantially. Sodium 152-158 angiogenin Homo sapiens 36-39 14624277-7 2003 The most important functions mediated by AT1 receptors include: vasoconstriction, induction of the production and release of aldosterone, renal reabsorption of sodium, cardiac cellular growth, proliferation of vascular smooth muscle, increase of peripheral noradrenergic action and the central activity of the sympathetic nervous system, stimulation of vasopressin release, and inhibition of renin release from the kidney. Sodium 160-166 angiotensin II receptor type 1 Homo sapiens 41-44 12900438-11 2003 An altered interaction of D1 and AT1 receptors may play a role in the impaired sodium excretion and enhanced vasoconstriction in hypertension. Sodium 79-85 angiotensin II receptor, type 1a Rattus norvegicus 33-36 12913255-1 2003 The renin-angiotensin cascade plays an important role in blood pressure control and sodium homeostasis. Sodium 84-90 renin Rattus norvegicus 4-9 12793982-11 2003 With both sodium supplements, decreased AT1 mRNA levels in the kidney and in the placenta were observed. Sodium 10-16 angiotensin II receptor, type 1a Rattus norvegicus 40-43 10702801-7 2000 Expression of a Ras effector mutant (RasV12S35) that signals preferentially through Raf-1, although sufficient to confer TSH-independent proliferation, abolished hormone-regulated expression of thyroglobulin and the sodium/iodide symporter. Sodium 216-222 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 84-89 12832517-5 2003 Acting on postsynaptic orexin type 2 receptors, orexin activates a sodium-calcium exchange current, thereby depolarizing the cell and increasing its firing frequency. Sodium 67-73 hypocretin Mus musculus 23-29 12832517-5 2003 Acting on postsynaptic orexin type 2 receptors, orexin activates a sodium-calcium exchange current, thereby depolarizing the cell and increasing its firing frequency. Sodium 67-73 hypocretin Mus musculus 48-54 12719443-11 2003 Taken together, these findings support the hypothesis that endothelin plays an important role in regulating sodium excretion through activation of ETB receptors. Sodium 108-114 endothelin receptor type B Rattus norvegicus 147-150 12754708-6 2003 Recently, we described de novo mutations of the neuronal sodium channel alpha-subunit gene SCN1A in seven isolated SMEI patients. Sodium 57-63 sodium voltage-gated channel alpha subunit 1 Homo sapiens 91-96 12805306-0 2003 Degeneration of the amygdala/piriform cortex and enhanced fear/anxiety behaviors in sodium pump alpha2 subunit (Atp1a2)-deficient mice. Sodium 84-90 ATPase, Na+/K+ transporting, alpha 2 polypeptide Mus musculus 112-118 10679502-9 2000 The renoprotective effects of HRI were at least in part due to improved renal hemodynamics and distal tubular function, since HRI shifted renal pressure-diuresis/natriuresis curves leftward by approximately 35 mm Hg, increased glomerular filtration rate and renal blood flow, and shifted the fractional water and sodium excretion curves leftward. Sodium 313-319 eukaryotic translation initiation factor 2 alpha kinase 1 Homo sapiens 30-33 10679502-9 2000 The renoprotective effects of HRI were at least in part due to improved renal hemodynamics and distal tubular function, since HRI shifted renal pressure-diuresis/natriuresis curves leftward by approximately 35 mm Hg, increased glomerular filtration rate and renal blood flow, and shifted the fractional water and sodium excretion curves leftward. Sodium 313-319 eukaryotic translation initiation factor 2 alpha kinase 1 Homo sapiens 126-129 10600659-0 2000 Modulation of the intrahepatic renin-angiotensin system after stimulation of the gastric sodium monitor in the rat. Sodium 89-95 renin Rattus norvegicus 31-36 11714411-1 2000 Inhibition of the sodium-hydrogen exchanger (NHE) is a powerful experimental tool to inhibit sodium and calcium accumulation within the ischemic myocyte and halt progression of cell ischemia to cell necrosis. Sodium 18-24 solute carrier family 9 member C1 Homo sapiens 45-48 10646118-0 2000 Stimulation of sodium-dependent phosphate transport and signaling mechanisms induced by basic fibroblast growth factor in MC3T3-E1 osteoblast-like cells. Sodium 15-21 fibroblast growth factor 2 Mus musculus 88-118 10646118-4 2000 The results indicate that bFGF is a potent and selective stimulator of sodium-dependent Pi transport in these cells. Sodium 71-77 fibroblast growth factor 2 Mus musculus 26-30 10544029-3 1999 The cDNA encoding the high-affinity sodium-dependent human carnitine transporter OCTN2 has recently been cloned. Sodium 36-42 solute carrier family 22 member 5 Homo sapiens 81-86 10553907-7 1999 The neurotrophin-induced depolarization resulted from the activation of a sodium ion conductance which was reversibly blocked by K-252a, a protein kinase blocker which prefers tyrosine kinase Trk receptors. Sodium 74-80 neurotrophic receptor tyrosine kinase 1 Homo sapiens 192-195 10535413-8 1999 These results suggest that both AT1 and AT2 receptor subtypes in the PVN are involved in ANG II-related urine, sodium, and potassium excretion, and that the inhibitory responses to AT2 blockade are predominant. Sodium 111-117 angiotensin II receptor, type 1a Rattus norvegicus 32-35 10535413-8 1999 These results suggest that both AT1 and AT2 receptor subtypes in the PVN are involved in ANG II-related urine, sodium, and potassium excretion, and that the inhibitory responses to AT2 blockade are predominant. Sodium 111-117 angiotensin II receptor, type 2 Rattus norvegicus 40-43 10489110-11 1999 CONCLUSIONS: In PIH, elevated hANP might be important as a counterbalance to the presence of the active vasopressors and sodium retention. Sodium 121-127 pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included) Homo sapiens 16-19 10444581-9 1999 In conclusion, in this rat CRF model: 1) increased fractional sodium excretion is associated with altered expression of proximal tubule Na transporter expression (NHE-3, NaPi-II, and Na-K-ATPase), consistent with glomerulotubular imbalance in the face of increased single-nephron glomerular filtration rate; and 2) compensatory increases in BSC-1 and TSC expression per nephron occur in distal segments. Sodium 62-68 solute carrier family 9 member A3 Rattus norvegicus 163-168 10444581-9 1999 In conclusion, in this rat CRF model: 1) increased fractional sodium excretion is associated with altered expression of proximal tubule Na transporter expression (NHE-3, NaPi-II, and Na-K-ATPase), consistent with glomerulotubular imbalance in the face of increased single-nephron glomerular filtration rate; and 2) compensatory increases in BSC-1 and TSC expression per nephron occur in distal segments. Sodium 62-68 solute carrier family 12 member 3 Rattus norvegicus 351-354 10491734-2 1999 Of the three classes of sodium-phosphate cotransporters expressed in the mammalian kidney, the type II transporter, NPT2/Npt2 reflects the characteristics of apical sodium-dependent phosphate transport, and is a target for regulation. Sodium 24-30 solute carrier family 34 member 1 Homo sapiens 116-120 10491734-2 1999 Of the three classes of sodium-phosphate cotransporters expressed in the mammalian kidney, the type II transporter, NPT2/Npt2 reflects the characteristics of apical sodium-dependent phosphate transport, and is a target for regulation. Sodium 24-30 solute carrier family 34 member 1 Homo sapiens 121-125 10432233-0 1999 Effect of calbindin D 28K on sodium transport by the luminal membrane of the rabbit nephron. Sodium 29-35 calbindin Oryctolagus cuniculus 10-19 12644265-7 2003 The HeLa cells expressing the RBE4 OCTN2 cDNA showed a sixfold increase in L-carnitine uptake and a fourfold increase in TEA uptake in a sodium-containing buffer. Sodium 137-143 solute carrier family 22 member 5 Homo sapiens 35-40 12763861-4 2003 CHIF, in contrast, augments its apparent affinity for sodium. Sodium 54-60 FXYD domain containing ion transport regulator 4 Homo sapiens 0-4 12615950-3 2003 AtDUR3 contains 14 putative transmembrane-spanning domains and represents an individual member in Arabidopsis that belongs to a superfamily of sodium-solute symporters. Sodium 143-149 urea-proton symporter DEGRADATION OF UREA 3 (DUR3) Arabidopsis thaliana 0-6 12924167-1 2003 A sodium-proton exchanger (NHE) is a membrane transport system taking part in intracellular sodium homeostasis. Sodium 2-8 solute carrier family 9 member C1 Homo sapiens 27-30 12569258-5 2003 A significant dependence (P < 0.05) between diastolic (DBP) or systolic (SBP) blood pressure and sodium intake was found in 16 and 5% of the participants, respectively. Sodium 100-106 selenium binding protein 1 Homo sapiens 76-79 10336520-2 1999 When expressed in Xenopus laevis oocytes, OAT1 mediated sodium-independent uptake of OTA (Km = 2.1 microM). Sodium 56-62 solute carrier family 22 (organic anion transporter), member 6 Mus musculus 42-46 12534970-2 2003 Both PACAP and NGF elicited rapid neurite outgrowth, which was accompanied by induction of cell excitability and the development of both sodium and calcium currents. Sodium 137-143 adenylate cyclase activating polypeptide 1 Rattus norvegicus 5-10 12502561-0 2002 The cardiac sodium-calcium exchanger associates with caveolin-3. Sodium 12-18 caveolin 3 Bos taurus 53-63 12195126-14 2002 Measurement of plasma renin activity, which was suppressed and stimulated, respectively, by high and low sodium intake, indicated that the effects on SBP and renal function induced by ICV RU28318 were independent from the level of activation of the renin-angiotensin system. Sodium 105-111 renin Rattus norvegicus 22-27 12408185-5 2002 Recently, a human gene, SLC22A5, encoding a sodium-dependent high-affinity carnitine transporter OCTN2 was cloned from human kidney and shown to be mutated in systemic carnitine deficiency. Sodium 44-50 solute carrier family 22 member 5 Homo sapiens 24-31 12408185-5 2002 Recently, a human gene, SLC22A5, encoding a sodium-dependent high-affinity carnitine transporter OCTN2 was cloned from human kidney and shown to be mutated in systemic carnitine deficiency. Sodium 44-50 solute carrier family 22 member 5 Homo sapiens 97-102 10404735-11 1999 The pHi recovery after acidification was sodium-dependent and inhibited by N-hexamethylene amiloride. Sodium 41-47 glucose-6-phosphate isomerase Homo sapiens 4-7 10201881-6 1999 Activation of luminal AT1 receptors stimulates tubular sodium reabsorption rate. Sodium 55-61 angiotensin II receptor, type 1a Rattus norvegicus 22-25 10201881-10 1999 Blockade of intrarenal AT1 receptors elicited significant increases in GFR, renal blood flow, sodium excretion, and fractional sodium excretion, suggesting synergistic actions on tubular transport and vascular smooth muscle cells. Sodium 94-100 angiotensin II receptor, type 1a Rattus norvegicus 23-26 10201881-10 1999 Blockade of intrarenal AT1 receptors elicited significant increases in GFR, renal blood flow, sodium excretion, and fractional sodium excretion, suggesting synergistic actions on tubular transport and vascular smooth muscle cells. Sodium 127-133 angiotensin II receptor, type 1a Rattus norvegicus 23-26 9950790-0 1999 Control of adrenal cell proliferation by AT1 receptors in response to angiotensin II and low-sodium diet. Sodium 93-99 angiotensin II receptor, type 1a Rattus norvegicus 41-44 9950829-4 1999 In proximal colon, dietary sodium depletion enhanced both NHE2 and NHE3 isoform-specific Na+/H+ exchange activities, protein expression, and mRNA abundance. Sodium 27-33 solute carrier family 9 member A3 Rattus norvegicus 67-71 9950829-5 1999 In contrast, in distal colon both NHE2 and NHE3 isoform-specific Na+/H+ exchange activities, protein expression, and mRNA abundance were inhibited by sodium depletion. Sodium 150-156 solute carrier family 9 member A3 Rattus norvegicus 43-47 12069945-10 2002 During WI + ANG II-low and WI + ANG II-high, an increase in C(Li) was prevented that was otherwise observed during WI, and fractional distal reabsorption of sodium was facilitated. Sodium 157-163 angiogenin Homo sapiens 32-35 9950831-9 1999 In females, expression of the sodium-dependent taurocholate peptide (Ntcp) and mRNA were selectively decreased to 46 +/- 9 and 54 +/- 4% (P < 0.01), respectively, and the organic anion transporter peptide (Oatp) and Na+-K+-ATPase alpha-subunit were not significantly different. Sodium 30-36 solute carrier family 10 member 1 Rattus norvegicus 69-73 12069945-13 2002 Furthermore, infusion of ANG II during WI prevents an otherwise induced increase in C(Li) and facilitates the fractional distal reabsorption of sodium, probably via an effect on aldosterone release. Sodium 144-150 angiogenin Homo sapiens 25-28 9950831-11 1999 In conclusion, these studies demonstrated that decreased sodium-dependent bile salt uptake in female hepatocytes was due to decreased membrane lipid fluidity and a selective decrease in Ntcp. Sodium 57-63 solute carrier family 10 member 1 Rattus norvegicus 186-190 10188997-15 1999 In conclusion, renal AT2 receptors oppose the sodium and water excretion induced by acute increases in blood pressure and this action cannot be directly explained by changes in cyclic GMP. Sodium 46-52 angiotensin II receptor, type 2 Rattus norvegicus 21-24 12358141-6 2002 (b) After adjustment for age, SBP and DBP showed a significant positive association with body mass index, urinary sodium (Na) excretion, and total cholesterol (TC) to high-density lipoprotein (HDL) cholesterol ratio (TC/HDL). Sodium 114-120 selenium binding protein 1 Homo sapiens 30-33 10029036-2 1999 OBJECTIVE: Because of the known sodium and water retention associated with growth hormone (GH) therapy, it is crucial to evaluate the safety of GH after brain injury. Sodium 32-38 gonadotropin releasing hormone receptor Rattus norvegicus 75-89 12065749-5 2002 When expressed in Xenopus laevis oocytes, mOAT2 mediated the high affinity transport of glutarate (K(m) = 15.8 +/- 3.2 microM) and prostaglandin E2 (K(m) = 5.2 +/- 0.5 nM) in a sodium-independent manner. Sodium 177-183 solute carrier family 22 (organic anion transporter), member 7 Mus musculus 42-47 10029036-2 1999 OBJECTIVE: Because of the known sodium and water retention associated with growth hormone (GH) therapy, it is crucial to evaluate the safety of GH after brain injury. Sodium 32-38 gonadotropin releasing hormone receptor Rattus norvegicus 91-93 12086636-2 2002 In generalized epilepsy with febrile seizures plus, an autosomal dominant epilepsy syndrome, mutations in three genes coding for voltage-gated sodium channel alpha or beta1 subunits (SCN1A, SCN2A, SCN1B) and one GABA receptor subunit gene (GABRG2) have been identified. Sodium 143-149 sodium voltage-gated channel alpha subunit 1 Homo sapiens 183-188 12086636-2 2002 In generalized epilepsy with febrile seizures plus, an autosomal dominant epilepsy syndrome, mutations in three genes coding for voltage-gated sodium channel alpha or beta1 subunits (SCN1A, SCN2A, SCN1B) and one GABA receptor subunit gene (GABRG2) have been identified. Sodium 143-149 sodium voltage-gated channel beta subunit 1 Homo sapiens 197-202 12086636-3 2002 Here, we characterize the functional effects of three mutations in the human neuronal sodium channel alpha subunit SCN1A by heterologous expression with its known accessory subunits, beta1 and beta2, in cultured mammalian cells. Sodium 86-92 sodium voltage-gated channel alpha subunit 1 Homo sapiens 115-120 12086636-4 2002 SCN1A mutations alter channel inactivation, resulting in persistent inward sodium current. Sodium 75-81 sodium voltage-gated channel alpha subunit 1 Homo sapiens 0-5 12223070-3 2002 Sodium-hydrogen exchange (NHE) is a key target for the treatment of heart failure. Sodium 0-6 solute carrier family 9 member C1 Homo sapiens 26-29 12186749-5 2002 Observed alterations in Na(+) and K(+) concentrations in erythrocytes were associated with significantly (p<001) increased Ouabain-sensitive sodium efflux rate and rate constants in erythrocytes from PIH women. Sodium 144-150 pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included) Homo sapiens 203-206 9927610-2 1999 NTR1 couples to Galphaq to stimulate phospholipase C and its binding affinity for neurotensin is decreased by sodium ions and GTP analogs. Sodium 110-116 neurotensin receptor 1 Homo sapiens 0-4 9927610-6 1999 We demonstrate that the presence of the Asp residue determines by itself the occurrence of the sodium effect on neurotensin affinity for both wild-type and mutated NTR1 and -2. Sodium 95-101 neurotensin receptor 1 Homo sapiens 164-175 9887076-8 1999 In contrast, chronic metabolic alkalosis, regardless of whether it is associated with high sodium intake or not, leads to an appropriate adaptation of NHE-3 activity, which involves a decrease in NHE-3 protein and mRNA abundance. Sodium 91-97 solute carrier family 9 member A3 Rattus norvegicus 151-156 9887082-1 1999 In the present study, we determined the effect of epidermal growth factor (EGF; 10 microgram/100 g body wt) on sodium gradient-dependent phosphate transport (Na-Pi cotransport) regulation in suckling (12-day-old) and weaned (24-day-old) rats. Sodium 111-117 epidermal growth factor like 1 Rattus norvegicus 50-73 9887082-1 1999 In the present study, we determined the effect of epidermal growth factor (EGF; 10 microgram/100 g body wt) on sodium gradient-dependent phosphate transport (Na-Pi cotransport) regulation in suckling (12-day-old) and weaned (24-day-old) rats. Sodium 111-117 epidermal growth factor like 1 Rattus norvegicus 75-78 10336138-0 1999 Hypo-osmolarity stimulates and high sodium concentration inhibits thyrotropin-releasing hormone secretion from rat hypothalamus. Sodium 36-42 thyrotropin releasing hormone Rattus norvegicus 66-95 12070427-2 2002 In this study we examined the effect of leptin on renal Na+, K+-ATPase responsible for active tubular sodium reabsorption, and compared the renal effects of leptin in lean and obese rats. Sodium 102-108 leptin Rattus norvegicus 40-46 12070427-11 2002 CONCLUSIONS: Leptin stimulates natriuresis primarily by inhibiting tubular sodium reabsorption. Sodium 75-81 leptin Rattus norvegicus 13-19 12030914-11 2002 During the course of a progressive fall in plasma sodium concentration (P = 0.001), there was a delayed activation of renin-aldosterone which was inversely correlated with declining levels of plasma ANP/BNP (P < 0.002). Sodium 50-56 natriuretic peptide B Homo sapiens 203-206 9843897-2 1998 In the normotensive animals (n = 8) an intravenous bolus of 400 microgram/kg of leptin produced a significant six- to sevenfold elevation in sodium excretion compared with controls (n = 8). Sodium 141-147 leptin Rattus norvegicus 80-86 9951557-6 1998 Previous administration of the AT1 receptor antagonist DuP753 into the SON decreased water (65%, N = 10, P < 0.01) and sodium intake (81%, N = 8, P < 0.01) induced by the injection of ANG II (10 nmol) into the MSA. Sodium 122-128 angiotensin II receptor, type 1a Rattus norvegicus 31-34 9951557-9 1998 These results suggest that both AT1 and V1 receptors within the SON may be involved in water and sodium intake induced by the activation of ANG II receptors within the MSA. Sodium 97-103 angiotensin II receptor, type 1a Rattus norvegicus 32-42 9826738-2 1998 To investigate whether mineralocorticoids regulate the expression of the thiazide-sensitive Na-Cl cotransporter (TSC), the chief apical sodium entry pathway of distal convoluted tubule cells, we prepared an affinity-purified, peptide-directed antibody to TSC. Sodium 136-142 solute carrier family 12 member 3 Rattus norvegicus 73-111 9826738-2 1998 To investigate whether mineralocorticoids regulate the expression of the thiazide-sensitive Na-Cl cotransporter (TSC), the chief apical sodium entry pathway of distal convoluted tubule cells, we prepared an affinity-purified, peptide-directed antibody to TSC. Sodium 136-142 solute carrier family 12 member 3 Rattus norvegicus 113-116 9807968-1 1998 Over the past few years, it has been shown that the cardiac myocyte plasma membrane sodium ion/hydrogen ion exchanger (NHE) plays an important role in the maintenance of intracellular pH, sodium, and calcium ion homeostasis. Sodium 84-90 solute carrier family 9 member C1 Homo sapiens 119-122 9807968-1 1998 Over the past few years, it has been shown that the cardiac myocyte plasma membrane sodium ion/hydrogen ion exchanger (NHE) plays an important role in the maintenance of intracellular pH, sodium, and calcium ion homeostasis. Sodium 188-194 solute carrier family 9 member C1 Homo sapiens 119-122 9814852-1 1998 Erythrocyte sodium hydrogen exchanger (NHE) represents one of a limited number of sodium entry pathway in erythrocytes. Sodium 12-18 solute carrier family 9 member C1 Homo sapiens 39-42 9855025-6 1998 Additionally, research has indicated that the AT1 receptor modulates cardiac contractility and glomerular filtration, increases renal tubular sodium reabsorption, and cardiac and vascular hypertrophy. Sodium 142-148 angiotensin II receptor type 1 Homo sapiens 46-49 9694847-15 1998 This plant glycoside also inhibited the SDCT1-specific sodium leak in the absence of substrate, indicating that at least one Na+ binds to the transporter before the substrate. Sodium 55-61 solute carrier family 13 member 2L homeolog Xenopus laevis 40-45 9685390-0 1998 Molecular and functional identification of sodium ion-dependent, high affinity human carnitine transporter OCTN2. Sodium 43-49 solute carrier family 22 member 5 Homo sapiens 107-112 9685390-6 1998 When OCTN2 was expressed in HEK293 cells, uptake of L-[3H]carnitine was strongly enhanced in a sodium-dependent manner with Km value of 4.34 microM, whereas typical substrates for previously known organic cation transporters, tetraethylammonium and guanidine, were not good substitutes. Sodium 95-101 solute carrier family 22 member 5 Homo sapiens 5-10 9688688-13 1998 The data demonstrate that ANG II mediates jejunal sodium and water absorption by an action at the AT2 receptor involving cGMP formation. Sodium 50-56 angiotensin II receptor, type 2 Rattus norvegicus 98-101 9888564-3 1998 In the present study the effects of dietary sodium changes on PAMP and adrenomedullin receptor expression was investigated. Sodium 44-50 G protein-coupled receptor 182 Rattus norvegicus 71-94 9697698-6 1998 We now report linkage, in another large GEFS+ family, to chromosome region 19q13.1 and identification of a mutation in the voltage-gated sodium (Na+)-channel beta1 subunit gene (SCN1B). Sodium 137-143 sodium voltage-gated channel beta subunit 1 Homo sapiens 178-183 9644212-8 1998 These findings suggest that sodium deficiency stimulates adrenal AT1A and AT1B receptor mRNA levels primarily via an ANGII-AT1-independent mechanism. Sodium 28-34 angiotensin II receptor, type 1a Rattus norvegicus 65-69 9644212-8 1998 These findings suggest that sodium deficiency stimulates adrenal AT1A and AT1B receptor mRNA levels primarily via an ANGII-AT1-independent mechanism. Sodium 28-34 angiotensin II receptor, type 1a Rattus norvegicus 65-68 9668069-10 1998 Furthermore, lithium inhibition under saturating sodium concentrations showed hyperbolic kinetics, suggesting that one of the three cation binding sites in NaDC-1 has a higher affinity for Li+ than Na+. Sodium 49-55 solute carrier family 13 member 2L homeolog Xenopus laevis 156-162 9651206-0 1998 The sodium channel Scn8a is the major contributor to the postnatal developmental increase of sodium current density in spinal motoneurons. Sodium 4-10 sodium channel, voltage-gated, type VIII, alpha Mus musculus 19-24 9651206-3 1998 For mice lacking a functional Scn8a sodium channel gene, motoneuronal sodium current density was comparable at P0 to that of normal mice but failed to increase from P0 to P8. Sodium 36-42 sodium channel, voltage-gated, type VIII, alpha Mus musculus 30-35 9688838-0 1998 Mechanisms of EGF-induced stimulation of sodium reabsorption by alveolar epithelial cells. Sodium 41-47 epidermal growth factor like 1 Rattus norvegicus 14-17 10085711-3 1998 Recent findings in African-Americans who are a model of sodium-sensitive population, reveal a strong association between Sma I polymorphism at intron 2 (the polymorphic site is identical for Hpa II restriction enzyme) or both Sma I and Sca I polymorphism at exon 3 of ANP precursor gene and essential hypertension. Sodium 56-62 survival of motor neuron 1, telomeric Homo sapiens 121-124 10085711-3 1998 Recent findings in African-Americans who are a model of sodium-sensitive population, reveal a strong association between Sma I polymorphism at intron 2 (the polymorphic site is identical for Hpa II restriction enzyme) or both Sma I and Sca I polymorphism at exon 3 of ANP precursor gene and essential hypertension. Sodium 56-62 survival of motor neuron 1, telomeric Homo sapiens 226-229 9636153-2 1998 Previous work has shown that yeast cells deficient in Ppz1 protein phosphatase or overexpressing Hal3p, a novel regulatory protein of unknown function, exhibit increased resistance to sodium and lithium, whereas cells lacking Hal3p display increased sensitivity. Sodium 184-190 phosphopantothenoylcysteine decarboxylase complex subunit SIS2 Saccharomyces cerevisiae S288C 97-102 9582411-9 1998 The results thus demonstrate that epithelial cells have an unusual capacity to adjust rap- idly to variations in sodium intake. Sodium 113-119 LDL receptor related protein associated protein 1 Gallus gallus 86-89 12008990-7 2002 Variables associated with higher energy-adjusted saturated fat intake with marginal statistical significance (P=.05-.10) included attendance at schools with a higher percentage of students receiving free or reduced-price lunch, usual breakfast location other than home or school, and less knowledge about low-fat, low-sodium foods. Sodium 318-324 FAT atypical cadherin 1 Homo sapiens 59-62 11940708-1 2002 Mutations in the neuronal voltage-gated sodium channel alpha-subunit type I gene (SCN1A) were found responsible for severe myoclonic epilepsy in infancy (SMEI). Sodium 40-46 sodium voltage-gated channel alpha subunit 1 Homo sapiens 82-87 11904438-7 2002 These findings provide a mechanism for the D(1) receptor coupling defect in the kidney and may explain the inability of the kidney to properly excrete sodium in genetic hypertension. Sodium 151-157 dopamine receptor D1 Mus musculus 43-56 11884374-3 2002 The addition of antibodies against caveolin-3 to the cell"s cytoplasm via the pipette solution abrogated this direct G protein-induced increase in sodium current, whereas antibodies to caveolin-1 or caveolin-2 did not. Sodium 147-153 caveolin 3 Homo sapiens 35-45 11832333-7 2002 In conclusion, we demonstrate that the age-related decrease in intestinal sodium-dependent P(i) absorption correlates with decreased NaP(i)-IIb mRNA expression. Sodium 74-80 solute carrier family 34 member 2 Homo sapiens 133-143 11868817-4 2002 NHE3 is an apical membrane NHE responsible for sodium absorption in renal proximal tubule and intestinal epithelium. Sodium 47-53 solute carrier family 9 member A3 Rattus norvegicus 0-4 11891977-2 2002 The purpose of this work was to quantify the effect of interleukin-1 (IL-1beta)-induced macromolecule depletion on the residual quadrupolar interaction (RQI) of sodium in bovine cartilage plugs. Sodium 161-167 interleukin 1 beta Bos taurus 70-78 12373543-0 2002 Repeated topical application of growth hormone attenuates blood-spinal cord barrier permeability and edema formation following spinal cord injury: an experimental study in the rat using Evans blue, ([125])I-sodium and lanthanum tracers. Sodium 207-213 gonadotropin releasing hormone receptor Rattus norvegicus 32-46 11823106-4 2002 A missense mutation was identified in the voltage-gated sodium (Na(+))-channel beta 1 subunit gene, SCN1B at chromosome 19p13.1 in generalized epilepsy with the febrile seizures plus type 1 (GEFS+1) family. Sodium 56-62 sodium voltage-gated channel beta subunit 1 Homo sapiens 100-105 11799079-6 2002 In contrast, GH treatment normalized impaired diuresis (vehicle 10.8+/-0.6 mL/d, GH 15.8+/-0.7 mL/d; P<0.05) and sodium excretion (vehicle 1.5+/-0.1 mmol/d, GH 2.2+/-0.1 mmol/d; P<0.001) in shunt-operated rats, with a similar increase of fractional sodium excretion. Sodium 116-122 gonadotropin releasing hormone receptor Rattus norvegicus 13-15 11799079-6 2002 In contrast, GH treatment normalized impaired diuresis (vehicle 10.8+/-0.6 mL/d, GH 15.8+/-0.7 mL/d; P<0.05) and sodium excretion (vehicle 1.5+/-0.1 mmol/d, GH 2.2+/-0.1 mmol/d; P<0.001) in shunt-operated rats, with a similar increase of fractional sodium excretion. Sodium 255-261 gonadotropin releasing hormone receptor Rattus norvegicus 13-15 11799079-11 2002 However, GH improved renal function by increasing diuresis and sodium excretion. Sodium 63-69 gonadotropin releasing hormone receptor Rattus norvegicus 9-11 11731622-5 2001 After 2 wk of sodium restriction, plasma aldosterone increased (1.51 +/- 0.27 ng/ml) and potassium remained on average at 4.5 +/- 0.2 mEq/liter, with aldosterone synthase mRNA expressed intensively in Agtr1a+/+, but not detectable in Agtr1a-/- cells. Sodium 14-20 cytochrome P450, family 11, subfamily b, polypeptide 2 Mus musculus 150-170 11731622-6 2001 Simultaneous sodium restriction and losartan treatment caused increases in plasma potassium (5.5 +/- 0.1 mEq/liter) and aldosterone (1.84 +/- 0.38 ng/ml), with both Agtr1a-/- and Agtr1a+/+ cells intensively expressing aldosterone synthase mRNA. Sodium 13-19 cytochrome P450, family 11, subfamily b, polypeptide 2 Mus musculus 218-238 11703584-18 2001 Finally, during low sodium intake (without induction of TGF), the regulation of basal Af-Art resistance by macula densa nNOS suggests that NO in the macula densa helps maintain renal blood flow during the high renin secretion caused by low sodium intake. Sodium 240-246 nitric oxide synthase 1, neuronal Mus musculus 120-124 11703600-0 2001 Coordinated down-regulation of NBC-1 and NHE-3 in sodium and bicarbonate loading. Sodium 50-56 solute carrier family 9 member A3 Rattus norvegicus 41-46 11457832-5 2001 Third, a gln3 gat1 mutant displays a pronounced sensitivity to high concentrations of lithium and sodium. Sodium 98-104 Gat1p Saccharomyces cerevisiae S288C 14-18 11507017-2 2001 Increasing sodium intake from approximately 200 to 1,000 microeq/day significantly decreased plasma renin concentration from 472 +/- 96 to 304 +/- 83 ng ANG I. ml(-1). Sodium 11-17 angiogenin, ribonuclease, RNase A family, 5 Mus musculus 153-156 11496062-2 2001 Recently, a novel such form of human hypertension caused by gain-of-function mutation in the mineralocorticoid receptor, the mediator of aldosterone-induced sodium transport in the distal nephron, has been described, with the notable finding being that pregnancy causes a severe worsening of blood pressure. Sodium 157-163 nuclear receptor subfamily 3 group C member 2 Homo sapiens 93-119 11571491-11 2001 Water and sodium depletion and water, NaCl and food deprivation induced sodium appetite, which in the short term depends on cerebral angiotensinergic activity mediated by the activation of AT1 receptors. Sodium 10-16 angiotensin II receptor, type 1a Rattus norvegicus 189-192 11571491-11 2001 Water and sodium depletion and water, NaCl and food deprivation induced sodium appetite, which in the short term depends on cerebral angiotensinergic activity mediated by the activation of AT1 receptors. Sodium 72-78 angiotensin II receptor, type 1a Rattus norvegicus 189-192 11716294-6 2001 According to the postulate that erythrocyte sodium-lithium countertransport (NLCT) might be one mode of operation of the ubiquitous NHE, and following the trail of previous investigations of NLCT association with hypertension and diabetic nephropathy, several studies have confirmed elevated NHE activity in different cell types in patients with essential hypertension. Sodium 44-50 solute carrier family 9 member C1 Homo sapiens 132-135 11716294-6 2001 According to the postulate that erythrocyte sodium-lithium countertransport (NLCT) might be one mode of operation of the ubiquitous NHE, and following the trail of previous investigations of NLCT association with hypertension and diabetic nephropathy, several studies have confirmed elevated NHE activity in different cell types in patients with essential hypertension. Sodium 44-50 solute carrier family 9 member C1 Homo sapiens 292-295 11509486-9 2001 On the contrary, low-sodium diet increased by 50% both LV betaARK1 protein (densitometry units: normal sodium, 26.5+/-0.9; low sodium, 35.7+/-1.6; P<0.05) and activity (fmol/mg per minute: normal sodium, 6.49+/-1.17; low sodium, 9.15+/-0.93; P<0.05). Sodium 21-27 G protein-coupled receptor kinase 2 Rattus norvegicus 58-66 11446717-7 2001 Renin gene expression significantly increased in rats fed with the low sodium diet compared with the standard diet group, and significantly decreased in rats fed the high sodium diet Renal denervation significantly reduced renin mRNA levels in rats receiving the low sodium diet, but did not produce any significant change in normal or high-sodium groups. Sodium 71-77 renin Rattus norvegicus 0-5 11446717-7 2001 Renin gene expression significantly increased in rats fed with the low sodium diet compared with the standard diet group, and significantly decreased in rats fed the high sodium diet Renal denervation significantly reduced renin mRNA levels in rats receiving the low sodium diet, but did not produce any significant change in normal or high-sodium groups. Sodium 171-177 renin Rattus norvegicus 0-5 11446717-7 2001 Renin gene expression significantly increased in rats fed with the low sodium diet compared with the standard diet group, and significantly decreased in rats fed the high sodium diet Renal denervation significantly reduced renin mRNA levels in rats receiving the low sodium diet, but did not produce any significant change in normal or high-sodium groups. Sodium 171-177 renin Rattus norvegicus 0-5 11446717-7 2001 Renin gene expression significantly increased in rats fed with the low sodium diet compared with the standard diet group, and significantly decreased in rats fed the high sodium diet Renal denervation significantly reduced renin mRNA levels in rats receiving the low sodium diet, but did not produce any significant change in normal or high-sodium groups. Sodium 171-177 renin Rattus norvegicus 0-5 11446717-8 2001 CONCLUSION: The activation of renin gene expression during sodium depletion in rats is dependent on the presence of the renal nerves, while the suppression of renin gene expression during a sodium load seems to be due to the macula densa mechanism alone. Sodium 59-65 renin Rattus norvegicus 30-35 11446717-8 2001 CONCLUSION: The activation of renin gene expression during sodium depletion in rats is dependent on the presence of the renal nerves, while the suppression of renin gene expression during a sodium load seems to be due to the macula densa mechanism alone. Sodium 190-196 renin Rattus norvegicus 159-164 11457957-0 2001 The wheat cDNA LCT1 generates hypersensitivity to sodium in a salt-sensitive yeast strain. Sodium 50-56 uncharacterized protein LOC542821 Triticum aestivum 15-19 11412807-13 2001 A strong positive correlation was observed between blood pressure (SBP and DBP) and body mass index, total serum cholesterol and sodium to potassium ratio. Sodium 129-135 selenium binding protein 1 Homo sapiens 67-70 11396936-4 2001 The freshly regenerated sodium form of Chelex-100 also removes the iron atom from native soybean lipoxygenase 3, but only in sodium bicarbonate buffer at pH 8.0. Sodium 24-30 seed linoleate 9S-lipoxygenase-3 Glycine max 97-111 11359211-0 2001 De novo mutations in the sodium-channel gene SCN1A cause severe myoclonic epilepsy of infancy. Sodium 25-31 sodium voltage-gated channel alpha subunit 1 Homo sapiens 45-50 11359211-5 2001 Missense mutations in the gene that codes for a neuronal voltage-gated sodium-channel alpha-subunit (SCN1A) were identified in families with generalized epilepsy with febrile seizures plus (GEFS+). Sodium 71-77 sodium voltage-gated channel alpha subunit 1 Homo sapiens 101-106 11390018-0 2001 Blockade of pancreatic polypeptide-sensitive neuropeptide Y (NPY) receptors by agonist peptides is prevented by modulators of sodium transport. Sodium 126-132 pancreatic polypeptide Homo sapiens 12-34 11402167-1 2001 The SOS3 (for SALT OVERLY SENSITIVE3) calcium binding protein and SOS2 protein kinase are required for sodium and potassium ion homeostasis and salt tolerance in Arabidopsis. Sodium 103-109 Calcium-binding EF-hand family protein Arabidopsis thaliana 4-8 11402167-1 2001 The SOS3 (for SALT OVERLY SENSITIVE3) calcium binding protein and SOS2 protein kinase are required for sodium and potassium ion homeostasis and salt tolerance in Arabidopsis. Sodium 103-109 Calcium-binding EF-hand family protein Arabidopsis thaliana 14-36 11304512-2 2001 Plasma renin activity was increased in rats fed a low sodium diet and decreased in those fed a high sodium diet. Sodium 54-60 renin Rattus norvegicus 7-12 11304512-2 2001 Plasma renin activity was increased in rats fed a low sodium diet and decreased in those fed a high sodium diet. Sodium 100-106 renin Rattus norvegicus 7-12 11267661-4 2001 In addition to the previously reported estrone-3-sulfate, we demonstrate that mouse Oatp1 mediates sodium-independent uptake of the anionic steroid conjugates dehydroepiandrosterone sulfate (K(m) approximately 8 microM) and estradiol-17-glucuronide (K(m) approximately 5 microM) and also of the prostaglandin PGE(2). Sodium 99-105 solute carrier organic anion transporter family, member 1a1 Mus musculus 84-89 11257506-2 2001 It is found in most cells at millimolar levels after uptake via the sodium-dependent carrier, OCTN2. Sodium 68-74 solute carrier family 22 member 5 Homo sapiens 94-99 28095242-5 2001 In contrast, RAS blockade coupled with reduced sodium diet (0.2%) significantly regresses cardiac hypertrophy, impairs animal growth and is associated with elevated plasma renin and dramatically suppressed plasma angiotensinogen levels. Sodium 47-53 renin Rattus norvegicus 172-177 11208593-1 2001 Aldosterone regulates renal sodium reabsorption through binding to the mineralocorticoid receptor (MR). Sodium 28-34 nuclear receptor subfamily 3 group C member 2 Homo sapiens 71-97 11208593-1 2001 Aldosterone regulates renal sodium reabsorption through binding to the mineralocorticoid receptor (MR). Sodium 28-34 nuclear receptor subfamily 3 group C member 2 Homo sapiens 99-101 11160999-4 2001 The third blood pressure QTL (QTL region 2) was close to the centromere between 1p11 and 1q12, which includes the candidate gene Slc9a3 for sodium/hydrogen exchange. Sodium 140-146 solute carrier family 9 member A3 Rattus norvegicus 129-135 11133517-8 2001 Sodium and chloride contents in the inner medulla in Clcnk1-/- mice were at about one-half the levels observed in Clcnk1+/+ mice. Sodium 0-6 chloride channel, voltage-sensitive Ka Mus musculus 53-59 11102483-4 2000 We show here that exposure to GDNF can significantly increase both slowly inactivating and persistent TTX-R sodium currents, which are paralleled by increases in SNS and NaN mRNA and protein levels, in axotomized DRG neurons in vitro. Sodium 108-114 glial cell line derived neurotrophic factor Mus musculus 30-34 11102483-6 2000 Finally, we demonstrate that GDNF upregulates the persistent TTX-R current in SNS-null mice, thus demonstrating that the upregulated persistent sodium current is not produced by SNS. Sodium 144-150 glial cell line derived neurotrophic factor Mus musculus 29-33 1409479-14 1992 As regards renal functional reserve, response to the antidiuretic hormone in case of water restriction, or stimulation of the renin-angiotensin system in response to decrease of sodium intake, it is clear that the renal cells responsible for glomerular filtration, tubular transport or synthesis and release of peptidic hormones exhibit functional alterations that are age-related. Sodium 178-184 renin Rattus norvegicus 126-131 1630068-9 1992 The response to sodium depletion suggests a volume-dependent component, which may result from elevated aldosterone levels, possibly due to enhanced adrenal renin expression. Sodium 16-22 renin Rattus norvegicus 156-161 1319542-4 1992 In response to hANP, patients with HbA1 greater than 8.5% had decreased responses of urinary volume and sodium excretion in comparison to patients with HbA1 less than 8.5% (p less than 0.05) in whom renal responses to hANP did not differ from controls. Sodium 104-110 hemoglobin subunit alpha 1 Homo sapiens 35-39 1322994-4 1992 Readdition of external sodium resulted in a rapid pHi recovery, which was almost completely amiloride-sensitive in the absence of CO2/HCO3- but only slightly influenced by amiloride in its presence. Sodium 23-29 glucose-6-phosphate isomerase Homo sapiens 50-53 1322994-6 1992 The pHi recovery after an intracellular acid load was completely dependent on extracellular sodium. Sodium 92-98 glucose-6-phosphate isomerase Homo sapiens 4-7 1322994-10 1992 Analysis of the sodium dependence of the pHi recovery after NH4Cl prepulse revealed Vmax = 0.57 pH units/min, Km = 39.7 mmol/liter extracellular sodium for the amiloride-sensitive component and Vmax = 0.19 pH units/min, Km = 14.3 mmol/liter extracellular sodium for the amiloride-insensitive component. Sodium 16-22 glucose-6-phosphate isomerase Homo sapiens 41-44 1322994-10 1992 Analysis of the sodium dependence of the pHi recovery after NH4Cl prepulse revealed Vmax = 0.57 pH units/min, Km = 39.7 mmol/liter extracellular sodium for the amiloride-sensitive component and Vmax = 0.19 pH units/min, Km = 14.3 mmol/liter extracellular sodium for the amiloride-insensitive component. Sodium 145-151 glucose-6-phosphate isomerase Homo sapiens 41-44 1322994-10 1992 Analysis of the sodium dependence of the pHi recovery after NH4Cl prepulse revealed Vmax = 0.57 pH units/min, Km = 39.7 mmol/liter extracellular sodium for the amiloride-sensitive component and Vmax = 0.19 pH units/min, Km = 14.3 mmol/liter extracellular sodium for the amiloride-insensitive component. Sodium 145-151 glucose-6-phosphate isomerase Homo sapiens 41-44 1501236-0 1992 Partial purification of a potassium channel with low permeability for sodium from tonoplast membranes of Hordeum vulgare cv. Sodium 70-76 encodes membrane spanning domains H5-S6 Hordeum vulgare 26-43 1498715-12 1992 This effect may relate to a marked reduction in the pressor effectiveness of the renin-angiotensin system by low sodium intake per se or by associated metabolic or other changes. Sodium 113-119 renin Rattus norvegicus 81-86 1312532-15 1992 The carboxy terminus of the potential polypeptide encoded by ORF2 has an amino acid sequence similar to that of the gamma subunit of oxaloacetate decarboxylase, which is involved in sodium ion transport in Klebsiella pneumoniae. Sodium 182-188 Orf2 Klebsiella pneumoniae 61-65 1835307-2 1991 In young, 4-wk-old Wistar-Kyoto rats (WKY) an increase in dietary sodium induced a dose-related increase in left ventricular (LV) weight (+10 and +24% after 4 wk of 342 or 1,370 mumol Na+/g diets, respectively). Sodium 66-72 sodium voltage-gated channel alpha subunit 7 Rattus norvegicus 184-189 1894615-2 1991 We found that this recovery is mediated by sodium-independent bicarbonate/chloride exchange: intracellular pH (pHi) recovery from alkaline load is inhibited by the anion exchange inhibitor 4,4"-diisothiocyanostilbene disulfonic acid, lack of bicarbonate, or lack of chloride. Sodium 43-49 glucose-6-phosphate isomerase 1 Mus musculus 111-114 1663977-4 1991 These results suggest that, in addition to atrial natriuretic factor, BNP may be a new and important natriuretic peptide which regulates sodium homeostasis in man during increased sodium intake. Sodium 137-143 natriuretic peptide B Homo sapiens 70-73 1663977-4 1991 These results suggest that, in addition to atrial natriuretic factor, BNP may be a new and important natriuretic peptide which regulates sodium homeostasis in man during increased sodium intake. Sodium 180-186 natriuretic peptide B Homo sapiens 70-73 1802684-4 1991 The high dose of ET-3 significantly increased the perfusion pressure, fractional sodium excretion and synthesis of prostaglandins (PGs) consistently with a significant reduction in the glomerular filtration rate (GFR). Sodium 81-87 endothelin 3 Rattus norvegicus 17-21 1802684-6 1991 These findings suggest that a low dose of ET-3 can increase the glomerular capillary ultrafiltration coefficient and that ET-3 exerts an influence on sodium and water handing in the rat PK. Sodium 150-156 endothelin 3 Rattus norvegicus 122-126 2045141-4 1991 Rats fed the high sodium diets were characterized by high plasma copper concentrations and ceruloplasmin activities compared with their respective control sodium rats. Sodium 18-24 ceruloplasmin Rattus norvegicus 91-104 2045141-5 1991 The magnitude of the sodium-induced rise in plasma copper and ceruloplasmin was affected by dietary copper intake; however, dietary copper intake had no effect on the development of hypertension in the high sodium groups. Sodium 21-27 ceruloplasmin Rattus norvegicus 62-75 1909336-2 1991 PC12 cells cultured for 13 days in the presence of nerve growth factor (NGF) and beta-xyloside, and labeled during days 11-13 with sodium [35S]sulfate, showed an 8- to 11-fold increase in [35S]sulfate-labeled macromolecules released into the culture medium. Sodium 131-137 nerve growth factor Rattus norvegicus 51-70 1909336-2 1991 PC12 cells cultured for 13 days in the presence of nerve growth factor (NGF) and beta-xyloside, and labeled during days 11-13 with sodium [35S]sulfate, showed an 8- to 11-fold increase in [35S]sulfate-labeled macromolecules released into the culture medium. Sodium 131-137 nerve growth factor Rattus norvegicus 72-75 1878323-6 1991 Average reactivities during CONFLICT + SODIUM periods were 11.2/7.9% delta for SBP/DBP (systolic/diastolic blood pressure, mmHg), and -5.65% delta for HR (heart rate, BPM). Sodium 39-45 selenium binding protein 1 Homo sapiens 79-82 2020021-7 1991 These results indicate that arginine vasopressin alters the mode of a loop diuretic-sensitive transporter from Na+: Cl- cotransport to Na+: K+: 2Cl- cotransport in the mouse MTAL with the latter providing a distinct metabolic advantage for sodium transport. Sodium 240-246 arginine vasopressin Mus musculus 28-48 1653774-1 1991 This study was undertaken to evaluate the effect of chronic renal failure as well as dialysate sodium concentration during haemodialysis on membrane ATPase activity and erythrocyte sodium and potassium concentration. Sodium 95-101 dynein axonemal heavy chain 8 Homo sapiens 149-155 2281947-1 1990 Activation of the renin-angiotensin system has been shown to arouse both water and sodium intake in the rat. Sodium 83-89 renin Rattus norvegicus 18-23 2281947-2 1990 The following experiments examine the contributions of the peripheral and central renin-angiotensin systems to the expression of sodium appetite in the adrenal-intact rat. Sodium 129-135 renin Rattus norvegicus 82-87 2096199-3 1990 The sodium/creatinine ratio [r = 0.10 (P less than 0.001)] and sodium/potassium ratio [r = 0.11 (P less than 0.001)] were positively correlated with SBP. Sodium 4-10 selenium binding protein 1 Homo sapiens 149-152 2096199-3 1990 The sodium/creatinine ratio [r = 0.10 (P less than 0.001)] and sodium/potassium ratio [r = 0.11 (P less than 0.001)] were positively correlated with SBP. Sodium 63-69 selenium binding protein 1 Homo sapiens 149-152 2175373-4 1990 A major cellular interaction is apparent in the proximal tubule where inhibition of sodium transport by ANF appears to be Ang II-dependent. Sodium 84-90 angiogenin Homo sapiens 122-125 1703080-3 1990 The sodium current, INa, was investigated at reduced extracellular Na+ (30 mM) in the presence of Cd2+ to block the calcium current, ICa, and with Cs+ substituted for K+ to reduce the K+ currents, IK. Sodium 4-10 alpha-internexin Cavia porcellus 20-23 2222970-4 1990 In Wistar rats, which were fed a high sodium diet (3.5%), BP significantly increased (P less than .01) from 106 +/- 4 to 128 +/- 8 mm Hg in parallel to an elevation of the CaM activator from 1.57 +/- 0.14 to 2.80 +/- 0.18 U. WKY, SHR, and Dahl salt-sensitive (DS/JR) and salt-resistant (DR/JR) rats were given low (0.15%) or high (2.5%) Ca diets, both with 1% sodium. Sodium 38-44 calmodulin 1 Rattus norvegicus 172-175 2222970-4 1990 In Wistar rats, which were fed a high sodium diet (3.5%), BP significantly increased (P less than .01) from 106 +/- 4 to 128 +/- 8 mm Hg in parallel to an elevation of the CaM activator from 1.57 +/- 0.14 to 2.80 +/- 0.18 U. WKY, SHR, and Dahl salt-sensitive (DS/JR) and salt-resistant (DR/JR) rats were given low (0.15%) or high (2.5%) Ca diets, both with 1% sodium. Sodium 360-366 calmodulin 1 Rattus norvegicus 172-175 2164443-2 1990 In mice a new inhibitor of DHO-DH, Brequinar sodium (DUP-785, NSC 368390) depleted the plasma uridine concentration to 40% within 2 h, followed by a small rebound after 7-9 days. Sodium 45-51 dihydroorotate dehydrogenase Mus musculus 27-33 1979036-3 1990 Stimulation of beta 1-adrenergic receptor with isoproterenol and beta 2-adrenergic antagonist ICI 118.551 inhibited the fractional reabsorption of sodium, chloride and magnesium, the fluid reabsorption being changed insignificantly. Sodium 147-153 adrenoceptor beta 1 Homo sapiens 15-41 1979036-3 1990 Stimulation of beta 1-adrenergic receptor with isoproterenol and beta 2-adrenergic antagonist ICI 118.551 inhibited the fractional reabsorption of sodium, chloride and magnesium, the fluid reabsorption being changed insignificantly. Sodium 147-153 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 65-71 2206912-6 1990 For instance sodium depletion increases the expression of renal angiotensinogen (as well as renin mRNA), as does high potassium intake and androgen administration. Sodium 13-19 renin Rattus norvegicus 92-97 2200107-2 1990 Since alteration in ion fluxes is crucial for endocrine cell activation and is a denominator of cell death, and since IL-1 was recently shown to increase the total sodium content in a murine pre-B-lymphocyte cell line, we investigated the effect of recombinant human IL-1 beta (rhIL-1 beta) on the cytosolic free sodium concentration (fNa+i) in rat islets. Sodium 164-170 interleukin 1 complex Mus musculus 118-122 2187092-4 1990 Renin secretion was lower in Hypox than in normal and sodium (Na) deprived rats. Sodium 54-60 renin Rattus norvegicus 0-5 2176808-4 1990 Recent theories as to the etiology of PIH include the suggestion that vascular tone may be increased as a result of inhibition of active sodium transport in vascular smooth muscle. Sodium 137-143 pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included) Homo sapiens 38-41 2153127-3 1990 In the absence of bicarbonate, lowering the sodium content of the medium led to decreased pHi and elimination of the difference between round and spread cells. Sodium 44-50 glucose-6-phosphate isomerase 1 Mus musculus 90-93 2153415-2 1990 Now we have observed that monensin, a sodium ionophore, also elevates the ACE activity of these cells. Sodium 38-44 angiotensin I converting enzyme Bos taurus 74-77 2302564-4 1990 We found that no treatment was as effective as NGF, and mitotic inhibitors and 8-bromocyclic AMP reduced the efficacy of NGF at increasing both sodium currents and ACh responses. Sodium 144-150 nerve growth factor Rattus norvegicus 121-124 2302564-5 1990 Some treatments were able to selectively reduce or enhance the ability of NGF to induce ACh responses or sodium currents. Sodium 105-111 nerve growth factor Rattus norvegicus 74-77 2105661-8 1990 These data are consistent with previous results from cultured cells in which altered extracellular sodium, but not urea, leads to rapid changes in aldose reductase mRNA and slow changes (days) in aldose reductase. Sodium 99-105 aldo-keto reductase family 1 member B1 Rattus norvegicus 147-163 2105661-8 1990 These data are consistent with previous results from cultured cells in which altered extracellular sodium, but not urea, leads to rapid changes in aldose reductase mRNA and slow changes (days) in aldose reductase. Sodium 99-105 aldo-keto reductase family 1 member B1 Rattus norvegicus 196-212 2405715-7 1990 These results demonstrate that endogenous angiotensin II is capable of providing a positive modulatory influence on neurally mediated release of adrenal epinephrine, an effect that may require a chronic activation of the renin-angiotensin system as occurs naturally with restricted dietary sodium intake. Sodium 290-296 renin Rattus norvegicus 221-226 9694563-3 1998 Using in situ hybridisation methods, it was demonstrated that transcription of the (pro)renin gene is regulated by sodium status, and is increased specifically in the zona glomerulosa by a low sodium diet. Sodium 115-121 renin Rattus norvegicus 88-93 1708016-5 1990 The metabolic clearance rate of VIP and its theoretical secretion rate increased after intravenous sodium loading in rabbits on a low salt diet (MCR, p less than 0.025; SR, p less than 0.05). Sodium 99-105 VIP peptides Oryctolagus cuniculus 32-35 1708016-6 1990 We conclude, therefore, that in rabbits on a low-salt diet, intravenous sodium increases VIP metabolism, causing a decrease in plasma levels that may explain the difference in sodium excretion. Sodium 72-78 VIP peptides Oryctolagus cuniculus 89-92 9694563-3 1998 Using in situ hybridisation methods, it was demonstrated that transcription of the (pro)renin gene is regulated by sodium status, and is increased specifically in the zona glomerulosa by a low sodium diet. Sodium 193-199 renin Rattus norvegicus 88-93 33798941-10 2021 Sodium channel neuronal type 1a (SCN1A) mRNA expression-level ratios increased when valproic acid was supplemented to cells. Sodium 0-6 sodium voltage-gated channel alpha subunit 1 Homo sapiens 33-38 9582047-7 1998 DATA SYNTHESIS: In 58 trials of hypertensive persons, the effect of reduced sodium intake as measured by urinary sodium excretion (mean, 118 mmol/24 h) on SBP was 3.9 mm Hg (95% confidence interval [CI], 3.0-4.8 mm Hg) (P<.001) and on DBP was 1.9 mm Hg (95% CI, 1.3-2.5 mm Hg) (P<.001). Sodium 76-82 selenium binding protein 1 Homo sapiens 155-158 9582047-7 1998 DATA SYNTHESIS: In 58 trials of hypertensive persons, the effect of reduced sodium intake as measured by urinary sodium excretion (mean, 118 mmol/24 h) on SBP was 3.9 mm Hg (95% confidence interval [CI], 3.0-4.8 mm Hg) (P<.001) and on DBP was 1.9 mm Hg (95% CI, 1.3-2.5 mm Hg) (P<.001). Sodium 113-119 selenium binding protein 1 Homo sapiens 155-158 9582047-8 1998 In 56 trials of normotensive persons, the effect of reduced sodium intake (mean, 160 mmol/24 h) on SBP was 1.2 mm Hg (95% CI, 0.6-1.8 mm Hg) (P<.001) and on DBP was 0.26 mm Hg (95% CI, -0.3-0.9 mm Hg) (P=.12). Sodium 60-66 selenium binding protein 1 Homo sapiens 99-102 9857377-4 1998 The renal immunocytochemical distribution of the Ang II/AVP receptor to the outer medullary thick ascending limb tubules and inner medullary collecting ducts suggests a prominent role in renal tubular sodium and fluid reabsorption. Sodium 201-207 angiogenin Homo sapiens 49-52 33811695-3 2021 The aim of this study was to investigate the effect of EVs from renal proximal tubule (HK2) and collecting duct cells (HCD) on intra- and intersegment modulation of extracellular ATP levels, the underlying molecular mechanisms, and the impact on the expression of the alpha subunit of the epithelial sodium channel (alphaENaC). Sodium 300-306 hexokinase 2 Homo sapiens 87-90 33766679-2 2021 The sodium leak channel (NALCN), a non-selective cation channel, mediates the background Na+ leak conductance and controls neuronal excitability and rhythmic behaviors. Sodium 4-10 sodium leak channel, non-selective Rattus norvegicus 25-30 33801115-2 2021 TRPV1"s activation increases the transport of calcium and sodium ions, leading to the excitation of sensory neurons and the perception of pain. Sodium 58-64 transient receptor potential cation channel subfamily V member 1 Homo sapiens 0-5 33815353-0 2021 Mice Heterozygous for the Sodium Channel Scn8a (Nav1.6) Have Reduced Inflammatory Responses During EAE and Following LPS Challenge. Sodium 26-32 sodium channel, voltage-gated, type VIII, alpha Mus musculus 48-54 33803193-1 2021 The SCN5A gene encodes the alpha-subunit of the voltage-gated cardiac sodium channel (NaV1.5), a key player in cardiac action potential depolarization. Sodium 70-76 sodium voltage-gated channel alpha subunit 5 Rattus norvegicus 4-9 33803193-1 2021 The SCN5A gene encodes the alpha-subunit of the voltage-gated cardiac sodium channel (NaV1.5), a key player in cardiac action potential depolarization. Sodium 70-76 sodium voltage-gated channel alpha subunit 5 Rattus norvegicus 86-92 33236643-4 2021 While this persistent sodium current (INaP) contributes to normal physiological functioning of neurons, accumulating evidence indicates a particularly pathogenic role for an elevated INaP in epilepsy (reviewed previously1). Sodium 22-28 NFKB inhibitor zeta Homo sapiens 38-42 33236643-5 2021 Due to significant advances over the past decade of epilepsy research concerning the importance of INaP in sodium channelopathies, this review seeks to summarize recent evidence and highlight promising novel anti-seizure medication strategies through preferentially targeting INaP. Sodium 107-113 NFKB inhibitor zeta Homo sapiens 99-103 33031824-7 2021 Finally, using two hypertrophy models, either a physiological response to endurance training or a pathological response to myocardial infarction, we show that TRPM4 plays a role in regulating transient calcium amplitudes and leads to the development of cellular arrhythmias potentially in cooperation with the Sodium-calcium exchange (NCX). Sodium 310-316 transient receptor potential cation channel, subfamily M, member 4 Mus musculus 159-164 24140414-0 2013 Sodium-hydrogen exchangers (NHE) in human cardiovascular diseases: interfering strategies and their therapeutic applications. Sodium 0-6 solute carrier family 9 member C1 Homo sapiens 28-31 24140414-1 2013 Sodium-hydrogen exchangers (NHE) are among the main regulators of cell volume and intracellular concentration of hydrogen and sodium ions. Sodium 126-132 solute carrier family 9 member C1 Homo sapiens 28-31 24140414-2 2013 By indirectly affecting sodium/calcium exchange across the plasma membrane, NHE can also influence the intracellular concentration of calcium. Sodium 24-30 solute carrier family 9 member C1 Homo sapiens 76-79 34952274-2 2022 However, sluggish reaction kinetics for large-radius sodium ions hinders the practical application of layered tin-based anodes such as tin disulfide (SnS2) in SIBs. Sodium 53-59 sodium voltage-gated channel alpha subunit 11 Homo sapiens 150-154 34750860-5 2022 The TTX-resistant sodium current recorded in this study was mainly carried by the Nav1.8 sodium channel isoform because the Nav1.9 current was inhibited by the -65 mV holding potential that we used throughout the study. Sodium 18-24 sodium voltage-gated channel alpha subunit 11 Homo sapiens 124-130 34970102-3 2021 Caused by a defective sodium-dependent phosphate transport protein due to loss-of-function variants of the SLC34A2 gene, PAM is an autosomal recessive transmitted disorder, and as such has a high correlation to consanguinity. Sodium 22-28 solute carrier family 34 member 2 Homo sapiens 107-114 34890198-0 2021 Manipulating the Phase Compositions of Na3(VO1-xPO4)2F1+2x (0 <= x <= 1) and Their Synergistic Effects with Reduced Graphene Oxide toward High-Rate Sodium-Ion Batteries. Sodium 148-154 exportin 4 Homo sapiens 47-51 34935140-4 2021 Canonical actions of the MR take place in epithelial cells of kidney, colon and sweat glands and contribute to sodium reabsorption, potassium secretion and extracellular volume homeostasis. Sodium 111-117 nuclear receptor subfamily 3 group C member 2 Homo sapiens 25-27 34936222-7 2022 Elevated bile acids were the mechanism of liver injury, as bile acid reduction by SC-435, an inhibitor of the ileal apical sodium-dependent bile acid transporter, prevented liver injury. Sodium 123-129 glucosidase beta 2 Mus musculus 59-68 34936222-7 2022 Elevated bile acids were the mechanism of liver injury, as bile acid reduction by SC-435, an inhibitor of the ileal apical sodium-dependent bile acid transporter, prevented liver injury. Sodium 123-129 glucosidase beta 2 Mus musculus 140-149 34889107-7 2021 Elevation of the urinary potassium-to-sodium excretion ratio, reflective of mineralocorticoid receptor activity, was only observed in participants with renin-independent aldosteronism. Sodium 38-44 nuclear receptor subfamily 3 group C member 2 Homo sapiens 76-102 34929720-1 2022 Depolarizing sodium (Na+) leak currents carried by the NALCN channel regulate the resting membrane potential of many neurons to modulate respiration, circadian rhythm, locomotion and pain sensitivity1-8. Sodium 13-19 sodium leak channel, non-selective Homo sapiens 55-60 9429665-2 1997 The three transport pathways of importance for the control of pHi are a sodium-coupled bicarbonate transport, a Na,H-exchanger and a Cl,HCO3- exchange. Sodium 72-78 glucose-6-phosphate isomerase Homo sapiens 62-65 9389507-8 1997 Furthermore, the labeling intensity of the medulla (AT2 receptors) was much stronger in adrenal sections from rats kept on a low sodium regimen than from controls. Sodium 129-135 angiotensin II receptor, type 2 Rattus norvegicus 52-55 9374809-3 1997 Blockade of AT1 receptors with valsartan increased slightly sodium and water excretion at low renal perfusion pressure (RPP). Sodium 60-66 angiotensin II receptor, type 1a Rattus norvegicus 12-15 9406970-4 1997 Blockade of sodium-dependent action potentials within the SCN prevented NPY- but not muscimol-induced phase advances. Sodium 12-18 pro-neuropeptide Y Mesocricetus auratus 72-75 9406970-5 1997 These data, along with our previous finding that bicuculline blocks NPY-induced phase advances, suggest that NPY requires sodium-dependent action potentials within GABAergic neurons in order to phase-shift the circadian pacemaker. Sodium 122-128 pro-neuropeptide Y Mesocricetus auratus 68-71 9406970-5 1997 These data, along with our previous finding that bicuculline blocks NPY-induced phase advances, suggest that NPY requires sodium-dependent action potentials within GABAergic neurons in order to phase-shift the circadian pacemaker. Sodium 122-128 pro-neuropeptide Y Mesocricetus auratus 109-112 9354334-0 1997 Altered subthreshold sodium currents and disrupted firing patterns in Purkinje neurons of Scn8a mutant mice. Sodium 21-27 sodium channel, voltage-gated, type VIII, alpha Mus musculus 90-95 9354334-6 1997 Evidently Scn8a channels carry most subthreshold sodium current and are crucial for repetitive firing. Sodium 49-55 sodium channel, voltage-gated, type VIII, alpha Mus musculus 10-15 9314415-1 1997 We have previously shown that sodium restriction upregulates the genes encoding angiotensin II receptor (AT1) subtypes, AT1A and AT1B, in the adrenal gland and that this upregulation is mediated by activation of the AT1 receptor. Sodium 30-36 angiotensin II receptor, type 1a Rattus norvegicus 105-108 9314415-1 1997 We have previously shown that sodium restriction upregulates the genes encoding angiotensin II receptor (AT1) subtypes, AT1A and AT1B, in the adrenal gland and that this upregulation is mediated by activation of the AT1 receptor. Sodium 30-36 angiotensin II receptor, type 1a Rattus norvegicus 120-124 9314415-1 1997 We have previously shown that sodium restriction upregulates the genes encoding angiotensin II receptor (AT1) subtypes, AT1A and AT1B, in the adrenal gland and that this upregulation is mediated by activation of the AT1 receptor. Sodium 30-36 angiotensin II receptor, type 1a Rattus norvegicus 120-123 9314415-2 1997 There are multiple interactions between the renin-angiotensin and the adrenergic nervous systems; thus, we conducted the present experiment to investigate whether low sodium-induced upregulation of adrenal AT1A and AT1B is modulated by the alpha1-adrenoreceptor. Sodium 167-173 angiotensin II receptor, type 1a Rattus norvegicus 206-210 9314415-11 1997 These data suggest that the sympathetic nervous system exerts an inhibitory action, via activation of the alpha1-adrenoreceptor, on AT1A and AT1B gene expression in the adrenal gland during sodium depletion. Sodium 190-196 angiotensin II receptor, type 1a Rattus norvegicus 132-136 9349392-1 1997 OBJECTIVE: This study examines the relative ability of sodium current (INa)-stimulated reverse mode Na/Ca exchange and the L-type calcium current (ICa) to trigger calcium-induced calcium release (CICR) in guinea-pig ventricular myocytes. Sodium 55-61 alpha-internexin Cavia porcellus 71-74 34992485-2 2021 More than 80% of DS cases are linked to mutations in genes which encode voltage-gated sodium channel subunits, SCN1A and SCN1B, which encode the Nav1.1alpha subunit and Nav1.1beta1 subunit, respectively. Sodium 86-92 sodium voltage-gated channel alpha subunit 1 Homo sapiens 111-116 34992485-2 2021 More than 80% of DS cases are linked to mutations in genes which encode voltage-gated sodium channel subunits, SCN1A and SCN1B, which encode the Nav1.1alpha subunit and Nav1.1beta1 subunit, respectively. Sodium 86-92 sodium voltage-gated channel beta subunit 1 Homo sapiens 121-126 9218502-18 1997 These data demonstrate that activation of the renin- angiotensin system during sodium depletion increases renal nitric oxide production through stimulation by Ang II at the angiotensin AT2 receptor. Sodium 79-85 renin Rattus norvegicus 46-51 9218502-18 1997 These data demonstrate that activation of the renin- angiotensin system during sodium depletion increases renal nitric oxide production through stimulation by Ang II at the angiotensin AT2 receptor. Sodium 79-85 angiotensin II receptor, type 2 Rattus norvegicus 185-188 9214404-16 1997 Since sodium depletion elevates peripheral renin activity, our experiments suggest a role for the renin-angiotensin system in the expression of TGF-beta1 and matrix proteins in CsA-induced renal fibrosis of rats on a LSD. Sodium 6-12 renin Rattus norvegicus 43-48 9214404-16 1997 Since sodium depletion elevates peripheral renin activity, our experiments suggest a role for the renin-angiotensin system in the expression of TGF-beta1 and matrix proteins in CsA-induced renal fibrosis of rats on a LSD. Sodium 6-12 renin Rattus norvegicus 98-103 9626756-3 1997 The best characterized transport system is a 50-51 kDa sodium-dependent taurocholate cotransporting polypeptide (ntcp), which mediates the sodium-dependent uptake of conjugated bile acids at the sinusoidal plasma membrane of hepatocytes. Sodium 55-61 solute carrier family 10 member 1 Rattus norvegicus 113-117 34918049-6 2021 ETB blockade increases both BP and sodium retention. Sodium 35-41 endothelin receptor type B Rattus norvegicus 0-3 34918429-4 2022 Compressed sensing-based (CS-based) methods have been shown to accelerate sodium imaging and/or improve sodium image quality significantly. Sodium 74-80 citrate synthase Homo sapiens 26-28 34918429-4 2022 Compressed sensing-based (CS-based) methods have been shown to accelerate sodium imaging and/or improve sodium image quality significantly. Sodium 104-110 citrate synthase Homo sapiens 26-28 34918429-5 2022 In this manuscript, the basic concepts of CS and how CS might be applied to improve sodium MRI are described, and the historical milestones of CS-based sodium MRI are briefly presented. Sodium 84-90 citrate synthase Homo sapiens 42-44 34918429-5 2022 In this manuscript, the basic concepts of CS and how CS might be applied to improve sodium MRI are described, and the historical milestones of CS-based sodium MRI are briefly presented. Sodium 84-90 citrate synthase Homo sapiens 53-55 34918429-5 2022 In this manuscript, the basic concepts of CS and how CS might be applied to improve sodium MRI are described, and the historical milestones of CS-based sodium MRI are briefly presented. Sodium 152-158 citrate synthase Homo sapiens 143-145 34918429-6 2022 Representative advanced techniques and evaluation methods are discussed in detail, followed by an expose of clinical applications in multiple anatomical regions and diseases as well as thoughts and suggestions on potential future research prospects of CS in sodium MRI. Sodium 258-264 citrate synthase Homo sapiens 252-254 34854298-6 2021 When used as the anode materials for Na+ storage, the M-MoS2@HCS anode presents durable and rapid sodium storage properties. Sodium 98-104 holocarboxylase synthetase Homo sapiens 61-64 34854298-10 2021 The excellent sodium storage capability of the MoS2@HCS electrode is explained by the special structural design, which reveals great potential to accelerate the practical applications of transition-metal dichalcogenide electrodes for sodium storage. Sodium 14-20 holocarboxylase synthetase Homo sapiens 52-55 34854298-10 2021 The excellent sodium storage capability of the MoS2@HCS electrode is explained by the special structural design, which reveals great potential to accelerate the practical applications of transition-metal dichalcogenide electrodes for sodium storage. Sodium 234-240 holocarboxylase synthetase Homo sapiens 52-55 34904226-2 2022 The purpose of the present study was to determine how the inhibition of basolateral Kir 4.1/Kir 5.1 heteromeric K+ channel affects epithelial sodium channel (ENaC)-mediated Na+ transport in the principal cells of cortical collecting duct (CCD). Sodium 142-148 potassium inwardly-rectifying channel, subfamily J, member 16 Rattus norvegicus 92-99 33258401-1 2021 Acid-sensing ion channel 3 (ASIC3) belongs to the epithelial sodium channel/degenerin (ENaC/DEG) superfamily. Sodium 61-67 acid-sensing (proton-gated) ion channel 3 Mus musculus 0-26 33258401-1 2021 Acid-sensing ion channel 3 (ASIC3) belongs to the epithelial sodium channel/degenerin (ENaC/DEG) superfamily. Sodium 61-67 acid-sensing (proton-gated) ion channel 3 Mus musculus 28-33 34737802-7 2021 TRPA1 has a high permeability to Ca2+, sodium and potassium ions as a non-selective cation channel and the Ca2+ influx mediated by TRPA1 is involved in a variety of biological processes. Sodium 39-45 transient receptor potential cation channel subfamily A member 1 Homo sapiens 0-5 34737802-7 2021 TRPA1 has a high permeability to Ca2+, sodium and potassium ions as a non-selective cation channel and the Ca2+ influx mediated by TRPA1 is involved in a variety of biological processes. Sodium 39-45 transient receptor potential cation channel subfamily A member 1 Homo sapiens 131-136 34758144-4 2021 Here we show that mepyramine directly inhibits a variety of voltage-gated sodium channels, including the Tetrodotoxin-sensitive isoforms and the main isoforms (Nav1.7, Nav1.8, and Nav1.9) of nociceptors. Sodium 74-80 sodium voltage-gated channel alpha subunit 11 Homo sapiens 180-186 34657443-8 2021 In conclusion, the present study demonstrates that in the early stage of leptin receptor-deficient diabetes, the upregulation of macula densa NOS1 inhibits TGF and increases glomerular filtration rate, which counteracts renal sodium retention and limits the rise in blood pressure. Sodium 226-232 nitric oxide synthase 1, neuronal Mus musculus 142-146 34657443-7 2021 Genetic knockout of macula densa NOS1 restored the TGF response and attenuated glomerular hyperfiltration in db/db mice but also further reduced fractional renal sodium excretion and substantially increased blood pressure. Sodium 162-168 nitric oxide synthase 1, neuronal Mus musculus 33-37 9171961-2 1997 Stimulation of the gastric sodium monitor has been reported to cause a decrease in renal nerve activity and also a decrease in plasma renin activity in renal venous blood. Sodium 27-33 renin Rattus norvegicus 134-139 9171961-3 1997 This suggests that changes in sympathetic nerve activity and in the intrarenal renin-angiotensin system may mediate the natriuresis that occurs following gastric sodium administration. Sodium 162-168 renin Rattus norvegicus 79-84 9176324-2 1997 To determine if nNOS is a critical component in renin stimulation induced by dietary sodium restriction, rats received either normal sodium or a sodium-restricted diet (0.03%) for 7 days and subsequently were or were not treated with the selective inhibitor of nNOS 7-nitroindazole (7-NI) either acutely (50 mg/kg body wt ip) on the final day or chronically (20 mg/kg body wt ip 2 x/day) over the final 5 days. Sodium 85-91 renin Rattus norvegicus 48-53 9143369-1 1997 The sodium/myo-inositol cotransporter (SMIT) is a plasma membrane protein catalyzing transfer of myo-inositol into cells against a considerable concentration gradient using the electrochemical potential of sodium across the cell membrane. Sodium 4-10 LOC100856716 Canis lupus familiaris 39-43 9170003-0 1997 Sodium intake regulates renin gene expression differently in the hypothalamus and kidney of rats. Sodium 0-6 renin Rattus norvegicus 24-29 9170003-1 1997 OBJECTIVE: To elucidate the different effects of sodium intake on renin messenger RNA (mRNA) in the hypothalamus and the kidney and to investigate the role of hypothalamic renin in sodium-induced hypertension. Sodium 49-55 renin Rattus norvegicus 66-71 9170003-1 1997 OBJECTIVE: To elucidate the different effects of sodium intake on renin messenger RNA (mRNA) in the hypothalamus and the kidney and to investigate the role of hypothalamic renin in sodium-induced hypertension. Sodium 181-187 renin Rattus norvegicus 172-177 9170003-2 1997 DESIGN AND METHODS: We investigated the expression of the renin gene in the hypothalamus and the kidney of rats with altered sodium intake and those administered either deoxycorticosterone acetate (DOCA) or sodium. Sodium 125-131 renin Rattus norvegicus 58-63 9170003-2 1997 DESIGN AND METHODS: We investigated the expression of the renin gene in the hypothalamus and the kidney of rats with altered sodium intake and those administered either deoxycorticosterone acetate (DOCA) or sodium. Sodium 207-213 renin Rattus norvegicus 58-63 9170003-7 1997 RESULTS: A high sodium intake for 10 days increased the renin mRNA in the hypothalamus; the hypothalamic renin mRNA had not been suppressed after 8 weeks of a high sodium intake despite the lowering in renal renin mRNA. Sodium 16-22 renin Rattus norvegicus 56-61 9170003-7 1997 RESULTS: A high sodium intake for 10 days increased the renin mRNA in the hypothalamus; the hypothalamic renin mRNA had not been suppressed after 8 weeks of a high sodium intake despite the lowering in renal renin mRNA. Sodium 16-22 renin Rattus norvegicus 105-110 9170003-7 1997 RESULTS: A high sodium intake for 10 days increased the renin mRNA in the hypothalamus; the hypothalamic renin mRNA had not been suppressed after 8 weeks of a high sodium intake despite the lowering in renal renin mRNA. Sodium 16-22 renin Rattus norvegicus 105-110 9170003-10 1997 The constant expression of the renin gene in the hypothalamus during a chronic high sodium load might be related at least in part to the mechanism of the activated brain renin-angiotensin system in sodium-induced hypertension. Sodium 84-90 renin Rattus norvegicus 31-36 9170003-10 1997 The constant expression of the renin gene in the hypothalamus during a chronic high sodium load might be related at least in part to the mechanism of the activated brain renin-angiotensin system in sodium-induced hypertension. Sodium 84-90 renin Rattus norvegicus 170-175 9170003-10 1997 The constant expression of the renin gene in the hypothalamus during a chronic high sodium load might be related at least in part to the mechanism of the activated brain renin-angiotensin system in sodium-induced hypertension. Sodium 198-204 renin Rattus norvegicus 31-36 9170003-10 1997 The constant expression of the renin gene in the hypothalamus during a chronic high sodium load might be related at least in part to the mechanism of the activated brain renin-angiotensin system in sodium-induced hypertension. Sodium 198-204 renin Rattus norvegicus 170-175 9106700-8 1997 RESULTS: On intraluminal infusion of PYY, increased absorption of water, sodium, and chloride was observed in the colon. Sodium 73-79 peptide YY Canis lupus familiaris 37-40 9118703-7 1997 These concentrations of TGF-alpha in pulmonary edema fluid have potent in vivo and in vitro effects on alveolar epithelial sodium transport and alveolar epithelial cell motility. Sodium 123-129 transforming growth factor alpha Homo sapiens 24-33 34981441-10 2021 The cystatin C ((area under the curve (AUC)=0.853) performance was better than that of the creatinine (AUC=0.699), Child-Turcotte-Pugh (CTP) (AUC=0.661), and model for end-stage liver disease-sodium (MELD-Na) (AUC=0.641). Sodium 192-198 cystatin C Homo sapiens 4-14 9084968-2 1997 Enhanced permeability of plasma membranes for sodium (e.g. sodium-hydrogen exchange, NHE) may predict the subset of diabetic patients for whom intensive modalities of treatment are indicated despite their potential risk. Sodium 46-52 solute carrier family 9 member C1 Homo sapiens 85-88 34880650-1 2021 Plasma membrane sodium-hydrogen exchangers (NHE) transport Na+ into cells in exchange for H+. Sodium 16-22 solute carrier family 9 member C1 Homo sapiens 44-47 34403723-1 2021 Intestinal absorption of vitamin C in humans is mediated via the sodium-dependent vitamin C transporters (hSVCT1 and hSVCT2). Sodium 65-71 solute carrier family 23 member 2 Homo sapiens 117-123 9062366-0 1997 Regulation of angiotensin II receptor AT1 subtypes in renal afferent arterioles during chronic changes in sodium diet. Sodium 106-112 angiotensin II receptor, type 1a Rattus norvegicus 38-41 34921521-8 2021 In the combined data set plasma sodium level was significantly associated with ECFV (B (SE) = 0.10 (0.04), p = 0.02), and systolic blood pressure (SBP, B (SE) = 0.73 (0.26), p = 0.006), independent of ECFV. Sodium 32-38 selenium binding protein 1 Homo sapiens 147-150 34921521-11 2021 Finally, plasma sodium level is associated with SBP, independent of ECFV and diet. Sodium 16-22 selenium binding protein 1 Homo sapiens 48-51 34779863-13 2021 The mechanism may be involved that paternal PM2.5 exposure-associated oxidative stress induces the elevated renal GRK4 level, leading to the enhanced AT1R expression and its-mediated sodium retention, consequently causes hypertension in male offspring. Sodium 183-189 angiotensin II receptor, type 1a Rattus norvegicus 150-154 9062366-13 1997 Total AT1 receptor mRNA expression was suppressed by low sodium intake to 66% of control levels, whereas it was increased to 132% of control by high-sodium diet, as indicated by ribonuclease protection assay. Sodium 57-63 angiotensin II receptor, type 1a Rattus norvegicus 6-9 34775762-0 2021 Ultrahigh Rate and Ultralong Life Span Sodium Storage of FePS3 Enabled by the Space Confinement Effect of Layered Expanded Graphite. Sodium 39-45 sodium voltage-gated channel alpha subunit 11 Homo sapiens 57-62 9062366-16 1997 Chronic changes in sodium intake caused parallel regulation of expression and amount of receptor protein of the two AT1 receptor genes that modulate receptor function and altered reactivity of renal vessels to ANG II. Sodium 19-25 angiotensin II receptor, type 1a Rattus norvegicus 116-119 34884494-5 2021 The mechanism by which these drugs exert their cardioprotective effects is unknown, although recent studies have shown that cardiovascular homeostasis occurs through the interplay of the sodium-hydrogen exchangers (NHE), specifically NHE1 and NHE3, with SGLT2i. Sodium 187-193 solute carrier family 9 member C1 Homo sapiens 215-218 8988947-6 1997 Regression analyses confirmed direct independent relations of body mass index, alcohol intake, sodium, and ratio of sodium to potassium to SBP and DBP, and an inverse relation of potassium to SBP and DBP. Sodium 116-122 selenium binding protein 1 Homo sapiens 139-142 9039118-0 1997 Cyclooxygenase-2 mediates increased renal renin content induced by low-sodium diet. Sodium 71-77 prostaglandin-endoperoxide synthase 2 Mus musculus 0-16 34840979-0 2021 Downregulation of Rap1GAP Expression Activates the TGF-beta/Smad3 Pathway to Inhibit the Expression of Sodium/Iodine Transporter in Papillary Thyroid Carcinoma Cells. Sodium 103-109 RAP1 GTPase activating protein Homo sapiens 18-25 34840979-0 2021 Downregulation of Rap1GAP Expression Activates the TGF-beta/Smad3 Pathway to Inhibit the Expression of Sodium/Iodine Transporter in Papillary Thyroid Carcinoma Cells. Sodium 103-109 transforming growth factor alpha Homo sapiens 51-59 34840979-0 2021 Downregulation of Rap1GAP Expression Activates the TGF-beta/Smad3 Pathway to Inhibit the Expression of Sodium/Iodine Transporter in Papillary Thyroid Carcinoma Cells. Sodium 103-109 SMAD family member 3 Homo sapiens 60-65 34834529-12 2021 SLC24A3 is a sodium-calcium regulator of cells, and high SLC24A3 levels are associated with poor prognosis. Sodium 13-19 solute carrier family 24 member 3 Homo sapiens 0-7 34553376-8 2021 The inhibition of gasping by lamotrigine was accompanied by a significant reduction of the persistent sodium current (INap) in PreBotC neurons. Sodium 102-108 NFKB inhibitor zeta Homo sapiens 118-122 34778257-8 2021 Further analysis revealed that renal Fgfr1/klotho/extracellular signal-regulated kinases 1/2 signaling was activated in AAV-Fgf23 mice, resulting in downregulation of sodium-phosphate cotransporter NaPi2a and NaPi2c and suppression of Cyp27b1, further supporting the bioactivity of cardiac-derived iFgf23. Sodium 167-173 fibroblast growth factor receptor 1 Mus musculus 37-42 34778257-8 2021 Further analysis revealed that renal Fgfr1/klotho/extracellular signal-regulated kinases 1/2 signaling was activated in AAV-Fgf23 mice, resulting in downregulation of sodium-phosphate cotransporter NaPi2a and NaPi2c and suppression of Cyp27b1, further supporting the bioactivity of cardiac-derived iFgf23. Sodium 167-173 mitogen-activated protein kinase 3 Mus musculus 50-92 9039118-9 1997 Thus, increased renal renin content in response to dietary sodium restriction appears to require the induction of cyclooxygenase-2, while neuronal nitric oxide synthase appears to affect basal but not stimulated renal renin content. Sodium 59-65 prostaglandin-endoperoxide synthase 2 Mus musculus 114-130 9050969-1 1997 OBJECTIVE: To examine the mechanisms affecting proximal tubule sodium reabsorption, we studied the gene expression and functional changes of the Na+/H+-exchanger 3 (NHE3) and its gene expression in spontaneously hypertensive rats (SHR). Sodium 63-69 solute carrier family 9 member A3 Rattus norvegicus 165-169 9210182-7 1997 Thus, calcitonin inhibition of sodium/potassium transport through synaptic membranes supports a regulatory role of this peptide on neurotransmission. Sodium 31-37 calcitonin-related polypeptide alpha Rattus norvegicus 6-16 8989127-5 1996 Urine volume and urine sodium excretion increased significantly during hBNP infusion when compared with placebo infusion (90 +/- 38 versus 67 +/- 27 mL/h and 2.6 +/- 2.4 versus 1.4 +/- 1.2 mEq/h, respectively, both P < .05 versus placebo), whereas creatinine clearance and urinary potassium excretion did not change. Sodium 23-29 natriuretic peptide B Homo sapiens 71-75 8986922-0 1996 Regulation of type 1 angiotensin II receptor and its subtype gene expression in kidney by sodium loading and angiotensin II infusion. Sodium 90-96 angiotensin II receptor, type 1a Rattus norvegicus 14-44 8961265-1 1996 The mineralocorticoid receptor (MR) is a ligand-dependent transcription factor involved in the regulation of sodium homeostasis. Sodium 109-115 nuclear receptor subfamily 3 group C member 2 Homo sapiens 4-30 8961265-1 1996 The mineralocorticoid receptor (MR) is a ligand-dependent transcription factor involved in the regulation of sodium homeostasis. Sodium 109-115 nuclear receptor subfamily 3 group C member 2 Homo sapiens 32-34 8945984-5 1996 Dietary sodium manipulation between postnatal days (PD) 6 and 18 significantly influenced renal renin gene expression, with low-sodium diet increasing renin mRNA on PD12 and PD18 and high-sodium diet decreasing renin mRNA on PD18. Sodium 8-14 renin Rattus norvegicus 96-101 8945984-5 1996 Dietary sodium manipulation between postnatal days (PD) 6 and 18 significantly influenced renal renin gene expression, with low-sodium diet increasing renin mRNA on PD12 and PD18 and high-sodium diet decreasing renin mRNA on PD18. Sodium 8-14 renin Rattus norvegicus 151-156 8945984-5 1996 Dietary sodium manipulation between postnatal days (PD) 6 and 18 significantly influenced renal renin gene expression, with low-sodium diet increasing renin mRNA on PD12 and PD18 and high-sodium diet decreasing renin mRNA on PD18. Sodium 8-14 renin Rattus norvegicus 151-156 8945984-5 1996 Dietary sodium manipulation between postnatal days (PD) 6 and 18 significantly influenced renal renin gene expression, with low-sodium diet increasing renin mRNA on PD12 and PD18 and high-sodium diet decreasing renin mRNA on PD18. Sodium 128-134 renin Rattus norvegicus 151-156 8945984-5 1996 Dietary sodium manipulation between postnatal days (PD) 6 and 18 significantly influenced renal renin gene expression, with low-sodium diet increasing renin mRNA on PD12 and PD18 and high-sodium diet decreasing renin mRNA on PD18. Sodium 128-134 renin Rattus norvegicus 151-156 8945984-5 1996 Dietary sodium manipulation between postnatal days (PD) 6 and 18 significantly influenced renal renin gene expression, with low-sodium diet increasing renin mRNA on PD12 and PD18 and high-sodium diet decreasing renin mRNA on PD18. Sodium 128-134 renin Rattus norvegicus 151-156 8945984-5 1996 Dietary sodium manipulation between postnatal days (PD) 6 and 18 significantly influenced renal renin gene expression, with low-sodium diet increasing renin mRNA on PD12 and PD18 and high-sodium diet decreasing renin mRNA on PD18. Sodium 128-134 renin Rattus norvegicus 151-156 8945984-9 1996 These results demonstrate that 1) the peripheral and central renin-angiotensin systems do not have a common ontogenetic pattern of development, 2) they are independently regulated in response to dietary sodium variations, and 3) young WKY and SHR share very similar ontogenetic patterns of angiotensinogen and renin gene expression. Sodium 203-209 renin Rattus norvegicus 61-66 34089591-1 2021 BACKGROUND: We have previously shown that high salt stimulates the expression of miR-429 in the renal medulla, which induces mRNA decay of HIF prolyl-hydroxylase 2 (PHD2), an enzyme to promote the degradation of hypoxia inducible factor (HIF)-1alpha, and increases the HIF-1alpha-mediated activation of antihypertensive genes in the renal medulla, consequently promoting extra sodium excretion. Sodium 377-383 microRNA 429 Rattus norvegicus 81-88 8969885-0 1996 AT1 receptors and cell proliferation in rat adrenals: effects of angiotensin infusion, low sodium diet and losartan. Sodium 91-97 angiotensin II receptor, type 1a Rattus norvegicus 0-3 34089591-7 2021 Functionally, overexpression of miR-429 transgene in the renal medulla significantly improved pressure natriuretic response, enhanced urinary sodium excretion and reduced sodium retention upon extra sodium loading, and consequently, attenuated the salt-sensitive hypertension in Dahl S rats. Sodium 142-148 microRNA 429 Rattus norvegicus 32-39 34089591-7 2021 Functionally, overexpression of miR-429 transgene in the renal medulla significantly improved pressure natriuretic response, enhanced urinary sodium excretion and reduced sodium retention upon extra sodium loading, and consequently, attenuated the salt-sensitive hypertension in Dahl S rats. Sodium 171-177 microRNA 429 Rattus norvegicus 32-39 34089591-7 2021 Functionally, overexpression of miR-429 transgene in the renal medulla significantly improved pressure natriuretic response, enhanced urinary sodium excretion and reduced sodium retention upon extra sodium loading, and consequently, attenuated the salt-sensitive hypertension in Dahl S rats. Sodium 199-205 microRNA 429 Rattus norvegicus 32-39 9086315-5 1996 Sodium loading increased SBP and decreased HR in all high physical activity subjects but not in low physical activity subjects (p < 0.05). Sodium 0-6 selenium binding protein 1 Homo sapiens 25-28 34533953-3 2021 Here, we utilized a new approach to study the effect of lithium as a drug on the protein interaction network of GSK-3beta as a hub protein and computed the affinities of GSK-3beta to its partners in the presence of lithium or sodium ions. Sodium 226-232 glycogen synthase kinase 3 alpha Homo sapiens 112-121 34533953-3 2021 Here, we utilized a new approach to study the effect of lithium as a drug on the protein interaction network of GSK-3beta as a hub protein and computed the affinities of GSK-3beta to its partners in the presence of lithium or sodium ions. Sodium 226-232 glycogen synthase kinase 3 alpha Homo sapiens 170-179 9086315-8 1996 These data suggest that high physical activity levels do not attenuate but rather exaggerate SBP response to a sodium load. Sodium 111-117 selenium binding protein 1 Homo sapiens 93-96 34533953-4 2021 For this purpose, ensembles of GSK-3beta protein structures were created in the presence of either lithium or sodium ions using adaptive tempering molecular dynamics simulations. Sodium 110-116 glycogen synthase kinase 3 alpha Homo sapiens 31-40 8986915-1 1996 OBJECTIVES: To determine the possible relationship between the degree of dietary sodium intake and the development of renal failure during blockade of the renin-angiotensin system. Sodium 81-87 renin Rattus norvegicus 155-160 8694907-0 1996 Nerve growth factor increases sodium current in pancreatic beta cells. Sodium 30-36 nerve growth factor Rattus norvegicus 0-19 34522919-3 2021 Highly selective and fully reversible pH optodes as well as Na+- and K+-selective optodes are obtained only when the most hydrophobic sensing chemicals are used (e.g., sodium ionophore VIII vs. sodium ionophore VI). Sodium 168-174 cytochrome c oxidase subunit 8A Homo sapiens 185-189 8770082-9 1996 Blockade of the binding of ANG II to the AT1 receptor by losartan prevents the increases in AT1A and AT1B mRNA expression and the AT1 receptor density induced by sodium depletion, suggesting that these changes in the adrenal gland are mediated by activation of the AT1 receptor. Sodium 162-168 angiotensin II receptor, type 1a Rattus norvegicus 41-44 8663325-2 1996 Analysis of a transgene-induced mutation at the mouse med locus led to the identification of the novel voltage-gated sodium channel gene Scn8a (Burgess, D. L., Kohrman, D. C., Galt, J., Plummer, N. W., Jones, J. M., Spear, B., and Meisler, M. H.(1995) Nat. Sodium 117-123 sodium channel, voltage-gated, type VIII, alpha Mus musculus 137-142 34640291-4 2021 The HA nanofibers and the MgP nanosheets were synthesized using a hydrothermal homogeneous precipitation method and tuning the crystallization of the sodium-magnesium-phosphate ternary system, respectively. Sodium 150-156 matrix Gla protein Homo sapiens 26-29 8770890-12 1996 The differential tissue-specific regulation of OTR gene expression may represent a mechanism by which circulating OT can assume a multifunctional role in both reproduction and sodium homeostasis. Sodium 176-182 oxytocin receptor Rattus norvegicus 47-50 8650545-4 1996 The PKD2 protein has amino acid similarity with PKD1, the Caenorhabditis elegans homolog of PKD1, and the family of voltage-activated calcium (and sodium) channels, and it contains a potential calcium-binding domain. Sodium 147-153 Polycystin-2 Caenorhabditis elegans 4-8 8928815-5 1996 ISC decreased, with a sensitivity to apical inhibitors of sodium transport in the order benzamil > amiloride > 5-(N-ethyl-N-isopropyl) amiloride in MDSF +/- EGF, and was completely inhibited by the addition of basolateral ouabain. Sodium 58-64 epidermal growth factor like 1 Rattus norvegicus 163-166 34617884-3 2021 We have shown that enhancing endosomal acidification by inhibiting the EE-specific sodium-hydrogen exchanger 6 (NHE6) restores vesicular trafficking and normalizes synaptic homeostasis. Sodium 83-89 solute carrier family 9 (sodium/hydrogen exchanger), member 6 Mus musculus 112-116 34755109-0 2021 Persistent sodium currents in SCN1A developmental and degenerative epileptic dyskinetic encephalopathy. Sodium 11-17 sodium voltage-gated channel alpha subunit 1 Homo sapiens 30-35 34755109-1 2021 Pathogenic variants in the voltage-gated sodium channel gene (SCN1A) are amongst the most common genetic causes of childhood epilepsies. Sodium 41-47 sodium voltage-gated channel alpha subunit 1 Homo sapiens 62-67 34549350-7 2021 Finally, we experimentally validate our top-scoring de novo mutation NP_001243143.1:p.Phe309Ser in the sodium/potassium-transporting ATPase ATP1A3 to disrupt protein binding with different partners. Sodium 103-109 ATPase Na+/K+ transporting subunit alpha 3 Homo sapiens 140-146 8928815-6 1996 Net sodium flux and Na+, K+ -ATPase activity both increased approximately 50% in the presence of EGF. Sodium 4-10 epidermal growth factor like 1 Rattus norvegicus 97-100 8928815-7 1996 These results indicate that 1) EGF decreases tight junctional permeability and increases active sodium transport by AEC monolayers via basolaterally located EGF receptors, and 2) the pathways for AEC sodium entry and exit (+/- EGF) are apical high amiloride affinity sodium channels and basolateral sodium pumps. Sodium 96-102 epidermal growth factor like 1 Rattus norvegicus 31-34 8785398-8 1996 In water-deprived, sodium-loaded, and potassium-loaded rats, the inner medullary sorbitol content increased significantly in accordance with the rise in the enzymatic activity and the level of aldose reductase mRNA. Sodium 19-25 aldo-keto reductase family 1 member B1 Rattus norvegicus 193-209 8592155-0 1996 Differential effects of nerve growth factor on expression of choline acetyltransferase and sodium-coupled choline transport in basal forebrain cholinergic neurons in culture. Sodium 91-97 nerve growth factor Rattus norvegicus 24-43 34475263-1 2021 Mutations in the voltage-gated sodium channel gene SCN1A are associated with human epilepsy disorders, but how most of these mutations alter channel properties and result in seizures is unknown. Sodium 31-37 sodium voltage-gated channel alpha subunit 1 Homo sapiens 51-56 8726683-0 1996 Sodium induced regulation of angiotensin receptor 1A and 1B in rat kidney. Sodium 0-6 angiotensin II receptor, type 1a Rattus norvegicus 29-59 34512260-3 2021 The sodium leak channel (NALCN), a non-selective cation channel, mediates the background Na+ leak conductance and controls neuronal excitability. Sodium 4-10 sodium leak channel, non-selective Rattus norvegicus 25-30 34378910-0 2021 Bimetallic Sulfide SnS2/FeS2 Nanosheets as High-Performance Anode Materials for Sodium-Ion Batteries. Sodium 80-86 sodium voltage-gated channel alpha subunit 11 Homo sapiens 19-23 34378910-1 2021 Transition-metal sulfide SnS2 has aroused wide concern due to its high capacity and nanosheet structure, making it an attractive choice as the anode material in sodium-ion batteries. Sodium 161-167 sodium voltage-gated channel alpha subunit 11 Homo sapiens 25-29 34378910-5 2021 SnS2/FeS2/rGO bimetallic sulfide electrode boasts a capacity of 768.3 mA h g-1 at the current density of 0.1 A g-1, and 541.2 mA h g-1 at the current density of 1 A g-1 in sodium-ion batteries, which is superior to that of either single metal sulfide SnS2 or FeS2. Sodium 172-178 sodium voltage-gated channel alpha subunit 11 Homo sapiens 0-4 34378910-7 2021 The superior electrochemical performance of the SnS2/FeS2/rGO composite material makes it a promising candidate for sodium storage. Sodium 116-122 sodium voltage-gated channel alpha subunit 11 Homo sapiens 48-52 34349262-1 2021 MFSD2A is a sodium-dependent lysophosphatidylcholine symporter that is responsible for the uptake of docosahexaenoic acid into the brain1,2, which is crucial for the development and performance of the brain3. Sodium 12-18 POU domain, class 3, transcription factor 3 Mus musculus 131-139 9162438-9 1996 In these rats, the loss of the capability to down-regulate insulin receptor in the kidney when extracellular fluid volume is expanded can lead to further sodium retention and might play a role in the development and maintenance of hypertension. Sodium 154-160 insulin receptor Rattus norvegicus 59-75 8993847-9 1996 Centrally administered AngII may act on AT1 receptors in the median preoptic nucleus and elsewhere to induce drinking, sodium appetite, a sympathetic vasoconstrictor response and vasopressin secretion. Sodium 119-125 angiotensin II receptor, type 1a Rattus norvegicus 40-43 8993850-9 1996 The expression of the AT1 receptor is modulated at the mRNA and protein levels by many factors: conditions that increase levels of AngII (low sodium diet, renovascular hypertension, AngII infusion) up-regulate AT1 receptor mRNA levels and binding and increase aldosterone secretion. Sodium 142-148 angiotensin II receptor type 1 Homo sapiens 22-25 8993850-9 1996 The expression of the AT1 receptor is modulated at the mRNA and protein levels by many factors: conditions that increase levels of AngII (low sodium diet, renovascular hypertension, AngII infusion) up-regulate AT1 receptor mRNA levels and binding and increase aldosterone secretion. Sodium 142-148 angiotensin II receptor type 1 Homo sapiens 210-213 8770597-6 1996 In light of previous physiological tests that show that Khc mutations inhibit compound action potential propagation in segmental nerves, these data indicate that kinesin activity is required for normal inward sodium currents during neuronal action potentials. Sodium 209-215 Kinesin heavy chain Drosophila melanogaster 162-169 8832271-0 1996 Effect of aging and sodium deprivation on plasma concentration of aldosterone and on plasma renin activity in the rat. Sodium 20-26 renin Rattus norvegicus 92-97 8832271-1 1996 Age-related changes in plasma aldosterone and corticosterone concentrations as well as in plasma renin activity in response to 10 days of sodium deprivation were studied in old as compared to adult male Long-Evans rats. Sodium 138-144 renin Rattus norvegicus 97-102 8832271-6 1996 Furthermore, although plasma renin activity of senescent rats, fed either a normal or a sodium-deprived diet, was lower as compared to adult rats, the absolute and percent increases of this activity in response to sodium deprivation were, respectively, similar and higher in old as compared to adult rats and so could partially contribute to the higher aldosterone response. Sodium 88-94 renin Rattus norvegicus 29-34 8832271-6 1996 Furthermore, although plasma renin activity of senescent rats, fed either a normal or a sodium-deprived diet, was lower as compared to adult rats, the absolute and percent increases of this activity in response to sodium deprivation were, respectively, similar and higher in old as compared to adult rats and so could partially contribute to the higher aldosterone response. Sodium 214-220 renin Rattus norvegicus 29-34 7498983-1 1995 We previously demonstrated that type 1A angiotensin II (Ang II) receptor (AT1A) is the predominant renal subtype and is upregulated by a low sodium diet. Sodium 141-147 angiotensin II receptor, type 1a Rattus norvegicus 74-78 7498983-2 1995 We have now tested the hypothesis that upregulation of AT1A mRNA induced by sodium deficiency is renal specific and is mediated by activation of type 1 Ang II receptor (AT1). Sodium 76-82 angiotensin II receptor, type 1a Rattus norvegicus 55-59 7498983-2 1995 We have now tested the hypothesis that upregulation of AT1A mRNA induced by sodium deficiency is renal specific and is mediated by activation of type 1 Ang II receptor (AT1). Sodium 76-82 angiotensin II receptor, type 1a Rattus norvegicus 55-58 7498983-5 1995 Plasma renin activity was elevated by losartan treatment, sodium restriction, or the combination of the two versus control (P < .05). Sodium 58-64 renin Rattus norvegicus 7-12 7498983-6 1995 Northern blot analysis showed that the ratio of renal AT1A to glyceraldehyde 3-phosphate dehydrogenase (GAPDH) mRNA was increased by losartan treatment, sodium restriction, or the combination of the two versus control (P < .05). Sodium 153-159 angiotensin II receptor, type 1a Rattus norvegicus 54-58 7498983-7 1995 In contrast, the ratio of adrenal AT1A to GAPDH mRNA was increased only by sodium restriction versus three other groups (P < .05). Sodium 75-81 angiotensin II receptor, type 1a Rattus norvegicus 34-38 7498983-8 1995 Thus, sodium deficiency increases AT1A mRNA in both kidney and adrenal gland, while Ang II receptor blockade by losartan prevents low sodium-induced AT1A mRNA only in adrenal gland. Sodium 6-12 angiotensin II receptor, type 1a Rattus norvegicus 34-38 7498983-8 1995 Thus, sodium deficiency increases AT1A mRNA in both kidney and adrenal gland, while Ang II receptor blockade by losartan prevents low sodium-induced AT1A mRNA only in adrenal gland. Sodium 134-140 angiotensin II receptor, type 1a Rattus norvegicus 149-153 8903651-11 1995 The increases in urine flow and sodium excretion rate induced by losartan depend partially on AT2 receptors, kinins and prostaglandins. Sodium 32-38 angiotensin II receptor, type 2 Rattus norvegicus 94-97 8587258-6 1995 Sodium loss was higher using LNaD (72 +/- 11 mEq, P < 0.01) and CD2.5 (41 +/- 12 mEq, P < 0.05) than using CD1.5 (-18 +/- 8 mEq). Sodium 0-6 interleukin 2 receptor subunit alpha Homo sapiens 67-72 34128158-6 2021 The expression of BAFF and its receptors was analyzed via flow cytometry and sodium ion transport function, and cytokeratin-18 expression was detected through immunofluorescence staining. Sodium 77-83 tumor necrosis factor (ligand) superfamily, member 13b Mus musculus 18-22 34135733-0 2021 Deciphering in silico the Role of Mutated Na V 1.1 Sodium Channels in Enhancing Trigeminal Nociception in Familial Hemiplegic Migraine Type 3. Sodium 51-57 sodium voltage-gated channel alpha subunit 1 Homo sapiens 42-50 34135733-0 2021 Deciphering in silico the Role of Mutated Na V 1.1 Sodium Channels in Enhancing Trigeminal Nociception in Familial Hemiplegic Migraine Type 3. Sodium 51-57 sodium voltage-gated channel alpha subunit 1 Homo sapiens 106-141 34135733-1 2021 Familial hemiplegic migraine type 3 (FHM3) is caused by gain-of-function mutations in the SCN1A gene that encodes the alpha1 subunit of voltage-gated NaV1.1 sodium channels. Sodium 157-163 sodium voltage-gated channel alpha subunit 1 Homo sapiens 0-35 34135733-1 2021 Familial hemiplegic migraine type 3 (FHM3) is caused by gain-of-function mutations in the SCN1A gene that encodes the alpha1 subunit of voltage-gated NaV1.1 sodium channels. Sodium 157-163 sodium voltage-gated channel alpha subunit 1 Homo sapiens 37-41 34135733-1 2021 Familial hemiplegic migraine type 3 (FHM3) is caused by gain-of-function mutations in the SCN1A gene that encodes the alpha1 subunit of voltage-gated NaV1.1 sodium channels. Sodium 157-163 sodium voltage-gated channel alpha subunit 1 Homo sapiens 90-95 34079337-2 2021 The angiotensin I-converting enzyme (ACE1), angiotensin-converting enzyme 2 (ACE2), angiotensinogen (AGT) and receptors angiotensin II receptor type 1 (AGTR1) are key factors for SARS-CoV-2 entering in the cells, sodium and water retention with an increase blood pressure, promotion of fibrotic and inflammatory phenomena resulting in a cytokine storm. Sodium 213-219 angiotensin II receptor type 1 Homo sapiens 152-157 34113239-1 2021 Background Our aim was to investigate the effects of the protein expression and the function of sodium, potassium, and chloride co-transporter (NKCC1) in the dorsal root ganglion (DRG) after activation of transient receptor potential vanilloid 1 receptor (TRPV1) in capsaicin-induced acute inflammatory pain and the possible mechanism of action. Sodium 96-102 solute carrier family 12 member 2 Rattus norvegicus 144-149 34113239-1 2021 Background Our aim was to investigate the effects of the protein expression and the function of sodium, potassium, and chloride co-transporter (NKCC1) in the dorsal root ganglion (DRG) after activation of transient receptor potential vanilloid 1 receptor (TRPV1) in capsaicin-induced acute inflammatory pain and the possible mechanism of action. Sodium 96-102 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 205-254 34113239-1 2021 Background Our aim was to investigate the effects of the protein expression and the function of sodium, potassium, and chloride co-transporter (NKCC1) in the dorsal root ganglion (DRG) after activation of transient receptor potential vanilloid 1 receptor (TRPV1) in capsaicin-induced acute inflammatory pain and the possible mechanism of action. Sodium 96-102 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 256-261 34095364-7 2021 The functional relevance of one LBN-induced candidate gene, Scn7a, could be confirmed by an increase in the density of voltage-gated sodium (Nav) channel activated currents in hippocampal NG2+ cells. Sodium 133-139 sodium channel, voltage-gated, type VII, alpha Mus musculus 60-65 34847569-2 2021 Enterocyte ACE2 is coexpressed as the apical membrane trafficking partner obligatory for expression and activity of the B0AT1 sodium-dependent neutral amino acid transporter. Sodium 126-132 angiotensin converting enzyme 2 Homo sapiens 11-15 34847569-2 2021 Enterocyte ACE2 is coexpressed as the apical membrane trafficking partner obligatory for expression and activity of the B0AT1 sodium-dependent neutral amino acid transporter. Sodium 126-132 solute carrier family 6 member 19 Homo sapiens 120-125 7565698-3 1995 Overexpression of HAL3 improves growth of wild-type cells exposed to toxic concentrations of sodium and lithium and suppresses the salt sensitivity conferred by mutation of the calcium-dependent protein phosphatase calcineurin. Sodium 93-99 phosphopantothenoylcysteine decarboxylase complex subunit SIS2 Saccharomyces cerevisiae S288C 18-22 8719773-0 1995 Renin gene expression in the aging kidney: effect of sodium restriction. Sodium 53-59 renin Rattus norvegicus 0-5 7576396-8 1995 The natriuretic effect of BNP was attributable to both an increase in filtered sodium load and a reduction of distal sodium reabsorption. Sodium 79-85 natriuretic peptide B Homo sapiens 26-29 7576396-8 1995 The natriuretic effect of BNP was attributable to both an increase in filtered sodium load and a reduction of distal sodium reabsorption. Sodium 117-123 natriuretic peptide B Homo sapiens 26-29 7576396-9 1995 These results suggest that BNP may contribute to maintain renal function and sodium excretion in patients with essential hypertension. Sodium 77-83 natriuretic peptide B Homo sapiens 27-30 7628645-1 1995 Homologous proteins (NBAT) which mediate sodium-independent transport of neutral as well as basic amino acids and cystine when expressed in Xenopus oocytes were recently cloned from mammalian kidneys. Sodium 41-47 solute carrier family 3 member 1 Homo sapiens 21-25 7608170-0 1995 Vasopressin-stimulated electrogenic sodium transport in A6 cells is linked to a Ca(2+)-mobilizing signal mechanism. Sodium 36-42 arginine vasopressin S homeolog Xenopus laevis 0-11 34927856-4 2021 Upon charging, sodium will be uniformly deposited onto the Ag@C substrate and afterwards functions as a real SMA, thus inheriting the intrinsic merits of SMA and enhancing safety simultaneously. Sodium 15-21 survival of motor neuron 1, telomeric Homo sapiens 109-112 34927856-4 2021 Upon charging, sodium will be uniformly deposited onto the Ag@C substrate and afterwards functions as a real SMA, thus inheriting the intrinsic merits of SMA and enhancing safety simultaneously. Sodium 15-21 survival of motor neuron 1, telomeric Homo sapiens 154-157 35296155-0 2022 Na+-Retaining Action of COX-2 (Cyclooxygenase-2)/EP1 Pathway in the Collecting Duct via Activation of Intrarenal Renin-Angiotensin-Aldosterone System and Epithelial Sodium Channel. Sodium 165-171 prostaglandin-endoperoxide synthase 2 Mus musculus 24-29 35296155-0 2022 Na+-Retaining Action of COX-2 (Cyclooxygenase-2)/EP1 Pathway in the Collecting Duct via Activation of Intrarenal Renin-Angiotensin-Aldosterone System and Epithelial Sodium Channel. Sodium 165-171 prostaglandin-endoperoxide synthase 2 Mus musculus 31-47 35430875-10 2022 During the second week of Ang II infusion when blood pressures between groups diverged, DC AT1aR KO mice excreted less sodium than WTs. Sodium 119-125 angiotensin II receptor type 1 Homo sapiens 91-96 35430875-12 2022 CONCLUSIONS: Following activation of the renin angiotensin system, AT1aR stimulation on DCs suppresses renal DC maturation and T cell activation with consequent protection from sodium retention and blood pressure elevation. Sodium 177-183 angiotensin II receptor type 1 Homo sapiens 67-72 35537891-1 2022 AIMS: To determine national prevalence of sodium-glucose contransporter-2 inhibitor (SGLT2i) and glucagon-like peptide-1 receptor agonist (GLP1RA) use among adults with type 2 diabetes mellitus (T2DM). Sodium 42-48 glucagon like peptide 1 receptor Homo sapiens 139-145 7661335-12 1995 We found that the volume-augmenting effect of HHL per millilitre infused solution was more than four times that of HA and HES, primarily as a result of increasing plasma osmolality due to an increase of plasma sodium levels. Sodium 210-216 hes family bHLH transcription factor 1 Homo sapiens 46-49 7576598-0 1995 The secretion of parathyroid hormone-related protein in the saliva of sheep and its effects on the salivary clearance of phosphate, calcium, magnesium, potassium and sodium ions. Sodium 166-172 parathyroid hormone-related protein Ovis aries 17-52 35344088-0 2022 Sodium retention in the nephrotic syndrome and the non-enzymatic function of prostasin. Sodium 0-6 serine protease 8 Homo sapiens 77-86 35621227-2 2022 We have identified a novel drug for hyperphosphatemia, EOS789, that interacts with several sodium-dependent phosphate transporters (NaPi-IIb, PiT-1, and PiT-2) known to contribute to intestinal phosphate absorption. Sodium 91-97 solute carrier family 34 member 2 Rattus norvegicus 132-140 35624145-3 2022 Thirteen kinases were found to activate sodium/hydrogen exchanger (NHE1) in normal hematopoietic progenitors, of which FLT3-ITD, KRASG12D, and BTK phosphorylated NHE1 maintained alkaline intracellular pH (pHi) and supported survival of AML cells. Sodium 40-46 glucose-6-phosphate isomerase Homo sapiens 205-208 35557557-1 2022 Mutations in the SCN8A gene encoding the voltage-gated sodium channel alpha-subunit Nav1. Sodium 55-61 sodium channel, voltage-gated, type VIII, alpha Mus musculus 17-22 35528382-8 2022 The mRNA expression levels of the plasma membrane Ca ATPase 1b (PMCAlb) in the duodenum and the sodium (Na)/ Ca exchanger 1 (NCX1) in the duodenum and the jejunum were also enhanced to 1.57-2.86 times with the addition of 1,25-(OH)2-D3 (P<0.05). Sodium 96-102 solute carrier family 8 member A1 Gallus gallus 125-129 8590367-6 1995 The urinary excretion of sodium and calcium and serum free calcium at the 28th GW were much lower in a woman with PIH, despite of the taking of a calcium supplement, than in the normotensive calcium group. Sodium 25-31 pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included) Homo sapiens 114-117 35496913-6 2022 Previously, we found that SC family member, the sodium-hydrogen exchanger NHE6, was expressed in all wildtype cochlear tissues, and that Nhe6-knockout mice displayed moderate hearing loss. Sodium 48-54 solute carrier family 9 (sodium/hydrogen exchanger), member 6 Mus musculus 74-78 35496913-6 2022 Previously, we found that SC family member, the sodium-hydrogen exchanger NHE6, was expressed in all wildtype cochlear tissues, and that Nhe6-knockout mice displayed moderate hearing loss. Sodium 48-54 solute carrier family 9 (sodium/hydrogen exchanger), member 6 Mus musculus 137-141 35493997-12 2022 The increased salt-sensitivity in female E-Cul3 9 mice was associated with decreased renovascular relaxation and impaired natriuresis in response to a sodium load. Sodium 151-157 cullin 3 Mus musculus 43-47 7636889-8 1995 These results demonstrate that, in the CCD, aldosterone and AVP act synergistically to increase not only the apical sodium entry but also the basolateral Na(+)-K(+)-ATPase transport capacity: AVP allows a rapid recruitment and/or activation of an aldosterone-dependent pool of latent Na(+)-K(+)-ATPase. Sodium 116-122 arginine vasopressin Mus musculus 60-63 35406789-3 2022 The sensitivity of the detected sodium current to tetrodotoxin was between the values published for TTX-sensitive and TTX-insensitive channels, which suggests the co-existence of multiple NaV1 subtypes in the B cell membrane. Sodium 32-38 neuron navigator 1 Homo sapiens 188-192 35529087-4 2022 Aldosterone activates the mineralocorticoid receptor in the collecting duct to increase sodium reabsorption, resulting in increased blood pressure. Sodium 88-94 nuclear receptor subfamily 3 group C member 2 Homo sapiens 26-52 35362824-0 2022 Laser-Derived Interfacial Confinement Enables Planar Growth of 2D SnS2 on Graphene for High-Flux Electron/Ion Bridging in Sodium Storage. Sodium 122-128 sodium voltage-gated channel alpha subunit 11 Homo sapiens 66-70 35362824-3 2022 The face-to-face bridging of ultrathin SnS2 nanosheets on graphene enables the heterostructure huge covalent coupling area and high loading and thus renders unimpeded electron/ion transfer pathways and indestructible electrode structure, and impressive reversible capacity and rate capability for sodium-ion batteries, which rank among the top in records of the SnS2-based anodes. Sodium 297-303 sodium voltage-gated channel alpha subunit 11 Homo sapiens 39-43 35142111-0 2022 Tailoring the Void Space Using Nanoreactors on Carbon Fibers to Confine SnS2 Nanosheets for Ultrastable Lithium/Sodium-Ion Batteries. Sodium 112-118 sodium voltage-gated channel alpha subunit 11 Homo sapiens 72-76 35142111-5 2022 Thus, the SnS2 @C/CNF benefits greatly in structural stability and pseudocapacitive capacity for improved lithium/sodium storage performance. Sodium 114-120 sodium voltage-gated channel alpha subunit 11 Homo sapiens 10-14 35142111-6 2022 As a result of these improvements, the self-standing SnS2 @C/CNF film electrodes exhibit the highly stable capacity of 964.8 and 767.6 mAh g-1 at 0.2 A g-1 , and excellent capacity retention of 87.4% and 82.4% after 1000 cycles at high current density for lithium-ion batteries and sodium-ion batteries, respectively. Sodium 282-288 sodium voltage-gated channel alpha subunit 11 Homo sapiens 53-57 35407276-4 2022 This study reports the optimization of the synthesis of sodium superionic conductor-type Li1.5Al0.3Si0.2Ti1.7P2.8O12 (LASTP) solid electrolyte. Sodium 56-62 transglutaminase 1 Homo sapiens 89-92 35202587-1 2022 In cystic fibrosis (CF), excessive furin activity plays a critical role in the activation of the epithelial sodium channel (ENaC), dysregulation of which contributes to airway dehydration, ineffective mucociliary clearance (MCC), and mucus obstruction. Sodium 108-114 furin, paired basic amino acid cleaving enzyme Homo sapiens 35-40 7603774-1 1995 It has been reported that: 1) ovine growth hormone stimulates intestinal water, sodium, and chloride absorption and 2) specific growth hormone receptors are present in the rat intestine. Sodium 80-86 gonadotropin releasing hormone receptor Rattus norvegicus 36-50 7603774-1 1995 It has been reported that: 1) ovine growth hormone stimulates intestinal water, sodium, and chloride absorption and 2) specific growth hormone receptors are present in the rat intestine. Sodium 80-86 gonadotropin releasing hormone receptor Rattus norvegicus 128-142 7603774-6 1995 In vivo, growth hormone induced a rapid increase in the absorption rates of water, sodium, chloride, and potassium. Sodium 83-89 gonadotropin releasing hormone receptor Rattus norvegicus 9-23 7606877-8 1995 These results suggest that plasma BNP-32 plays an important role in the sodium-fluid balance and that secretion and metabolism of BNP may differ from those of ANP in the HD patients. Sodium 72-78 natriuretic peptide B Homo sapiens 34-37 7721446-1 1995 This study was designed to determine whether expression of renal messenger RNA (mRNA) encoding the two known angiotensin II type 1 (AT1) receptor subtypes (AT1A and AT1B) can be regulated by dietary sodium. Sodium 199-205 angiotensin II receptor, type 1a Rattus norvegicus 156-160 7721446-4 1995 By use of Northern blot analysis, renal mRNA levels for the AT1 and AT1A receptors in rats fed a low-sodium diet were found to be increased twofold (P < .05) compared with control. Sodium 101-107 angiotensin II receptor, type 1a Rattus norvegicus 60-63 7721446-4 1995 By use of Northern blot analysis, renal mRNA levels for the AT1 and AT1A receptors in rats fed a low-sodium diet were found to be increased twofold (P < .05) compared with control. Sodium 101-107 angiotensin II receptor, type 1a Rattus norvegicus 68-72 7625178-2 1995 Therefore, to effect a natriuresis, VIP may need to modulate the sodium conserving actions of the renin angiotensin system (RAS) by another means. Sodium 65-71 VIP peptides Oryctolagus cuniculus 36-39 7625178-6 1995 These studies were performed in rabbits on low, normal and high sodium diets, as dietary sodium has been shown to affect the metabolism of both VIP and Ang II. Sodium 89-95 VIP peptides Oryctolagus cuniculus 144-147 7625178-8 1995 VIP decreased Ang II catabolism in rabbits on low (P < 0.05) and normal sodium diets (P < 0.05). Sodium 75-81 VIP peptides Oryctolagus cuniculus 0-3 7625178-10 1995 In contrast, in rabbits on a high sodium diet VIP increased the rate of catabolism of Ang II (P < 0.001). Sodium 34-40 VIP peptides Oryctolagus cuniculus 46-49 7625178-11 1995 Thus we conclude that the effect of VIP on sodium excretion may be modulated by its effects on Ang II metabolism. Sodium 43-49 VIP peptides Oryctolagus cuniculus 36-39 7625178-12 1995 The decrease in Ang II catabolism seen in rabbits on low and normal sodium diets may prevent or ameliorate any natriuresis while the more rapid degradation of Ang II which occurs in dietary sodium excess may enhance the natriuretic effect of VIP. Sodium 190-196 VIP peptides Oryctolagus cuniculus 242-245 7741532-6 1995 Subcutaneous infusion of ACTH (Synacthen) at 2.8 micrograms/day for 7 days by mini-osmotic pump increased sodium intake five-fold and water intake three- or four-fold. Sodium 106-112 pro-opiomelanocortin-alpha Mus musculus 25-29 7989609-13 1994 When animals were chronically sodium restricted, the level of COX-2 in the region of the macula densa increased threefold (from 0.86 +/- 0.08 to 2.52 +/- 0.43/mm2) and the total area of the COX-2 immunoreactive cells in cortex increased from 34 microns2/mm2 of cortex to 226 microns2/mm2 of cortex. Sodium 30-36 cytochrome c oxidase II, mitochondrial Rattus norvegicus 62-67 7989609-13 1994 When animals were chronically sodium restricted, the level of COX-2 in the region of the macula densa increased threefold (from 0.86 +/- 0.08 to 2.52 +/- 0.43/mm2) and the total area of the COX-2 immunoreactive cells in cortex increased from 34 microns2/mm2 of cortex to 226 microns2/mm2 of cortex. Sodium 30-36 cytochrome c oxidase II, mitochondrial Rattus norvegicus 190-195 7989609-14 1994 The intrarenal distribution of COX-2 and its increased expression in response to sodium restriction suggest that in addition to its proposed role in inflammatory and growth responses, this enzyme may play an important role in the regulation of salt, volume, and blood pressure homeostasis. Sodium 81-87 cytochrome c oxidase II, mitochondrial Rattus norvegicus 31-36 7966619-1 1994 The amphotropic murine retrovirus receptor Ram-1 shows significant sequence similarity to the gibbon ape leukemia virus (GALV) receptor Glvr-1, and both of these cell surface virus receptors normally function as sodium-dependent phosphate symporters. Sodium 212-218 recognized antigen from MCA-induced tumor 1 Mus musculus 43-48 35216442-1 2022 Angiotensin II (Ang II) type-2 receptors (AT2R) are expressed in the adult kidney, prominently in renal proximal tubule cells (RPTCs), and play an important role in opposing renal sodium (Na+) retention induced by Ang II stimulation of Ang II type-1 receptor (AT1R). Sodium 180-186 angiotensin II receptor, type 2 Rattus norvegicus 42-46 7966619-1 1994 The amphotropic murine retrovirus receptor Ram-1 shows significant sequence similarity to the gibbon ape leukemia virus (GALV) receptor Glvr-1, and both of these cell surface virus receptors normally function as sodium-dependent phosphate symporters. Sodium 212-218 solute carrier family 20, member 1 Mus musculus 136-142 7525476-9 1994 After sodium depletion, known to induce hyperactivity of the renin-angiotensin system, adrenal AT1A and AT1B receptor mRNA levels were increased by 60% and 110%, respectively. Sodium 6-12 renin Rattus norvegicus 61-66 35310859-10 2022 With the knowledge that using sodium-channel blockers simply exacerbates the seizure, the need for understanding the intrinsic nature of the NaV1.2 channel provides an important research topic in the future. Sodium 30-36 sodium channel, voltage-gated, type II, alpha Mus musculus 141-147 7525476-9 1994 After sodium depletion, known to induce hyperactivity of the renin-angiotensin system, adrenal AT1A and AT1B receptor mRNA levels were increased by 60% and 110%, respectively. Sodium 6-12 angiotensin II receptor, type 1a Rattus norvegicus 95-99 7943299-0 1994 Enhanced adrenal renin and aldosterone biosynthesis during sodium restriction in TGR (mREN2)27. Sodium 59-65 renin Rattus norvegicus 17-22 35280382-6 2022 To date, only 21 cases of FEPS3 caused by the sodium voltage-gated channel alpha subunit 11A (SCN11A) gene mutation have been reported. Sodium 46-52 sodium voltage-gated channel alpha subunit 11 Homo sapiens 26-31 35280382-6 2022 To date, only 21 cases of FEPS3 caused by the sodium voltage-gated channel alpha subunit 11A (SCN11A) gene mutation have been reported. Sodium 46-52 sodium voltage-gated channel alpha subunit 11 Homo sapiens 94-100 7943299-1 1994 The aim of the study was to investigate the relationships between tissue renin and the steroid production in the adrenal cortex during dietary sodium restriction in the transgenic rat (TGR) (mREN2)27. Sodium 143-149 renin Rattus norvegicus 73-78 7943299-4 1994 Sodium restriction caused sustained increases of adrenal renin activity (from 28.5 +/- 3.5 to 87.5 +/- 4.5 ng.mg protein-1.h-1 on day 7) and of adrenal renin mRNA (+63 +/- 13 and +43 +/- 7% on days 4 and 7, respectively), whereas plasma renin activity (from 3.3 +/- 0.3 to 4.4 +/- 0.6 ng.ml-1.h-1) and renal renin activity (from 0.85 +/- 0.25 to 0.7 +/- 0.4 microgram.mg protein-1.h-1) did not change. Sodium 0-6 renin Rattus norvegicus 57-62 7943299-4 1994 Sodium restriction caused sustained increases of adrenal renin activity (from 28.5 +/- 3.5 to 87.5 +/- 4.5 ng.mg protein-1.h-1 on day 7) and of adrenal renin mRNA (+63 +/- 13 and +43 +/- 7% on days 4 and 7, respectively), whereas plasma renin activity (from 3.3 +/- 0.3 to 4.4 +/- 0.6 ng.ml-1.h-1) and renal renin activity (from 0.85 +/- 0.25 to 0.7 +/- 0.4 microgram.mg protein-1.h-1) did not change. Sodium 0-6 renin Rattus norvegicus 152-157 35136380-4 2022 This case-control (100 control: 101patients) study evaluated the association of sodium channel genes SCN1A and SCN2A with drug-resistant epilepsy. Sodium 80-86 sodium voltage-gated channel alpha subunit 1 Homo sapiens 101-106 7943299-4 1994 Sodium restriction caused sustained increases of adrenal renin activity (from 28.5 +/- 3.5 to 87.5 +/- 4.5 ng.mg protein-1.h-1 on day 7) and of adrenal renin mRNA (+63 +/- 13 and +43 +/- 7% on days 4 and 7, respectively), whereas plasma renin activity (from 3.3 +/- 0.3 to 4.4 +/- 0.6 ng.ml-1.h-1) and renal renin activity (from 0.85 +/- 0.25 to 0.7 +/- 0.4 microgram.mg protein-1.h-1) did not change. Sodium 0-6 renin Rattus norvegicus 152-157 7943299-4 1994 Sodium restriction caused sustained increases of adrenal renin activity (from 28.5 +/- 3.5 to 87.5 +/- 4.5 ng.mg protein-1.h-1 on day 7) and of adrenal renin mRNA (+63 +/- 13 and +43 +/- 7% on days 4 and 7, respectively), whereas plasma renin activity (from 3.3 +/- 0.3 to 4.4 +/- 0.6 ng.ml-1.h-1) and renal renin activity (from 0.85 +/- 0.25 to 0.7 +/- 0.4 microgram.mg protein-1.h-1) did not change. Sodium 0-6 renin Rattus norvegicus 152-157 7968444-1 1994 The biexponential relaxation behavior of the sodium nucleus affects the accuracy of quantitative measurement of in vivo tissue sodium concentration (TSC). Sodium 45-51 solute carrier family 12 member 3 Rattus norvegicus 149-152 2803669-6 1989 In contrast to NaCl, a high dietary intake of sodium with anions other than chloride (NaAA) fails to produce hypertension in the Dahl-S rat. Sodium 46-52 N-acylethanolamine acid amidase Rattus norvegicus 86-90 2517056-6 1989 No correlation between intra-RBC sodium and BP was found; (2) Plasma sodium concentration in HBP was much lower than that in NBP. Sodium 69-75 heme binding protein 1 Homo sapiens 93-96 2517056-8 1989 Of those children with FH- the 4-hour sodium excretion in HBP was higher than that in NBP, but no significant difference was found between HBP and NBP of the FH+ children in the 4-hour urinary sodium excretions. Sodium 38-44 heme binding protein 1 Homo sapiens 58-61 7968444-2 1994 Theoretical analysis and in vivo experimental results are used to demonstrate the extent of the large bias in the measured TSC that arises when the relaxation behavior in vivo differs significantly from that of the calibration standards which is when a significant fraction of the total sodium signal decays with a relaxation time much shorter than the echo time (TE) used for imaging. Sodium 287-293 solute carrier family 12 member 3 Rattus norvegicus 123-126 7963510-4 1994 RESULTS: Plasma levels of BNP and ANP increased significantly on the high sodium intake compared with when the patients were on their normal diet. Sodium 74-80 natriuretic peptide B Homo sapiens 26-29 7963510-6 1994 In contrast, plasma BNP and ANP decreased on the low sodium intake, but were not significantly different compared with when the patients were on their normal diet. Sodium 53-59 natriuretic peptide B Homo sapiens 20-23 7963510-8 1994 Compared with the normal diet, BNP and ANP plasma levels showed similar percentage decreases on the low sodium intake and similar percentage increases on the high sodium intake. Sodium 104-110 natriuretic peptide B Homo sapiens 31-34 7963510-9 1994 CONCLUSIONS: These findings suggest that BNP and ANP are released in response to a common stimulus during changes in dietary sodium intake. Sodium 125-131 natriuretic peptide B Homo sapiens 41-44 7963510-10 1994 The changes in plasma BNP and ANP observed with sodium restriction and sodium loading indicate the potential importance of BNP and ANP as a dual peptide system contributing to the maintenance of sodium balance and blood pressure regulation in patients with essential hypertension, during changes in dietary sodium intake. Sodium 48-54 natriuretic peptide B Homo sapiens 22-25 7963510-10 1994 The changes in plasma BNP and ANP observed with sodium restriction and sodium loading indicate the potential importance of BNP and ANP as a dual peptide system contributing to the maintenance of sodium balance and blood pressure regulation in patients with essential hypertension, during changes in dietary sodium intake. Sodium 48-54 natriuretic peptide B Homo sapiens 123-126 7963510-10 1994 The changes in plasma BNP and ANP observed with sodium restriction and sodium loading indicate the potential importance of BNP and ANP as a dual peptide system contributing to the maintenance of sodium balance and blood pressure regulation in patients with essential hypertension, during changes in dietary sodium intake. Sodium 71-77 natriuretic peptide B Homo sapiens 123-126 7963510-10 1994 The changes in plasma BNP and ANP observed with sodium restriction and sodium loading indicate the potential importance of BNP and ANP as a dual peptide system contributing to the maintenance of sodium balance and blood pressure regulation in patients with essential hypertension, during changes in dietary sodium intake. Sodium 71-77 natriuretic peptide B Homo sapiens 123-126 7963510-10 1994 The changes in plasma BNP and ANP observed with sodium restriction and sodium loading indicate the potential importance of BNP and ANP as a dual peptide system contributing to the maintenance of sodium balance and blood pressure regulation in patients with essential hypertension, during changes in dietary sodium intake. Sodium 71-77 natriuretic peptide B Homo sapiens 123-126 8031857-9 1994 The results confirm that EGF promotes uptake of both sodium and glucose by the jejunal mucosal cells, and suggest the effect of EGF on glucose and sodium is mediated through the brush-border membrane glucose-sodium transporter. Sodium 53-59 epidermal growth factor like 1 Rattus norvegicus 25-28 8031857-9 1994 The results confirm that EGF promotes uptake of both sodium and glucose by the jejunal mucosal cells, and suggest the effect of EGF on glucose and sodium is mediated through the brush-border membrane glucose-sodium transporter. Sodium 147-153 epidermal growth factor like 1 Rattus norvegicus 25-28 8031857-9 1994 The results confirm that EGF promotes uptake of both sodium and glucose by the jejunal mucosal cells, and suggest the effect of EGF on glucose and sodium is mediated through the brush-border membrane glucose-sodium transporter. Sodium 147-153 epidermal growth factor like 1 Rattus norvegicus 128-131 8031857-11 1994 The short-term effects of EGF on glucose and sodium transport by the small intestine may have potential therapeutic implications. Sodium 45-51 epidermal growth factor like 1 Rattus norvegicus 26-29 8023885-3 1994 To study further the regulation of gene expression in sodium-transporting epithelia by corticosteroids, we have cloned an amiloride-binding protein (ABP) cDNA from rat descending colon and kidney. Sodium 54-60 amine oxidase, copper containing 1 Rattus norvegicus 149-152 2677316-10 1989 Caffeine and 1,3-dipropyl-8-(p-sulfophenyl)xanthine potentiated the increase in plasma renin activity produced by furosemide (to 120 +/- 15 and 147 +/- 21 ng Al/ml/hr, respectively), whereas having no significant effects on urinary volume, sodium excretion or blood pressure. Sodium 240-246 renin Rattus norvegicus 87-92 2553185-2 1989 The time course of the blockade of sodium currents (INa) by the antiarrhythmic agents, lignocaine and SUN 1165, was studied in single myocytes isolated enzymatically from guinea-pig atrium, by a new concentration-jump termed as a "concentration-clamp" technique. Sodium 35-41 alpha-internexin Cavia porcellus 52-55 2677137-4 1989 Plasma renin activity (PRA) in SHR and WKY was increased similarly by sodium depletion and by treatment with captopril. Sodium 70-76 renin Rattus norvegicus 7-12 2677137-6 1989 Both sodium depletion and captopril treatment caused significant increases in the kidney renin mRNA in SHR and WKY. Sodium 5-11 renin Rattus norvegicus 89-94 2770278-7 1989 Twenty-four hours after injury, BUN, creatinine, and fractional sodium excretion values were less in FDP-treated rats than in control rats (P less than 0.001, P less than 0.005, and P less than 0.001, respectively) and not different from values observed in sham-operated rats. Sodium 64-70 fructose-bisphosphatase 1 Rattus norvegicus 101-104 8175974-3 1994 Exploration of segmental sodium handling by the lithium clearance technique showed that the natriuretic effect of BNP was due to both an increase in filtered sodium load and a reduced distal sodium reabsorption. Sodium 25-31 natriuretic peptide B Homo sapiens 114-117 8175974-3 1994 Exploration of segmental sodium handling by the lithium clearance technique showed that the natriuretic effect of BNP was due to both an increase in filtered sodium load and a reduced distal sodium reabsorption. Sodium 158-164 natriuretic peptide B Homo sapiens 114-117 8175974-4 1994 These results indicate that the high plasma BNP levels observed in disease states, such as heart failure, may contribute to the regulation of renal hemodynamics and sodium excretion. Sodium 165-171 natriuretic peptide B Homo sapiens 44-47 7922761-1 1994 To find changes in activity of red-cell sodium-lithium counter transport (RBC Na+/Li+CT) in IgA nephropathology (IgAN) and renal hypertension (RHT), we measured the activity of RBC Na+/Li+CT in 21 patients with IgAN and 13 patients with RHT and compared it with that in 23 normal persons and 17 essential hypertension (EHT) patients by improved Canessa"s method. Sodium 40-46 IGAN1 Homo sapiens 113-117 2681965-6 1989 To this end, increased excretion of sodium and chloride, and stimulation of urinary flow are less pronounced with CGRP than with calcitonin. Sodium 36-42 calcitonin-related polypeptide alpha Rattus norvegicus 114-118 2681965-6 1989 To this end, increased excretion of sodium and chloride, and stimulation of urinary flow are less pronounced with CGRP than with calcitonin. Sodium 36-42 calcitonin-related polypeptide alpha Rattus norvegicus 129-139 2791336-4 1989 Rats receiving the low sodium diet had significantly higher plasma renin activity than rats receiving the high sodium diet. Sodium 23-29 renin Rattus norvegicus 67-72 2510668-0 1989 [Effects of sodium depletion in rats actively immunized against renin]. Sodium 12-18 renin Rattus norvegicus 64-69 2510668-1 1989 The influence of active immunization against renin on systolic blood pressure in response to a dietary sodium restriction was assessed in normotensive rats (WKY) and spontaneously hypertensive rats (SHR). Sodium 103-109 renin Rattus norvegicus 45-50 2510668-11 1989 These results confirm the importance of an efficient renin-angiotensin system in the adaptative response to sodium restriction. Sodium 108-114 renin Rattus norvegicus 53-58 2548914-1 1989 Sodium-dependent intracellular pH (pHi) regulation was compared in granulosa cells from the three largest avian ovarian follicles by monitoring the pHi with biscarboxyethylcarboxyfluorescein, a dye whose fluorescence increases with alkalinity. Sodium 0-6 glucose-6-phosphate isomerase Homo sapiens 35-38 2548914-1 1989 Sodium-dependent intracellular pH (pHi) regulation was compared in granulosa cells from the three largest avian ovarian follicles by monitoring the pHi with biscarboxyethylcarboxyfluorescein, a dye whose fluorescence increases with alkalinity. Sodium 0-6 glucose-6-phosphate isomerase Homo sapiens 148-151 2544093-1 1989 We studied the effects of isoproterenol (ISP), dibutyryl adenosine 3",5"-cyclic monophosphate (DBcAMP), and forskolin on the sodium current (INa) of guinea pig ventricular myocytes using the tight-seal, whole cell voltage-clamp method. Sodium 125-131 alpha-internexin Cavia porcellus 141-144 2660590-0 1989 Modification of glycosylation of renin in sodium-depleted and captopril-treated rats. Sodium 42-48 renin Rattus norvegicus 33-38 2660590-8 1989 These results show that the predominant release of renin C, with the longest half-life (35 min) in the plasma, contributes to the increased plasma renin concentration in sodium-depleted and captopril-treated rats. Sodium 170-176 renin Rattus norvegicus 51-56 2660590-8 1989 These results show that the predominant release of renin C, with the longest half-life (35 min) in the plasma, contributes to the increased plasma renin concentration in sodium-depleted and captopril-treated rats. Sodium 170-176 renin Rattus norvegicus 147-152 2661429-2 1989 In sodium-replete rats the infusion of the renin inhibitor CP71362 (100 micrograms/kg/min) decreased blood pressure by 13 +/- 1 mm Hg (p less than 0.0001), reduced plasma renin activity to undetectable levels, but did not lower plasma angiotensin II. Sodium 3-9 renin Rattus norvegicus 43-48 2661432-2 1989 In the present study, experiments were designed to test the hypothesis that acute volume expansion with isotonic sodium chloride stimulates the production of DA within the kidney, which in turn acts on specific DA1 receptors to promote sodium excretion. Sodium 113-119 RT1 class II, locus Da Rattus norvegicus 211-214 7922761-1 1994 To find changes in activity of red-cell sodium-lithium counter transport (RBC Na+/Li+CT) in IgA nephropathology (IgAN) and renal hypertension (RHT), we measured the activity of RBC Na+/Li+CT in 21 patients with IgAN and 13 patients with RHT and compared it with that in 23 normal persons and 17 essential hypertension (EHT) patients by improved Canessa"s method. Sodium 40-46 IGAN1 Homo sapiens 211-215 8147862-0 1994 Protein kinase C is crucial for the stimulation of sodium-dependent phosphate transport by parathyroid hormone-related peptide in osteoblast-like cells. Sodium 51-57 parathyroid hormone like hormone Homo sapiens 91-126 8147862-7 1994 These results indicate that the messenger system mediated by PKC, rather than adenylate cyclase or cytosolic calcium, plays a crucial role in the regulation of sodium-dependent Pi transport by PTHrP in the osteoblast-like cells. Sodium 160-166 parathyroid hormone like hormone Homo sapiens 193-198 8125563-1 1994 Atrial natriuretic factor induces renal sodium excretion by several mechanisms, including inhibition of angiotensin II-stimulated sodium reabsorption in the proximal tubule. Sodium 40-46 natriuretic peptides A Oryctolagus cuniculus 0-25 2655664-8 1989 Infusion of renin form 4 increased urine volume and sodium excretion significantly. Sodium 52-58 renin Rattus norvegicus 12-17 2655477-0 1989 Effect of epidermal growth factor on sodium transport in the cortical collecting tubule. Sodium 37-43 pro-epidermal growth factor Oryctolagus cuniculus 10-33 2655477-4 1989 Peritubular EGF in concentrations of 0.1 to 100 ng/ml (1.7 X 10(-11) to 1.7 X 10(-8) M) decreased sodium reabsorption, measured as 22Na absorption from the lumen, by 44-59%. Sodium 98-104 pro-epidermal growth factor Oryctolagus cuniculus 12-15 2655477-7 1989 Pretreatment of the tubules with ouabain eliminated the effect of EGF on sodium transport. Sodium 73-79 pro-epidermal growth factor Oryctolagus cuniculus 66-69 2655477-12 1989 We conclude that EGF inhibits active sodium absorption in CCT via receptors located at the basolateral membrane. Sodium 37-43 pro-epidermal growth factor Oryctolagus cuniculus 17-20 2655479-4 1989 The depressor response to neither agent changed over the next 40 h. The pressor response to angiotensin II was blunted significantly by 8 h and also did not change over the next 40 h. The findings indicate that the rapid tempo of sodium homeostasis in the rat is matched by an equally rapid tempo of activation of the renin-angiotensin system, although the factors responsible for aldosterone release are probably more complex. Sodium 230-236 renin Rattus norvegicus 318-323 2651516-6 1989 In contrast, severe sodium restriction blunted or prevented the development of hypertension in SHR and was associated with (1) marked increases in plasma renin activity (2) increased maintenance of blood pressure by the renin-angiotensin system (as assessed by captopril), and (3) a marked decrease in the blood pressure response to angiotensin II. Sodium 20-26 renin Rattus norvegicus 154-159 2651516-6 1989 In contrast, severe sodium restriction blunted or prevented the development of hypertension in SHR and was associated with (1) marked increases in plasma renin activity (2) increased maintenance of blood pressure by the renin-angiotensin system (as assessed by captopril), and (3) a marked decrease in the blood pressure response to angiotensin II. Sodium 20-26 renin Rattus norvegicus 220-225 2977165-3 1988 In the high-sodium state, renal renin mRNA decreased, but it increased in the low-sodium state. Sodium 12-18 renin Rattus norvegicus 32-37 2977165-4 1988 A further increase in renin mRNA was seen in the low-sodium state after captopril administration. Sodium 53-59 renin Rattus norvegicus 22-27 2856469-7 1988 Sodium loading in the presence of reduced renal mass (unilateral nephrectomy) or mineralocorticoid administration produced renin suppression and resulted in down-regulation of vascular ANP receptors. Sodium 0-6 renin Rattus norvegicus 123-128 3041306-4 1988 The plasma renin concentration responses to immobilization and a low-sodium diet were also reduced. Sodium 69-75 renin Rattus norvegicus 11-16 3045293-0 1988 Effect of sodium intake on urinary renin excretion in rats. Sodium 10-16 renin Rattus norvegicus 35-40 3045293-1 1988 The present study was carried out to investigate the effect of sodium intake on urinary renin excretion in rats. Sodium 63-69 renin Rattus norvegicus 88-93 3045293-4 1988 Low sodium intake for 4 weeks resulted in a 16-fold increase in urinary renin excretion and led to a 15-fold increase in plasma renin activity. Sodium 4-10 renin Rattus norvegicus 72-77 3045293-4 1988 Low sodium intake for 4 weeks resulted in a 16-fold increase in urinary renin excretion and led to a 15-fold increase in plasma renin activity. Sodium 4-10 renin Rattus norvegicus 128-133 3045293-6 1988 In contrast, high sodium intake for 4 weeks decreased urinary renin excretion, plasma renin activity and renal renin content to about 20%, 25% and 35% of the control level, respectively. Sodium 18-24 renin Rattus norvegicus 62-67 3045293-6 1988 In contrast, high sodium intake for 4 weeks decreased urinary renin excretion, plasma renin activity and renal renin content to about 20%, 25% and 35% of the control level, respectively. Sodium 18-24 renin Rattus norvegicus 86-91 3045293-6 1988 In contrast, high sodium intake for 4 weeks decreased urinary renin excretion, plasma renin activity and renal renin content to about 20%, 25% and 35% of the control level, respectively. Sodium 18-24 renin Rattus norvegicus 86-91 3045293-8 1988 The molecular weight of renin in the urine from rats on low or high sodium intake was 40,000, the value being identical with that from control rats. Sodium 68-74 renin Rattus norvegicus 24-29 3252965-2 1988 During a late diuretic phase, the excretion of N-acetyl-beta-D-glucosaminidase in the urine increased in accordance with increases of sodium excretion and urine flow, and then decreased to the normal range on the 20th day of the disease. Sodium 134-140 O-GlcNAcase Homo sapiens 47-78 3298045-4 1987 Sodium depletion resulted in increased renin expression in the kidney, heart, and adrenal, but not in the submandibular gland and testis. Sodium 0-6 renin Rattus norvegicus 39-44 3555117-0 1987 Renin secretory effects of N6-cyclohexyladenosine: effects of dietary sodium. Sodium 70-76 renin Rattus norvegicus 0-5 2953032-3 1987 Data from clearance studies in anesthetized rabbits demonstrate that ANP administration can produce a significant increase in absolute and percentage sodium excretion (42.0 +/- 5.9----64.6 +/- 10.2 mu eq/min, P less than 0.01, and 1.97 +/- 0.28----3.12 +/- 0.35%, P less than 0.001, respectively) without increasing GFR (16.8 +/- 2.1----16.1 +/- 2.5 cc/min, P greater than 0.30). Sodium 150-156 natriuretic peptides A Oryctolagus cuniculus 69-72 2953032-7 1987 These findings suggest that ANP can inhibit sodium transport without increasing whole-kidney GFR or RPF, but does not directly inhibit transport in the proximal straight tubule. Sodium 44-50 natriuretic peptides A Oryctolagus cuniculus 28-31 3030698-8 1987 Captopril administration in sodium-depleted rats increased plasma concentrations of renin, des-angiotensin I-angiotensinogen, and angiotensin I and decreased plasma angiotensinogen concentration measured by both methods. Sodium 28-34 renin Rattus norvegicus 84-89 3030698-10 1987 The angiotensinogen liver content and in vitro angiotensinogen release were decreased in sodium-depleted rats treated with a converting enzyme inhibitor, and these parameters were negatively correlated to in vivo plasma levels of renin, angiotensin I, and des-angiotensin I-angiotensinogen. Sodium 89-95 renin Rattus norvegicus 230-235 2959417-14 1987 It is proposed that ANP acts via a mediator to alter sodium movement across terminal segments of the nephron. Sodium 53-59 natriuretic peptides A Oryctolagus cuniculus 20-23 3553783-3 1987 The decrease in intraerythrocyte sodium concentration could have resulted from the observed increase in sodium, potassium-ATPase pump activity. Sodium 33-39 dynein axonemal heavy chain 8 Homo sapiens 122-128 3539793-4 1986 Intravenous administration of U-71038 to conscious, sodium-depleted monkeys caused dose-related decreases of blood pressure and plasma renin activity without affecting heart rate. Sodium 52-58 renin Rattus norvegicus 135-140 3539793-5 1986 Similarly, the oral administration of U-71038 at 50 mg/kg to conscious, sodium-depleted monkeys elicited a pronounced hypotension and decrease in plasma renin activity that persisted for 5 hours. Sodium 72-78 renin Rattus norvegicus 153-158 3539795-1 1986 We previously showed that adrenal renin is highest in the rat zona glomerulosa (ZG) and that low sodium or high potassium and nephrectomy increase adrenal ZG renin and aldosterone. Sodium 97-103 renin Rattus norvegicus 158-163 3533999-6 1986 These findings provide evidence for sodium regulation of renal renin and angiotensinogen mRNA expressions, which supports potential existence of an intrarenally regulated RAS and suggest that different factors regulate renal and hepatic angiotensinogen. Sodium 36-42 renin Rattus norvegicus 63-68 3529827-0 1986 The effect of sodium load on the development of hypertension, plasma renin and kininogen in rats with renal artery constriction. Sodium 14-20 kininogen 2-like 1 Rattus norvegicus 79-88 3012198-1 1986 Earlier experiments have shown that in sodium depleted hypertensive rats with bilaterally constricted renal arteries the arterial pressure normalized after blockade of the renin-angiotensin system; simultaneously acute renal failure occurred. Sodium 39-45 renin Rattus norvegicus 172-177 3084468-0 1986 Effect of interleukin-1 on intracellular concentration of sodium, calcium, and potassium in 70Z/3 cells. Sodium 58-64 interleukin 1 complex Mus musculus 10-23 3084468-2 1986 An early intracellular event caused by exposure to IL-1 is an amiloride-sensitive progressive rise in the total concentration of intracellular sodium ([Na]i), caused by influx of Na+ from outside, and a transient fall in total intracellular calcium. Sodium 143-149 interleukin 1 complex Mus musculus 51-55 3521182-3 1986 Combined restriction of sodium, potassium and chloride elicited a decreased activity of the enzyme(s) involved in late steps in aldosterone biosynthesis, an elevation of plasma renin activity to excessively high levels and a substantial hypokalaemia. Sodium 24-30 renin Rattus norvegicus 177-182 3521516-6 1986 Plasma renin activity was markedly higher in adrenalectomized rats than in the sham-operated rats even after sodium supplementation. Sodium 109-115 renin Rattus norvegicus 7-12 3082358-3 1986 Porcine proinsulin and a cross-linked derivative of bovine insulin are less effective than porcine insulin in stimulating the short-circuit current (SCC), indicating the specificity appropriate for activation of sodium transport through an insulin receptor. Sodium 212-218 insulin receptor Bos taurus 240-256 3011343-11 1986 Ouabain-sensitive sodium efflux, i.e. "Na-K ATPase", is mainly regulated by its substrate, [Nai]. Sodium 18-24 dynein axonemal heavy chain 8 Homo sapiens 44-51 2438484-3 1986 Renin expression in kidney, heart, and adrenal are stimulated by sodium depletion and beta-adrenergic agonist. Sodium 65-71 renin Rattus norvegicus 0-5 2438484-8 1986 Sodium depletion stimulates renin angiotensinogen mRNA expression but does not influence hepatic angiotensinogen mRNA levels. Sodium 0-6 renin Rattus norvegicus 28-33 2856715-0 1985 The effect of sodium intake on the renin response to dopamine in superfused rat renal cortical cells. Sodium 14-20 renin Rattus norvegicus 35-40 2856715-5 1985 Rats on a low sodium diet showed a higher basal cellular renin release and an enhanced renin response to dopamine (10(-7), 10(-6) mol/l) compared with the normal sodium diet group. Sodium 14-20 renin Rattus norvegicus 57-62 2856715-5 1985 Rats on a low sodium diet showed a higher basal cellular renin release and an enhanced renin response to dopamine (10(-7), 10(-6) mol/l) compared with the normal sodium diet group. Sodium 14-20 renin Rattus norvegicus 87-92 2856715-6 1985 Rats on a high sodium diet, in contrast, showed a lower cellular renin release and a decreased sensitivity to dopamine (10(-7), 10(-6) mol/l) compared with the normal sodium diet group. Sodium 15-21 renin Rattus norvegicus 65-70 2856715-7 1985 These results demonstrate that the renin response to dopamine is dependent upon sodium intake. Sodium 80-86 renin Rattus norvegicus 35-40 3908312-6 1985 Following a 1-hour infusion of angiotensin II in sodium-depleted and captopril-treated rats, plasma renin concentration decreased by 84% whereas no significant changes in either renal renin concentration or renin mRNA content were observed. Sodium 49-55 renin Rattus norvegicus 100-105 3908312-7 1985 These results show that sodium depletion and captopril treatment increase the level of renin gene transcription and renin biosynthesis. Sodium 24-30 renin Rattus norvegicus 87-92 3908312-7 1985 These results show that sodium depletion and captopril treatment increase the level of renin gene transcription and renin biosynthesis. Sodium 24-30 renin Rattus norvegicus 116-121 2994494-1 1985 Parathyroid hormone (PTH), through the generation of cAMP, inhibits the transport of sodium, bicarbonate, and water in the proximal convoluted tubule. Sodium 85-91 parathyroid hormone Oryctolagus cuniculus 0-19 2994494-1 1985 Parathyroid hormone (PTH), through the generation of cAMP, inhibits the transport of sodium, bicarbonate, and water in the proximal convoluted tubule. Sodium 85-91 parathyroid hormone Oryctolagus cuniculus 21-24 4063547-3 1985 The overactivity of the renin-angiotensin system in sodium-depleted rats was demonstrated by the fall in mean arterial pressure (15 +/- 2 vs 0.5 +/- 1 mmHg in sodium-depleted and control rats, respectively), after blocking the converting enzyme with BPP9a (SQ 20881) and also by evaluating plasma renin activity (10 +/- 8 vs 3.0 +/- 0.6 ng AI ml-1 h-1 in sodium-depleted and control rats, respectively). Sodium 52-58 renin Rattus norvegicus 24-29 4063547-3 1985 The overactivity of the renin-angiotensin system in sodium-depleted rats was demonstrated by the fall in mean arterial pressure (15 +/- 2 vs 0.5 +/- 1 mmHg in sodium-depleted and control rats, respectively), after blocking the converting enzyme with BPP9a (SQ 20881) and also by evaluating plasma renin activity (10 +/- 8 vs 3.0 +/- 0.6 ng AI ml-1 h-1 in sodium-depleted and control rats, respectively). Sodium 52-58 renin Rattus norvegicus 297-302 4063547-3 1985 The overactivity of the renin-angiotensin system in sodium-depleted rats was demonstrated by the fall in mean arterial pressure (15 +/- 2 vs 0.5 +/- 1 mmHg in sodium-depleted and control rats, respectively), after blocking the converting enzyme with BPP9a (SQ 20881) and also by evaluating plasma renin activity (10 +/- 8 vs 3.0 +/- 0.6 ng AI ml-1 h-1 in sodium-depleted and control rats, respectively). Sodium 159-165 renin Rattus norvegicus 24-29 4063547-3 1985 The overactivity of the renin-angiotensin system in sodium-depleted rats was demonstrated by the fall in mean arterial pressure (15 +/- 2 vs 0.5 +/- 1 mmHg in sodium-depleted and control rats, respectively), after blocking the converting enzyme with BPP9a (SQ 20881) and also by evaluating plasma renin activity (10 +/- 8 vs 3.0 +/- 0.6 ng AI ml-1 h-1 in sodium-depleted and control rats, respectively). Sodium 159-165 renin Rattus norvegicus 24-29 2579215-2 1985 The persistent sodium current (INaP) attained its steady level within 2-4 ms of a step change in voltage at every potential where it could be examined directly [to about 40 mV positive to resting potential (RP)]. Sodium 15-21 NFKB inhibitor zeta Homo sapiens 31-35 3001555-1 1985 The renin angiotensin aldosterone system (RAAS) is activated during the early phase of renal adaptation to sodium restriction. Sodium 107-113 renin Rattus norvegicus 4-9 11540097-0 1985 Reduced phenylalanine ammonia-lyase and tyrosine ammonia-lyase activities and lignin synthesis in wheat grown under low pressure sodium lamps. Sodium 129-135 wali4 Triticum aestivum 8-35 6236930-6 1984 An altered interaction between the calcium-calmodulin system and sodium handling by the plasma membrane in SHR may play a role in the pathogenesis of hypertension. Sodium 65-71 calmodulin 1 Rattus norvegicus 43-53 6084759-6 1984 As expected, rats maintained on the low-sodium regimen for either 5 or 21 days had marked stimulation of plasma renin activity and increased angiotensin I, angiotensin II, and aldosterone formation. Sodium 40-46 renin Rattus norvegicus 112-117 6098235-1 1984 The relationship between sodium homeostasis and the renin-angiotensin system was assessed through the use of two angiotensin-converting enzyme inhibitors (captopril and enalapril) in the rat. Sodium 25-31 renin Rattus norvegicus 52-57 6509555-4 1984 We have found that the chick embryo: (1) can use exogenously applied choline for the synthesis of acetylcholine; (2) possesses a true acetylcholinesterase, which is predominantly in the form of the 4-6s monomer; and (3) can take up exogenous choline through a sodium-dependent, high-affinity choline transport system. Sodium 260-266 acetylcholinesterase (Cartwright blood group) Gallus gallus 134-154 6540174-0 1984 Potassium-39 and sodium-23 NMR studies of cation binding to phosvitin. Sodium 17-23 casein kinase 2 beta Homo sapiens 60-69 6329658-0 1984 Role of the renin-angiotensin system in the regulation of late steps in aldosterone biosynthesis by sodium intake of potassium-deficient rats. Sodium 100-106 renin Rattus norvegicus 12-17 6329658-1 1984 The role of the renin-angiotensin system in the adaptation of late steps in aldosterone biosynthesis to sodium intake was studied in potassium-deficient rats. Sodium 104-110 renin Rattus norvegicus 16-21 6329658-6 1984 Accordingly, the renin-angiotensin system plays an important but limited role in the control of late steps of aldosterone biosynthesis by sodium intake. Sodium 138-144 renin Rattus norvegicus 17-22 27786021-0 1984 The Inhibition of Rat Renin in Sodium Depleted and Renal Hypertensive Rats. Sodium 31-37 renin Rattus norvegicus 22-27 27786021-2 1984 Studies were undertaken in order to demonstrate the role of the renin-angiotensin system for blood pressure homeostasis in sodium depleted and renal hypertensive (acute and chronic) rats. Sodium 123-129 renin Rattus norvegicus 64-69 6399313-1 1984 Intracranial renin is a potent stimulus to sodium appetite and thirst, the effects being mediated by local generation of angiotensin II. Sodium 43-49 renin Rattus norvegicus 13-18 6360871-1 1983 Effect on urinary prostaglandin E2 and plasma renin in response to variations in sodium intake and in relation to blood pressure. Sodium 81-87 renin Rattus norvegicus 46-51 6368017-0 1983 Molecular characterization of renin in plasma and kidney of sodium-restricted rats. Sodium 60-66 renin Rattus norvegicus 30-35 6632176-5 1983 The prolonged half time (t 1/2 alpha) in the hypertensives tended to be shortened after sodium depletion induced by either low sodium diet or diuretics (1.04 +/- 0.22, p less than 0.001). Sodium 88-94 interleukin 1 receptor like 1 Homo sapiens 25-36 6632176-5 1983 The prolonged half time (t 1/2 alpha) in the hypertensives tended to be shortened after sodium depletion induced by either low sodium diet or diuretics (1.04 +/- 0.22, p less than 0.001). Sodium 127-133 interleukin 1 receptor like 1 Homo sapiens 25-36 6187220-3 1983 Plasma renin activity (PRA) was increased by furosemide and also by the low-sodium diet. Sodium 76-82 renin Rattus norvegicus 7-12 6187220-6 1983 These results suggest that furosemide and low-sodium diet act on the kidney to release renin via protease production. Sodium 46-52 renin Rattus norvegicus 87-92 7115771-0 1982 Studies on the role of protein synthesis and of sodium on the regulation of ornithine decarboxylase activity. Sodium 48-54 ornithine decarboxylase 1 Homo sapiens 76-99 7115771-14 1982 These results, the finding that alpha-aminoisobutyric acid stimulates ornithine decarboxylase activity and that sodium is required for the stimulation of ornithine decarboxylase activity are discussed in relation to the "A" amino acid transport system. Sodium 112-118 ornithine decarboxylase 1 Homo sapiens 154-177 6182339-5 1982 Sodium loading depressed plasma and kidney renin but did not alter intrarenal AII. Sodium 0-6 renin Rattus norvegicus 43-48 6750722-0 1982 Calcium and renin release: inhibition of low sodium-induced renin secretion by high calcium concentration in rat kidney perfusion. Sodium 45-51 renin Rattus norvegicus 12-17 6750722-0 1982 Calcium and renin release: inhibition of low sodium-induced renin secretion by high calcium concentration in rat kidney perfusion. Sodium 45-51 renin Rattus norvegicus 60-65 6750722-4 1982 When the renin release is previously increased by low sodium concentration (Na+: 110 mM/l) however, perfusion with high calcium buffer (Ca++: 5 mM/l) significantly inhibits this stimulation. Sodium 54-60 renin Rattus norvegicus 9-14 6124857-0 1982 Effect of sodium ions on cyclic AMP and cyclic GMP levels in mouse parotid acini. Sodium 10-16 5'-nucleotidase, cytosolic II Mus musculus 47-50 7040241-2 1982 Stimulation of active renin was accompanied by either an increase (low sodium diet), no change (pentobarbital anesthesia plus hemorrhage), or fall (pentobarbital anesthesia) in the plasma levels of inactive renin, while suppression of active renin was accompanied by a fall (high sodium diet) or mild but nonsignificant increases (clonidine or saline infusion) of the inactive enzyme. Sodium 71-77 renin Rattus norvegicus 22-27 7040241-2 1982 Stimulation of active renin was accompanied by either an increase (low sodium diet), no change (pentobarbital anesthesia plus hemorrhage), or fall (pentobarbital anesthesia) in the plasma levels of inactive renin, while suppression of active renin was accompanied by a fall (high sodium diet) or mild but nonsignificant increases (clonidine or saline infusion) of the inactive enzyme. Sodium 280-286 renin Rattus norvegicus 22-27 6281614-9 1982 These data suggest that growth hormone and triiodothyronine may both be calorigenic through their effect on the sodium pumping mechanism in the call membrane. Sodium 112-118 gonadotropin releasing hormone receptor Rattus norvegicus 24-38 7245818-2 1981 Moreover, the intracellular sodium concentration seems to have influence also on the peripheral insulin content after glucose load as it was shown by the negative correlation of the quotient Na(Plasma)/Na(Ery) with the insulin concentration surface in the rabbits. Sodium 28-34 insulin Oryctolagus cuniculus 96-103 7245818-2 1981 Moreover, the intracellular sodium concentration seems to have influence also on the peripheral insulin content after glucose load as it was shown by the negative correlation of the quotient Na(Plasma)/Na(Ery) with the insulin concentration surface in the rabbits. Sodium 28-34 insulin Oryctolagus cuniculus 219-226 6174024-3 1981 At higher concentrations of sodium and potassium ions, ATPase of normal and nitrofurantoin resistant Vibrio el tor responded quite differently. Sodium 28-34 dynein axonemal heavy chain 8 Homo sapiens 55-61 7024508-2 1981 Sodium depletion which occurred in cattle following exteriorization of a parotid duct produced depression of both plasma and salivary sodium, acidosis, elevated plasma aldosterone and renin activity. Sodium 0-6 renin Bos taurus 184-189 6777378-10 1980 However, at acid pH, or in presence of low levels of K+, sodium extrusion requires both "ATP" and the proton-motive force. Sodium 57-63 ATPase phospholipid transporting 8A2 Homo sapiens 89-93 7004728-4 1980 Active renin increased with delivery of extra sodium by microperfusion to the macula densa and this increase was similar to that achieved with acidification. Sodium 46-52 renin Rattus norvegicus 7-12 7004728-6 1980 In rats pretreated with an inhibitor of protein synthesis active renin increased when extra sodium was delivered to the macula densa. Sodium 92-98 renin Rattus norvegicus 65-70 7000955-0 1980 Increased sodium appetite in adrenalectomized or hypophysectomized rats after intracranial injections of renin or angiotensin II. Sodium 10-16 renin Rattus norvegicus 105-110 7000955-6 1980 These results demonstrated that the delayed sodium appetite induced by renin or angiotensin II is not secondary to the stimulation of release of hormones from the pituitary gland or adrenal cortex. Sodium 44-50 renin Rattus norvegicus 71-76 7003100-0 1980 Studies on the mechanism of renin release from rat kidney slices: calcium, sodium and metabolic inhibition. Sodium 75-81 renin Rattus norvegicus 28-33 7003100-9 1980 Medium sodium depletion caused a significant inhibition of renin release. Sodium 7-13 renin Rattus norvegicus 59-64 396613-2 1979 Perfusion with low sodium buffer (110 mM/l) produced a significant increase in renin secretion compared with control experiments (Na+:135 mM/l). Sodium 19-25 renin Rattus norvegicus 79-84 396613-3 1979 Since the presence of tubules seems necessary for such an effect to take place, it suggests that the high renin secretion stimulated by a low sodium buffer centers in the Macula densa. Sodium 142-148 renin Rattus norvegicus 106-111 396613-4 1979 Perfusion with high sodium buffer (170 mM/l; osmolarity 350 mOs/l) induces a stimulation on renin release. Sodium 20-26 renin Rattus norvegicus 92-97 396613-6 1979 All this suggests that high sodium buffer, independently of its osmotic effect, has an inhibitory role on renin release. Sodium 28-34 renin Rattus norvegicus 106-111 227278-0 1979 Effect of sodium restriction on plasma renin activity and renin granules in rat kidney. Sodium 10-16 renin Rattus norvegicus 39-44 227278-0 1979 Effect of sodium restriction on plasma renin activity and renin granules in rat kidney. Sodium 10-16 renin Rattus norvegicus 58-63 227278-1 1979 The present study was carried out to procure detailed information on the relationship between chronic sodium restriction and renin content of kidneys at a subcellular level in the rat. Sodium 102-108 renin Rattus norvegicus 125-130 227278-5 1979 Low sodium intake for 4 wk resulted in a 12.4-fold increase in plasma renin activity and led to a 2.6-fold increase in renin activity of the RG fraction. Sodium 4-10 renin Rattus norvegicus 70-75 227278-5 1979 Low sodium intake for 4 wk resulted in a 12.4-fold increase in plasma renin activity and led to a 2.6-fold increase in renin activity of the RG fraction. Sodium 4-10 renin Rattus norvegicus 119-124 227278-7 1979 These results provide evidence for increased renin activity in storage granules following chronic sodium restriction. Sodium 98-104 renin Rattus norvegicus 45-50 211515-0 1978 Regulation of aldosterone secretion by the renin-angiotensin system during sodium restriction in rats. Sodium 75-81 renin Rattus norvegicus 43-48 211515-4 1978 The absolute dependence of adrenal glomerulosa cell responses on angiotensin II formation indicates that the renin-angiotensin system is the primary regulator of aldosterone secretion during physiological fluctuations in sodium intake. Sodium 221-227 renin Rattus norvegicus 109-114 666023-9 1978 The authors conclude that the anesthetic agents studied increase renin release in the sodium-depleted rat. Sodium 86-92 renin Rattus norvegicus 65-70 645374-7 1978 The results indicate that administration of insulin affects bile formation by stimulating the active transport of sodium across the canalicular membrane. Sodium 114-120 insulin Felis catus 44-51 215928-1 1978 The effect of L-norepinephrine (NE) on renin release by slices of kidney cortex from sodium-replete and sodium-deficient rats was studied in vitro. Sodium 85-91 renin Rattus norvegicus 39-44 215928-2 1978 The rate of renin release by slices from sodium-deficient rats in the absence of added NE increased in proportion to the length of dietary sodium restriction and was significantly greater at all times than release by slices from sodium-replete animals. Sodium 41-47 renin Rattus norvegicus 12-17 215928-2 1978 The rate of renin release by slices from sodium-deficient rats in the absence of added NE increased in proportion to the length of dietary sodium restriction and was significantly greater at all times than release by slices from sodium-replete animals. Sodium 139-145 renin Rattus norvegicus 12-17 215928-2 1978 The rate of renin release by slices from sodium-deficient rats in the absence of added NE increased in proportion to the length of dietary sodium restriction and was significantly greater at all times than release by slices from sodium-replete animals. Sodium 139-145 renin Rattus norvegicus 12-17 215928-9 1978 These data indicate that sodium deprivation enhances the sensitivity of the renin-secreting cells to catecholamine stimulation, and are consistent with the hypothesis that the increase in renin secretion produced by NE is mediated via cyclic AMP. Sodium 25-31 renin Rattus norvegicus 76-81 215928-9 1978 These data indicate that sodium deprivation enhances the sensitivity of the renin-secreting cells to catecholamine stimulation, and are consistent with the hypothesis that the increase in renin secretion produced by NE is mediated via cyclic AMP. Sodium 25-31 renin Rattus norvegicus 188-193 23429-0 1977 The role of bicarbonate, chloride and sodium ions in the regulation of intracellular pH in snail neurones. Sodium 38-44 glucose-6-phosphate isomerase Homo sapiens 85-87 589929-4 1977 Phaeochromocytoma suppressed the usual elevated plasma renin activity observed during sodium deprivation. Sodium 86-92 renin Rattus norvegicus 55-60 589929-6 1977 Studies in isolated perfused kidneys indicated that sodium-deprived phaeochromocytoma rats released substantially less renin than sodium-deprived control rats despite an almost identical renal renin content in both sets of animals. Sodium 52-58 renin Rattus norvegicus 119-124 142633-3 1977 Previous reports of activation of the NaK ATPase at low potassium and high sodium are probably not due to phenytoin but to a potassium contamination in the phenytoin solution. Sodium 75-81 dynein axonemal heavy chain 8 Homo sapiens 42-48 299947-5 1977 These values correspond to a density of about 700,000 sodium channels per node--i.e., about 12,000 per mum2 of nodal membrane. Sodium 54-60 trafficking protein particle complex subunit 1 Homo sapiens 103-107 132454-9 1976 It can be concluded from these studies that the decreased sodium efflux in the erythrocytes of patients with hyperthyroidism is associated with a decrease in the activity of the ouabain-sensitive component of ATPase in the erythrocyte membrane. Sodium 58-64 dynein axonemal heavy chain 8 Homo sapiens 209-215 5201-7 1976 The alpha-adrenergic blocking drug phentolamine prevented clonidine suppression of renin release in sodium-depleted rats and was partially effective in normal rats. Sodium 100-106 renin Rattus norvegicus 83-88 5201-9 1976 Clozapine, a new neuroleptic agent with alpha-adrenergic blocking activity, or phenoxybenzamine blocked the effect of clonidine on renin release in both sodium-depleted and normal rats. Sodium 153-159 renin Rattus norvegicus 131-136 1261210-12 1976 It is concluded that the observed findings are compatible with an action of sodium-loading on the sensitivity of the smooth muscle cell to angiotensin, on the resting of the renin-angiotensin system, on the rate of inactivation of angiotensin and on a change in initial length of the muscle fibre. Sodium 76-82 renin Rattus norvegicus 174-179 1255521-0 1976 Effect of renin-angiotensin system on sodium intake. Sodium 38-44 renin Rattus norvegicus 10-15 2926-6 1976 These results suggest a central nervous system site for sodium, beta-adrenergic, and cholinergic receptors in altering renin release and blood pressure. Sodium 56-62 renin Rattus norvegicus 119-124 1192571-3 1975 The plasma renin activity of normal and sodium-depleted rats was reduced after the administration of clonidine (100 mug/kg, iv) by 22.8% and 34.4%, respectively. Sodium 40-46 renin Rattus norvegicus 11-16 1192571-8 1975 The data presented in this paper are consistent with the conclusion that clonidine acts at some site in the sympathetic nervous system of sodium-depleted rats to inhibit renal nerve activity with a resultant suppression of renin secretion and a reduction of the angiotensin II-maintained arterial blood pressure. Sodium 138-144 renin Rattus norvegicus 223-228 1204570-5 1975 Thus, in the absence of anesthesia, the renin-angiotensin-aldosterone system of the rat responds, as in other species, to a sodium load. Sodium 124-130 renin Rattus norvegicus 40-45 813373-7 1975 Both hypertensive MtT tumor-bearing animals and normotensive controls on a sodium deficient diet had a conspicuous increase of renal content of renin. Sodium 75-81 renin Rattus norvegicus 144-149 1194132-0 1975 Toxicity of sodium and chloride ions to Rhizobium spp. Sodium 12-18 histocompatibility minor 13 Homo sapiens 50-53 126237-2 1975 Sodium and potassium ion-activated adenosine triphosphatase is the enzyme responsible for the active transport of sodium and potassium across the plasma membrane. Sodium 114-120 ATPase Na+/K+ transporting subunit beta 1 Homo sapiens 35-59 1168128-4 1975 Bovine growth hormone and ovine prolactin produce essentially similar effects in intact rats: significant increases in fluid, sodium and calcium transport in the duodenum; in fluid, sodium and potassium transport in the jejunum; in sodium, chloride, potassium and calcium transport in the ileum. Sodium 126-132 gonadotropin releasing hormone receptor Rattus norvegicus 7-21 1168128-4 1975 Bovine growth hormone and ovine prolactin produce essentially similar effects in intact rats: significant increases in fluid, sodium and calcium transport in the duodenum; in fluid, sodium and potassium transport in the jejunum; in sodium, chloride, potassium and calcium transport in the ileum. Sodium 182-188 gonadotropin releasing hormone receptor Rattus norvegicus 7-21 1168128-4 1975 Bovine growth hormone and ovine prolactin produce essentially similar effects in intact rats: significant increases in fluid, sodium and calcium transport in the duodenum; in fluid, sodium and potassium transport in the jejunum; in sodium, chloride, potassium and calcium transport in the ileum. Sodium 182-188 gonadotropin releasing hormone receptor Rattus norvegicus 7-21 1168128-5 1975 Growth hormone also significantly increased fluid, sodium and chloride transport in the colon. Sodium 51-57 gonadotropin releasing hormone receptor Rattus norvegicus 0-14 124056-2 1975 Strophanthine K, an inhibitor of (Na-+--K-+) -activated ATP-ase, prevented the activating effect of adrenaline on sodium transport, and in the medium with a low concentration of this ion--it only partially inhibited its actibating effect. Sodium 114-120 dynein axonemal heavy chain 8 Homo sapiens 56-63 124056-4 1975 It is supposed that (Na-+--K-+)-activated ATP-ase was directly involved in the action mechanism of catecholamines on the system of active sodium transport in frog skin. Sodium 138-144 dynein axonemal heavy chain 8 Homo sapiens 42-49 234807-2 1975 Changes in sodium and potassium balance were related to changes in blood pressure, plasma renin activity, hematocrit, and kidney histology. Sodium 11-17 renin Rattus norvegicus 90-95 234807-4 1975 Plasma renin activity remained markedly suppressed both at the fourth week (0.33 plus or minus 0.02 ng/ml hour-1) when the sodium balance was positive and the kidney biopsy negative and at the end of the experiment (0.35 plus or minus 0.36 ng/ml hour-1) when the sodium balance was negative and the kidney histology revealed malignant vasculitis. Sodium 123-129 renin Rattus norvegicus 7-12 234807-4 1975 Plasma renin activity remained markedly suppressed both at the fourth week (0.33 plus or minus 0.02 ng/ml hour-1) when the sodium balance was positive and the kidney biopsy negative and at the end of the experiment (0.35 plus or minus 0.36 ng/ml hour-1) when the sodium balance was negative and the kidney histology revealed malignant vasculitis. Sodium 263-269 renin Rattus norvegicus 7-12 4279584-0 1974 Participation of cytidine triphosphate in sodium-dependent phosphorylation, transphosphorylation, and hydrolysis: evidence for two hydrolytic sites in sodium ion-plus potassium ion-dependent adenosine triphosphatase. Sodium 151-157 ATPase Na+/K+ transporting subunit beta 1 Homo sapiens 191-215 4273225-0 1973 Urea and sodium: effect on microsomal ATPase in different parts of the kidney. Sodium 9-15 dynein axonemal heavy chain 8 Homo sapiens 38-44 4319969-8 1970 Therefore, the effect seems to be mediated by a direct influence of potassium ions on renal renin secretion, perhaps via induced changes in sodium load to the macula densa.These studies point to an important role for potassium in the regulation of renin secretion. Sodium 140-146 renin Rattus norvegicus 248-253 4242765-0 1969 Effect of dehydration, starvation and sodium deprivation on microsomal ATPase in the kidney. Sodium 38-44 dynein axonemal heavy chain 8 Homo sapiens 71-77 4242427-0 1969 [Effect of sodium depletion on experimental renal hypertension and renin activity in rats]. Sodium 11-17 renin Rattus norvegicus 67-72 5684032-11 1968 The results of these experiments suggest that both calcium and sodium must act at the beta cell membrane or enter the cell before insulin release can occur in response to a variety of stimuli. Sodium 63-69 insulin Oryctolagus cuniculus 130-137 4235237-13 1968 High concentrations of sodium inhibited the microsomal ATPase activity irrespective of the previous conditions of adaptation.6. Sodium 23-29 dynein axonemal heavy chain 8 Homo sapiens 55-61 4223577-0 1966 Separation of adenosine diphosphate--adenosine triphosphate-exchange activity from the cerebral microsomal sodium-plus-potassium ion-stimulated adenosine triphosphatase. Sodium 107-113 ATPase Na+/K+ transporting subunit beta 1 Homo sapiens 144-168 4225829-0 1966 Studies on the activity of sodium and potassium activated ATP-ase in normal and leukemic granulocytes. Sodium 27-33 dynein axonemal heavy chain 8 Homo sapiens 58-65 14022085-0 1962 Distribution of glycogen, lipid and glucose-6-phosphate dehydrogenase activity in the adrenal cortex of the sodium-depleted rat: a histochemical study. Sodium 108-114 glucose-6-phosphate dehydrogenase Rattus norvegicus 36-69 13880309-0 1962 Glucose-6-phosphate dehydrogenase activity in the adrenal cortex of the sodium depleted rat: a histochemical study. Sodium 72-78 glucose-6-phosphate dehydrogenase Rattus norvegicus 0-33 13969508-0 1962 [Action of different inhibitors of L-DOPA decarboxylase on the water ration, diuresis and urinary sodium and potassium elimination in rats]. Sodium 98-104 dopa decarboxylase Rattus norvegicus 35-55 14006658-0 1961 The sensitivity of a kidney ATPase to ouabain and to sodium and potassium. Sodium 53-59 dynein axonemal heavy chain 8 Homo sapiens 28-34 13645748-0 1959 Increased renal pressor activity (renin) in sodium deficient rats and correlation with juxtaglomerular cell granulation. Sodium 44-50 renin Rattus norvegicus 34-39 13381905-0 1956 Urinary sodium and chloride determinations as an aid in the diagnosis of adrenal cortical insufficiency. Sodium 8-14 activation induced cytidine deaminase Homo sapiens 49-52 14920503-0 1952 Reduction of urinary sodium and potassium produced by hypophyseal growth hormone in normal female rats. Sodium 21-27 gonadotropin releasing hormone receptor Rattus norvegicus 66-80 14885451-0 1951 Effects of renin on excretion of sodium, chloride and water in the rat. Sodium 33-39 renin Rattus norvegicus 11-16 14864646-0 1951 Reduction of urinary sodium and potassium of diabetic rats produced by hypophyseal growth hormone. Sodium 21-27 gonadotropin releasing hormone receptor Rattus norvegicus 83-97 34054053-7 2021 As the reduction of systolic ARV was majorly derived from the change of mean SBP, diastolic ARV was significantly determined by urinary sodium-to-potassium ratio (beta coefficient +- standard error: 0.012 +- 0.004; P = 0.006) after adjusting for age, sex, smoking, mean DBP, BMI, and race. Sodium 136-142 selenium binding protein 1 Homo sapiens 77-80 34045310-2 2021 We have previously shown that the epithelial sodium channel ENaC/UNC-8 triggers an activity-dependent mechanism that drives the removal of presynaptic proteins liprin-alpha/SYD-2, Synaptobrevin/SNB-1, RAB-3 and Endophilin/UNC-57 in remodeling GABAergic neurons in C. elegans (Miller-Fleming et al., 2016). Sodium 45-51 Synaptobrevin-1 Caenorhabditis elegans 194-199 34038903-4 2020 Key Message: Sodium channel beta1- and its variant beta1B-subunits are encoded by SCN1B. Sodium 13-19 sodium voltage-gated channel beta subunit 1 Homo sapiens 82-87 34024107-8 2021 Therefore, the full cell of SnS2/GPE1/Na3V2(PO4)3 is evaluated and delivers good cycling stability of 500 cycles, holding a great prospect for the design and production of phosphorus-containing electrolytes for safer sodium-ion batteries. Sodium 217-223 sodium voltage-gated channel alpha subunit 11 Homo sapiens 28-32 33377278-12 2021 Angiotensin II antagonism alleviates CsA nephrotoxicity via the COX-2-dependent normalization of creatinine clearance and sodium excretion. Sodium 122-128 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 64-69 8125563-1 1994 Atrial natriuretic factor induces renal sodium excretion by several mechanisms, including inhibition of angiotensin II-stimulated sodium reabsorption in the proximal tubule. Sodium 130-136 natriuretic peptides A Oryctolagus cuniculus 0-25 8106444-8 1994 Zn(2+)-induced overexpression of PKC-delta- and PKC-epsilon-stimulated sodium-dependent phosphate uptake. Sodium 71-77 protein kinase C, epsilon Mus musculus 48-59 7507836-6 1994 We found that a low sodium intake increased plasma aldosterone levels from 5.5 to 236 ng/dl and led to 2.3- and 3.7-fold increases in the levels of adrenal ZG AT1 receptor protein and AT1 receptor mRNA, whereas a 11.8-fold increase was found in the level of P450c18 mRNA. Sodium 20-26 angiotensin II receptor, type 1a Rattus norvegicus 159-162 7507836-6 1994 We found that a low sodium intake increased plasma aldosterone levels from 5.5 to 236 ng/dl and led to 2.3- and 3.7-fold increases in the levels of adrenal ZG AT1 receptor protein and AT1 receptor mRNA, whereas a 11.8-fold increase was found in the level of P450c18 mRNA. Sodium 20-26 angiotensin II receptor, type 1a Rattus norvegicus 184-187 7507836-11 1994 Collectively, these results indicate that the increased aldosterone secretion induced by low sodium or high potassium intake involves concomitant increases in AT1 receptor and P450c18 mRNAs, which are effectively translated into their respective proteins, and that the expression of both proteins is mediated in part by AII. Sodium 93-99 angiotensin II receptor, type 1a Rattus norvegicus 159-162 7856932-5 1994 Comparison of plasma from 102 to 152 patients showed a good concordance for sodium with the Dimension ARS (y = 1x + 0). Sodium 76-82 RIEG2 Homo sapiens 102-105 8298079-1 1993 We present a biophysical model of a slowly inactivating potassium ion current IKS, based on recent voltage-clamp data from layer V pyramidal neurons in the cat sensorimotor cortex and show that the interplay between a persistent sodium current INaP and IKS is able to produce intrinsic membrane potential oscillations in the 10- to 50-frequency range. Sodium 229-235 NFKB inhibitor zeta Homo sapiens 244-248 8388735-5 1993 During the growth phase in glucose- and insulin-free medium, cells showed higher sodium-dependent glucose uptake. Sodium 81-87 insulin Oryctolagus cuniculus 40-47 8387081-7 1993 In sharp contrast, atrial extracts from sodium-depleted enalapril-treated rats displayed a pronounced band of hybridization, corresponding in size to that expected for renin mRNA. Sodium 40-46 renin Rattus norvegicus 168-173 8095371-1 1993 Since DA1 receptors regulate renal tubular sodium transport, it is possible that the reported defect in the coupling between the DA1 dopamine receptor and adenylyl cyclase (AC) in the proximal tubule (PT) is a mechanism for the increased sodium reabsorption in animal models of spontaneous hypertension. Sodium 43-49 RT1 class II, locus Da Rattus norvegicus 6-9 8095371-1 1993 Since DA1 receptors regulate renal tubular sodium transport, it is possible that the reported defect in the coupling between the DA1 dopamine receptor and adenylyl cyclase (AC) in the proximal tubule (PT) is a mechanism for the increased sodium reabsorption in animal models of spontaneous hypertension. Sodium 238-244 RT1 class II, locus Da Rattus norvegicus 6-9 8095371-1 1993 Since DA1 receptors regulate renal tubular sodium transport, it is possible that the reported defect in the coupling between the DA1 dopamine receptor and adenylyl cyclase (AC) in the proximal tubule (PT) is a mechanism for the increased sodium reabsorption in animal models of spontaneous hypertension. Sodium 238-244 RT1 class II, locus Da Rattus norvegicus 129-132 8389045-4 1993 Acute intravenous sodium chloride load induced a significant increase of the mean arterial pressure (MBP) only when the patients were on the high sodium diet. Sodium 18-24 myelin basic protein Homo sapiens 101-104 8389045-5 1993 This increase of the MBP was associated with a significantly lower increment of plasma ANP, cGMP, lower decrement of ALDO and PRA when compared to normal- or low- sodium intake. Sodium 163-169 myelin basic protein Homo sapiens 21-24 8380606-4 1993 Compared to placebo infusions, hBNP induced a greater than 2-fold increase in sodium excretion (P = 0.014) and suppressed plasma aldosterone (P < 0.004) to levels less than 50% of placebo values. Sodium 78-84 natriuretic peptide B Homo sapiens 31-35 8302455-9 1993 The decrease of Cin after infusion of AA was amplified by pre-equilibration on low-sodium diet (20 mmol Na/day). Sodium 83-89 pyridoxal phosphatase Homo sapiens 16-19 7906427-0 1993 D1 and D2 dopamine receptor modulation of sodium and potassium currents in rat neostriatal neurons. Sodium 42-48 dopamine receptor D2 Rattus norvegicus 7-27 8234540-1 1993 We explored the hypothesis that chronic blockage of adenosine (Ado) receptors might augment the renin response to sodium restriction. Sodium 114-120 renin Rattus norvegicus 96-101 1337728-3 1992 The channel state dependent blocking effects on cardiac sodium current (INa) of quinidine and disopyramide were studied under the whole cell variation of the patch clamp technique. Sodium 56-62 alpha-internexin Cavia porcellus 72-75 1335051-6 1992 In further experiments with L-Arg and L-Gly, this effect was associated with increased glomerular filtration rate, renal plasma flow, fractional sodium and free water excretion and urinary cyclic guanosine monophosphate. Sodium 145-151 Rho guanine nucleotide exchange factor 12 Homo sapiens 28-33 1282726-8 1992 Moreover, an ET-3 concentration (500 pmol/l), which induced a dramatic fall in tubular sodium load, led to an increase of fractional sodium excretion and to a decrease of renal oxygen consumption. Sodium 87-93 endothelin 3 Rattus norvegicus 13-17 1282726-8 1992 Moreover, an ET-3 concentration (500 pmol/l), which induced a dramatic fall in tubular sodium load, led to an increase of fractional sodium excretion and to a decrease of renal oxygen consumption. Sodium 133-139 endothelin 3 Rattus norvegicus 13-17 1338636-8 1992 In vitro, the effects of PTH(1-34), PTHrP(1-34) and PTHrP(1-141) on cAMP production and sodium-dependent phosphate transport (NaPiT) are similar in kidney cells, where NaPiT is specifically inhibited by either peptide. Sodium 88-94 parathyroid hormone like hormone Homo sapiens 36-41 1338636-8 1992 In vitro, the effects of PTH(1-34), PTHrP(1-34) and PTHrP(1-141) on cAMP production and sodium-dependent phosphate transport (NaPiT) are similar in kidney cells, where NaPiT is specifically inhibited by either peptide. Sodium 88-94 parathyroid hormone like hormone Homo sapiens 52-57 1573339-3 1992 There was a significant linear correlation between serum sodium and corrected sodium versus CPK (R = 0.585 and 0.713, respectively). Sodium 57-63 phosphatidylinositol-4-phosphate 3-kinase catalytic subunit type 2 alpha Homo sapiens 92-95 1371856-2 1992 On the fourth day of incubation with nerve growth factor, sodium potential-activated ionic currents appeared in the membranes of the most morphologically differentiated cells. Sodium 58-64 nerve growth factor Rattus norvegicus 37-56 1725739-6 1991 Alterations in plasma renin activity (PRA) were a consequence of PRC and PAC changes in thyroidectomized animals, as an increase in fractional sodium excretion (FENa) time course dependent, was found in these rats. Sodium 143-149 renin Rattus norvegicus 22-27 1804631-5 1991 Endogenous angiotensin formation was blocked by the angiotensin converting enzyme inhibitors captopril and ramiprilat and the activity of the endogenous renin-angiotensin system was modulated by variations in nutritional sodium load prior to the experiments. Sodium 221-227 renin Rattus norvegicus 153-158 1818950-0 1991 Insulin receptor concentration and gene expression are modulated by sodium intake in the rat kidney. Sodium 68-74 insulin receptor Rattus norvegicus 0-16 1772038-6 1991 We conclude that hepatic VIP metabolism is decreased by acute gastric sodium loading but it is not affected by chronic sodium intake. Sodium 70-76 VIP peptides Oryctolagus cuniculus 25-28 1659225-0 1991 Mechanism of sodium transport inhibition by epidermal growth factor in cortical collecting ducts. Sodium 13-19 pro-epidermal growth factor Oryctolagus cuniculus 44-67 1683170-1 1991 Renal dopamine DA1 receptors are linked to the regulation of sodium transport. Sodium 61-67 RT1 class II, locus Da Rattus norvegicus 15-18 1914098-4 1991 BNP infusion significantly increased urine volume (control, from 2.3 +/- 0.7 to 7.5 +/- 1.9 ml/min; CHF, from 0.8 +/- 0.2 to 5.3 +/- 1.0 ml/min; p less than 0.01, respectively), excretion of sodium (control, from 79.2 +/- 21.6 to 332.8 +/- 70.9 microEq/min; CHF, from 77.4 +/- 20.8 to 753.5 +/- 108.0 microEq/min; p less than 0.01, respectively), and excretion of chloride (control, from 72.5 +/- 18.4 to 256.0 +/- 43.3 microEq/min; CHF, from 74.0 +/- 19.6 to 708.8 +/- 103.3 microEq/min; p less than 0.01, respectively). Sodium 191-197 natriuretic peptide B Homo sapiens 0-3 1914098-5 1991 Urinary excretion of sodium and of chloride in response to BNP infusion was higher in patients with CHF than in control subjects (p less than 0.01, respectively). Sodium 21-27 natriuretic peptide B Homo sapiens 59-62 1877652-8 1991 DNX rats had a net accumulation of 2.54 meq more sodium than INN rats over 72 h. Significant inhibition of plasma renin activity within the first 24 h occurred only in rats receiving the LNa-to-HNa switch in sodium intake, and this response was not different between rats with innervated and denervated kidneys. Sodium 208-214 renin Rattus norvegicus 114-119 1661120-3 1991 In preoperative animals, urine volume and urinary sodium excretion increased greatly during ANP administration, but this natriuretic effect was strongly suppressed in TAH animals. Sodium 50-56 natriuretic peptides A Capra hircus 92-95 1656038-1 1991 The sodium dependence of recovery of cytoplasmic pH (pHi) after an acid load was studied in platelets from 15 patients with untreated essential hypertension (mean arterial pressure 117 +/- 2.3 mmHg, mean +/- SE) and in 15 normotensive controls (mean arterial pressure 90 +/- 2.2 mmHg). Sodium 4-10 glucose-6-phosphate isomerase Homo sapiens 53-56 1673100-12 1991 Primary cultures exhibited several differentiated functions of the proximal tubule cell: (a) PTH alone was able to induce a significant stimulation of adenylate cyclase activity, unlike isoproterenol, thyrocalcitonin, and arginine vasopressin, and (b) sodium-dependent alpha-methylglucoside (AMG) transport was detected. Sodium 252-258 parathyroid hormone Oryctolagus cuniculus 93-96 2061832-6 1991 Granular renin content was increased by chronic sodium deprivation and hypophysectomy. Sodium 48-54 renin Rattus norvegicus 9-14 1647796-1 1991 Plasma from normal humans and rats on a high sodium intake, and from patients and rats suffering from hereditary hypertension has an increased cytochemically detectable glucose-6-phosphate dehydrogenase (G6PD)-stimulating/Na-K-ATPase inhibiting activity. Sodium 45-51 glucose-6-phosphate dehydrogenase Rattus norvegicus 169-202 1647796-1 1991 Plasma from normal humans and rats on a high sodium intake, and from patients and rats suffering from hereditary hypertension has an increased cytochemically detectable glucose-6-phosphate dehydrogenase (G6PD)-stimulating/Na-K-ATPase inhibiting activity. Sodium 45-51 glucose-6-phosphate dehydrogenase Rattus norvegicus 204-208 2019995-1 1991 A-4, A-5 and HC-3 are experimental bis tertiary and quaternary amines which have been shown to be potent inhibitors of the sodium-dependent, high affinity choline uptake system. Sodium 123-129 laminin, alpha 5 Mus musculus 5-8 1999328-1 1991 It has been proposed that the initial event of sodium retention in cirrhosis is a peripheral arteriolar vasodilation causing underfilling of the arterial vascular compartment and stimulation of the renin-aldosterone and sympathetic nervous systems. Sodium 47-53 renin Rattus norvegicus 198-203 2054651-0 1991 Effects of calmodulin antagonists on sodium-dependent high-affinity choline uptake. Sodium 37-43 calmodulin 1 Rattus norvegicus 11-21 1854946-0 1991 [The effect of calcitonin on the mechanisms of urine formation and sodium excretion in normotensive and spontaneously hypertensive rats]. Sodium 67-73 calcitonin-related polypeptide alpha Rattus norvegicus 15-25 2213567-2 1990 Previous work in this laboratory has shown A-4 and A-5 to be inhibitors of the sodium-dependent, high affinity choline uptake system (SDHACU). Sodium 79-85 immunoglobulin kappa variable 1D-27 (pseudogene) Homo sapiens 43-46 2369117-0 1990 Extracellular ATP stimulates an amiloride-sensitive sodium influx in human lymphocytes. Sodium 52-58 ATPase phospholipid transporting 8A2 Homo sapiens 14-17 2369117-8 1990 Sodium influx was stimulated 7-fold by extracellular ATP but only 2.4-fold by hypertonic conditions which are known to activate Na(+)-H+ countertransport. Sodium 0-6 ATPase phospholipid transporting 8A2 Homo sapiens 53-56 2185278-5 1990 Administration of an aldose reductase inhibitor prevented reductions in both nerve myo-inositol content and endoneurial sodium-dependent 2-aminoisobutyric acid uptake. Sodium 120-126 aldo-keto reductase family 1 member B1 Oryctolagus cuniculus 21-37 2110974-12 1990 These results indicate that the hypotensive response induced by CGP 44 099 A in sodium-depleted rats is specifically due to the renin inhibition. Sodium 80-86 renin Rattus norvegicus 128-133 2331021-9 1990 These results suggest different roles for sodium and chloride in the regulation of the peripheral and central renin-angiotensin system in young rats. Sodium 42-48 renin Rattus norvegicus 110-115 2347119-0 1990 Sodium-dependent, ethylisopropylamiloride-sensitive mechanisms regulate intracellular pH in human vascular smooth muscle. Sodium 0-6 glucose-6-phosphate isomerase Homo sapiens 86-88 2184915-2 1990 Moderate sodium depletion (0.05% sodium in diet) significantly impaired growth rate and stimulated the renin-angiotensin system, but did not result in significant changes in peripheral or central angiotensin II receptors. Sodium 9-15 renin Rattus norvegicus 103-108 2184915-2 1990 Moderate sodium depletion (0.05% sodium in diet) significantly impaired growth rate and stimulated the renin-angiotensin system, but did not result in significant changes in peripheral or central angiotensin II receptors. Sodium 33-39 renin Rattus norvegicus 103-108 2184915-3 1990 In young rats, the impairment of the growth rate and the stimulation of the peripheral renin-angiotensin system were more notable after profound sodium depletion (0.005% sodium in diet). Sodium 145-151 renin Rattus norvegicus 87-92 2184915-3 1990 In young rats, the impairment of the growth rate and the stimulation of the peripheral renin-angiotensin system were more notable after profound sodium depletion (0.005% sodium in diet). Sodium 170-176 renin Rattus norvegicus 87-92 1708016-0 1990 Regulation of vasoactive intestinal peptide release and metabolism by sodium. Sodium 70-76 VIP peptides Oryctolagus cuniculus 14-43 1708016-1 1990 To determine whether vasoactive intestinal peptide (VIP) might act as a humoral mediator for a proposed portal or hepatic sodium monitor, we measured plasma VIP levels and urinary sodium excretion after portal and intravenous sodium loading in rabbits equilibrated on normal and low sodium diets. Sodium 122-128 VIP peptides Oryctolagus cuniculus 21-50 1708016-1 1990 To determine whether vasoactive intestinal peptide (VIP) might act as a humoral mediator for a proposed portal or hepatic sodium monitor, we measured plasma VIP levels and urinary sodium excretion after portal and intravenous sodium loading in rabbits equilibrated on normal and low sodium diets. Sodium 122-128 VIP peptides Oryctolagus cuniculus 52-55 2154581-7 1990 Thus, taking into account the cellular localization of the IsK protein, together with its electrophysiological properties, we discussed a possible function of the IsK protein, namely that this protein is involved in potassium permeation in the apical membrane of epithelial cells through the depolarizing effect of sodium entry. Sodium 315-321 potassium voltage-gated channel subfamily E regulatory subunit 1 Rattus norvegicus 163-166 2148203-5 1990 ET-3 infusion at 40 ng/kg/min increased sodium excretion (delta UNaV) by 0.14 +/- 0.08 microEq/min (p less than 0.05 compared to vehicle infusion) without affecting the glomerular filtration rate (GFR). Sodium 40-46 endothelin 3 Rattus norvegicus 0-4 2175824-0 1990 Pharmacological evidence for involvement of the sympathetic nervous system in the increase in renin secretion produced by a low sodium diet in rats. Sodium 128-134 renin Rattus norvegicus 94-99 2175824-1 1990 To determine the degree to which increased sympathetic activity contributes to the increase in renin secretion produced by a low sodium diet, the beta-adrenergic blocking drug propranolol or saline vehicle was injected through indwelling jugular cannulas in rats fed a normal diet and rats fed a low sodium diet for 9 days. Sodium 129-135 renin Rattus norvegicus 95-100 2175824-6 1990 The results indicate that increased sympathetic activity makes a substantial contribution to the increase in renin secretion produced by 9 days of dietary sodium restriction. Sodium 155-161 renin Rattus norvegicus 109-114 2104641-9 1990 These data suggest that myo-inositol content of glomerular mesangial cells, which is reduced by high concentrations of glucose, is maintained by two processes: a glucose-sensitive but sorbitol-insensitive process, sodium-dependent myo-inositol uptake; and a sorbitol (aldose reductase) sensitive process, myo-Inositol depletion under high glucose condition may induce dysfunction of mesangial cells seen in diabetes. Sodium 214-220 aldo-keto reductase family 1 member B1 Rattus norvegicus 268-284 2236972-2 1990 The role of proteinuria, hypoproteinemia, and renin-angiotensin-aldosterone system on sodium retention. Sodium 86-92 renin Rattus norvegicus 46-51 33818128-0 2021 Deletion of renal Nedd4-2 abolishes the effect of high sodium intake (HS) on Kir4.1, ENaC and NCC, and causes hypokalemia during HS. Sodium 55-61 potassium inwardly-rectifying channel, subfamily J, member 10 Mus musculus 77-83 33941260-8 2021 TRPC7 was found to be positively associated with the activity of ryanodine receptor 2 (RyR2), sarco/endoplasmic reticulum Ca2+-ATPase (SERCA), and sodium-calcium exchanger (NCX) but not hyperpolarization-activated, cyclic nucleotide-gated channel (HCN), and inositol trisphosphate receptor (IP3R). Sodium 147-153 transient receptor potential cation channel subfamily C member 7 Felis catus 0-5 33793981-0 2021 The sodium leak channel NALCN regulates cell excitability of pituitary endocrine cells. Sodium 4-10 sodium leak channel, non-selective Rattus norvegicus 24-29 33782967-3 2021 Transient receptor potential vanilloid 1 (TRPV1) channels are nonselective cation channels that permeate sodium and calcium. Sodium 105-111 transient receptor potential cation channel subfamily V member 1 Homo sapiens 0-40 33782967-3 2021 Transient receptor potential vanilloid 1 (TRPV1) channels are nonselective cation channels that permeate sodium and calcium. Sodium 105-111 transient receptor potential cation channel subfamily V member 1 Homo sapiens 42-47 33782967-10 2021 The results suggest that TRPV1 controls calcium release from the SR. By electrophysiology, TRPV1 blockade and functional knockdown of TRPV1 decreased the Na+ /Ca2+ exchanger (NCX) currents from both the forward and reverse modes, suggesting that sodium and calcium through TRPV1 stimulate the NCX activity. Sodium 246-252 transient receptor potential cation channel subfamily V member 1 Homo sapiens 25-30 33807852-5 2021 We have previously shown that high levels of sodium can induce the cl-Par-4 fragment to form highly compact, highly helical tetramers in vitro. Sodium 45-51 pro-apoptotic WT1 regulator Homo sapiens 70-75 34952274-5 2022 Owing to the significantly improved sodium ions transport kinetics and fast electronic conductive network, the PEG-SnS2/rGO composite presents a high capacitance contribution of 90.69% at a scan rate of 0.6 mV s-1. Sodium 36-42 sodium voltage-gated channel alpha subunit 11 Homo sapiens 115-119 34870751-0 2022 Proteolytic activation of the epithelial sodium channel (ENaC) by factor VII activating protease (FSAP) and its relevance for sodium retention in nephrotic mice. Sodium 41-47 hyaluronic acid binding protein 2 Mus musculus 98-102 34794320-1 2022 Background: How signals from activated angiotensin type-2 receptors (AT2R) mediate inhibition of sodium ion (Na+) reabsorption in renal proximal tubule cells (RPTCs) is currently unknown. Sodium 97-103 angiotensin II receptor, type 2 Rattus norvegicus 69-73 34679207-4 2022 Sodium metal batteries (SMB, NMB) with NST-Na and Na3 V2 (PO4 )3 (NVP) or sulfur cathodes give significantly improved energy, cycling and CE (> 99%). Sodium 0-12 neuromedin B Homo sapiens 29-32 34196792-10 2022 The coefficients of variations of measured vs. calculated sodium excretion were 25.3% vs. 25.8%, and the P30 of calculated sodium excretion was 100%. Sodium 123-129 centromere protein V Homo sapiens 105-108 34755678-3 2021 Here, we evaluate sodium transporters in uEVs as candidates of biomarkers of MR activity in the clinical setting. Sodium 18-24 nuclear receptor subfamily 3 group C member 2 Homo sapiens 77-79 34950618-3 2021 BNP functions to promote vasodilation, diuresis, and sodium release to regulate blood pressure. Sodium 53-59 natriuretic peptide B Homo sapiens 0-3 34866245-0 2021 In situ Fabrication of Porous Cox P Hierarchical Nanostructures on Carbon Fiber Cloth with Exceptional Performance for Sodium Storage. Sodium 119-125 cytochrome c oxidase subunit 8A Homo sapiens 30-33 34925043-1 2021 Variants of the SCN1A gene encoding the neuronal voltage-gated sodium channel NaV1.1 cause over 85% of all cases of Dravet syndrome, a severe and often pharmacoresistent epileptic encephalopathy with mostly infantile onset. Sodium 63-69 sodium voltage-gated channel alpha subunit 1 Homo sapiens 16-21 34925043-1 2021 Variants of the SCN1A gene encoding the neuronal voltage-gated sodium channel NaV1.1 cause over 85% of all cases of Dravet syndrome, a severe and often pharmacoresistent epileptic encephalopathy with mostly infantile onset. Sodium 63-69 sodium voltage-gated channel alpha subunit 1 Homo sapiens 78-84 34703915-8 2021 Sodium-dependent VC transporter 1 and 2 (SVCT1 and SVCT2) expressions were higher in ileum than in duodenum and jejunum (P < 0.05). Sodium 0-6 solute carrier family 23 member 2 Homo sapiens 51-56 34779863-8 2021 Both the mRNA and protein expression of GRK4 and its downstream target AT1R were increased in offspring of PM2.5-exposed paternal rats, which was reflected in its function because treatment with losartan, an AT1R antagonist, decreased the blood pressure and increased urine volume and sodium excretion. Sodium 285-291 angiotensin II receptor, type 1a Rattus norvegicus 71-75 34826216-1 2021 OBJECTIVE: SCN8A epileptic encephalopathy is caused predominantly by de novo gain-of-function mutations in the voltage-gated-sodium channel Nav 1.6. Sodium 125-131 sodium channel, voltage-gated, type VIII, alpha Mus musculus 11-16 34797252-0 2021 A Potential Treatment of Congenital Sodium Diarrhea in Patients With Activating GUCY2C Mutations. Sodium 36-42 guanylate cyclase 2C Homo sapiens 80-86 33275464-4 2021 Of note, a mutation in the voltage-gated sodium-channel gene alpha 1 subunit (SCN1A) has been found in around 85% of patients with Dravet syndrome. Sodium 41-47 sodium voltage-gated channel alpha subunit 1 Homo sapiens 78-83 33782571-1 2021 Evidence from human genetic pain disorders shows that voltage-gated sodium channel alpha-subtypes Nav1.7, Nav1.8 and Nav1.9 are important in the peripheral signalling of pain. Sodium 68-74 sodium voltage-gated channel alpha subunit 11 Homo sapiens 117-123 33937968-2 2021 Approximately 80% of patients with this syndrome present SCN1A pathogenic variants, which encodes an alpha subunit of a neural voltage-dependent sodium channel. Sodium 145-151 sodium voltage-gated channel alpha subunit 1 Homo sapiens 57-62 33895391-0 2021 Mutations in the sodium channel genes SCN1A, SCN3A, and SCN9A in children with epilepsy with febrile seizures plus(EFS+). Sodium 17-23 sodium voltage-gated channel alpha subunit 1 Homo sapiens 38-43 33895391-5 2021 RESULTS: We identified 10 putatively causative sodium channel gene variants in 49 patients with EFS+, including 8 variants in SCN1A (R500Q appeared twice), one in SCN3A and one in SCN9A. Sodium 47-53 sodium voltage-gated channel alpha subunit 1 Homo sapiens 126-131 33476711-11 2021 We conclude that acute HgCl2 exposure causes renal vasoconstriction that is associated with reduced endothelial vasodilator agonist- and flow-mediated responses and inhibition of NHE3-mediated sodium reabsorption. Sodium 193-199 solute carrier family 9 member A3 Rattus norvegicus 179-183 34544834-1 2021 SCN8A epileptic encephalopathy is a devastating epilepsy syndrome caused by mutant SCN8A which encodes the voltage-gated sodium channel NaV1.6. Sodium 121-127 sodium channel, voltage-gated, type VIII, alpha Mus musculus 0-5 34544834-1 2021 SCN8A epileptic encephalopathy is a devastating epilepsy syndrome caused by mutant SCN8A which encodes the voltage-gated sodium channel NaV1.6. Sodium 121-127 sodium channel, voltage-gated, type VIII, alpha Mus musculus 83-88 34544834-1 2021 SCN8A epileptic encephalopathy is a devastating epilepsy syndrome caused by mutant SCN8A which encodes the voltage-gated sodium channel NaV1.6. Sodium 121-127 sodium channel, voltage-gated, type VIII, alpha Mus musculus 136-142 34544834-6 2021 Aberrantly large persistent sodium currents, a hallmark of SCN8A mutations, were observed and were found to contribute directly to aberrant SST physiology in computational modeling and pharmacological experiments. Sodium 28-34 sodium channel, voltage-gated, type VIII, alpha Mus musculus 59-64 34523364-0 2021 Contribution of tetrodotoxin-sensitive voltage-gated sodium channels (NaV1) to action potential discharge from mouse esophageal tension mechanoreceptors. Sodium 53-59 neuron navigator 1 Mus musculus 70-74 34605518-0 2021 Sandwich-like SnS2/graphene multilayers for efficient lithium/sodium storage. Sodium 62-68 sodium voltage-gated channel alpha subunit 11 Homo sapiens 14-18 34605518-2 2021 Herein, we report utilization of monolayer SnS2 sheets within SnS2/graphene multilayers for efficient lithium and sodium storage. Sodium 114-120 sodium voltage-gated channel alpha subunit 11 Homo sapiens 43-47 34605518-2 2021 Herein, we report utilization of monolayer SnS2 sheets within SnS2/graphene multilayers for efficient lithium and sodium storage. Sodium 114-120 sodium voltage-gated channel alpha subunit 11 Homo sapiens 62-66 34605518-4 2021 It has been shown that the SnS2/graphene multilayer electrode has a large pseudocapacity contribution for enhanced lithium and sodium storage. Sodium 127-133 sodium voltage-gated channel alpha subunit 11 Homo sapiens 27-31 34988469-7 2021 We found that furosemide sensitive sodium transport (NKCC2) is only increased during late pregnancy, thiazide sensitive sodium transport (NDCBE/pendrin) is increased in all stages of pregnancy, and that benzamil sensitive sodium transport (ENaC) is increased beginning in mid-pregnancy. Sodium 120-126 solute carrier family 26 member 4 Rattus norvegicus 144-151 34343486-0 2021 Dysfunction of Cullin 3 RING E3 ubiquitin ligase causes vasoconstriction and increased sodium reabsorption in diabetes. Sodium 87-93 cullin 3 Mus musculus 15-23 34343486-9 2021 Increases in WNK4 abundance resulted in increased sodium reabsorption in the distal renal tubules. Sodium 50-56 WNK lysine deficient protein kinase 4 Mus musculus 13-17 34343486-10 2021 Thus, KLHL2/RhoBTB1/KLHL3 inactivation in the aortic tissues and kidney is a result of excessive activation of neddylation in hyperglycemia and hyperinsulinemia, which affects vascular tone and sodium reabsorption. Sodium 194-200 Rho-related BTB domain containing 1 Mus musculus 12-19 34746693-0 2021 SLO2.1/NALCN a sodium signaling complex that regulates uterine activity. Sodium 15-21 sodium leak channel, non-selective Homo sapiens 7-12 34375627-0 2021 Regulation of the voltage-dependent sodium channel NaV1.1 by AKT1. Sodium 36-42 sodium voltage-gated channel alpha subunit 1 Homo sapiens 51-57 33900854-1 2021 High-sodium-intake (HS) inhibited epithelial-sodium-channel (ENaC) in the aldosterone-sensitive-distal-nephron (ASDN) and Na+-Cl--cotransporter (NCC) by suppressing basolateral Kir4.1/Kir5.1 in the distal-convoluted-tubule (DCT) thereby increasing renal Na+ excretion but not affecting K+ excretion. Sodium 5-11 potassium inwardly-rectifying channel, subfamily J, member 10 Mus musculus 177-183 34375627-1 2021 The voltage-sensitive sodium channel NaV1.1 plays a critical role in regulating excitability of GABAergic neurons and mutations in the corresponding gene are associated to Dravet syndrome and other forms of epilepsy. Sodium 22-28 sodium voltage-gated channel alpha subunit 1 Homo sapiens 37-43 34389319-0 2021 The insecticide deltamethrin enhances sodium channel slow inactivation of human Nav1.9, Nav1.8 and Nav1.7. Sodium 38-44 sodium voltage-gated channel alpha subunit 11 Homo sapiens 80-86 34584093-2 2021 The previously solved structures of the outward facing (OF) conformation for AE1 (SLC4A1) and NBCe1 (SLC4A4) transporters revealed an identical overall fold despite their different transport modes (chloride/bicarbonate exchange versus sodium-carbonate cotransport). Sodium 235-241 solute carrier family 4 member 1 (Diego blood group) Homo sapiens 77-80 34584093-2 2021 The previously solved structures of the outward facing (OF) conformation for AE1 (SLC4A1) and NBCe1 (SLC4A4) transporters revealed an identical overall fold despite their different transport modes (chloride/bicarbonate exchange versus sodium-carbonate cotransport). Sodium 235-241 solute carrier family 4 member 1 (Diego blood group) Homo sapiens 82-88 34556045-9 2021 We found allele C of rs55742440 in SCN1B was statistically significantly associated with not achieving seizure-free with sodium channel blocking ASMs. Sodium 121-127 sodium voltage-gated channel beta subunit 1 Homo sapiens 35-40 34556045-11 2021 CONCLUSION: Single-nucleotide polymorphism in SCN1B was associated with the response to sodium channel blocking ASMs. Sodium 88-94 sodium voltage-gated channel beta subunit 1 Homo sapiens 46-51 34630451-2 2021 SOS3/CBL4 is a core component of the SOS pathway that senses calcium signaling of salinity stress to activate and recruit the protein kinase SOS2/CIPK24 to the plasma membrane to trigger sodium efflux by the Na/H exchanger SOS1/NHX7. Sodium 187-193 Calcium-binding EF-hand family protein Arabidopsis thaliana 0-4 34630451-2 2021 SOS3/CBL4 is a core component of the SOS pathway that senses calcium signaling of salinity stress to activate and recruit the protein kinase SOS2/CIPK24 to the plasma membrane to trigger sodium efflux by the Na/H exchanger SOS1/NHX7. Sodium 187-193 Calcium-binding EF-hand family protein Arabidopsis thaliana 5-9 34459253-0 2021 ATP1A3-Encoded Sodium-Potassium ATPase Subunit Alpha 3 D801N Variant Is Associated With Shortened QT Interval and Predisposition to Ventricular Fibrillation Preceded by Bradycardia. Sodium 15-21 ATPase Na+/K+ transporting subunit alpha 3 Homo sapiens 0-6 34459253-1 2021 Background Pathogenic variation in the ATP1A3-encoded sodium-potassium ATPase, ATP1A3, is responsible for alternating hemiplegia of childhood (AHC). Sodium 54-60 ATPase Na+/K+ transporting subunit alpha 3 Homo sapiens 39-45 34459253-1 2021 Background Pathogenic variation in the ATP1A3-encoded sodium-potassium ATPase, ATP1A3, is responsible for alternating hemiplegia of childhood (AHC). Sodium 54-60 ATPase Na+/K+ transporting subunit alpha 3 Homo sapiens 79-85 34252210-0 2021 Synergistic Engineering of Defects and Heterostructures Enhance Lithium/Sodium Storage Properties of F-SnO2-x-SnS2-x Nanocrystals Supported on N, S-graphene. Sodium 72-78 sodium voltage-gated channel alpha subunit 11 Homo sapiens 110-114 34573045-1 2021 During brain development, sodium-vitamin C transporter (SVCT2) has been detected primarily in radial glial cells in situ, with low-to-absent expression in cerebral cortex neuroblasts. Sodium 26-32 solute carrier family 23 member 2 Homo sapiens 56-61 34504954-2 2021 The sodium-dependent phosphate transporter NaPi2b encoded by SLC34A2 gene is expressed in 80-90% of epithelial ovarian cancers and used as a target for therapeutic antibodies XMT-1536, and XMT-1592, which are derived from MX35 antibodies and used in clinical trials for the treatment of ovarian and lung cancers. Sodium 4-10 solute carrier family 34 member 2 Homo sapiens 61-68 34278939-8 2021 In the "bang-sensitive" sodium channel mutant bangsenseless (bss), the LFP pattern was prolonged, and the temporal correlation between LFP oscillations and DLM discharges was altered. Sodium 24-30 paralytic Drosophila melanogaster 46-59 34353676-4 2021 In this review we describe the identification of a new epileptic encephalopathy caused by a de novo mutation in the SCN8A gene, which encodes for NaV1.6, a vital sodium channel in the central nervous system. Sodium 162-168 neuron navigator 1 Homo sapiens 146-150 34330444-5 2021 Herein, a nanobiosensor for detecting sodium and potassium ions using folic acid-functionalised reduced graphene oxide-modified RNase A gold nanoclusters (FA-rGO-RNase A/AuNCs) based on fluorescence "turn-off/turn-on" is presented. Sodium 38-44 ribonuclease A family member 1, pancreatic Homo sapiens 128-135 33886138-7 2021 The excellent cycling performance and rate capability demonstrated that the CoS 2 /S@N-HCS is a potential and prospective anode material for sodium-ion batteries. Sodium 141-147 holocarboxylase synthetase Homo sapiens 87-90 33886140-11 2021 Finally, it was shown that the anti-inflammatory effect of SVHRSP in microglia was Nav 1.6 dependent and was related to suppression of sodium current and probably the consequent Na+ /Ca2+ exchange. Sodium 135-141 sodium channel, voltage-gated, type VIII, alpha Mus musculus 83-90 33880743-3 2021 TGF-beta, by internalization of the epithelial sodium channel (ENaC), suppresses the anti-oxidant system, downregulates the cystic fibrosis transmembrane conductance regulator (CFTR), and activates the plasminogen activator inhibitor 1 (PAI-1) and nuclear factor-kappa-light-chain-enhancer of activated B cells (NF-kB). Sodium 47-53 transforming growth factor alpha Homo sapiens 0-8 33854040-0 2021 The ubiquitin ligase NEDD4-2/NEDD4L regulates both sodium homeostasis and fibrotic signaling to prevent end-stage renal disease. Sodium 51-57 ring finger protein 123 Mus musculus 4-20 34330444-5 2021 Herein, a nanobiosensor for detecting sodium and potassium ions using folic acid-functionalised reduced graphene oxide-modified RNase A gold nanoclusters (FA-rGO-RNase A/AuNCs) based on fluorescence "turn-off/turn-on" is presented. Sodium 38-44 ribonuclease A family member 1, pancreatic Homo sapiens 162-169 34330444-9 2021 Finally, a fluorescence "turn-on" sensing strategy is developed using the as-synthesised FA-rGO-RNase A/AuNCs to detect sodium and potassium ions. Sodium 120-126 ribonuclease A family member 1, pancreatic Homo sapiens 96-103 34589280-3 2021 In >80% of cases, the disease is caused by haploinsufficiency of the SCN1A gene, which encodes the alpha subunit of the Nav1.1 voltage-gated sodium channel. Sodium 141-147 sodium voltage-gated channel alpha subunit 1 Homo sapiens 69-74 33919841-0 2021 A Low-Sodium Diet Boosts Ang (1-7) Production and NO-cGMP Bioavailability to Reduce Edema and Enhance Survival in Experimental Heart Failure. Sodium 6-12 angiopoietin 1 Homo sapiens 25-33 33928137-9 2021 Conclusion: These findings support that the downregulation of CRL3 function disrupts the balance of vasoconstriction and vasodilation and aggravates excess reabsorption of sodium in PE. Sodium 172-178 interleukin 31 receptor A Mus musculus 62-66 33921209-0 2021 NFAT5 Is Involved in GRP-Enhanced Secretion of GLP-1 by Sodium. Sodium 56-62 glucagon Mus musculus 47-52 33921209-1 2021 Gastrin, secreted by G-cells, and glucagon-like peptide-1 (GLP-1), secreted by L-cells, may participate in the regulation of sodium balance. Sodium 125-131 glucagon Mus musculus 34-57 33921209-1 2021 Gastrin, secreted by G-cells, and glucagon-like peptide-1 (GLP-1), secreted by L-cells, may participate in the regulation of sodium balance. Sodium 125-131 glucagon Mus musculus 59-64 33921209-3 2021 A high-sodium diet increases serum GLP-1 levels in mice. Sodium 7-13 glucagon Mus musculus 35-40 33921209-4 2021 Increasing sodium concentration stimulates GLP-1 secretion from mouse ileum and L-cells. Sodium 11-17 glucagon Mus musculus 43-48 33921209-5 2021 GRP enhances the high sodium-induced increase in GLP-1 secretion. Sodium 22-28 glucagon Mus musculus 49-54 33921209-6 2021 High sodium increases cellular GLP-1 expression, while low and high sodium concentrations increase NFAT5 and GRPR expression. Sodium 5-11 glucagon Mus musculus 31-36 33921209-6 2021 High sodium increases cellular GLP-1 expression, while low and high sodium concentrations increase NFAT5 and GRPR expression. Sodium 68-74 gastrin releasing peptide receptor Mus musculus 109-113 33921209-7 2021 Silencing NFAT5 in L-cells abrogates the stimulatory effect of GRP on the high sodium-induced GLP-1 secretion and protein expression, and the sodium-induced increase in GRPR expression. Sodium 79-85 glucagon Mus musculus 94-99 33921209-7 2021 Silencing NFAT5 in L-cells abrogates the stimulatory effect of GRP on the high sodium-induced GLP-1 secretion and protein expression, and the sodium-induced increase in GRPR expression. Sodium 142-148 gastrin releasing peptide receptor Mus musculus 169-173 33921209-8 2021 GLP-1 and gastrin decrease the expression of Na+-K+/ATPase and increase the phosphorylation of sodium/hydrogen exchanger type 3 (NHE3) in human renal proximal tubule cells (hRPTCs). Sodium 95-101 glucagon like peptide 1 receptor Homo sapiens 0-5 33826405-2 2021 In non-excitable epithelial cells of the kidney tubule, for example, Kir1.1 (KCNJ1) and Kir4.1 (KCNJ10) are linked to sodium reabsorption in the thick ascending limb of Henle"s loop and distal convoluted tubule, respectively, and have been explored as novel-mechanism diuretic targets for managing hypertension and edema. Sodium 118-124 potassium inwardly rectifying channel subfamily J member 1 Homo sapiens 69-75 33826405-2 2021 In non-excitable epithelial cells of the kidney tubule, for example, Kir1.1 (KCNJ1) and Kir4.1 (KCNJ10) are linked to sodium reabsorption in the thick ascending limb of Henle"s loop and distal convoluted tubule, respectively, and have been explored as novel-mechanism diuretic targets for managing hypertension and edema. Sodium 118-124 potassium inwardly rectifying channel subfamily J member 1 Homo sapiens 77-82 34399820-4 2021 Whole exome sequencing showed a de novo heterozygous variant (c.4873-4881 duplication) in the SCN8A gene and an inherited heterozygous variant (c.952G > A) in the CACNA1H gene encoding for Nav1.6 voltage-gated sodium and Cav3.2 voltage-gated calcium channels, respectively. Sodium 210-216 calcium voltage-gated channel subunit alpha1 H Homo sapiens 163-170 34399820-4 2021 Whole exome sequencing showed a de novo heterozygous variant (c.4873-4881 duplication) in the SCN8A gene and an inherited heterozygous variant (c.952G > A) in the CACNA1H gene encoding for Nav1.6 voltage-gated sodium and Cav3.2 voltage-gated calcium channels, respectively. Sodium 210-216 neuron navigator 1 Homo sapiens 189-193 34348148-0 2021 Severe deficiency of the voltage-gated sodium channel NaV1.2 elevates neuronal excitability in adult mice. Sodium 39-45 sodium channel, voltage-gated, type II, alpha Mus musculus 54-60 34348148-1 2021 Scn2a encodes the voltage-gated sodium channel NaV1.2, a main mediator of neuronal action potential firing. Sodium 32-38 sodium channel, voltage-gated, type II, alpha Mus musculus 0-5 34335164-4 2021 Sodium leak channel (NALCN) is widely expressed in central nervous system and controls the basal excitability of neurons. Sodium 0-6 sodium leak channel, non-selective Homo sapiens 21-26 34356336-4 2021 Nevertheless, low-sodium-induced weight loss and sodium sparing function was similar in WT and Nox4-/- mice, disputing an important function of renal Nox4 in sodium handling. Sodium 158-164 NADPH oxidase 4 Mus musculus 150-154 33712547-0 2021 Comparative structural analysis of human Nav1.1 and Nav1.5 reveals mutational hotspots for sodium channelopathies. Sodium 91-97 sodium voltage-gated channel alpha subunit 1 Homo sapiens 41-47 33712547-1 2021 Among the nine subtypes of human voltage-gated sodium (Nav) channels, the brain and cardiac isoforms, Nav1.1 and Nav1.5, each carry more than 400 missense mutations respectively associated with epilepsy and cardiac disorders. Sodium 47-53 sodium voltage-gated channel alpha subunit 1 Homo sapiens 102-108 33570024-2 2021 Glycyrrhizin in licorice root activates the renal mineralocorticoid receptor increasing sodium reabsorption and potassium excretion. Sodium 88-94 nuclear receptor subfamily 3 group C member 2 Homo sapiens 50-76 33390050-0 2021 Thiazide-Sensitive NCC (Sodium-Chloride Cotransporter) in Human Metabolic Syndrome: Sodium Sensitivity and Potassium-Induced Natriuresis. Sodium 24-30 solute carrier family 12 member 3 Homo sapiens 19-22 33390050-0 2021 Thiazide-Sensitive NCC (Sodium-Chloride Cotransporter) in Human Metabolic Syndrome: Sodium Sensitivity and Potassium-Induced Natriuresis. Sodium 84-90 solute carrier family 12 member 3 Homo sapiens 19-22 33390050-1 2021 The thiazide-sensitive sodium-chloride cotransporter (NCC;SLC12A3) is central to sodium and blood pressure regulation. Sodium 23-29 solute carrier family 12 member 3 Homo sapiens 54-57 33390050-1 2021 The thiazide-sensitive sodium-chloride cotransporter (NCC;SLC12A3) is central to sodium and blood pressure regulation. Sodium 23-29 solute carrier family 12 member 3 Homo sapiens 58-65 33390050-2 2021 Metabolic syndrome induces NCC upregulation generating sodium-sensitive hypertension in experimental animal models. Sodium 55-61 solute carrier family 12 member 3 Homo sapiens 27-30 33460646-1 2021 Mutations in genes encoding the human brain-expressed voltage-gated sodium (NaV) channels NaV1.1, NaV1.2, and NaV1.6 are associated with a variety of human diseases including epilepsy, autism spectrum disorder, familial migraine, and other neurodevelopmental disorders. Sodium 68-74 sodium voltage-gated channel alpha subunit 1 Homo sapiens 90-96 34356336-8 2021 Our observations suggest that the control by this system is attenuated in Nox4-/- mice, resulting in lower blood pressure in response to low sodium. Sodium 141-147 NADPH oxidase 4 Mus musculus 74-78 34368091-0 2021 Conditioned Medium of Bone Marrow Mesenchymal Stem Cells Involved in Acute Lung Injury by Regulating Epithelial Sodium Channels via miR-34c. Sodium 112-118 microRNA 34c Mus musculus 132-139 34127616-7 2021 Western blots were run from testosterone treated postnatal day 7 animals to measure levels of chloride cotransporters sodium-potassium-chloride symporter (NKCC1) and chloride-potassium symporter 5 (KCC2). Sodium 118-124 solute carrier family 12 member 2 Rattus norvegicus 155-160 34195248-2 2021 It has been established that the Type IIb sodium-dependent phosphate cotransporters (NaPi-IIb) protein is the major sodium-dependent phosphate (Pi) transporter, which plays an important role in Pi uptake across the apical membrane of epithelial cells in the small intestine. Sodium 42-48 solute carrier family 34 member 2 Homo sapiens 85-93 34195248-2 2021 It has been established that the Type IIb sodium-dependent phosphate cotransporters (NaPi-IIb) protein is the major sodium-dependent phosphate (Pi) transporter, which plays an important role in Pi uptake across the apical membrane of epithelial cells in the small intestine. Sodium 116-122 solute carrier family 34 member 2 Homo sapiens 85-93 34412058-6 2021 STK-001 is an ASO that increases expression of the sodium channel gene SCN1A by exclusion of a poison exon. Sodium 51-57 sodium voltage-gated channel alpha subunit 1 Homo sapiens 71-76 33442688-2 2021 Plasmin, and other host proteases, may cleave the furin site of SARS-CoV-2 S protein and gamma subunits of epithelial sodium channels (gamma ENaC), resulting in an increment in virus infectivity and channel activity. Sodium 118-124 plasminogen Homo sapiens 0-7 33442688-2 2021 Plasmin, and other host proteases, may cleave the furin site of SARS-CoV-2 S protein and gamma subunits of epithelial sodium channels (gamma ENaC), resulting in an increment in virus infectivity and channel activity. Sodium 118-124 furin, paired basic amino acid cleaving enzyme Homo sapiens 50-55 33411788-8 2021 A similar pattern exists for the homologous sodium channel Nav1.6, encoded by Scn8a. Sodium 44-50 sodium channel, voltage-gated, type VIII, alpha Mus musculus 78-83 33414395-4 2021 We investigated the role of FAT10 in regulating the sodium channel Nav1.5, a major regulator of cardiac arrhythmias. Sodium 52-58 ubiquitin D Mus musculus 28-33 35259444-10 2022 These results suggested that uPA and plasmin are direct targets of DSS and YXHX in intervening NS sodium retention. Sodium 98-104 plasminogen activator, urokinase Rattus norvegicus 29-32 35259444-14 2022 CONCLUSION: Intervening in sodium retention by inhibiting uPA-mediated plasmin generation and plasmin activity in the kidneys could be possible mechanisms for DSS, as indicated by the results in PAN-induced nephrotic rats. Sodium 27-33 plasminogen activator, urokinase Rattus norvegicus 58-61 35588446-2 2022 However, whether CeA affects the nongenomic role of aldosterone (ALD) in regulating sodium intake at the NTS level remains unclear. Sodium 84-90 carcinoembryonic antigen gene family 4 Rattus norvegicus 17-20 33398797-10 2021 However, we identified glutamyl aminopeptidase (ENPEP), PLAU, EGF and Xaa-Pro aminopeptidase 2 precursor XPNPEP2 as key molecules of salt-sensitivity, through modulation of ENaC-dependent sodium reabsorption along the distal tubule. Sodium 188-194 glutamyl aminopeptidase Homo sapiens 23-46 33398797-10 2021 However, we identified glutamyl aminopeptidase (ENPEP), PLAU, EGF and Xaa-Pro aminopeptidase 2 precursor XPNPEP2 as key molecules of salt-sensitivity, through modulation of ENaC-dependent sodium reabsorption along the distal tubule. Sodium 188-194 X-prolyl aminopeptidase 2 Homo sapiens 70-94 33398797-10 2021 However, we identified glutamyl aminopeptidase (ENPEP), PLAU, EGF and Xaa-Pro aminopeptidase 2 precursor XPNPEP2 as key molecules of salt-sensitivity, through modulation of ENaC-dependent sodium reabsorption along the distal tubule. Sodium 188-194 X-prolyl aminopeptidase 2 Homo sapiens 105-112 32455507-7 2021 RESULTS: Uninduced nphs2Deltaipod *plg-/- mice had normal kidney function and sodium handling. Sodium 78-84 plasminogen Mus musculus 35-38 35588446-11 2022 CONCLUSION: The results verified that the complete CeA may play an important role in aldosterone to regulate the nongenomic effect on rapid sodium intake. Sodium 140-146 carcinoembryonic antigen gene family 4 Rattus norvegicus 51-54 35550517-1 2022 NALCN channel mediates sodium leak currents and is important for maintaining proper resting membrane potential. Sodium 23-29 sodium leak channel, non-selective Homo sapiens 0-5 33095056-13 2021 Sodium restriction impairs endothelial function, which is nitric oxide dependent, and increases vascular contractility in association with reduced vascular endothelial nitric oxide synthase and NOX4 expression in female mice ablating the baseline sex difference. Sodium 0-6 NADPH oxidase 4 Mus musculus 194-198 33283643-2 2021 Tenapanor is a non-binder, sodium/hydrogen exchanger isoform 3 (NHE3) inhibitor that reduces paracellular intestinal phosphate absorption. Sodium 27-33 solute carrier family 9 member A3 Rattus norvegicus 64-68 33730735-1 2021 INTRODUCTION: Sodium MRI (23Na MRI) derived biomarkers such as tissue sodium concentration (TSC) provide valuable information on cell function and brain tissue viability and has become a reliable tool for the assessment of brain tumors and ischemic stroke beyond pathoanatomical morphology. Sodium 14-20 solute carrier family 12 member 3 Rattus norvegicus 92-95 33730735-1 2021 INTRODUCTION: Sodium MRI (23Na MRI) derived biomarkers such as tissue sodium concentration (TSC) provide valuable information on cell function and brain tissue viability and has become a reliable tool for the assessment of brain tumors and ischemic stroke beyond pathoanatomical morphology. Sodium 70-76 solute carrier family 12 member 3 Rattus norvegicus 92-95 33165026-12 2021 Treatment with mitochondrial damage-associated molecular patterns decreased the expression of epithelial sodium channel alpha, zonula occludens-1, and occludin via the formyl peptide receptor-1/p38 pathway in the primary rat alveolar epithelial type II cells. Sodium 105-111 mitogen activated protein kinase 14 Rattus norvegicus 194-197 33402493-4 2021 After normalizing the signal intensity with that of the vitreous humor, relative tissue sodium concentration (rTSC) was measured after automated segmentation in the hippocampus, amygdala, basal ganglia, white matter (WM) and grey matter (GM) in both cerebral hemispheres. Sodium 88-94 solute carrier family 12 member 3 Rattus norvegicus 110-114 35514175-0 2022 Integrating Bi@C Nanospheres in Porous Hard Carbon Frameworks for Ultrafast Sodium Storage. Sodium 76-82 MIR155 host gene Homo sapiens 12-16 35509038-1 2022 BACKGROUND: Gitelman Syndrome (GS) is a hereditary tubulopathy associated with a biallelic inactivating mutations of the SLC12A3 gene encoding the thiazide-sensitive sodium-chloride cotransporter (NCCT). Sodium 166-172 solute carrier family 12 member 3 Homo sapiens 121-128 35509038-1 2022 BACKGROUND: Gitelman Syndrome (GS) is a hereditary tubulopathy associated with a biallelic inactivating mutations of the SLC12A3 gene encoding the thiazide-sensitive sodium-chloride cotransporter (NCCT). Sodium 166-172 solute carrier family 12 member 3 Homo sapiens 197-201 35503765-1 2022 Sodium-hydrogen exchangers (NHEs) tightly regulate intracellular pH (pHi), proliferation, migration and cell volume. Sodium 0-6 glucose-6-phosphate isomerase Homo sapiens 69-72 32968789-3 2020 The mechanisms by which SCN8A variants lead to epilepsy are poorly understood, although heterologous expression systems and mouse models have demonstrated altered sodium current properties. Sodium 163-169 sodium channel, voltage-gated, type VIII, alpha Mus musculus 24-29 32977294-1 2020 Dravet syndrome is an epileptic encephalopathy largely due to haploinsufficiency of the voltage-gated sodium channel Nav1.1 that is expressed primarily in GABAergic neurons. Sodium 102-108 sodium voltage-gated channel alpha subunit 1 Homo sapiens 117-123 33134290-0 2020 An SCN1B Variant Affects Both Cardiac-Type (NaV1.5) and Brain-Type (NaV1.1) Sodium Currents and Contributes to Complex Concomitant Brain and Cardiac Disorders. Sodium 76-82 sodium voltage-gated channel beta subunit 1 Homo sapiens 3-8 33134290-0 2020 An SCN1B Variant Affects Both Cardiac-Type (NaV1.5) and Brain-Type (NaV1.1) Sodium Currents and Contributes to Complex Concomitant Brain and Cardiac Disorders. Sodium 76-82 sodium voltage-gated channel alpha subunit 1 Homo sapiens 68-74 33134290-6 2020 We observed a decrease in sodium current density in cells co-expressing NaV1.5 or NaV1.1 and beta1D103V compared to beta1WT. Sodium 26-32 sodium voltage-gated channel alpha subunit 1 Homo sapiens 82-88 35398096-3 2022 We previously showed that the sodium-channel blocker carbamazepine (Carb) corrects KATP channel surface expression defects induced by PHHI-causing mutations in SUR1. Sodium 30-36 ATP binding cassette subfamily C member 8 Homo sapiens 160-164 35212221-7 2022 These findings strongly support the hypothesis that new benzo(d)isoxazole derivatives display anticonvulsant activity by selectively blocking voltage-gated sodium channel NaV1.1, which provides good alternatives for developing selective NaV1.1 channel blockers as antiseizure drugs in the future. Sodium 156-162 sodium voltage-gated channel alpha subunit 1 Homo sapiens 171-177 35074891-1 2022 BACKGROUND AND OBJECTIVES: Pathogenic variants in the neuronal sodium-channel alpha1-subunit gene (SCN1A) are the most frequent monogenic cause of epilepsy. Sodium 63-69 sodium voltage-gated channel alpha subunit 1 Homo sapiens 99-104 35110381-1 2022 ATP1A1 encodes the alpha1 subunit of the sodium-potassium ATPase, an electrogenic cation pump highly expressed in the nervous system. Sodium 41-47 dynein axonemal heavy chain 8 Homo sapiens 58-64 35329921-5 2022 For example, mutations in the CAV-3 gene promote ventricular arrhythmogenesis in long QT syndrome 9 by a combined decrease in the loss of the inward rectifier current (IK1) and gain of the late sodium current (INa-L). Sodium 194-200 caveolin 3 Homo sapiens 30-35 35359895-1 2022 Isolated hyperchloridrosis (HYCHL; OMIM 143860) is a rare autosomal recessive disorder caused by biallelic mutations in the carbonic anhydrase 12 (CA12; OMIM 603263) gene, which is characterized by abnormally high levels of salt in sweat that can lead to dehydration associated with low levels of sodium in the blood. Sodium 297-303 carbonic anhydrase 12 Homo sapiens 124-145 35359895-1 2022 Isolated hyperchloridrosis (HYCHL; OMIM 143860) is a rare autosomal recessive disorder caused by biallelic mutations in the carbonic anhydrase 12 (CA12; OMIM 603263) gene, which is characterized by abnormally high levels of salt in sweat that can lead to dehydration associated with low levels of sodium in the blood. Sodium 297-303 carbonic anhydrase 12 Homo sapiens 147-151 35359639-2 2022 Background: Dravet syndrome (DS) is a severe epileptic encephalopathy mainly caused by haploinsufficiency of the gene SCN1A, which encodes the voltage-gated sodium channel NaV1. Sodium 157-163 sodium voltage-gated channel alpha subunit 1 Homo sapiens 118-123 35256591-0 2022 mTORC1 induces plasma membrane depolarization and promotes preosteoblast senescence by regulating the sodium channel Scn1a. Sodium 102-108 CREB regulated transcription coactivator 1 Mus musculus 0-6 35234610-0 2022 NBI-921352, a first-in-class, NaV1.6 selective, sodium channel inhibitor that prevents seizures in Scn8a gain-of-function mice, and wild-type mice and rats. Sodium 48-54 neuron navigator 1 Mus musculus 30-34 32662793-0 2020 MOF-derived ultrasmall CoSe2 nanoparticles encapsulated by an N-doped carbon matrix and their superior lithium/sodium storage properties. Sodium 111-117 lysine acetyltransferase 8 Homo sapiens 0-3 35234610-1 2022 NBI-921352 (formerly XEN901) is a novel sodium channel inhibitor designed to specifically target NaV1.6 channels. Sodium 40-46 neuron navigator 1 Mus musculus 97-101 35234610-2 2022 Such a molecule provides a precision-medicine approach to target SCN8A-related epilepsy syndromes (SCN8A-RES), where gain-of-function (GoF) mutations lead to excess NaV1.6 sodium current, or other indications where NaV1.6 mediated hyper-excitability contributes to disease (Gardella and Moller, 2019; Johannesen et al., 2019; Veeramah et al., 2012). Sodium 172-178 sodium channel, voltage-gated, type VIII, alpha Mus musculus 65-70 35234610-2 2022 Such a molecule provides a precision-medicine approach to target SCN8A-related epilepsy syndromes (SCN8A-RES), where gain-of-function (GoF) mutations lead to excess NaV1.6 sodium current, or other indications where NaV1.6 mediated hyper-excitability contributes to disease (Gardella and Moller, 2019; Johannesen et al., 2019; Veeramah et al., 2012). Sodium 172-178 sodium channel, voltage-gated, type VIII, alpha Mus musculus 99-104 35234610-2 2022 Such a molecule provides a precision-medicine approach to target SCN8A-related epilepsy syndromes (SCN8A-RES), where gain-of-function (GoF) mutations lead to excess NaV1.6 sodium current, or other indications where NaV1.6 mediated hyper-excitability contributes to disease (Gardella and Moller, 2019; Johannesen et al., 2019; Veeramah et al., 2012). Sodium 172-178 sodium channel, voltage-gated, type VIII, alpha Mus musculus 165-171 34714114-0 2022 Renal NOXA1/NOX1 Signaling Regulates Epithelial Sodium Channel and Sodium Retention in Angiotensin II-induced Hypertension. Sodium 48-54 NADPH oxidase activator 1 Mus musculus 6-11 32538148-0 2020 An acute rise of plasma sodium concentration associates with syndecan-1 shedding during hemodialysis. Sodium 24-30 syndecan 1 Homo sapiens 61-71 32538148-3 2020 As sodium is a trigger for glycocalyx shedding, we now tested whether hemodialysis with higher dialysate sodium concentrations is associated with more syndecan-1 shedding compared with standard hemodialysis (SHD). Sodium 105-111 syndecan 1 Homo sapiens 151-161 32538148-4 2020 In this cross-over study in 29 patients, plasma syndecan-1 was repeatedly measured during SHD and during Hemocontrol hemodialysis (HHD) which is characterized by initially higher dialysate and plasma sodium levels. Sodium 200-206 syndecan 1 Homo sapiens 48-58 32538148-11 2020 Lower predialysis plasma sodium and osmolality were associated with greater intradialytic increases in syndecan-1 levels (both groups P=0.001). Sodium 25-31 syndecan 1 Homo sapiens 103-113 34714114-0 2022 Renal NOXA1/NOX1 Signaling Regulates Epithelial Sodium Channel and Sodium Retention in Angiotensin II-induced Hypertension. Sodium 48-54 NADPH oxidase 1 Mus musculus 12-16 32538148-12 2020 The rise in plasma syndecan-1 levels was more pronounced and occurred earlier during hemodialysis with higher plasma sodium levels. Sodium 117-123 syndecan 1 Homo sapiens 19-29 32538148-13 2020 Although we cannot proof that the rise in plasma syndecan-1 originates from the endothelial glycocalyx, our findings are compatible with sodium-driven endothelial glycocalyx-derived syndecan-1 shedding. Sodium 137-143 syndecan 1 Homo sapiens 182-192 34714114-0 2022 Renal NOXA1/NOX1 Signaling Regulates Epithelial Sodium Channel and Sodium Retention in Angiotensin II-induced Hypertension. Sodium 67-73 NADPH oxidase activator 1 Mus musculus 6-11 32387413-7 2020 SIGNIFICANCE: These results suggest that the depletion of SLC14alpha1 gene in mice may contribute to the HS-induced abnormality of sodium transportation in the CSF, and lead to the elevation of MAP, which eventually promote the development of salt-sensitive hypertension. Sodium 131-137 solute carrier family 14 (urea transporter), member 1 Mus musculus 58-69 32311027-1 2020 CONTEXT: Hypophosphatemia and metabolic bone disease are associated with Hereditary Hypophosphatemic Rickets with Hypercalciuria (HHRH) due to biallelic mutations of SLC34A3 encoding the NPT2C sodium-phosphate cotransporter and Nephrolithiasis/osteoporosis, hypophosphatemic 1 (NPHLOP1) due to monoallelic mutations in SLC34A1 encoding the NPT2A sodium-phosphate cotransporter. Sodium 193-199 solute carrier family 34 member 1 Homo sapiens 319-326 32311027-1 2020 CONTEXT: Hypophosphatemia and metabolic bone disease are associated with Hereditary Hypophosphatemic Rickets with Hypercalciuria (HHRH) due to biallelic mutations of SLC34A3 encoding the NPT2C sodium-phosphate cotransporter and Nephrolithiasis/osteoporosis, hypophosphatemic 1 (NPHLOP1) due to monoallelic mutations in SLC34A1 encoding the NPT2A sodium-phosphate cotransporter. Sodium 346-352 solute carrier family 34 member 1 Homo sapiens 319-326 32671946-1 2020 The voltage-gated sodium (Nav) channel complex is comprised of pore-forming alpha subunits (Nav1.1-1.9) and accessory regulatory proteins such as the intracellular fibroblast growth factor 14 (FGF14). Sodium 18-24 fibroblast growth factor 14 Homo sapiens 164-191 32671946-1 2020 The voltage-gated sodium (Nav) channel complex is comprised of pore-forming alpha subunits (Nav1.1-1.9) and accessory regulatory proteins such as the intracellular fibroblast growth factor 14 (FGF14). Sodium 18-24 fibroblast growth factor 14 Homo sapiens 193-198 34714114-0 2022 Renal NOXA1/NOX1 Signaling Regulates Epithelial Sodium Channel and Sodium Retention in Angiotensin II-induced Hypertension. Sodium 67-73 NADPH oxidase 1 Mus musculus 12-16 35264044-4 2022 GnRHR was activated in cultured MDA-MB-231 and MDA-MB-468 cells by leuprolide acetate and antagonized by elagolix sodium. Sodium 114-120 gonadotropin releasing hormone receptor Homo sapiens 0-5 32387285-5 2020 We employed whole-cell patch-clamp electrophysiology to measure sodium currents in HEK-293 cells stably expressing Nav1.6 channels and intrinsic excitability of MSNs in the brain slice preparation. Sodium 64-70 neuron navigator 1 Homo sapiens 115-119 35163352-8 2022 Cultured lymphatic endothelial cells (LECs) were used to assess direct sodium effects on NKCC1. Sodium 71-77 solute carrier family 12 member 2 Rattus norvegicus 89-94 35163352-12 2022 In LECs, high sodium reduced phosphorylated NKCC1 and SPAK, an upstream activating kinase of NKCC1, and eNOS, a downstream effector of lymphatic contractility. Sodium 14-20 solute carrier family 12 member 2 Rattus norvegicus 44-49 35163352-14 2022 High sodium within the renal interstitium following proteinuric injury is associated with impaired renal lymphatic pumping that may, in part, involve the SPAK-NKCC1-eNOS pathway, which may contribute to sodium retention and reduce lymphatic responsiveness to furosemide. Sodium 5-11 solute carrier family 12 member 2 Rattus norvegicus 159-164 35163352-14 2022 High sodium within the renal interstitium following proteinuric injury is associated with impaired renal lymphatic pumping that may, in part, involve the SPAK-NKCC1-eNOS pathway, which may contribute to sodium retention and reduce lymphatic responsiveness to furosemide. Sodium 203-209 solute carrier family 12 member 2 Rattus norvegicus 159-164 35118146-0 2021 Fibroblast Growth Factor 1 Reduces Pulmonary Vein and Atrium Arrhythmogenesis via Modification of Oxidative Stress and Sodium/Calcium Homeostasis. Sodium 119-125 fibroblast growth factor 1 Oryctolagus cuniculus 0-26 32581296-1 2020 Mutations in the voltage-gated sodium channel Nav1.1 (SCN1A) are linked to various epileptic phenotypes with different severities, however, the consequences of newly identified SCN1A variants on patient phenotype is uncertain so far. Sodium 31-37 sodium voltage-gated channel alpha subunit 1 Homo sapiens 46-52 32581296-1 2020 Mutations in the voltage-gated sodium channel Nav1.1 (SCN1A) are linked to various epileptic phenotypes with different severities, however, the consequences of newly identified SCN1A variants on patient phenotype is uncertain so far. Sodium 31-37 sodium voltage-gated channel alpha subunit 1 Homo sapiens 54-59 32581296-1 2020 Mutations in the voltage-gated sodium channel Nav1.1 (SCN1A) are linked to various epileptic phenotypes with different severities, however, the consequences of newly identified SCN1A variants on patient phenotype is uncertain so far. Sodium 31-37 sodium voltage-gated channel alpha subunit 1 Homo sapiens 177-182 35062349-11 2022 A whole-cell patch-clamp analysis suggested that HERV-W ENV enhanced sodium influx through DRD2. Sodium 69-75 dopamine receptor D2 Homo sapiens 91-95 35023666-12 2022 CONCLUSION: Our findings indicate that apelin is involved in the fine regulation of sodium balance in the renal collecting duct by opposing the effects of aldosterone, likely by activation of ENaC ubiquitination. Sodium 84-90 apelin Mus musculus 39-45 34982741-8 2022 The first SNP, rs77149046, located in the endosome-lysosome associated apoptosis and autophagy regulator family member 2 (ELAPOR2) gene, conferred an HR of 5.40 (CI, 3.23-9.02; p = 1.32x10-10), followed by 4 SNPs within the region coding for sodium-dependent taurine and beta-alanine transporter (SLC6A6), with HRs ranging from 3.35 to 3.43. Sodium 242-248 solute carrier family 6 member 6 Homo sapiens 297-303 35466629-11 2022 CONCLUSIONS: Serum visfatin significantly decreased the sodium and chloride levels whereas the levels of potassium remained unaffected. Sodium 56-62 nicotinamide phosphoribosyltransferase Homo sapiens 19-27 2812277-2 1989 After 2 weeks of sodium deprivation, the peripheral angiotensin system was activated as shown by increased plasma renin activity (4-fold) and plasma aldosterone concentration (approximately 40-fold). Sodium 17-23 renin Rattus norvegicus 114-119 2733594-4 1989 Signal intensities after addition of small quantities of K+ and Mg2+ to the hemolysates were significantly larger than that expected from dilution of the sample, implying that the additions have resulted in the release of formerly invisible sodium. Sodium 241-247 mucin 7, secreted Homo sapiens 64-67 2651649-0 1989 Endogenous adenosine restrains renin release during sodium restriction. Sodium 52-58 renin Rattus norvegicus 31-36 2651649-1 1989 The purpose of this study was to determine the role of endogenous adenosine in controlling renin release during both a normal and low sodium diet. Sodium 134-140 renin Rattus norvegicus 91-96 2651649-4 1989 DPSPX significantly increased arterial and renal venous levels of renin in both groups of animals; however, statistical analysis of the data (2-factor analysis of variance) indicated that DPSPX increased aortic and renal venous levels of renin more in rats fed a low sodium diet compared to rats fed a normal sodium diet. Sodium 267-273 renin Rattus norvegicus 238-243 2651649-4 1989 DPSPX significantly increased arterial and renal venous levels of renin in both groups of animals; however, statistical analysis of the data (2-factor analysis of variance) indicated that DPSPX increased aortic and renal venous levels of renin more in rats fed a low sodium diet compared to rats fed a normal sodium diet. Sodium 309-315 renin Rattus norvegicus 238-243 2649097-3 1989 In response to sodium depletion and captopril treatment, the expression of mRNAs encoding rat renin were in a tissue-specific manner. Sodium 15-21 renin Rattus norvegicus 94-99 2649097-4 1989 The level of kidney renin mRNA remarkably increased in sodium-depleted rats treated with captopril, whereas that of brain renin mRNA definitely decreased. Sodium 55-61 renin Rattus norvegicus 20-25 2691126-3 1989 Its intensity and duration are dose-dependent; they are increased in the presence of stimulation of the renin-angiotensin system (renovascular hypertension, sodium depletion). Sodium 157-163 renin Rattus norvegicus 104-109 32164457-8 2020 SIRT1 and AMPK also act on sodium transport mechanisms to reduce intracellular sodium concentrations. Sodium 27-33 protein kinase AMP-activated catalytic subunit alpha 2 Homo sapiens 10-14 32164457-8 2020 SIRT1 and AMPK also act on sodium transport mechanisms to reduce intracellular sodium concentrations. Sodium 79-85 protein kinase AMP-activated catalytic subunit alpha 2 Homo sapiens 10-14 2692881-2 1989 In comparison with normal pregnant women and normal non-pregnant women, women with PIH showed an increase in heart rate, suggesting an increased peripheral sympathetic tone, and an initial derangement in renal function as shown by the increase in serum uric acid and reduction in sodium excretion and total and fractional calcium excretion at any given level of sodium excretion. Sodium 280-286 pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included) Homo sapiens 83-86 2692881-2 1989 In comparison with normal pregnant women and normal non-pregnant women, women with PIH showed an increase in heart rate, suggesting an increased peripheral sympathetic tone, and an initial derangement in renal function as shown by the increase in serum uric acid and reduction in sodium excretion and total and fractional calcium excretion at any given level of sodium excretion. Sodium 362-368 pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included) Homo sapiens 83-86 32529312-5 2020 Recent research has proposed that decreased TCF4 expression can lead to the increased translation of the sodium channel Nav1.8. Sodium 105-111 transcription factor 4 Homo sapiens 44-48 2692882-2 1989 The levels of, and responses of, renal renin and renal renin mRNA to sodium deficient diet and to sodium deficient diet plus Captopril treatment were compared in S and R rats. Sodium 69-75 renin Rattus norvegicus 55-60 32521252-0 2020 Dynamic Palmitoylation of the Sodium-Calcium Exchanger Modulates Its Structure, Affinity for Lipid-Ordered Domains, and Inhibition by XIP. Sodium 30-36 late endosomal/lysosomal adaptor, MAPK and MTOR activator 5 Homo sapiens 134-137 2692882-4 1989 Sodium deficient diet caused a modest increase, and sodium deficient diet plus Captopril caused a very large increase in both renal renin and renal renin mRNA in both strains. Sodium 52-58 renin Rattus norvegicus 132-137 2692882-4 1989 Sodium deficient diet caused a modest increase, and sodium deficient diet plus Captopril caused a very large increase in both renal renin and renal renin mRNA in both strains. Sodium 52-58 renin Rattus norvegicus 148-153 31578830-3 2020 Here, we found that TXNIP expression induced by sodium butyrate (NaBu) was TRAF6-dependent. Sodium 65-69 LOC222344 Homo sapiens 75-80 31578830-6 2020 NaBu reinforced the interaction of TRAF6/TXNIP as well as TXNIP" polyubiquitylation. Sodium 0-4 LOC222344 Homo sapiens 35-40 20504460-1 1989 Sodium- and energy-dependent accumulation of [(3)H]l-glutamic acid (Glu) into rat cerebral cortical slices was inhibited by relatively high concentrations (40-100 ?M) of calmodulin antagonists, such as N-(6-aminohexyl)-1-naphthalenesulfonamide and N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide, in concentration-dependent and noncompetitive manners. Sodium 0-6 calmodulin 1 Rattus norvegicus 170-180 31578830-7 2020 Moreover, treated with NaBu, the A549 cells with TRAF6/TXNIP double knockdown showed an enhanced protein expression of E-cadherin comparing to cells with single gene or negative knockdown. Sodium 23-27 LOC222344 Homo sapiens 49-54 31578830-10 2020 Our results revealed TRAF6 regulated the expression and polyubiquitylation of TXNIP in a NaBu-dependent manner, alleviating tumorigenesis of TRAF6. Sodium 89-93 LOC222344 Homo sapiens 21-26 31578830-10 2020 Our results revealed TRAF6 regulated the expression and polyubiquitylation of TXNIP in a NaBu-dependent manner, alleviating tumorigenesis of TRAF6. Sodium 89-93 LOC222344 Homo sapiens 141-146 2976957-0 1988 Atrial natriuretic peptide inhibits water and sodium intake in rabbits. Sodium 46-52 natriuretic peptides A Oryctolagus cuniculus 0-26 31916329-10 2020 Enhanced AMPK/SIRT1 signaling may also contribute to the action of SGLT2 inhibitors to interfere with sodium transport mechanisms. Sodium 102-108 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 9-13 3174385-3 1988 (3) pHi-Recovery after an acute intracellular acid load (by means of NH4Cl-prepulse) was reversibly blocked by 1 mM amiloride and was dependent on the presence of sodium. Sodium 163-169 glucose-6-phosphate isomerase Homo sapiens 4-7 32154868-0 2020 mTORC1 Deficiency Modifies Volume Homeostatic Responses to Dietary Sodium in a Sex-Specific Manner. Sodium 67-73 CREB regulated transcription coactivator 1 Mus musculus 0-6 32154868-2 2020 Dietary sodium can upregulate mTORC1 signaling in cardiac and renal tissue, and inhibition of mTOR can prevent aldosterone associated, salt-induced hypertension. Sodium 8-14 CREB regulated transcription coactivator 1 Mus musculus 30-36 31904424-2 2020 In the heart, the protein CASK (Calcium/CAlmodulin-dependent Serine protein Kinase) negatively regulates the main cardiac sodium channel, NaV1.5, which carries the sodium current (INa) by preventing its anterograde trafficking. Sodium 164-170 calcium/calmodulin dependent serine protein kinase Homo sapiens 26-30 31904424-2 2020 In the heart, the protein CASK (Calcium/CAlmodulin-dependent Serine protein Kinase) negatively regulates the main cardiac sodium channel, NaV1.5, which carries the sodium current (INa) by preventing its anterograde trafficking. Sodium 164-170 calcium/calmodulin dependent serine protein kinase Homo sapiens 32-82 32752588-0 2020 PI3K/Akt and ERK1/2 pathways are responsible for sodium butyrateinduced inhibition of neuronal apoptosis in rats with cerebral infarction. Sodium 49-55 mitogen activated protein kinase 3 Rattus norvegicus 13-19 31420581-10 2020 Sodium to potassium ratio was positively associated with SBP (P10-P50, P80) and DBP (P70-P90) in males, and was positively associated with SBP(P10-P70, P90) in females. Sodium 0-6 coilin Homo sapiens 71-74 32006563-7 2020 SAM/NaHS significantly increased the number of surviving cells, whereas CaM weakened the protection induced by SAM/NaHS. Sodium 115-119 calcium/calmodulin dependent protein kinase II gamma Homo sapiens 72-75 32006563-10 2020 Co-Immunoprecipitation and immunoblotting were conducted to demonstrate that SAM/NaHS suppressed the assembly of CaMKII with the ASK1-MKK3-p38 signal module after cerebral I/R, which decreased the phosphorylation of p38. Sodium 81-85 calcium/calmodulin dependent protein kinase II gamma Homo sapiens 113-119 32006563-11 2020 In contrast, CaM significantly inhibited the effects of SAM/NaHS. Sodium 60-64 calcium/calmodulin dependent protein kinase II gamma Homo sapiens 13-16 32006563-12 2020 Taken together, the results suggested that SAM/NaHS could suppress cerebral I/R injury by downregulating p38 phosphorylation via decreasing the assembly of CaMKII with the ASK1-MKK3-p38 signal module. Sodium 47-51 calcium/calmodulin dependent protein kinase II gamma Homo sapiens 156-162 32232280-7 2020 The enhanced Li+ diffusion kinetics in the 3D interconnected network endows CGN with better rate performance than GNS as lithium-ion battery anode material, and Na+ adsorption dominates the Na+ storage in CGN as sodium-ion battery anode material. Sodium 212-218 cingulin Homo sapiens 205-208 32290310-8 2020 To date, this study is the most comprehensive investigation conducted to determine if the TRPV1-rs8065080 genotype relates to sodium intake and health markers influenced by sodium intake. Sodium 126-132 transient receptor potential cation channel subfamily V member 1 Homo sapiens 90-95 32290310-8 2020 To date, this study is the most comprehensive investigation conducted to determine if the TRPV1-rs8065080 genotype relates to sodium intake and health markers influenced by sodium intake. Sodium 173-179 transient receptor potential cation channel subfamily V member 1 Homo sapiens 90-95 32290310-10 2020 In addition to further research across other ages and cultures, the TRPV1-rs8065080 genotype may interact with other ion channels, and so further studies are required to determine if polymorphic variations influence sodium intake, diet and health. Sodium 216-222 transient receptor potential cation channel subfamily V member 1 Homo sapiens 68-73 32213629-2 2020 A high-salt diet (HSD) can stimulate immunity through the nuclear factor of activated T cells 5 (Nfat5)-signaling pathway, especially in the skin, where sodium is stored. Sodium 153-159 nuclear factor of activated T cells 5 Homo sapiens 58-95 32213629-2 2020 A high-salt diet (HSD) can stimulate immunity through the nuclear factor of activated T cells 5 (Nfat5)-signaling pathway, especially in the skin, where sodium is stored. Sodium 153-159 nuclear factor of activated T cells 5 Homo sapiens 97-102 3174385-4 1988 The velocity of pHi recovery increased with increasing sodium concentrations with an apparent Km for external sodium of about 30 mM and a Vmax of about 0.35 pH units/min. Sodium 55-61 glucose-6-phosphate isomerase Homo sapiens 16-19 3174385-4 1988 The velocity of pHi recovery increased with increasing sodium concentrations with an apparent Km for external sodium of about 30 mM and a Vmax of about 0.35 pH units/min. Sodium 110-116 glucose-6-phosphate isomerase Homo sapiens 16-19 3260077-9 1988 These data indicate that macrophages, via IL 1 secretion, are capable of modulation of sodium-linked solute transport in proximal tubular epithelium. Sodium 87-93 interleukin 1 complex Mus musculus 42-46 2450203-4 1988 The limitation of SRF was accompanied by use- and voltage-dependent reduction of maximal rate of rise (Vmax) of sodium-dependent action potentials. Sodium 112-118 serum response factor Mus musculus 18-21 31950564-2 2020 The beta3-subunit (encoded by the SCN3B gene) is an important physiological regulator of the heart-specific sodium channel, Nav1.5. Sodium 108-114 sodium voltage-gated channel beta subunit 3 Homo sapiens 34-39 32115039-0 2020 Compensation of high-pressure processing for the solubility of sodium-reduced chicken breast myosin with three anion types of potassium salts. Sodium 63-69 myosin, heavy chain 7B, cardiac muscle, beta Gallus gallus 93-99 31831582-1 2020 BACKGROUND: Pulmonary alveolar microlithiasis (PAM) is caused by genetic variants in the SLC34A2 gene, which encodes the sodium-dependent phosphate transport protein 2B. Sodium 121-127 solute carrier family 34 member 2 Homo sapiens 89-96 31977198-4 2020 Using mild oxidants, such as [CoCp2][PF6] or [FeCp2][Al{OC(CF3)3}4], yields the discrete salts [1][A] (A = PF6-, Al{OC(CF3)3}4-), whereas the anion exchange of [1][PF6] with NaBPh4 yields [1][BPh4]. Sodium 174-180 sperm associated antigen 17 Homo sapiens 37-40 2962940-5 1988 Atrial natriuretic peptide also elicited a significant increment in urine volume and urinary sodium excretion, while nifedipine was devoid of any significant effects on renal hemodynamics and renal excretory function during the experimental period. Sodium 93-99 natriuretic peptides A Oryctolagus cuniculus 0-26 31734346-12 2020 Na2S2O3 significantly attenuated shock-induced impairment of lung mechanics and gas exchange (plateau and positive end-expiratory pressure at 72 hours p = 0.0006/p = 0.0264; Horovitz index at 48 hours p = 0.0261), which coincided with a higher tissue GCR expression (p = 0.0415). Sodium 0-7 nuclear receptor subfamily 3 group C member 1 Sus scrofa 251-254 31734346-13 2020 During resuscitation from hemorrhagic shock Na2S2O3 attenuated shock-induced acute lung injury in co-morbid swine, most likely due to a GCR expression related mechanism. Sodium 44-51 nuclear receptor subfamily 3 group C member 1 Sus scrofa 136-139 31704583-7 2020 Mechanistically, NaHS upregulated SIRT1 expression, but inhibited activation of TGF-beta1/Smad3 signaling in vivo and in vitro. Sodium 17-21 SMAD family member 3 Homo sapiens 90-95 3166114-5 1988 The NRC group was the only one able to increase the urinary excretion of kallikrein in response to the sodium load. Sodium 103-109 nuclear receptor coactivator 6 Rattus norvegicus 4-7 31908951-1 2020 Introduction: Hartnup disorder is caused by a deficiency of the sodium dependent B0 AT1 neutral amino acid transporter in the proximal kidney tubules and jejunum. Sodium 64-70 solute carrier family 6 member 19 Homo sapiens 81-87 31864286-6 2019 On the contrary, the blockade of sodium pump or Na+/Ca+ exchanger during hypoxia-ischemia may cause further intracellular sodium accumulation and consequent osmotic cell death. Sodium 122-128 nascent polypeptide-associated complex alpha polypeptide Mus musculus 48-54 31799617-11 2019 These studies revealed that the knockout of Kcnj16 markedly altered RAAS regulation and function, suggesting Kir5.1 as a key regulator of the RAAS, particularly when exposed to changes in dietary sodium and potassium content. Sodium 196-202 potassium inwardly-rectifying channel, subfamily J, member 16 Rattus norvegicus 44-50 31799617-11 2019 These studies revealed that the knockout of Kcnj16 markedly altered RAAS regulation and function, suggesting Kir5.1 as a key regulator of the RAAS, particularly when exposed to changes in dietary sodium and potassium content. Sodium 196-202 potassium inwardly-rectifying channel, subfamily J, member 16 Rattus norvegicus 109-115 31933626-6 2019 Using Western blot studies and high-resolution confocal microscopy in the prefrontal frontal cortex (PFC), our data indicate disrupted expression of different isoforms of the voltage-gated sodium channels (NaV) at the AIS, whereas other components of AIS such as ankyrin-G and fibroblast growth factor 14 (FGF14) and contactin-associated protein 1 (Caspr) in BTBR were comparable to those in wild-type control mice. Sodium 189-195 contactin associated protein-like 1 Mus musculus 317-347 31510893-7 2019 The function of the sodium hydrogen exchanger (NHE) and sodium calcium exchanger (NCX) are driven by sodium gradients. Sodium 20-26 solute carrier family 9 member C1 Homo sapiens 47-50 31653700-0 2019 The KDEL receptor has a role in the biogenesis and trafficking of the epithelial sodium channel (ENaC). Sodium 81-87 KDEL endoplasmic reticulum protein retention receptor 1 Homo sapiens 4-17 31509436-16 2019 Nod2 deficiency functionally impairs adaptation to short bowel syndrome via a lesser increase of epithelial sodium pore permeability, altered epithelial barrier function, and the microbiome.NEW & NOTEWORTHY NOD2 gene mutations are associated with the development of severe short bowel syndrome and intestinal failure. Sodium 108-114 nucleotide-binding oligomerization domain containing 2 Mus musculus 0-4 3690353-9 1987 Circadian rhythms, stress and dietary sodium were utilized in this study to induce physiological variations in serum ALD and CORT. Sodium 38-44 cortistatin Rattus norvegicus 125-129 3311989-7 1987 Serum renin activity was lower in SHR than in WKY following acute decreases in serum sodium at 8 weeks, but it was the same for both strains at 18 weeks. Sodium 85-91 renin Rattus norvegicus 6-11 2442134-10 1987 I report here that cells grown under conditions in which sodium ATPase is not induced can still expel sodium ions. Sodium 57-63 ATPase Enterococcus faecalis 64-70 2442134-18 1987 I propose that streptococci have two independent systems for sodium extrusion: an inducible sodium ATPase and a constitutive sodium/proton antiporter. Sodium 61-67 ATPase Enterococcus faecalis 99-105 2886872-5 1987 Less severe sodium restriction (17 mumol Na/g) resulted in a reduction in hypertension development when initiated at 2, 4, and 7 weeks of age, but not at 10 weeks of age. Sodium 12-18 sodium voltage-gated channel alpha subunit 7 Rattus norvegicus 41-45 3300372-8 1987 They also suggest that the serotonergic pathway does mediate the increases in renin secretion produced by immobilization, head-up tilt, and a low-sodium diet. Sodium 146-152 renin Rattus norvegicus 78-83 2948755-4 1987 During sodium depletion, the rise in plasma renin activity which determines an increment in the circulating concentration of angiotensin II was accompanied by a rise in aldosterone secretion as expected. Sodium 7-13 renin Rattus norvegicus 44-49 2948755-7 1987 Since the increase in plasma aldosterone levels in sodium-depleted rats is mainly dependent on the activation of the renin-angiotensin system, we conclude that ANP may modulate the effect of endogenous as well as exogenous angiotensin II on plasma aldosterone secretion. Sodium 51-57 renin Rattus norvegicus 117-122 3465434-6 1986 Like promyelocyte inhibitin, H.Ep2 inhibitin reduced sodium efflux and influx by equivalent amounts suggesting thereby that it is a sodium/sodium exchange inhibitor. Sodium 53-59 prostaglandin E receptor 2 Homo sapiens 31-34 31162688-4 2019 Here, we review the evidence of PACAP-dependent modulation of calcium- and voltage-gated potassium currents, hyperpolarization-activated cation currents, calcium currents, and voltage-gated sodium currents. Sodium 190-196 adenylate cyclase activating polypeptide 1 Homo sapiens 32-37 31550081-1 2019 SnS2 has been widely studied as an anode material for sodium-ion batteries (SIBs) based on the high theoretical capacity and layered structure. Sodium 54-60 sodium voltage-gated channel alpha subunit 11 Homo sapiens 0-4 31188746-2 2019 Recently, also defects in the SLC34A1 gene, encoding for the renal sodium-phosphate transporter NaPi-IIa, were associated with the disease. Sodium 67-73 solute carrier family 34 member 1 Homo sapiens 30-37 31188746-2 2019 Recently, also defects in the SLC34A1 gene, encoding for the renal sodium-phosphate transporter NaPi-IIa, were associated with the disease. Sodium 67-73 solute carrier family 34 member 1 Homo sapiens 96-104 31708756-8 2019 Furthermore, NaHS recovered autophagic flux in the hippocampus of B2M-exposed rats, as evidenced by decreases in the ratio of autophagosome to autolysosome and the expression of p62 protein in the hippocampus. Sodium 13-17 KH RNA binding domain containing, signal transduction associated 1 Rattus norvegicus 178-181 31663064-0 2019 Ghrelin-Induced Sodium Reabsorption Is Mediated by PKA and Microtubule-Dependent alphaENaC Translocation in Female Rats. Sodium 16-22 ghrelin and obestatin prepropeptide Rattus norvegicus 0-7 31663064-1 2019 Intrarenal ghrelin infusion activates ghrelin receptors in the kidney collecting duct (CD) to increase alpha epithelial sodium (Na+) channel (alphaENaC)-dependent Na+ reabsorption in vivo, but the underlying mechanisms are unknown. Sodium 120-126 ghrelin and obestatin prepropeptide Rattus norvegicus 11-18 31663064-1 2019 Intrarenal ghrelin infusion activates ghrelin receptors in the kidney collecting duct (CD) to increase alpha epithelial sodium (Na+) channel (alphaENaC)-dependent Na+ reabsorption in vivo, but the underlying mechanisms are unknown. Sodium 120-126 ghrelin and obestatin prepropeptide Rattus norvegicus 38-45 31166814-2 2019 LRRK2 facilitates calcium extrusion exchanger and sodium-calcium exchanger activity and hence influences intracellular Ca2+ concentration in dendritic cells (DCs). Sodium 50-56 leucine-rich repeat kinase 2 Mus musculus 0-5 31469828-4 2019 We simulate the blockade of a persistent sodium current (INaP), proposed to underlie rhythm generation in pre-Botzinger complex (pre-BotC) respiratory neurons, via two distinct pharmacological mechanisms: (1) pore obstruction mediated by tetrodotoxin and (2) altered inactivation dynamics mediated by riluzole. Sodium 41-47 NFKB inhibitor zeta Homo sapiens 57-61 3039090-1 1986 In 24 normotensive male volunteers (age 20-25 years) reduction of sodium intake from 200 to 50 mmol/day over 2 weeks resulted in a 14% fall of alpha 2-adrenoceptors of platelets from 209.5 to 179.4 fmol/mg (P less than 0.01) and in a 16% rise of beta 2-adrenoceptors of lymphocytes from 13.3 to 16.2 fmol/mg (P less than 0.05) which was reversible by 2 weeks of high sodium intake. Sodium 66-72 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 246-252 2874562-8 1986 The accumulation of Ca2+ is decreased by sodium ions and totally inhibited by monensin. Sodium 41-47 carbonic anhydrase 2 Bos taurus 20-23 3717543-11 1986 From the literature it is known that beta 2-mimetics can aggravate the increased water and sodium retention during pregnancy and cause pulmonary edema by an additional increase in pulmonary artery pressure. Sodium 91-97 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 37-43 3009208-2 1986 Basal levels of plasma renin activity of both types of hypertensive rats were suppressed by sodium loading. Sodium 92-98 renin Rattus norvegicus 23-28 3511734-4 1986 Plasma renin activity (PRA) was elevated fourfold after 6 wk of sodium restriction and was unchanged by renal denervation. Sodium 64-70 renin Rattus norvegicus 7-12 3532691-0 1986 Renin-angiotensin system and renal excretory function under conditions of hypovolemia and limited sodium intake. Sodium 98-104 renin Rattus norvegicus 0-5 3766163-4 1986 After sodium depletion significant activation of renin-angiotensin-aldosterone system and insignificantly increased kallikrein excretion without changes in prostaglandin excretion and plasma vasopressin were found. Sodium 6-12 renin Rattus norvegicus 49-54 3913755-8 1985 Afferent and efferent renal nerve activity appear to be closely related since recent experiments by our group have provided further evidence of the existence of neural renorenal reflexes by which one kidney exerts a tonic inhibitory effect on the release of renin from juxtaglomerular cells and on tubular sodium and water reabsorption of the contralateral kidney. Sodium 306-312 renin Rattus norvegicus 258-263 3908312-5 1985 After 15 days of sodium depletion and captopril treatment, plasma renin concentration increased 46-fold, renal renin concentration only 1.5-fold, and renin mRNA content increased about threefold. Sodium 17-23 renin Rattus norvegicus 66-71 2857853-2 1985 Fat mass is calculated by subtracting daily fluid (calculated from sodium and potassium balances) and protein mass changes from daily weight changes. Sodium 67-73 FAT atypical cadherin 1 Homo sapiens 0-3 30821358-3 2019 The voltage-gated cardiac sodium channel complex is responsible for the generation and conduction of the cardiac action potential, and composed of the main pore-forming alpha-subunit Nav 1.5 (encoded by the SCN5A gene) and one or more auxiliary beta-subunits, including Nav beta1 to Nav beta4 encoded by SCN1B to SCN4B, respectively. Sodium 26-32 sodium voltage-gated channel beta subunit 1 Homo sapiens 304-309 30895530-0 2019 Role of the putative PKC phosphorylation sites of the type IIc sodium-dependent phosphate transporter in parathyroid hormone regulation. Sodium 63-69 parathyroid hormone Mus musculus 105-124 3893559-16 1985 The amino acids that induce ornithine decarboxylase as well as those that promote polyamine uptake utilize the sodium dependent A and N transport systems. Sodium 111-117 ornithine decarboxylase 1 Homo sapiens 28-51 31012184-4 2019 Increasing sodium level improved feed conversion ratio (FCR) linearly and quadratically. Sodium 11-17 FCR Gallus gallus 56-59 2857711-11 1985 (ii) KtrII and the Na+-ATPase are induced in parallel when cells are grown on media rich in sodium, particularly under conditions that limit the generation of a proton potential. Sodium 92-98 ATPase Enterococcus faecalis 23-29 30997950-0 2019 Surface-Confined SnS2 @C@rGO as High-Performance Anode Materials for Sodium- and Potassium-Ion Batteries. Sodium 69-75 sodium voltage-gated channel alpha subunit 11 Homo sapiens 17-21 31230006-4 2019 Plasmin may activate the epithelial sodium channel and cause impaired sodium excretion and contribute to hypertension. Sodium 36-42 plasminogen Homo sapiens 0-7 2982285-1 1985 Parathyroid hormone (PTH) and cAMP inhibit sodium, water, and bicarbonate reabsorption in the proximal tubule. Sodium 43-49 parathyroid hormone Oryctolagus cuniculus 0-19 31002656-11 2019 Consistent with these assertions, Vitamin C is known to be highly concentrated within mitochondria, by a specific transporter, namely SVCT2, in a sodium-coupled manner. Sodium 146-152 solute carrier family 23 member 2 Homo sapiens 134-139 31069052-6 2019 Among emerging treatment options currently under clinical investigation are local botulinum neurotoxin type A injections and a novel sodium channel blocker (CNV1014802) that selectively blocks the Na v1.7 sodium channel. Sodium 133-139 immunoglobulin lambda variable 2-23 Homo sapiens 200-204 2982285-1 1985 Parathyroid hormone (PTH) and cAMP inhibit sodium, water, and bicarbonate reabsorption in the proximal tubule. Sodium 43-49 parathyroid hormone Oryctolagus cuniculus 21-24 31069052-6 2019 Among emerging treatment options currently under clinical investigation are local botulinum neurotoxin type A injections and a novel sodium channel blocker (CNV1014802) that selectively blocks the Na v1.7 sodium channel. Sodium 205-211 immunoglobulin lambda variable 2-23 Homo sapiens 200-204 6100750-0 1984 Altered active sodium and calcium transport by heart sarcolemmal membranes from young spontaneously hypertensive rats: modulation by calmodulin. Sodium 15-21 calmodulin 1 Rattus norvegicus 133-143 6328982-4 1984 The relationship between sodium homeostasis and the renin-angiotensin system was assessed through the use of captopril in the rat. Sodium 25-31 renin Rattus norvegicus 52-57 6328982-8 1984 They suggest that the renin-angiotensin system is probably indispensable in preventing sodium loss when dietary sodium is suppressed. Sodium 87-93 renin Rattus norvegicus 22-27 6328982-8 1984 They suggest that the renin-angiotensin system is probably indispensable in preventing sodium loss when dietary sodium is suppressed. Sodium 112-118 renin Rattus norvegicus 22-27 6707633-4 1984 Mg2+ incorporation is also promoted by nigericin in the presence of potassium or sodium ions, indicating that Mg2+ accumulation is also dependent upon the transmembrane pH gradient. Sodium 81-87 mucin 7, secreted Homo sapiens 0-3 30772377-0 2019 UBC9 regulates cardiac sodium channel Nav1.5 ubiquitination, degradation and sodium current density. Sodium 23-29 ubiquitin conjugating enzyme E2 I Homo sapiens 0-4 30772377-0 2019 UBC9 regulates cardiac sodium channel Nav1.5 ubiquitination, degradation and sodium current density. Sodium 77-83 ubiquitin conjugating enzyme E2 I Homo sapiens 0-4 30772377-6 2019 Overexpression of UBC9 significantly decreased Nav1.5 expression and reduced sodium current densities, whereas knockdown of UBC9 expression significantly enhanced Nav1.5 expression and increased sodium current densities, in both HEK293 cells and primary neonatal cardiomyocytes. Sodium 77-83 ubiquitin conjugating enzyme E2 I Homo sapiens 18-22 30772377-6 2019 Overexpression of UBC9 significantly decreased Nav1.5 expression and reduced sodium current densities, whereas knockdown of UBC9 expression significantly enhanced Nav1.5 expression and increased sodium current densities, in both HEK293 cells and primary neonatal cardiomyocytes. Sodium 195-201 ubiquitin conjugating enzyme E2 I Homo sapiens 124-128 6093165-1 1984 Disturbances in body water and electrolytes that trigger sodium appetite, such as sodium depletion or hypovolemia, are potent activators of the renin-angiotensin system. Sodium 57-63 renin Rattus norvegicus 144-149 6093165-1 1984 Disturbances in body water and electrolytes that trigger sodium appetite, such as sodium depletion or hypovolemia, are potent activators of the renin-angiotensin system. Sodium 82-88 renin Rattus norvegicus 144-149 6308123-5 1983 The G6PD-stimulating activity of hypothalamic extracts from rats which had been on a high sodium intake for 4 weeks were approximately 150 times more active than those obtained from rats which had been on a low sodium diet. Sodium 90-96 glucose-6-phosphate dehydrogenase Rattus norvegicus 4-8 30556625-3 2019 The crown-ether complexes of sodium (1-Na) and potassium (1-K) exhibited different structures, with sodium preferring coordination to the nitrogen end, whereas potassium binds in an unusual eta2 -coordination mode to the two central carbon atoms. Sodium 29-35 DNA polymerase iota Homo sapiens 190-194 6308123-5 1983 The G6PD-stimulating activity of hypothalamic extracts from rats which had been on a high sodium intake for 4 weeks were approximately 150 times more active than those obtained from rats which had been on a low sodium diet. Sodium 211-217 glucose-6-phosphate dehydrogenase Rattus norvegicus 4-8 6621776-2 1983 In neurons and most glial cells L-CSA uptake is inhibited by acidic amino acids, L-glutamate and L-aspartate and requires sodium ions; however the sodium dependence varies from one cell type to the other. Sodium 122-128 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 34-37 30791470-6 2019 OtMgtE shares homology with the mammalian SLC41A1 magnesium/sodium antiporter, which has previously been implicated in maintaining clock period. Sodium 60-66 solute carrier family 41 member 1 Homo sapiens 42-49 6621776-2 1983 In neurons and most glial cells L-CSA uptake is inhibited by acidic amino acids, L-glutamate and L-aspartate and requires sodium ions; however the sodium dependence varies from one cell type to the other. Sodium 147-153 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 34-37 6303178-1 1983 Both the inhibition of renin release by sodium chloride and salt-sensitive hypertension have been attributed to sodium. Sodium 40-46 renin Rattus norvegicus 23-28 6341542-6 1983 This potent and specific stimulation of sodium intake by oral treatment with an inhibitor of the renin-angiotensin system may be caused by a paradoxical increase in the synthesis of angiotensin II in the brain. Sodium 40-46 renin Rattus norvegicus 97-102 6837658-9 1983 This effect of sodium on vascular reactivity could be the explanation for the favorable effect of a strongly sodium-restricted diet in lowering the incidence of eclampsia in women with PIH. Sodium 15-21 pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included) Homo sapiens 185-188 6837658-9 1983 This effect of sodium on vascular reactivity could be the explanation for the favorable effect of a strongly sodium-restricted diet in lowering the incidence of eclampsia in women with PIH. Sodium 109-115 pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included) Homo sapiens 185-188 6348254-0 1983 Renin-induced sodium appetite: effects on sodium balance and mediation by angiotensin in the rat. Sodium 14-20 renin Rattus norvegicus 0-5 6348254-0 1983 Renin-induced sodium appetite: effects on sodium balance and mediation by angiotensin in the rat. Sodium 42-48 renin Rattus norvegicus 0-5 6348254-11 1983 Preoptic injection of renin caused some increase in sodium excretion but this was small compared with the stimulating effect on sodium appetite.7. Sodium 52-58 renin Rattus norvegicus 22-27 6348254-13 1983 Increased intakes of water and 2.7% NaCl caused by renin resulted in the rats going into and remaining in positive fluid and sodium balance throughout the 24 h experiment.8. Sodium 125-131 renin Rattus norvegicus 51-56 6348254-17 1983 In conclusion, renin injected into the preoptic region or third ventricle is a potent stimulus to sodium appetite as well as thirst. Sodium 98-104 renin Rattus norvegicus 15-20 6756166-0 1982 Prostaglandin in renin release during sodium deprivation. Sodium 38-44 renin Rattus norvegicus 17-22 6756166-1 1982 This study was designed to examine the role of prostaglandins in the macula densa-mediated increase in plasma renin activity (PRA) during dietary sodium deprivation in rats. Sodium 146-152 renin Rattus norvegicus 110-115 6982423-2 1982 Very early responses to EGF, such as increased sodium fluxes5 and stimulation of tyrosine phosphorylation6, have been proposed to mediate some or all of EGF"s effects. Sodium 47-53 epidermal growth factor like 1 Rattus norvegicus 24-27 30735520-1 2019 Mutations in the SCN1A gene, which encodes for the voltage-gated sodium channel NaV1.1, cause Dravet syndrome, a severe developmental and epileptic encephalopathy. Sodium 65-71 sodium voltage-gated channel alpha subunit 1 Homo sapiens 17-22 30735520-1 2019 Mutations in the SCN1A gene, which encodes for the voltage-gated sodium channel NaV1.1, cause Dravet syndrome, a severe developmental and epileptic encephalopathy. Sodium 65-71 sodium voltage-gated channel alpha subunit 1 Homo sapiens 80-86 6982423-2 1982 Very early responses to EGF, such as increased sodium fluxes5 and stimulation of tyrosine phosphorylation6, have been proposed to mediate some or all of EGF"s effects. Sodium 47-53 epidermal growth factor like 1 Rattus norvegicus 153-156 7119865-2 1982 In the absence of NGF, PC12 cells are electrically inexcitable, while after several weeks of NGF treatment, they develop sodium action potentials. Sodium 121-127 nerve growth factor Rattus norvegicus 93-96 30159893-2 2019 As the key regulator of tumor cell volume, sodium-potassium-chloride cotransporter 1 (NKCC1) expression increases along with the malignancy of the glioma, and NKCC1 has been implicated in glioblastoma invasion. Sodium 43-49 solute carrier family 12, member 2 Mus musculus 86-91 30619835-0 2018 In-situ Grown SnS2 Nanosheets on rGO as an Advanced Anode Material for Lithium and Sodium Ion Batteries. Sodium 83-89 sodium voltage-gated channel alpha subunit 11 Homo sapiens 14-18 30487736-11 2018 The Nav1.6 channel blocker, 4,9-anhydrotetrodotoxin, reduced a component of sodium current in immature and mature calyces. Sodium 76-82 neuron navigator 1 Homo sapiens 4-8 30346691-0 2018 Hierarchical Carbon@SnS2 Aerogel with "Skeleton/Skin" Architectures as a High-Capacity, High-Rate Capability and Long Cycle Life Anode for Sodium Ion Storage. Sodium 139-145 sodium voltage-gated channel alpha subunit 11 Homo sapiens 20-24 30111855-0 2018 An interesting cross-talk between the glucagon-like peptide-1 receptor axis and angiotensin receptor pathway for modulation of renal sodium handling in obesity. Sodium 133-139 glucagon like peptide 1 receptor Homo sapiens 38-70 30152599-0 2018 SnS2 Nanosheets Coating on Nanohollow Cubic CoS2 /C for Ultralong Life and High Rate Capability Half/Full Sodium-Ion Batteries. Sodium 106-112 sodium voltage-gated channel alpha subunit 11 Homo sapiens 0-4 30242241-0 2018 Genome-wide analysis of polymorphism x sodium interaction effect on blood pressure identifies a novel 3"-BCL11B gene desert locus. Sodium 39-45 BAF chromatin remodeling complex subunit BCL11B Homo sapiens 105-111 30242241-5 2018 We found that an interaction between a novel 3"-BCL11B gene desert locus and daily sodium consumption was significantly associated with systolic blood pressure in both discovery and replication cohorts under the recessive model. Sodium 83-89 BAF chromatin remodeling complex subunit BCL11B Homo sapiens 48-54 30371202-11 2018 This suggests that sGC downregulation occurs outside the renal vasculature, increases renal sodium retention, and contributes to nitrate resistance of sunitinib-induced hypertension. Sodium 92-98 guanylate cyclase 1 soluble subunit alpha 1 Rattus norvegicus 19-22 29603851-1 2018 This study aimed to identify the optimal dose of the endothelin-1 receptor antagonist atrasentan with maximal albuminuria reduction and minimal signs of sodium retention, as manifested by increase in bodyweight. Sodium 153-159 endothelin receptor type A Homo sapiens 53-74 29704292-5 2018 In addition, activation of HCA1 significantly blocked the fast inactivating sodium current and increased the delay from inactivation to a conducting state of the sodium channel. Sodium 76-82 HCA1 Homo sapiens 27-31 29998261-0 2018 A versatile strategy for ultrathin SnS2 nanosheets confined in a N-doped graphene sheet composite for high performance lithium and sodium-ion batteries. Sodium 131-137 sodium voltage-gated channel alpha subunit 11 Homo sapiens 35-39 29489494-2 2018 Recently, the role of aldosterone and the activity of its receptor [mineralocorticoid receptor (MR)] in the clinical outcome for treatment with standard antidepressants has been shown including low systolic blood pressure and a low concentration of plasma sodium (Na), both of which appear to be related to therapy resistance to standard antidepressants. Sodium 256-262 nuclear receptor subfamily 3 group C member 2 Homo sapiens 68-94 29489494-2 2018 Recently, the role of aldosterone and the activity of its receptor [mineralocorticoid receptor (MR)] in the clinical outcome for treatment with standard antidepressants has been shown including low systolic blood pressure and a low concentration of plasma sodium (Na), both of which appear to be related to therapy resistance to standard antidepressants. Sodium 256-262 nuclear receptor subfamily 3 group C member 2 Homo sapiens 96-98 7049917-0 1982 Effects of chronic sodium depletion on canine brain renin and cathepsin D activities. Sodium 19-25 cathepsin D Canis lupus familiaris 62-73 29947535-1 2018 Renal medullary endothelin B receptors (ET(B)) mediate sodium excretion and blood pressure (BP) control. Sodium 55-61 endothelin receptor type B Rattus norvegicus 16-38 29947535-1 2018 Renal medullary endothelin B receptors (ET(B)) mediate sodium excretion and blood pressure (BP) control. Sodium 55-61 endothelin receptor type B Rattus norvegicus 40-45 29888331-3 2018 We report a pyrolyzed polyacrylonitrile/selenium disulfide (pPAN/SeS2) composite with dramatically enhanced active material content (63 wt %) and superior performances for both lithium and sodium storage. Sodium 189-195 peter pan homolog Homo sapiens 60-64 6763275-1 1982 In this study we have shown that sodium deprivation of rats increased the number of specific granules and renin activity in atria. Sodium 33-39 renin Rattus norvegicus 106-111 29793596-9 2018 Serum sodium and lactate concentrations and serum osmolality were higher in the TBI-HSL than in the TBI-saline group. Sodium 6-12 lipase E, hormone sensitive type Rattus norvegicus 84-87 6763275-2 1982 Sodium loading and DOCA treatment were found to lower the number of granules and renin activity. Sodium 0-6 renin Rattus norvegicus 81-86 6756681-0 1982 Secretion control for active and inactive renin: interactions with calcium and sodium ions. Sodium 79-85 renin Rattus norvegicus 42-47 6756695-2 1982 Sodium depletion increased total and active renin in the juxtaglomerular apparatus and approximately one third of the renin was in an inactive form in sodium depletion. Sodium 0-6 renin Rattus norvegicus 44-49 6756695-2 1982 Sodium depletion increased total and active renin in the juxtaglomerular apparatus and approximately one third of the renin was in an inactive form in sodium depletion. Sodium 151-157 renin Rattus norvegicus 118-123 6756695-3 1982 Sodium loading decreased active and total renin and there was no inactive renin present. Sodium 0-6 renin Rattus norvegicus 42-47 6756695-5 1982 Haemorrhage caused a release of active renin in both sodium states and did not alter the renin content of the J.G.A. Sodium 53-59 renin Rattus norvegicus 39-44 7188049-0 1982 Renin-angiotensin-aldosterone system in hyper- and hypothyroid rats during sodium depletion. Sodium 75-81 renin Rattus norvegicus 0-5 29782051-4 2018 Functional characterization of several SCN8A encephalopathy variants has shown that elevated persistent sodium current is one of several common biophysical defects. Sodium 104-110 sodium channel, voltage-gated, type VIII, alpha Mus musculus 39-44 29782051-7 2018 We evaluated the therapeutic effect of GS967 in the Scn8aN1768D/+ mouse model carrying an SCN8A patient mutation that results in elevated persistent sodium current. Sodium 149-155 sodium channel, voltage-gated, type VIII, alpha Mus musculus 90-95 29782051-13 2018 SIGNIFICANCE: Persistent sodium current modulators like GS967 may be an effective precision targeting strategy for SCN8A encephalopathy and other functionally similar channelopathies when elevated persistent sodium current is the primary dysfunction. Sodium 25-31 sodium channel, voltage-gated, type VIII, alpha Mus musculus 115-120 29782051-13 2018 SIGNIFICANCE: Persistent sodium current modulators like GS967 may be an effective precision targeting strategy for SCN8A encephalopathy and other functionally similar channelopathies when elevated persistent sodium current is the primary dysfunction. Sodium 208-214 sodium channel, voltage-gated, type VIII, alpha Mus musculus 115-120 29700291-6 2018 Protectin DX markedly regulated alveolar fluid clearance by upregulating sodium channel and Na, K-ATPase protein expression levels in vivo and in vitro. Sodium 73-79 CD59 molecule Rattus norvegicus 0-9 29700291-8 2018 In addition, protectin DX enhanced the subcellular distribution of sodium channels and Na, K-ATPase, which were specifically localized to the apical and basal membranes of primary rat ATII cells. Sodium 67-73 CD59 molecule Rattus norvegicus 13-22 29700291-10 2018 Protectin DX stimulates alveolar fluid clearance through a mechanism partly dependent on alveolar epithelial sodium channel and Na, K-ATPase activation via the ALX/PI3K/Nedd4-2 signaling pathway. Sodium 109-115 CD59 molecule Rattus norvegicus 0-9 6795609-3 1981 TRH was found to be taken up via a process sharing many of the properties of a high affinity transport system, viz: (1) saturation kinetics; (2) high affinity kinetic constants (Km1 = 1.06 X 10(-5) M, Km2 = 5.6 X 10(-6) M); (3) temperature sensitivity (Q10 = 1.48); (4) dependency on the sodium concentration in the incubation medium; and (5) tissue/medium ratios greater than 1. Sodium 288-294 thyrotropin releasing hormone Rattus norvegicus 0-3 29400008-4 2018 The incorporation of Mg2+ into intrinsic Na+ vacancies in Na-ion layers can lead to a high-performance P2-type cathode material for sodium-ion batteries. Sodium 132-138 mucin 7, secreted Homo sapiens 21-24 29295803-0 2018 Differential effects on sodium current impairments by distinct SCN1A mutations in GABAergic neurons derived from Dravet syndrome patients. Sodium 24-30 sodium voltage-gated channel alpha subunit 1 Homo sapiens 63-68 29153712-6 2018 The SnS2/RGO composite exhibits great application potential as an anode for sodium ion batteries with the advantages of unique structure and superior sodium storage performance. Sodium 76-82 sodium voltage-gated channel alpha subunit 11 Homo sapiens 4-8 29153712-6 2018 The SnS2/RGO composite exhibits great application potential as an anode for sodium ion batteries with the advantages of unique structure and superior sodium storage performance. Sodium 150-156 sodium voltage-gated channel alpha subunit 11 Homo sapiens 4-8 6789664-5 1981 And, perfusion with 0.5 mM cholate only produced sodium secretion in PEM rats. Sodium 49-55 Rhox homeobox family member 5 Rattus norvegicus 69-72 7018257-0 1981 Effects of sodium intake and Goldblatt hypertension on renin release in rat kidney slices. Sodium 11-17 renin Rattus norvegicus 55-60 7018257-2 1981 The low sodium diet significantly elevated plasma and kidney renin activity (KRA) and base-line renin release (BRR). Sodium 8-14 renin Rattus norvegicus 61-66 7018257-2 1981 The low sodium diet significantly elevated plasma and kidney renin activity (KRA) and base-line renin release (BRR). Sodium 8-14 renin Rattus norvegicus 96-101 7009830-0 1981 Influence of dietary sodium on renin angiotensin system involvement in sodium nitroprusside hypotension in conscious rats. Sodium 21-27 renin Rattus norvegicus 31-36 6269812-1 1981 Observations with both captopril and teprotide suggest interplay of the renin angiotensin and sympathetic nervous systems during sodium depletion. Sodium 129-135 renin Rattus norvegicus 72-77 7004910-0 1980 [Interaction of catecholamines and the renin-angiotensin system in regulating sodium reabsorption in the rat kidney]. Sodium 78-84 renin Rattus norvegicus 39-44 7004910-4 1980 It is suggested that the renin-angiotensin system may be directly involved into the mechanism of catecholamine-stimulated sodium reabsorption by the rat kidney. Sodium 122-128 renin Rattus norvegicus 25-30 7430266-2 1980 After properly timed preincubations to control the size of internal amino acid pools, the activity of systems A, ASC, L, and Ly+ has been discriminated by measurements of amino acid uptake (initial entry rate) in the presence and absence of sodium and of transport-specific model substrates. Sodium 241-247 steroid sulfatase Mus musculus 113-116 29380651-1 2018 The negative slope conductance created by the persistent sodium current (INaP) prolongs the decay phase of excitatory postsynaptic potentials (EPSPs). Sodium 57-63 NFKB inhibitor zeta Homo sapiens 73-77 28842436-14 2017 Listen to this article"s corresponding podcast at http://ajpheart.podbean.com/e/camkii-dependent-regulation-of-atrial-late-sodium-current-and-excitability/ . Sodium 123-129 calcium/calmodulin dependent protein kinase II gamma Homo sapiens 80-86 28687226-3 2017 Inhibition of PI3K affects multiple plateau currents, reducing IKr, IKs, and ICaL while increasing the persistent sodium current (INaP). Sodium 114-120 NFKB inhibitor zeta Homo sapiens 130-134 6158822-0 1980 Role of the renin-angiotensin system in the adaptation of aldosterone biosynthesis to sodium restriction in the rat. Sodium 86-92 renin Rattus norvegicus 12-17 28951361-1 2017 OBJECTIVE: To investigate the opioidergic mechanism of the central nucleus of the amygdala (CeA) for regulating sodium appetite in rats. Sodium 112-118 carcinoembryonic antigen gene family 4 Rattus norvegicus 92-95 28951361-5 2017 CONCLUSION: micro-opioid receptors in the CeA are involved in the excitatory regulation of sodium appetite to mediate sodium intake. Sodium 91-97 carcinoembryonic antigen gene family 4 Rattus norvegicus 42-45 28951361-5 2017 CONCLUSION: micro-opioid receptors in the CeA are involved in the excitatory regulation of sodium appetite to mediate sodium intake. Sodium 118-124 carcinoembryonic antigen gene family 4 Rattus norvegicus 42-45 28928410-1 2017 The renin-angiotensin system (RAS) plays a key role in the control of vasoconstriction as well as sodium and fluid retention mediated mainly by angiotensin (Ang) II acting at the AT1 receptor (AT1R). Sodium 98-104 angiotensin II receptor type 1 Homo sapiens 193-197 28928636-8 2017 Our results show that in both conditions, Smn-deficient cells displayed lower action potential threshold, greater action potential amplitudes, and larger density of voltage-dependent sodium currents than cells with normal Smn-levels. Sodium 183-189 survival motor neuron 1 Mus musculus 42-45 28445205-6 2017 Our results demonstrated that inhibition of miR-429 remarkably increased the levels of PHD2, which disrupted PHD2-associated adaptive activation of HIF-1alpha-mediated gene expression in response to high salt in the renal medulla and consequently inhibited urinary sodium excretion, enhanced sodium retention in response to chronic sodium overloading, and as a result, produced a salt-sensitive hypertension. Sodium 265-271 microRNA 429 Rattus norvegicus 44-51 28445205-6 2017 Our results demonstrated that inhibition of miR-429 remarkably increased the levels of PHD2, which disrupted PHD2-associated adaptive activation of HIF-1alpha-mediated gene expression in response to high salt in the renal medulla and consequently inhibited urinary sodium excretion, enhanced sodium retention in response to chronic sodium overloading, and as a result, produced a salt-sensitive hypertension. Sodium 292-298 microRNA 429 Rattus norvegicus 44-51 28445205-6 2017 Our results demonstrated that inhibition of miR-429 remarkably increased the levels of PHD2, which disrupted PHD2-associated adaptive activation of HIF-1alpha-mediated gene expression in response to high salt in the renal medulla and consequently inhibited urinary sodium excretion, enhanced sodium retention in response to chronic sodium overloading, and as a result, produced a salt-sensitive hypertension. Sodium 292-298 microRNA 429 Rattus norvegicus 44-51 28836382-0 2017 Sodium appetite elicited by low-sodium diet is dependent on p44/42 mitogen-activated protein kinase (extracellular signal-regulated kinase 1/2) activation in the brain. Sodium 0-6 interferon induced protein 44 Homo sapiens 60-63 28836382-0 2017 Sodium appetite elicited by low-sodium diet is dependent on p44/42 mitogen-activated protein kinase (extracellular signal-regulated kinase 1/2) activation in the brain. Sodium 32-38 interferon induced protein 44 Homo sapiens 60-63 28836382-1 2017 Sodium appetite is regulated by several signalling molecules, among which angiotensin II (Ang II) serves as a key driver of robust salt intake by binding to Ang II type 1 receptors (AT1R) in several regions in the brain. Sodium 0-6 angiotensin II receptor type 1 Homo sapiens 157-180 28836382-1 2017 Sodium appetite is regulated by several signalling molecules, among which angiotensin II (Ang II) serves as a key driver of robust salt intake by binding to Ang II type 1 receptors (AT1R) in several regions in the brain. Sodium 0-6 angiotensin II receptor type 1 Homo sapiens 182-186 28836382-7 2017 This result indicates that low-sodium diet consumption activates the MAPK pathway via Ang II/AT1R signalling on the laminae terminalis. Sodium 31-37 angiotensin II receptor type 1 Homo sapiens 93-97 6158822-1 1980 The purpose of the present study was to evaluate the role of the renin-angiotensin system in the secretion of aldosterone during restriction of dietary sodium intake. Sodium 152-158 renin Rattus norvegicus 65-70 6158822-9 1980 Plasma renin activity was increased both by sodium depletion and CEI. Sodium 44-50 renin Rattus norvegicus 7-12 6992601-5 1980 The low-sodium diet increased plasma renin activity to about the same level in one- and two-kidney normotensive rats. Sodium 8-14 renin Rattus norvegicus 37-42 6992601-6 1980 However, the increase in plasma renin activity elicited by dietary sodium restriction was markedly less in one-kidney Goldblatt hypertension. Sodium 67-73 renin Rattus norvegicus 32-37 6154896-2 1980 Nerve growth factor (NGF), a polypeptide trophic factor for peripheral sympathetic and sensory neurones, has also been reported to be a potent stimulus to thirst and sodium appetite when injected into the brain of the rat. Sodium 166-172 nerve growth factor Rattus norvegicus 0-19 6154896-2 1980 Nerve growth factor (NGF), a polypeptide trophic factor for peripheral sympathetic and sensory neurones, has also been reported to be a potent stimulus to thirst and sodium appetite when injected into the brain of the rat. Sodium 166-172 nerve growth factor Rattus norvegicus 21-24 6154896-5 1980 We report here that NGF-induced thirst and sodium appetite, as well as increased blood pressure and increase ornithine decarboxylase activity in the brain and liver, depend on the formation of AII (see also ref. Sodium 43-49 nerve growth factor Rattus norvegicus 20-23 6988533-4 1980 After 5 months the PRA was significantly higher in the lead-treated group even on a 1% NaCl diet, but the difference between groups disappeared on an Na-free diet; that is, the renin response to sodium deprivation was blunted. Sodium 195-201 renin Rattus norvegicus 177-182 6248654-2 1980 On the sodium loading, the blood pressure increased gradually and plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were decreased. Sodium 7-13 renin Rattus norvegicus 73-78 6995690-7 1980 These results indicate that changes in fractional renin release are induced by sodium balance variation, and these changes are preserved in vitro only in sodium-loaded states. Sodium 79-85 renin Rattus norvegicus 50-55 6995690-7 1980 These results indicate that changes in fractional renin release are induced by sodium balance variation, and these changes are preserved in vitro only in sodium-loaded states. Sodium 154-160 renin Rattus norvegicus 50-55 7411436-0 1980 Increased sodium appetite in the rat induced by intracranial administration of components of the renin-angiotensin system. Sodium 10-16 renin Rattus norvegicus 97-102 7418541-3 1980 The main purpose of the study was to find out how a reduction or an increase of total body sodium and the associated changes of renin production can influence the vascular response to angiotensin and to catecholamines. Sodium 91-97 renin Rattus norvegicus 128-133 6991209-5 1980 During sodium-depletion, blood pressure maintenance became renin-dependent; sodium-loading caused a decrease of renin-angiotensin activity in renovascular hypertension. Sodium 7-13 renin Rattus norvegicus 59-64 6991209-5 1980 During sodium-depletion, blood pressure maintenance became renin-dependent; sodium-loading caused a decrease of renin-angiotensin activity in renovascular hypertension. Sodium 76-82 renin Rattus norvegicus 112-117 6991209-6 1980 A weak direct correlation between depressor response to saralasin and the plasma renin activity could be established in the different sodium-depleted and sodium-loaded states. Sodium 134-140 renin Rattus norvegicus 81-86 28488023-2 2017 The rotavirus enterotoxin nonstructural protein 4 (NSP4) directly inhibits glucose-mediated sodium absorption. Sodium 92-98 serine protease 57 Homo sapiens 51-55 6991209-6 1980 A weak direct correlation between depressor response to saralasin and the plasma renin activity could be established in the different sodium-depleted and sodium-loaded states. Sodium 154-160 renin Rattus norvegicus 81-86 232088-8 1979 However, there appears to be an abnormal relationship between renin and exchangeable sodium in the two-kidney hypertensive responders that could contribute to the maintenance of the hypertension. Sodium 85-91 renin Rattus norvegicus 62-67 28762720-0 2017 Rationally Incorporated MoS2/SnS2 Nanoparticles on Graphene Sheets for Lithium-Ion and Sodium-Ion Batteries. Sodium 87-93 sodium voltage-gated channel alpha subunit 11 Homo sapiens 29-33 398416-2 1979 In the current study, renal renin of rats was increased by chronic sodium deprivation and decreased by chronic sodium loading and DOCA administration. Sodium 67-73 renin Rattus norvegicus 28-33 28731330-2 2017 We have previously modeled mammalian members of the SLC13 family, including the Na+/dicarboxylate cotransporter NaDC1 (SLC13A2), based on a structure of the bacterial homologue VcINDY in an inward-facing conformation with one sodium ion bound at the Na1 site. Sodium 226-232 solute carrier family 13 member 2 Homo sapiens 112-117 28731330-2 2017 We have previously modeled mammalian members of the SLC13 family, including the Na+/dicarboxylate cotransporter NaDC1 (SLC13A2), based on a structure of the bacterial homologue VcINDY in an inward-facing conformation with one sodium ion bound at the Na1 site. Sodium 226-232 solute carrier family 13 member 2 Homo sapiens 119-126 28731318-0 2017 Ultrafast Ionic Liquid-Assisted Microwave Synthesis of SnO Microflowers and Their Superior Sodium-Ion Storage Performance. Sodium 91-97 strawberry notch homolog 1 Homo sapiens 55-58 28515174-1 2017 The thiazide-sensitive sodium chloride cotransporter NCC is important for maintaining serum sodium (Na+) and, indirectly, serum potassium (K+) levels. Sodium 23-29 solute carrier family 12 member 3 Homo sapiens 53-56 28516268-2 2017 In a panel of human cancer cell lines, which express the system L transporters LAT1 and LAT2, GPNA inhibits the sodium-independent influx of leucine and glutamine. Sodium 112-118 linker for activation of T cells family member 2 Homo sapiens 88-92 28274929-1 2017 The thiazide-sensitive NaCl cotransporter (NCC), located apically in distal convoluted tubule epithelia, regulates the fine-tuning of renal sodium excretion. Sodium 140-146 solute carrier family 12 member 3 Homo sapiens 43-46 27936281-2 2017 In general, the organic anion transporting polypeptides (OATP; SLCO) represent a superfamily of uptake transporters that mediate the sodium-independent transport of a diverse range of amphipathic organic compounds including bile salts, steroid conjugates, thyroid hormones, anionic peptides, numerous drugs and other xenobiotic substances. Sodium 133-139 solute carrier organic anion transporter family member 1A2 Homo sapiens 16-55 27936281-2 2017 In general, the organic anion transporting polypeptides (OATP; SLCO) represent a superfamily of uptake transporters that mediate the sodium-independent transport of a diverse range of amphipathic organic compounds including bile salts, steroid conjugates, thyroid hormones, anionic peptides, numerous drugs and other xenobiotic substances. Sodium 133-139 solute carrier organic anion transporter family member 1A2 Homo sapiens 57-61 28492364-5 2017 Mechanistically, TCR stimulation induced rapid sodium influx in Napahyh/hyh CD4 T cells, which reduced intracellular ATP, [ATP]i. Depletion of [ATP]i inhibited mTORC2 dependent NFkappaB activation in Napahyh/hyh cells but ablation of Orai1 restored it. Sodium 47-53 CREB regulated transcription coactivator 2 Mus musculus 160-166 28429929-0 2017 Flexible Paper-like Free-Standing Electrodes by Anchoring Ultrafine SnS2 Nanocrystals on Graphene Nanoribbons for High-Performance Sodium Ion Batteries. Sodium 131-137 sodium voltage-gated channel alpha subunit 11 Homo sapiens 68-72 398416-2 1979 In the current study, renal renin of rats was increased by chronic sodium deprivation and decreased by chronic sodium loading and DOCA administration. Sodium 111-117 renin Rattus norvegicus 28-33 522895-1 1979 Bilateral adrenalectomy combined with a sodium-deficient diet caused a time-dependent increase in plasma renin concentration in rats. Sodium 40-46 renin Rattus norvegicus 105-110 523796-0 1979 Effects of acute hemodialysis-induced changes in sodium balance on the renin-angiotensin system in renovascular and spontaneously hypertensive rats. Sodium 49-55 renin Rattus norvegicus 71-76 523796-1 1979 In two-kidney Goldblatt hypertensive, spontaneously hypertensive, and normotensive control rats the activity of the renin-angiotensin system was tested during variation of sodium balance. Sodium 172-178 renin Rattus norvegicus 116-121 523796-5 1979 During sodium depletion blood pressure maintenance became renin-dependent; sodium loading caused a decrease of renin-angiotensin activity in renovascular hypertension. Sodium 7-13 renin Rattus norvegicus 58-63 523796-5 1979 During sodium depletion blood pressure maintenance became renin-dependent; sodium loading caused a decrease of renin-angiotensin activity in renovascular hypertension. Sodium 75-81 renin Rattus norvegicus 111-116 314308-1 1979 The responses of isolated frog skin to 5-hydroxytryptamine (increased active sodium transport and decreased passive chloride permeability) are diminished by incubation with the enzymes neuraminidase and N-acetylneuraminic acid aldolase but only in the absence of Ca2+ and presence of EDTA. Sodium 77-83 neuraminidase 1 Homo sapiens 185-198 223439-7 1979 Among 56 white infants whose mother"s mean BP was above the median for this population, infant sodium intake correlated with infant SBP (r = .31, p less than .009). Sodium 95-101 selenium binding protein 1 Homo sapiens 132-135 223439-8 1979 Among 32 black infants, regardless of parents" BP, sodium intake was negatively correlated with SBP (r = -.36, p less than .021). Sodium 51-57 selenium binding protein 1 Homo sapiens 96-99 495153-6 1979 During high sodium intake, the plasma renin activity in subtotally nephrectomized rats was suppressed to one fifth of that in sham-operated animals, but the renin substrate activity did not increase markedly. Sodium 12-18 renin Rattus norvegicus 38-43 477254-8 1979 Animals fed on a sodium-deficient diet for 8 days had markedly higher concentrations of intrarenal ANG II, plasma renin activity and kidney renin concentration than sodium-replete animals. Sodium 17-23 renin Rattus norvegicus 114-119 477254-8 1979 Animals fed on a sodium-deficient diet for 8 days had markedly higher concentrations of intrarenal ANG II, plasma renin activity and kidney renin concentration than sodium-replete animals. Sodium 17-23 renin Rattus norvegicus 140-145 477254-10 1979 After oral sodium loading for 3 weeks, rats had suppressed plasma renin activity and kidney renin concentration but unchanged intrarenal ANG II when compared with animals on a normal sodium intake. Sodium 11-17 renin Rattus norvegicus 66-71 477254-10 1979 After oral sodium loading for 3 weeks, rats had suppressed plasma renin activity and kidney renin concentration but unchanged intrarenal ANG II when compared with animals on a normal sodium intake. Sodium 11-17 renin Rattus norvegicus 92-97 87396-0 1979 Side-specific effects of sodium on (Na,K)-ATPase. Sodium 25-31 dynein axonemal heavy chain 8 Homo sapiens 42-48 16068187-11 1979 It also describes for the first time a second phenomenon produced by intracranial administration of NGF, namely an intense appetite for aversive concentrations of sodium solutions. Sodium 163-169 nerve growth factor Rattus norvegicus 100-103 28431667-4 2017 However, emerging evidence suggests that GLP-1 RA can also have direct effects in the kidney, including inhibiting NHE3-dependent sodium reabsorption in the proximal tubule. Sodium 130-136 glucagon like peptide 1 receptor Homo sapiens 41-46 439071-4 1979 In immature rats this effect of hCG was dose-dependent and time-related and the accumulated fluid contained high levels of potassium and phosphate; levels of sodium, calcium and protein were similar to those in serum. Sodium 158-164 hypertrichosis 2 (generalised, congenital) Homo sapiens 32-35 28082350-0 2017 Secretin is involved in sodium conservation through the renin-angiotensin-aldosterone system. Sodium 24-30 secretin Mus musculus 0-8 28273873-6 2017 CSK rs1378942 and CSK-MIR4513 rs3784789 were significantly modified by urinary sodium-potassium excretion ratio. Sodium 79-85 C-terminal Src kinase Homo sapiens 0-3 28273873-6 2017 CSK rs1378942 and CSK-MIR4513 rs3784789 were significantly modified by urinary sodium-potassium excretion ratio. Sodium 79-85 C-terminal Src kinase Homo sapiens 18-21 28273873-8 2017 The present study results indicated that the mutant alleles of CSK rs1378942 and CSK-MIR4513 rs3784789 had the strongest protective effects against hypertension in the middle group of 24 h estimated urinary sodium-potassium excretion ratio. Sodium 207-213 C-terminal Src kinase Homo sapiens 63-66 28273873-8 2017 The present study results indicated that the mutant alleles of CSK rs1378942 and CSK-MIR4513 rs3784789 had the strongest protective effects against hypertension in the middle group of 24 h estimated urinary sodium-potassium excretion ratio. Sodium 207-213 C-terminal Src kinase Homo sapiens 81-84 762115-5 1979 Uptake by one system was sensitive to DL-beta-2-aminobicyclo[2,2,1]-heptane-2-carboxylic acid, was sodium-independent, and appeared to be mediated by system L. The second unassigned system was characterized by sodium dependence, insensitivity to 2-aminoisobutyric acid and 2-(methylamino)isobutyric acid, and was inhibited by alanine, serine, cysteine, and other amino acids. Sodium 99-105 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 41-47 28103016-0 2017 SnS2 Nanowall Arrays toward High-Performance Sodium Storage. Sodium 45-51 sodium voltage-gated channel alpha subunit 11 Homo sapiens 0-4 28103016-7 2017 The superior sodium storage capability of the SnS2 NWA electrode could be attributed to outstanding electrode design and a rational growth process, which favor fast electron and Na-ion transport, as well as provide steady structure for elongated cycling. Sodium 13-19 sodium voltage-gated channel alpha subunit 11 Homo sapiens 46-50 27009112-3 2017 The aim of this study was to determine whether the lowering of dialysate sodium (Na) levels is effective on LV systolic and diastolic parameters and BNP in the maintenance of hemodialysis patients. Sodium 73-79 natriuretic peptide B Homo sapiens 149-152 420931-5 1979 The following occurred in 8 to 12 weeks with the restoration of the 11-OCS and sodium level in the plasma: renin JGC activity became normal, RLA activity in MC disappeared, and the initial ultrastructure of both of these cells was restored. Sodium 79-85 renin Rattus norvegicus 107-112 27924781-7 2017 All the currently available surveys in literature state the potential applicability of SnS2 as the anode material for reversible lithium/sodium ion batteries (LIBs/NIBs) but there is a lack of equivalent studies on electrochemical capacitors. Sodium 137-143 sodium voltage-gated channel alpha subunit 11 Homo sapiens 87-91 421968-2 1979 One possible mechanism that may explain the decreased PRA is an increased delivery of sodium to the macula densa produced by the glucose osmotic diuresis, resulting in decreased renin release. Sodium 86-92 renin Rattus norvegicus 178-183 28101449-5 2017 RESULTS: The intake of high sodium produced a slight but significant increase in MAP and differentially regulated components of the renal renin-angiotensin system (RAS). Sodium 28-34 renin Rattus norvegicus 138-143 27544874-1 2017 Facilitatory and inhibitory mechanisms in the central nucleus of the amygdala (CeA) and the lateral parabrachial nucleus (LPBN), respectively, are important for the control of sodium and water intake. Sodium 176-182 carcinoembryonic antigen gene family 4 Rattus norvegicus 79-82 28332265-7 2017 There was a significant involvement of alpha1A -adrenoceptor in carrying out renal tubular antinatriuretic and antidiuretic response in Wistar Kyoto rats on normal sodium diet (WKYNNa). Sodium 164-170 adrenoceptor alpha 1A Rattus norvegicus 39-60 439781-2 1979 In sodium repleted animals indomethacin did not change systolic blood pressure (BP) although plasma renin activity was decreased. Sodium 3-9 renin Rattus norvegicus 100-105 27479742-2 2017 NFAT5, a relative of nuclear factor kappaB and the calcineurin-activated NFATc transcription factors, protects mammalian cells from hyperosmotic stress caused by the elevation of extracellular sodium levels. Sodium 193-199 nuclear factor of activated T cells 5 Homo sapiens 0-5 28008944-6 2016 JNK and CDK5 inhibitor attenuated increases in Nav1.6 sodium currents induced by overexpression of APP. Sodium 54-60 neuron navigator 1 Homo sapiens 47-51 28008944-7 2016 Nav1.6 sodium currents were increased by APPT668E (mutant Thr to Glu) and decreased by T668A (mutant Thr to ALa) mutant, respectively. Sodium 7-13 neuron navigator 1 Homo sapiens 0-4 390990-4 1979 Plasma renin and blood angiotensin I were closely linearly related over the range of sodium intakes. Sodium 85-91 renin Rattus norvegicus 7-12 215214-0 1978 Activation by lithium ions of the inside sodium sites in (Na+ + K+)-ATPase. Sodium 41-47 dynein axonemal heavy chain 8 Homo sapiens 68-74 31796-5 1978 These results suggest that inhibition of renin by sodium is dependent on an intrarenal effect of chloride. Sodium 50-56 renin Rattus norvegicus 41-46 699502-10 1978 A low sodium diet elevated both plasma and aortic renin and retarded the progressive increase of blood pressure in the spontaneously hypertensive rat. Sodium 6-12 renin Rattus norvegicus 50-55 27627464-1 2016 The nociceptive noxious heat-activated receptor - TRPV1, conducts calcium and sodium, thus producing a depolarizing receptor potential, leading to activation of nociceptive neurons. Sodium 78-84 transient receptor potential cation channel subfamily V member 1 Homo sapiens 50-55 27627464-2 2016 TRPV1-mediated calcium and sodium influx is negatively modulated by calcium, via calcium-dependent desensitization of TRPV1 channels. Sodium 27-33 transient receptor potential cation channel subfamily V member 1 Homo sapiens 0-5 27627464-2 2016 TRPV1-mediated calcium and sodium influx is negatively modulated by calcium, via calcium-dependent desensitization of TRPV1 channels. Sodium 27-33 transient receptor potential cation channel subfamily V member 1 Homo sapiens 118-123 27571932-10 2016 Moreover, BNP (100 nM) increased the transient inward current, sodium currents, sodium-calcium exchanger currents, and L-type calcium current; but reduced late sodium currents and the Na-K pump in PV cardiomyocytes. Sodium 63-69 natriuretic peptide B Homo sapiens 10-13 871165-6 1977 These observations, along with those reported previously in sodium-depleted rats, point to an important overall role for the renin-angiotensin system in the control of aldosterone secretion in the rat. Sodium 60-66 renin Rattus norvegicus 125-130 851195-6 1977 It is concluded that a) low perfusate calcium and high magnesium concentrations stimulate renin release, b) kidneys removed from sodium-deprived rats released substantially more renin thatn those from sodium-loaded rats, and c) changing perfusate sodium concentration alters sodium excretion, but does not affect renin release. Sodium 129-135 renin Rattus norvegicus 178-183 851195-6 1977 It is concluded that a) low perfusate calcium and high magnesium concentrations stimulate renin release, b) kidneys removed from sodium-deprived rats released substantially more renin thatn those from sodium-loaded rats, and c) changing perfusate sodium concentration alters sodium excretion, but does not affect renin release. Sodium 129-135 renin Rattus norvegicus 178-183 837868-6 1977 Ptasssium loading also increased plasma renin concentration which was correlated with the sodium excretion rate (r = 0.64, P less than 0.01). Sodium 90-96 renin Rattus norvegicus 40-45 137674-2 1977 In this study, the enzyme responsible for active sodium transport--Na/K-ATPase and a nonspecific ATPase Mg-ATPase--were assayed in the placenta and in maternal and fetal (cord) erythrocytes of pregnant women with and without pre-eclampsia. Sodium 49-55 dynein axonemal heavy chain 8 Homo sapiens 72-78 1071719-10 1976 Decreasing sodium concentration from 140 to 110 mol/l with constant osmolarity of 305 mosmol/l stimulated renin release by a direct effect on juxtaglomerular cells. Sodium 11-17 renin Rattus norvegicus 106-111 1071589-9 1976 The fact that both plasma renin levels and exchangeable sodium levels increase according to this method, suggests that hypertension in the two-kidney model is renin-dependent. Sodium 56-62 renin Rattus norvegicus 159-164 1071623-4 1976 of renin strikingly reduced kallikrein excretion (P less than 0-01) but considerably increased sodium excretion (P less than 0-001). Sodium 95-101 renin Rattus norvegicus 3-8 1071628-0 1976 Renin-angiotensin and kallikrein-kinin systems in sodium homeostasis and hypertension in rats. Sodium 50-56 renin Rattus norvegicus 0-5 1071628-4 1976 Rats given a sodium load (NaCl solution, 20 g/l, to drink) for 28 days showed acute and prolonged significant falls in urinary kallikrein excretion associated with suppression of plasma renin and angiotensin. Sodium 13-19 renin Rattus norvegicus 186-191 1071628-6 1976 Conversely sodium-depleted rats showed increases in urinary kallikrein excretion, associated with rises in plasma renin and angiotensin. Sodium 11-17 renin Rattus norvegicus 114-119 1071639-2 1976 Renal hypertensive rats with a normal or suppressed activity of the renin-angiotensin system develop vascular lesions which are similar to those observed in spontaneously hypertensive rats on high sodium diet. Sodium 197-203 renin Rattus norvegicus 68-73 186664-2 1976 Animals on a sodium-deficient diet had a significant decrease of serum sodium levels with a concomitant increase of renal renin granules. Sodium 13-19 renin Rattus norvegicus 122-127 62828-1 1976 In Duchenne muscular dystrophy the activity of (Na+ + K+)ATPase in erythrocyte ghosts is reduced and its reaction to ouabain is paradoxical both in low sodium and high sodium systems. Sodium 152-158 dynein axonemal heavy chain 8 Homo sapiens 57-63 27990272-2 2016 The monoclonal antibody SVmab1 was recently published to bind the Na V1.7 DII voltage sensor domain and block human Na V1.7 sodium currents in heterologous cells. Sodium 124-130 immunoglobulin lambda variable 2-23 Homo sapiens 119-123 27882351-4 2016 Here, we tested this hypothesis in vivo by inserting a human gain-of-function mutation in the mouse NaV1.2-encoding gene Scn2a that is known to increase NaV1.2-mediated persistent sodium currents. Sodium 180-186 sodium channel, voltage-gated, type II, alpha Mus musculus 100-106 27882351-4 2016 Here, we tested this hypothesis in vivo by inserting a human gain-of-function mutation in the mouse NaV1.2-encoding gene Scn2a that is known to increase NaV1.2-mediated persistent sodium currents. Sodium 180-186 sodium channel, voltage-gated, type II, alpha Mus musculus 121-126 27882351-4 2016 Here, we tested this hypothesis in vivo by inserting a human gain-of-function mutation in the mouse NaV1.2-encoding gene Scn2a that is known to increase NaV1.2-mediated persistent sodium currents. Sodium 180-186 neuron navigator 1 Mus musculus 100-104 27895596-12 2016 Reciprocal modulation of the inwardly rectifying potassium current and the fast inward sodium current may have a functional role in allowing cardiac tissue to remain excitable when IK1 is upregulated. Sodium 87-93 IKAROS family zinc finger 1 Homo sapiens 181-184 27582096-0 2016 Loss of endothelin B receptor function impairs sodium excretion in a time- and sex-dependent manner. Sodium 47-53 endothelin receptor type B Rattus norvegicus 8-29 27582096-3 2016 Therefore, this study was designed to test the hypothesis that ETB receptor activation contributes to the diurnal control of sodium excretion and that sex differences contribute to this control as well. Sodium 125-131 endothelin receptor type B Rattus norvegicus 63-66 62828-1 1976 In Duchenne muscular dystrophy the activity of (Na+ + K+)ATPase in erythrocyte ghosts is reduced and its reaction to ouabain is paradoxical both in low sodium and high sodium systems. Sodium 168-174 dynein axonemal heavy chain 8 Homo sapiens 57-63 993320-8 1976 Two steroids, 16beta-hydroxy-dehydroepiandrosterone and 16-oxo-androstenediol, recently shown to have sodium-retaining activity in the rat, and also implicated in low-renin "essential" hypertension in man, showed no competitive binding activity. Sodium 102-108 renin Rattus norvegicus 167-172 26912587-1 2016 The subthreshold activity of hippocampal CA1 pyramidal neurons is regulated by the persistent sodium current (INaP) and the h-current (Ih), carried by tetrodotoxin-sensitive sodium channels and hyperpolarization-activated cyclic-nucleotide-gated channels, respectively. Sodium 94-100 NFKB inhibitor zeta Homo sapiens 110-114 978043-12 1976 Sodium restriction stimulated the renin angiotensin system markedly, whereas high sodium intake suppressed it. Sodium 0-6 renin Rattus norvegicus 34-39 978043-13 1976 After subtotal nephrectomy, elevation of blood pressure, renal hypertrophy, and suppression of the renin-angiotensin system are closely related to sodium intake. Sodium 147-153 renin Rattus norvegicus 99-104 965491-2 1976 Sodium deprivation caused marked increases in plasma renin, blood angiotensin II, and plasma aldosterone, and was accompanied by a significant increase (+74%) in the number of specific angiotensin II receptor sites per adrenal cortical cell. Sodium 0-6 renin Rattus norvegicus 53-58 27230512-10 2016 The significantly larger furosemide-induced decrease in medullary R2* levels in the healthy group and unaffected contralateral kidneys of the VUR group points towards more intense renal sodium transport in these kidneys. Sodium 186-192 VUR Homo sapiens 142-145 27635179-11 2016 Cox proportional hazard analysis revealed that BNP increase at the time of discharge was an independent predictor of 6-month all-cause mortality after adjustment for age, sodium at discharge, creatinine at discharge and New York Heart Association (NYHA) class at discharge (hazard ratio 34.49; 95% confidence intervals: 4.55 - 261.06; P = 0.001). Sodium 171-177 natriuretic peptide B Homo sapiens 47-50 27564657-8 2016 Dermatan sulfate and polyphosphates with sodium as counter ion (Na-PolyP700, Na-PolyP100 and Na-PolyP70) enhanced plasmin-mediated but not thrombin-mediated TAFI activation. Sodium 41-47 plasminogen Homo sapiens 114-121 26872488-2 2016 Herein, we demonstrated in cultured cells and in vivo that increased levels of extracellular Pi activated the AKT/mammalian target of rapamycin complex 1 (mTORC1) pathway by suppressing membrane-bound phosphatase and tensin homolog (PTEN) levels in a manner requiring the sodium-dependent Pi transporter PiT-1. Sodium 272-278 CREB regulated transcription coactivator 1 Mus musculus 155-161 27320123-0 2016 Lithium-Rich Layered Oxide Li1.18 Ni0.15 Co0.15 Mn0.52 O2 as the Cathode Material for Hybrid Sodium-Ion Batteries. Sodium 93-99 transglutaminase 1 Homo sapiens 27-30 27320123-1 2016 Li-rich layered oxide Li1.18 Ni0.15 Co0.15 Mn0.52 O2 (LNCM) is, for the first time, examined as the positive electrode for hybrid sodium-ion battery and its Na(+) storage properties are comprehensively studied in terms of galvanostatic charge-discharge curves, cyclic voltammetry and rate capability. Sodium 130-136 transglutaminase 1 Homo sapiens 22-25 27323774-0 2016 AT2 Receptor Activation Prevents Sodium Retention and Reduces Blood Pressure in Angiotensin II-Dependent Hypertension. Sodium 33-39 angiotensin II receptor type 2 Homo sapiens 0-3 27252474-2 2016 Nax is a sodium (Na(+)) level sensor in the brain, and the transient receptor potential vanilloid (TRPV) channels TRPV1 and TRPV4 have been proposed to function as osmosensors. Sodium 9-15 sodium channel, voltage-gated, type VII, alpha Mus musculus 0-3 27648015-7 2016 Patients in a higher log-transformed BNP level tertile were more likely to be older, to have a higher frequency of cardiac comorbidities, pulse pressure, C-reactive protein levels, and proteinuria, and to have lower serum sodium, kidney function, and serum albumin (p < 0.05). Sodium 222-228 natriuretic peptide B Homo sapiens 37-40 25994218-9 2016 CONCLUSIONS: Dominant gain-of-function GUCY2C mutations lead to elevated intracellular cyclic guanosine monophosphate levels and could explain the chronic diarrhoea as a result of decreased intestinal sodium and water absorption and increased chloride secretion. Sodium 201-207 guanylate cyclase 2C Homo sapiens 39-45 26647426-6 2016 Compared with control mice, mice with macula densa-specific knockout of all nitric oxide synthase 1 isoforms (MD-NOS1KO) had a significantly enhanced tubuloglomerular feedback response and after acute volume expansion, significantly reduced GFR, urine flow, and sodium excretion. Sodium 262-268 nitric oxide synthase 1, neuronal Mus musculus 76-99 27038931-0 2016 Stromal Cell-Derived Factor 1 Increases Tetrodotoxin-Resistant Sodium Currents Nav1.8 and Nav1.9 in Rat Dorsal Root Ganglion Neurons via Different Mechanisms. Sodium 63-69 C-X-C motif chemokine ligand 12 Rattus norvegicus 0-29 27136376-6 2016 Electrochemical tests demonstrated that sodium-ion-functionalized GO (GNa) has shown outstanding Na-storage performance in terms of excellent rate capability and long-term cycle life (110 mAh g(-1) after 600 cycles at 1 A g(-1) ) owing to its high BET area, appropriate mesopore, high degree of disorder, and improved electrical conductivity. Sodium 40-46 delta/notch like EGF repeat containing Homo sapiens 248-251 27059077-6 2016 Furthermore, IK1-enhanced iPS-CMs expressing the F97C-CAV3 long QT9 mutation compared with wild-type CAV3 demonstrated an increase in AP duration and late sodium current. Sodium 155-161 IKAROS family zinc finger 1 Homo sapiens 13-16 27059077-6 2016 Furthermore, IK1-enhanced iPS-CMs expressing the F97C-CAV3 long QT9 mutation compared with wild-type CAV3 demonstrated an increase in AP duration and late sodium current. Sodium 155-161 caveolin 3 Homo sapiens 54-58 26880295-7 2016 The effect of high BNP levels on the risk of all-cause mortality was significantly greater in the subgroup of patients with a non-hypertensive etiology, low creatinine levels (<1.3mg/dL), and high sodium levels (>=135mEq/L) than in those without these factors (P=0.024, P<0.001, and P<0.001 for the interaction, respectively). Sodium 200-206 natriuretic peptide B Homo sapiens 19-22 26880295-8 2016 CONCLUSIONS: The present analysis shows that underlying etiology of heart failure (i.e., hypertensive), renal function, and sodium levels should be considered for assessing the clinical significance of elevated BNP levels on admission in relation to the risk of adverse outcome after hospitalization for AHFS. Sodium 124-130 natriuretic peptide B Homo sapiens 211-214 26818798-0 2016 High maternal sodium intake alters sex-specific renal renin-angiotensin system components in newborn Wistar offspring. Sodium 14-20 renin Rattus norvegicus 54-59 26567011-5 2016 We characterized the kinetic properties of system XAG (sodium-dependent) and systems xc- (sodium-independent) [3H]-L-glutamate uptake in the striatum and hippocampus of HIV-1 gp120 transgenic mice, an established model of HIV neuropathology. Sodium 90-96 Envelope surface glycoprotein gp160, precursor Human immunodeficiency virus 1 175-180 27000037-7 2016 Cultured cardiomyocytes from neonatal mice express messenger RNA (mRNA) for Nav1.2, 1.3, 1.5, 1.8, and 1.9 and generate TTX-sensitive sodium currents. Sodium 134-140 sodium channel, voltage-gated, type II, alpha Mus musculus 76-82 26786162-4 2016 Nav1.5 N-terminal domain, by itself (the 132 aa peptide) (Nter), exerts a "chaperone-like" effect that increases sodium (I(Na)) and inward rectifier potassium (I(K1)) currents by enhancing the expression of Nav1.5, Kir2.1, and Kir2.2 channels as demonstrated in Chinese hamster ovary (CHO) cells and in rat cardiomyocytes. Sodium 113-119 potassium inwardly rectifying channel subfamily J member 2 Homo sapiens 215-221 26951941-4 2016 We showed that the inhibitory effect of E2 on ANGII-induced water and sodium intake requires the ERK1/2 and JNK signaling pathways. Sodium 70-76 mitogen activated protein kinase 3 Rattus norvegicus 97-103 26933188-2 2016 Recent work has shown stimulation of sodium retention by urinary plasmin during nephrotic syndrome. Sodium 37-43 plasminogen Homo sapiens 65-72 27147650-6 2016 The decrease of Kir4.1 conductance reduced the sodium transients but increased the amplitudes of somatic GTCs. Sodium 47-53 potassium inwardly-rectifying channel, subfamily J, member 10 Mus musculus 16-22 26859646-6 2016 RESULTS: Activation of hTRPA1 by carvacrol and hTRPV1 by capsaicin produced a QX-314-independent reduction of sodium current amplitudes. Sodium 110-116 transient receptor potential cation channel subfamily A member 1 Homo sapiens 23-29 26859646-6 2016 RESULTS: Activation of hTRPA1 by carvacrol and hTRPV1 by capsaicin produced a QX-314-independent reduction of sodium current amplitudes. Sodium 110-116 transient receptor potential cation channel subfamily V member 1 Homo sapiens 47-53 26667412-4 2016 Signaling through dopamine D1 receptor and angiotensin II type I receptor (AT1R) reciprocally modulates renal sodium excretion and blood pressure. Sodium 110-116 angiotensin II receptor type 1 Homo sapiens 75-79 26475588-4 2016 The classic RAS comprises the ACE-ANG II-AT1R axis that promotes vasoconstriction; water intake; sodium retention; and increased oxidative stress, fibrosis, cellular growth, and inflammation. Sodium 97-103 angiogenin Homo sapiens 34-37 26475588-4 2016 The classic RAS comprises the ACE-ANG II-AT1R axis that promotes vasoconstriction; water intake; sodium retention; and increased oxidative stress, fibrosis, cellular growth, and inflammation. Sodium 97-103 angiotensin II receptor type 1 Homo sapiens 41-45 26760974-6 2016 During a 1-hour 3.86% mini-peritoneal equilibration test (mini-PET), AQP1fl/fl; Cdh5-Cre+ mice exhibited strongly decreased indices for AQP1-related transcellular water transport (43.0% in net ultrafiltration, 93.0% in sodium sieving and 57.9% in free water transport) compared to controls. Sodium 219-225 aquaporin 1 Mus musculus 69-73 26760974-6 2016 During a 1-hour 3.86% mini-peritoneal equilibration test (mini-PET), AQP1fl/fl; Cdh5-Cre+ mice exhibited strongly decreased indices for AQP1-related transcellular water transport (43.0% in net ultrafiltration, 93.0% in sodium sieving and 57.9% in free water transport) compared to controls. Sodium 219-225 aquaporin 1 Mus musculus 136-140 26742644-10 2016 In up-co-expression module, SCN3B (sodium channel, voltage gated, type III beta subunit) was enriched in GO:0006814 ~ sodium ion transport. Sodium 35-41 sodium voltage-gated channel beta subunit 3 Homo sapiens 28-33 26728597-0 2016 Regulation of SCN3B/scn3b by Interleukin 2 (IL-2): IL-2 modulates SCN3B/scn3b transcript expression and increases sodium current in myocardial cells. Sodium 114-120 sodium voltage-gated channel beta subunit 3 Homo sapiens 14-19 26728597-0 2016 Regulation of SCN3B/scn3b by Interleukin 2 (IL-2): IL-2 modulates SCN3B/scn3b transcript expression and increases sodium current in myocardial cells. Sodium 114-120 sodium voltage-gated channel beta subunit 3 Homo sapiens 20-25 26515654-2 2016 CS is caused by mutations in the SLC9A6 gene, which encodes a multipass transmembrane sodium (potassium)-hydrogen exchanger 6 (NHE6) protein, functional in early recycling endosomes. Sodium 86-92 solute carrier family 9 (sodium/hydrogen exchanger), member 6 Mus musculus 33-39 26515654-2 2016 CS is caused by mutations in the SLC9A6 gene, which encodes a multipass transmembrane sodium (potassium)-hydrogen exchanger 6 (NHE6) protein, functional in early recycling endosomes. Sodium 86-92 solute carrier family 9 (sodium/hydrogen exchanger), member 6 Mus musculus 127-131 26324851-0 2016 Aldosterone synthase knockout mouse as a model for sodium-induced endothelial sodium channel up-regulation in vascular endothelium. Sodium 51-57 cytochrome P450, family 11, subfamily b, polypeptide 2 Mus musculus 0-20 26668301-1 2016 The mineralocorticoid receptor (MR) and its ligand aldosterone are the principal modulators of hormone-regulated renal sodium reabsorption. Sodium 119-125 nuclear receptor subfamily 3 group C member 2 Homo sapiens 4-30 26668301-1 2016 The mineralocorticoid receptor (MR) and its ligand aldosterone are the principal modulators of hormone-regulated renal sodium reabsorption. Sodium 119-125 nuclear receptor subfamily 3 group C member 2 Homo sapiens 32-34 26487194-3 2015 Herein, ultrathin two-dimensional SnS2 nanosheets (3-4 nm in thickness) are synthesized via a facile refluxing process toward enhanced sodium storage. Sodium 135-141 sodium voltage-gated channel alpha subunit 11 Homo sapiens 34-38 26559902-4 2015 Importantly, we show that Caprin-2 knockdown in the hypothalamus decreases urine output and fluid intake, and increases urine osmolality, urine sodium concentration, and plasma AVP levels. Sodium 144-150 caprin family member 2 Homo sapiens 26-34 26495835-2 2015 In this issue of the JCI, a study by Zhang and associates shows that consumption of a high-sodium diet induces expression of cyclooxygenase-2 (COX-2) in macrophages, resulting in enhanced levels of prostaglandin E2 (PGE2), autocrine activation of the macrophage E-prostanoid 4 (EP4) receptor, and subsequent triggering of parallel pathways in the kidney and in skin that help dispose of excess sodium. Sodium 91-97 prostaglandin-endoperoxide synthase 2 Mus musculus 125-141 26495835-2 2015 In this issue of the JCI, a study by Zhang and associates shows that consumption of a high-sodium diet induces expression of cyclooxygenase-2 (COX-2) in macrophages, resulting in enhanced levels of prostaglandin E2 (PGE2), autocrine activation of the macrophage E-prostanoid 4 (EP4) receptor, and subsequent triggering of parallel pathways in the kidney and in skin that help dispose of excess sodium. Sodium 91-97 prostaglandin-endoperoxide synthase 2 Mus musculus 143-148 26495835-2 2015 In this issue of the JCI, a study by Zhang and associates shows that consumption of a high-sodium diet induces expression of cyclooxygenase-2 (COX-2) in macrophages, resulting in enhanced levels of prostaglandin E2 (PGE2), autocrine activation of the macrophage E-prostanoid 4 (EP4) receptor, and subsequent triggering of parallel pathways in the kidney and in skin that help dispose of excess sodium. Sodium 394-400 prostaglandin-endoperoxide synthase 2 Mus musculus 125-141 26330489-1 2015 The pharmacological action of peroxisome proliferator-activated receptor (PPAR)gamma in promoting sodium and water retention is well documented as highlighted by the major side-effect of body weight gain and edema associated with thiazolidinedione use. Sodium 98-104 peroxisome proliferator activated receptor gamma Mus musculus 74-78 26350587-0 2015 Combined Experimental and Computational Studies of a Na2 Ni1-x Cux Fe(CN)6 Cathode with Tunable Potential for Aqueous Rechargeable Sodium-Ion Batteries. Sodium 131-137 cut like homeobox 1 Homo sapiens 63-66 26350587-1 2015 Herein, potential-tunable Na2 Ni1-x Cux Fe(CN)6 nanoparticles with three-dimensional frameworks and large interstitial spaces were synthesized as alternative cathode materials for aqueous sodium-ion batteries by controlling the molar ratio of Ni(II) to Cu(II) at ambient temperature. Sodium 188-194 cut like homeobox 1 Homo sapiens 36-39 965491-6 1976 A decrease in receptor affinity was noted after 6 wk of either low sodium or low potassium intake, when the renin and angiotensin II levels were increased by 104-129%. Sodium 67-73 renin Rattus norvegicus 108-132 970153-4 1976 For the animals reacting with an increased sodium output a decrease in plasma renin activity was found together with an increase in glomerular filtration rate. Sodium 43-49 renin Rattus norvegicus 78-83 970153-6 1976 The animals not reacting with an increased sodium output had a higher initial plasma renin activity, which did not change during 1 M NaCl infusion. Sodium 43-49 renin Rattus norvegicus 85-90 939004-5 1976 Lowering sodium concentration inhibited renin release by one-half, even when osmolality was kept constant. Sodium 9-15 renin Rattus norvegicus 40-45 25770092-1 2015 BACKGROUND: The kidney, via its regulation of sodium excretion, which is modulated by humoral factors, including the dopamine and renin-angiotensin systems, keeps the blood pressure in the normal range. Sodium 46-52 renin Rattus norvegicus 130-135 954653-2 1976 Circadian rhythms of plasma aldosterone, prolactin, and corticosterone concentrations and of serum renin activity were demonstrated during a regular sodium diet. Sodium 149-155 renin Rattus norvegicus 99-104 988976-0 1976 Change in plasma renin substrate in lithium-intoxicated nephrectomized rats, and the effect of sodium on plasma renin and plasma renin substrate in lithium-intoxicated rats. Sodium 95-101 renin Rattus norvegicus 112-117 988976-0 1976 Change in plasma renin substrate in lithium-intoxicated nephrectomized rats, and the effect of sodium on plasma renin and plasma renin substrate in lithium-intoxicated rats. Sodium 95-101 renin Rattus norvegicus 112-117 1269103-8 1976 We conclude that a portion of saralasin-elicited renin release in sodium-depleted rats is mediated by hypotensive activation of the carotid baroreceptor reflex which increases sympathetic nervous activity in the kidney. Sodium 66-72 renin Rattus norvegicus 49-54 26173747-2 2015 In the proximal tubule, the Na(+) /H(+) Exchanger 3 (NHE3) is responsible for normal protein reabsorption and the reabsorption of approximately 70% of the renal sodium load. Sodium 161-167 solute carrier family 9 member A3 Rattus norvegicus 28-51 26173747-2 2015 In the proximal tubule, the Na(+) /H(+) Exchanger 3 (NHE3) is responsible for normal protein reabsorption and the reabsorption of approximately 70% of the renal sodium load. Sodium 161-167 solute carrier family 9 member A3 Rattus norvegicus 53-57 133480-1 1976 Using quantitative cytochemistry, activities of Na, K-ATPase, succinate dehydrogenase (SDH) and alpha-keto-glutarate dehydrogenase (alpha-KDH) was investigated in cells of renal tubules at different levels of sodium reabsorption in the kidney. Sodium 209-215 oxoglutarate dehydrogenase Rattus norvegicus 132-141 33051988-4 2021 We identified MeuNaTxalpha-1, a sodium channel-selective scorpion alpha-toxin from Mesobuthus eupeus, which affected both PKA-II and ERK1/2. Sodium 32-38 mitogen activated protein kinase 3 Rattus norvegicus 133-139 33051988-7 2021 Application of inhibitors and toxin mutants with altered sodium channel selectivity demonstrated that signaling activation in sensory neurons depends on NaV 1.2 isoform. Sodium 57-63 sodium voltage-gated channel alpha subunit 2 Rattus norvegicus 153-160 33077905-1 2021 Aldosterone is a biological ligand for mineralocorticoid receptor (MR) that elevates blood pressure by promoting sodium reabsorption in the kidneys. Sodium 113-119 nuclear receptor subfamily 3 group C member 2 Homo sapiens 39-65 33077905-1 2021 Aldosterone is a biological ligand for mineralocorticoid receptor (MR) that elevates blood pressure by promoting sodium reabsorption in the kidneys. Sodium 113-119 nuclear receptor subfamily 3 group C member 2 Homo sapiens 67-69 33688893-3 2021 Herein, double-carbon confined cobalt germanium hydroxide (CGH@C/rGO) composites has been facilely synthesized with the supportion of l-ascorbic acid and graphene oxide (GO) as anode materials for sodium-ion storage. Sodium 197-203 hypertrichosis 2 (generalised, congenital) Homo sapiens 59-62 26133798-6 2015 Consistent with the predicted loss of function induced by the mutation, knock-down of PigK phenocopies maco touch insensitivity and leads to reduced sodium current (INa) amplitudes in sensory neurons. Sodium 149-155 phosphatidylinositol glycan anchor biosynthesis, class K Danio rerio 86-90 26133798-9 2015 In addition, for maco mutants, expression of wild-type pigk restricted to sensory neurons rescues sodium current amplitudes and action potential firing in sensory neurons. Sodium 98-104 phosphatidylinositol glycan anchor biosynthesis, class K Danio rerio 55-59 25780059-6 2015 We have demonstrated that renin and (P)RR are augmented in renal tissues from rats infused with Ang II and during sodium depletion, suggesting a physiological role in intrarenal RAS activation. Sodium 114-120 renin Rattus norvegicus 26-31 26609290-10 2015 The serum sodium and triglycerides (M+-SD = 165.8+-9.1 mmol/l, 5.1+-8.1 mmol/l respectively) were significantly higher compared with the control group (M+-SD = 137.5+-3.9 mmol/l, 0.7+-0.3 mmol/l and P < 0.001, P < 0.05 respectively). Sodium 10-16 MSD Homo sapiens 36-41 26609290-10 2015 The serum sodium and triglycerides (M+-SD = 165.8+-9.1 mmol/l, 5.1+-8.1 mmol/l respectively) were significantly higher compared with the control group (M+-SD = 137.5+-3.9 mmol/l, 0.7+-0.3 mmol/l and P < 0.001, P < 0.05 respectively). Sodium 10-16 MSD Homo sapiens 152-157 33711230-7 2021 For the glucagon receptor (a Class B GPCR) we observed enhanced ligand binding in electrospray buffers containing high concentrations of sodium, as opposed to ammonium acetate buffers. Sodium 137-143 glucagon receptor Homo sapiens 8-25 33199159-1 2021 INTRODUCTION: Dravet syndrome (DS) is severe myoclonic epilepsy in infancy and associated with a heterozygous mutation of the gene for the sodium channel alpha 1 subunit (SCN1A). Sodium 139-145 sodium voltage-gated channel alpha subunit 1 Homo sapiens 171-176 33394730-5 2021 The presentation of hypertension and increased sodium-chloride cotransporter (NCC) activity in chloride-insensitive WNK4 mice proved that WNK4 is inhibitable by physiological [Cl-]i in DCT. Sodium 47-53 WNK lysine deficient protein kinase 4 Mus musculus 138-142 33755985-5 2021 The naive form of renal dopaminergic framework is related with the expanded reabsorption of sodium resulting in downregulation of the ACE2 expression. Sodium 92-98 angiotensin converting enzyme 2 Homo sapiens 134-138 32642858-9 2021 Functional analyses in Xenopus oocytes indicated that this mutated SLC12A3 gene encodes a protein which fails to mediate normal sodium transport, and when this mutant gene was expressed in HEK293T cells, we observed significant increases in endoplasmic reticulum (ER)-stress pathway activation. Sodium 128-134 solute carrier family 12 member 3 Homo sapiens 67-74 25851853-7 2015 Patients with 20 units/gram creatinine or higher urinary N-acetyl-beta-glucosaminidase developed statistically lower minimum serum sodium concentration (median 126 vs. 134 mEq/L, p = 0.0053). Sodium 131-137 O-GlcNAcase Homo sapiens 57-86 32939791-3 2021 Patch clamp, western blot and RT-PCR studies were performed to investigate neuronal firing thresholds and sodium channel subtypes Nav1.2 and Nav1.6 expression. Sodium 106-112 sodium channel, voltage-gated, type II, alpha Mus musculus 130-136 25784523-8 2015 Treatment with HS/HSD led to higher admission systolic blood pressure, sodium, chloride, and osmolarity, whereas lactate, base deficit, fluid requirement, and hemoglobin levels were similar in all groups. Sodium 71-77 carbohydrate sulfotransferase 3 Homo sapiens 18-21 26142600-10 2015 T&A led to normalization of ADH and BNP, probably through a calcium- and sodium-dependent mechanism. Sodium 77-83 natriuretic peptide B Homo sapiens 40-43 32939791-6 2021 Neurons grown up on Matrigel showed increased levels of sodium channel protein expression of Nav1.2 and Nav1.6 compared to neurons on PDL. Sodium 56-62 sodium channel, voltage-gated, type II, alpha Mus musculus 93-99 33450050-4 2021 Its properties are reminiscent of those of the sodium leak channel NALCN. Sodium 47-53 sodium leak channel, non-selective Mus musculus 67-72 25855512-2 2015 The present study is designed to investigate whether angiotensin type 2 receptor (AT2R) activation with selective agonist C21 prevents high-sodium diet (HSD)-induced hypertension in obese animals. Sodium 140-146 angiotensin II receptor, type 2 Rattus norvegicus 53-80 25855512-2 2015 The present study is designed to investigate whether angiotensin type 2 receptor (AT2R) activation with selective agonist C21 prevents high-sodium diet (HSD)-induced hypertension in obese animals. Sodium 140-146 angiotensin II receptor, type 2 Rattus norvegicus 82-86 25970036-0 2015 Solid-State Fabrication of SnS2/C Nanospheres for High-Performance Sodium Ion Battery Anode. Sodium 67-73 sodium voltage-gated channel alpha subunit 11 Homo sapiens 27-31 25768006-9 2015 The obesity risk increased 7.06, 16.8, and 46.09-fold more in boys with GRK4 A486V, ACE, and SLC12A3 mutants as sodium intake increased. Sodium 112-118 solute carrier family 12 member 3 Homo sapiens 93-100 25888997-13 2015 CONCLUSION: The results of the present study demonstrated that a GLP-1 analog and a DPP4 inhibitor may have beneficial effects on renal sodium and water handling. Sodium 136-142 dipeptidylpeptidase 4 Rattus norvegicus 84-88 24899236-3 2015 Mutations of Kir channels cause human hereditary diseases collectively called Kir channelopathies, many of which are characterized by disorders of sodium and potassium homeostasis. Sodium 147-153 killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 4 Homo sapiens 13-16 24899236-3 2015 Mutations of Kir channels cause human hereditary diseases collectively called Kir channelopathies, many of which are characterized by disorders of sodium and potassium homeostasis. Sodium 147-153 killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 4 Homo sapiens 78-81 24899236-4 2015 Studies on these genetic Kir channelopathies have shed light on novel pathophysiological mechanisms, including renal sodium and potassium handling, potassium shifting in skeletal muscles, and aldosterone production in the adrenal glands. Sodium 117-123 killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 4 Homo sapiens 25-28 24899236-5 2015 Here, we review several recent advances in Kir channels and their clinical implications in sodium and potassium homeostasis. Sodium 91-97 killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 4 Homo sapiens 43-46 25641537-10 2015 At 6 months, a post hoc analysis based on the dietary sodium intake achieved (> or <= 1,500 mg/d) in all patients showed an association between a sodium intake <= 1,500 mg/d and improvement in BNP levels and KCCQ scores. Sodium 152-158 natriuretic peptide B Homo sapiens 202-205 25641537-11 2015 CONCLUSIONS: A dietary intervention restricting sodium intake was feasible, and achievement of this sodium goal was associated with lower BNP levels and improved quality of life in patients with HF. Sodium 100-106 natriuretic peptide B Homo sapiens 138-141 24677068-6 2015 Analysis of splicing in DmNa v shows variants exhibit distinct gating properties including varying magnitudes of persistent sodium current (INaP). Sodium 124-130 paralytic Drosophila melanogaster 24-30 24677068-6 2015 Analysis of splicing in DmNa v shows variants exhibit distinct gating properties including varying magnitudes of persistent sodium current (INaP). Sodium 124-130 NFKB inhibitor zeta Homo sapiens 140-144 25616098-1 2015 AIM: Polymorphisms in the mineralocorticoid receptor may affect urinary sodium and potassium excretion. Sodium 72-78 nuclear receptor subfamily 3 group C member 2 Homo sapiens 26-52 24953135-2 2014 Although the MIT domains of CAPN7 were previously shown to interact with a subset of endosomal sorting complex required for transport (ESCRT)-III and ESCRT-III-related proteins, including charged multivesicular body protein 1 and increased sodium tolerance (IST)1, knowledge of the involvement of the protease in membrane trafficking has been limited. Sodium 240-246 calpain 7 Homo sapiens 28-33 24953135-2 2014 Although the MIT domains of CAPN7 were previously shown to interact with a subset of endosomal sorting complex required for transport (ESCRT)-III and ESCRT-III-related proteins, including charged multivesicular body protein 1 and increased sodium tolerance (IST)1, knowledge of the involvement of the protease in membrane trafficking has been limited. Sodium 240-246 IST1 factor associated with ESCRT-III Homo sapiens 258-263 24842923-9 2014 Taken together, acute AT2R stimulation enhanced renal vasodilatation and sodium excretion without concomitant alterations in glomerular filtration rate in female hypertensive rats. Sodium 73-79 angiotensin II receptor, type 2 Rattus norvegicus 22-26 25068403-8 2014 Circulating miRNA-34a in the hepatic vein correlated with ALT, CHE and sodium excretion after TIPS. Sodium 71-77 microRNA 34a Homo sapiens 12-21 24903104-3 2014 METHODS AND RESULTS: In rats, AT2R activation with intravenous C-21 increased urinary sodium excretion by 10-fold (P<0.0001); this natriuresis was abolished by direct renal interstitial infusion of specific AT2R antagonist PD-123319. Sodium 86-92 angiotensin II receptor, type 2 Rattus norvegicus 30-34 24829503-7 2014 These changes in nesfatin-1/NucB2 mRNA expression were positively correlated with plasma sodium concentration, plasma osmolality, and total protein levels in all of the examined nuclei. Sodium 89-95 nucleobindin 2 Rattus norvegicus 17-27 24829503-7 2014 These changes in nesfatin-1/NucB2 mRNA expression were positively correlated with plasma sodium concentration, plasma osmolality, and total protein levels in all of the examined nuclei. Sodium 89-95 nucleobindin 2 Rattus norvegicus 28-33 24785188-0 2014 Sodium and potassium regulate endothelial phospholipase C-gamma and Bmx. Sodium 0-6 BMX non-receptor tyrosine kinase Rattus norvegicus 68-71 24803536-2 2014 WNK1 is at the top of a kinase cascade, leading to phosphorylation of several cotransporters, in particular those transporting sodium, potassium, and chloride (NKCC), sodium and chloride (NCC), and potassium and chloride (KCC). Sodium 127-133 WNK lysine deficient protein kinase 1 Homo sapiens 0-4 33450050-12 2021 These biophysical attributes, together with the expression of the sodium-leak channel Nalcn transcript in CCs, state credible the contribution of NALCN. Sodium 66-72 sodium leak channel, non-selective Mus musculus 86-91 33378794-0 2021 Knockout of sodium channel Nax delays re-epithelializathion of splinted murine excisional wounds. Sodium 12-18 sodium channel, voltage-gated, type VII, alpha Mus musculus 27-30 33378794-3 2021 Our lab previously demonstrated that the atypical sodium channel Nax (encoded by Scn7a) responds to wound-induced epidermal dehydration, resulting in molecular cascades that drive pro-inflammatory signaling. Sodium 50-56 sodium channel, voltage-gated, type VII, alpha Mus musculus 65-68 33378794-3 2021 Our lab previously demonstrated that the atypical sodium channel Nax (encoded by Scn7a) responds to wound-induced epidermal dehydration, resulting in molecular cascades that drive pro-inflammatory signaling. Sodium 50-56 sodium channel, voltage-gated, type VII, alpha Mus musculus 81-86 33838996-11 2021 CONCLUSIONS: Sodium restriction significantly reduces SBP and DBP in patients with T2DM. Sodium 13-19 selenium binding protein 1 Homo sapiens 54-57 33465740-4 2021 In addition, accumulating evidence have revealed that MB diminishes voltage-gated sodium channel currents. Sodium 82-88 myoglobin Rattus norvegicus 54-56 33577799-0 2021 Inhibition of the epithelial sodium channel (ENaC) by connexin 30 involves stimulation of clathrin-mediated endocytosis. Sodium 29-35 gap junction protein beta 6 Homo sapiens 54-65 33577799-1 2021 Mice lacking connexin 30 (Cx30) display increased epithelial sodium channel (ENaC) activity in the distal nephron and develop salt-sensitive hypertension. Sodium 61-67 gap junction protein beta 6 Homo sapiens 13-24 33577799-1 2021 Mice lacking connexin 30 (Cx30) display increased epithelial sodium channel (ENaC) activity in the distal nephron and develop salt-sensitive hypertension. Sodium 61-67 gap junction protein beta 6 Homo sapiens 26-30 33145656-8 2021 Thus, RhoA might be considered as a potential negative regulator of sodium channels cardiac isoform NaV1.5. Sodium 68-74 sodium voltage-gated channel alpha subunit 5 Rattus norvegicus 100-106 24955166-8 2014 RESULTS: The sodium current density of ventricular cardiomyocytes from Rheb1 cKO mice was decreased by about 60%. Sodium 13-19 Ras homolog enriched in brain Mus musculus 71-76 24955166-11 2014 Moreover, the sodium current, in general, was recovered much slower in Rheb1 cKO mice than that of the controls. Sodium 14-20 Ras homolog enriched in brain Mus musculus 71-76 24955166-13 2014 CONCLUSION: Sodium currents are decreased in Rheb1 cKO mice, which might be responsible for the phenotype of arrhythima in Rheb1 cKO mice. Sodium 12-18 Ras homolog enriched in brain Mus musculus 45-50 24955166-13 2014 CONCLUSION: Sodium currents are decreased in Rheb1 cKO mice, which might be responsible for the phenotype of arrhythima in Rheb1 cKO mice. Sodium 12-18 Ras homolog enriched in brain Mus musculus 123-128 24508524-3 2014 Risperidone inhibited both endogenous and NaV1.6-mediated sodium currents at concentrations that are expected around active synaptic release sites owing to its strong accumulation in synaptic vesicles. Sodium 58-64 neuron navigator 1 Mus musculus 42-46 24552576-3 2014 Sulfonylurea receptor 1 (Sur1) is a transmembrane protein that, when activated in the central nervous system, allows for unregulated sodium influx into cells, a process that has been linked to cytotoxic edema formation in ischemic stroke, subarachnoid hemorrhage, spinal cord injury, traumatic brain injury, and, most recently, brain metastases. Sodium 133-139 ATP binding cassette subfamily C member 8 Homo sapiens 0-23 24552576-3 2014 Sulfonylurea receptor 1 (Sur1) is a transmembrane protein that, when activated in the central nervous system, allows for unregulated sodium influx into cells, a process that has been linked to cytotoxic edema formation in ischemic stroke, subarachnoid hemorrhage, spinal cord injury, traumatic brain injury, and, most recently, brain metastases. Sodium 133-139 ATP binding cassette subfamily C member 8 Homo sapiens 25-29 32826759-3 2021 Several voltage-gated sodium (NaV) and calcium (CaV) channels are implicated in the etiology of chronic pain, particularly NaV1.1, NaV1.3, NaV1.7-NaV1.9, CaV2.2 and CaV3.2. Sodium 22-28 sodium voltage-gated channel alpha subunit 1 Homo sapiens 123-129 32826759-3 2021 Several voltage-gated sodium (NaV) and calcium (CaV) channels are implicated in the etiology of chronic pain, particularly NaV1.1, NaV1.3, NaV1.7-NaV1.9, CaV2.2 and CaV3.2. Sodium 22-28 sodium voltage-gated channel alpha subunit 11 Homo sapiens 146-152 32826759-3 2021 Several voltage-gated sodium (NaV) and calcium (CaV) channels are implicated in the etiology of chronic pain, particularly NaV1.1, NaV1.3, NaV1.7-NaV1.9, CaV2.2 and CaV3.2. Sodium 22-28 calcium voltage-gated channel subunit alpha1 B Homo sapiens 154-160 32826759-3 2021 Several voltage-gated sodium (NaV) and calcium (CaV) channels are implicated in the etiology of chronic pain, particularly NaV1.1, NaV1.3, NaV1.7-NaV1.9, CaV2.2 and CaV3.2. Sodium 22-28 calcium voltage-gated channel subunit alpha1 H Homo sapiens 165-171 33614016-7 2021 The main ions involved in PH are calcium ion (Ca2+), potassium ion (K+), sodium ion (Na+) and chloride ion (Cl-). Sodium 73-79 phenylalanine hydroxylase Homo sapiens 26-28 33472641-6 2021 High sodium diet increased expression of nuclear factor of activated t-cells 5 (NFAT5)-a transcription factor responsive to changes in osmolarity-and moderately sulfated heparan sulfate in skin of healthy controls. Sodium 5-11 nuclear factor of activated T cells 5 Homo sapiens 41-78 33472641-6 2021 High sodium diet increased expression of nuclear factor of activated t-cells 5 (NFAT5)-a transcription factor responsive to changes in osmolarity-and moderately sulfated heparan sulfate in skin of healthy controls. Sodium 5-11 nuclear factor of activated T cells 5 Homo sapiens 80-85 33436636-5 2021 We revealed that the intracellular domain of NRG1 interacts with the cytoplasmic loop 1 of Nav1.1, a sodium channel critical for the excitability of GABAergic interneurons, and inhibits Nav currents. Sodium 101-107 neuregulin 1 Mus musculus 45-49 33585337-1 2021 Gitelman syndrome (GS) is a hereditary renal tubulopathy caused by mutations in the SLC12A3 gene which encodes the thiazide-sensitive apical sodium-chloride cotransporter. Sodium 141-147 solute carrier family 12 member 3 Homo sapiens 84-91 23802191-5 2014 Studies in Aqp1 mice have shown that deletion of AQP1 is reflected by a 50% decrease in ultrafiltration and a disappearance of the sodium sieving. Sodium 131-137 aquaporin 1 Mus musculus 49-53 24352520-0 2014 Missense mutations in plakophilin-2 cause sodium current deficit and associate with a Brugada syndrome phenotype. Sodium 42-48 plakophilin 2 Homo sapiens 22-35 24522961-0 2014 Hierarchical mesoporous SnO microspheres as high capacity anode materials for sodium-ion batteries. Sodium 78-84 strawberry notch homolog 1 Homo sapiens 24-27 24522961-4 2014 When applied as anode materials in Na-ion batteries, SnO microspheres exhibited high reversible sodium storage capacity, good cyclability and a satisfactory high rate performance. Sodium 96-102 strawberry notch homolog 1 Homo sapiens 53-56 24522961-7 2014 The high sodium storage capacity and good electrochemical performance could be ascribed to the unique hierarchical mesoporous architecture of SnO microspheres. Sodium 9-15 strawberry notch homolog 1 Homo sapiens 142-145 24380846-0 2014 Cx46 hemichannels contribute to the sodium leak conductance in lens fiber cells. Sodium 36-42 gap junction protein, alpha 3 Mus musculus 0-4 24179170-0 2014 Sodium transport is modulated by p38 kinase-dependent cross-talk between ENaC and Na,K-ATPase in collecting duct principal cells. Sodium 0-6 mitogen activated protein kinase 14 Rattus norvegicus 33-36 23900806-0 2014 Increased dietary sodium induces COX2 expression by activating NFkappaB in renal medullary interstitial cells. Sodium 18-24 prostaglandin-endoperoxide synthase 2 Mus musculus 33-37 23900806-2 2014 Selective blockade of renal medullary COX2 activity in rats causes salt-sensitive hypertension, suggesting a role for renal medullary COX2 in maintaining systemic sodium balance. Sodium 163-169 prostaglandin-endoperoxide synthase 2 Mus musculus 38-42 23900806-2 2014 Selective blockade of renal medullary COX2 activity in rats causes salt-sensitive hypertension, suggesting a role for renal medullary COX2 in maintaining systemic sodium balance. Sodium 163-169 prostaglandin-endoperoxide synthase 2 Mus musculus 134-138 23900806-8 2014 These data therefore suggest that renal medullary interstitial cell NFkappaB plays an important role in mediating renal medullary COX2 expression and promoting renal PGE2 synthesis in response to increased dietary sodium. Sodium 214-220 prostaglandin-endoperoxide synthase 2 Mus musculus 130-134 24520203-2 2014 Chronic sodium deprivation enhances renin secretion from the kidney, due to recruitment of additional cells from the afferent renal microvasculature to become renin-producing rather than just increasing release from existing juxtaglomerular (JG) cells. Sodium 8-14 renin Rattus norvegicus 36-41 24520203-2 2014 Chronic sodium deprivation enhances renin secretion from the kidney, due to recruitment of additional cells from the afferent renal microvasculature to become renin-producing rather than just increasing release from existing juxtaglomerular (JG) cells. Sodium 8-14 renin Rattus norvegicus 159-164 24520203-5 2014 We hypothesized that non-JG cells in renal microvessels recruited to produce renin in response to chronic dietary sodium restriction would demonstrate the calcium paradox, characteristic of the JG cell phenotype. Sodium 114-120 renin Rattus norvegicus 77-82 24520203-6 2014 Histology showed recruitment of upstream arteriolar renin in response to sodium restriction compared to normal-diet rats. Sodium 73-79 renin Rattus norvegicus 52-57 24520203-7 2014 Renin fluorescence intensity increased 53% in cortices of sodium-restricted rats (P<0.001). Sodium 58-64 renin Rattus norvegicus 0-5 24520203-9 2014 Basal renin release from normal sodium-diet rat microvessels in normal calcium media was 298.1+-44.6 ng AngI/mL/hour/mg protein, and in low-calcium media increased 39% to 415.9+-71.4 ng AngI/mL/hour/mg protein (P<0.025). Sodium 32-38 renin Rattus norvegicus 6-11 24520203-10 2014 Renin released from sodium-restricted rat microvessels increased 50% compared to samples from normal-diet rats (P<0.04). Sodium 20-26 renin Rattus norvegicus 0-5 24409169-5 2014 The classic RAS can be defined as the ACE-Ang II-AT1R axis that promotes vasoconstriction, sodium retention, and other mechanisms to maintain blood pressure, as well as increased oxidative stress, fibrosis, cellular growth, and inflammation in pathological conditions. Sodium 91-97 angiogenin Homo sapiens 42-45 24409169-5 2014 The classic RAS can be defined as the ACE-Ang II-AT1R axis that promotes vasoconstriction, sodium retention, and other mechanisms to maintain blood pressure, as well as increased oxidative stress, fibrosis, cellular growth, and inflammation in pathological conditions. Sodium 91-97 angiotensin II receptor type 1 Homo sapiens 49-53 29979251-1 2021 PURPOSE: To report the presence of drusen in infancy, in a patient with Type 1 retinopathy of prematurity and a rare congenital sodium diarrhea secondary to a sporadic GUCY2C mutation. Sodium 128-134 guanylate cyclase 2C Homo sapiens 168-174 24190904-1 2014 BACKGROUND: In response to high salt intake, transcription factor hypoxia-inducible factor (HIF) 1alpha activates many antihypertensive genes, such as heme oxygenase 1 (HO-1) 1 and cyclooxygenase 2 (COX-2) in the renal medulla, which is an important molecular adaptation to promote extra sodium excretion. Sodium 288-294 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 181-197 24190904-1 2014 BACKGROUND: In response to high salt intake, transcription factor hypoxia-inducible factor (HIF) 1alpha activates many antihypertensive genes, such as heme oxygenase 1 (HO-1) 1 and cyclooxygenase 2 (COX-2) in the renal medulla, which is an important molecular adaptation to promote extra sodium excretion. Sodium 288-294 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 199-204 24746040-2 2014 Experimental studies have identified two mechanisms potentially involved in this activity: one based on the persistent sodium current (INaP) and the other involving calcium (ICa) and/or calcium-activated nonspecific cation (ICAN) currents. Sodium 119-125 NFKB inhibitor zeta Homo sapiens 135-139 24215100-4 2013 Compounds 2 and 16 that blocked sodium permeation in Na(v)1.7 with IC50 values of 7 and 9 muM, respectively, are among the most potent clathrodin analogs discovered so far. Sodium 32-38 immunoglobulin lambda variable 2-23 Homo sapiens 53-61 24354396-7 2013 Leptin-treated LA myocytes showed a larger sodium current, but a smaller ultra-rapid delayed rectifier potassium current, and sodium-calcium exchanger current than the control. Sodium 43-49 leptin Oryctolagus cuniculus 0-6 24354396-7 2013 Leptin-treated LA myocytes showed a larger sodium current, but a smaller ultra-rapid delayed rectifier potassium current, and sodium-calcium exchanger current than the control. Sodium 126-132 leptin Oryctolagus cuniculus 0-6 24354396-8 2013 Leptin-treated and control LA myocytes exhibited a similar late sodium current, inward rectifier potassium current, transient outward current and L-type calcium current. Sodium 64-70 leptin Oryctolagus cuniculus 0-6 24040819-1 2013 The most relevant biological action of aldosterone in epithelial tissues is the regulation of sodium reabsorption through binding to the mineralocorticoid receptor (MR). Sodium 94-100 nuclear receptor subfamily 3 group C member 2 Homo sapiens 137-163 24040819-1 2013 The most relevant biological action of aldosterone in epithelial tissues is the regulation of sodium reabsorption through binding to the mineralocorticoid receptor (MR). Sodium 94-100 nuclear receptor subfamily 3 group C member 2 Homo sapiens 165-167 24126278-8 2013 Sodium, P, and Ca content and the interaction between content of NDF x Na were positively associated with excreta moisture. Sodium 0-6 neuregulin 1 Homo sapiens 65-68 24260444-5 2013 Selective inhibition of calcium channels and sodium/calcium exchange activity significantly diminished ELOA"s bactericidal activity, similar to what we have observed with HAMLET. Sodium 45-51 elongin A Homo sapiens 103-107 23660476-9 2013 In particular, miR-210 seemed to be more closely related than miR-30a to the pathological mechanisms of HF, including the calcium signaling, vascular smooth muscle contraction, transforming growth factor-beta signaling, and aldosterone-regulated sodium reabsorption pathways. Sodium 246-252 microRNA 210 Homo sapiens 15-22 33273469-0 2020 Structure of voltage-modulated sodium-selective NALCN-FAM155A channel complex. Sodium 31-37 sodium leak channel, non-selective Homo sapiens 48-53 33273469-2 2020 The NALCN channel mediates sodium leak currents, which positively adjust resting membrane potential towards depolarization. Sodium 27-33 sodium leak channel, non-selective Homo sapiens 4-9 33273469-6 2020 We find that the non-canonical architecture of NALCN selectivity filter dictates its sodium selectivity and calcium block, and that the asymmetric arrangement of two functional voltage sensors confers the modulation by membrane potential. Sodium 85-91 sodium leak channel, non-selective Mus musculus 47-52 33142317-0 2020 CACNA1H Calcium Channel Mutations in Primary Aldosteronism - Is Sodium the Culprit? Sodium 64-70 calcium voltage-gated channel subunit alpha1 H Homo sapiens 0-7 25602406-0 2013 Reduction of methyl isothiocyanate atmospheric emissions after application of metam sodium by shank injection. Sodium 84-90 SH3 and multiple ankyrin repeat domains 2 Homo sapiens 94-99 24005896-0 2013 A common polymorphism in the tissue kallikrein gene is associated with increased urinary excretions of calcium and sodium in Japanese volunteers. Sodium 115-121 kallikrein 1 Homo sapiens 29-46 24400138-1 2013 Sodium-dependent ascorbic acid membrane transporters SLC23A1 and SLC23A2 mediate ascorbic acid (vitamin C) transport into cells. Sodium 0-6 solute carrier family 23 member 2 Homo sapiens 65-72 24073915-2 2013 Meanwhile, replacement of sodium ion with an ammonium amphiphile 1 gives a lipid complex 1[Eu(nta)4] which shows distinct changes: its luminescence quantum yield Phi is remarkably increased to ~0.6 above the water content of ~60 vol. Sodium 26-32 glucose-6-phosphate isomerase Homo sapiens 162-165 24075186-1 2013 Sodium leak channel, nonselective (NALCN) is a voltage-independent and cation-nonselective channel that is mainly responsible for the leaky sodium transport across neuronal membranes and controls neuronal excitability. Sodium 140-146 sodium leak channel, non-selective Homo sapiens 35-40 24088384-1 2013 BACKGROUND: The human mineralocorticoid receptor (MR) is one of the main components of the renin-angiotensin-aldosterone system (RAAS), the system that regulates the body exchange of water and sodium. Sodium 193-199 nuclear receptor subfamily 3 group C member 2 Homo sapiens 22-48 24088384-1 2013 BACKGROUND: The human mineralocorticoid receptor (MR) is one of the main components of the renin-angiotensin-aldosterone system (RAAS), the system that regulates the body exchange of water and sodium. Sodium 193-199 nuclear receptor subfamily 3 group C member 2 Homo sapiens 50-52 23692342-4 2013 Previous results showed that leptin caused a partial blockade of sodium (I(Na)) and h-current (I(H)) in PPN neurons. Sodium 65-71 leptin Rattus norvegicus 29-35 32529661-9 2020 Taken together, PCTR1 upregulates sodium channels" expression via activating the ALX/cAMP/P-Akt/Nedd4-2 pathway and increases Na, K-ATPase expression and activity to promote alveolar fluid clearance. Sodium 34-40 NEDD4 like E3 ubiquitin protein ligase Rattus norvegicus 96-103 32346123-3 2020 Ang-(1-7), an alternative RAS product, counteracts Ang II by stimulating sodium excretion, vasodilation, and nitric oxide, thus contributing to lower BP. Sodium 73-79 angiopoietin 1 Homo sapiens 0-8 33189042-2 2020 The disease is mainly caused by heterozygous loss-of-function mutation of SCN1A gene encoding alpha subunit of the sodium channel Nav1.1. Sodium 115-121 sodium voltage-gated channel alpha subunit 1 Homo sapiens 74-79 33255592-0 2020 SnS2 Nanocrystalline-Anchored Three-Dimensional Graphene for Sodium Batteries with Improved Rate Performance. Sodium 61-67 sodium voltage-gated channel alpha subunit 11 Homo sapiens 0-4 33255592-1 2020 Tin disulfide (SnS2) is regarded as one of the most suitable candidates as the electrode material for sodium-ion batteries (SIBs). Sodium 102-108 sodium voltage-gated channel alpha subunit 11 Homo sapiens 15-19 33255592-7 2020 The excellent performance of the novel SnS2/3DG composite is attributed to the porous structure, which not only promoted the infiltration of electrolytes and hindered volume expansion for the porous structure, but also improved the conductivity of the whole electrode, demonstrating that the SnS2/3DG composite is a prospective anode for the next generation of sodium-ion batteries. Sodium 361-367 sodium voltage-gated channel alpha subunit 11 Homo sapiens 39-43 33581704-15 2020 An insufficient BNP response to sodium intake might be one of the underlying causes of MHT in obese cases. Sodium 32-38 natriuretic peptide B Homo sapiens 16-19 33156304-0 2020 In situ chemically encapsulated and controlled SnS2 nanocrystal composites for durable lithium/sodium-ion batteries. Sodium 95-101 sodium voltage-gated channel alpha subunit 11 Homo sapiens 47-51 33165811-7 2021 Consistent with the previous results, sodium cantharidinate treatment decreased Bcl-2 and mitochondrial cytochrome-c protein expression, as well as phosphorylation of MDM2; meanwhile, it increased the levels of cleaved-caspase-3, cleaved-caspase-9, cleaved-PARP, Bax, and phosphorylated p53, thus inducing the apoptosis of pancreatic cancer cells. Sodium 38-44 collagen type XI alpha 2 chain Homo sapiens 257-261 32619119-4 2020 We then identify an enrichment of ALS-associated mutations in another sodium channel, SCN7A, from whole genome sequencing data of 4495 ALS patients and 1925 controls passing multiple testing correction (67 variants, p = 0.0002, Firth logistic regression). Sodium 70-76 sodium voltage-gated channel alpha subunit 7 Homo sapiens 86-91 23698230-0 2013 Intrarenal ghrelin receptors regulate ENaC-dependent sodium reabsorption by a cAMP-dependent pathway. Sodium 53-59 ghrelin and obestatin prepropeptide Rattus norvegicus 11-18 23698230-2 2013 The infusion of ghrelin into the renal interstitium stimulates distal nephron-dependent sodium reabsorption in normal rats, but the mechanism is unknown. Sodium 88-94 ghrelin and obestatin prepropeptide Rattus norvegicus 16-23 23698230-6 2013 In the presence of amiloride, renal interstitial ghrelin failed to reduce urine sodium excretion, suggesting that ghrelin-induced sodium reabsorption is dependent on intact ENaC activity. Sodium 130-136 ghrelin and obestatin prepropeptide Rattus norvegicus 114-121 23816375-0 2013 Role of angiotensin II type 1 receptors in the subfornical organ in the pressor responses to central sodium in rats. Sodium 101-107 angiotensin II receptor, type 1a Rattus norvegicus 8-29 32979291-5 2020 Mouse models have suggested that Scn2a-, Scn3a-, and Scn8a-linked DEE variants are, in general, gain of function, resulting in increased persistent or resurgent sodium current (INa ) and pyramidal neuron hyperexcitability. Sodium 161-167 sodium channel, voltage-gated, type II, alpha Mus musculus 33-38 32979291-5 2020 Mouse models have suggested that Scn2a-, Scn3a-, and Scn8a-linked DEE variants are, in general, gain of function, resulting in increased persistent or resurgent sodium current (INa ) and pyramidal neuron hyperexcitability. Sodium 161-167 sodium channel, voltage-gated, type VIII, alpha Mus musculus 53-58 32335140-2 2020 Heterozygous loss-of-function mutations in one allele of SCN1A, the gene encoding the voltage-gated sodium channel 1.1 (NaV1.1), lead to DS. Sodium 100-106 sodium voltage-gated channel alpha subunit 1 Homo sapiens 57-62 32335140-2 2020 Heterozygous loss-of-function mutations in one allele of SCN1A, the gene encoding the voltage-gated sodium channel 1.1 (NaV1.1), lead to DS. Sodium 100-106 sodium voltage-gated channel alpha subunit 1 Homo sapiens 120-126 32768677-0 2020 Sodium current abnormalities and deregulation of Wnt/beta-catenin signaling in iPSC-derived cardiomyocytes generated from patient with arrhythmogenic cardiomyopathy harboring compound genetic variants in plakophilin 2 gene. Sodium 0-6 plakophilin 2 Homo sapiens 204-217 32768677-2 2020 Inhibitors of GSK3B were reported to restore sodium current and improve heart function in various arrhythmogenic cardiomyopathy models, but mechanisms underlying this effect remain unclear. Sodium 45-51 glycogen synthase kinase 3 beta Homo sapiens 14-19 32768677-5 2020 iPSC-derived cardiomyocytes from patient carrying two genetic variants in PKP2 gene demonstrated that PKP2 haploinsufficiency due to frameshift variant, in combination with the missense variant expressed from the second allele, was associated with decreased Wnt/beta-catenin activity and reduced sodium current. Sodium 296-302 plakophilin 2 Homo sapiens 74-78 32768677-5 2020 iPSC-derived cardiomyocytes from patient carrying two genetic variants in PKP2 gene demonstrated that PKP2 haploinsufficiency due to frameshift variant, in combination with the missense variant expressed from the second allele, was associated with decreased Wnt/beta-catenin activity and reduced sodium current. Sodium 296-302 plakophilin 2 Homo sapiens 102-106 32768677-7 2020 Inhibition of GSK3B led to the restoration of both Wnt/beta-catenin signaling activity and sodium current density in patient-specific cardiomyocytes while GSK3B activation led to the reduction of sodium current density. Sodium 91-97 glycogen synthase kinase 3 beta Homo sapiens 14-19 32768677-7 2020 Inhibition of GSK3B led to the restoration of both Wnt/beta-catenin signaling activity and sodium current density in patient-specific cardiomyocytes while GSK3B activation led to the reduction of sodium current density. Sodium 196-202 glycogen synthase kinase 3 beta Homo sapiens 155-160 32768677-8 2020 Moreover, we found that upon inhibition GSK3B sodium current was restored through Wnt/beta-catenin-independent mechanism. Sodium 46-52 glycogen synthase kinase 3 beta Homo sapiens 40-45 32768677-9 2020 CONCLUSION: We propose that alterations in GSK3B-Wnt/beta-catenin signaling pathways lead to regulation of sodium current implying its role in molecular pathogenesis of arrhythmogenic cardiomyopathy. Sodium 107-113 glycogen synthase kinase 3 beta Homo sapiens 43-48 32016826-3 2020 In our previous study, NaF exposure decreased IR expressions in olfactory bulb (OB) and hippocampus after Y-maze test in male mice. Sodium 23-26 insulin receptor Mus musculus 46-48 32016826-7 2020 The protein and mRNA expression levels of the IR were significantly decreased in the OB and hippocampus of the NaF-treated mice. Sodium 111-114 insulin receptor Mus musculus 46-48 32016826-9 2020 Taken together, these results indicated that Y-maze test could promote the expression levels of IR protein and mRNA in the OB and hippocampus, while NaF had a stronger inhibitory effect, which resulted in adverse effects on the expression levels of IR in the OB and hippocampus of male mice. Sodium 149-152 insulin receptor Mus musculus 249-251 32040846-2 2020 Transient receptor potential vanilloid 1 (TRPV1) as a Ca2+ permeable cation channel is activated by capsaicin and reactive oxygen species (ROS), although it is blocked by capsazepine and sodium selenite (Na-Se). Sodium 204-209 transient receptor potential cation channel subfamily V member 1 Homo sapiens 0-40 32040846-2 2020 Transient receptor potential vanilloid 1 (TRPV1) as a Ca2+ permeable cation channel is activated by capsaicin and reactive oxygen species (ROS), although it is blocked by capsazepine and sodium selenite (Na-Se). Sodium 204-209 transient receptor potential cation channel subfamily V member 1 Homo sapiens 42-47 32949224-10 2020 Furthermore, we hypothesize that mild edema may especially progress to severe edema in patients with sodium channel mutations which may represent an important mechanism to investigate in the context of understanding the significantly elevated risk of SUDEP in patients with SCN1A mutations. Sodium 101-107 sodium voltage-gated channel alpha subunit 1 Homo sapiens 274-279 32960505-6 2020 The increase in CD69 was strongly correlated to increases in 24-hour urinary sodium excretion (r = .93, P = .02). Sodium 77-83 CD69 molecule Homo sapiens 16-20 32592815-7 2020 An increase in natriuresis was observed after treatment with hydrochlorothiazide, but not amiloride, a change observed in parallel with increased phosphorylated sodium-chloride cotransporter (NCC). Sodium 161-167 solute carrier family 12 member 3 Rattus norvegicus 192-195 33254575-7 2020 ACE2 mediated dysregulation of sodium dependent glucose transporter (SGLT1 or SLC5A1) in the intestinal epithelium also links it to the pathogenesis of diabetes mellitus which can be a possible reason for the associated mortality in COVID-19 patients with diabetes. Sodium 31-37 angiotensin converting enzyme 2 Homo sapiens 0-4 32698188-0 2020 Structure of the human sodium leak channel NALCN. Sodium 23-29 sodium leak channel, non-selective Homo sapiens 43-48 23991143-8 2013 With no clear indication that the kidneys of salt-exposed offspring retained more sodium per se, we conducted a preliminary investigation of their gastrointestinal electrolyte handling and found increased expression of proximal colon solute carrier family 9 (sodium/hydrogen exchanger), member 3 (SLC9A3) together with altered faecal characteristics and electrolyte handling, relative to control offspring. Sodium 259-265 solute carrier family 9 member A3 Rattus norvegicus 297-303 23977363-1 2013 Melanocyte-stimulating hormones, alpha-, beta- and gamma-MSH, regulate important physiological functions including energy homeostasis, inflammation and sodium metabolism. Sodium 152-158 pro-opiomelanocortin-alpha Mus musculus 33-60 23977363-2 2013 Previous studies have shown that alpha-MSH increases sodium excretion and promotes vascular function in rodents, but it is unexplored whether these characteristics of alpha-MSH could translate into therapeutic benefits in the treatment of hypertension. Sodium 53-59 pro-opiomelanocortin-alpha Mus musculus 33-42 23966951-4 2013 The P2X4 receptor has been linked to epithelial sodium transport in the nephron and expression levels of the P2X7 receptor are up-regulated in certain pathophysiological states. Sodium 48-54 purinergic receptor P2X 4 Homo sapiens 4-8 33079488-0 2020 Structural Engineering of SnS2 Encapsulated in Carbon Nanoboxes for High-Performance Sodium/Potassium-Ion Batteries Anodes. Sodium 85-91 sodium voltage-gated channel alpha subunit 11 Homo sapiens 26-30 32758497-3 2020 In this study, eight human sodium channel subtypes, hNav1.1- hNav1.8, were expressed in HEK293 or ND7/23 cells and tested on the chemically synthesized TsIIIA. Sodium 27-33 sodium voltage-gated channel alpha subunit 1 Homo sapiens 52-59 33178316-4 2020 A total of nine genes (Nav1.1-Nav1.9) have been recognized to encode practical sodium channel isoforms. Sodium 79-85 sodium voltage-gated channel alpha subunit 1 Homo sapiens 23-29 33178316-4 2020 A total of nine genes (Nav1.1-Nav1.9) have been recognized to encode practical sodium channel isoforms. Sodium 79-85 sodium voltage-gated channel alpha subunit 11 Homo sapiens 30-36 33192558-5 2020 We hypothesized that in dermal fibroblasts (DFs) high-sodium concentration activates the COX-2/PGE2 pathway and also that PGE2 increases the production of HA. Sodium 54-60 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 89-94 33192558-9 2020 Sodium excess activates the COX-2/PGE2 pathway in DFs, and COX-2 inhibition decreases the synthesis of HA. Sodium 0-6 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 28-33 32898233-4 2021 METHODS AND RESULTS: Using human cardiac tissues, transcriptomic correlative analyses between IRX5 and genes involved in cardiac electrical activity showed that in human ventricular compartment, IRX5 expression strongly correlated to the expression of major actors of cardiac conduction, including the sodium channel, Nav1.5, and Connexin 40 (Cx40). Sodium 302-308 iroquois homeobox 5 Homo sapiens 195-199 23747447-2 2013 TGA and (23)Na MAS NMR suggested the formation of new hydrated sodium phase, which is likely responsible for the high activity of the catalyst. Sodium 63-69 T-box transcription factor 1 Homo sapiens 0-3 23628455-11 2013 The renin-angiotensin-aldosterone system participates in the impaired coronary relaxation in aged SHR, but does not partake in this deleterious effect under increased salt intake, indicating that age could differentiate the effects of high sodium intake in coronary arteries of SHR. Sodium 240-246 renin Rattus norvegicus 4-9 23753418-1 2013 D3 dopamine receptor (D3R)-deficient mice have renin-dependent hypertension associated with sodium retention, but the hypertension is mild. Sodium 92-98 dopamine receptor D3 Mus musculus 0-20 23753418-1 2013 D3 dopamine receptor (D3R)-deficient mice have renin-dependent hypertension associated with sodium retention, but the hypertension is mild. Sodium 92-98 dopamine receptor D3 Mus musculus 22-25 23541953-0 2013 Caveolin-3 suppresses late sodium current by inhibiting nNOS-dependent S-nitrosylation of SCN5A. Sodium 27-33 caveolin 3 Homo sapiens 0-10 23541953-0 2013 Caveolin-3 suppresses late sodium current by inhibiting nNOS-dependent S-nitrosylation of SCN5A. Sodium 27-33 nitric oxide synthase 1 Homo sapiens 56-60 23558339-3 2013 Single-channel analysis in freshly isolated split-open tubules demonstrated that the InsR-KO mice have significantly lower ENaC activity compared to their wild-type (C57BL/6J) littermates when animals were fed either normal or sodium-deficient diets. Sodium 227-233 insulin receptor Mus musculus 85-89 23608660-3 2013 The collecting duct (CD) is the site of daily fine-tune regulation of sodium balance, and led us to hypothesize that a CD-specific deletion of NOS1 would result in an impaired ability to excrete a sodium load leading to a salt-sensitive blood pressure phenotype. Sodium 70-76 nitric oxide synthase 1, neuronal Mus musculus 143-147 23608660-3 2013 The collecting duct (CD) is the site of daily fine-tune regulation of sodium balance, and led us to hypothesize that a CD-specific deletion of NOS1 would result in an impaired ability to excrete a sodium load leading to a salt-sensitive blood pressure phenotype. Sodium 197-203 nitric oxide synthase 1, neuronal Mus musculus 143-147 23344129-0 2013 Urinary prostasin in normotensive individuals: correlation with the aldosterone to renin ratio and urinary sodium. Sodium 107-113 serine protease 8 Homo sapiens 8-17 26877914-8 2013 The change in serum sodium concentration was correlated with postdialysis SBP (r=0.304, P<0.005) and pulse pressure (r=0.299, P<0.005). Sodium 20-26 selenium binding protein 1 Homo sapiens 74-77 26877914-9 2013 Predialysis SBP (r = 0.317, P<0.005) and pulse pressure (r=0.324, P=0.001) were also correlated with the postdialysis serum sodium change. Sodium 127-133 selenium binding protein 1 Homo sapiens 12-15 23501259-0 2013 Fat and salt contents affect the in-mouth temporal sodium release and saltiness perception of chicken sausages. Sodium 51-57 FAT atypical cadherin 1 Gallus gallus 0-3 24967239-3 2013 After ingestion of a salty meal, GN and UGN are secreted into the intestinal lumen, where they inhibit sodium absorption and induce anion and water secretion. Sodium 103-109 guanylate cyclase activator 2b (retina) Mus musculus 40-43 23430254-7 2013 Conversely to angiotensin 2 receptor, PAR2 is involved in the regulation of sodium and potassium balance in the context of either stimulation or nonstimulation of the renin/angiotensin/aldosterone system. Sodium 76-82 F2R like trypsin receptor 1 Homo sapiens 38-42 23324064-1 2013 INTRODUCTION: Over the last two decades, the known functions of the mineralocorticoid receptor (MR) have expanded beyond regulation of sodium and potassium in epithelial cells to encompass physiological and pathophysiological effects in many tissues throughout the body. Sodium 135-141 nuclear receptor subfamily 3, group C, member 2 Mus musculus 68-94 23324064-1 2013 INTRODUCTION: Over the last two decades, the known functions of the mineralocorticoid receptor (MR) have expanded beyond regulation of sodium and potassium in epithelial cells to encompass physiological and pathophysiological effects in many tissues throughout the body. Sodium 135-141 nuclear receptor subfamily 3, group C, member 2 Mus musculus 96-98 23314744-0 2013 Sodium-dependent modulation of systemic and urinary renalase expression and activity in the rat remnant kidney. Sodium 0-6 renalase, FAD-dependent amine oxidase Rattus norvegicus 52-60 23314744-2 2013 RESULTS: The reduced circulating renalase levels in 3/4nx rats during normal-sodium intake were accompanied by increased plasma renalase activity. Sodium 77-83 renalase, FAD-dependent amine oxidase Rattus norvegicus 33-41 23314744-3 2013 The sodium-induced increase of blood pressure in 3/4nx rats was accompanied by significant decreases in circulating renalase levels and activity as well as by a significant decrease in cardiac renalase levels in 3/4nx rats but not in Sham rats. Sodium 4-10 renalase, FAD-dependent amine oxidase Rattus norvegicus 116-124 23314744-3 2013 The sodium-induced increase of blood pressure in 3/4nx rats was accompanied by significant decreases in circulating renalase levels and activity as well as by a significant decrease in cardiac renalase levels in 3/4nx rats but not in Sham rats. Sodium 4-10 renalase, FAD-dependent amine oxidase Rattus norvegicus 193-201 23314744-5 2013 During high-sodium intake, urinary renalase levels increased in both 3/4nx and Sham groups by three-fold whereas urinary renalase activity increased in 3/4nx and Sham rats by greater than twelve-fold and greater than four-fold, respectively. Sodium 12-18 renalase, FAD-dependent amine oxidase Rattus norvegicus 35-43 23314744-8 2013 Differences in systemic and urinary renalase levels and activity between 3/4nx and Sham rats during high-sodium intake may contribute to activation of the sympathetic nervous system, hypertension and enhanced cardiovascular risk in CKD but do not appear to account for the decrease in renal dopaminergic activity in the rat remnant kidney. Sodium 105-111 renalase, FAD-dependent amine oxidase Rattus norvegicus 36-44 23255722-1 2013 The sodium/calcium exchanger (NCX) is a widespread transporter that exchanges sodium and calcium ions across excitable membranes. Sodium 4-10 T cell leukemia, homeobox 2 Mus musculus 30-33 23255722-2 2013 Normally, NCX mainly operates in its "forward" mode, harnessing the electrochemical gradient of sodium ions to expel calcium. Sodium 96-102 T cell leukemia, homeobox 2 Mus musculus 10-13 23255722-3 2013 During membrane depolarization or elevated internal sodium levels, NCX can instead switch the direction of net flux to expel sodium and allow calcium entry. Sodium 52-58 T cell leukemia, homeobox 2 Mus musculus 67-70 23255722-3 2013 During membrane depolarization or elevated internal sodium levels, NCX can instead switch the direction of net flux to expel sodium and allow calcium entry. Sodium 125-131 T cell leukemia, homeobox 2 Mus musculus 67-70 23255722-7 2013 Simulations, supported by experimental manipulations, showed that accumulation of intracellular sodium drove NCX into reverse mode. Sodium 96-102 T cell leukemia, homeobox 2 Mus musculus 109-112 23129822-7 2013 In the acute experiment, the increases in expression of osteopontin, MCP-1, alpha-SMA, TGF-beta and collagen III were significantly reduced by dietary sodium restriction. Sodium 151-157 C-C motif chemokine ligand 2 Rattus norvegicus 69-74 23129822-7 2013 In the acute experiment, the increases in expression of osteopontin, MCP-1, alpha-SMA, TGF-beta and collagen III were significantly reduced by dietary sodium restriction. Sodium 151-157 actin gamma 2, smooth muscle Rattus norvegicus 82-85 23240817-4 2013 We show higher HKT1;1 expression in abi4 mutant plants and lower levels of expression in ABI4-overexpressing plants, resulting in reduced accumulation of sodium ions in the shoot of abi4 mutants. Sodium 154-160 high-affinity K+ transporter 1 Arabidopsis thaliana 15-21 23240817-5 2013 HKT1;1 encodes a sodium transporter which is known to unload sodium ions from the root xylem stream into the xylem parenchyma stele cells. Sodium 17-23 high-affinity K+ transporter 1 Arabidopsis thaliana 0-6 23325664-0 2013 Polysulfide chemistry in sodium-sulfur batteries and related systems--a computational study by G3X(MP2) and PCM calculations. Sodium 25-31 tryptase pseudogene 1 Homo sapiens 99-102 23417379-1 2013 Non-dystrophic myotonias (NDM) are characterised by muscle stiffness during voluntary movement owing to delayed skeletal muscle relaxation caused by mutations in the chloride (CLCN1) and sodium (SCN4A) skeletal muscle channel genes. Sodium 187-193 sodium voltage-gated channel alpha subunit 4 Homo sapiens 195-200 24555036-4 2013 METHODS: In this short study, we (1) compared the biophysical properties of the sodium current (I Na) generated by the mouse Na v1.5 (mNa v1.5) and human Na v1.5 (hNa v1.5) constructs that were expressed in HEK293 cells, and (2) investigated the possible alterations of the biophysical properties of the human Na v1.5 construct that was modified with specific epitopes. Sodium 80-86 immunoglobulin lambda variable 2-18 Homo sapiens 128-132 24555036-4 2013 METHODS: In this short study, we (1) compared the biophysical properties of the sodium current (I Na) generated by the mouse Na v1.5 (mNa v1.5) and human Na v1.5 (hNa v1.5) constructs that were expressed in HEK293 cells, and (2) investigated the possible alterations of the biophysical properties of the human Na v1.5 construct that was modified with specific epitopes. Sodium 80-86 sodium voltage-gated channel alpha subunit 5 Homo sapiens 135-142 24555036-4 2013 METHODS: In this short study, we (1) compared the biophysical properties of the sodium current (I Na) generated by the mouse Na v1.5 (mNa v1.5) and human Na v1.5 (hNa v1.5) constructs that were expressed in HEK293 cells, and (2) investigated the possible alterations of the biophysical properties of the human Na v1.5 construct that was modified with specific epitopes. Sodium 80-86 immunoglobulin lambda variable 2-18 Homo sapiens 138-142 24555036-4 2013 METHODS: In this short study, we (1) compared the biophysical properties of the sodium current (I Na) generated by the mouse Na v1.5 (mNa v1.5) and human Na v1.5 (hNa v1.5) constructs that were expressed in HEK293 cells, and (2) investigated the possible alterations of the biophysical properties of the human Na v1.5 construct that was modified with specific epitopes. Sodium 80-86 sodium voltage-gated channel alpha subunit 5 Homo sapiens 135-142 23364694-3 2013 Here we show that the Caenorhabditis elegans tmc-1 gene encodes a sodium sensor that functions specifically in salt taste chemosensation. Sodium 66-72 Transmembrane channel-like protein 1 Caenorhabditis elegans 45-50 23364694-6 2013 When expressed in mammalian cell culture, C. elegans TMC-1 generates a predominantly cationic conductance activated by high extracellular sodium but not by other cations or uncharged small molecules. Sodium 138-144 Transmembrane channel-like protein 1 Caenorhabditis elegans 53-58 23393317-8 2013 In summary, these results suggest that SPAK mediates the effect of vasopressin on sodium reabsorption along the distal nephron. Sodium 82-88 serine/threonine kinase 39 Mus musculus 39-43 23010574-5 2012 This study showed that the conjugation of sodium taurocholates selectively blocked interaction with antithrombin III (ATIII) while enhancing the binding with VEGF. Sodium 42-48 serpin family C member 1 Homo sapiens 100-116 23010574-5 2012 This study showed that the conjugation of sodium taurocholates selectively blocked interaction with antithrombin III (ATIII) while enhancing the binding with VEGF. Sodium 42-48 serpin family C member 1 Homo sapiens 118-123 32898233-7 2021 In accordance with the prolonged QRS interval observed in Hamamy Syndrome patients, a slower ventricular action potential depolarization due to sodium current reduction was observed on electrophysiological analyses performed on patient-derived cardiomyocytes, confirming the functional role of IRX5 in electrical conduction. Sodium 144-150 iroquois homeobox 5 Homo sapiens 294-298 32755467-10 2020 Collectively, these results suggest that endogenous GLP-1R signaling exerts a physiologically relevant effect on BP control, which may be attributable, in part, to its tonic actions on the proximal tubule NHE3-mediated sodium reabsorption, intrarenal renin-angiotensin system, and insulin sensitivity. Sodium 219-225 solute carrier family 9 member A3 Rattus norvegicus 205-209 31659629-0 2020 IL-1 promotes alpha-epithelial Sodium Channel (alpha-ENaC) expression in murine lung epithelial cells: involvement of NF-kappaB. Sodium 31-37 interleukin 1 complex Mus musculus 0-4 32705197-2 2020 Taurine"s influx and efflux are mainly mediated through the ubiquitous expression of the sodium/chloride-dependent taurine transporter, located on the plasma membrane. Sodium 89-95 solute carrier family 6 (neurotransmitter transporter, taurine), member 6 Mus musculus 115-134 32835124-7 2020 Additionally, Furin intracellular levels are largely dependent on concentration of intracellular ions, notably sodium, potassium, and magnesium. Sodium 111-117 furin, paired basic amino acid cleaving enzyme Homo sapiens 14-19 23232097-11 2012 Taken together, our results suggest that UBP16 is involved in salt tolerance in Arabidopsis by modulating sodium transport activity and repressing cell death at least partially through modulating SMH1stability and activity. Sodium 106-112 ubiquitin-specific protease 16 Arabidopsis thaliana 41-46 23002235-1 2012 The epithelial Na(+) channel (ENaC) in the aldosterone-sensitive distal nephron (ASDN) is under tonic inhibition by a local purinergic signaling system responding to changes in dietary sodium intake. Sodium 185-191 sodium channel, nonvoltage-gated 1 alpha Mus musculus 4-28 23002235-1 2012 The epithelial Na(+) channel (ENaC) in the aldosterone-sensitive distal nephron (ASDN) is under tonic inhibition by a local purinergic signaling system responding to changes in dietary sodium intake. Sodium 185-191 sodium channel, nonvoltage-gated 1 alpha Mus musculus 30-34 23002235-3 2012 We tested here whether ATP secreted through connexin channels in a coupled manner with K(+) efflux through BK(Ca) channels is required for inhibitory purinergic regulation of ENaC in response to increases in sodium intake. Sodium 208-214 sodium channel, nonvoltage-gated 1 alpha Mus musculus 175-179 23002235-6 2012 As a consequence, ENaC activity, particularly in the presence of high sodium intake, is inappropriately elevated in BK-beta4 null mice. Sodium 70-76 sodium channel, nonvoltage-gated 1 alpha Mus musculus 18-22 23002235-10 2012 These results demonstrate that the ATP secreted in the ASDN in a BK(Ca) channel-dependent manner is physiologically available for purinergic inhibition of ENaC in response to changes in sodium homeostasis. Sodium 186-192 sodium channel, nonvoltage-gated 1 alpha Mus musculus 155-159 23002235-11 2012 Impaired sodium excretion resulting form loss of normal purinergic regulation of ENaC in BK-beta4 null mice likely contributes to their elevated blood pressure. Sodium 9-15 sodium channel, nonvoltage-gated 1 alpha Mus musculus 81-85 22989884-3 2012 Once activated by WNK1, OSR1 and SPAK phosphorylate and stimulate the sodium, potassium, two chloride co-transporters, NKCC1 and NKCC2, and also affect other related ion co-transporters. Sodium 70-76 solute carrier family 12 member 2 Homo sapiens 119-124 22977235-11 2012 Consequently, SPAK(-/-) mice are highly sensitive to dietary salt restriction, displaying prolonged negative sodium balance and hypotension. Sodium 109-115 serine/threonine kinase 39 Mus musculus 14-18 23033373-3 2012 Under normal sodium intake (0.32% Na(+)), ENaC open probability (P(o)) was modestly elevated in B1R, B2R(-/-) mice compared with wild-type mice. Sodium 13-19 sodium channel, nonvoltage-gated 1 alpha Mus musculus 42-46 23033373-9 2012 We concluded that BK cascade has its own specific role in blunting ENaC activity, particularly under conditions of elevated sodium intake. Sodium 124-130 sodium channel, nonvoltage-gated 1 alpha Mus musculus 67-71 32770034-5 2020 This effect was also obtained using the other ROCK inhibitor Fasudil as well as with knocking down the expression of ROCK-1 or ROCK-2, but was prevented by the inhibition of NaV1.5 voltage-gated sodium channel activity. Sodium 195-201 Rho associated coiled-coil containing protein kinase 1 Homo sapiens 117-123 32770034-5 2020 This effect was also obtained using the other ROCK inhibitor Fasudil as well as with knocking down the expression of ROCK-1 or ROCK-2, but was prevented by the inhibition of NaV1.5 voltage-gated sodium channel activity. Sodium 195-201 Rho associated coiled-coil containing protein kinase 2 Homo sapiens 127-133 32439321-1 2020 Salt-Overly-Sensitive (SOS) signaling module comprising the sodium-transport protein SOS1 and the regulatory proteins SOS2 and SOS3, is well known as the central salt excretion system that helps plants against salt accumulation. Sodium 60-66 Calcium-binding EF-hand family protein Arabidopsis thaliana 127-131 32830219-11 2020 Our data show that TTX-S sodium channel Nav1.6 is involved in the functional changes of dorsal root ganglion neurons following vincristine treatment and it contributes to the maintenance of vincristine-induced mechanical allodynia. Sodium 25-31 sodium channel, voltage-gated, type VIII, alpha Mus musculus 40-46 23373225-3 2012 RESULT: On the 7th day, the neuron-like cells derived from ginsenoside Rg1 (20 mg x L(-1))-induced NSCs show: (1) The resting membrane potential: (-45.70 +/- 2.63) mV, the membrane capacitance: (26.89 +/- 1.91) pF, the membrane input impedance: (877.51 +/- 20.44) MH (P < 0.05 compared with the control group, respectively); (2) The detection rate of inward sodium current which is rapidly activated and inactivated in voltage-dependence was 50%, and its average peak value was (711.48 +/- 158.03) pA (P < 0.05 compared with the control group); (3) The outward potassium currents were composed of rapidly activated and inactivated transient outward potassium current and delayed rectifier outward potassium current, and its average peak value was (1 070.42 +/- 177.18) pA (P < 0.05 compared with the control group). Sodium 361-367 protein phosphatase 1 regulatory subunit 3A Homo sapiens 71-74 23035147-6 2012 Compared with the major G allele, the BDKRB2 rs11847625 minor C allele was significantly associated with increased systolic blood pressure responses to low-sodium intervention (P = 0.0001). Sodium 156-162 bradykinin receptor B2 Homo sapiens 38-44 23035147-8 2012 Seven highly correlated ECE1 SNPs were shown to increase the diastolic blood pressure response to low-sodium intervention (P values ranged from 0.0003 to 0.002), with 2 haplotypes containing these 7 SNPs also associated with this same phenotype (P values ranged from 0.0004 to 0.002). Sodium 102-108 endothelin converting enzyme 1 Homo sapiens 24-28 22587908-8 2012 The high-sodium diet also induced Ang II, TGF-beta(1) and alpha-SMA overexpression and decreased eNOS expression in the renal cortex and medulla. Sodium 9-15 actin gamma 2, smooth muscle Rattus norvegicus 58-67 22455658-4 2012 The purpose of the present study was to test the hypothesis that inhibiting sodium absorption via the epithelial sodium channel (ENaC) will increase ocular hydration in both normal as well as in animals with experimentally induced dry eye. Sodium 76-82 sodium channel, nonvoltage-gated 1 alpha Mus musculus 129-133 21424526-3 2012 Its expression is modulated by salt intake, and urinary renalase may regulate catecholamines levels and effect renal sodium and phosphate transport. Sodium 117-123 renalase, FAD-dependent amine oxidase Rattus norvegicus 56-64 22373544-4 2012 We establish the membrane ions" contributions (sodium, potassium, calcium and iron) mediated by water to the antagonism of these drugs at the 5-HT1A receptor. Sodium 47-53 5-hydroxytryptamine receptor 1A Homo sapiens 142-157 22238420-8 2012 Altering two amino acid residues in TsHKT1;2 to mimic the AtHKT1 sequence resulted in enhanced sodium uptake and loss of the TsHKT1;2 intrinsic K(+) transporter activity. Sodium 95-101 high-affinity K+ transporter 1 Arabidopsis thaliana 58-64 22344440-4 2012 We report on the conversion of synthesis gas to C(2) through C(4) olefins with selectivity up to 60 weight percent, using catalysts that constitute iron nanoparticles (promoted by sulfur plus sodium) homogeneously dispersed on weakly interactive alpha-alumina or carbon nanofiber supports. Sodium 192-198 complement C2 Homo sapiens 48-52 22344440-4 2012 We report on the conversion of synthesis gas to C(2) through C(4) olefins with selectivity up to 60 weight percent, using catalysts that constitute iron nanoparticles (promoted by sulfur plus sodium) homogeneously dispersed on weakly interactive alpha-alumina or carbon nanofiber supports. Sodium 192-198 complement C4A (Rodgers blood group) Homo sapiens 61-65 22203739-11 2012 We conclude that sodium depletion upregulates renal PRR expression via the cGMP-PKG signaling pathway by enhancing binding of cAMP response element binding protein 1, nuclear factor-kappaB p65, and c-Jun to PRR promotor. Sodium 17-23 cAMP responsive element binding protein 1 Rattus norvegicus 126-165 32232733-3 2020 Understanding of the pathophysiology of edema is still evolving with recent research elucidating newer mechanism of sodium retention through plasmin mediated epithelial sodium channel activation in collecting duct. Sodium 116-122 plasminogen Homo sapiens 141-148 32652890-2 2020 Herein, we identify the involvement of sodium/glucose co-transporter gene (SGLT2) in disrupted cellular Ca2+ -homeostasis, and mitochondrial dysfunction in age-associated cardiac dysfunction. Sodium 39-45 solute carrier family 5 member 2 Rattus norvegicus 75-80 31506013-1 2020 SLC5A8 is a sodium-coupled monocarboxylate and ketone transporter expressed in various epithelial cells. Sodium 12-18 solute carrier family 5 (iodide transporter), member 8 Mus musculus 0-6 32624180-3 2020 We discovered a novel inhibitor, EOS789, that interacts with several sodium-dependent phosphate transporters (NaPi-IIb, PiT-1, and PiT-2) known to contribute to intestinal phosphate absorption. Sodium 69-75 solute carrier family 34 member 2 Rattus norvegicus 110-118 32680508-3 2020 We tested the hypothesis that short palate lung and nasal epithelial clone 1 (SPLUNC1)-epithelial sodium channel (ENaC) interactions at the plasma membrane are required to reduce Bcc burden in normal airways. Sodium 98-104 BPI fold containing family A member 1 Homo sapiens 78-85 32596999-10 2020 Sodium, chloride, and magnesium concentrations increased progressively with distance ran, suggesting that these electrolytes are primarily being lost as exercising dogs salivate. Sodium 0-6 RAN, member RAS oncogene family Canis lupus familiaris 85-88 21993890-0 2012 Effect of high and low sodium intake on urinary aquaporin-2 excretion in healthy humans. Sodium 23-29 aquaporin 2 Homo sapiens 48-59 22677781-2 2012 In many organ systems, this activity is regulated by membrane-bound sodium/calcium (Na(+)/Ca(2+)) exchangers, which include the NCX and NCKX [sodium/calcium-potassium (Na(+)/Ca(2+)-K(+)) exchanger] proteins. Sodium 68-74 solute carrier family 24 member 1 Homo sapiens 136-140 22591021-4 2012 The increases in water and sodium absorption via AQP2 and ENaC after furosemide treatment most likely are compensatory phenomena to antagonize water and sodium depletion. Sodium 27-33 aquaporin 2 Homo sapiens 49-53 22591021-4 2012 The increases in water and sodium absorption via AQP2 and ENaC after furosemide treatment most likely are compensatory phenomena to antagonize water and sodium depletion. Sodium 153-159 aquaporin 2 Homo sapiens 49-53 22174313-7 2011 To determine whether an alternative therapy would be more appropriate, we characterized cardiomyocytes from Mecp2(Null/Y) mice and found increased persistent sodium current, which was normalized when cells were treated with the sodium channel-blocking anti-seizure drug phenytoin. Sodium 158-164 methyl CpG binding protein 2 Mus musculus 108-113 21943787-1 2011 Brugada Syndrome (BS) is a cardiac ion channel disorder linked to loss of function mutation in the SCN5A gene which affects the sodium current. Sodium 128-134 sodium voltage-gated channel alpha subunit 5 Homo sapiens 99-104 21945676-0 2011 Blocking of sodium and potassium ion-dependent adenosine triphosphatase-alpha1 with ouabain and vanadate suppresses cell-cell fusion during RANKL-mediated osteoclastogenesis. Sodium 12-18 tumor necrosis factor (ligand) superfamily, member 11 Mus musculus 140-145 21704303-5 2011 The phase of steady increase was blocked without major effect on the plateau by KB-R 7943, a sodium/calcium exchange (NCX) inhibitor. Sodium 93-99 T cell leukemia, homeobox 2 Mus musculus 118-121 21705762-0 2011 Post-transcriptional silencing of SCN1B and SCN2B genes modulates late sodium current in cardiac myocytes from normal dogs and dogs with chronic heart failure. Sodium 71-77 sodium voltage-gated channel beta subunit 2 Canis lupus familiaris 44-49 21840964-6 2011 Importantly, we also expressed the peptide spanning the H558R polymorphism with 8 additional BrS Na(v)1.5 mutations with reduced currents and demonstrated that the peptide was able to restore significant sodium currents in 4 of them. Sodium 204-210 immunoglobulin lambda variable 2-18 Homo sapiens 97-105 32431059-0 2020 A Flexible Film with SnS2 Nanoparticles Chemically Anchored on 3D-Graphene Framework for High Areal Density and High Rate Sodium Storage. Sodium 122-128 sodium voltage-gated channel alpha subunit 11 Homo sapiens 21-25 32452762-2 2020 We report that SARS-CoV-2 has evolved a unique S1/S2 cleavage site, absent in any previous coronavirus sequenced, resulting in the striking mimicry of an identical FURIN-cleavable peptide on the human epithelial sodium channel alpha-subunit (ENaC-alpha). Sodium 212-218 furin, paired basic amino acid cleaving enzyme Homo sapiens 164-169 32587934-11 2020 The Cancer Genome Atlas analysis demonstrated concomitant NFAT5 amplification and overexpression (P < 0.0001) that correlated with increased expression of sodium/myo-inositol transporter SLC5A3 (r 2 = 0.237, P < 0.0001) and 14 other regulatory proteins (P < 0.05) previously shown to interact with NFAT5. Sodium 155-161 nuclear factor of activated T cells 5 Homo sapiens 58-63 32587934-11 2020 The Cancer Genome Atlas analysis demonstrated concomitant NFAT5 amplification and overexpression (P < 0.0001) that correlated with increased expression of sodium/myo-inositol transporter SLC5A3 (r 2 = 0.237, P < 0.0001) and 14 other regulatory proteins (P < 0.05) previously shown to interact with NFAT5. Sodium 155-161 solute carrier family 5 member 3 Homo sapiens 187-193 32587934-11 2020 The Cancer Genome Atlas analysis demonstrated concomitant NFAT5 amplification and overexpression (P < 0.0001) that correlated with increased expression of sodium/myo-inositol transporter SLC5A3 (r 2 = 0.237, P < 0.0001) and 14 other regulatory proteins (P < 0.05) previously shown to interact with NFAT5. Sodium 155-161 nuclear factor of activated T cells 5 Homo sapiens 298-303 32027092-1 2020 The sodium channel NaX (encoded by the SCN7A gene) was originally identified in the heart and skeletal muscle and is structurally similar to the other voltage-gated sodium channels but does not appear to be voltage gated. Sodium 4-10 sodium voltage-gated channel alpha subunit 7 Homo sapiens 39-44 21788423-0 2011 Inhibition of Navbeta4 peptide-mediated resurgent sodium currents in Nav1.7 channels by carbamazepine, riluzole, and anandamide. Sodium 50-56 sodium voltage-gated channel beta subunit 4 Homo sapiens 14-22 21784856-1 2011 Serum- and glucocorticoid-regulated kinase 1 (sgk1) participates in diverse biological processes, including cell growth, apoptosis, and sodium homeostasis. Sodium 136-142 serum/glucocorticoid regulated kinase 1 Mus musculus 0-44 21784856-1 2011 Serum- and glucocorticoid-regulated kinase 1 (sgk1) participates in diverse biological processes, including cell growth, apoptosis, and sodium homeostasis. Sodium 136-142 serum/glucocorticoid regulated kinase 1 Mus musculus 46-50 21784856-2 2011 In the cortical collecting duct of the kidney, sgk1 regulates sodium transport by stimulating the epithelial sodium channel (ENaC). Sodium 62-68 serum/glucocorticoid regulated kinase 1 Mus musculus 47-51 21784856-2 2011 In the cortical collecting duct of the kidney, sgk1 regulates sodium transport by stimulating the epithelial sodium channel (ENaC). Sodium 62-68 sodium channel, nonvoltage-gated 1 alpha Mus musculus 125-129 21273195-3 2011 Cardiac sodium current reduction caused by SCN5A mutations may facilitate AFib by slowing intra-atrial conduction and inducing structural changes, but also prevent it by suppressing atrial ectopic activity. Sodium 8-14 sodium voltage-gated channel alpha subunit 5 Homo sapiens 43-48 21467193-7 2011 Understanding of MR-regulatory mechanisms could therefore lead to new therapeutic strategies for the management of sodium loss in preterms and neonates. Sodium 115-121 nuclear receptor subfamily 3, group C, member 2 Mus musculus 17-19 21340731-0 2011 Scutellarin blocks sodium current in freshly isolated mouse hippocampal CA1 neurons. Sodium 19-25 carbonic anhydrase 1 Mus musculus 72-75 21340731-2 2011 To explore the therapeutic mechanism of Scu, we investigated the impact of Scu on sodium current (I(Na)) of freshly isolated mouse hippocampal CA1 neurons using the whole-cell patch clamp technique. Sodium 82-88 carbonic anhydrase 1 Mus musculus 143-146 21493770-6 2011 Isolated brush border membranes from gsk3(KI) mice showed less sodium-dependent phosphate transport and Na-phosphate co-transporter expression. Sodium 63-69 glycogen synthase kinase 3 beta Mus musculus 37-41 32027092-1 2020 The sodium channel NaX (encoded by the SCN7A gene) was originally identified in the heart and skeletal muscle and is structurally similar to the other voltage-gated sodium channels but does not appear to be voltage gated. Sodium 19-22 sodium voltage-gated channel alpha subunit 7 Homo sapiens 39-44 32027092-1 2020 The sodium channel NaX (encoded by the SCN7A gene) was originally identified in the heart and skeletal muscle and is structurally similar to the other voltage-gated sodium channels but does not appear to be voltage gated. Sodium 165-171 sodium voltage-gated channel alpha subunit 7 Homo sapiens 39-44 31874233-7 2020 Changes in pHi recovery due to intracellular acidification and alkalization induced by NH4Cl prepulse and Na-acetate prepulse, respectively, were detected by microspectrofluorimetry with the pH-sensitive fluorescent dye BCECF. Sodium 106-116 glucose-6-phosphate isomerase Homo sapiens 11-14 32300368-6 2020 The findings of this study revealed that groundwater in the north of the West Bank comply with several drinking water requirements including total hardness, pH, and sodium and chloride content. Sodium 165-171 B cell scaffold protein with ankyrin repeats 1 Homo sapiens 78-82 32226389-6 2020 Such electrophysiological changes could be attributed to an increase in inward sodium current density and a decrease in funny current densities, which is consistent with the observed up- and downregulated SCN1B and HCN2/4 transcripts, respectively. Sodium 79-85 sodium voltage-gated channel beta subunit 1 Homo sapiens 205-210 32210813-7 2020 Consistent with a conserved structure-function amongst sodium-dependent neurotransmitter transporters, S1 residues A73, A77 (G100 in hSERT), N78, V148 (I150 in hSERT), N153, G320, F329 (Y331 in d DAT), N350, and G423 are conserved in DAT and SERT, indicating they likely play conserved functional roles. Sodium 55-61 Serotonin transporter Drosophila melanogaster 134-138 31901456-3 2020 In this study, a functional sodium alginate (SA) dressing with H2S-releasing property (SA/JK-1) was fabricated by incorporating JK-1 molecule, a pH-dependent H2S donor, into SA sponge. Sodium 28-34 reticulophagy regulator 1 Homo sapiens 90-94 31901456-3 2020 In this study, a functional sodium alginate (SA) dressing with H2S-releasing property (SA/JK-1) was fabricated by incorporating JK-1 molecule, a pH-dependent H2S donor, into SA sponge. Sodium 28-34 reticulophagy regulator 1 Homo sapiens 128-132 31930721-4 2020 Treatment with 10 mM NaF induced a significant difference in the production of ROS, triggered the expression of cleaved caspase-3 and upregulated the mRNA expression of Fas-L in regular L-929 cells. Sodium 21-24 Fas ligand (TNF superfamily, member 6) Mus musculus 169-174 31957111-5 2020 Furthermore, we found that NaB inhibited migration and induced AMPK/mTOR pathway-activated autophagy and reactive oxygen species (ROS) overproduction via the miR-139-5p/Bmi-1 axis. Sodium 27-30 BMI1 proto-oncogene, polycomb ring finger Homo sapiens 169-174 31836481-0 2020 Protein kinase D2 regulates epithelial sodium channel activity and aldosterone non-genomic responses in renal cortical collecting duct cells. Sodium 39-45 protein kinase D2 Rattus norvegicus 0-17 31997705-2 2020 Objective: This study aimed to delineate in pre-hypertensive SHR kidneys the receptor and/or post-receptor defect causing impaired AT2R signaling and renal sodium (Na+) retention by utilizing the selective AT2R agonist Compound 21 (C-21). Sodium 156-162 angiotensin II receptor, type 2 Rattus norvegicus 206-210 21190943-0 2011 Reduced sodium channel Na(v)1.1 levels in BACE1-null mice. Sodium 8-14 beta-site APP cleaving enzyme 1 Mus musculus 42-47 21190943-2 2011 We have previously identified the contribution of elevated BACE1 activity to voltage-gated sodium channel Na(v)1.1 density and neuronal function. Sodium 91-97 beta-site APP cleaving enzyme 1 Mus musculus 59-64 21190943-3 2011 Here, we analyzed physiological changes in sodium channel metabolism in BACE1-null mice. Sodium 43-49 beta-site APP cleaving enzyme 1 Mus musculus 72-77 21190943-13 2011 Together, our data show that endogenous BACE1 activity regulates total and surface levels of voltage-gated sodium channels in mouse brains. Sodium 107-113 beta-site APP cleaving enzyme 1 Mus musculus 40-45 21051419-2 2011 Screening of SCN5A-the gene encoding the alpha-subunit of the cardiac sodium channel-has indicated that disturbances of the sodium current may play a central role in the mechanism of lone AF. Sodium 70-76 sodium voltage-gated channel alpha subunit 5 Homo sapiens 13-18 21173039-6 2011 The results suggest that activity of these three carriers is sodium/potassium-independent and affected differently by changes in pHo and DeltaPsi: Oatp1a1 was confirmed to be an electroneutral anion exchanger, whereas the function of both OATP1B1 and OATP1B3 was markedly affected by the magnitude of DeltaPsi. Sodium 61-67 solute carrier organic anion transporter family member 1B1 Homo sapiens 239-246 21609529-5 2011 RESULTS: In transfected HEK293 cells, the nonsense mutation in SCN5A inhibited the expression level of full-length protein, and the sodium currents from the mutant channels were less than 3% of the wild-type level. Sodium 132-138 sodium voltage-gated channel alpha subunit 5 Homo sapiens 63-68 21098479-2 2011 The transporter GAT-1 mediates electrogenic cotransport of GABA, sodium, and chloride. Sodium 65-71 solute carrier family 6 (neurotransmitter transporter), member 1 S homeolog Xenopus laevis 16-21 21088576-11 2011 SUMMARY: SPAK is a recently identified regulator of NCC and, hence, sodium reabsorption in the distal nephron. Sodium 68-74 serine/threonine kinase 39 Mus musculus 9-13 22216116-4 2011 Pravastatin is a hydrophilic statin that is selectively taken up by a sodium-independent organic anion transporter protein-1B1 (OATP1B1) exclusively expressed in liver. Sodium 70-76 solute carrier organic anion transporter family member 1B1 Homo sapiens 128-135 20937801-2 2010 Dipeptide transport by AtPTR1 and AtPTR5 was found to be electrogenic and dependent on protons but not sodium. Sodium 103-109 peptide transporter 1 Arabidopsis thaliana 23-29 22127746-2 2010 In order to better clarify the human tissue distribution of expression of SGLT2 and related members of this cotransporter class, we performed TaqMan (Applied Biosystems, Foster City, CA, USA) quantitative polymerase chain reaction (PCR) analysis of SGLT2 and other sodium/glucose transporter genes on RNAs from 72 normal tissues from three different individuals. Sodium 266-272 solute carrier family 5 member 2 Homo sapiens 74-79 20717920-4 2010 Interestingly, increased extracellular Pi resulted in activation of the Raf/MEK/ERK pathway and expression of EGR1, which involved type III sodium/phosphate (Na(+)/Pi) cotransporter PiT-1. Sodium 140-146 early growth response 1 Homo sapiens 110-114 32123746-4 2020 Here, we probed the existence of internal and functionally important sodium ions in the dopamine D2 receptor, using molecular dynamics simulations. Sodium 69-75 dopamine receptor D2 Homo sapiens 88-108 31870150-4 2020 Moreover, NaB promotes toll-like receptor 2 (TLR2) expression. Sodium 10-13 toll like receptor 2 Sus scrofa 23-43 31870150-4 2020 Moreover, NaB promotes toll-like receptor 2 (TLR2) expression. Sodium 10-13 toll like receptor 2 Sus scrofa 45-49 31870150-5 2020 TLR2 silencing inhibits the pBD3 and pEP2C expression induced by NaB but does not abolish the histone deacetylase (HDAC) inhibitory activity of NaB. Sodium 65-68 toll like receptor 2 Sus scrofa 0-4 31870150-10 2020 This study showed that NaB simultaneously induces pBD3 and pEP2C via TLR2 and EGFR in IPEC J2 cells without increasing the risk of a harmful inflammatory response. Sodium 23-26 toll like receptor 2 Sus scrofa 69-73 31433752-2 2020 In pathophysiological conditions, over activation of RAAS leads to an increase in the concentration of Angiotensin II (AngII) and over activation of Angiotensin Type 1 Receptor (AT1R) resulting in vasoconstriction, sodium retention and change in myocyte growth. Sodium 215-221 angiotensin II receptor type 1 Homo sapiens 149-176 31433752-2 2020 In pathophysiological conditions, over activation of RAAS leads to an increase in the concentration of Angiotensin II (AngII) and over activation of Angiotensin Type 1 Receptor (AT1R) resulting in vasoconstriction, sodium retention and change in myocyte growth. Sodium 215-221 angiotensin II receptor type 1 Homo sapiens 178-182 32407275-0 2020 The sodium channel Nav1.7 is involved in paclitaxel-induced peripheral neuropathy though ERK1/2 signaling in rats. Sodium 4-10 mitogen activated protein kinase 3 Rattus norvegicus 89-95 32402638-1 2020 The mineralocorticoid receptor (MR) has classically been studied in the renal epithelium for its role in regulating sodium and water balance and, subsequently, blood pressure. Sodium 116-122 nuclear receptor subfamily 3 group C member 2 Homo sapiens 4-30 32402638-1 2020 The mineralocorticoid receptor (MR) has classically been studied in the renal epithelium for its role in regulating sodium and water balance and, subsequently, blood pressure. Sodium 116-122 nuclear receptor subfamily 3 group C member 2 Homo sapiens 32-34 31838698-11 2020 Desorption studies with 0.1 M NaOH indicate that ZnO:Alx% can be regenerated effectively. Sodium 30-34 hematopoietic SH2 domain containing Homo sapiens 53-56 21139332-3 2010 When expressed in X. oocytes, RPL3 mediated the high affinity transport of [(3)H]digoxin (K(m) = 213.3 +- 46.8 nM) in a time-, concentration-, and sodium-dependent manners. Sodium 147-153 ribosomal protein L3 L homeolog Xenopus laevis 30-34 21085628-0 2010 A coastal cline in sodium accumulation in Arabidopsis thaliana is driven by natural variation of the sodium transporter AtHKT1;1. Sodium 19-25 high-affinity K+ transporter 1 Arabidopsis thaliana 120-128 20535627-8 2010 Aldosterone and transforming growth factor-beta1 reciprocally regulate expression of prostasin, PN-1, and ENaC in renal epithelial cell, resulting in sodium retention or natriuresis, respectively. Sodium 150-156 serpin family E member 2 Homo sapiens 96-100 20838240-4 2010 Therefore, we investigated the expression patterns of KCC2 and its functional opponent, the chloride influx-mediating sodium-potassium chloride cotransporter 1 (NKCC1), in the superoxide dismutase 1 (SOD1-G93A) mouse model of ALS. Sodium 118-124 solute carrier family 12, member 5 Mus musculus 54-58 20838445-1 2010 Previously, cell type-specific expression of AtHKT1;1, a sodium transporter, improved sodium (Na(+)) exclusion and salinity tolerance in Arabidopsis. Sodium 86-94 high-affinity K+ transporter 1 Arabidopsis thaliana 45-53 20629553-10 2010 Sunitinib treatment of RET/PTC1 cell lines, in combination, with forskolin induced expression of the sodium (Na)/iodide (I) symporter (NIS) and the transcription factors that bind the NIS upstream enhancer. Sodium 101-107 ret proto-oncogene Homo sapiens 23-26 20580637-0 2010 Estradiol attenuates multiple tetrodotoxin-sensitive sodium currents in isolated gonadotropin-releasing hormone neurons. Sodium 53-59 gonadotropin releasing hormone 1 Mus musculus 81-111 31928904-1 2020 The four voltage-gated sodium channels SCN1/2/3/8A have been associated with heterogeneous types of developmental disorders, each presenting with disease specific temporal and cell type specific gene expression. Sodium 23-29 sodium voltage-gated channel alpha subunit 1 Homo sapiens 39-50 20558140-6 2010 Mutation A130V dramatically decreased the cardiac sodium current density when expressed in HEK293/Na(v)1.5 stable cell line, but did not have significant effect on kinetics of activation, inactivation, and channel recovery from inactivation. Sodium 50-56 immunoglobulin lambda variable 2-18 Homo sapiens 98-106 31786985-8 2020 In an intraperitoneal saline challenge test at day 7 of Ang II, FLT3L-/- mice excreted higher proportions of the injected volume and sodium than WTs. Sodium 133-139 FMS-like tyrosine kinase 3 ligand Mus musculus 64-69 31746362-6 2020 Of the eleven HDACs (HDAC1-11) studied, only the mRNA expression of HDAC2 was attenuated by NaBu in NRK-52E cells under the HG condition. Sodium 92-96 histone deacetylase 1 Rattus norvegicus 21-29 31746362-6 2020 Of the eleven HDACs (HDAC1-11) studied, only the mRNA expression of HDAC2 was attenuated by NaBu in NRK-52E cells under the HG condition. Sodium 92-96 histone deacetylase 2 Rattus norvegicus 68-73 31746362-7 2020 Overexpression of HDAC2 offset the anti-apoptotic effect of NaBu. Sodium 60-64 histone deacetylase 2 Rattus norvegicus 18-23 31746362-10 2020 Mechanistically, NaBu acted as an antioxidant in HG-induced NRK-52E cells and suppressed HG-induced apoptosis of NRK-52E cells through inhibiting HDAC2 by virtue of its anti-oxidative property. Sodium 17-21 histone deacetylase 2 Rattus norvegicus 146-151 31550457-4 2020 Recent studies demonstrated that intrinsic and synaptic properties of GABAergic interneurons and excitatory cells are regulated by a slowly inactivating or non-inactivating sodium current (i.e., persistent sodium current, INaP), suggesting that INaP is involved in gamma oscillations. Sodium 173-179 NFKB inhibitor zeta Homo sapiens 222-226 31550457-4 2020 Recent studies demonstrated that intrinsic and synaptic properties of GABAergic interneurons and excitatory cells are regulated by a slowly inactivating or non-inactivating sodium current (i.e., persistent sodium current, INaP), suggesting that INaP is involved in gamma oscillations. Sodium 173-179 NFKB inhibitor zeta Homo sapiens 245-249 31550457-4 2020 Recent studies demonstrated that intrinsic and synaptic properties of GABAergic interneurons and excitatory cells are regulated by a slowly inactivating or non-inactivating sodium current (i.e., persistent sodium current, INaP), suggesting that INaP is involved in gamma oscillations. Sodium 206-212 NFKB inhibitor zeta Homo sapiens 245-249 31765958-1 2020 PURPOSE: The vast majority of mutations responsible for epilepsy syndromes such as genetic epilepsy with febrile seizures plus (GEFS+) and Dravet syndrome (DS) occur in the gene encoding the type 1 alpha subunit of neuronal voltage-gated sodium channel (SCN1A). Sodium 238-244 sodium voltage-gated channel alpha subunit 1 Homo sapiens 254-259 33148866-7 2020 A mutation within the SCN1B encoding genes, which is responsible for channelopathy within the voltage-dependent Nav sodium channels, may be considered as a potential cause for this state. Sodium 116-122 sodium voltage-gated channel beta subunit 1 Homo sapiens 22-27 31892729-1 2019 Ginsenoside Rb1 exerts its pharmacological action by regulating sodium, potassium and calcium ion channels in the membranes of nerve cells. Sodium 64-70 RB transcriptional corepressor 1 Homo sapiens 12-15 31701738-6 2019 More importantly, BF-1 affords high sensitivity for monitoring Sec stimulated by Na2SeO3 in tumor-bearing mice. Sodium 81-88 eukaryotic elongation factor, selenocysteine-tRNA-specific Mus musculus 63-66 31892185-1 2019 BACKGROUND: Natriuretic peptides (NPs), including brain natriuretic peptide (BNP), are neurohormones involved in the regulation of water-sodium balance and the maintenance of cardiovascular homeostasis. Sodium 137-143 natriuretic peptide B Homo sapiens 50-75 31892185-1 2019 BACKGROUND: Natriuretic peptides (NPs), including brain natriuretic peptide (BNP), are neurohormones involved in the regulation of water-sodium balance and the maintenance of cardiovascular homeostasis. Sodium 137-143 natriuretic peptide B Homo sapiens 77-80 20335314-0 2010 mPGES-1 deletion impairs aldosterone escape and enhances sodium appetite. Sodium 57-63 prostaglandin E synthase Mus musculus 0-7 31835299-8 2019 In addition, ion analysis showed that opr7opr8 accumulated less sodium but more potassium in the leaves than WT but more sodium and less potassium in the roots than WT, suggesting that JA deficiency causes higher salt stress to the roots but less stress to the leaves of the seedlings. Sodium 64-70 12-oxophytodienoate reductase7 Zea mays 38-46 31835299-8 2019 In addition, ion analysis showed that opr7opr8 accumulated less sodium but more potassium in the leaves than WT but more sodium and less potassium in the roots than WT, suggesting that JA deficiency causes higher salt stress to the roots but less stress to the leaves of the seedlings. Sodium 121-127 12-oxophytodienoate reductase7 Zea mays 38-46 31703480-7 2019 In addition, findings showed that in NaF and EAO groups, macrophages and T cells both significantly secreted IL-17A, and the protein and mRNA levels of cytokines (IL-6 and TGF-beta) were significantly increased. Sodium 37-40 transforming growth factor, beta 1 Mus musculus 172-180 31791063-9 2019 Many solute carriers (SLC) that are potential prodrug targets were present on both cellular surfaces, whereas putative sodium-coupled neutral amino acid transporter 7 (SNAT7) and riboflavin transporter (RFT3) were enriched on the basolateral and sodium- and chloride-dependent neutral and basic amino acid transporter (ATB0+) on the apical membrane. Sodium 119-125 solute carrier family 52 member 2 Homo sapiens 203-207 31791063-9 2019 Many solute carriers (SLC) that are potential prodrug targets were present on both cellular surfaces, whereas putative sodium-coupled neutral amino acid transporter 7 (SNAT7) and riboflavin transporter (RFT3) were enriched on the basolateral and sodium- and chloride-dependent neutral and basic amino acid transporter (ATB0+) on the apical membrane. Sodium 246-252 solute carrier family 52 member 2 Homo sapiens 203-207 31006168-1 2019 AIM: In nephrotic syndrome, aberrantly filtered plasminogen (plg) is converted to active plasmin by tubular urokinase-type plasminogen activator (uPA) and thought to lead to sodium retention by proteolytic activation of the epithelial sodium channel (ENaC). Sodium 174-180 plasminogen Mus musculus 61-64 31904117-1 2019 SCN1A, encoding the alpha 1 subunit of the sodium channel, is associated with several epilepsy syndromes and a range of other diseases. Sodium 43-49 sodium voltage-gated channel alpha subunit 1 Homo sapiens 0-5 31904118-1 2019 De novo mutations of the neuronal sodium channel SCN8A have been identified in approximately 2% of individuals with epileptic encephalopathy. Sodium 34-40 sodium channel, voltage-gated, type VIII, alpha Mus musculus 49-54 31370103-14 2019 The failure in functionality of the mutated GlyT2 is most probably due to structural changes localised in close proximity to the sodium-binding site of the transporter. Sodium 129-135 solute carrier family 6 member 5 Homo sapiens 44-49 31445158-1 2019 Dravet syndrome (DS) is an early onset refractory epilepsy typically caused by de novo heterozygous variants in SCN1A encoding the alpha-subunit of the neuronal sodium channel Nav1.1. Sodium 161-167 sodium voltage-gated channel alpha subunit 1 Homo sapiens 176-182 31795491-3 2019 The encoded proteins Kelch-like 3 and Cullin 3 interact to form a ring-like complex to ubiquitinate WNK-kinase 4, which, in normal circumstances, interacts with the sodium chloride co-symporter (NCC), the epithelial sodium channel (ENaC), and the renal outer medullary potassium channel (ROMK) in an inhibitory manner to maintain normokalaemia and normotension. Sodium 165-171 cullin 3 Homo sapiens 38-46 31795491-3 2019 The encoded proteins Kelch-like 3 and Cullin 3 interact to form a ring-like complex to ubiquitinate WNK-kinase 4, which, in normal circumstances, interacts with the sodium chloride co-symporter (NCC), the epithelial sodium channel (ENaC), and the renal outer medullary potassium channel (ROMK) in an inhibitory manner to maintain normokalaemia and normotension. Sodium 165-171 potassium inwardly rectifying channel subfamily J member 1 Homo sapiens 288-292 31490586-4 2019 The sodium and sulphate ions embedded inside MOG are sufficient enough for the charge storage. Sodium 4-10 myelin oligodendrocyte glycoprotein Homo sapiens 45-48 20335314-10 2010 Together, these results suggest an important role of mPGES-1 in antagonizing the sodium-retaining action of Aldo at the levels of both the central nervous system and the kidney. Sodium 81-87 prostaglandin E synthase Mus musculus 53-60 20486282-6 2010 Carriers of the rare A allele of rs5479 in the hydroxysteroid (11-beta) dehydrogenase 2 gene had decreased DBP responses to low sodium (P=0.00004). Sodium 128-134 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 47-87 31525968-2 2019 The efficacy of these drugs is thought to be due to the block of sodium channels on excitatory neurons, primarily NaV1.6 and NaV1.2. Sodium 65-71 sodium channel, voltage-gated, type VIII, alpha Mus musculus 114-120 31525968-2 2019 The efficacy of these drugs is thought to be due to the block of sodium channels on excitatory neurons, primarily NaV1.6 and NaV1.2. Sodium 65-71 sodium channel, voltage-gated, type II, alpha Mus musculus 125-131 31730524-7 2019 Mg2+ can maintain the lens sodium pump activity and antioxidant status and block the calcium channels and release of glutamate in nerve endings. Sodium 27-33 mucin 7, secreted Homo sapiens 0-3 32009801-12 2019 Coagulation experiments in animals (mice and rats) revealed that Na2SeO3 can reduce the coagulation time of BMSCs in a concentration-dependent manner, which is related to the high expression of hematopoietic factors (SDF-1alpha, GM-CSF, IL-7, IL-8, IL-11, and SCF). Sodium 65-72 interleukin 11 Rattus norvegicus 249-254 20385770-3 2010 We demonstrate that SORLA is expressed in epithelial cells of the thick ascending limb (TAL) of Henle"s loop and that lack of receptor expression in this cell type in SORLA-deficient mice results in an inability to properly reabsorb sodium and chloride during osmotic stress. Sodium 233-239 sortilin-related receptor, LDLR class A repeats-containing Mus musculus 20-25 20339117-5 2010 The SCN5A mutation F1473S expressed in HEK293 cells presented a right-ward shift of steady-state inactivation, enlarged window current, and huge sustained sodium current. Sodium 155-161 sodium voltage-gated channel alpha subunit 5 Homo sapiens 4-9 20049896-0 2010 EGF and its related growth factors mediate sodium transport in mpkCCDc14 cells via ErbB2 (neu/HER-2) receptor. Sodium 43-49 epidermal growth factor Mus musculus 0-3 20049896-0 2010 EGF and its related growth factors mediate sodium transport in mpkCCDc14 cells via ErbB2 (neu/HER-2) receptor. Sodium 43-49 erb-b2 receptor tyrosine kinase 2 Mus musculus 83-88 20049896-0 2010 EGF and its related growth factors mediate sodium transport in mpkCCDc14 cells via ErbB2 (neu/HER-2) receptor. Sodium 43-49 erb-b2 receptor tyrosine kinase 2 Mus musculus 90-93 20049896-12 2010 Thus, we conclude that EGF and its related growth factors are important for maintaining transepithelial Na(+) transport and that EGF biphasically modulates sodium transport in mpkCCD(c14) cells via the ErbB2 receptor. Sodium 156-162 epidermal growth factor Mus musculus 129-132 20164394-0 2010 Augmented sodium currents contribute to the enhanced excitability of small diameter capsaicin-sensitive sensory neurons isolated from Nf1+/- mice. Sodium 10-16 neurofibromin 1 Mus musculus 134-137 20164394-9 2010 These results demonstrate that enhanced production of action potentials in Nf1+/- neurons results, in part, from larger current densities and a depolarized voltage dependence of steady-state inactivation for I(Na) that potentially leads to a greater availability of sodium channels at voltages near the firing threshold for the action potential. Sodium 266-272 neurofibromin 1 Mus musculus 75-78 20088828-1 2010 The type IIa renal sodium-dependent phosphate (Na/Pi) co-transporter Npt2a is implicated in the control of serum phosphate levels. Sodium 19-25 solute carrier family 34 (sodium phosphate), member 1 Mus musculus 69-74 20029090-10 2010 Sodium binds more weakly to both sites and activates HDAC8 to a lesser extent than potassium. Sodium 0-6 histone deacetylase 8 Homo sapiens 53-58 21286276-4 2010 Leptin has a dose- and time-dependent effect on urinary sodium excretion. Sodium 56-62 leptin Homo sapiens 0-6 20023383-2 2010 The miR-8 family of miRNAs plays a key role in this process by precisely regulating the activity of NHERF1, a regulator of sodium hydrogen exchange that also serves as an adaptor protein linked to the actin cytoskeleton. Sodium 123-129 SLC9A3 regulator 1a Danio rerio 100-106 19906950-0 2010 ANP-mediated inhibition of distal nephron fractional sodium reabsorption in wild-type and mice overexpressing natriuretic peptide receptor. Sodium 53-59 natriuretic peptide type A Mus musculus 0-3 19906950-3 2010 The lower dose of ANP (0.1 ng x g body wt(-1) x min(-1), n = 6) increased distal sodium delivery (DSD, 2.4 +/- 0.4 vs. 1.6 +/- 0.2 mueq/min, P < 0.05) but did not change fractional reabsorption of DSD compared with control (86.3 +/- 2.0 vs. 83.9 +/- 3.6%, P > 0.05), thus limiting the magnitude of the natriuresis. Sodium 81-87 natriuretic peptide type A Mus musculus 18-21 19906950-5 2010 In Npr1 gene-duplicated four-copy mice (n = 6), the lower dose of ANP increased urinary sodium excretion (0.6 +/- 0.1 vs. 0.3 +/- 0.1 mueq/min, P < 0.05) and decreased fractional reabsorption of DSD compared with control (72.2 +/- 3.4%, P < 0.05) at similar mean arterial pressures (91 +/- 6 vs. 92 +/- 3 mmHg, P > 0.05). Sodium 88-94 natriuretic peptide type A Mus musculus 66-69 19906950-6 2010 These results provide in vivo evidence that ANP-mediated increases in DSD alone exert modest effects on sodium excretion and that inhibition of fractional reabsorption of distal sodium delivery is requisite for the augmented natriuresis in response to the higher dose of ANP or in Npr1 gene-duplicated mice. Sodium 104-110 natriuretic peptide type A Mus musculus 44-47 19906950-6 2010 These results provide in vivo evidence that ANP-mediated increases in DSD alone exert modest effects on sodium excretion and that inhibition of fractional reabsorption of distal sodium delivery is requisite for the augmented natriuresis in response to the higher dose of ANP or in Npr1 gene-duplicated mice. Sodium 178-184 natriuretic peptide type A Mus musculus 44-47 31722722-1 2019 BACKGROUND: In multiple sclerosis (MS) and in the experimental autoimmune encephalomyelitis (EAE) model of MS, the Nav1.6 voltage-gated sodium (Nav) channel isoform has been implicated as a primary contributor to axonal degeneration. Sodium 136-142 neuron navigator 1 Mus musculus 115-119 20054145-0 2010 Importance of ENaC-mediated sodium transport in alveolar fluid clearance using genetically-engineered mice. Sodium 28-34 sodium channel, nonvoltage-gated 1 alpha Mus musculus 14-18 19851106-7 2010 Further research awaits the characterization of additional mechanisms of action of leptin, including its interface with other important endocrine and hemodynamic sodium-volume regulatory systems, in both health and disease, particularly in obesity and related comorbidities. Sodium 162-168 leptin Homo sapiens 83-89 20043279-1 2010 Sodium transport via epithelial sodium channels (ENaC) expressed in alveolar epithelial cells (AEC) provides the driving force for removal of fluid from the alveolar space. Sodium 0-6 sodium channel, nonvoltage-gated 1 alpha Mus musculus 49-53 20043279-4 2010 Deficiency of CAP1/Prss8 in AEC induced in vitro a 40% decrease in ENaC-mediated sodium currents. Sodium 81-87 protease, serine 8 (prostasin) Mus musculus 19-24 20043279-4 2010 Deficiency of CAP1/Prss8 in AEC induced in vitro a 40% decrease in ENaC-mediated sodium currents. Sodium 81-87 sodium channel, nonvoltage-gated 1 alpha Mus musculus 67-71 20043279-5 2010 Sodium-driven alveolar fluid clearance (AFC) was reduced in CAP1/Prss8-deficient mice, due to a 48% decrease in amiloride-sensitive clearance, and was less sensitive to beta(2)-agonist treatment. Sodium 0-6 protease, serine 8 (prostasin) Mus musculus 65-70 20043279-8 2010 This study reveals that CAP1 plays a crucial role in the regulation of ENaC-mediated alveolar sodium and water transport and in mouse lung fluid balance. Sodium 94-100 sodium channel, nonvoltage-gated 1 alpha Mus musculus 71-75 20038812-4 2010 We demonstrated that a paroxysmal extreme pain disorder (PEPD) mutation in the human peripheral neuronal sodium channel Nav1.7, a paramyotonia congenita (PMC) mutation in the human skeletal muscle sodium channel Nav1.4, and a long-QT3/SIDS mutation in the human cardiac sodium channel Nav1.5 all substantially increased the amplitude of resurgent sodium currents in an optimized adult rat-derived dorsal root ganglion neuronal expression system. Sodium 197-203 sodium voltage-gated channel alpha subunit 4 Homo sapiens 212-218 20038812-4 2010 We demonstrated that a paroxysmal extreme pain disorder (PEPD) mutation in the human peripheral neuronal sodium channel Nav1.7, a paramyotonia congenita (PMC) mutation in the human skeletal muscle sodium channel Nav1.4, and a long-QT3/SIDS mutation in the human cardiac sodium channel Nav1.5 all substantially increased the amplitude of resurgent sodium currents in an optimized adult rat-derived dorsal root ganglion neuronal expression system. Sodium 197-203 sodium voltage-gated channel alpha subunit 5 Homo sapiens 285-291 20038812-4 2010 We demonstrated that a paroxysmal extreme pain disorder (PEPD) mutation in the human peripheral neuronal sodium channel Nav1.7, a paramyotonia congenita (PMC) mutation in the human skeletal muscle sodium channel Nav1.4, and a long-QT3/SIDS mutation in the human cardiac sodium channel Nav1.5 all substantially increased the amplitude of resurgent sodium currents in an optimized adult rat-derived dorsal root ganglion neuronal expression system. Sodium 197-203 sodium voltage-gated channel alpha subunit 4 Homo sapiens 212-218 20038812-4 2010 We demonstrated that a paroxysmal extreme pain disorder (PEPD) mutation in the human peripheral neuronal sodium channel Nav1.7, a paramyotonia congenita (PMC) mutation in the human skeletal muscle sodium channel Nav1.4, and a long-QT3/SIDS mutation in the human cardiac sodium channel Nav1.5 all substantially increased the amplitude of resurgent sodium currents in an optimized adult rat-derived dorsal root ganglion neuronal expression system. Sodium 197-203 sodium voltage-gated channel alpha subunit 5 Homo sapiens 285-291 20038812-4 2010 We demonstrated that a paroxysmal extreme pain disorder (PEPD) mutation in the human peripheral neuronal sodium channel Nav1.7, a paramyotonia congenita (PMC) mutation in the human skeletal muscle sodium channel Nav1.4, and a long-QT3/SIDS mutation in the human cardiac sodium channel Nav1.5 all substantially increased the amplitude of resurgent sodium currents in an optimized adult rat-derived dorsal root ganglion neuronal expression system. Sodium 197-203 sodium voltage-gated channel alpha subunit 4 Homo sapiens 212-218 20038812-4 2010 We demonstrated that a paroxysmal extreme pain disorder (PEPD) mutation in the human peripheral neuronal sodium channel Nav1.7, a paramyotonia congenita (PMC) mutation in the human skeletal muscle sodium channel Nav1.4, and a long-QT3/SIDS mutation in the human cardiac sodium channel Nav1.5 all substantially increased the amplitude of resurgent sodium currents in an optimized adult rat-derived dorsal root ganglion neuronal expression system. Sodium 197-203 sodium voltage-gated channel alpha subunit 5 Homo sapiens 285-291 20090362-0 2010 Genetic variations in the sodium balance-regulating genes ENaC, NEDD4L, NDFIP2 and USP2 influence blood pressure and hypertension. Sodium 26-32 ubiquitin specific peptidase 2 Homo sapiens 83-87 20024379-1 2009 The prediction and characterization of the single-electron sodium bond complexes Y-C...Na-H [Y = H(3), H(3)CH(2), (H(3)C)(2)H and (H(3)C)(3)] have been investigated for the first time by using MP2/6-311++G(d,p), MP2/6-311++G(2d,2p) and MP2/aug-cc-pVDZ methods. Sodium 59-65 tryptase pseudogene 1 Homo sapiens 193-196 20024379-1 2009 The prediction and characterization of the single-electron sodium bond complexes Y-C...Na-H [Y = H(3), H(3)CH(2), (H(3)C)(2)H and (H(3)C)(3)] have been investigated for the first time by using MP2/6-311++G(d,p), MP2/6-311++G(2d,2p) and MP2/aug-cc-pVDZ methods. Sodium 59-65 tryptase pseudogene 1 Homo sapiens 212-215 20024379-1 2009 The prediction and characterization of the single-electron sodium bond complexes Y-C...Na-H [Y = H(3), H(3)CH(2), (H(3)C)(2)H and (H(3)C)(3)] have been investigated for the first time by using MP2/6-311++G(d,p), MP2/6-311++G(2d,2p) and MP2/aug-cc-pVDZ methods. Sodium 59-65 tryptase pseudogene 1 Homo sapiens 212-215 19657284-0 2009 Blocking the salt-inducible kinase 1 network prevents the increases in cell sodium transport caused by a hypertension-linked mutation in human alpha-adducin. Sodium 76-82 salt inducible kinase 1 Homo sapiens 13-36 19657284-1 2009 OBJECTIVES: Because a newly described salt-inducible kinase 1 (SIK1) network is responsible for increases in active cell sodium transport in response to elevated intracellular sodium, we hypothesized that this network could mediate the effects of the mutant (hypertensive) form of alpha-adducin on Na,K-ATPase activity. Sodium 121-127 salt inducible kinase 1 Homo sapiens 38-61 19657284-1 2009 OBJECTIVES: Because a newly described salt-inducible kinase 1 (SIK1) network is responsible for increases in active cell sodium transport in response to elevated intracellular sodium, we hypothesized that this network could mediate the effects of the mutant (hypertensive) form of alpha-adducin on Na,K-ATPase activity. Sodium 121-127 salt inducible kinase 1 Homo sapiens 63-67 19657284-1 2009 OBJECTIVES: Because a newly described salt-inducible kinase 1 (SIK1) network is responsible for increases in active cell sodium transport in response to elevated intracellular sodium, we hypothesized that this network could mediate the effects of the mutant (hypertensive) form of alpha-adducin on Na,K-ATPase activity. Sodium 176-182 salt inducible kinase 1 Homo sapiens 38-61 19657284-1 2009 OBJECTIVES: Because a newly described salt-inducible kinase 1 (SIK1) network is responsible for increases in active cell sodium transport in response to elevated intracellular sodium, we hypothesized that this network could mediate the effects of the mutant (hypertensive) form of alpha-adducin on Na,K-ATPase activity. Sodium 176-182 salt inducible kinase 1 Homo sapiens 63-67 19657284-7 2009 CONCLUSION: The SIK1 network may constitute an alternative target by which agents can modulate active sodium transport in renal epithelia and avoid the increases in systemic blood pressure that are associated with genetic mutations in the human alpha-adducin molecule. Sodium 102-108 salt inducible kinase 1 Homo sapiens 16-20 19741019-0 2009 Proinsulin C-peptide reduces diabetes-induced glomerular hyperfiltration via efferent arteriole dilation and inhibition of tubular sodium reabsorption. Sodium 131-137 insulin 2 Rattus norvegicus 11-20 19843921-2 2009 Accordingly, experimental studies suggest that BrS-linked SCN5A mutations reduce sodium current more at fast heart rates. Sodium 81-87 sodium voltage-gated channel alpha subunit 5 Homo sapiens 58-63 19562367-5 2009 Moreover, in Xenopus oocytes coexpressing 4F2hc and y(+)LAT2, leucine exerts a marked inhibition of arginine transport, partially dependent on sodium, while no inhibition is seen in oocytes expressing CAT1. Sodium 143-149 solute carrier family 7 (amino acid transporter light chain, y+L system), member 6 L homeolog Xenopus laevis 42-60 19606473-4 2009 Loss-of-function mutations in SCN5A, which encodes the alpha-subunit of the Na(v)1.5 sodium ion channel conducting the depolarizing I(Na) current, causes 15-20% of BrS cases. Sodium 85-91 sodium voltage-gated channel alpha subunit 5 Homo sapiens 30-35 19657969-0 2009 Sodium translocation by the iminoglycinuria associated imino transporter (SLC6A20). Sodium 0-6 solute carrier family 6 member 20 Homo sapiens 74-81 20409966-0 2009 A HMGCR polymorphism is associated with relations between blood pressure and urinary sodium and potassium ratio in the Epic-Norfolk Study. Sodium 85-91 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 2-7 20409966-6 2009 Our results suggest that the SNP rs17238540 in the HMGCR is associated with the BP response to urinary sodium: potassium ratio, the magnitude of the association differing according to possession of the G allele. Sodium 103-109 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 51-56 19247687-0 2009 SIK1/SOS2 networks: decoding sodium signals via calcium-responsive protein kinase pathways. Sodium 29-35 salt inducible kinase 1 Homo sapiens 0-4 19247687-4 2009 The specific ionic stress (elevated intracellular sodium) is followed by changes in intracellular calcium; the calcium signals are sensed by calcium-binding proteins and lead to activation of SIK1 or SOS2. Sodium 50-56 salt inducible kinase 1 Homo sapiens 192-196 19297452-12 2009 This TGF-alpha- or EGF-induced increase in sodium current is abolished by a phosphatidylinositol 3-kinase (PI-3 kinase) inhibitor, LY294002, suggesting that PI-3 kinase is involved in the activation of sodium transport. Sodium 43-49 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha L homeolog Xenopus laevis 76-105 19297452-12 2009 This TGF-alpha- or EGF-induced increase in sodium current is abolished by a phosphatidylinositol 3-kinase (PI-3 kinase) inhibitor, LY294002, suggesting that PI-3 kinase is involved in the activation of sodium transport. Sodium 43-49 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha L homeolog Xenopus laevis 107-118 19297452-12 2009 This TGF-alpha- or EGF-induced increase in sodium current is abolished by a phosphatidylinositol 3-kinase (PI-3 kinase) inhibitor, LY294002, suggesting that PI-3 kinase is involved in the activation of sodium transport. Sodium 43-49 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha L homeolog Xenopus laevis 157-168 19307188-6 2009 Surprisingly, when yeast cells were challenged with lithium, a tracer for sodium, the main effect of the mutations in AtNHX1 was a reduction in the amount of compartmentalized lithium. Sodium 74-80 Na+/H+ exchanger 1 Arabidopsis thaliana 118-124 19106216-1 2009 The mineralocorticoid receptor (MR) is a major regulator of renal sodium reabsorption and body fluid homeostasis. Sodium 66-72 nuclear receptor subfamily 3, group C, member 2 Mus musculus 4-30 19106216-1 2009 The mineralocorticoid receptor (MR) is a major regulator of renal sodium reabsorption and body fluid homeostasis. Sodium 66-72 nuclear receptor subfamily 3, group C, member 2 Mus musculus 32-34 19193726-8 2009 In distal epithelia, significant increases in proteolytic cleavage products of alpha-epithelial Na(+) channel (ENaC) and gamma-ENaC were observed, suggesting enhanced tubular sodium reabsorption. Sodium 175-181 sodium channel, nonvoltage-gated 1 alpha Mus musculus 79-109 19193726-8 2009 In distal epithelia, significant increases in proteolytic cleavage products of alpha-epithelial Na(+) channel (ENaC) and gamma-ENaC were observed, suggesting enhanced tubular sodium reabsorption. Sodium 175-181 sodium channel, nonvoltage-gated 1 alpha Mus musculus 111-115 19193726-10 2009 Our data indicate that ENaC-mediated sodium entry may be the rate-limiting step in proteinuric sodium retention. Sodium 37-43 sodium channel, nonvoltage-gated 1 alpha Mus musculus 23-27 19193726-10 2009 Our data indicate that ENaC-mediated sodium entry may be the rate-limiting step in proteinuric sodium retention. Sodium 95-101 sodium channel, nonvoltage-gated 1 alpha Mus musculus 23-27 18752973-5 2009 A post mortem DNA sequencing of the LQTS-associated genes revealed a novel missense mutation in the SCN5A gene coding for the cardiac sodium channel, voltage gated, type V, alpha subunit. Sodium 134-140 sodium voltage-gated channel alpha subunit 5 Homo sapiens 100-105 31722722-3 2019 The persistent influx of sodium through Nav1.6 is believed to reverse the function of NCX, resulting in an increased influx of damaging Ca2+ ions. Sodium 25-31 neuron navigator 1 Mus musculus 40-44 31613590-2 2019 Herein, we investigated the most favorable dehydrogenation pathway for each ABH3 system and found that NaCaH3 was the most attractive ABH3 system. Sodium 103-109 alkB homolog 3, alpha-ketoglutarate dependent dioxygenase Homo sapiens 76-80 31613590-2 2019 Herein, we investigated the most favorable dehydrogenation pathway for each ABH3 system and found that NaCaH3 was the most attractive ABH3 system. Sodium 103-109 alkB homolog 3, alpha-ketoglutarate dependent dioxygenase Homo sapiens 134-138 31545435-9 2019 Furthermore, NaHS suppressed HG-induced TG accumulation by activating AMPK. Sodium 13-17 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 70-74 31278928-1 2019 SCN8A epileptic encephalopathy is a severe genetic epilepsy syndrome caused by de novo gain-of-function mutations of SCN8A encoding the voltage-gated sodium (Na) channel (VGSC) NaV1.6. Sodium 150-156 sodium channel, voltage-gated, type VIII, alpha Mus musculus 0-5 31278928-1 2019 SCN8A epileptic encephalopathy is a severe genetic epilepsy syndrome caused by de novo gain-of-function mutations of SCN8A encoding the voltage-gated sodium (Na) channel (VGSC) NaV1.6. Sodium 150-156 sodium channel, voltage-gated, type VIII, alpha Mus musculus 117-122 31632551-0 2019 Pre-B-cell colony enhancing factor regulates the alveolar epithelial sodium-water transport system through the ERK and AKT pathways. Sodium 69-75 nicotinamide phosphoribosyltransferase Homo sapiens 0-34 31632551-3 2019 We previously demonstrated that pre-B-cell colony enhancing factor (PBEF) increases alveolar capillary permeability and inhibits the sodium-water transport system. Sodium 133-139 nicotinamide phosphoribosyltransferase Homo sapiens 32-66 31632551-3 2019 We previously demonstrated that pre-B-cell colony enhancing factor (PBEF) increases alveolar capillary permeability and inhibits the sodium-water transport system. Sodium 133-139 nicotinamide phosphoribosyltransferase Homo sapiens 68-72 31632551-4 2019 However, the specific mechanism by which PBEF inhibits the sodium-water transport system is unclear. Sodium 59-65 nicotinamide phosphoribosyltransferase Homo sapiens 41-45 31632551-6 2019 The impact of PBEF on the expression of genes and proteins implicated in sodium transport and its effect on the activation status of the ERK, P38, and AKT signaling pathways were explored in HPAEpiC by real-time fluorescent PCR and western blotting. Sodium 73-79 nicotinamide phosphoribosyltransferase Homo sapiens 14-18 31632551-12 2019 In conclusion, PBEF inhibited the sodium-water transport system by activation of ERK and suppression of AKT signaling. Sodium 34-40 nicotinamide phosphoribosyltransferase Homo sapiens 15-19 31508914-1 2019 The salt sensitivity of the blood pressure (SSBP) is defined as a rise or fall in blood pressure induced by a change in sodium intake. Sodium 120-126 single stranded DNA binding protein 1 Homo sapiens 44-48 31508914-3 2019 The SSBP may lead to underestimation of the beneficial effect of sodium restriction in some patients in meta-analyzes. Sodium 65-71 single stranded DNA binding protein 1 Homo sapiens 4-8 31439819-2 2019 In terrestrial vertebrates, the MR mediates sodium homeostasis by aldosterone and also acts as a receptor for cortisol. Sodium 44-50 nuclear receptor subfamily 3, group C, member 2 Danio rerio 32-34 31564962-3 2019 The genesis and propagation of action potentials is dependent on voltage-gated sodium channels, in particular, Nav1.7, Nav1.8 and Nav1.9. Sodium 79-85 sodium voltage-gated channel alpha subunit 11 Homo sapiens 130-136 31257701-0 2019 Metallic-State SnS2 Nanosheets with Expanded Lattice Spacing for High-Performance Sodium-Ion Batteries. Sodium 82-88 sodium voltage-gated channel alpha subunit 11 Homo sapiens 15-19 31257701-2 2019 The expanded lattice spacing efficiently enhanced the electrochemical performance of the SnS2 for sodium-ion batteries owing to the change electron state density and energy band structure. Sodium 98-104 sodium voltage-gated channel alpha subunit 11 Homo sapiens 89-93 31551682-1 2019 Voltage-gated sodium channel Nav1.9 is a threshold channel that regulates action potential firing. Sodium 14-20 sodium voltage-gated channel alpha subunit 11 Homo sapiens 29-35 31172810-4 2019 The objective of this study was to determine the role of CD161a+/CD68+ macrophages and renal sympathetic nerves in cholinergic-hypertension and renal sodium retention. Sodium 150-156 Cd68 molecule Rattus norvegicus 65-69 31313673-6 2019 Studies seeking to elucidate the molecular mechanisms by which Cullin 3 mutations lead to dysregulation of renal sodium transport will be discussed. Sodium 113-119 cullin 3 Mus musculus 63-71 31350809-7 2019 Urinary sodium was significantly associated with SBP (beta = 1.08, P = .018) after adjustment for potential confounders. Sodium 8-14 selenium binding protein 1 Homo sapiens 49-52 31323180-0 2019 Sandwich-like SnS2/Graphene/SnS2 with Expanded Interlayer Distance as High-Rate Lithium/Sodium-Ion Battery Anode Materials. Sodium 88-94 sodium voltage-gated channel alpha subunit 11 Homo sapiens 14-18 31323180-0 2019 Sandwich-like SnS2/Graphene/SnS2 with Expanded Interlayer Distance as High-Rate Lithium/Sodium-Ion Battery Anode Materials. Sodium 88-94 sodium voltage-gated channel alpha subunit 11 Homo sapiens 28-32 31507534-1 2019 The mineralocorticoid receptor (MR) was originally identified as a regulator of blood pressure, able to modulate renal sodium handling in response to its principal ligand aldosterone. Sodium 119-125 nuclear receptor subfamily 3 group C member 2 Homo sapiens 4-30 19272188-11 2009 In conclusion, the SCN5A channel defect related to Brugada syndrome might be diverse but all resulted in a decrease of sodium current. Sodium 119-125 sodium voltage-gated channel alpha subunit 5 Homo sapiens 19-24 19075100-8 2009 Thus, TRPV4 activation decreases blood pressure in rats given a normal-sodium diet. Sodium 71-77 transient receptor potential cation channel, subfamily V, member 4 Rattus norvegicus 6-11 19133985-10 2009 CONCLUSIONS AND IMPLICATIONS: F 15845 is a selective, potent blocker of the persistent sodium current, generated by the human Na(v)1.5 channel isoforms, and prevents cardiac angina in animal models. Sodium 87-93 immunoglobulin lambda variable 2-18 Homo sapiens 126-134 19013186-4 2009 Under normal circumstances, endogenous GCs alone do not induce sodium transport in MC responsive epithelia yet these same GCs are able to activate MR and induce sodium transport if the enzyme 11beta-HSD2 is inhibited. Sodium 161-167 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 192-203 19013186-8 2009 What is clear is that a dual role for 11beta-HSD2 is emerging; first as the putative "guardian" over the MR reducing GC binding, and second as a source for 11-dehydro-GCs, which may serve as endogenously and locally produced "spironolactone-like substances", which may thus attenuate aldosterone-induced sodium transport. Sodium 304-310 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 38-49 19004798-5 2008 Sodium use was increased in ant communities further inland, as was preference for the baits with the highest sodium concentration. Sodium 0-6 solute carrier family 25 member 6 Homo sapiens 28-31 19004798-7 2008 We suggest that the geography of ant activity is shaped by sodium toxicity near the shore and by sodium deficit farther inland. Sodium 59-65 solute carrier family 25 member 6 Homo sapiens 33-36 19004798-7 2008 We suggest that the geography of ant activity is shaped by sodium toxicity near the shore and by sodium deficit farther inland. Sodium 97-103 solute carrier family 25 member 6 Homo sapiens 33-36 31507534-1 2019 The mineralocorticoid receptor (MR) was originally identified as a regulator of blood pressure, able to modulate renal sodium handling in response to its principal ligand aldosterone. Sodium 119-125 nuclear receptor subfamily 3 group C member 2 Homo sapiens 32-34 31389935-0 2019 Reversible uptake and release of sodium ions in layered SnS2-reduced graphene oxide composites for neuromorphic devices. Sodium 33-39 sodium voltage-gated channel alpha subunit 11 Homo sapiens 56-60 31389935-3 2019 Here, we suggest a biomimetic three-terminal electrochemical artificial synapse that is operated by a conductance change in response to intercalation of sodium (Na+) ions into a layered SnS2-reduced graphene oxide (RGO) composite channel. Sodium 153-159 sodium voltage-gated channel alpha subunit 11 Homo sapiens 186-190 31474871-4 2019 Following diet switch to low sodium, Nr3c1 Pax8/LC1 mice exhibit a transient but significant reduction in the activity of NCC and expression of NHE3 and NKCC2 accompanied by significant increased Spak activity. Sodium 29-35 paired box 8 Mus musculus 43-47 31409833-2 2019 Among these channels, the leak sodium channel NALCN plays a crucial role in the maintenance of the resting membrane potential. Sodium 31-37 sodium leak channel, non-selective Homo sapiens 46-51 19808282-8 2008 Renal effects of AM2 included increased excretion of sodium (P<0.05), cAMP (P<0.01), and creatinine (P<0.05), with augmented creatinine clearance (P<0.05), and a trend for urine output to rise (P=0.068). Sodium 53-59 adrenomedullin 2 Homo sapiens 17-20 19552070-6 2008 The poor water quality belonged to categories of B1, B2, B3, C1 and C2, which were either having accumulation of salts (high EC) or high sodium adsorption ratio (SAR) and residual sodium carbonate (RSC). Sodium 137-143 heterogeneous nuclear ribonucleoprotein C Homo sapiens 49-70 31375080-1 2019 BACKGROUND: Renal proximal tubular sodium and glucose reabsorption are regulated by the sodium-glucose cotransporter (SGLT2). Sodium 35-41 solute carrier family 5 member 2 Rattus norvegicus 118-123 32154769-8 2019 Results revealed that both high and low sodium diet with low and high renin levels respectively block the influence of candesartan on CBF autoregulation. Sodium 40-46 renin Rattus norvegicus 70-75 18413781-5 2008 Signaling array analysis reveals that AVP stimulation of AVR- and NAVR-specific Cos1 transfectants results in diametrical activation as well as coactivation of signaling pathways known to mediate renal sodium and water balance. Sodium 202-208 NLR family pyrin domain containing 6 Homo sapiens 57-60 18413781-5 2008 Signaling array analysis reveals that AVP stimulation of AVR- and NAVR-specific Cos1 transfectants results in diametrical activation as well as coactivation of signaling pathways known to mediate renal sodium and water balance. Sodium 202-208 NLR family pyrin domain containing 6 Homo sapiens 66-70 18452873-2 2008 Mutations in KCNQ1-, KCNH2-, and KCNA5-encoded potassium channels and SCN5A-encoded sodium channels have been reported in familial AF. Sodium 84-90 sodium voltage-gated channel alpha subunit 5 Homo sapiens 70-75 18277387-10 2008 Co-treatment of OVX rats with PIO and PPAR-alpha ligand, fenofibrate, a putative inducer of CYP4A, restored not only the impaired sodium excretion but also the downregulated CYP4A expression. Sodium 130-136 peroxisome proliferator activated receptor alpha Rattus norvegicus 38-48 18277387-14 2008 Furthermore, PPAR-alpha ligands can provide a novel strategy for preventing the PIO-induced sodium retention. Sodium 92-98 peroxisome proliferator activated receptor alpha Rattus norvegicus 13-23 18468451-2 2008 Increased distal tubule sodium and water reabsorption through the epithelial sodium channel (ENaC) and aquaporin-2 (AQP-2) have been suggested to play mechanistic roles. Sodium 24-30 aquaporin 2 Rattus norvegicus 103-114 18468451-2 2008 Increased distal tubule sodium and water reabsorption through the epithelial sodium channel (ENaC) and aquaporin-2 (AQP-2) have been suggested to play mechanistic roles. Sodium 24-30 aquaporin 2 Rattus norvegicus 116-121 18468451-12 2008 However, later reduction in AQP-2 and alpha-ENaC may represent an attempt to re-establish sodium and water balance. Sodium 90-96 aquaporin 2 Rattus norvegicus 28-33 18378609-0 2008 Cardiac sodium channel (SCN5A) variants associated with atrial fibrillation. Sodium 8-14 sodium voltage-gated channel alpha subunit 5 Homo sapiens 24-29 18378609-2 2008 Here, we tested the hypothesis that vulnerability to AF is associated with variation in SCN5A, the gene encoding the cardiac sodium channel. Sodium 125-131 sodium voltage-gated channel alpha subunit 5 Homo sapiens 88-93 18242854-0 2008 Mutation of sodium channel SCN3A in a patient with cryptogenic pediatric partial epilepsy. Sodium 12-18 sodium voltage-gated channel alpha subunit 3 Homo sapiens 27-32 18247577-1 2008 Sodium-dependent vitamin C transporters, SVCT1 and SVCT2, are the only two known proteins for the uptake of ascorbate, the active form of vitamin C. Sodium 0-6 solute carrier family 23 member 1 Homo sapiens 41-46 18247577-7 2008 Among eight other mutations of His51 in hSVCT1, significant sodium-dependent ascorbate transport activity was only observed with asparagine or tyrosine replacement. Sodium 60-66 solute carrier family 23 member 1 Homo sapiens 40-46 18247577-10 2008 The importance of TM1 is further strengthened by the comparable loss of sodium-dependent ascorbate transport activity upon the mutation of adjacent conserved Gln50 and the apparent change in substrate specificity in the hSVCT1-His51Gln mutation, which showed a specific increase in sodium-independent dehydroascorbate transport. Sodium 282-288 solute carrier family 23 member 1 Homo sapiens 220-226 18178722-11 2008 The data support the hypothesis that endothelial Cav-1, likely through an effect on eNOS activity, plays a prominent role in the regulation of vascular function during substantial changes in dietary sodium intake. Sodium 199-205 caveolin 1, caveolae protein Mus musculus 49-54 18178722-11 2008 The data support the hypothesis that endothelial Cav-1, likely through an effect on eNOS activity, plays a prominent role in the regulation of vascular function during substantial changes in dietary sodium intake. Sodium 199-205 nitric oxide synthase 3, endothelial cell Mus musculus 84-88 17892895-0 2008 Changes in action potentials and intracellular ionic homeostasis in a ventricular cell model related to a persistent sodium current in SCN5A mutations underlying LQT3. Sodium 117-123 sodium channel protein type 5 subunit alpha Cavia porcellus 135-140 17892895-0 2008 Changes in action potentials and intracellular ionic homeostasis in a ventricular cell model related to a persistent sodium current in SCN5A mutations underlying LQT3. Sodium 117-123 sodium voltage-gated channel alpha subunit 5 Homo sapiens 162-166 17967976-9 2007 Compared with wild-type GPD1-L, GPD1-L mutations coexpressed with SCN5A in heterologous HEK cells produced a significantly reduced sodium current (P<0.01). Sodium 131-137 sodium voltage-gated channel alpha subunit 5 Homo sapiens 66-71 31113930-0 2019 Estrogen negatively regulates the renal epithelial sodium channel (ENaC) by promoting Derlin-1 expression and AMPK activation. Sodium 51-57 derlin 1 Rattus norvegicus 86-94 30917747-2 2019 The sodium/proton exchanger (NHE) and the sodium/bicarbonate cotransporter (NBC) regulate the intracellular pH and, indirectly, the intracellular sodium concentration ([Na+]). Sodium 4-10 solute carrier family 9 member C1 Homo sapiens 29-32 17884088-5 2007 In acutely dissociated ventricular myocytes, loss of beta1 expression resulted in a approximately 1.6-fold increase in both peak and persistent sodium current while channel gating and kinetics were unaffected. Sodium 144-150 hemoglobin, beta adult major chain Mus musculus 53-58 29986598-1 2019 INTRODUCTION: Familial hemiplegic migraine 3 is an autosomal dominant headache disorder associated with aura and transient hemiparesis, caused by mutations of the neuronal voltage-gated sodium channel Nav1.1. Sodium 186-192 sodium voltage-gated channel alpha subunit 1 Homo sapiens 201-207 17823376-1 2007 Natriuretic peptides such as B-type natriuretic peptide (BNP) are important cardioprotective hormones with essential functions in sodium excretion, water balance and blood pressure regulation. Sodium 130-136 natriuretic peptide type B Mus musculus 29-55 17823376-1 2007 Natriuretic peptides such as B-type natriuretic peptide (BNP) are important cardioprotective hormones with essential functions in sodium excretion, water balance and blood pressure regulation. Sodium 130-136 natriuretic peptide type B Mus musculus 57-60 18850166-0 2007 Genomic and functional analysis of the sodium-dependent vitamin C transporter SLC23A1-SVCT1. Sodium 39-45 solute carrier family 23 member 1 Homo sapiens 78-85 18850166-0 2007 Genomic and functional analysis of the sodium-dependent vitamin C transporter SLC23A1-SVCT1. Sodium 39-45 solute carrier family 23 member 1 Homo sapiens 86-91 17882401-6 2007 [(3)H]-NA transport by both isoforms showed the typical properties of an NAT because it was dependent on sodium and chloride and inhibited with almost identical K (i) values by various NAT substrates and inhibitors. Sodium 105-111 solute carrier family 38, member 3 Mus musculus 73-76 30759345-1 2019 The voltage-gated cardiac sodium channel, Nav1.5, is the key component that controls cardiac excitative electrical impulse and propagation. Sodium 26-32 sodium voltage-gated channel alpha subunit 5 Rattus norvegicus 42-48 17652085-8 2007 The stimulatory effect of NDRG2 was preserved in oocytes maintained in a low sodium bath solution to prevent sodium feedback inhibition. Sodium 77-83 NDRG family member 2 Homo sapiens 26-31 31933849-11 2019 The Muller cells exhibited signs of dedifferentiation, as paired box 6 (PAX6) and SRY box 2 (SOX2) were expressed by NaIO3 stimulated Muller glia proliferation and overexpression of proliferating cell nuclear antigen (PCNA). Sodium 117-122 paired box 6 Rattus norvegicus 58-70 31933849-11 2019 The Muller cells exhibited signs of dedifferentiation, as paired box 6 (PAX6) and SRY box 2 (SOX2) were expressed by NaIO3 stimulated Muller glia proliferation and overexpression of proliferating cell nuclear antigen (PCNA). Sodium 117-122 paired box 6 Rattus norvegicus 72-76 30559144-0 2019 Kir4.1/Kir5.1 Activity Is Essential for Dietary Sodium Intake-Induced Modulation of Na-Cl Cotransporter. Sodium 48-54 potassium inwardly-rectifying channel, subfamily J, member 10 Mus musculus 0-6 29859229-3 2019 One of the most frequent causes of hyperekplexia are mutations in the SLC6A5 gene, encoding the neuronal glycine transporter 2 (GlyT2), a key component of inhibitory glycinergic presynapses involved in synaptic glycine recycling though sodium and chloride-dependent co-transport. Sodium 236-242 solute carrier family 6 member 5 Homo sapiens 70-76 29859229-3 2019 One of the most frequent causes of hyperekplexia are mutations in the SLC6A5 gene, encoding the neuronal glycine transporter 2 (GlyT2), a key component of inhibitory glycinergic presynapses involved in synaptic glycine recycling though sodium and chloride-dependent co-transport. Sodium 236-242 solute carrier family 6 member 5 Homo sapiens 105-126 29859229-3 2019 One of the most frequent causes of hyperekplexia are mutations in the SLC6A5 gene, encoding the neuronal glycine transporter 2 (GlyT2), a key component of inhibitory glycinergic presynapses involved in synaptic glycine recycling though sodium and chloride-dependent co-transport. Sodium 236-242 solute carrier family 6 member 5 Homo sapiens 128-133 30629417-0 2019 Two-Dimensional Hybrid Composites of SnS2 with Graphene and Graphene Oxide for Improving Sodium Storage: A First-Principles Study. Sodium 89-95 sodium voltage-gated channel alpha subunit 11 Homo sapiens 37-41 30629699-4 2019 NKCC1 brings sodium and chloride into the cell, possibly worsening ion dyshomeostasis. Sodium 13-19 solute carrier family 12 member 2 Rattus norvegicus 0-5 30306852-6 2019 More specifically, GSK-3beta-sensitive cellular transport regulation involves various calcium, chloride, sodium, and potassium ion channels, as well as a number of Na+-coupled cellular carriers including excitatory amino acid transporters EAAT2, 3 and 4, high-affinity Na+ coupled glucose carriers SGLT1, creatine transporter 1 CreaT1, and the type II sodium/phosphate cotransporter NaPi-IIa. Sodium 105-111 glycogen synthase kinase 3 alpha Homo sapiens 19-28 30306852-6 2019 More specifically, GSK-3beta-sensitive cellular transport regulation involves various calcium, chloride, sodium, and potassium ion channels, as well as a number of Na+-coupled cellular carriers including excitatory amino acid transporters EAAT2, 3 and 4, high-affinity Na+ coupled glucose carriers SGLT1, creatine transporter 1 CreaT1, and the type II sodium/phosphate cotransporter NaPi-IIa. Sodium 352-358 glycogen synthase kinase 3 alpha Homo sapiens 19-28 29949063-4 2019 Basal Isc in oviduct epithelium in response to apical ATPe comprises both chloride secretion and sodium absorption and has distinct temporal phases. Sodium 97-103 ATP synthase F1 subunit epsilon Homo sapiens 54-58 30442022-9 2018 Key messages Sodium consumption correlated positively with CV risk factors: age, smoking, SBP, BMI and LDL-cholesterol. Sodium 13-19 selenium binding protein 1 Homo sapiens 90-93 30442022-11 2018 Sodium consumption as a continuous variable was independently associated with AF events when age, BMI, smoking, SBP, LAD, LVMI and the use of any antihypertensive therapy were considered. Sodium 0-6 selenium binding protein 1 Homo sapiens 112-115 30323262-0 2018 Association of Kir genes with blood pressure responses to dietary sodium intervention: the GenSalt study. Sodium 66-72 killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 4 Homo sapiens 15-18 30323262-3 2018 We aimed to investigate the associations of Kir genes with BP responses to dietary sodium intervention. Sodium 83-89 killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 4 Homo sapiens 44-47 30323262-6 2018 Both single-marker and gene-based analyses were performed to explore the associations between Kir gene variants and BP responses to dietary sodium interventions. Sodium 140-146 killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 4 Homo sapiens 94-97 30333031-1 2018 BACKGROUND: Sodium/hydrogen exchanger 1 (NHE1), encoded by the SLC9A1 gene (SoLute Carrier family 9A1) in humans, is the main H+ efflux mechanism in maintaining alkaline intracellular pH (pHi) and Warburg effects in glioma. Sodium 12-18 glucose-6-phosphate isomerase Homo sapiens 188-191 30192914-1 2018 Activation of the mineralocorticoid receptor (MR) in the distal nephron by its ligand, aldosterone, plays an important role in sodium reabsorption and blood pressure regulation. Sodium 127-133 nuclear receptor subfamily 3 group C member 2 Homo sapiens 18-44 17724164-6 2007 All three mutants exhibited significant attenuation of the EGF-induced inhibition of sodium current. Sodium 85-91 epidermal growth factor Canis lupus familiaris 59-62 17493914-2 2007 This initial high concentration is commonly attributed to the ubiquitous chloride cotransporter NKCC1, which uses a sodium gradient to accumulate chloride. Sodium 116-122 solute carrier family 12 member 2 Homo sapiens 96-101 17532793-10 2007 However, nociceptin produced a rapid and marked increase in urine flow (V) and a decrease in urinary sodium excretion rate. Sodium 101-107 prepronociceptin Rattus norvegicus 9-19 17576410-5 2007 However, Na(v)1.1 is retained inside the cells and cell surface expression of the Na(v)1 alpha-subunits and sodium current densities are markedly reduced in both neuroblastoma cells and adult hippocampal neurons from BACE1-transgenic mice. Sodium 108-114 beta-site APP cleaving enzyme 1 Mus musculus 217-222 17576410-6 2007 BACE1, by cleaving beta2, thus regulates Na(v)1 alpha-subunit levels and controls cell-surface sodium current densities. Sodium 95-101 beta-site APP cleaving enzyme 1 Mus musculus 0-5 17475815-0 2007 Impairment of sodium balance in mice deficient in renal principal cell mineralocorticoid receptor. Sodium 14-20 nuclear receptor subfamily 3, group C, member 2 Mus musculus 71-97 17475815-1 2007 Germline inactivation of the mineralocorticoid receptor (MR) gene in mice results in postnatal lethality as a result of massive loss of sodium and water. Sodium 136-142 nuclear receptor subfamily 3, group C, member 2 Mus musculus 29-55 17475815-1 2007 Germline inactivation of the mineralocorticoid receptor (MR) gene in mice results in postnatal lethality as a result of massive loss of sodium and water. Sodium 136-142 nuclear receptor subfamily 3, group C, member 2 Mus musculus 57-59 17475815-9 2007 These results demonstrate that inactivation of MR in CD and late CNT can be compensated under standard diet but no longer when sodium supply is limited. Sodium 127-133 nuclear receptor subfamily 3, group C, member 2 Mus musculus 47-49 17244889-8 2007 Finally, we demonstrated that tubular VMAT-1 mRNA and protein expression were significantly upregulated during a high-sodium diet. Sodium 118-124 solute carrier family 18 member A1 Rattus norvegicus 38-44 30192914-1 2018 Activation of the mineralocorticoid receptor (MR) in the distal nephron by its ligand, aldosterone, plays an important role in sodium reabsorption and blood pressure regulation. Sodium 127-133 nuclear receptor subfamily 3 group C member 2 Homo sapiens 46-48 29923768-7 2018 However, intrarenal GR siRNA infusion prevented angiotensin II-mediated sodium retention on day 1, induced a continuously negative cumulative sodium balance compared with angiotensin II alone, and reduced BP chronically. Sodium 72-78 growth hormone secretagogue receptor Rattus norvegicus 20-22 17497345-1 2007 This study examined the effect of leptin on renal ouabain-resistant Na(+)-ATPase, which drives the reabsorption of about 10% of sodium transported in the proximal tubule. Sodium 128-134 leptin Homo sapiens 34-40 17226797-4 2007 These neurons express mineralocorticoid receptors and the enzyme 11-beta-hydroxysteroid dehydrogenase type 2 (HSD2), which makes them selectively sensitive to aldosterone-an adrenal hormone that modulates sodium appetite. Sodium 205-211 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 65-108 17226797-4 2007 These neurons express mineralocorticoid receptors and the enzyme 11-beta-hydroxysteroid dehydrogenase type 2 (HSD2), which makes them selectively sensitive to aldosterone-an adrenal hormone that modulates sodium appetite. Sodium 205-211 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 110-114 17226797-12 2007 HSD2 neurons may be part of an ascending pathway involved in the salt-seeking behavior of sodium-depleted rats. Sodium 90-96 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 0-4 17210841-6 2007 Five variants (S216L, T1304M, F1486L, F2004L, and P2006A) exhibited significantly increased persistent sodium currents (range, 0.5% to 1.7% of peak current) typical of SCN5A mutations associated with long-QT syndrome. Sodium 103-109 sodium voltage-gated channel alpha subunit 5 Homo sapiens 168-173 17340569-3 2007 FAB mass spectra of these compounds produced abundant sodium-adducted molecules [M+Na]+ from a mixture of 3-nitrobenzyl alcohol and sodium iodide. Sodium 54-60 FA complementation group B Homo sapiens 0-3 17124532-7 2006 CaMKIIdelta(C) markedly increased persistent (late) inward I(Na) and intracellular Na(+) concentration (as measured by the Na(+) indicator sodium-binding benzofuran isophthalate [SBFI]), which was prevented by CaMKII inhibition in the case of acute CaMKIIdelta(C) overexpression. Sodium 139-145 calcium/calmodulin-dependent protein kinase II, delta Mus musculus 0-6 17082480-1 2006 Long QT syndrome (LQTS) type 3 (LQT3), typified by the DeltaKPQ mutation (LQT3 mutation in which amino acid residues 1505 to 1507 [KPQ] are deleted), is caused by increased sodium entry during the action potential plateau resulting from mutation-altered inactivation of the Na(v)1.5 channel. Sodium 173-179 sodium voltage-gated channel alpha subunit 5 Homo sapiens 32-36 17082480-1 2006 Long QT syndrome (LQTS) type 3 (LQT3), typified by the DeltaKPQ mutation (LQT3 mutation in which amino acid residues 1505 to 1507 [KPQ] are deleted), is caused by increased sodium entry during the action potential plateau resulting from mutation-altered inactivation of the Na(v)1.5 channel. Sodium 173-179 sodium voltage-gated channel alpha subunit 5 Homo sapiens 74-78 17095726-2 2006 The present study examined the role of mPGES-1 in regulation of sodium balance and blood pressure in the settings of salt loading and angiotensin II infusion. Sodium 64-70 prostaglandin E synthase Mus musculus 39-46 17095726-3 2006 mPGES-1 -/- mice developed severe and progressive hypertension associated with an inappropriate increase in sodium balance when fed a high-salt diet. Sodium 108-114 prostaglandin E synthase Mus musculus 0-7 16705152-1 2006 Sodium-dependent phosphate transport in NHERF-1(-/-) proximal tubule cells does not increase when grown in a low phosphate media and is resistant to the normal inhibitory effects of parathyroid hormone (PTH). Sodium 0-6 solute carrier family 9 (sodium/hydrogen exchanger), member 3 regulator 1 Mus musculus 40-47 16705152-3 2006 NHERF-1 null cells have decreased sodium-dependent phosphate transport compared with wild-type cells. Sodium 34-40 solute carrier family 9 (sodium/hydrogen exchanger), member 3 regulator 1 Mus musculus 0-7 16897044-3 2006 Accordingly, the ability of sgk1 (-/-) mice to decrease urinary sodium output during salt depletion is impaired. Sodium 64-70 serum/glucocorticoid regulated kinase 1 Mus musculus 28-32 17111037-7 2006 PC2 and its homologue, polycystin-L (PCL), are nonselective cation channels permeable to potassium, sodium, and calcium. Sodium 100-106 polycystin 2 like 1, transient receptor potential cation channel Homo sapiens 23-35 17111037-7 2006 PC2 and its homologue, polycystin-L (PCL), are nonselective cation channels permeable to potassium, sodium, and calcium. Sodium 100-106 polycystin 2 like 1, transient receptor potential cation channel Homo sapiens 37-40 16937603-9 2006 Sodium excretion significantly increased after exercise training in the ACE II (114 +/- 22 vs 169 +/- 39 mEq/day, P=.04), but not in the ID (100 +/- 8 vs 133 +/- 17 mEq/day, P=.12) or DD (113 +/- 18 vs 138 +/- 11 mEq/day, P=.13) genotype groups. Sodium 0-6 H3 histone pseudogene 6 Homo sapiens 222-227 16937603-10 2006 In the II genotype group, the increase in sodium excretion was significantly and inversely correlated with decreases in 24-hour diastolic (r= -.88, P=.02) and mean (r= -.95, P=.004) BP. Sodium 42-48 tumor protein, translationally-controlled 1 Homo sapiens 148-153 16613846-9 2006 Our studies show that aldosterone increases the expression of 14-3-3beta, which interacts with phospho-Nedd4-2 to block its interaction with ENaC, thus enhancing sodium absorption by increasing apical membrane ENaC density. Sodium 162-168 neural precursor cell expressed, developmentally down-regulated gene 4-like Mus musculus 103-110 16799398-15 2006 Diabetic animals supplemented with C-peptide exhibit better renal function resulting in reduced urinary sodium waste and protein excretion together with reduction of the diabetes-induced glomerular hyperfiltration. Sodium 104-110 insulin 2 Rattus norvegicus 35-44 16540484-0 2006 Calcium regulation of sodium hypersensitivities of sos3 and athkt1 mutants. Sodium 22-28 high-affinity K+ transporter 1 Arabidopsis thaliana 60-66 30170187-1 2018 The central nucleus of the amygdala (CeA) is a critical region in regulating sodium intake, and interestingly, purinergic receptors reportedly related to fluid balance, are also expressed in CeA. Sodium 77-83 carcinoembryonic antigen gene family 4 Rattus norvegicus 37-40 30170187-2 2018 In this study, we investigated whether the purinergic mechanisms of CeA were involved in regulating sodium intake. Sodium 100-106 carcinoembryonic antigen gene family 4 Rattus norvegicus 68-71 30231508-1 2018 The mineralocorticoid receptor (MR) was first identified as a blood pressure regulator, modulating renal sodium handling in response to its principal ligand aldosterone. Sodium 105-111 nuclear receptor subfamily 3 group C member 2 Homo sapiens 4-30 30354328-9 2018 Cycle threshold values for MR-regulated targets ( SCNN1A, SCNN1G, TSC22D3) changed after sodium loading, and MR-regulated targets ( SCNN1A, SCNN1G, SGK1, and TSC22D3) correlated significantly with serum aldosterone and inversely with urinary sodium excretion. Sodium 89-95 TSC22 domain family member 3 Homo sapiens 66-73 30167850-1 2018 NALCN is a conserved cation channel, which conducts a permanent sodium leak current and regulates resting membrane potential and neuronal excitability. Sodium 64-70 sodium leak channel, non-selective Homo sapiens 0-5 29677807-0 2018 Electrochemical Properties of Micron-Sized SnO Anode Using a Glyme-Based Electrolyte for Sodium-Ion Battery. Sodium 89-95 strawberry notch homolog 1 Homo sapiens 43-46 29677807-1 2018 Tin monoxide (SnO) anodes are promising candidates for use in sodium-ion batteries because of their high theoretical capacities and stable cycle performance. Sodium 62-68 strawberry notch homolog 1 Homo sapiens 14-17 29677807-9 2018 The electrode composed of micron-sized SnO is a potential candidate for use in sodium-ion batteries. Sodium 79-85 strawberry notch homolog 1 Homo sapiens 39-42 29847236-12 2018 The voltage-dependent sodium channel NaV1.9 plays a unique role in controlling afferent excitability. Sodium 22-28 sodium voltage-gated channel alpha subunit 11 Homo sapiens 37-43 30029710-5 2018 Most of articles in this review reported that 2.6-3 g/day of dietary sodium is effective for decreased BNP, renin, and aldosterone (neurohormonal) plasma levels in patients with HF. Sodium 69-75 natriuretic peptide B Homo sapiens 103-106 29991598-9 2018 The only major difference between Nav1.6-null and wild-type neurons was a strong reduction in persistent sodium current. Sodium 105-111 neuron navigator 1 Homo sapiens 34-38 29505789-6 2018 We examined the mechanisms underlying these effects, with poly I:C significantly reducing peak sodium current, an effect dependent on the MyD88-independent TRIF dependent pathway. Sodium 95-101 MYD88 innate immune signal transduction adaptor Homo sapiens 138-143 29717862-0 2018 MOF-Templated N-Doped Carbon-Coated CoSe2 Nanorods Supported on Porous CNT Microspheres with Excellent Sodium-Ion Storage and Electrocatalytic Properties. Sodium 103-109 lysine acetyltransferase 8 Homo sapiens 0-3 29666849-0 2018 A rational microstructure design of SnS2-carbon composites for superior sodium storage performance. Sodium 72-78 sodium voltage-gated channel alpha subunit 11 Homo sapiens 36-40 29666849-5 2018 The sodium storage mechanism of SnS2 was systematically studied through CV, ex situ XPS, and ex situ HRTEM characterization studies, disclosing the reversible conversion and alloying reactions of SnS2 during sodiation/desodiation processes. Sodium 4-10 sodium voltage-gated channel alpha subunit 11 Homo sapiens 32-36 29666849-5 2018 The sodium storage mechanism of SnS2 was systematically studied through CV, ex situ XPS, and ex situ HRTEM characterization studies, disclosing the reversible conversion and alloying reactions of SnS2 during sodiation/desodiation processes. Sodium 4-10 sodium voltage-gated channel alpha subunit 11 Homo sapiens 196-200 29666849-6 2018 Moreover, ex situ TEM was further applied to clarify the relationships between the SnS2-C microstructure and sodium storage performance. Sodium 109-115 sodium voltage-gated channel alpha subunit 11 Homo sapiens 83-87 29447844-1 2018 The central nucleus of the amygdala (CeA) is critical in the regulation of sodium appetite. Sodium 75-81 carcinoembryonic antigen gene family 4 Rattus norvegicus 37-40 29327011-0 2018 Highly reversible and fast sodium storage boosted by improved interfacial and surface charge transfer derived from the synergistic effect of heterostructures and pseudocapacitance in SnO2-based anodes. Sodium 27-33 strawberry notch homolog 1 Homo sapiens 183-186 16713495-2 2006 Patients with hereditary NDI bearing mutations in AVPR2, the gene coding for the arginine vasopressin 2 receptor, or in AQP2, the gene coding for the vasopressin-sensitive water channel, have a pure NDI phenotype with loss of water, but normal conservation of sodium, potassium, chloride, and calcium. Sodium 260-266 aquaporin 2 Homo sapiens 120-124 16633672-8 2006 Furthermore, this force field is used to study the effects of sodium cations on the adsorption behavior of larger alkanes, such as C(4)-C(7), in MOR-type zeolites. Sodium 62-68 opioid receptor mu 1 Homo sapiens 145-148 16107787-2 2006 Three gene products of the sodium-calcium exchanger family NCX1, NCX2, and NCX3 couple, in a bidirectional way, the movement of these ions across the cell membrane during cerebral ischemia. Sodium 27-33 solute carrier family 8 member A3 Rattus norvegicus 75-79 16213693-5 2006 The SAPS II score requires 17 static variables (e.g. serum sodium), which are collected within the first day of the patient"s admission. Sodium 59-65 src kinase associated phosphoprotein 2 Homo sapiens 4-8 16357110-2 2006 There are two sodium-dependent membrane transporters encoded by SLC23A1 and SLC23A2, which have key roles in human vitamin C metabolism and which control dietary uptake, reabsorption, and tissue distribution of vitamin C. Sodium 14-20 solute carrier family 23 member 1 Homo sapiens 64-71 16174867-11 2006 The increased targeting of ENaC and AQP2 likely represents direct or compensatory effects to increase sodium and water reabsorption and to prevent volume depletion in response to prolonged ANP infusion. Sodium 102-108 aquaporin 2 Rattus norvegicus 36-40 17183188-8 2006 Sodium overload increased the expression of: RANTES (38.4.3 +/- 0.8 vs. 2.9 +/- 0.6%, p < 0.001), transforming-growth-factor-beta(1) (35.3 +/- 1.0 vs. 5.0 +/- 0.7%, p < 0.001), alpha-smooth muscle actin (15.6 +/- 0.7 vs. 3.1 +/- 0.3%, p < 0.001), NF-kappaB (9.4 +/- 1.3 to 2.2 +/- 0.5 cells/mm(2), p < 0.001), HIF-1alpha (38.2 +/- 1.7 to 8.4 +/- 0.8 cells/mm(2), p < 0.001) and angiotensin II (35.9 +/- 1.3 to 8.2 +/- 0.5%, p < 0.001). Sodium 0-6 actin gamma 2, smooth muscle Rattus norvegicus 183-208 29352161-0 2018 The action of a negative allosteric modulator at the dopamine D2 receptor is dependent upon sodium ions. Sodium 92-98 dopamine receptor D2 Homo sapiens 53-73 16874452-5 2006 In the animal model of CIM the Nav1.5 sodium channel isoform is upregulated, but the majority of sodium current is still carried by Nav1.4 sodium channels. Sodium 38-44 sodium voltage-gated channel alpha subunit 5 Homo sapiens 31-37 16550618-4 2006 FAB-MS spectra produced a significant abundance of the sodium adducts [M+Na]+ and [M+2Na-H]+ from a mixture of m-NBA and NaI. Sodium 55-61 FA complementation group B Homo sapiens 0-3 16359386-8 2005 These findings show that AtHKT1 selectively unloads sodium directly from xylem vessels to xylem parenchyma cells. Sodium 52-58 high-affinity K+ transporter 1 Arabidopsis thaliana 25-31 16359386-10 2005 Thus AtHKT1 reduces the sodium content in xylem vessels and leaves, thereby playing a central role in protecting plant leaves from salinity stress. Sodium 24-30 high-affinity K+ transporter 1 Arabidopsis thaliana 5-11 29352161-1 2018 Sodium ions (Na+) allosterically modulate the binding of orthosteric agonists and antagonists to many class A G protein-coupled receptors, including the dopamine D2 receptor (D2R). Sodium 0-6 dopamine receptor D2 Homo sapiens 153-173 30081699-4 2018 Using a rational design strategy, we identified a heptamer peptide harboring CRMP2"s SUMO motif that disrupted the CRMP2-Ubc9 interaction, inhibited CRMP2 SUMOylation, inhibited NaV1.7 membrane trafficking, and specifically inhibited NaV1.7 sodium influx in sensory neurons. Sodium 241-247 ubiquitin conjugating enzyme E2 I Homo sapiens 121-125 30081699-4 2018 Using a rational design strategy, we identified a heptamer peptide harboring CRMP2"s SUMO motif that disrupted the CRMP2-Ubc9 interaction, inhibited CRMP2 SUMOylation, inhibited NaV1.7 membrane trafficking, and specifically inhibited NaV1.7 sodium influx in sensory neurons. Sodium 241-247 neuron navigator 1 Homo sapiens 178-182 29491733-2 2018 In arabidopsis, the Ca2+ activated SOS3 interacts with SOS2 which further activates SOS1, a Na+/H+ antiporter, responsible for removing toxic sodium ions from the cells. Sodium 142-148 Calcium-binding EF-hand family protein Arabidopsis thaliana 35-39 30175793-0 2018 [6]-Gingerol Induces Amiloride-Sensitive Sodium Absorption in the Rat Colon via the Capsaicin Receptor TRPV1 in Colonic Mucosa. Sodium 41-47 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 103-108 15958719-5 2005 The sodium-dependent component of 2,4-D uptake coincided with the PAH-sensitive component, indicating uptake mediated by organic anion transporter subtype (Oat) 3. Sodium 4-10 solute carrier family 22 member 8 Rattus norvegicus 121-162 30175793-2 2018 Recently, our group observed that the serosal administration of [6]-gingerol stimulated electrogenic sodium absorption in the rat colon via the capsaicin receptor, TRPV1. Sodium 101-107 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 144-162 30175793-5 2018 We compared the effect of [6]-gingerol on TRPV1-dependent colonic sodium absorption in the colon preparation with or without muscle layer. Sodium 66-72 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 42-47 16105937-4 2005 Leptin adversely shifts the renal pressure-natriuresis curve, leading to relative sodium retention. Sodium 82-88 leptin Homo sapiens 0-6 28732557-2 2017 In contrast with classical cable theory predictions, the persistent sodium current (INaP), a non-inactivating mode of the voltage-dependent sodium current, paradoxically increases Rin and taum when activated. Sodium 68-74 NFKB inhibitor zeta Homo sapiens 84-88 16061744-1 2005 BACKGROUND: The Y1102 polymorphism of the cardiac sodium channel (SCN5A) gene has been found in 13% of black Americans. Sodium 50-56 sodium voltage-gated channel alpha subunit 5 Homo sapiens 66-71 16054936-9 2005 Whole-cell recordings in transiently transfected tsA201 cells expressing the highly homologous SCN5A sodium channel showed that the mutation induces a two-fold to four-fold accelerated recovery from fast inactivation without altering any of the other channel parameters investigated. Sodium 101-107 sodium voltage-gated channel alpha subunit 5 Homo sapiens 95-100 21783565-0 2005 Enhancement of sodium metabisulfite on sodium currents in acutely isolated rat hippocampal CA1 neurons. Sodium 15-21 carbonic anhydrase 1 Rattus norvegicus 91-94 28732557-2 2017 In contrast with classical cable theory predictions, the persistent sodium current (INaP), a non-inactivating mode of the voltage-dependent sodium current, paradoxically increases Rin and taum when activated. Sodium 140-146 NFKB inhibitor zeta Homo sapiens 84-88 28959816-1 2017 Tin disulfide (SnS2) has emerged as a promising anode material for lithium/sodium ion batteries (LIBs/SIBs) due to its unique layered structure, outstanding electrochemical properties and low cost. Sodium 75-81 sodium voltage-gated channel alpha subunit 11 Homo sapiens 15-19 28509725-7 2017 SBP reduction was positively related to increasing urinary sodium and PP levels for patients in both groups but increased faster with increasing PP in HCTZ than in telmisartan (P = 0.0238 for group x PP). Sodium 59-65 selenium binding protein 1 Homo sapiens 0-3 28718687-1 2017 The cardiac voltage-gated sodium channel (gene: SCN5A, protein: NaV1.5) is responsible for the sodium current that initiates the cardiomyocyte action potential. Sodium 26-32 sodium voltage-gated channel alpha subunit 5 Rattus norvegicus 48-53 15882659-4 2005 Mutations in SCN5A cause a functional reduction in the availability of cardiac sodium current in Brugada syndrome. Sodium 79-85 sodium voltage-gated channel alpha subunit 5 Homo sapiens 13-18 28718687-1 2017 The cardiac voltage-gated sodium channel (gene: SCN5A, protein: NaV1.5) is responsible for the sodium current that initiates the cardiomyocyte action potential. Sodium 26-32 sodium voltage-gated channel alpha subunit 5 Rattus norvegicus 64-70 28506883-10 2017 Our findings indicate the involvement of NKA-SRc-Kinase-Ras-Raf-ERK1/2 pathway in the downregulation of NHE3 by cardiotonic steroids in the renal proximal tubule, promoting a reduction of proximal sodium reabsorption and natriuresis. Sodium 197-203 mitogen activated protein kinase 3 Rattus norvegicus 64-70 28506883-10 2017 Our findings indicate the involvement of NKA-SRc-Kinase-Ras-Raf-ERK1/2 pathway in the downregulation of NHE3 by cardiotonic steroids in the renal proximal tubule, promoting a reduction of proximal sodium reabsorption and natriuresis. Sodium 197-203 solute carrier family 9 member A3 Rattus norvegicus 104-108 28343377-9 2017 Under voltage-clamp mode, incubation of CORT enhanced voltage-gated sodium current density of the recorded neurons. Sodium 68-74 cortistatin Rattus norvegicus 40-44 15696543-2 2005 Two configurations of the unbound form of BuChE differing in the presence or absence of a sodium ion inside the protein gorge were simulated for 10 and 5 ns, respectively. Sodium 90-96 butyrylcholinesterase Homo sapiens 42-47 28343377-10 2017 Pre-incubation of GF109203X, an inhibitor of protein kinase C, blocked the CORT-induced hyperexcitability and potentiation of sodium currents. Sodium 126-132 cortistatin Rattus norvegicus 75-79 27624713-8 2017 Cox proportional hazard analysis revealed that a higher BNP at T1 independently predicts 6-month mortality (hazard ratio 1.95, 95 % CI 1.067-3.578, P = 0.03) after adjustment for age, sodium, creatinine, and NYHA class-all at discharge. Sodium 184-190 natriuretic peptide B Homo sapiens 56-59 28591032-6 2017 In a multivariate Cox-proportional regression analysis, discharge sodium level had the strongest significant relationship with long-term mortality (hazard ratio [HR] as continuous variable = 1.06, 95% confidence interval [CI]: 1.01-1.11, P = .026; HR as categorical variable = 1.71; 95% CI: 1.06-2.75; P = .028), but baseline and nadir sodium had no prognostic impact on long-term mortality after adjustment. Sodium 66-72 cytochrome c oxidase subunit 8A Homo sapiens 18-21 28593901-8 2017 Sequence analysis of the CUL3 gene demonstrated a previously unreported heterozygous c.1377+2T>3 mutation, confirming the diagnosis of PHAII-E. We highlight the importance of the determination of plasma aldosterone and plasma renin activity in the context of persistent sodium and potassium imbalances in children. Sodium 273-279 cullin 3 Homo sapiens 25-29 15489254-7 2005 J Endocrinol 175: 343-347, 2002), they could involve cAMP-mediated activation of the cystic fibrosis transmembrane conductance regulator chloride channel, which drives sodium secretion in the IMCD. Sodium 168-174 CF transmembrane conductance regulator Rattus norvegicus 85-136 15590761-2 2005 However, the roles of uroguanylin in nephrotic syndrome, which is associated with sodium and water retention, have not been determined. Sodium 82-88 guanylate cyclase activator 2B Rattus norvegicus 22-33 15590761-5 2005 The plasma levels and renal and intestinal mRNA expression of uroguanylin at the periods of sodium retention and remarkable natriuresis also were evaluated. Sodium 92-98 guanylate cyclase activator 2B Rattus norvegicus 62-73 15590761-7 2005 When the urinary excretion of ir-uroguanylin and sodium peaked, the plasma level of ir-uroguanylin also increased compared with that of the control group. Sodium 49-55 guanylate cyclase activator 2B Rattus norvegicus 87-98 15590761-8 2005 Uroguanylin mRNA expression in the kidney increased during the period of sodium retention and then decreased during the period of remarkable natriuresis. Sodium 73-79 guanylate cyclase activator 2B Rattus norvegicus 0-11 28391629-20 2017 AUTHORS" CONCLUSIONS: Sodium reduction from an average high usual sodium intake level (201 mmol/day) to an average level of 66 mmol/day, which is below the recommended upper level of 100 mmol/day (5.8 g salt), resulted in a decrease in SBP/DBP of 1/0 mmHg in white participants with normotension and a decrease in SBP/DBP of 5.5/2.9 mmHg in white participants with hypertension. Sodium 22-28 selenium binding protein 1 Homo sapiens 236-239 28391629-20 2017 AUTHORS" CONCLUSIONS: Sodium reduction from an average high usual sodium intake level (201 mmol/day) to an average level of 66 mmol/day, which is below the recommended upper level of 100 mmol/day (5.8 g salt), resulted in a decrease in SBP/DBP of 1/0 mmHg in white participants with normotension and a decrease in SBP/DBP of 5.5/2.9 mmHg in white participants with hypertension. Sodium 22-28 selenium binding protein 1 Homo sapiens 314-317 27906747-2 2017 RECENT FINDINGS: AT2R activation prevents sodium (Na) retention and lowers blood pressure in the Ang II infusion model of experimental hypertension and prevents salt-sensitive hypertension in the obese Zucker rat model of obesity and the metabolic syndrome. Sodium 42-48 angiotensin II receptor, type 2 Rattus norvegicus 17-21 28134511-0 2017 Sulfate-Centered Sodium-Icosahedron-Templated Uranyl Peroxide Phosphate Cages with Uranyl Bridged by mu-eta1:eta2 Peroxide. Sodium 17-23 DNA polymerase iota Homo sapiens 109-113 15673310-10 2005 CONCLUSION: This study highlights the role of this HSD11B2 polymorphism in sodium handling and is consistent with a role in the BP response to thiazide diuretics. Sodium 75-81 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 51-58 15642860-4 2005 DESIGN: The coding regions of 6 genes that cause peripheral neuropathy and regions of the muscle sodium channel gene (SCN4A) were sequenced. Sodium 97-103 sodium voltage-gated channel alpha subunit 4 Homo sapiens 118-123 15486051-2 2005 We tested the hypothesis that sodium excretion is reduced in response to a sodium load during combined P(4)-E(2) treatment, but P(4) administration alone has little effect on sodium regulation. Sodium 30-36 solute carrier family 10 member 4 Homo sapiens 103-107 15486051-2 2005 We tested the hypothesis that sodium excretion is reduced in response to a sodium load during combined P(4)-E(2) treatment, but P(4) administration alone has little effect on sodium regulation. Sodium 75-81 solute carrier family 10 member 4 Homo sapiens 103-107 15486051-9 2005 Compared with GnRH antagonist alone, P(4)-E(2) treatment increased distal sodium reabsorption and transiently decreased proximal sodium reabsorption, whereas P(4) treatment did not alter either distal or proximal sodium reabsorption. Sodium 74-80 solute carrier family 10 member 4 Homo sapiens 37-41 15486051-9 2005 Compared with GnRH antagonist alone, P(4)-E(2) treatment increased distal sodium reabsorption and transiently decreased proximal sodium reabsorption, whereas P(4) treatment did not alter either distal or proximal sodium reabsorption. Sodium 129-135 solute carrier family 10 member 4 Homo sapiens 37-41 15486051-9 2005 Compared with GnRH antagonist alone, P(4)-E(2) treatment increased distal sodium reabsorption and transiently decreased proximal sodium reabsorption, whereas P(4) treatment did not alter either distal or proximal sodium reabsorption. Sodium 129-135 solute carrier family 10 member 4 Homo sapiens 37-41 15486051-13 2005 In summary, we found that P(4)-E(2) treatment decreased sodium excretion via either renin-angiotensin-Ald system stimulation or direct effects on kidney tubules. Sodium 56-62 solute carrier family 10 member 4 Homo sapiens 26-30 15623826-0 2005 Growth hormone and epidermal growth factor upregulate specific sodium-dependent glutamine uptake systems in human intestinal C2BBe1 cells. Sodium 63-69 epidermal growth factor Homo sapiens 19-42 15614025-1 2004 OBJECTIVE: Angiotensin II and aldosterone, generated by the angiotensin-converting enzyme (ACE) and aldosterone synthase (CYP11B2), respectively, not only regulate sodium and water homeostasis, but also influence vascular remodeling in response to high blood pressure. Sodium 164-170 cytochrome P450 family 11 subfamily B member 2 Homo sapiens 100-120 15614025-1 2004 OBJECTIVE: Angiotensin II and aldosterone, generated by the angiotensin-converting enzyme (ACE) and aldosterone synthase (CYP11B2), respectively, not only regulate sodium and water homeostasis, but also influence vascular remodeling in response to high blood pressure. Sodium 164-170 cytochrome P450 family 11 subfamily B member 2 Homo sapiens 122-129 15338391-7 2004 In conclusion, our data show that increased sodium intake during pregnancy induces a reduction of alpha-SM-actin, fibronectin, and PCNA expression in the renal cortex tubulointerstitium and glomeruli of neonatal rats. Sodium 44-50 fibronectin 1 Rattus norvegicus 114-125 15486089-5 2004 Using microarray mapping, a sodium overaccumulation mutant FN1148 was identified as having a 523-bp genomic deletion within the second exon and intron of the AtHKT1 gene. Sodium 28-34 high-affinity K+ transporter 1 Arabidopsis thaliana 158-164 15486089-6 2004 Further cosegregation, complementation, and comparative analyses among different salt-sensitive mutants confirmed that the deletion within the AtHKT1 gene is responsible for the sodium overaccumulation in shoots and leaf sodium sensitivity of the FN1148 mutant. Sodium 178-184 high-affinity K+ transporter 1 Arabidopsis thaliana 143-149 15486089-6 2004 Further cosegregation, complementation, and comparative analyses among different salt-sensitive mutants confirmed that the deletion within the AtHKT1 gene is responsible for the sodium overaccumulation in shoots and leaf sodium sensitivity of the FN1148 mutant. Sodium 221-227 high-affinity K+ transporter 1 Arabidopsis thaliana 143-149 15493939-1 2004 Reduction of the five-coordinate iron(II) dihalide complexes (iPrPDI)FeX2 (iPrPDI = ((2,6-CHMe2)2C6H3N=CMe)2C5H3N; X = Cl, Br) with sodium amalgam under 1 atm of dinitrogen afforded the square pyramidal, high spin iron(0) bis(dinitrogen) complex (iPrPDI)Fe(N2)2. Sodium 132-138 stabilin 2 Homo sapiens 69-73 28218286-0 2017 Vinculin variant M94I identified in sudden unexplained nocturnal death syndrome decreases cardiac sodium current. Sodium 98-104 vinculin Homo sapiens 0-8 28218286-7 2017 In HEK293 cells with pH 7.4, VCL-M94I caused ~30% decrease in peak sodium current (INa) amplitude compared to WT; under acidotic conditions (pH 7.0) typically found with hypoxia during sleep apnea, M94I resulted in 37% reduction in peak INa compared to WT and the combination of VCL-M94I and pH 7.0 decreased peak INa by ~56% compared to WT at pH 7.4. Sodium 67-73 vinculin Homo sapiens 29-32 28098459-0 2017 Two-Dimensional SnO Anodes with a Tunable Number of Atomic Layers for Sodium Ion Batteries. Sodium 70-76 strawberry notch homolog 1 Homo sapiens 16-19 15317600-4 2004 RESULTS: Cin and CPAH were not significantly different during euglycaemia (period I of Study 1) in DM1 and controls, whereas fractional excretion of sodium was decreased in DM1 (1.84 +/- 0.75 vs. 2.36 +/- 0.67%; P < 0.05) due to an increase in fractional distal tubular reabsorption of sodium (94.01 +/- 1.94 vs. 92.24 +/- 2.47%; P < 0.05). Sodium 149-155 immunoglobulin heavy diversity 1-7 Homo sapiens 173-176 15317600-5 2004 A comparison of changes during Study 1 and Study 2 revealed acute hyperglycaemia did not change renal haemodynamics significantly, while fractional distal tubular reabsorption of sodium increased (DM1: P < 0.05; C: P < 0.01) and fractional excretion of sodium decreased (P < 0.01) in both groups. Sodium 179-185 immunoglobulin heavy diversity 1-7 Homo sapiens 197-200 15317600-9 2004 CONCLUSION: This study demonstrates that DM1 without renal haemodynamic alterations is associated with impaired renal sodium handling. Sodium 118-124 immunoglobulin heavy diversity 1-7 Homo sapiens 41-44 15234075-5 2004 These results imply that AlCl3 could affect the activation and inactivation courses of sodium current and potassium current of rat hippocampal CA1 neurons, which may contribute to damage of the central nervous system by aluminum. Sodium 87-93 carbonic anhydrase 1 Rattus norvegicus 143-146 15246823-0 2004 Dietary sodium regulates angiotensin AT1a and AT1b mRNA expression in mouse brain. Sodium 8-14 angiotensin II receptor, type 1b Mus musculus 46-50 27627464-4 2016 The functional interplay between TRPV1, MCU and NCLX, in controlling the cytosolic and mitochondrial calcium and sodium transients and subsequently the nociceptive excitability, is poorly understood. Sodium 113-119 transient receptor potential cation channel subfamily V member 1 Homo sapiens 33-38 27627464-6 2016 We show that the propagation of the TRPV1-induced cytosolic calcium and sodium fluxes into mitochondria is dependent on coordinated activity of NCLX and MCU. Sodium 72-78 transient receptor potential cation channel subfamily V member 1 Homo sapiens 36-41 27571932-10 2016 Moreover, BNP (100 nM) increased the transient inward current, sodium currents, sodium-calcium exchanger currents, and L-type calcium current; but reduced late sodium currents and the Na-K pump in PV cardiomyocytes. Sodium 80-86 natriuretic peptide B Homo sapiens 10-13 27841351-3 2016 Here, using experimental and modelling approaches, we show how the activation of glycogen synthase kinase 3 (GSK3) contributes to neuronal excitability through regulation of the persistent sodium current (INaP). Sodium 189-195 NFKB inhibitor zeta Homo sapiens 205-209 27510906-9 2016 Moreover, these findings support the notion that NHE3 dephosphorylation at serine 552 may represent a key event in the regulation of renal proximal tubule sodium handling by ANG II in the presence of natriuretic hormones that promote cAMP accumulation and transporter phosphorylation. Sodium 155-161 solute carrier family 9 member A3 Rattus norvegicus 49-53 27600292-8 2016 Our study indicates that this "ghrelin-Sirt1 system" may participate in regulating sodium reabsorption in the distal nephron. Sodium 83-89 ghrelin and obestatin prepropeptide Rattus norvegicus 31-38 27561861-7 2016 Nut consumption was mainly from incorporated sources (65%), which were higher in added sugar (p < .001) and sodium (p < .001), and lower in nut quantity (p < .001) than stand-alone sources. Sodium 111-117 NUT midline carcinoma family member 1 Homo sapiens 0-3 27561861-8 2016 Nut consumers consumed more daily added sugar (p = .004) and sodium (p = .04) than non-consumers. Sodium 61-67 NUT midline carcinoma family member 1 Homo sapiens 0-3 27229121-3 2016 How loss of Myo5b results in increased stool loss of chloride (Cl(-)) and sodium (Na(+)) is unknown. Sodium 74-80 myosin VB Homo sapiens 12-17 27214555-3 2016 In the proximal tubule (PT) of the kidney, claudin-2 mediates paracellular sodium reabsorption. Sodium 75-81 claudin 2 Mus musculus 43-52 27214555-5 2016 We found that claudin-2-null mice conserve sodium to the same extent as WT mice, even during profound dietary sodium depletion, as a result of the upregulation of transcellular Na-K-2Cl transport activity in the thick ascending limb of Henle. Sodium 43-49 claudin 2 Mus musculus 14-23 27214555-5 2016 We found that claudin-2-null mice conserve sodium to the same extent as WT mice, even during profound dietary sodium depletion, as a result of the upregulation of transcellular Na-K-2Cl transport activity in the thick ascending limb of Henle. Sodium 110-116 claudin 2 Mus musculus 14-23 26223346-1 2016 A recent study from the United Kingdom indicates an association between pre hemodialysis (HD) serum sodium (SNa(+)) and systolic and diastolic blood pressure (SBP and DBP) in chronic HD patients. Sodium 100-106 selenium binding protein 1 Homo sapiens 159-162 27355484-11 2016 The accumulated ATPe activates P2X receptors, followed by sodium influx, resulting in cell swelling, which in turn further activates ATP release. Sodium 58-64 ATP synthase F1 subunit epsilon Homo sapiens 16-20 15169846-0 2004 Functional interaction between extracellular sodium, potassium and inactivation gating in HERG channels. Sodium 45-51 potassium voltage-gated channel subfamily H member 2 Homo sapiens 90-94 15253107-4 2004 PPAR-alpha is known to regulate cytochrome P450 gene expression, and may possibly affect sodium retention in the kidney. Sodium 89-95 peroxisome proliferator activated receptor alpha Rattus norvegicus 0-10 14759559-0 2004 Internalization of neuropeptide Y Y1 and Y5 and of pancreatic polypeptide Y4 receptors is inhibited by lithium in preference to sodium and potassium ions. Sodium 128-134 RNA, Ro60-associated Y5 Homo sapiens 19-43 14700527-0 2004 Effects of hydrogen peroxide on sodium current in acutely isolated rat hippocampal CA1 neurons. Sodium 32-38 carbonic anhydrase 1 Rattus norvegicus 83-86 14984931-1 2004 Microsomal epoxide hydrolase (mEH) is a bifunctional protein that plays a crucial role in the metabolism of numerous xenobiotics as well as in mediating the hepatic sodium-dependent uptake of bile acids that are involved in numerous physiological processes including the regulation of cholesterol metabolism. Sodium 165-171 epoxide hydrolase 1 Homo sapiens 0-28 27339867-5 2016 Arterial stiffness increased with higher sodium reabsorption in the distal tubule, in the presence of AGTR2 G allele with the opposite tendency in A allele carriers. Sodium 41-47 angiotensin II receptor type 2 Homo sapiens 102-107 27339867-7 2016 CONCLUSIONS: The relation between sodium reabsorption in the distal tubule and the development of arterial stiffness depends on the AGTR2 G1675A polymorphism in blood pressure independent fashion. Sodium 34-40 angiotensin II receptor type 2 Homo sapiens 132-137 26764207-3 2016 We aimed to investigate how diabetes and SGLT2 inhibition affect TNa and sodium transport-dependent oxygen consumption [Formula: see text] along the whole nephron. Sodium 73-79 solute carrier family 5 member 2 Rattus norvegicus 41-46 14610227-3 2004 OATP-B-mediated uptake of estrone-3-sulfate was independent of sodium, chloride, bicarbonate, or glutathione, whereas the proton ionophore carbonylcyanide p-trifluoromethoxyphenylhydrazone exhibited a pH-dependent inhibitory effect, suggesting that a proton gradient is a driving force for OATP-B. Sodium 63-69 solute carrier organic anion transporter family member 2B1 Homo sapiens 0-6 26886564-13 2016 These findings suggest that mineralocorticoid receptor antagonists may be of preferential benefit in counteracting the BP effects of high dietary sodium. Sodium 146-152 nuclear receptor subfamily 3 group C member 2 Homo sapiens 28-54 14984796-0 2004 Sodium deficiency and salt appetite in ICR: CD1 mice. Sodium 0-6 CD1 antigen complex Mus musculus 44-47 14676229-3 2004 High throughput genetic analysis found a sodium channel gene (LQT3) mutation. Sodium 41-47 sodium voltage-gated channel alpha subunit 5 Homo sapiens 62-66 14654249-3 2003 Inhibition of 11beta-HSD2, which may cause cortisol-dependent activation of the mineralocorticoid receptor with sodium retention and hypertension, was observed for several compounds, with diethylcarbamate being the most potent inhibitor (IC50 6.3 microM). Sodium 112-118 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 14-25 14653952-0 2003 Blockade of paeoniflorin on sodium current in mouse hippocampal CA1 neurons. Sodium 28-34 carbonic anhydrase 1 Mus musculus 64-67 14689370-1 2003 In the kidney, neutral endopeptidase (NEP) is implicated in the metabolism of several peptides involved in blood pressure and sodium homeostasis control, such as the atrial natriuretic peptide, bradykinin and angiotensin I. Sodium 126-132 natriuretic peptide type A Mus musculus 166-192 14643057-3 2003 Ye and co-workers recently showed that the mRNA expression of the genes for the last enzyme of the aldosterone pathway, aldosterone synthase, is regulated by sodium depletion, as is the case in the adrenal gland. Sodium 158-164 cytochrome P450 family 11 subfamily B member 2 Homo sapiens 120-140 26994581-9 2016 We suggest that inhibition of glucose metabolism with ensuing loss of ATP is a neurotoxic mechanism of hyperosmolar sodium, whereas increased uptake of extracellular neuroactive amino acids and reduced intracellular [Ca(2+)] may, if they occur in vivo, contribute to the cerebral dysfunction and delirium described in hypernatremia. Sodium 116-122 ATPase phospholipid transporting 8A2 Homo sapiens 70-73 26850381-5 2016 A realistic model for the mechanism of the exchanger"s allosteric regulation should not only address this property, but also it should explain the distinctive behavior of Drosophila melanogaster"s sodium/calcium exchanger, CALX, for which Ca(2+) -binding to CBD1 inhibits Ca(2+) exchange. Sodium 197-203 defensin beta 1 Canis lupus familiaris 258-262 12869367-8 2003 ANG II increased ANG IR by 60 +/- 7 pmol/ml, blood pressure by 30%, increased plasma aldosterone markedly (to 345 +/- 72 pg/ml), and plasma vasopressin transiently, while reducing glomerular filtration rate (40 +/- 2 to 33 +/- 2 ml/min), sodium excretion (50 +/- 7 to 16 +/- 4 micromol/min), and urine flow. Sodium 238-244 ANG Canis lupus familiaris 0-3 12869367-12 2003 It is concluded that 1) plasma clearances of ANG III and ANG IV are higher than those of ANG II; 2) ANG III is more potent than ANG II in eliciting immediate sodium and potassium retention, as well as aldosterone secretion, particularly at low concentrations; and 3) the complexity of the ANG III dose-response relationships provides indirect evidence that several effector mechanisms are involved. Sodium 158-164 ANG Canis lupus familiaris 45-48 14569097-1 2003 The role of SGLT2 (the gene for a renal sodium-dependent glucose transporter) in renal glucosuria was evaluated. Sodium 40-46 solute carrier family 5 member 2 Homo sapiens 12-17 14523039-0 2003 Congenital sick sinus syndrome caused by recessive mutations in the cardiac sodium channel gene (SCN5A). Sodium 76-82 sodium voltage-gated channel alpha subunit 5 Homo sapiens 97-102 14523039-4 2003 Based on prior associations with disorders of cardiac rhythm and conduction, we screened the alpha subunit of the cardiac sodium channel (SCN5A) as a candidate gene in ten pediatric patients from seven families who were diagnosed with congenital SSS during the first decade of life. Sodium 122-128 sodium voltage-gated channel alpha subunit 5 Homo sapiens 138-143 14619194-4 2003 Mutations in SCN5A, responsible for Brugada syndrome, cause a functional reduction in the availability of cardiac sodium current. Sodium 114-120 sodium voltage-gated channel alpha subunit 5 Homo sapiens 13-18 12742089-3 2003 It was demonstrated that, as in several other transporters, sodium binding and release by GAT1, GAT3 and BGT-1, the canine homolog of GAT2, resulted in the appearance of presteady-state currents. Sodium 60-66 solute carrier family 6 (neurotransmitter transporter), member 1 S homeolog Xenopus laevis 90-94 12775716-4 2003 Activation of the aldosterone system by a low sodium diet up-regulated the expression of PKG II, however, it did not change PKG I expression in adrenal cortex. Sodium 46-52 protein kinase cGMP-dependent 1 Rattus norvegicus 89-94 12881590-2 2003 In peripheral epithelial tissues, sodium and water transport is regulated by corticosteroids and the 11beta-hydroxysteroid dehydrogenase (11beta-HSD) isozymes (11beta-HSD1 activating cortisol from cortisone, 11beta-HSD2 inactivating cortisol to cortisone). Sodium 34-40 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 208-219 12697273-0 2003 Sodium ions and GTP decrease the potency of [Nphe1]N/OFQ(1-13)NH2 in blocking nociceptin/orphanin FQ receptors coupled to cyclic AMP in N1E-115 neuroblastoma cells and rat olfactory bulb. Sodium 0-6 prepronociceptin Rattus norvegicus 78-88 12697273-0 2003 Sodium ions and GTP decrease the potency of [Nphe1]N/OFQ(1-13)NH2 in blocking nociceptin/orphanin FQ receptors coupled to cyclic AMP in N1E-115 neuroblastoma cells and rat olfactory bulb. Sodium 0-6 prepronociceptin Rattus norvegicus 89-100 26923164-0 2016 The type III transporters (PiT-1 and PiT-2) are the major sodium-dependent phosphate transporters in the mice and human brains. Sodium 58-64 solute carrier family 20, member 1 Mus musculus 27-32 26553454-0 2016 Effects of sodium ions on rat thyrocyte (FRTL-5 cells) swelling- and thyrotropin-activated taurine efflux dependent on cAMP and Epac. Sodium 11-17 Rap guanine nucleotide exchange factor 3 Rattus norvegicus 128-132 12466144-5 2003 Treatment of infected tissue with selective COX inhibitors revealed that COX-1 and -2 must be blocked to restore electroneutral sodium absorption, although the transporter involved did not appear to be the expected Na(+)/H(+) exchanger 3 isoform. Sodium 128-134 cytochrome c oxidase subunit I Bos taurus 73-85 14584380-1 2003 Subclinical mastitis, defined as raised milk sodium/potassium (Na/K) ratio is common and associated with poor infant growth and increased mother-to-child HIV transmission. Sodium 45-51 TANK binding kinase 1 Homo sapiens 63-67 27372528-8 2016 Mixed-effects multivariable linear regression models assessed the association of SBP and DBP with sodium intake. Sodium 98-104 selenium binding protein 1 Homo sapiens 81-84 27372528-11 2016 Significant (P < 0.01) increases in SBP and DBP were evident in men, but not women with increasing quintile of sodium intake. Sodium 114-120 selenium binding protein 1 Homo sapiens 39-42 27372528-12 2016 After multivariable adjustments, sodium intake was independently associated with SBP, but not DBP, in both sexes. Sodium 33-39 selenium binding protein 1 Homo sapiens 81-84 27372528-14 2016 CONCLUSION: In a South Indian population, the dietary intake of sodium was higher than recommendations by major dietary guidelines and was an independent predictor of SBP. Sodium 64-70 selenium binding protein 1 Homo sapiens 167-170 26727380-0 2016 Inhibition of NHE3-mediated Sodium Absorption in the Gut Reduced Cardiac End-organ Damage Without Deteriorating Renal Function in Obese Spontaneously Hypertensive Rats. Sodium 28-34 solute carrier family 9 member A3 Rattus norvegicus 14-18 26727380-2 2016 The sodium-proton-exchanger subtype 3 (NHE3) is an important mediator of intestinal sodium absorption. Sodium 4-10 solute carrier family 9 member A3 Rattus norvegicus 39-43 26727380-3 2016 The compound SAR is a new specific NHE3 inhibitor with extremely low oral absorbability leading to decreased sodium absorption in the gut and substantial systolic blood pressure reduction. Sodium 109-115 solute carrier family 9 member A3 Rattus norvegicus 35-39 26727380-10 2016 Reduction of intestinal sodium absorption by selective NHE3 inhibition in the gut lowered high blood pressure and reduced LV remodeling without deteriorating renal functional and structural parameters in SHR-ob. Sodium 24-30 solute carrier family 9 member A3 Rattus norvegicus 55-59 27149052-0 2016 Interaction according to urinary sodium excretion level on the association between ATP2B1 rs17249754 and incident hypertension: the Korean genome epidemiology study. Sodium 33-39 ATPase plasma membrane Ca2+ transporting 1 Homo sapiens 83-89 12446715-2 2003 GAT-1 expressed in Xenopus laevis oocytes exhibits sodium-dependent GABA-induced inward currents reflecting electrogenic sodium-coupled transport. Sodium 51-57 solute carrier family 6 (neurotransmitter transporter), member 1 S homeolog Xenopus laevis 0-5 12446715-2 2003 GAT-1 expressed in Xenopus laevis oocytes exhibits sodium-dependent GABA-induced inward currents reflecting electrogenic sodium-coupled transport. Sodium 121-127 solute carrier family 6 (neurotransmitter transporter), member 1 S homeolog Xenopus laevis 0-5 12446715-8 2003 The cation leak currents mediated by wild-type GAT-1 were inhibited by low millimolar sodium concentrations in a noncompetitive manner. Sodium 86-92 solute carrier family 6 (neurotransmitter transporter), member 1 S homeolog Xenopus laevis 47-52 12446715-11 2003 Thus, transmembrane domain I of GAT-1 contains determinants controlling both sodium-coupled GABA flux and the cation leak pathway as well as the interconversion of these distinct modes. Sodium 77-83 solute carrier family 6 (neurotransmitter transporter), member 1 S homeolog Xenopus laevis 32-37 27149052-1 2016 OBJECTIVE: We examined an interaction according to the estimated 24-h urinary sodium excretion on the association between ATP2B1 rs17249754 and incident hypertension. Sodium 78-84 ATPase plasma membrane Ca2+ transporting 1 Homo sapiens 122-128 27149052-6 2016 We utilized Cox proportional hazard models to test an interaction according to urinary sodium excretion on the association between ATP2B1 rs17249754 and incident hypertension. Sodium 87-93 ATPase plasma membrane Ca2+ transporting 1 Homo sapiens 131-137 27149052-10 2016 CONCLUSIONS: In this 6-year longitudinal study, our findings suggest that excessive sodium intake estimated from urinary sodium excretion significantly modified the risk of developing hypertension associated with ATP2B1 rs17249754 genetic trait. Sodium 84-90 ATPase plasma membrane Ca2+ transporting 1 Homo sapiens 213-219 27149052-10 2016 CONCLUSIONS: In this 6-year longitudinal study, our findings suggest that excessive sodium intake estimated from urinary sodium excretion significantly modified the risk of developing hypertension associated with ATP2B1 rs17249754 genetic trait. Sodium 121-127 ATPase plasma membrane Ca2+ transporting 1 Homo sapiens 213-219 27149052-11 2016 That is, carriers with ATP2B1 rs17249754 homozygote mutant allele may be at higher risk of hypertension, when they consume excessive sodium intake. Sodium 133-139 ATPase plasma membrane Ca2+ transporting 1 Homo sapiens 23-29 28053652-4 2016 Our simulation results showed that (1) CaMKII overexpression facilitates EADs through the prolongation of late sodium current"s (INaL) deactivation progress; (2) the combined effect of CaMKII overexpression and activation of beta-adrenergic signaling pathway further increases the risk of EADs, where EADs could occur at shorter cycle length (2000 ms versus 4000 ms) and lower rapid delayed rectifier K+ current (IKr) blockage (77% versus 85%). Sodium 111-117 calcium/calmodulin dependent protein kinase II gamma Homo sapiens 39-45 12525183-1 2003 The Na/Ca-K exchanger (NCKX) utilizes the inward sodium gradient and outward potassium gradient for Ca(2+) extrusion; two distinct NCKX isoforms are expressed in the outer segments of retinal rod (NCKX1) and cone (NCKX2) photoreceptors, respectively, where NCKX extrudes Ca(2+) that enters photoreceptors via the cGMP-gated channels. Sodium 49-55 solute carrier family 24 member 1 Homo sapiens 23-27 12390967-4 2002 While five patients had a clinical diagnosis of myotonia congenita, the patient with the F428S mutation exhibited symptoms characteristic of paramyotonia congenita--a condition usually thought to be caused by mutations in the sodium channel gene SCN4A. Sodium 226-232 sodium voltage-gated channel alpha subunit 4 Homo sapiens 246-251 12107065-11 2002 In summary, these studies suggest that ANG II causes H(+)-ATPase inhibition and an increase of cell sodium due to activation of Na(+)/H(+) exchange. Sodium 100-106 angiogenin Oryctolagus cuniculus 39-42 12160190-5 2002 RESULTS: Sodium restriction increased PAI-1 levels from 32.1 +/- 2.5 ng/mL to 39.8 +/- 3.2 ng/mL (P = .009). Sodium 9-15 serpin family E member 1 Homo sapiens 38-43 12031708-3 2002 We hypothesized that the rate-dependent shortening of the QT interval may be attributed to the kinetic properties of inactivation the late sodium current (I(Na)) in LQT3. Sodium 139-145 sodium voltage-gated channel alpha subunit 5 Homo sapiens 165-169 11967240-1 2002 An apical serine protease, channel-activating protease 1 (CAP1), augments sodium transport in A6 cells. Sodium 74-80 protease, serine 8 (prostasin) Mus musculus 27-56 11967240-1 2002 An apical serine protease, channel-activating protease 1 (CAP1), augments sodium transport in A6 cells. Sodium 74-80 protease, serine 8 (prostasin) Mus musculus 58-62 11967240-15 2002 In conclusion, although prostasin is present in M-1 cells and probably augments sodium transport in these cells, serine proteases probably have other effects (eg, resistance) in the collecting duct in addition to effects on sodium channels. Sodium 80-86 protease, serine 8 (prostasin) Mus musculus 24-33 11826163-9 2002 Interestingly, AC-modified hH1 channels inactivated completely if the external solution did not contain sodium ions. Sodium 104-110 H1.5 linker histone, cluster member Homo sapiens 27-30 26515056-3 2016 We have previously shown that HCN2 may transport ammonium (NH4 (+)), besides sodium (Na(+)), in the rat distal nephron. Sodium 77-83 hyperpolarization activated cyclic nucleotide gated potassium and sodium channel 2 Rattus norvegicus 30-34 27010539-8 2016 Caspase-1 inhibitor, Ac-YVAD-CMK and deletion of Nlrp3 or Asc gene abolished MSU-induced decreases in renal sodium excretion and MBF. Sodium 108-114 caspase 1 Mus musculus 0-9 27010539-8 2016 Caspase-1 inhibitor, Ac-YVAD-CMK and deletion of Nlrp3 or Asc gene abolished MSU-induced decreases in renal sodium excretion and MBF. Sodium 108-114 steroid sulfatase Mus musculus 58-61 26365358-4 2015 We show that IL-13 impairs ENaC-dependent sodium transport by activating the JAK1/2-STAT6 signalling pathway. Sodium 42-48 Janus kinase 1 Mus musculus 77-83 26365358-4 2015 We show that IL-13 impairs ENaC-dependent sodium transport by activating the JAK1/2-STAT6 signalling pathway. Sodium 42-48 signal transducer and activator of transcription 6 Mus musculus 84-89 26432356-4 2015 In this report, evidence is presented that (1) both the recently discovered cAMP-regulated transcriptional coactivators (CRTCs) and salt-inducible kinase 1 (SIK1) contribute to the transcriptional regulation of atp1b1 in renal proximal tubule (RPT) cells and (2) renal effectors, including norepinephrine, dopamine, prostaglandins, and sodium, play a role. Sodium 336-342 ATPase Na+/K+ transporting subunit beta 1 Homo sapiens 211-217 26173672-7 2015 Furthermore, ETA-R inhibition reduced the diabetes-induced glomerular hyperfiltration and increased the urinary sodium excretion. Sodium 112-118 endothelin receptor type A Rattus norvegicus 13-18 11826163-11 2002 The results also imply that the reduced inactivation of AC-modified hH1 channels at least partially depends on the presence of extracellular sodium. Sodium 141-147 H1.5 linker histone, cluster member Homo sapiens 68-71 15618652-2 2002 This phenotype is caused by a missense mutation (Leu352Arg) of a sodium-dependent carnitine/organic cation transporter, Octn2 (Slc22a5). Sodium 65-71 solute carrier family 22 (organic cation transporter), member 5 Mus musculus 120-125 15618652-2 2002 This phenotype is caused by a missense mutation (Leu352Arg) of a sodium-dependent carnitine/organic cation transporter, Octn2 (Slc22a5). Sodium 65-71 solute carrier family 22 (organic cation transporter), member 5 Mus musculus 127-134 11457832-5 2001 Third, a gln3 gat1 mutant displays a pronounced sensitivity to high concentrations of lithium and sodium. Sodium 98-104 nitrogen-responsive transcriptional regulator GLN3 Saccharomyces cerevisiae S288C 9-13 11482976-3 2001 At low ionic strengths, the apoferritin second virial coefficient initially decreases with increasing sodium ion concentration, as DLVO theory predicts. Sodium 102-108 ferritin heavy chain 1 Homo sapiens 28-39 11472309-4 2001 Sodium excretion increased sixfold after COMT inhibition, eightfold after administration of the D1-like agonist, whereas it was similar to control after MAO inhibition and infusion of DA precursor. Sodium 0-6 catechol-O-methyltransferase Rattus norvegicus 41-45 11390018-0 2001 Blockade of pancreatic polypeptide-sensitive neuropeptide Y (NPY) receptors by agonist peptides is prevented by modulators of sodium transport. Sodium 126-132 neuropeptide Y Homo sapiens 45-59 11388780-1 2001 We developed a new hypothesis claiming that natriuresis of fasting is not only caused by diminished insulin resistance and hyperinsulinaemia with the subsequent reduction of renal sodium retention but it can also be attributed to the function of the leptin-NPY system. Sodium 180-186 leptin Homo sapiens 250-256 11388780-4 2001 NPY has been demonstrated to be intimately involved in the regulation of renal functions; under various experimental conditions it increased urine flow rate and urinary sodium excretion presumably through stimulating the synthesis and/or release of other natriuretic factors.3. Sodium 169-175 neuropeptide Y Homo sapiens 0-3 11392001-4 2001 Insulin and leptin increase sympathetic tone which results in sodium retention and hyper-responsiveness of blood vessels. Sodium 62-68 leptin Homo sapiens 12-18 11274952-0 2001 Effect of the antimalarial drug halofantrine in the long QT syndrome due to a mutation of the cardiac sodium channel gene SCN5A. Sodium 102-108 sodium voltage-gated channel alpha subunit 5 Homo sapiens 122-127 11264553-2 2001 ADM-induced natriuresis is caused by an increase in glomerular filtration rate and a decrease in distal tubular sodium reabsorption. Sodium 112-118 adrenomedullin Canis lupus familiaris 0-3 11264553-6 2001 Intrarenal infusion of ADM (1 and 25 ng/kg/min) induced an increase in urinary sodium excretion in the normal control dogs (change in urinary sodium excretion [Delta UNaV], +94.5 microEq/min during 1 ng/kg/min ADM infusion and +128.1 microEq/min during 25 ng/kg/min ADM infusion). Sodium 79-85 adrenomedullin Canis lupus familiaris 23-26 11264553-6 2001 Intrarenal infusion of ADM (1 and 25 ng/kg/min) induced an increase in urinary sodium excretion in the normal control dogs (change in urinary sodium excretion [Delta UNaV], +94.5 microEq/min during 1 ng/kg/min ADM infusion and +128.1 microEq/min during 25 ng/kg/min ADM infusion). Sodium 142-148 adrenomedullin Canis lupus familiaris 23-26 11264553-7 2001 In the acute heart failure dogs, intrarenal ADM infusion resulted in an attenuated increase in urinary sodium excretion (Delta UNaV, +44.8 microEq/min during 1 ng/kg/min ADM infusion and +51.8 microEq/min during 25 ng/kg/min ADM infusion). Sodium 103-109 adrenomedullin Canis lupus familiaris 44-47 11264553-10 2001 This study provides insight into humoral mechanisms that may promote sodium retention in heart failure via a renal hyporesponsiveness to natriuretic actions of ADM. Sodium 69-75 adrenomedullin Canis lupus familiaris 160-163 11169461-0 2001 Epidermal growth factor regulates the transition from basal sodium absorption to anion secretion in cultured endometrial epithelial cells. Sodium 60-66 epidermal growth factor Homo sapiens 0-23 26260990-4 2015 Pendrin has been shown to support sodium reabsorption in the distal nephron and compensate for loss of the sodium-chloride cotransporter. Sodium 34-40 solute carrier family 26 member 4 Rattus norvegicus 0-7 26260990-12 2015 Additionally, pendrin coupled to the sodium-dependent chloride-bicarbonate exchanger (NDCBE) mediates thiazide-sensitive sodium reabsorption in the cortical collecting duct. Sodium 37-43 solute carrier family 26 member 4 Rattus norvegicus 14-21 26260990-17 2015 Given that NCC expression is decreased in late pregnancy, an increased thiazide sensitivity may be due to inhibition of upregulated pendrin-NDCBE-coupled sodium reabsorption. Sodium 154-160 solute carrier family 26 member 4 Rattus norvegicus 132-139 26120029-7 2015 The results suggest that water and sodium ingestion in response to hypovolemic/hypotensive stimuli are disturbed in nephrotic rats, and provide evidence that the disordered behaviors reflect disturbances of the peripheral renin-angiotensin-aldosterone system. Sodium 35-41 renin Rattus norvegicus 222-227 26408173-11 2015 Using a reduced expression system in DRG neurons, we isolated recombinant human Nav1.6 sodium currents in rat DRG neurons and found that overexpression of Navbeta4 enhanced Nav1.6 INaR generation. Sodium 87-93 neuron navigator 1 Homo sapiens 80-84 11211741-8 2001 Lack of adequately functional renal alpha 2B AR is thought to preclude reabsorption of sodium. Sodium 87-93 adrenergic receptor, alpha 2b Mus musculus 36-47 26160054-3 2015 BNP and ANP, acting through a guanylyl cyclase receptor, increase sodium and water excretion by the kidney, induce vasodilation, reduce blood pressure, counteract the bioactivity of the renin-angiotensin-aldosterone and sympathetic nervous systems and possess anti-hypertrophic and anti-fibrotic properties. Sodium 66-72 natriuretic peptide B Homo sapiens 0-3 26347659-1 2015 To counter the development of salt-sensitive hypertension, multiple brain G-protein-coupled receptor (GPCR) systems are activated to facilitate sympathoinhibition, sodium homeostasis, and normotension. Sodium 164-170 G protein-coupled bile acid receptor 1 Rattus norvegicus 74-100 26347659-1 2015 To counter the development of salt-sensitive hypertension, multiple brain G-protein-coupled receptor (GPCR) systems are activated to facilitate sympathoinhibition, sodium homeostasis, and normotension. Sodium 164-170 G protein-coupled bile acid receptor 1 Rattus norvegicus 102-106 26019035-3 2015 Hepatic nuclear receptors are known to modulate genes controlling BA metabolism; thus, in this work we aimed to compare the expression of liver nuclear receptors -farnesoid X (FXR), small heterodimer partner (SHP) and liver X alpha (LXRalpha) receptors- and BA transporters -sodium+/taurocholate cotransporting polypeptide (NTCP) and bile salt export pump (BSEP)- in liver biopsy samples of patients with simple steatosis (SS) and NASH. Sodium 275-281 nuclear receptor subfamily 1 group H member 3 Homo sapiens 233-241 11483305-0 2001 Sodium currents in isolated rat CA1 pyramidal and dentate granule neurones in the post-status epilepticus model of epilepsy. Sodium 0-6 carbonic anhydrase 1 Rattus norvegicus 32-35 11483305-3 2001 In these animals we determined the properties of voltage-dependent sodium currents in acutely isolated CA1 pyramidal neurones and dentate granule cells using the whole-cell voltage-clamp technique. Sodium 67-73 carbonic anhydrase 1 Rattus norvegicus 103-106 11166117-6 2001 Hippocampal CA1 neurons isolated from presymptomatic Q54 mice exhibited increased persistent sodium current which may underlie hyperexcitability in the hippocampus. Sodium 93-99 carbonic anhydrase 1 Mus musculus 12-15 11150514-8 2000 Our findings uphold the idea that LQT3 is related to a persistent sodium current whereas reduction in the expression level of cardiac sodium channels is one of the biophysical characteristics of Brugada syndrome. Sodium 66-72 sodium voltage-gated channel alpha subunit 5 Homo sapiens 34-38 1495010-5 1992 When selected compounds were administered intravenously to sodium-deficient rhesus monkeys (Macaca mulatta) at 0.06-1 mg/kg, they reduced plasma renin activity by 87-94%. Sodium 59-65 renin Macaca mulatta 145-150 1376926-4 1992 This is based on the following results: (i) Injection of in vitro transcripts from 4F2hc cDNA (4F2hc cRNA) into oocytes stimulates up to 10-fold the sodium-independent uptake of L-arginine and up to 4.1-fold the sodium-dependent uptake of L-leucine. Sodium 149-155 solute carrier family 3 member 2 Homo sapiens 83-88 1376926-4 1992 This is based on the following results: (i) Injection of in vitro transcripts from 4F2hc cDNA (4F2hc cRNA) into oocytes stimulates up to 10-fold the sodium-independent uptake of L-arginine and up to 4.1-fold the sodium-dependent uptake of L-leucine. Sodium 149-155 solute carrier family 3 member 2 Homo sapiens 95-100 25827430-7 2015 For example, one standard deviation higher log-UAGT/Cr ratio (1.2 mug/g) was associated with a 5.0-mmHg (95% confidence interval 2.3-7.8) higher SBP at the end of the high-sodium intervention, after adjusting for multiple covariates (P = 0.003). Sodium 173-179 selenium binding protein 1 Homo sapiens 146-149 25827430-8 2015 In addition, one standard deviation higher log-UAGT/Cr ratio was associated with a 1.6-mmHg increase in age-adjusted and sex-adjusted SBP from the low-sodium intervention to the high-sodium intervention (95% confidence interval 0.1-3.1, P = 0.04). Sodium 151-157 selenium binding protein 1 Homo sapiens 134-137 25701775-1 2015 BACKGROUND: The human cardiac action potential in atrial and ventricular cells is initiated by a fast-activating, fast-inactivating sodium current generated by the SCN5A/Nav1.5 channel in association with its beta1/SCN1B subunit. Sodium 132-138 sodium voltage-gated channel beta subunit 1 Homo sapiens 215-220 25931204-2 2015 Aldosterone and vasopressin modulate ion transporters and channels crucial in sodium (Na) and water reabsorption such as the epithelium Na channel and the renal thiazide-sensitive NaCl cotransporter (NCC). Sodium 78-84 solute carrier family 12 member 3 Homo sapiens 180-198 25931204-2 2015 Aldosterone and vasopressin modulate ion transporters and channels crucial in sodium (Na) and water reabsorption such as the epithelium Na channel and the renal thiazide-sensitive NaCl cotransporter (NCC). Sodium 78-84 solute carrier family 12 member 3 Homo sapiens 200-203 26064449-2 2015 Sodium-hydrogen exchange (NHE) is an important contributor to pHi control in PASMCs. Sodium 0-6 solute carrier family 9 member C1 Homo sapiens 26-29 1376926-4 1992 This is based on the following results: (i) Injection of in vitro transcripts from 4F2hc cDNA (4F2hc cRNA) into oocytes stimulates up to 10-fold the sodium-independent uptake of L-arginine and up to 4.1-fold the sodium-dependent uptake of L-leucine. Sodium 212-218 solute carrier family 3 member 2 Homo sapiens 83-88 1376926-4 1992 This is based on the following results: (i) Injection of in vitro transcripts from 4F2hc cDNA (4F2hc cRNA) into oocytes stimulates up to 10-fold the sodium-independent uptake of L-arginine and up to 4.1-fold the sodium-dependent uptake of L-leucine. Sodium 212-218 solute carrier family 3 member 2 Homo sapiens 95-100 1376926-6 1992 (ii) Basal and 4F2hc cRNA-stimulated sodium-independent uptake of L-arginine is completely inhibited by L-leucine in the presence of sodium. Sodium 37-43 solute carrier family 3 member 2 Homo sapiens 15-20 1376926-6 1992 (ii) Basal and 4F2hc cRNA-stimulated sodium-independent uptake of L-arginine is completely inhibited by L-leucine in the presence of sodium. Sodium 133-139 solute carrier family 3 member 2 Homo sapiens 15-20 1376926-7 1992 Similarly, the basal and 4F2hc cRNA-stimulated sodium-dependent uptake of L-leucine is entirely inhibited by L-arginine. Sodium 47-53 solute carrier family 3 member 2 Homo sapiens 25-30 1376926-8 1992 (iii) The stimulation of sodium-independent uptake of L-arginine and the stimulation of sodium-dependent uptake of L-leucine induced by injection of 4F2hc cRNA are both completely inhibited by dibasic L amino acids and to a lesser extent by D-ornithine. Sodium 25-31 solute carrier family 3 member 2 Homo sapiens 149-154 1376926-8 1992 (iii) The stimulation of sodium-independent uptake of L-arginine and the stimulation of sodium-dependent uptake of L-leucine induced by injection of 4F2hc cRNA are both completely inhibited by dibasic L amino acids and to a lesser extent by D-ornithine. Sodium 88-94 solute carrier family 3 member 2 Homo sapiens 149-154 1376926-9 1992 (iv) Both basal and 4F2hc cRNA-stimulated sodium-independent uptake of L-arginine show two additional characteristics of the system y+ transport activity: inhibition of L-arginine uptake by L-homoserine only in the presence of sodium and an increase in the inhibition exerted by L-histidine as the extracellular pH decreased. Sodium 42-48 solute carrier family 3 member 2 Homo sapiens 20-25 1376926-9 1992 (iv) Both basal and 4F2hc cRNA-stimulated sodium-independent uptake of L-arginine show two additional characteristics of the system y+ transport activity: inhibition of L-arginine uptake by L-homoserine only in the presence of sodium and an increase in the inhibition exerted by L-histidine as the extracellular pH decreased. Sodium 227-233 solute carrier family 3 member 2 Homo sapiens 20-25 1630066-2 1992 This dehydration-induced natriuresis occurs despite simultaneous hypovolemia, and it can be blocked by an experimentally-induced reduction in the sodium concentration of CSF, or by ablation of the periventricular tissue in the vicinity of the lamina terminalis. Sodium 146-152 colony stimulating factor 2 Homo sapiens 170-173 1315122-1 1992 Two polymorphic dinucleotide repeats--one (dGdA)n and one (dGdT)n--have been identified at the SCN4A locus, encoding the alpha-subunit of the adult skeletal muscle sodium channel. Sodium 164-170 sodium voltage-gated channel alpha subunit 4 Homo sapiens 95-100 1533215-8 1992 Comparison of the effects of altering end-expiratory pressure and infusing ANF indicates that a substantial part of the changes in sodium excretion during variations in end-expiratory pressure can be attributed to changes in plasma irANF. Sodium 131-137 natriuretic peptide A Canis lupus familiaris 75-78 1310898-1 1992 Paramyotonia congenita (PMC), a dominant disorder featuring cold-induced myotonia (muscle stiffness), has recently been genetically linked to a candidate gene, the skeletal muscle sodium channel gene SCN4A. Sodium 180-186 sodium voltage-gated channel alpha subunit 4 Homo sapiens 200-205 26064449-2 2015 Sodium-hydrogen exchange (NHE) is an important contributor to pHi control in PASMCs. Sodium 0-6 glucose-6-phosphate isomerase Homo sapiens 62-65 25656365-9 2015 The male-dominant expression of renal AQP1 in rats, which develops after puberty largely in the glycosylated form of the protein, may contribute to enhanced fluid reabsorption following the androgen- or progesterone-stimulated activities of sodium-reabsorptive mechanisms in proximal tubules. Sodium 241-247 aquaporin 1 Rattus norvegicus 38-42 25656367-3 2015 Since the sympathetic nervous system and intrarenal ANG II appear to act synergistically to mediate the process of sodium reabsorption, we hypothesized that low-frequency acute electrical stimulation of the renal nerve (ESRN) activates NHE3-mediated sodium reabsorption via ANG II AT1 receptor activation in Wistar rats. Sodium 250-256 solute carrier family 9 member A3 Rattus norvegicus 236-240 25656367-8 2015 Taken together, our results demonstrate that higher NHE3-mediated proximal tubular sodium reabsorption induced by ESRN occurs via intrarenal renin angiotensin system activation and triggering of the AT1 receptor/inhibitory G-protein signaling pathway, which leads to inhibition of cAMP formation and reduction of PKA activity. Sodium 83-89 solute carrier family 9 member A3 Rattus norvegicus 52-56 25615535-4 2015 METHODS: We used patch-clamp electrophysiology to record sodium currents from Na(v)1.2 channels stably expressed in HEK-293 cells. Sodium 57-63 immunoglobulin lambda variable 2-8 Homo sapiens 78-86 1539631-4 1992 2) In HCO3(-)-CO2-buffered solution, removal of extracellular sodium resulted in a depolarization [change in membrane resistance (delta V) = 31.3 +/- 2.8 mV] that was less marked in the absence of HCO3(-)-CO2 (delta V = 0.5 +/- 2.6 mV) and reduced by 4,4"-diisothiocyanostilbene-2,2"-disulfonic acid (DIDS) (delta V = 19.3 +/- 1.9 mV). Sodium 62-68 complement C2 Homo sapiens 6-17 1539631-4 1992 2) In HCO3(-)-CO2-buffered solution, removal of extracellular sodium resulted in a depolarization [change in membrane resistance (delta V) = 31.3 +/- 2.8 mV] that was less marked in the absence of HCO3(-)-CO2 (delta V = 0.5 +/- 2.6 mV) and reduced by 4,4"-diisothiocyanostilbene-2,2"-disulfonic acid (DIDS) (delta V = 19.3 +/- 1.9 mV). Sodium 62-68 complement C2 Homo sapiens 197-208 1539631-5 1992 3) Removal of extracellular HCO3(-)-CO2 led to a depolarization (delta V = 13.2 +/- 0.8 mV) that was abolished in the absence of extracellular sodium and inhibited by DIDS. Sodium 143-149 complement C2 Homo sapiens 28-39 25733376-1 2015 The mineralocorticoid receptor (MR) is a major regulator of blood pressure by modulating sodium balance and blood volume in the distal nephron. Sodium 89-95 nuclear receptor subfamily 3 group C member 2 Homo sapiens 4-30 25733376-1 2015 The mineralocorticoid receptor (MR) is a major regulator of blood pressure by modulating sodium balance and blood volume in the distal nephron. Sodium 89-95 nuclear receptor subfamily 3 group C member 2 Homo sapiens 32-34 25588850-10 2015 The DPP-4 inhibitor, vildagliptin, may elicit beneficial antihypertensive effects, including the improvement of abnormal circadian blood pressure pattern, by enhancing urinary sodium excretion. Sodium 176-182 dipeptidylpeptidase 4 Rattus norvegicus 4-9 25632083-6 2015 We report here the effects of muO -GVIIJ on 1) sodium currents of mouse NaV1.6 coexpressed with various combinations of NaVbeta-subunits in oocytes; 2) A- and C-CAPs of mouse and rat sciatic nerves; and 3) sodium currents of small and large neurons dissociated from rat dorsal root ganglia. Sodium 47-53 neuron navigator 1 Mus musculus 72-76 25861425-6 2015 A reduction of 28 mmol sodium excretion decreased SBP/DBP to 135.5 (+- 13.0)/82.5 (+- 12.8) (P < 0.001). Sodium 23-29 selenium binding protein 1 Homo sapiens 50-53 25504670-1 2015 BACKGROUND: Aldosterone, synthesized in the adrenal cortex by the enzyme CYP11B2, induces positive sodium balance and predisposes to hypertension. Sodium 99-105 cytochrome P450, family 11, subfamily b, polypeptide 2 Mus musculus 73-80 25367597-0 2015 Exfoliated-SnS2 restacked on graphene as a high-capacity, high-rate, and long-cycle life anode for sodium ion batteries. Sodium 99-105 sodium voltage-gated channel alpha subunit 11 Homo sapiens 11-15 25367597-1 2015 Designed as a high-capacity, high-rate, and long-cycle life anode for sodium ion batteries, exfoliated-SnS2 restacked on graphene is prepared by the hydrolysis of lithiated SnS2 followed by a facile hydrothermal method. Sodium 70-76 sodium voltage-gated channel alpha subunit 11 Homo sapiens 103-107 25615575-10 2015 Concordantly, lower ATP1A1 expression is expected to lower Na-reabsorption in the kidney thereby decreasing sodium-associated risk for hypertension and sodium-induced endothelial stiffness and dysfunction. Sodium 108-114 ATPase, Na+/K+ transporting, alpha 1 polypeptide Mus musculus 20-26 25615575-10 2015 Concordantly, lower ATP1A1 expression is expected to lower Na-reabsorption in the kidney thereby decreasing sodium-associated risk for hypertension and sodium-induced endothelial stiffness and dysfunction. Sodium 152-158 ATPase, Na+/K+ transporting, alpha 1 polypeptide Mus musculus 20-26 25603341-5 2015 Pre-treatment with phosphatase inhibitor sodium or thovanadate halted dephosphorylation of AKT and GSK3beta, and blocked ophiobolin O-induced G1 phase arrest. Sodium 41-47 glycogen synthase kinase 3 beta Homo sapiens 99-107 25393565-1 2015 Nax , an alpha-subunit of the sodium channel encoded by the SCN7A gene, has been deemed to be a sensor of the concentration of sodium in the brain and may be involved in salt intake behavior. Sodium 30-36 sodium voltage-gated channel alpha subunit 7 Homo sapiens 60-65 26612332-1 2015 Tubular transport of sodium (TNa+) and chloride (TCl-) is decreased in patients with chronic kidney disease. Sodium 21-27 C-type lectin domain family 3 member B Homo sapiens 29-32 25007996-1 2014 Ang II, the primary effector pleiotropic hormone of the renin-angiotensin system (RAS) cascade, mediates physiological control of blood pressure and electrolyte balance through its action on vascular tone, aldosterone secretion, renal sodium absorption, water intake, sympathetic activity and vasopressin release. Sodium 235-241 angiogenin Homo sapiens 0-3 25007170-5 2014 In addition, there is some evidence that GLP-1 receptor agonists and DPP-4 inhibitors mediate sodium excretion and diuresis to lower blood pressure. Sodium 94-100 glucagon like peptide 1 receptor Homo sapiens 41-55 24990699-4 2014 Such as, apelin/APJ system may be concerned in hyperfunction of the sympathetic nervous system, renin-angiotensin-aldosterone system, endothelial injury, excessive endothelin, sodium retention, vascular remodeling, insulin resistance elicit hypertension, as well as in hypertension-induced organ damaged. Sodium 176-182 apelin receptor Homo sapiens 16-19 25102326-4 2014 We hypothesize that the persistent sodium current (INaP), a subthreshold sodium current that can increase neuronal excitability, may in part account for the Abeta-induced neuronal hyperexcitation. Sodium 35-41 NFKB inhibitor zeta Homo sapiens 51-55 25102326-4 2014 We hypothesize that the persistent sodium current (INaP), a subthreshold sodium current that can increase neuronal excitability, may in part account for the Abeta-induced neuronal hyperexcitation. Sodium 73-79 NFKB inhibitor zeta Homo sapiens 51-55 24841206-9 2014 Moreover, we found that trypsin IV is expressed in human renal epithelial cells and can increase ENaC-mediated sodium transport in cultured human airway epithelial cells. Sodium 111-117 serine protease 3 Homo sapiens 24-34 24573382-6 2014 Sodium channel blockers, pathways" inhibitors, and siRNA against tonicity-responsive enhancer binding protein (TonEBP) were used to identify the mechanisms of sodium effects on endothelium. Sodium 159-165 nuclear factor of activated T cells 5 Homo sapiens 111-117 24573382-9 2014 Sodium-induced increase in monocytic cell adhesion was mediated by reactive oxygen species and the endothelial nitric oxygen synthase, and was sensitive to the knockdown of TonEBP. Sodium 0-6 nuclear factor of activated T cells 5 Homo sapiens 173-179 24652800-7 2014 Functional analyses showed that Bmal1(lox/lox)/Ren1(d)Cre mice exhibited multiple abnormalities, including increased urine volume, changes in the circadian rhythm of urinary sodium excretion, increased GFR, and significantly reduced plasma aldosterone levels. Sodium 174-180 lysyl oxidase Mus musculus 38-41 24729405-0 2014 Sn4+x P3 @ amorphous Sn-P composites as anodes for sodium-ion batteries with low cost, high capacity, long life, and superior rate capability. Sodium 51-57 XPC complex subunit, DNA damage recognition and repair factor Homo sapiens 0-8 24729405-1 2014 Sn4+x P3 @ amorphous Sn-P composites are a promising cheap anode material for sodium-ion batteries with high capacity (502 mA h g(-1) at a current density of 100 mA g(-1)), long cycling stability (92.6% capacity retention up to 100 cycles), and high rate capability (165 mA h g(-1) at the 10C rate). Sodium 78-84 XPC complex subunit, DNA damage recognition and repair factor Homo sapiens 0-8 24677348-0 2014 Layered SnS2-reduced graphene oxide composite--a high-capacity, high-rate, and long-cycle life sodium-ion battery anode material. Sodium 95-101 sodium voltage-gated channel alpha subunit 11 Homo sapiens 8-12 24904279-2 2014 This review focuses on the sodium leak, G protein-coupled receptors (GPCRs)-activated NALCN channel that is predominantly expressed in neurons where it regulates the resting membrane potential and neuronal excitability. Sodium 27-33 sodium leak channel, non-selective Homo sapiens 86-91 1309946-5 1992 The single channel conductance of hH1 to sodium ions is about twice that of the homologous rat channel and hH1 is more resistant to block by tetrodotoxin (IC50 = 5.7 microM). Sodium 41-47 H1.5 linker histone, cluster member Homo sapiens 34-37 1309946-5 1992 The single channel conductance of hH1 to sodium ions is about twice that of the homologous rat channel and hH1 is more resistant to block by tetrodotoxin (IC50 = 5.7 microM). Sodium 41-47 H1.5 linker histone, cluster member Homo sapiens 107-110 1824254-7 1991 However, the effect of IFN-gamma on intracellular pH and DNA synthesis was transient and pretreatment with IFN markedly inhibited the ability of GM-CSF, M-CSF, and IL-3 to activate the sodium/hydrogen antiport. Sodium 185-191 colony stimulating factor 2 Homo sapiens 145-151 1824254-7 1991 However, the effect of IFN-gamma on intracellular pH and DNA synthesis was transient and pretreatment with IFN markedly inhibited the ability of GM-CSF, M-CSF, and IL-3 to activate the sodium/hydrogen antiport. Sodium 185-191 colony stimulating factor 1 Homo sapiens 146-151 1824254-7 1991 However, the effect of IFN-gamma on intracellular pH and DNA synthesis was transient and pretreatment with IFN markedly inhibited the ability of GM-CSF, M-CSF, and IL-3 to activate the sodium/hydrogen antiport. Sodium 185-191 interleukin 3 Homo sapiens 164-168 1659972-8 1991 Apical ouabain (10(-4) M) and sodium replacement in the bathing medium reduced the AB and net flux of AA significantly suggesting the requirement of a functioning Na(+)-K(+)-ATPase on the apical side membrane of the RPE. Sodium 30-36 ribulose-phosphate 3-epimerase Bos taurus 216-219 1655094-10 1991 Additional in vivo experiments showed that oral administration of the specific 5-lipoxygenase inhibitor L-651,392 to rats prevented the increase in urine flow rate (pre, 5.7 +/- 0.1; post, 6.6 +/- 0.8 microL/min), and in absolute (pre, 0.33 +/- 0.04; post, 0.37 +/- 0.05 microEq/min) and fractional (pre, 0.10 +/- 0.02; post, 0.11 +/- 0.03%) sodium excretion caused by bolus i.v. Sodium 342-348 arachidonate 5-lipoxygenase Rattus norvegicus 79-93 1873917-7 1991 Sodium restriction increased PAI, PAII, and PRA, but did not alter UV-AI and UV-AII. Sodium 0-6 serpin family E member 1 Homo sapiens 29-32 1831368-6 1991 With the highest infusion dose, ANF (95-126) increased urinary sodium excretion to at least twice the levels observed with alpha ANF (99-126) in both groups of dogs (P less than .05). Sodium 63-69 natriuretic peptide A Canis lupus familiaris 32-35 1831368-8 1991 These results indicate that ANF (95-126) is more potent than alpha ANF (99-126) for the promotion of a natriuresis, particularly in AV fistula dogs with compensated high-output heart failure, in which the sodium excretory actions of alpha ANF (99-126) were attenuated markedly. Sodium 205-211 natriuretic peptide A Canis lupus familiaris 28-31 1900957-3 1991 The TNF-infused dogs (n = 4) had marked polyuria and natriuresis in comparison with those in the control group (n = 12) (urine output, 35.3 +/- 4.1 versus 3.7 +/- 0.5 millimeters per kilogram per six hours p less than 0.01; sodium excretion, 2.82 +/- 0.27 versus 0.75 +/- 0.19, p less than 0.01). Sodium 224-230 tumor necrosis factor Canis lupus familiaris 4-7 1998202-10 1991 2-PAM exhibited a 4-fold more potent in vitro inhibition of 3H-quinuclidinyl benzilate (3H-QNB) binding and sodium-dependent high-affinity Ch uptake (HACU) than did HI-6 in brain tissues. Sodium 108-114 peptidylglycine alpha-amidating monooxygenase Rattus norvegicus 2-5 24594434-10 2014 Overall, our data indicate that intracellular SVCT2 is localized in mitochondria, is sensitive to an intracellular microenvironment low in sodium and high in potassium, and functions as a low-affinity ascorbic acid transporter. Sodium 139-145 solute carrier family 23 member 2 Homo sapiens 46-51 24710520-6 2014 On the other hand, the expression of Slc20a1 encoding the sodium/phosphate (Na+/Pi) co-transporter Pit1 was increased in osteoblasts and osteocytes from adult Hyp mice, but not in Hyp fetal bones. Sodium 58-64 solute carrier family 20, member 1 Mus musculus 37-44 24338820-4 2014 Renal functional reserve is reduced in COX2np-treated rats since their renal response to an increase in plasma amino acids levels is abolished, and their renal ability to eliminate a sodium load is impaired (P < 0.05). Sodium 183-189 cytochrome c oxidase II, mitochondrial Rattus norvegicus 39-43 24338820-6 2014 However, the prolonged high-sodium intake at 9-11 mo of age leads to a greater proteinuria in male than in female (114 +- 12 mug/min vs. 72 +- 8 mug/min; P < 0.05) COX2np-treated rats. Sodium 28-34 cytochrome c oxidase II, mitochondrial Rattus norvegicus 167-171 24338820-8 2014 In summary, these results indicate that the reduction of COX2 activity during nephrogenic period programs for the development of an ANG II-dependent hypertension, reduces renal functional reserve to a similar extent in both sexes, and increases proteinuria in males but not in females when there is a prolonged increment in sodium intake. Sodium 324-330 cytochrome c oxidase II, mitochondrial Rattus norvegicus 57-61 24308971-1 2014 The dopamine D3 receptor (D3R) is crucial in the regulation of blood pressure and sodium balance, in that Drd3 gene ablation in mice results in hypertension and failure to excrete a dietary salt load. Sodium 82-88 dopamine receptor D3 Mus musculus 4-24 24308971-1 2014 The dopamine D3 receptor (D3R) is crucial in the regulation of blood pressure and sodium balance, in that Drd3 gene ablation in mice results in hypertension and failure to excrete a dietary salt load. Sodium 82-88 dopamine receptor D3 Mus musculus 106-110 24308971-3 2014 We now offer and describe a novel mechanism by which D3R decreases sodium transport in the long term by inhibiting the deubiquitinylating activity of ubiquitin-specific peptidase 48 (USP48), thereby promoting Na(+)-H(+) exchanger (NHE)-3 degradation. Sodium 67-73 ubiquitin specific peptidase 48 Mus musculus 150-181 24308971-3 2014 We now offer and describe a novel mechanism by which D3R decreases sodium transport in the long term by inhibiting the deubiquitinylating activity of ubiquitin-specific peptidase 48 (USP48), thereby promoting Na(+)-H(+) exchanger (NHE)-3 degradation. Sodium 67-73 ubiquitin specific peptidase 48 Mus musculus 183-188 24327600-6 2014 Although GLP1 infusion increased the urinary sodium excretion markedly, there were no significant changes in either proANP or proBNP concentrations. Sodium 45-51 glucagon like peptide 1 receptor Homo sapiens 9-13 24327600-7 2014 When GLP1 infusion was stopped, sodium excretion declined rapidly. Sodium 32-38 glucagon like peptide 1 receptor Homo sapiens 5-9 24714077-5 2014 Neutrophils acidified by an ammonium prepulse showed an EIPA-resistant recovery of pHi that was inhibited by the blocker of the anionic transporters SITS or the Na(+)/HCO3(-) cotransporter (NBC) selective inhibitor S0859, and abolished when sodium was removed from the extracellular medium. Sodium 241-247 glucose-6-phosphate isomerase Homo sapiens 83-86 24275769-9 2014 The mineralocorticoid receptor interacts with cav-1 and is modulated by sodium intake. Sodium 72-78 nuclear receptor subfamily 3 group C member 2 Homo sapiens 4-30 2149525-4 1990 During the control period and at weeks, 2, 6, and 8 post-CBDL all dogs responded to ANF with a significant change in sodium excretion (delta UNaV, 50-240 mu equiv./min). Sodium 117-123 natriuretic peptide A Canis lupus familiaris 84-87 2076204-9 1990 The kallikrein activity responded differently to pH, to metal ions (zinc and copper), and to the sodium/potassium ratio, depending on the concomitant presence or absence of UT-like material. Sodium 97-103 kallikrein 1-related peptidase b9 Mus musculus 4-14 2167025-8 1990 Chronic ACE inhibition significantly attenuated the conductance responses to SNS and slightly decreased responses to NE in sodium-depleted rabbits. Sodium 123-129 angiotensin-converting enzyme Oryctolagus cuniculus 8-11 2361480-6 1990 As previously reported for GH, IGF-1 also increased GFR and reduced urinary sodium excretion. Sodium 76-82 insulin-like growth factor 1 Rattus norvegicus 31-36 2184672-5 1990 One of these monokines, interleukin 1, induces a natriuresis by direct inhibition of collecting duct sodium reabsorption. Sodium 101-107 interleukin 1 alpha Homo sapiens 24-37 2160828-2 1990 In initial studies to characterize Na+/H+ exchange in FRTL-5 cell suspensions, the recovery of a resting pHi in acid-loaded cells was shown to be dependent upon the presence of extracellular Na+, was enhanced by the presence of the sodium ionophore monensin and was abolished by amiloride, an antagonist of Na+/H+ antiport activity. Sodium 232-238 glucose-6-phosphate isomerase Rattus norvegicus 105-108 2383642-5 1990 The results were compared with observations of crystallographic ordered water sites from x-ray diffraction studies on G and C containing small molecules, and in crystal structure determinations of the sodium, calcium, and ammonium salts of rGpC. Sodium 201-207 glycophorin C Rattus norvegicus 240-244 2383642-9 1990 The calculated one- and two-water bridges in the rGpC hydration complex coincide in a number of cases to those observed in the ordered water structure of the sodium rGpC crystal hydrate. Sodium 158-164 glycophorin C Rattus norvegicus 49-53 2383642-9 1990 The calculated one- and two-water bridges in the rGpC hydration complex coincide in a number of cases to those observed in the ordered water structure of the sodium rGpC crystal hydrate. Sodium 158-164 glycophorin C Rattus norvegicus 165-169 23708151-2 2014 The bioavailability of this vitamin depends upon the nutritional intake and its uptake by cells, mainly through the sodium-dependent transporters SVCT1/Svct1 and SVCT2/Svct2 (human/rat). Sodium 116-122 solute carrier family 23 member 2 Homo sapiens 162-167 2298725-6 1990 264, 213-219) described the requirement for a sodium ion influx in the down-modulation of the EGF receptor stimulated by a non-TPA-type tumor promoter, palytoxin, in Swiss 3T3 cells. Sodium 46-52 epidermal growth factor Mus musculus 94-97 2298725-9 1990 In each of these experiments, the loss of 125I-EGF binding occurred to a similar extent and at a similar rate in the presence or absence of sodium. Sodium 140-146 epidermal growth factor Mus musculus 47-50 1983458-1 1990 Studies were undertaken to characterize the participation of specific alpha-1,alpha-2 and beta adrenoceptors of the lateral hypothalamic area (LHA) in the urinary excretion of sodium and potassium. Sodium 176-182 adrenoceptor alpha 1D Homo sapiens 70-77 1983458-2 1990 Alpha-1 and alpha-2 LHA receptors were shown to participate in the regulation of renal sodium and potassium excretion. Sodium 87-93 adrenoceptor alpha 1D Homo sapiens 0-7 1983458-3 1990 The effects of noradrenaline microinjection (30 nmol in 1 microliter) into the LHA on urinary sodium excretion (UNaV) are blocked by previous injection of the alpha-1 antagonist prazosin (4 nmol in 1 microliter) from 3.22 +/- 0.25 to 0.59 +/- 0.04 microEq min-1 100 g body weight-1. Sodium 94-100 adrenoceptor alpha 1D Homo sapiens 159-166 2136843-6 1990 Long-term, low dose infusion directly into the renal artery of conscious dogs supports a physiological action of ANF to promote urinary sodium excretion. Sodium 136-142 natriuretic peptide A Canis lupus familiaris 113-116 1697368-4 1990 The augmentation of urine volume and urinary sodium excretion may also be related to the hypotensive effects of ACE inhibitors, and this mechanism might be explained by the renal blood flow increase and augmented activity in the renal kallikrein-kinin system. Sodium 45-51 angiotensin I converting enzyme Canis lupus familiaris 112-115 33788620-0 2021 Sodium sensitivity of KNa channels in mouse CA1 neurons. Sodium 0-6 carbonic anhydrase 1 Mus musculus 44-47 33940220-0 2021 Mineralocorticoid receptor modulation by dietary sodium influences NAFLD development in mice. Sodium 49-55 nuclear receptor subfamily 3, group C, member 2 Mus musculus 0-26 33940220-3 2021 We aimed to evaluate the effect of MR modulation by sodium intake in liver injury in experimental models of NAFLD. Sodium 52-58 nuclear receptor subfamily 3, group C, member 2 Mus musculus 35-37 33797191-1 2021 Biallelic loss-of-function (LoF) of SLC13A5 (solute carrier family 13, member 5) induced deficiency in sodium/citrate transporter (NaCT) causes autosomal recessive developmental epileptic encephalopathy 25 with hypoplastic amelogenesis imperfecta (DEE25; MIM #615905). Sodium 103-109 solute carrier family 13 member 5 Homo sapiens 131-135 33764691-10 2021 CONCLUSIONS: The linkage mutation SCN5A R965C-R1309H led to a more dramatically reduced current density, as well as more significant depolarisation-shifted activation and hyperpolarisation-shifted inactivation in sodium channels than R965C or R1309H alone, which potentially explain this complex familial arrhythmia syndrome. Sodium 213-219 sodium voltage-gated channel alpha subunit 5 Homo sapiens 34-39 23708151-2 2014 The bioavailability of this vitamin depends upon the nutritional intake and its uptake by cells, mainly through the sodium-dependent transporters SVCT1/Svct1 and SVCT2/Svct2 (human/rat). Sodium 116-122 solute carrier family 23 member 2 Homo sapiens 168-173 24026042-0 2014 High sodium augments angiotensin II-induced vascular smooth muscle cell proliferation through the ERK 1/2-dependent pathway. Sodium 5-11 mitogen activated protein kinase 3 Rattus norvegicus 98-105 24026042-7 2014 Ang II (100 nmol l(-1)) significantly increased ERK 1/2 phosphorylation and cell proliferation in the both medium containing standard sodium and high sodium. Sodium 134-140 mitogen activated protein kinase 3 Rattus norvegicus 48-55 24555708-5 2014 The major food sources of sodium were commercially prepared and processed foods for both CBC and ABC (59.9% and 54.7% of sodium, respectively). Sodium 26-32 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 89-100 24555708-5 2014 The major food sources of sodium were commercially prepared and processed foods for both CBC and ABC (59.9% and 54.7% of sodium, respectively). Sodium 121-127 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 89-100 24555708-6 2014 Condiments contributed substantially to dietary sodium intake of CBC and ABC (27.8% and 35.1% of sodium, respectively). Sodium 48-54 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 73-76 24555708-6 2014 Condiments contributed substantially to dietary sodium intake of CBC and ABC (27.8% and 35.1% of sodium, respectively). Sodium 97-103 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 73-76 24124190-0 2013 Identification of the SPLUNC1 ENaC-inhibitory domain yields novel strategies to treat sodium hyperabsorption in cystic fibrosis airway epithelial cultures. Sodium 86-92 BPI fold containing family A member 1 Homo sapiens 22-29 23676421-12 2013 CONCLUSIONS: Dietary sodium is positively associated with fluid consumption and predicted SSB consumption in consumers of SSBs. Sodium 21-27 small RNA binding exonuclease protection factor La Homo sapiens 90-93 23552861-0 2013 Mice carrying ubiquitin-specific protease 2 (Usp2) gene inactivation maintain normal sodium balance and blood pressure. Sodium 85-91 ubiquitin specific peptidase 2 Mus musculus 14-43 23552861-0 2013 Mice carrying ubiquitin-specific protease 2 (Usp2) gene inactivation maintain normal sodium balance and blood pressure. Sodium 85-91 ubiquitin specific peptidase 2 Mus musculus 45-49 23412700-0 2013 Reduced sodium transport with nasal administration of the prostasin inhibitor camostat in subjects with cystic fibrosis. Sodium 8-14 serine protease 8 Homo sapiens 58-67 23412700-10 2013 CONCLUSIONS: This study establishes the proof of concept that a reduction in sodium transport in the human CF airway can be achieved through inhibition of prostasin activity, identifying a potential therapeutic target in the disease. Sodium 77-83 serine protease 8 Homo sapiens 155-164 23719923-3 2013 Experimental evidence demonstrates that in addition to its classic role in the regulating sodium handling in the kidney, functional MR is expressed in the blood vessels and contributes to hypertension, vascular inflammation and remodeling, and atherogenesis. Sodium 90-96 nuclear receptor subfamily 3 group C member 2 Homo sapiens 132-134 33814411-6 2021 The antioxidant effect of loading with water with saturation with molecular hydrogen leads to a decrease in the loss of sodium ions due to an improvement in its reabsorption and beta2-microglobulin in the proximal tubule, a decrease in lipid peroxidation in the renal cortex was noted, the degree of its damage by an increase in the K+/Na+ ratio and a decrease in degree of edema. Sodium 120-126 beta-2 microglobulin Rattus norvegicus 178-197 33235263-4 2020 Previous work suggests that interstitial edema in the heart can acutely promote ventricular arrhythmias by disrupting ventricular myocyte intercalated disk (ID) nanodomains rich in cardiac sodium channels (NaV1.5) and slowing cardiac conduction. Sodium 189-195 sodium voltage-gated channel alpha subunit 5 Homo sapiens 206-212 33034205-0 2020 Machine learning-based QSAR models to predict sodium ion channel (Nav 1.5) blockers. Sodium 46-52 sodium voltage-gated channel alpha subunit 5 Homo sapiens 66-73 33034205-2 2020 The voltage-gated sodium ion channel 1.5 (Nav 1.5), a target known for arrhythmic drugs, causes adverse cardiac complications when the channel is blocked. Sodium 18-24 sodium voltage-gated channel alpha subunit 5 Homo sapiens 42-49 33762787-0 2021 Sodium Channel Myotonia and a Novel Gly701Asp Mutation in the SCN4A Gene: From an Ophthalmological Symptom to a Familial Disease. Sodium 0-6 sodium voltage-gated channel alpha subunit 4 Homo sapiens 62-67 33762787-4 2021 The child and family members underwent genetic testing, which was negative for CLCN1 mutations but was positive for a novel heterozygotic Gly701Asp mutation in the SCN4A gene, compatible with sodium channel myotonia. Sodium 192-198 sodium voltage-gated channel alpha subunit 4 Homo sapiens 164-169 34969185-2 2021 The SLC6A20 protein product (Sodium-dependent Imino Transporter 1 (SIT1)) is involved in the transport of amino acids, including glycine. Sodium 29-35 solute carrier family 6 member 20 Homo sapiens 4-11 34964123-2 2021 Glucose is taken up by apical sodium-glucose cotransporters SGLT2 and SGLT1 whereas SGLT5 and potentially SGLT4 and GLUT5 have been implicated in apical fructose uptake. Sodium 30-36 solute carrier family 5 member 2 Homo sapiens 60-65 34964123-8 2021 Moreover, renal glucose retention is coupled to sodium retention through SGLT2 and SGLT1, which induces secondary deleterious effects. Sodium 48-54 solute carrier family 5 member 2 Homo sapiens 73-78 34086898-3 2021 This mutation reduced expression of cardiomyocyte sodium channel Nav1.5 via Nedd4-2 E3 ubiquitin ligase-induced ubiquitination and degradation. Sodium 50-56 sodium voltage-gated channel alpha subunit 5 Homo sapiens 65-71 34949099-1 2022 BACKGROUND: Variants in the SCN5A gene, that encodes the cardiac sodium channel, Nav1.5, are associated with a highly arrhythmogenic form of dilated cardiomyopathy (DCM). Sodium 65-71 sodium voltage-gated channel alpha subunit 5 Homo sapiens 28-33 34949099-1 2022 BACKGROUND: Variants in the SCN5A gene, that encodes the cardiac sodium channel, Nav1.5, are associated with a highly arrhythmogenic form of dilated cardiomyopathy (DCM). Sodium 65-71 sodium voltage-gated channel alpha subunit 5 Homo sapiens 81-87 34988095-10 2021 SGLT2i improve blood pressure through a negative sodium and water balance and possibly by inhibiting the sympathetic nervous system. Sodium 49-55 solute carrier family 5 member 2 Homo sapiens 0-5 34975470-5 2021 Moreover, based on the molecular docking and molecular dynamic simulation, the binding free energies of the constructed systems were calculated, and the binding sites of GAS on the sodium channels (NaV1.7 and NaV1.8) were preliminarily determined. Sodium 181-187 sodium voltage-gated channel alpha subunit 9 Rattus norvegicus 198-204 34904226-2 2022 The purpose of the present study was to determine how the inhibition of basolateral Kir 4.1/Kir 5.1 heteromeric K+ channel affects epithelial sodium channel (ENaC)-mediated Na+ transport in the principal cells of cortical collecting duct (CCD). Sodium 142-148 potassium inwardly-rectifying channel, subfamily J, member 10 Rattus norvegicus 84-91 33258401-1 2021 Acid-sensing ion channel 3 (ASIC3) belongs to the epithelial sodium channel/degenerin (ENaC/DEG) superfamily. Sodium 61-67 sodium channel, nonvoltage-gated 1 alpha Mus musculus 87-91 33345742-11 2021 PPPs are caused by mutations in skeletal muscle calcium channel CaV1.1 gene (CACNA1S), sodium channel NaV1.4 gene (SCN4A), and potassium channels Kir2.1, Kir3.4 genes (KCNJ2, KCNJ5), including HypoPP1, HypoPP2, NormoPP, HyperPP, and ATS, which have significant clinical and genetic heterogeneity. Sodium 87-93 sodium voltage-gated channel alpha subunit 4 Homo sapiens 115-120 23590941-2 2013 Among them, the Slo1 and C. elegans SLO-2 channels are gated by calcium (Ca ( 2+) ), while mammalian Slo2 channels are activated by both sodium (Na (+) ) and chloride (Cl (-) ). Sodium 137-143 BK channel;Calcium-activated potassium channel slo-1 Caenorhabditis elegans 16-20 23195037-6 2013 Moreover, renal restricted subcapsular infusion of Snx5-specific siRNA (vs. mock siRNA) decreases sodium excretion (Delta=-0.2+-0.005 mEq/mg creatinine) and further elevates the systolic blood pressure (Delta=48+-5 mm Hg) in spontaneously hypertensive rats, indicating that SNX5 depletion impairs renal D1R function. Sodium 98-104 sorting nexin 5 Rattus norvegicus 51-55 23376999-3 2013 PiT1 (or SLC20A1) is a constitutively expressed, high-affinity sodium-dependent phosphate import protein. Sodium 63-69 solute carrier family 20, member 1 Mus musculus 0-4 23376999-0 2013 Mice lacking the sodium-dependent phosphate import protein, PiT1 (SLC20A1), have a severe defect in terminal erythroid differentiation and early B cell development. Sodium 17-23 solute carrier family 20, member 1 Mus musculus 60-64 23376999-0 2013 Mice lacking the sodium-dependent phosphate import protein, PiT1 (SLC20A1), have a severe defect in terminal erythroid differentiation and early B cell development. Sodium 17-23 solute carrier family 20, member 1 Mus musculus 66-73 23376999-3 2013 PiT1 (or SLC20A1) is a constitutively expressed, high-affinity sodium-dependent phosphate import protein. Sodium 63-69 solute carrier family 20, member 1 Mus musculus 9-16 23619363-5 2013 Moreover, the renal responses to high serum Ang II observed in wild-type mice, including intrarenal Ang II accumulation, sodium and water retention, and activation of ion transporters in the loop of Henle (NKCC2) and distal nephron (NCC, ENaC, and pendrin) as well as the transporter activating kinases SPAK and OSR1, were effectively prevented in mice that lack kidney ACE. Sodium 121-127 angiogenin, ribonuclease, RNase A family, 5 Mus musculus 44-47 23283969-5 2013 CYP2C44 epoxygenase knockdown blunted the sodium transport effects of EGF, and its 14,15-EET metabolite rescued the knockdown phenotype. Sodium 42-48 epidermal growth factor Homo sapiens 70-73 23106982-1 2013 We have identified QDR2 in a screening for genes able to confer tolerance to sodium and/or lithium stress upon overexpression. Sodium 77-83 cation transporter Saccharomyces cerevisiae S288C 19-23 22952014-3 2013 Among them, OCTN2 is a sodium-dependent, high-affinity transporter of carnitine, and a functional defect of OCTN2 due to genetic mutation causes primary systemic carnitine deficiency (SCD). Sodium 23-29 solute carrier family 22 (organic cation transporter), member 5 Mus musculus 12-17 23257389-7 2013 CONCLUSIONS: The Val110Ile mutation of SCN3B is a relatively common cause of SCN5A-negative BrS in Japan, which has a reduced sodium current because of the loss of cell surface expression of Nav1.5. Sodium 126-132 sodium voltage-gated channel alpha subunit 5 Homo sapiens 77-82 22680232-3 2013 We suggest that gastrin is involved in the regulation of blood pressure, possibly via the regulation of sodium and water metabolism and/or renin-angiotensin-aldosterone system. Sodium 104-110 gastrin Homo sapiens 16-23 22966789-9 2013 The increases in water and sodium absorption via AQP2 and ENaC after furosemide most likely are compensatory phenomena to antagonize water and sodium depletion. Sodium 27-33 aquaporin 2 Homo sapiens 49-53 22966789-9 2013 The increases in water and sodium absorption via AQP2 and ENaC after furosemide most likely are compensatory phenomena to antagonize water and sodium depletion. Sodium 143-149 aquaporin 2 Homo sapiens 49-53 23042029-4 2013 RECENT FINDINGS: This review provides an overview of recent findings in this area: the transcriptional control of SGLT2 expression in human proximal tubular cells implicates a number of cytokines in the alteration of SGLT2 expression; experimental data show that SGLT2 inhibition may correct early detrimental effects of diabetes by reducing proximal tubular sodium and glucose transport, suggesting a possible renoprotective effect independent of the glucose lowering effects of these agents; and the nonglycaemic effects of SGLT2 inhibitors may have an impact on renal outcomes. Sodium 359-365 solute carrier family 5 member 2 Homo sapiens 114-119 23160444-2 2013 The focus of this review is to integrate these models and to propose a scheme for the control of sodium excretion by the collecting duct and the endothelin/ETB/NOS system. Sodium 97-103 endothelin receptor type B Mus musculus 156-159 23160444-8 2013 SUMMARY: In the collecting duct, the ET1/nitric oxide pathways are intimately linked, and deletion of collecting duct ET1, ETB receptor or NOS1beta results in a salt-sensitive phenotype, which is at least partially dependent on dysregulation of sodium and water reabsorption. Sodium 245-251 endothelin 1 Mus musculus 118-121 23160444-8 2013 SUMMARY: In the collecting duct, the ET1/nitric oxide pathways are intimately linked, and deletion of collecting duct ET1, ETB receptor or NOS1beta results in a salt-sensitive phenotype, which is at least partially dependent on dysregulation of sodium and water reabsorption. Sodium 245-251 endothelin receptor type B Mus musculus 123-126 23232097-4 2012 Plants lacking UBP16 were hypersensitive to salt stress and accumulated more sodium and less potassium. Sodium 77-83 ubiquitin-specific protease 16 Arabidopsis thaliana 15-20 22766068-7 2012 Over-expression of hSGLT3 in COS-7 cells increased intracellular sodium concentration by 3-fold without affecting glucose transport. Sodium 65-71 solute carrier family 5 member 4 Homo sapiens 19-25 22766068-8 2012 Activation of hSGLT3 with DNJ (50muM) increased sodium uptake in HK-2 cells by 5.5 fold and this effect could be completely blocked with SGLT inhibitor phlorizin (50muM). Sodium 48-54 solute carrier family 5 member 4 Homo sapiens 14-20 22766068-10 2012 Up-regulation of the expression of SGLT3 in the proximal tubule in diabetic patients may contribute to the elevated sodium transport in this segment of the nephron that has been postulated to promote hyperfiltration and renal injury. Sodium 116-122 solute carrier family 5 member 4 Homo sapiens 35-40 22686594-5 2012 Taken together, integrated analysis of omics data demonstrated that water and sodium reabsorption could be reduced by decreased extracellular osmolality per se, through decreased levels of ABC transporters and IRS2, which play a potential role in the transport of organic osmolytes, BCAA, glucose, and trafficking of epithelial sodium channel. Sodium 78-84 insulin receptor substrate 2 Homo sapiens 210-214 22467310-0 2012 Increases in intracellular sodium activate transcription and gene expression via the salt-inducible kinase 1 network in an atrial myocyte cell line. Sodium 27-33 salt inducible kinase 1 Homo sapiens 85-108 22467310-11 2012 These data obtained in a cardiac cell line suggest that increases in intracellular sodium could influence myocardial growth by controlling transcriptional activation and gene expression throughout the activation of the SIK1 network. Sodium 83-89 salt inducible kinase 1 Homo sapiens 219-223 22665796-1 2012 The epithelial Na(+) channel (ENaC) in the aldosterone-sensitive distal nephron (ASDN) is under negative-feedback regulation by the renin-angiotensin-aldosterone system in protection of sodium balance and blood pressure. Sodium 186-192 sodium channel, nonvoltage-gated 1 alpha Mus musculus 4-28 34943889-2 2021 The solute carrier family 13 member 5 (SLC13A5), a sodium-coupled citrate transporter, plays an important role in intracellular citrate homeostasis that is associated with a number of metabolic syndromes and neurological disorders. Sodium 51-57 solute carrier family 13 member 5 Homo sapiens 4-37 34943889-2 2021 The solute carrier family 13 member 5 (SLC13A5), a sodium-coupled citrate transporter, plays an important role in intracellular citrate homeostasis that is associated with a number of metabolic syndromes and neurological disorders. Sodium 51-57 solute carrier family 13 member 5 Homo sapiens 39-46 34463415-1 2021 AIMS: The selective sodium-glucose cotransporter 2 inhibitor empagliflozin increases urinary glucose, sodium excretion, and urinary volume, and reduces plasma glucose in type 2 diabetes mellitus (T2DM) patients. Sodium 102-108 solute carrier family 5 member 2 Homo sapiens 20-50 34657443-8 2021 In conclusion, the present study demonstrates that in the early stage of leptin receptor-deficient diabetes, the upregulation of macula densa NOS1 inhibits TGF and increases glomerular filtration rate, which counteracts renal sodium retention and limits the rise in blood pressure. Sodium 226-232 leptin receptor Mus musculus 73-88 34289398-0 2021 The potential roles of osmotic and non-osmotic sodium handling in mediating effects of SGLT2 inhibitors on heart failure. Sodium 47-53 solute carrier family 5 member 2 Homo sapiens 87-92 34297135-1 2021 In different large-scale clinic outcome trials, sodium (Na+)/glucose co-transporter 2 (SGLT2) inhibitors showed profound cardiac- and renal-protective effects, making them revolutionary treatments for heart failure and kidney disease. Sodium 48-54 solute carrier family 5 member 2 Homo sapiens 56-85 34297135-1 2021 In different large-scale clinic outcome trials, sodium (Na+)/glucose co-transporter 2 (SGLT2) inhibitors showed profound cardiac- and renal-protective effects, making them revolutionary treatments for heart failure and kidney disease. Sodium 48-54 solute carrier family 5 member 2 Homo sapiens 87-92 34403723-1 2021 Intestinal absorption of vitamin C in humans is mediated via the sodium-dependent vitamin C transporters (hSVCT1 and hSVCT2). Sodium 65-71 solute carrier family 23 member 1 Homo sapiens 106-112 34378097-1 2021 INTRODUCTION: Mutations of the skeletal muscle sodium channel gene SCN4A are associated with several neuromuscular disorders including hyper/hypokaliemic periodic paralysis, paramyotonia congenita and sodium channel myotonia. Sodium 47-53 sodium voltage-gated channel alpha subunit 4 Homo sapiens 67-72 34378097-1 2021 INTRODUCTION: Mutations of the skeletal muscle sodium channel gene SCN4A are associated with several neuromuscular disorders including hyper/hypokaliemic periodic paralysis, paramyotonia congenita and sodium channel myotonia. Sodium 201-207 sodium voltage-gated channel alpha subunit 4 Homo sapiens 67-72 34583417-9 2021 In terms of biochemistry, MIS-C patients had lower levels of albumin, sodium and alanine aminotransferase and higher levels of creatinine than KD patients. Sodium 70-76 anti-Mullerian hormone Homo sapiens 26-29 34837866-1 2021 Revealing the role of the sodium HKT1;5 transporter in plant adaptive responses to varying soil salinity. Sodium 26-32 high-affinity K+ transporter 1 Arabidopsis thaliana 33-37 34837866-8 2021 AtHKT1; 1 (Arabidopsis thaliana) and HKT1; 5 (cereal crops) "exclude" Na+ from the xylem into xylem parenchyma in the root, reducing shoot Na+ and hence, confer sodium tolerance. Sodium 161-167 high-affinity K+ transporter 1 Arabidopsis thaliana 0-9 34837866-8 2021 AtHKT1; 1 (Arabidopsis thaliana) and HKT1; 5 (cereal crops) "exclude" Na+ from the xylem into xylem parenchyma in the root, reducing shoot Na+ and hence, confer sodium tolerance. Sodium 161-167 high-affinity K+ transporter 1 Arabidopsis thaliana 37-41 34837866-9 2021 However, more recent data from Arabidopsis and crop species show that AtHKT1;1/HKT1;5 alleles have a strong genetic association with "shoot sodium accumulation" and concomitant salt tolerance. Sodium 140-146 high-affinity K+ transporter 1 Arabidopsis thaliana 70-76 34837866-9 2021 However, more recent data from Arabidopsis and crop species show that AtHKT1;1/HKT1;5 alleles have a strong genetic association with "shoot sodium accumulation" and concomitant salt tolerance. Sodium 140-146 high-affinity K+ transporter 1 Arabidopsis thaliana 79-83 34916958-0 2021 Sensory Afferent Renal Nerve Activated Galphai2 Subunit Proteins Mediate the Natriuretic, Sympathoinhibitory and Normotensive Responses to Peripheral Sodium Challenges. Sodium 150-156 G protein subunit alpha i2 Rattus norvegicus 39-47 34916958-1 2021 We have previously reported that brain Galphai2 subunit proteins are required to maintain sodium homeostasis and are endogenously upregulated in the hypothalamic paraventricular nucleus (PVN) in response to increased dietary salt intake to maintain a salt resistant phenotype in rats. Sodium 90-96 G protein subunit alpha i2 Rattus norvegicus 39-47 34916958-5 2021 Furthermore, in response to chronically elevated dietary sodium intake, endogenous up-regulation of PVN specific Galphai2 proteins does not involve the AV3V region and is mediated by the sensory afferent renal nerves to counter the development of the salt sensitivity of blood pressure (MAP (mmHg) 4% NaCl; Sham ADNX 124 +- 4 vs. ADNX 145 +- 4, p < 0.05; Sham AV3V 125 +- 4 vs. AV3V 121 +- 5). Sodium 57-63 G protein subunit alpha i2 Rattus norvegicus 113-121 34916958-7 2021 Collectively, our data suggest that in response to alterations in whole body sodium the peripheral sensory afferent renal nerves, but not the central AV3V sodium sensitive region, evoke the up-regulation and activation of PVN Galphai2 protein gated pathways to maintain a salt resistant phenotype. Sodium 77-83 G protein subunit alpha i2 Rattus norvegicus 226-234 34779863-13 2021 The mechanism may be involved that paternal PM2.5 exposure-associated oxidative stress induces the elevated renal GRK4 level, leading to the enhanced AT1R expression and its-mediated sodium retention, consequently causes hypertension in male offspring. Sodium 183-189 G protein-coupled receptor kinase 4 Rattus norvegicus 114-118 34843967-0 2022 Mechanistic insights into the interaction of cardiac sodium channel Nav1.5 with MOG1 and a new molecular mechanism for Brugada syndrome. Sodium 53-59 sodium voltage-gated channel alpha subunit 5 Homo sapiens 68-74 34843967-1 2022 BACKGROUND: Mutations in cardiac sodium channel Nav1.5 cause Brugada syndrome (BrS). Sodium 33-39 sodium voltage-gated channel alpha subunit 5 Homo sapiens 48-54 34374996-1 2021 Nowadays sodium-based energy storage systems (Na-based ESSs) have been widely researched as it possesses the possibility to replace traditional energy storage media to become next generation energy storage system. Sodium 9-15 NADH:ubiquinone oxidoreductase subunit B11 Homo sapiens 55-59 34374996-2 2021 However, due to the irreversible loss of sodium ions in the first cycle, development of Na-based ESSs is limited. Sodium 41-47 NADH:ubiquinone oxidoreductase subunit B11 Homo sapiens 97-101 34868940-0 2021 Elevated Sodium Pump alpha3 Subunit Expression Promotes Colorectal Liver Metastasis via the p53-PTEN/IGFBP3-AKT-mTOR Axis. Sodium 9-15 phosphatase and tensin homolog Homo sapiens 96-100 34868940-0 2021 Elevated Sodium Pump alpha3 Subunit Expression Promotes Colorectal Liver Metastasis via the p53-PTEN/IGFBP3-AKT-mTOR Axis. Sodium 9-15 insulin like growth factor binding protein 3 Homo sapiens 101-107 34868940-8 2021 Conclusions: Elevated expression of the sodium pump alpha3 subunit promotes CRC liver metastasis via the PTEN/IGFBP3-mediated mTOR pathway, suggesting that sodium pump alpha3 could represent a critical prognostic marker and/or therapeutic target for this disease. Sodium 40-46 phosphatase and tensin homolog Homo sapiens 105-109 34868940-8 2021 Conclusions: Elevated expression of the sodium pump alpha3 subunit promotes CRC liver metastasis via the PTEN/IGFBP3-mediated mTOR pathway, suggesting that sodium pump alpha3 could represent a critical prognostic marker and/or therapeutic target for this disease. Sodium 40-46 insulin like growth factor binding protein 3 Homo sapiens 110-116 34562870-1 2021 BACKGROUND AND AIMS: To study euglycemic diabetic ketoacidosis (euDKA) outcomes associated with sodium-glucose co-transporter 2 inhibitors (SGLT2is) METHODS: Review of 72 euDKA cases in T2DM between September 2015 and January 2020 (PUBMED). Sodium 96-102 solute carrier family 5 member 2 Homo sapiens 140-145 34725782-9 2021 These findings include SGLT2-iss-mediated reductions in the expression of hypertrophic foetal genes and diastolic myofilaments stiffness, increases in global phosphorylation of myofilament regulatory proteins (in HFpEF), inhibition of cardiac late sodium channel current and Na+/H+ exchanger activity, metabolic shifts, and effects on calcium cycling. Sodium 248-254 solute carrier family 5 member 2 Homo sapiens 23-28 34427958-8 2021 Sodium channel blockers significantly shortened QTc both in LQT3 and LQT2 patients, while the QTc shortening effect in LQT3 was superior to that in LQT2 (57.39 ms vs. 36.61 ms). Sodium 0-6 sodium voltage-gated channel alpha subunit 5 Homo sapiens 60-64 34427958-8 2021 Sodium channel blockers significantly shortened QTc both in LQT3 and LQT2 patients, while the QTc shortening effect in LQT3 was superior to that in LQT2 (57.39 ms vs. 36.61 ms). Sodium 0-6 potassium voltage-gated channel subfamily H member 2 Homo sapiens 69-73 34427958-8 2021 Sodium channel blockers significantly shortened QTc both in LQT3 and LQT2 patients, while the QTc shortening effect in LQT3 was superior to that in LQT2 (57.39 ms vs. 36.61 ms). Sodium 0-6 sodium voltage-gated channel alpha subunit 5 Homo sapiens 119-123 34427958-10 2021 CONCLUSIONS: sodium channel blockers can be useful both in LQT3 and LQT2 patients. Sodium 13-19 sodium voltage-gated channel alpha subunit 5 Homo sapiens 59-63 34427958-10 2021 CONCLUSIONS: sodium channel blockers can be useful both in LQT3 and LQT2 patients. Sodium 13-19 potassium voltage-gated channel subfamily H member 2 Homo sapiens 68-72 34507633-1 2021 Sodium/glucose cotransporter 2 (SGLT2) is a renal low-affinity high-capacity sodium/glucose cotransporter expressed in the apical membrane of the early segment of proximal tubules. Sodium 77-83 solute carrier family 5 member 2 Homo sapiens 0-30 34507633-1 2021 Sodium/glucose cotransporter 2 (SGLT2) is a renal low-affinity high-capacity sodium/glucose cotransporter expressed in the apical membrane of the early segment of proximal tubules. Sodium 77-83 solute carrier family 5 member 2 Homo sapiens 32-37 34507633-2 2021 SGLT2 reabsorbs filtered glucose in the kidney, and its inhibitors represent a new class of oral medications used for type 2 diabetes mellitus, which act by increasing glucose and sodium excretion in urine, thereby reducing blood glucose levels. Sodium 180-186 solute carrier family 5 member 2 Homo sapiens 0-5 34778257-8 2021 Further analysis revealed that renal Fgfr1/klotho/extracellular signal-regulated kinases 1/2 signaling was activated in AAV-Fgf23 mice, resulting in downregulation of sodium-phosphate cotransporter NaPi2a and NaPi2c and suppression of Cyp27b1, further supporting the bioactivity of cardiac-derived iFgf23. Sodium 167-173 solute carrier family 34 (sodium phosphate), member 1 Mus musculus 198-204 34754936-3 2021 This condition is associated with mutations in several pathologic genes including the most notable mutation in the SCN5A gene, which encodes for a voltage-gated cardiac sodium channel. Sodium 169-175 sodium voltage-gated channel alpha subunit 5 Homo sapiens 115-120 34697091-4 2021 A plasmid designed to silence epithelial sodium channel (ENaC) hyperactivity, which causes airway surface dehydration and mucus stasis, was intratracheally administered via DNA-MPP to evaluate therapeutic effects in vivo with or without pretreatment with hypertonic saline, a clinically used mucus-rehydrating agent. Sodium 41-47 sodium channel, nonvoltage-gated 1 alpha Mus musculus 57-61 34744721-6 2021 Methods: Electrophysiological experiments were performed by means of the patch-clamp technique using heterologously expressed human heart muscle sodium channels (hNav1.5), which are among the most common subtypes of VGSCs occurring in tumor cells. Sodium 145-151 sodium voltage-gated channel alpha subunit 5 Homo sapiens 162-169 34677420-2 2021 The solute carrier family 13 member 5 (SLC13A5), a sodium-coupled citrate transporter highly expressed in the mammalian liver with relatively low levels in the testis and brain, imports citrate from extracellular spaces into the cells. Sodium 51-57 solute carrier family 13 member 5 Homo sapiens 4-37 34677420-2 2021 The solute carrier family 13 member 5 (SLC13A5), a sodium-coupled citrate transporter highly expressed in the mammalian liver with relatively low levels in the testis and brain, imports citrate from extracellular spaces into the cells. Sodium 51-57 solute carrier family 13 member 5 Homo sapiens 39-46 34293127-3 2021 OBJECTIVES: We hypothesized that a low-sodium DASH diet improves (lowers) biomarkers of inflammation (C-reactive protein (CRP) and soluble urokinase plasminogen activator receptor (suPAR)) and mineral metabolism (phosphorus and fibroblast growth factor-23 (FGF23)). Sodium 39-45 plasminogen activator, urokinase receptor Homo sapiens 139-179 34927950-1 2021 The degradation mechanism in a sodium cell of a layered Na0.48 Al0.03 Co0.18 Ni0.18 Mn0.47 O2 (NCAM) cathode with P3/P2 structure is investigated by revealing the changes in microstructure and composition upon cycling. Sodium 31-37 neural cell adhesion molecule 1 Homo sapiens 95-99 34089062-1 2021 Mutations of SPINT2, the gene encoding the integral membrane, Kunitz-type serine inhibitor HAI-2, primarily affect the intestine, while sparing many other HAI-2-expressing tissues, causing sodium loss in patients with syndromic congenital sodium diarrhea. Sodium 189-195 serine peptidase inhibitor, Kunitz type 2 Homo sapiens 13-19 34089062-1 2021 Mutations of SPINT2, the gene encoding the integral membrane, Kunitz-type serine inhibitor HAI-2, primarily affect the intestine, while sparing many other HAI-2-expressing tissues, causing sodium loss in patients with syndromic congenital sodium diarrhea. Sodium 239-245 serine peptidase inhibitor, Kunitz type 2 Homo sapiens 13-19 34603048-3 2021 The etiology of ionic imbalances resulting from stroke-induced ischemia and acidosis includes the dysregulation of multiple plasma membrane transport proteins, such as increased activity of sodium-potassium-chloride cotransporter-1 (NKCC-1). Sodium 190-196 solute carrier family 12 member 2 Homo sapiens 233-239 34525352-2 2021 Recent studies have observed that deficiency of the sodium-dependent citrate transporter (NaCT), encoded by SLC13A5, dysregulates hepatic metabolism and drives pediatric epilepsy. Sodium 52-58 solute carrier family 13 member 5 Homo sapiens 90-94 34525352-2 2021 Recent studies have observed that deficiency of the sodium-dependent citrate transporter (NaCT), encoded by SLC13A5, dysregulates hepatic metabolism and drives pediatric epilepsy. Sodium 52-58 solute carrier family 13 member 5 Homo sapiens 108-115 22665796-1 2012 The epithelial Na(+) channel (ENaC) in the aldosterone-sensitive distal nephron (ASDN) is under negative-feedback regulation by the renin-angiotensin-aldosterone system in protection of sodium balance and blood pressure. Sodium 186-192 sodium channel, nonvoltage-gated 1 alpha Mus musculus 30-34 22665796-8 2012 The absence of aldosterone combined with elevated AVP release compromises normal feedback regulation of ENaC in Adx mice in response to changes in sodium intake. Sodium 147-153 sodium channel, nonvoltage-gated 1 alpha Mus musculus 104-108 26069764-2 2012 Patients with congenital NDI bearing mutations in the vasopressin 2 receptor gene, AVPR2, or in the aquaporin-2 gene, AQP2, have a pure NDI phenotype with loss of water but normal conservation of sodium, potassium, chloride and calcium. Sodium 196-202 aquaporin 2 Homo sapiens 100-111 34566847-0 2021 Therapeutic Potential of Sodium Channel Blockers as a Targeted Therapy Approach in KCNA1-Associated Episodic Ataxia and a Comprehensive Review of the Literature. Sodium 25-31 potassium voltage-gated channel subfamily A member 1 Homo sapiens 83-88 34502151-5 2021 Meanwhile, we also shown that the expression sodium-dependent neutral amino acid transporter 2 (SNAT2) for Ser and excitatory amino acid transporter 4 (EAAT4) for Glu was also significantly elevated during infection. Sodium 45-51 solute carrier family 1 (high affinity aspartate/glutamate transporter), member 6 Mus musculus 115-150 34502151-5 2021 Meanwhile, we also shown that the expression sodium-dependent neutral amino acid transporter 2 (SNAT2) for Ser and excitatory amino acid transporter 4 (EAAT4) for Glu was also significantly elevated during infection. Sodium 45-51 solute carrier family 1 (high affinity aspartate/glutamate transporter), member 6 Mus musculus 152-157 34099506-8 2021 Finally, we show that endogenous polyamines constrain INaP availability in both somato-dendritic and axonal compartments of non-dialyzed cortical neurons.SIGNIFICANCE STATEMENT:The most salient characteristic of neuronal sodium channels is fast inactivation. Sodium 221-227 nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, zeta Mus musculus 54-58 34064873-3 2021 The mechanism of action of CG"s toxicity is inhibition of Na+/K+-ATPase (the sodium-potassium pump, NKA), which disrupts the ionic homeostasis leading to elevated Ca2+ concentration resulting in cell death. Sodium 77-83 NKA Bos taurus 100-103 34195526-4 2021 However, a recent study about urine sodium excretion in the presence of an SGLT2 inhibitor did not show any increases in urine sodium excretion. Sodium 36-42 solute carrier family 5 member 2 Homo sapiens 75-80 34194835-12 2021 Conclusion: This study revealed that FGF13 could stabilize microtubules to modulate sodium channel function in DRG neurons and modulate inflammatory pain. Sodium 84-90 fibroblast growth factor 13 Mus musculus 37-42 34194835-13 2021 This study provides a novel mechanism for FGF13 modulation of sodium channel function and suggests that FGF13 might be a novel target for inflammatory pain treatment. Sodium 62-68 fibroblast growth factor 13 Mus musculus 42-47 34194835-13 2021 This study provides a novel mechanism for FGF13 modulation of sodium channel function and suggests that FGF13 might be a novel target for inflammatory pain treatment. Sodium 62-68 fibroblast growth factor 13 Mus musculus 104-109 35612552-4 2022 Here, we studied the cardiac sodium channel, Nav1.5, using charge-neutralizing mutations and voltage-clamp fluorometry. Sodium 29-35 sodium voltage-gated channel alpha subunit 5 Homo sapiens 45-51 35506380-2 2022 Although aldosterone activates MR to increase epithelial sodium channel (ENaC) activity, glucocorticoids also activate MR but are metabolized by 11betaHSD2 (11beta-hydroxysteroid dehydrogenase type 2). Sodium 57-63 sodium channel, nonvoltage-gated 1 alpha Mus musculus 73-77 35397174-4 2022 SCN5A encodes the cardiac Nav 1.5 sodium channel. Sodium 34-40 sodium voltage-gated channel alpha subunit 5 Homo sapiens 0-5 35397174-4 2022 SCN5A encodes the cardiac Nav 1.5 sodium channel. Sodium 34-40 sodium voltage-gated channel alpha subunit 5 Homo sapiens 26-33 35305865-1 2022 PURPOSE: Up to 30% of patients with Brugada syndrome (BrS) carry loss-of-function (LoF) variants in the cardiac sodium channel gene SCN5A encoding for the protein NaV1.5. Sodium 112-118 sodium voltage-gated channel alpha subunit 5 Homo sapiens 132-137 35305865-1 2022 PURPOSE: Up to 30% of patients with Brugada syndrome (BrS) carry loss-of-function (LoF) variants in the cardiac sodium channel gene SCN5A encoding for the protein NaV1.5. Sodium 112-118 sodium voltage-gated channel alpha subunit 5 Homo sapiens 163-169 35512853-2 2022 Inhibition of amiloride-sensitive epithelial sodium ion channel (ENaC) has now been considered as a potential therapeutic target against COPD. Sodium 45-51 sodium channel, nonvoltage-gated 1 alpha Mus musculus 65-69 35621227-2 2022 We have identified a novel drug for hyperphosphatemia, EOS789, that interacts with several sodium-dependent phosphate transporters (NaPi-IIb, PiT-1, and PiT-2) known to contribute to intestinal phosphate absorption. Sodium 91-97 solute carrier family 20 member 2 Rattus norvegicus 153-158 26069764-2 2012 Patients with congenital NDI bearing mutations in the vasopressin 2 receptor gene, AVPR2, or in the aquaporin-2 gene, AQP2, have a pure NDI phenotype with loss of water but normal conservation of sodium, potassium, chloride and calcium. Sodium 196-202 aquaporin 2 Homo sapiens 118-122 22590457-7 2012 (ii) A Brugada syndrome, that may directly cause ventricular fibrillation due to reduced sodium current through Nav1.5 channels. Sodium 89-95 sodium voltage-gated channel alpha subunit 5 Homo sapiens 112-118 35633140-1 2022 Recessive mutations in the SLC13A5 gene encoding the sodium-dependent citrate transporter are a recently identified cause of developmental and epileptic encephalopathy. Sodium 53-59 solute carrier family 13 member 5 Homo sapiens 27-34 22052157-4 2012 Specifically, we compute the fast Fourier transform for a family of current traces at different step potentials for the inward rectifying potassium channel, K(ir)2.1, and the channel encoding the cardiac fast sodium current, Na(v)1.5. Sodium 209-215 immunoglobulin lambda variable 2-18 Homo sapiens 225-233 35607934-0 2022 Electrolyte Sieving Chemistry in Suppressing Gas Evolution of Sodium Metal Batteries. Sodium 62-74 gastrin Homo sapiens 45-48 22260870-1 2012 We reported previously that sensory neurons isolated from mice with a heterozygous mutation of the Nf1 gene (Nf1+/-) exhibited greater excitability and increased sodium current densities compared with wildtype mice. Sodium 162-168 neurofibromin 1 Mus musculus 99-102 22260870-1 2012 We reported previously that sensory neurons isolated from mice with a heterozygous mutation of the Nf1 gene (Nf1+/-) exhibited greater excitability and increased sodium current densities compared with wildtype mice. Sodium 162-168 neurofibromin 1 Mus musculus 109-112 22260870-10 2012 These results demonstrate that the increased expression levels of Nav1.7, Nav1.8, and perhaps Nav1.1 in the Nf1+/- DRG make the largest contribution to the increased sodium current density and thus give rise to the enhanced excitability. Sodium 166-172 neurofibromin 1 Mus musculus 108-111 22209345-4 2012 We have previously shown that estradiol administered to the female mouse modulates sodium currents in fluorescently-labeled GnRH neurons. Sodium 83-89 gonadotropin releasing hormone 1 Mus musculus 124-128 35471735-3 2022 Herein, a liquid metal interfacial engineering strategy is reported for the synthesis of porous carbon using CCl4 as the carbon precursor and sodium-potassium alloy (NaK) as the reducing agent, which is superior to traditional synthetic methods because it enables the engineering of a highly active liquid metal alloy microemulsion to directly generate porous carbon at ambient temperature. Sodium 142-148 TANK binding kinase 1 Homo sapiens 166-169 22209345-6 2012 The direct application of estradiol modulated a tetrodotoxin-sensitive sodium current in isolated GnRH neurons from both young and aged animals. Sodium 71-77 gonadotropin releasing hormone 1 Mus musculus 98-102 22088435-3 2012 Experimental data indicate that the sodium/hydrogen ion exchanger isoform 4 (NHE4; Scl9a4) is a sodium/ammonia exchanger and plays a major role in this process. Sodium 36-42 solute carrier family 9 (sodium/hydrogen exchanger), member 4 Mus musculus 77-81 35456996-1 2022 Nav1.5 is the pore forming alpha-subunit of the cardiac voltage-gated sodium channel that initiates cardiac action potential and regulates the human heartbeat. Sodium 70-76 sodium voltage-gated channel alpha subunit 5 Homo sapiens 0-6 22088435-3 2012 Experimental data indicate that the sodium/hydrogen ion exchanger isoform 4 (NHE4; Scl9a4) is a sodium/ammonia exchanger and plays a major role in this process. Sodium 96-102 solute carrier family 9 (sodium/hydrogen exchanger), member 4 Mus musculus 77-81 22089104-1 2012 BACKGROUND: Aldosterone (ALDO), a critical regulator of sodium homeostasis, mediates its effects via activation of the mineralocorticoid receptor (MR) through mechanisms that are not entirely clear. Sodium 56-62 nuclear receptor subfamily 3, group C, member 2 Mus musculus 119-145 22089104-1 2012 BACKGROUND: Aldosterone (ALDO), a critical regulator of sodium homeostasis, mediates its effects via activation of the mineralocorticoid receptor (MR) through mechanisms that are not entirely clear. Sodium 56-62 nuclear receptor subfamily 3, group C, member 2 Mus musculus 147-149 35394010-2 2022 Among these, the cardiac sodium channel SCN5A undergoes fetal-to-adult isoform switching around birth. Sodium 25-31 sodium voltage-gated channel alpha subunit 5 Homo sapiens 40-45 22184322-0 2012 Cyp2c44 epoxygenase is essential for preventing the renal sodium absorption during increasing dietary potassium intake. Sodium 58-64 cytochrome P450, family 2, subfamily c, polypeptide 23 Mus musculus 0-7 22195582-2 2012 The plasma membrane (PM) Na+/H+ antiporter (SOS1) is involved in salt tolerance, presumably in sodium extrusion; the vacuolar type I H+-PPase AVP1 is involved in vacuolar sodium sequestration, but its overexpression has also been shown to alter the abundance and activity of the PM H+-ATPase. Sodium 95-101 sodium proton exchanger, putative (NHX7) (SOS1) Arabidopsis thaliana 44-48 35465610-0 2022 Identification of Sodium Transients Through NaV1.5 Channels as Regulators of Differentiation in Immortalized Dorsal Root Ganglia Neurons. Sodium 18-24 sodium voltage-gated channel alpha subunit 5 Homo sapiens 44-50 35129370-6 2022 The increased sodium retention is associated with altered expression of glucocorticoid and mineralocorticoid receptors, increased serum aldosterone, and increased medullary endothelin-1 compared to control (CNTL) mice. Sodium 14-20 endothelin 1 Mus musculus 173-185 35401866-2 2022 One common observation is that cortical neurons become overexcited with abnormal running of sodium and potassium ions cross membrane in raised body temperature condition, Considering that astrocyte Kir4.1 channel play a critical role in maintaining extracellular homeostasis of ionic concentrations and electrochemical potentials of neurons by fast depletion of extracellular potassium ions, we examined here the potential role of temperature-dependent Kir4.1 channel in astrocytes in causing FS. Sodium 92-98 potassium inwardly rectifying channel subfamily J member 10 Homo sapiens 198-204 35401866-2 2022 One common observation is that cortical neurons become overexcited with abnormal running of sodium and potassium ions cross membrane in raised body temperature condition, Considering that astrocyte Kir4.1 channel play a critical role in maintaining extracellular homeostasis of ionic concentrations and electrochemical potentials of neurons by fast depletion of extracellular potassium ions, we examined here the potential role of temperature-dependent Kir4.1 channel in astrocytes in causing FS. Sodium 92-98 potassium inwardly rectifying channel subfamily J member 10 Homo sapiens 453-459 35013551-1 2022 The sodium (Na+):multivitamin transporter (SMVT), encoded by SLC5A6, belongs to the sodium:solute symporter family and is required for the Na+-dependent uptake of biotin (vitamin B7), pantothenic acid (vitamin B5), the vitamin-like substance alpha-lipoic acid, and iodide. Sodium 4-10 solute carrier family 5 member 6 Homo sapiens 43-47 35013551-1 2022 The sodium (Na+):multivitamin transporter (SMVT), encoded by SLC5A6, belongs to the sodium:solute symporter family and is required for the Na+-dependent uptake of biotin (vitamin B7), pantothenic acid (vitamin B5), the vitamin-like substance alpha-lipoic acid, and iodide. Sodium 4-10 solute carrier family 5 member 6 Homo sapiens 61-67 35013551-1 2022 The sodium (Na+):multivitamin transporter (SMVT), encoded by SLC5A6, belongs to the sodium:solute symporter family and is required for the Na+-dependent uptake of biotin (vitamin B7), pantothenic acid (vitamin B5), the vitamin-like substance alpha-lipoic acid, and iodide. Sodium 84-90 solute carrier family 5 member 6 Homo sapiens 43-47 35013551-1 2022 The sodium (Na+):multivitamin transporter (SMVT), encoded by SLC5A6, belongs to the sodium:solute symporter family and is required for the Na+-dependent uptake of biotin (vitamin B7), pantothenic acid (vitamin B5), the vitamin-like substance alpha-lipoic acid, and iodide. Sodium 84-90 solute carrier family 5 member 6 Homo sapiens 61-67 35177789-1 2022 Mineralocorticoid receptor (MR) and its ligand aldosterone play a central role in controlling blood pressure by promoting sodium reabsorption in the kidney. Sodium 122-128 nuclear receptor subfamily 3, group C, member 2 Mus musculus 0-26 35177789-1 2022 Mineralocorticoid receptor (MR) and its ligand aldosterone play a central role in controlling blood pressure by promoting sodium reabsorption in the kidney. Sodium 122-128 nuclear receptor subfamily 3, group C, member 2 Mus musculus 28-30 35202650-0 2022 Development of high-affinity nanobodies specific for NaV1.4 and NaV1.5 voltage-gated sodium channel isoforms. Sodium 85-91 sodium voltage-gated channel alpha subunit 5 Homo sapiens 64-70 35048187-5 2022 In addition, Slc7a5 is a transporter for the first-line anti-allodynic gabapentinoid drugs and binds to ion channels implicated in nociception and chronic pain including the voltage-gated sodium channel Nav1.7 and the voltage-gated potassium channels Kv1.1 and Kv1.2. Sodium 188-194 solute carrier family 7 member 5 Homo sapiens 13-19 35093717-1 2022 Mutations leading to haploinsufficiency in SCN5A, the gene encoding the cardiac sodium channel Nav1.5 alpha-subunit, are involved in life-threatening cardiac disorders. Sodium 80-86 sodium voltage-gated channel alpha subunit 5 Homo sapiens 43-48 35247843-2 2022 25% of BrS patients carry a mutation in the SCN5A gene, encoding the cardiac specific voltage-gated sodium channel Nav1.5. Sodium 100-106 sodium voltage-gated channel alpha subunit 5 Homo sapiens 44-49 35247843-2 2022 25% of BrS patients carry a mutation in the SCN5A gene, encoding the cardiac specific voltage-gated sodium channel Nav1.5. Sodium 100-106 sodium voltage-gated channel alpha subunit 5 Homo sapiens 115-121 35281930-0 2022 Effects of Sodium-Glucose Cotransporter 2 Inhibitors on Water and Sodium Metabolism. Sodium 66-72 solute carrier family 5 member 2 Homo sapiens 11-41 35281930-1 2022 Sodium-glucose cotransporter 2 (SGLT2) inhibitors exert hypoglycemic and diuretic effects by inhibiting the absorption of sodium and glucose from the proximal tubule. Sodium 122-128 solute carrier family 5 member 2 Homo sapiens 0-30 35281930-1 2022 Sodium-glucose cotransporter 2 (SGLT2) inhibitors exert hypoglycemic and diuretic effects by inhibiting the absorption of sodium and glucose from the proximal tubule. Sodium 122-128 solute carrier family 5 member 2 Homo sapiens 32-37 35281930-2 2022 Currently available data indicate that SGLT2 inhibitors transiently enhance urinary sodium excretion and urinary volume. Sodium 84-90 solute carrier family 5 member 2 Homo sapiens 39-44 35063775-3 2022 Type-III sodium-dependent Pi transporters, PiT-1 (encoded by SLC20A1) and PiT-2 (encoded by SLC20A2), are distributed throughout the tissues of the body, including the central nervous system, and are known to be responsible for extracellular to intracellular Pi transport. Sodium 9-15 solute carrier family 20 member 1 Homo sapiens 43-48 35063775-3 2022 Type-III sodium-dependent Pi transporters, PiT-1 (encoded by SLC20A1) and PiT-2 (encoded by SLC20A2), are distributed throughout the tissues of the body, including the central nervous system, and are known to be responsible for extracellular to intracellular Pi transport. Sodium 9-15 solute carrier family 20 member 1 Homo sapiens 61-68 35063775-3 2022 Type-III sodium-dependent Pi transporters, PiT-1 (encoded by SLC20A1) and PiT-2 (encoded by SLC20A2), are distributed throughout the tissues of the body, including the central nervous system, and are known to be responsible for extracellular to intracellular Pi transport. Sodium 9-15 solute carrier family 20 member 2 Homo sapiens 74-79 35063775-3 2022 Type-III sodium-dependent Pi transporters, PiT-1 (encoded by SLC20A1) and PiT-2 (encoded by SLC20A2), are distributed throughout the tissues of the body, including the central nervous system, and are known to be responsible for extracellular to intracellular Pi transport. Sodium 9-15 solute carrier family 20 member 2 Homo sapiens 92-99 35242892-9 2022 This might reflect a temporal increase of sodium driven phosphate reabsorption in the proximal tubule of the kidney caused by increased sodium availability in response to SGLT2 inhibition. Sodium 42-48 solute carrier family 5 member 2 Homo sapiens 171-176 35242892-9 2022 This might reflect a temporal increase of sodium driven phosphate reabsorption in the proximal tubule of the kidney caused by increased sodium availability in response to SGLT2 inhibition. Sodium 136-142 solute carrier family 5 member 2 Homo sapiens 171-176 35607336-0 2022 Takotsubo cardiomyopathy and Brugada syndrome in a patient with a novel loss-of-function variant in the cardiac sodium channel Nav1.5. Sodium 112-118 sodium voltage-gated channel alpha subunit 5 Homo sapiens 127-133 35022275-5 2022 HBV/HCV coinfection and HBx, HBV preS2, HCV Core, and HCV NS2/3 overexpression increased TGF-beta1 mRNA levels in sodium taurocholate cotransporting polypeptide-Huh7.5.1 cells compared with controls. Sodium 114-120 X protein Hepatitis B virus 24-27 35113333-6 2022 A key mechanism is tubuloglomerular feedback in which SGLT2 inhibitors cause more sodium to pass along the nephron: the sodium is sensed by macula cells which act via adenosine to constrict afferent glomerular arterioles, thereby protecting glomeruli by reducing intraglomerular pressure. Sodium 82-88 solute carrier family 5 member 2 Homo sapiens 54-59 35113333-6 2022 A key mechanism is tubuloglomerular feedback in which SGLT2 inhibitors cause more sodium to pass along the nephron: the sodium is sensed by macula cells which act via adenosine to constrict afferent glomerular arterioles, thereby protecting glomeruli by reducing intraglomerular pressure. Sodium 120-126 solute carrier family 5 member 2 Homo sapiens 54-59 2529785-10 1989 Restoration of RPP but not blockade of intrarenal ANG II resulted in a restoration of the response of sodium excretion and glomerular filtration rate to ANF. Sodium 102-108 natriuretic peptide A Canis lupus familiaris 153-156 2529778-5 1989 During the 0.01-micrograms.kg-1.min-1 infusion, the plasma concentration of ANF rose approximately threefold (from 68 +/- 7 to 207 +/- 14 pg/ml), with no change in urine flow rate, sodium excretion, or arterial pressure. Sodium 181-187 natriuretic peptide A Canis lupus familiaris 76-79 2529778-7 1989 At the highest dose of ANF (0.3 micrograms.kg-1.min-1) urine flow rose by 0.62 +/- 0.16 ml/min, P less than 0.05, and sodium excretion rose by 139 +/- 30 mu eq/min, P less than 0.05, whereas plasma levels of ANF rose to 2,436 +/- 320 pg/ml. Sodium 118-124 natriuretic peptide A Canis lupus familiaris 23-26 2608159-0 1989 Sodium and potassium uptake in primary cultures of rat astroglial cells induced by long-term exposure to the basic astroglial growth factor (AGF2). Sodium 0-6 myotrophin Rattus norvegicus 126-139 2570066-2 1989 Previous studies have shown that palytoxin, a non-(12-O-tetradecanoylphorbol-13-acetate)-type tumor promoter, is able to down-modulate the epidermal growth factor (EGF) receptor through a sodium-dependent pathway in Swiss 3T3 cells. Sodium 188-194 epidermal growth factor receptor Mus musculus 139-177 2570066-10 1989 These results suggest that sodium may act as a second messenger in the signal transduction mechanism by which palytoxin modulates the EGF receptor. Sodium 27-33 epidermal growth factor receptor Mus musculus 134-146 2528918-10 1989 The present results suggest that the ANF endocrine system may represent one chronic compensatory mechanism to achieve sodium balance in heart failure when there is concomitant normalization of the renin-aldosterone system. Sodium 118-124 natriuretic peptide A Canis lupus familiaris 37-40 2533478-4 1989 In 6 healthy dogs, while histamine 4.0 micrograms/min free base on average was being infused into a femoral vein, the infusion of ANP increased sodium excretion by 168 microEq/min, compared to 160 microEq/min when the same dose of histamine was being infused into the portal vein (portal pressure increased by 46% or 6 cm H2O). Sodium 144-150 natriuretic peptide A Canis lupus familiaris 130-133 2526402-9 1989 With these higher plasma ANF levels in overloaded animals, we observed, 2 hr after declamping, considerably improved renal function recovery in terms of glomerular filtration rate--37.5% +/- 8.7 versus 11.8 +/- 3.9%; urinary sodium excretion rate--53.89 mu eq/min versus 5.36 +/- 1.2 mu eq/min (P less than 0.01); total Na reabsorption rate--1.2 +/- 0.23 meq/min versus 0.28 +/- 0.09 meq/min (P less than 0.01) (group II vs. controls, respectively). Sodium 225-231 natriuretic peptide A Canis lupus familiaris 25-28 2525348-1 1989 To examine whether release of atrial natriuretic factor (ANF) can explain the increase in sodium excretion during supraventricular tachycardia, we compared the natriuretic responses with right atrial pacing tachycardia and ANF infusion in six barbiturate-anesthetized dogs. Sodium 90-96 natriuretic peptide A Canis lupus familiaris 30-55 2525348-1 1989 To examine whether release of atrial natriuretic factor (ANF) can explain the increase in sodium excretion during supraventricular tachycardia, we compared the natriuretic responses with right atrial pacing tachycardia and ANF infusion in six barbiturate-anesthetized dogs. Sodium 90-96 natriuretic peptide A Canis lupus familiaris 57-60 2546649-1 1989 The effects of scorpion toxin on the voltage-dependent sodium current (INa) of CA1 pyramidal neurons isolated from rat hippocampus were studied under the single-electrode voltage-clamp condition using a "concentration-clamp" technique. Sodium 55-61 internexin neuronal intermediate filament protein, alpha Rattus norvegicus 71-74 2546649-1 1989 The effects of scorpion toxin on the voltage-dependent sodium current (INa) of CA1 pyramidal neurons isolated from rat hippocampus were studied under the single-electrode voltage-clamp condition using a "concentration-clamp" technique. Sodium 55-61 carbonic anhydrase 1 Rattus norvegicus 79-82 2725018-4 1989 Intracellular pH (pHi) was changed by manipulating the bicarbonate/CO2 ratio of the incubation medium, or by adding amiloride, a hydrogen/sodium antiport blocker. Sodium 138-144 glucose-6-phosphate isomerase Rattus norvegicus 14-16 2725018-4 1989 Intracellular pH (pHi) was changed by manipulating the bicarbonate/CO2 ratio of the incubation medium, or by adding amiloride, a hydrogen/sodium antiport blocker. Sodium 138-144 glucose-6-phosphate isomerase Rattus norvegicus 18-21 2523950-3 1989 sodium load (240 mmol NaCl/fetus) on fetal ANP; the second group acted as controls. Sodium 0-6 natriuretic peptide A Bos taurus 43-46 2523950-8 1989 sodium load, fetal plasma ANP correlated significantly with fetal plasma sodium concentrations (r = 0.96; n = 12) and with fetal plasma osmolality (r = 0.94; n = 12). Sodium 73-79 natriuretic peptide A Bos taurus 26-29 2523950-10 1989 These results suggest that ANP secretion is stimulated during pregnancy in cows, and that, in the bovine fetus, a hypertonic sodium load appears to be a potent stimulus for ANP release. Sodium 125-131 natriuretic peptide A Bos taurus 173-176 3234636-3 1988 The 22Na ouabain-insensitive efflux rate constant which reflects passive sodium efflux was raised in insulin treated diabetes (0.92 [0.42-1.73] versus 0.79 [0.28-1.49] h-1, p less than 0.01). Sodium 73-79 H1.5 linker histone, cluster member Homo sapiens 168-171 2833308-3 1988 When freshly isolated alveolar type II cells were acid loaded with nigericin in sodium-free buffer, the pHi dropped to 6.59 +/- 0.04 and remained low in sodium-free buffer. Sodium 80-86 glucose-6-phosphate isomerase Rattus norvegicus 104-107 2833308-5 1988 Amiloride (0.1 mM) inhibited the sodium-induced increase in pHi. Sodium 33-39 glucose-6-phosphate isomerase Rattus norvegicus 60-63 2965517-1 1988 The hypothesis that an increase in plasma sodium concentration (PNa) causes an increase in circulating atrial natriuretic polypeptide (ANP) was examined in conscious dogs. Sodium 42-48 natriuretic peptide A Canis lupus familiaris 135-138 3034330-1 1987 Using 4,4"-diisothiocyanostilbene-2,2"-disulfonate (DIDS) and tributyltin the sodium transport pathway activated by shrinkage in dog red blood cells is shown to behave as expected for an electroneutral Na+/H+ exchanger. Sodium 78-84 solute carrier family 9 member A1 Canis lupus familiaris 202-218 3555119-0 1987 Interleukin-1 decreases renal sodium reabsorption: possible mechanism of endotoxin-induced natriuresis. Sodium 30-36 interleukin 1 alpha Homo sapiens 0-13 2953252-5 1987 Although atrial natriuretic peptide increased absolute and fractional urine flow rate and urinary sodium excretion in conscious heart-failure dogs and nephrotic rats, the responses were markedly blunted. Sodium 98-104 natriuretic peptide A Canis lupus familiaris 9-35 2952021-7 1987 It is suggested that following the initial period of sodium retention in this experimental mental model of heart failure, chronic endocrine adjustments for the reestablishment of sodium balance involve an increase in ANF which subsequently can exert a tonic inhibitory action on the renin-aldosterone axis. Sodium 179-185 natriuretic peptide A Canis lupus familiaris 217-220 2952021-8 1987 It is concluded that the ANF endocrine system might function as an effective chronic compensatory mechanism to help promote sodium and water excretion in dogs with an AV fistula through the suppression of the renin-aldosterone system and possibly through its direct renal actions. Sodium 124-130 natriuretic peptide A Canis lupus familiaris 25-28 3555912-4 1987 The inappropriate sodium retention, weight gain, and blood pressure increase following salt loading in idiopathic edema is thus associated with a blunted increase in the glomerular filtration and urinary dopamine excretion rates, as well as plasma dopamine-beta-hydroxylase non-suppressibility by saline. Sodium 18-24 dopamine beta-hydroxylase Homo sapiens 248-273 2949886-5 1986 ANP specifically reduced renal vascular resistance and increased sodium excretion. Sodium 65-71 natriuretic peptide A Canis lupus familiaris 0-3 3018411-10 1986 They also suggest a role for sodium transport and for phosphorylation-dephosphorylation mechanisms in the mode of action of ANF. Sodium 29-35 natriuretic peptide A Bos taurus 124-127 3099700-0 1986 [Hypotensive effect of a human anti-renin monoclonal antibody (4G1D8) in the sodium-depleted alert marmoset]. Sodium 77-83 renin Callithrix jacchus 36-41 2872085-5 1986 When ANF was infused directly into the renal artery of anesthetized beagles, a dose-dependent natriuresis and calciuresis were observed with maximal fractional sodium excretion averaging approximately 8%. Sodium 160-166 natriuretic peptide A Canis lupus familiaris 5-8 3082358-3 1986 Porcine proinsulin and a cross-linked derivative of bovine insulin are less effective than porcine insulin in stimulating the short-circuit current (SCC), indicating the specificity appropriate for activation of sodium transport through an insulin receptor. Sodium 212-218 insulin Bos taurus 8-18 3082358-3 1986 Porcine proinsulin and a cross-linked derivative of bovine insulin are less effective than porcine insulin in stimulating the short-circuit current (SCC), indicating the specificity appropriate for activation of sodium transport through an insulin receptor. Sodium 212-218 insulin Bos taurus 11-18 3082358-3 1986 Porcine proinsulin and a cross-linked derivative of bovine insulin are less effective than porcine insulin in stimulating the short-circuit current (SCC), indicating the specificity appropriate for activation of sodium transport through an insulin receptor. Sodium 212-218 insulin Bos taurus 59-66 3004779-0 1986 Hypothalamic beta 2-adrenoceptor control of renal sympathetic nerve activity and urinary sodium excretion in conscious, spontaneously hypertensive rats. Sodium 89-95 adrenoceptor beta 2 Rattus norvegicus 13-32 3817330-2 1986 Intravenous infusion of 1 clinical unit (CU; 82 pmol/kg/h) of secretin inhibited jejunal absorption of water, sodium and glucose compared to control period. Sodium 110-116 SCT Canis lupus familiaris 62-70 3817330-5 1986 Thus it seems that secretin inhibits the absorption of water, sodium and glucose from the jejunum of dogs and caerulein, added to secretin, reverses the effect of secretin. Sodium 62-68 SCT Canis lupus familiaris 19-27 2424780-0 1986 Histochemical demonstration of sodium-dependent glutamate uptake in brain tissues by glutamate dehydrogenase reaction. Sodium 31-37 glutamate dehydrogenase 1 Homo sapiens 85-108 2424780-3 1986 The GDH catalyzed sodium-dependent increase in formazan production is suggested to be a consequence of the sodium dependence of glutamate uptake in glutamatergic brain structures supplying the enzyme with substrate. Sodium 18-24 glutamate dehydrogenase 1 Homo sapiens 4-7 2424780-3 1986 The GDH catalyzed sodium-dependent increase in formazan production is suggested to be a consequence of the sodium dependence of glutamate uptake in glutamatergic brain structures supplying the enzyme with substrate. Sodium 107-113 glutamate dehydrogenase 1 Homo sapiens 4-7 3970646-4 1985 The Dead Sea has a uniquely high concentration of calcium, magnesium, sodium, potassium, and chloride. Sodium 70-76 S13 erythroblastosis (avian) oncogene homolog Homo sapiens 9-12 6090604-12 1984 Sag observed in response to a depolarizing current pulse is due to activation of a slow outward current, which superimposes on and partially counters the persistent sodium current. Sodium 165-171 S-antigen visual arrestin Homo sapiens 0-3 6489438-1 1984 SKF 64139, an inhibitor of phenylethanolamine-N-methyltransferase (PNMT), has a marked hypotensive effect in models of sodium-dependent hypertension. Sodium 119-125 phenylethanolamine-N-methyltransferase Rattus norvegicus 27-65 6489438-1 1984 SKF 64139, an inhibitor of phenylethanolamine-N-methyltransferase (PNMT), has a marked hypotensive effect in models of sodium-dependent hypertension. Sodium 119-125 phenylethanolamine-N-methyltransferase Rattus norvegicus 67-71 6290747-5 1982 Animal experiments (sodium depletion, sodium loading, adrenalectomy) bring about marked APA alterations in the glomeruli and in the JGA. Sodium 20-26 glutamyl aminopeptidase Rattus norvegicus 88-91 6290747-5 1982 Animal experiments (sodium depletion, sodium loading, adrenalectomy) bring about marked APA alterations in the glomeruli and in the JGA. Sodium 38-44 glutamyl aminopeptidase Rattus norvegicus 88-91 6290645-10 1982 Active sodium transport (delta k x Nac) increased in a sigmoidal and saturable way with intracellular Na+ and with extracellular K+ concentrations. Sodium 7-13 synuclein alpha Homo sapiens 35-38 6276440-1 1982 TWO SODIUM TRANSPORT SYSTEMS HAVE BEEN ANALYZED IN THIS WORK: the voltage-sensitive sodium channel and the (Na(+), K(+)) ATPase pump. Sodium 4-10 TANK binding kinase 1 Homo sapiens 107-127 6974244-0 1981 Action of caerulein, gastrin 17, pentagastrin, and secretin on the active transport of sodium by the frog skin. Sodium 87-93 gastrin Homo sapiens 21-28 6974244-1 1981 Frog skin was mounted in an Ussing chamber and the actions of caerulein, gastrin, pentagastrin, and secretin on the active transport of sodium were studied using the short-circuit current method. Sodium 136-142 gastrin Homo sapiens 73-80 20487773-3 1980 When put together, all the results seem to give sense to the hypothesis according to which the conformation of the protein controlling the sodium conductance of the axonal membrane and for which the name sodium conductin has been coined is directly related to its net phosphorylation state. Sodium 139-145 axin 2 Homo sapiens 211-220 7374952-0 1980 The mechanism of neuronal noradrenaline and dopamine beta-hydroxylase release by a sodium-deficient solution substituted with urea. Sodium 83-89 dopamine beta-hydroxylase Homo sapiens 44-69 7423122-6 1980 Sodium is currently difficult to detect at concentrations below 50 mMl-1 whereas other elements can be detected in the 2-5 mMl-1 range. Sodium 0-6 MuLV-induced myeloid leukemia 1 Mus musculus 67-72 500638-6 1979 This sodium-specific cooperative modification of the STX binding site (the hypothetical "ion selectivity filter" of the axonal Na+ gate) may be indicative of some as yet undefined regulatory mechanism of the Na+ gate in mammalian myelinated axons. Sodium 5-11 ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 2 Homo sapiens 53-56 227518-0 1979 Sodium independent GABA receptor binding in peripheral nervous tissue [proceedings]. Sodium 0-6 GABA type A receptor-associated protein Homo sapiens 19-32 204498-5 1978 As with other opiate agonists, 5--10 mM sodium selectively decreases the binding of 3H-methionine enkephalin. Sodium 40-46 proenkephalin Rattus norvegicus 98-108 605360-2 1977 Gastrin converted the normal mucosal absorption of water and sodium into a net secretion. Sodium 61-67 gastrin Homo sapiens 0-7 605360-3 1977 The colonic response to gastrin was done-related with respect to sodium, and the effects were greater when it was added to the serosal side. Sodium 65-71 gastrin Homo sapiens 24-31 605360-5 1977 At a concentration of 800pg/ml, gastrin signficantly reduced the normal movement of sodium from mucosa to serosa (absorption) but significantly increased serosal to mucosal movement (secretion). Sodium 84-90 gastrin Homo sapiens 32-39 1264237-0 1976 Letter: Evidence for two sodium sites on the external aspect of Na-K pump in human erythrocytes. Sodium 25-31 TANK binding kinase 1 Homo sapiens 64-68 1244223-4 1976 Dietary sodium depletion, a stimulus for catecholamine secretion, produced only a small increase in serum DBH activity in supine normal volunteers (26.5 +/- 10.4 to 33.9 +/- 11.4, P less than 0.05; n = 7) and in five adrenalectomized patients (33.0 +/- 12.7 to 44.1 +/- 15.2, P = 0.06). Sodium 8-14 dopamine beta-hydroxylase Homo sapiens 106-109 1148287-8 1975 Phospholipase A is known to block the sodium activation and pronase to eliminate the sodium inactivation. Sodium 38-44 phospholipase A and acyltransferase 1 Homo sapiens 0-15 1148287-8 1975 Phospholipase A is known to block the sodium activation and pronase to eliminate the sodium inactivation. Sodium 85-91 phospholipase A and acyltransferase 1 Homo sapiens 0-15 1122917-6 1975 The experiments indicated that the replacement of sodium by calcium as the ionic environment of fibrous elastin produced a configurational change towards increasing hydrophobic character. Sodium 50-56 elastin Bos taurus 104-111 5051202-0 1972 [The effect of sodium- and calcium chloride mineral water from the Spalis spring (Druskininkai health resort) on serum pseudocholinesterase activity and the protein-synthesizing function of the liver in experimental acute toxic hepatitis]. Sodium 15-21 butyrylcholinesterase Homo sapiens 119-139 4652490-0 1972 [The reliability of the simultaneous determination of sodium, potassium and chloride in serum with the automatic analyser C 4 (Perkin Elmer)]. Sodium 54-60 complement C4A (Rodgers blood group) Homo sapiens 122-125 5783010-6 1969 The relation between membrane potential and dV/dt of the spike was steepened by oxytocin, suggesting that oxytocin increased the number of normally sparse sodium gates in the myometrial membrane. Sodium 155-161 oxytocin Oryctolagus cuniculus 80-88 5783010-6 1969 The relation between membrane potential and dV/dt of the spike was steepened by oxytocin, suggesting that oxytocin increased the number of normally sparse sodium gates in the myometrial membrane. Sodium 155-161 oxytocin Oryctolagus cuniculus 106-114 5689153-0 1968 Effect of a synthetic gastrin-like pentapeptide upon the intestinal transport of sodium, potassium, and water. Sodium 81-87 gastrin Homo sapiens 22-29 5912660-0 1966 Potassium, sodium, and chlorides in gastrin-stimulated gastric secretion in man. Sodium 11-17 gastrin Homo sapiens 36-43 13729732-0 1961 Sodium dependence of intermedin action on melanophores in tissue culture. Sodium 0-6 adrenomedullin 2 Homo sapiens 21-31 14480163-0 1961 [Modification of the enzymatic activity of amylase, phosphatase and cholinesterase under the influence of hypnotic and sedative drugs (sodium bromide, luminal sodium, chloral hydrate, urethane and sodium amytal)]. Sodium 135-141 butyrylcholinesterase Homo sapiens 68-82 21993890-2 2012 In rats, the AQP2 expression varies with sodium intake. Sodium 41-47 aquaporin 2 Rattus norvegicus 13-17 13584585-0 1958 [Sodium & potassium in myocardial & skeletal muscular tissue in experimental infection of mice by Coxsackie viruses (strains B1, B3, B4, B5)]. Sodium 1-7 B.burgdorferi-associated arthritis 5 Mus musculus 133-147 21993890-3 2012 In humans, the effect of sodium intake on u-AQP2 and the underlying mechanisms have not previously been studied. Sodium 25-31 aquaporin 2 Homo sapiens 44-48 22084095-6 2012 Furthermore, the SP signaling could alter action potential thresholds and modulate the expression of TTX-resistant sodium currents in medium-sized muscle nociceptors. Sodium 115-121 tachykinin 1 Mus musculus 17-19 13525672-7 1958 The inhibition of sodium extrusion by physostigmine was correlated with the inhibition of the intracellular cholinesterase. Sodium 18-24 butyrylcholinesterase Homo sapiens 108-122 13087227-0 1953 Effect of cholinesterase inhibitors and atropine on active sodium transport across frog skin. Sodium 59-65 butyrylcholinesterase Homo sapiens 10-24 34045310-2 2021 We have previously shown that the epithelial sodium channel ENaC/UNC-8 triggers an activity-dependent mechanism that drives the removal of presynaptic proteins liprin-alpha/SYD-2, Synaptobrevin/SNB-1, RAB-3 and Endophilin/UNC-57 in remodeling GABAergic neurons in C. elegans (Miller-Fleming et al., 2016). Sodium 45-51 Degenerin unc-8 Caenorhabditis elegans 65-70 34045310-2 2021 We have previously shown that the epithelial sodium channel ENaC/UNC-8 triggers an activity-dependent mechanism that drives the removal of presynaptic proteins liprin-alpha/SYD-2, Synaptobrevin/SNB-1, RAB-3 and Endophilin/UNC-57 in remodeling GABAergic neurons in C. elegans (Miller-Fleming et al., 2016). Sodium 45-51 Liprin-alpha Caenorhabditis elegans 160-172 34045310-2 2021 We have previously shown that the epithelial sodium channel ENaC/UNC-8 triggers an activity-dependent mechanism that drives the removal of presynaptic proteins liprin-alpha/SYD-2, Synaptobrevin/SNB-1, RAB-3 and Endophilin/UNC-57 in remodeling GABAergic neurons in C. elegans (Miller-Fleming et al., 2016). Sodium 45-51 Liprin-alpha Caenorhabditis elegans 173-178 34045310-2 2021 We have previously shown that the epithelial sodium channel ENaC/UNC-8 triggers an activity-dependent mechanism that drives the removal of presynaptic proteins liprin-alpha/SYD-2, Synaptobrevin/SNB-1, RAB-3 and Endophilin/UNC-57 in remodeling GABAergic neurons in C. elegans (Miller-Fleming et al., 2016). Sodium 45-51 Endophilin-A homolog Caenorhabditis elegans 222-228 34044026-2 2021 The goal of the pilot project was to create evidence-based guidelines for use of sodium-glucose transport protein 2 inhibitors (SGLT2-I) when managing very high risk T2D patients, evidenced by the presence of both CVD and CKD. Sodium 81-87 solute carrier family 5 member 2 Homo sapiens 128-133 33951626-1 2021 The sodium-dependent phosphate transporter, SLC20A1, is required for elevated inorganic phosphate (Pi) induced vascular smooth muscle cell (VSMC) matrix mineralization and phenotype transdifferentiation. Sodium 4-10 solute carrier family 20 member 1 Homo sapiens 44-51 32453275-0 2021 TAS2R38 Haplotype Predicts 24-Hour Urinary Sodium Excretion in Patients With Heart Failure and Their Family Caregivers. Sodium 43-49 taste 2 receptor member 38 Homo sapiens 0-7 32453275-3 2021 OBJECTIVE: Our purpose was to examine if TAS2R38 haplotype predicted salt taste sensitivity and dietary sodium intake among patients with HF. Sodium 104-110 taste 2 receptor member 38 Homo sapiens 41-48 33951591-1 2021 The SCN5A gene, located on chromosome 3p21, has 28 exons and is a member of the human voltage-gated sodium channel gene family. Sodium 100-106 sodium voltage-gated channel alpha subunit 5 Homo sapiens 4-9 33895391-0 2021 Mutations in the sodium channel genes SCN1A, SCN3A, and SCN9A in children with epilepsy with febrile seizures plus(EFS+). Sodium 17-23 sodium voltage-gated channel alpha subunit 3 Homo sapiens 45-50 33895391-5 2021 RESULTS: We identified 10 putatively causative sodium channel gene variants in 49 patients with EFS+, including 8 variants in SCN1A (R500Q appeared twice), one in SCN3A and one in SCN9A. Sodium 47-53 sodium voltage-gated channel alpha subunit 3 Homo sapiens 163-168 20430871-7 2010 Inhibition of the sodium/hydrogen exchanger 3 (NHE3) had an additive effect to AICAR, suggesting that the AMPK effect is not via NHE3. Sodium 18-24 protein kinase AMP-activated catalytic subunit alpha 2 Homo sapiens 106-110 19955850-1 2010 BACKGROUND/AIMS: Aldosterone and the mineralocorticoid receptor (MR) play a major role in sodium balance and blood pressure control. Sodium 90-96 nuclear receptor subfamily 3 group C member 2 Homo sapiens 37-63 19955850-1 2010 BACKGROUND/AIMS: Aldosterone and the mineralocorticoid receptor (MR) play a major role in sodium balance and blood pressure control. Sodium 90-96 nuclear receptor subfamily 3 group C member 2 Homo sapiens 65-67 20125035-7 2010 RESULTS: SNPs rs2282623 and rs746886 of the APLNR gene were significantly associated with DBP (both P = 0.002) and mean arterial pressure (MAP) (P = 0.001 and 0.005, respectively) responses to low-sodium intervention. Sodium 197-203 apelin receptor Homo sapiens 44-49 20125035-8 2010 Six SNPs of the ACE2 gene were significantly associated with SBP, DBP, or MAP responses to low-sodium intervention. Sodium 95-101 angiotensin converting enzyme 2 Homo sapiens 16-20 20125035-8 2010 Six SNPs of the ACE2 gene were significantly associated with SBP, DBP, or MAP responses to low-sodium intervention. Sodium 95-101 selenium binding protein 1 Homo sapiens 61-64 20125035-10 2010 Haplotype analysis indicated the A-T-T haplotype of APLNR SNPs rs721608-rs2282623-rs746886 was associated with decreased DBP and MAP responses to low-sodium intervention (P = 0.001 and 0.003, respectively), whereas G-C-C was associated with increased SBP and MAP responses to high-sodium intervention (P = 0.004 and 0.01, respectively). Sodium 150-156 apelin receptor Homo sapiens 52-57 20125035-10 2010 Haplotype analysis indicated the A-T-T haplotype of APLNR SNPs rs721608-rs2282623-rs746886 was associated with decreased DBP and MAP responses to low-sodium intervention (P = 0.001 and 0.003, respectively), whereas G-C-C was associated with increased SBP and MAP responses to high-sodium intervention (P = 0.004 and 0.01, respectively). Sodium 150-156 selenium binding protein 1 Homo sapiens 251-254 20125035-10 2010 Haplotype analysis indicated the A-T-T haplotype of APLNR SNPs rs721608-rs2282623-rs746886 was associated with decreased DBP and MAP responses to low-sodium intervention (P = 0.001 and 0.003, respectively), whereas G-C-C was associated with increased SBP and MAP responses to high-sodium intervention (P = 0.004 and 0.01, respectively). Sodium 281-287 apelin receptor Homo sapiens 52-57 20125035-10 2010 Haplotype analysis indicated the A-T-T haplotype of APLNR SNPs rs721608-rs2282623-rs746886 was associated with decreased DBP and MAP responses to low-sodium intervention (P = 0.001 and 0.003, respectively), whereas G-C-C was associated with increased SBP and MAP responses to high-sodium intervention (P = 0.004 and 0.01, respectively). Sodium 281-287 selenium binding protein 1 Homo sapiens 251-254 20125035-11 2010 CONCLUSION: This large family-based study indicates that genetic variants in the APLNR and ACE2 genes are significantly associated with BP responses to dietary sodium intervention. Sodium 160-166 apelin receptor Homo sapiens 81-86 20125035-11 2010 CONCLUSION: This large family-based study indicates that genetic variants in the APLNR and ACE2 genes are significantly associated with BP responses to dietary sodium intervention. Sodium 160-166 angiotensin converting enzyme 2 Homo sapiens 91-95 20036246-0 2010 Modulation of canine cardiac sodium current by Apelin. Sodium 29-35 apelin Canis lupus familiaris 47-53 20036246-5 2010 We tested the effects of apelin on the cardiac sodium current (I(Na)) using patch clamp technique on cardiac myocytes acutely dissociated from dog ventricle. Sodium 47-53 apelin Canis lupus familiaris 25-31 20036246-8 2010 The effects of apelin on I(Na) amplitude were linked to activation of protein kinase C. Apelin also increased I(Na) "window" current by up to 600% suggesting that changes in intracellular sodium may contribute to the apelin inotropic effects. Sodium 188-194 apelin Canis lupus familiaris 15-21 20036246-8 2010 The effects of apelin on I(Na) amplitude were linked to activation of protein kinase C. Apelin also increased I(Na) "window" current by up to 600% suggesting that changes in intracellular sodium may contribute to the apelin inotropic effects. Sodium 188-194 apelin Canis lupus familiaris 88-94 20583536-1 2010 Aldosterone plays an important role in blood pressure homeostasis, the regulation of circulating volume, and the maintenance of the sodium-potassium balance by binding to the mineralocorticoid receptor (MR). Sodium 132-138 nuclear receptor subfamily 3 group C member 2 Homo sapiens 175-201 20583536-1 2010 Aldosterone plays an important role in blood pressure homeostasis, the regulation of circulating volume, and the maintenance of the sodium-potassium balance by binding to the mineralocorticoid receptor (MR). Sodium 132-138 nuclear receptor subfamily 3 group C member 2 Homo sapiens 203-205 19962419-0 2010 Sodium permeability and sensitivity induced by mutations in the selectivity filter of the KcsA channel towards Kir channels. Sodium 0-6 killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 4 Homo sapiens 111-114 19944461-0 2010 SLP-2 negatively modulates mitochondrial sodium-calcium exchange. Sodium 41-47 synaptotagmin like 2 Homo sapiens 0-5 20447295-3 2010 Ranolazine appears to produce its anti-angina effect through blocking the late sodium current associated with the voltage-gated sodium channel, Na(v) 1.5. Sodium 79-85 sodium voltage-gated channel alpha subunit 5 Rattus norvegicus 144-153 19776173-9 2009 We conclude that GLP-1 receptor agonists modulate sodium homeostasis in the kidney, most likely by affecting NHE3 activity. Sodium 50-56 glucagon like peptide 1 receptor Homo sapiens 17-31 19567370-9 2009 We conclude that CNKSR3, a homologue of scaffold proteins involved in MAPK pathway regulation, is a direct target of MR and is required for the maintenance of transepithelial sodium transport in the kidney. Sodium 175-181 nuclear receptor subfamily 3 group C member 2 Homo sapiens 117-119 19406178-1 2009 Ouabain is a cardiotonic glycoside that inhibits the sodium potassium ATPase pump leading to sodium accumulation in nerve terminals. Sodium 53-59 dynein axonemal heavy chain 8 Homo sapiens 70-76 19664597-7 2009 NPC2 might regulate sodium reabsorption in the terminal nephron by interacting with ENaC-Nedd4L system. Sodium 20-26 NPC intracellular cholesterol transporter 2 Homo sapiens 0-4 21918182-2 2012 Compromise of ET-1 signaling or ETB receptors in the CD cause sodium retention and increase blood pressure. Sodium 62-68 endothelin 1 Mus musculus 14-18 33731449-2 2021 This process is supported by a diverse complement of sodium, potassium, and calcium channels (CaV). Sodium 53-59 caveolin 1, caveolae protein Mus musculus 94-97 33899737-4 2021 We demonstrated that the essential factor controlling the diversity of the discharge pattern of embryonic V1R is the ratio of a persistent sodium conductance to a delayed rectifier potassium conductance. Sodium 139-145 vomeronasal 1 receptor 51 Mus musculus 106-109 21918182-2 2012 Compromise of ET-1 signaling or ETB receptors in the CD cause sodium retention and increase blood pressure. Sodium 62-68 endothelin receptor type B Mus musculus 32-35 21964404-6 2012 Here, we demonstrate that bupivacaine and quinidine, blockers of four-transmembrane domain, two-pore potassium (K2P) channels, inhibit both amiloride-sensitive sodium absorption and forskolin-stimulated anion secretion in polarized, normal human bronchial epithelial cells at lower concentrations when applied to the mucosal surface than when applied to the serosal surface. Sodium 160-166 keratin 76 Homo sapiens 112-115 33965302-1 2021 Skeletal muscle sodium channelopathies due to SCN4A gene mutations have a broad clinical spectrum. Sodium 16-22 sodium voltage-gated channel alpha subunit 4 Homo sapiens 46-51 33854040-0 2021 The ubiquitin ligase NEDD4-2/NEDD4L regulates both sodium homeostasis and fibrotic signaling to prevent end-stage renal disease. Sodium 51-57 neural precursor cell expressed, developmentally down-regulated gene 4-like Mus musculus 21-28 33854040-0 2021 The ubiquitin ligase NEDD4-2/NEDD4L regulates both sodium homeostasis and fibrotic signaling to prevent end-stage renal disease. Sodium 51-57 neural precursor cell expressed, developmentally down-regulated gene 4-like Mus musculus 29-35 33864813-13 2021 The increased urine excretion of glucose and sodium was mediated by decreased renal SGLT2 expression due to inactivation of the IKKalpha/beta/NF-kappaB-induced inflammatory response. Sodium 45-51 conserved helix-loop-helix ubiquitous kinase Mus musculus 128-141 22366772-5 2012 The ability to transport ingested vitamin C from the intestines into blood is limited by the saturable sodium-dependent vitamin C transporter (SVCT1) and thus very high intakes and the use of supplements are often erroneously considered to be of greater benefit that they really are. Sodium 103-109 solute carrier family 23 member 1 Homo sapiens 143-148 33928121-6 2021 In addition, comparative substrate profiles of two related sodium neutral amino acid transporters known as SNAT1 and SNAT2, revealed the latter as a significant leucine accumulator. Sodium 59-65 solute carrier family 38 member 1 Homo sapiens 107-112 33921209-8 2021 GLP-1 and gastrin decrease the expression of Na+-K+/ATPase and increase the phosphorylation of sodium/hydrogen exchanger type 3 (NHE3) in human renal proximal tubule cells (hRPTCs). Sodium 95-101 gastrin Homo sapiens 10-17 33826405-2 2021 In non-excitable epithelial cells of the kidney tubule, for example, Kir1.1 (KCNJ1) and Kir4.1 (KCNJ10) are linked to sodium reabsorption in the thick ascending limb of Henle"s loop and distal convoluted tubule, respectively, and have been explored as novel-mechanism diuretic targets for managing hypertension and edema. Sodium 118-124 potassium inwardly rectifying channel subfamily J member 10 Homo sapiens 88-94 33826405-2 2021 In non-excitable epithelial cells of the kidney tubule, for example, Kir1.1 (KCNJ1) and Kir4.1 (KCNJ10) are linked to sodium reabsorption in the thick ascending limb of Henle"s loop and distal convoluted tubule, respectively, and have been explored as novel-mechanism diuretic targets for managing hypertension and edema. Sodium 118-124 potassium inwardly rectifying channel subfamily J member 10 Homo sapiens 96-102 23594971-1 2012 Epithelial sodium channels (ENaC) are ion transporters in the aldosterone-sensitive distal nephron that play an important role in sodium reabsorption in the terminal nephron. Sodium 11-17 sodium channel, nonvoltage-gated 1 alpha Mus musculus 28-32 33828490-0 2021 A Heart Failure-Associated SCN5A Splice Variant Leads to a Reduction in Sodium Current Through Coupled-Gating With the Wild-Type Channel. Sodium 72-78 sodium voltage-gated channel alpha subunit 5 Homo sapiens 27-32 33828490-1 2021 Nav1.5, encoded by the gene SCN5A, is the predominant voltage-gated sodium channel expressed in the heart. Sodium 68-74 sodium voltage-gated channel alpha subunit 5 Homo sapiens 0-6 33828490-1 2021 Nav1.5, encoded by the gene SCN5A, is the predominant voltage-gated sodium channel expressed in the heart. Sodium 68-74 sodium voltage-gated channel alpha subunit 5 Homo sapiens 28-33 33828490-6 2021 It was previously reported that reduction in cardiac sodium currents (INa), observed in HF, could be due to the increased expression of an SCN5A splice variant - E28D, which results in a truncated sodium channel (Nav1.5-G1642X). Sodium 53-59 sodium voltage-gated channel alpha subunit 5 Homo sapiens 139-144 33828490-6 2021 It was previously reported that reduction in cardiac sodium currents (INa), observed in HF, could be due to the increased expression of an SCN5A splice variant - E28D, which results in a truncated sodium channel (Nav1.5-G1642X). Sodium 53-59 sodium voltage-gated channel alpha subunit 5 Homo sapiens 213-219 33730389-9 2021 In the peripheral nervous system, we revealed that the TLR4/NF-kappaB signaling pathway induced upregulation of voltage-gated sodium channel 1.7 (Nav1.7) in DRGs, triggering peripheral hyperalgesia in SMIR-induced CPSP. Sodium 126-132 sodium voltage-gated channel alpha subunit 9 Rattus norvegicus 146-152 33712541-9 2021 The structural analysis presented here, with a focus on the impact of mutations on inactivation and late sodium current, establishes a structure-function relationship for the mechanistic understanding of Nav1.5 channelopathies. Sodium 105-111 sodium voltage-gated channel alpha subunit 5 Homo sapiens 204-210 33712547-0 2021 Comparative structural analysis of human Nav1.1 and Nav1.5 reveals mutational hotspots for sodium channelopathies. Sodium 91-97 sodium voltage-gated channel alpha subunit 5 Homo sapiens 52-58 33712547-1 2021 Among the nine subtypes of human voltage-gated sodium (Nav) channels, the brain and cardiac isoforms, Nav1.1 and Nav1.5, each carry more than 400 missense mutations respectively associated with epilepsy and cardiac disorders. Sodium 47-53 sodium voltage-gated channel alpha subunit 5 Homo sapiens 113-119 33486984-3 2021 Here, we investigate whether NPR-C regulates Ang II (angiotensin II)-induced hypertension through sodium transporters activity. Sodium 98-104 natriuretic peptide receptor 3 Mus musculus 29-34 33486984-11 2021 These results demonstrate that NPR-C signaling regulates NCC function contributing to sodium retention-mediated elevated blood pressure, which suggests that NPR-C is a promising candidate for the treatment of sodium retention-related hypertension. Sodium 86-92 natriuretic peptide receptor 3 Mus musculus 31-36 33486984-11 2021 These results demonstrate that NPR-C signaling regulates NCC function contributing to sodium retention-mediated elevated blood pressure, which suggests that NPR-C is a promising candidate for the treatment of sodium retention-related hypertension. Sodium 86-92 natriuretic peptide receptor 3 Mus musculus 157-162 33486984-11 2021 These results demonstrate that NPR-C signaling regulates NCC function contributing to sodium retention-mediated elevated blood pressure, which suggests that NPR-C is a promising candidate for the treatment of sodium retention-related hypertension. Sodium 209-215 natriuretic peptide receptor 3 Mus musculus 31-36 33486984-11 2021 These results demonstrate that NPR-C signaling regulates NCC function contributing to sodium retention-mediated elevated blood pressure, which suggests that NPR-C is a promising candidate for the treatment of sodium retention-related hypertension. Sodium 209-215 natriuretic peptide receptor 3 Mus musculus 157-162 33651170-7 2021 Genetic analysis of the proband, his father, and his younger brother revealed a missense mutation, D1275N, in SCN5A, a gene which encodes sodium ion channel protein, are related to cardiomyopathy and arrhythmia. Sodium 138-144 sodium voltage-gated channel alpha subunit 5 Homo sapiens 110-115 33533125-3 2021 An eco-friendly and biodegradable sodium-ion secondary battery (SIB) is developed through extensive material screening followed by the synthesis of biodegradable electrodes and their seamless assembly with an unconventional biodegradable separator, electrolyte, and package. Sodium 34-40 ciliogenesis associated kinase 1 Homo sapiens 3-6 33633824-1 2021 Background: The urinary sodium potassium (NaK) ratio is associated with dietary sodium and potassium intake and blood pressure, and it also reflects the activity of aldosterone. Sodium 24-30 TANK binding kinase 1 Homo sapiens 42-45 32721227-1 2021 AIM: Sodium-glucose co-transporter 2 inhibitors (SGLT2is) provide renal protection in patients with type 2 diabetes mellitus (T2DM). Sodium 5-11 solute carrier family 5 member 2 Homo sapiens 49-54 33356113-3 2021 This method involves immersing the graphene in solutions of [K(15-crown-5)2]Na prepared by dissolving a sodium-potassium (NaK) alloy in a 15-crown-5 solution. Sodium 104-110 TANK binding kinase 1 Homo sapiens 122-125 33488393-3 2020 Our previous work identified adenoviral gene transfer of Hcn2 and SkM1, encoding a "funny current" and skeletal fast sodium current, respectively, as a potent combination to induce short-term biological pacing in dogs with atrioventricular block. Sodium 117-123 sodium voltage-gated channel alpha subunit 4 Homo sapiens 66-70 33095056-0 2021 Dietary sodium restriction sex specifically impairs endothelial function via mineralocorticoid receptor-dependent reduction in NO bioavailability in Balb/C mice. Sodium 8-14 nuclear receptor subfamily 3, group C, member 2 Mus musculus 77-103 33095056-12 2021 Utilizing sodium restriction as a method to increase plasma aldosterone levels in healthy female mice, we demonstrated that female mice are more susceptible to vascular damage via MR activation in the vascular endothelium only.NEW & NOTEWORTHY Female sex confers improved endothelial relaxation and vascular constriction responses in female Balb/C mice compared with males under baseline conditions. Sodium 10-16 nuclear receptor subfamily 3, group C, member 2 Mus musculus 180-182 33095056-14 2021 Mineralocorticoid receptor antagonism ablates sodium restriction-induced endothelial dysfunction, but not increased vascular contractility, in female mice. Sodium 46-52 nuclear receptor subfamily 3, group C, member 2 Mus musculus 0-26 33065235-1 2021 We previously showed that increased epithelial sodium channel (ENaC) activity in endothelial cells induced by oxidized low-density lipoprotein (ox-LDL) contributes to vasculature dysfunction. Sodium 47-53 sodium channel, nonvoltage-gated 1 alpha Mus musculus 63-67 33127751-11 2021 Significance Statement Activation of G protein-coupled estrogen receptor1 (GPER1) in the renal medulla of female rats evokes natriuresis via endothelin receptors A and/or B, suggesting that GPER1 and endothelin signaling pathways help efficient sodium excretion in females. Sodium 245-251 G protein-coupled estrogen receptor 1 Rattus norvegicus 37-73 33127751-11 2021 Significance Statement Activation of G protein-coupled estrogen receptor1 (GPER1) in the renal medulla of female rats evokes natriuresis via endothelin receptors A and/or B, suggesting that GPER1 and endothelin signaling pathways help efficient sodium excretion in females. Sodium 245-251 G protein-coupled estrogen receptor 1 Rattus norvegicus 75-80 33127751-11 2021 Significance Statement Activation of G protein-coupled estrogen receptor1 (GPER1) in the renal medulla of female rats evokes natriuresis via endothelin receptors A and/or B, suggesting that GPER1 and endothelin signaling pathways help efficient sodium excretion in females. Sodium 245-251 G protein-coupled estrogen receptor 1 Rattus norvegicus 190-195 32726130-1 2020 We investigated voltage-gated sodium channel (NaV1) subunits that regulate action potential initiation in the nerve terminals of vagal nodose C-fibers innervating the esophagus. Sodium 30-36 neuron navigator 1 Cavia porcellus 46-50 33098508-4 2020 Cotransfection with wild-type Rac1 resulted in a minor decrease in sodium current. Sodium 67-73 ras-related C3 botulinum toxin substrate 1 Cricetulus griseus 30-34 32828039-3 2020 Moreover autoimmune axonal neuropathies due to nodal voltage gated sodium channels dysfunction/disruption may show slowing of conduction velocity, even in the demyelinating range, possibly due to prolongation of the depolarization time required to reach the threshold for action potential regeneration at subsequent nodes. Sodium 67-73 nodal growth differentiation factor Homo sapiens 47-52 33134290-0 2020 An SCN1B Variant Affects Both Cardiac-Type (NaV1.5) and Brain-Type (NaV1.1) Sodium Currents and Contributes to Complex Concomitant Brain and Cardiac Disorders. Sodium 76-82 sodium voltage-gated channel alpha subunit 5 Homo sapiens 44-50 33134290-6 2020 We observed a decrease in sodium current density in cells co-expressing NaV1.5 or NaV1.1 and beta1D103V compared to beta1WT. Sodium 26-32 sodium voltage-gated channel alpha subunit 5 Homo sapiens 72-78 33013490-2 2020 ERp29 regulates the biosynthesis and trafficking of several transmembrane and secretory proteins, including the cystic fibrosis transmembrane conductance regulator (CFTR), the epithelial sodium channel (ENaC), thyroglobulin, connexin 43 hemichannels, and proinsulin. Sodium 187-193 endoplasmic reticulum protein 29 Homo sapiens 0-5 32673289-4 2020 Three new, inducible murine models were used to determine that HDAC1 and HDAC2 in the kidney epithelium are necessary for maintaining epithelial integrity and maintaining fluid-electrolyte balance during increased dietary sodium intake. Sodium 222-228 histone deacetylase 1 Mus musculus 63-68 32673289-5 2020 Moreover, single nucleus RNA sequencing determined that epithelial HDAC1 and HDAC2 are necessary for expression of many sodium or water transporters and channels. Sodium 120-126 histone deacetylase 1 Mus musculus 67-72 32631918-5 2020 Scnn1b-Tg mice overexpress the epithelial Na+ channel (ENaC) in their lungs, driving increased sodium absorption that causes lung pathology similar to CF. Sodium 95-101 sodium channel, nonvoltage-gated 1 alpha Mus musculus 31-53 32631918-5 2020 Scnn1b-Tg mice overexpress the epithelial Na+ channel (ENaC) in their lungs, driving increased sodium absorption that causes lung pathology similar to CF. Sodium 95-101 sodium channel, nonvoltage-gated 1 alpha Mus musculus 55-59 31743556-1 2020 Manipulating the level of expression of SOS1, a protein which regulates the movement and distribution of sodium ions, has been shown to enhance the salinity tolerance of a number of plant species, but its involvement in the response to hypoxia is less well established. Sodium 105-111 sodium proton exchanger, putative (NHX7) (SOS1) Arabidopsis thaliana 40-44 32775992-0 2020 In Reply to "Do SGLT-2 Inhibitors Act Only Through a Functional Tubuloglomerular Feedback Induced by the Increased Outflow of Sodium?" Sodium 126-132 solute carrier family 5 member 2 Homo sapiens 16-22 32715162-10 2020 Perhaps the strongest evidence linking LAT1 to pain is its interactions with key voltage-gated ion channels connected to nociception, namely the voltage-gated potassium channels Kv1.1 and Kv1.2 and the voltage-gated sodium channel Nav1.7. Sodium 216-222 solute carrier family 7 member 5 Homo sapiens 39-43 32164457-11 2020 SGLT2 inhibitors reverse this maladaptive signaling by triggering a state of fasting and hypoxia mimicry, which includes activation of SIRT1, AMPK and HIF-2alpha, enhanced autophagic flux, reduced cellular stress, decreased sodium influx into cells, and restoration of mitochondrial homeostasis. Sodium 224-230 solute carrier family 5 member 2 Homo sapiens 0-5 32569262-5 2020 We demonstrate this methodology using a well-established disease-gene pair, the cardiac sodium channel gene SCN5A and the heart arrhythmia Brugada syndrome. Sodium 88-94 sodium voltage-gated channel alpha subunit 5 Homo sapiens 108-113 32802705-6 2020 The proposed mechanisms for the renoprotective effects of SGLT2 inhibitors include the action of tubulo-glomerular feedback system and attenuation of hypoxia and metabolic stress in proximal tubular cells mediated through the inhibition of excessive glucose and sodium reabsorption, increased erythropoiesis, or increased ketone body production. Sodium 262-268 solute carrier family 5 member 2 Homo sapiens 58-63 31916329-0 2020 Interplay of AMPK/SIRT1 Activation and Sodium Influx Inhibition Mediates the Renal Benefits of SGLT2 Inhibitors in Type 2 Diabetes: a Novel Conceptual Framework. Sodium 39-45 solute carrier family 5 member 2 Homo sapiens 95-100 31916329-5 2020 Instead, the reduction in intraglomerular pressures may be related to an action of SGLT2 inhibitors to interfere with the activity of sodium-hydrogen exchanger isoform 3 (NHE-3), thereby inhibiting proximal tubular sodium reabsorption and promoting tubuloglomerular feedback. Sodium 134-140 solute carrier family 5 member 2 Homo sapiens 83-88 31916329-10 2020 Enhanced AMPK/SIRT1 signaling may also contribute to the action of SGLT2 inhibitors to interfere with sodium transport mechanisms. Sodium 102-108 solute carrier family 5 member 2 Homo sapiens 67-72 31916329-11 2020 The dual effects of SGLT2 inhibitors on AMPK/SIRT1 activation and renal tubular sodium transport may explain their protective effects on the kidney in type 2 diabetes. Sodium 80-86 solute carrier family 5 member 2 Homo sapiens 20-25 32154868-2 2020 Dietary sodium can upregulate mTORC1 signaling in cardiac and renal tissue, and inhibition of mTOR can prevent aldosterone associated, salt-induced hypertension. Sodium 8-14 mechanistic target of rapamycin kinase Mus musculus 30-34 31904424-2 2020 In the heart, the protein CASK (Calcium/CAlmodulin-dependent Serine protein Kinase) negatively regulates the main cardiac sodium channel, NaV1.5, which carries the sodium current (INa) by preventing its anterograde trafficking. Sodium 164-170 sodium voltage-gated channel alpha subunit 5 Homo sapiens 138-144 31420581-10 2020 Sodium to potassium ratio was positively associated with SBP (P10-P50, P80) and DBP (P70-P90) in males, and was positively associated with SBP(P10-P70, P90) in females. Sodium 0-6 coiled-coil domain containing 8 Homo sapiens 89-92 31420581-10 2020 Sodium to potassium ratio was positively associated with SBP (P10-P50, P80) and DBP (P70-P90) in males, and was positively associated with SBP(P10-P70, P90) in females. Sodium 0-6 coiled-coil domain containing 8 Homo sapiens 152-155 32006563-9 2020 Compared with the I/R group, the number of Iba1-positive microglia in the SAM/NaHS groups significantly decreased. Sodium 78-82 allograft inflammatory factor 1 Homo sapiens 43-47 32006563-10 2020 Co-Immunoprecipitation and immunoblotting were conducted to demonstrate that SAM/NaHS suppressed the assembly of CaMKII with the ASK1-MKK3-p38 signal module after cerebral I/R, which decreased the phosphorylation of p38. Sodium 81-85 mitogen-activated protein kinase kinase kinase 5 Homo sapiens 129-133 32006563-12 2020 Taken together, the results suggested that SAM/NaHS could suppress cerebral I/R injury by downregulating p38 phosphorylation via decreasing the assembly of CaMKII with the ASK1-MKK3-p38 signal module. Sodium 47-51 mitogen-activated protein kinase kinase kinase 5 Homo sapiens 172-176 32276507-0 2020 Changes of Resurgent Na+ Currents in the Nav1.4 Channel Resulting from an SCN4A Mutation Contributing to Sodium Channel Myotonia. Sodium 105-111 sodium voltage-gated channel alpha subunit 4 Homo sapiens 41-47 32276507-0 2020 Changes of Resurgent Na+ Currents in the Nav1.4 Channel Resulting from an SCN4A Mutation Contributing to Sodium Channel Myotonia. Sodium 105-111 sodium voltage-gated channel alpha subunit 4 Homo sapiens 74-79 32276507-2 2020 Mutations in the SCN4A gene encoding the alpha-subunit of the voltage-gated sodium channel Nav1.4 have been reported to be responsible for sodium channel myotonia (SCM). Sodium 76-82 sodium voltage-gated channel alpha subunit 4 Homo sapiens 17-22 32276507-2 2020 Mutations in the SCN4A gene encoding the alpha-subunit of the voltage-gated sodium channel Nav1.4 have been reported to be responsible for sodium channel myotonia (SCM). Sodium 76-82 sodium voltage-gated channel alpha subunit 4 Homo sapiens 91-97 32276507-2 2020 Mutations in the SCN4A gene encoding the alpha-subunit of the voltage-gated sodium channel Nav1.4 have been reported to be responsible for sodium channel myotonia (SCM). Sodium 139-145 sodium voltage-gated channel alpha subunit 4 Homo sapiens 17-22 32276507-2 2020 Mutations in the SCN4A gene encoding the alpha-subunit of the voltage-gated sodium channel Nav1.4 have been reported to be responsible for sodium channel myotonia (SCM). Sodium 139-145 sodium voltage-gated channel alpha subunit 4 Homo sapiens 91-97 32208832-4 2020 High K+ intake stimulated ENaC in the late DCT/early connecting tubule (DCT2/CNT) and in the CCD whereas low sodium intake stimulated ENaC in the CCD but not in the DCT2/CNT. Sodium 109-115 sodium channel, nonvoltage-gated 1 alpha Mus musculus 134-138 32208832-5 2020 The deletion of MR abolished the stimulatory effect of high K+ and low sodium intake on ENaC, partially inhibited ENaC in DCT2/CNT but almost abolished ENaC activity in the CCD. Sodium 71-77 sodium channel, nonvoltage-gated 1 alpha Mus musculus 88-92 31918016-13 2020 CONCLUSIONS: NaFTV and QrLx treatment could decrease symptoms and inflammatory colitis, by decreasing of FICZ concentration and AhR signaling in colon, resulting in reducing the expression of IL-6, STAT3, and RORgammat, whereas increasing the expression of FOXP3, consequently reducing the proportion of Th17 cells and increasing the proportion of Treg cells, respectively. Sodium 13-18 forkhead box P3 Mus musculus 257-262 31972307-2 2020 We found that miR-574-5p and HIF-1alpha were up-regulated in gastric cancer cells cultured under 2% O2 or in medium containing CoCl2, and in muscle tissues of mice injected with NaNO2, indicating up-regulation of miR-574-5p in vitro or in vivo in response to hypoxic conditions. Sodium 178-183 hypoxia inducible factor 1, alpha subunit Mus musculus 29-39 32260115-2 2020 In both the kidney and tongue, the epithelial sodium channel (ENaC) is involved in sodium uptake and sensing. Sodium 46-52 sodium channel, nonvoltage-gated 1 alpha Mus musculus 62-66 32260115-2 2020 In both the kidney and tongue, the epithelial sodium channel (ENaC) is involved in sodium uptake and sensing. Sodium 83-89 sodium channel, nonvoltage-gated 1 alpha Mus musculus 62-66 31753654-4 2020 Sodium borohydride (NaBH4) was used to completely remove the PVP ligands from the surface of AgNWs and produce a clean AgNWs-AgNWs interface that effectively enhances the localized surface plasmon resonance (i.e., LSPR) was produced, greatly improving the SERS activity of the AgNWs thin film. Sodium 20-25 seryl-tRNA synthetase 1 Homo sapiens 256-260 31789848-2 2020 Recent studies from mice, rats and humans have shown that the sodium retention depends on urinary serine proteases and that it can be mitigated by blockers (amiloride, triamterene) of the epithelial sodium channel ENaC. Sodium 62-68 sodium channel, nonvoltage-gated 1 alpha Mus musculus 214-218 31789848-2 2020 Recent studies from mice, rats and humans have shown that the sodium retention depends on urinary serine proteases and that it can be mitigated by blockers (amiloride, triamterene) of the epithelial sodium channel ENaC. Sodium 199-205 sodium channel, nonvoltage-gated 1 alpha Mus musculus 214-218 31789848-9 2020 Experimental and clinical evidence indicate that aberrant proteolytic ENaC activation is a primary driver of sodium retention in nephrotic syndrome and contributes to hypertension in conditions with low-grade proteinuria. Sodium 109-115 sodium channel, nonvoltage-gated 1 alpha Mus musculus 70-74 31950564-0 2020 Supramolecular clustering of the cardiac sodium channel Nav1.5 in HEK293F cells, with and without the auxiliary beta3-subunit. Sodium 41-47 sodium voltage-gated channel alpha subunit 5 Homo sapiens 56-62 31950564-2 2020 The beta3-subunit (encoded by the SCN3B gene) is an important physiological regulator of the heart-specific sodium channel, Nav1.5. Sodium 108-114 sodium voltage-gated channel alpha subunit 5 Homo sapiens 124-130 31830809-4 2020 Here, we compared the rescue effects of an adeno-associated viral (AAV) vector coding for the multi-functional beta1 sodium channel auxiliary subunit (AAV- NaVbeta1) with a control vector lacking a transgene. Sodium 117-123 hemoglobin, beta adult major chain Mus musculus 111-116 19585586-1 2009 The neuronal voltage-gated sodium channel Na(v)1.1 encoded by the SCN1A gene plays an important role in the generation and propagation of action potentials in the central nervous system. Sodium 27-33 sodium voltage-gated channel alpha subunit 1 Homo sapiens 66-71 19593630-5 2009 There is evidence that the nociceptive (and sympathetic) axons die because nerve growth factor is not being produced by the target tissues; patients with congenital insensitivity to pain have mutations in the NTRK1 gene, the gene responsible for producing the TrkA receptor, but there is also evidence for mutations in the SCN9A gene, which codes for a specific subunit of the voltage-gated sodium channel. Sodium 391-397 neurotrophic receptor tyrosine kinase 1 Homo sapiens 209-214 19593630-5 2009 There is evidence that the nociceptive (and sympathetic) axons die because nerve growth factor is not being produced by the target tissues; patients with congenital insensitivity to pain have mutations in the NTRK1 gene, the gene responsible for producing the TrkA receptor, but there is also evidence for mutations in the SCN9A gene, which codes for a specific subunit of the voltage-gated sodium channel. Sodium 391-397 neurotrophic receptor tyrosine kinase 1 Homo sapiens 260-264 19609280-0 2009 Variations in the WNK1 gene modulates the effect of dietary intake of sodium and potassium on blood pressure determination. Sodium 70-76 WNK lysine deficient protein kinase 1 Homo sapiens 18-22 19609280-5 2009 In addition, we investigated the interactions between the haplotypes of the WNK1 gene and dietary sodium and potassium intake for determining inter-individual variations in blood pressure. Sodium 98-104 WNK lysine deficient protein kinase 1 Homo sapiens 76-80 19609280-6 2009 Our data support the hypothesis that part of the variation in blood pressure response to dietary sodium and potassium intake among individuals can be explained by variations in the WNK1 gene. Sodium 97-103 WNK lysine deficient protein kinase 1 Homo sapiens 181-185 19617444-1 2009 The mineralocorticoid receptor (MR) is a member of the nuclear receptor superfamily and is essential for controlling sodium transport in epithelial tissues such as the kidney and colon. Sodium 117-123 nuclear receptor subfamily 3 group C member 2 Homo sapiens 4-30 19617444-1 2009 The mineralocorticoid receptor (MR) is a member of the nuclear receptor superfamily and is essential for controlling sodium transport in epithelial tissues such as the kidney and colon. Sodium 117-123 nuclear receptor subfamily 3 group C member 2 Homo sapiens 32-34 19487301-3 2009 RESULTS: Of the 4 single nucleotide polymorphisms (SNPs) on the sodium bicarbonate cotransporter gene (SLC4A5), rs8179526 had a statistically significant interaction with cytosine/thymine (C/T) genotype by sodium status on systolic BP (SBP; p=.0077). Sodium 64-70 selenium binding protein 1 Homo sapiens 236-239 19487301-6 2009 DISCUSSION: A gene x environmental interaction with rs8179526 has a protective effect on SBP in African-American women with high sodium intake. Sodium 129-135 selenium binding protein 1 Homo sapiens 89-92 19487301-7 2009 Participants with C/T genotype of rs8179526 who consumed greater than 2,300 mg of sodium had lower SBP than those who consumed less than recommended. Sodium 82-88 selenium binding protein 1 Homo sapiens 99-102 19400878-1 2009 OBJECTIVE: We aimed to determine the type, frequency, and size of microchromosomal copy number variations (CNVs) affecting the neuronal sodium channel alpha 1 subunit gene (SCN1A) in Dravet syndrome (DS), other epileptic encephalopathies, and generalized epilepsy with febrile seizures plus (GEFS+). Sodium 136-142 sodium voltage-gated channel alpha subunit 1 Homo sapiens 173-178 19525971-2 2009 Here we show that the N-terminal core domains of increased sodium tolerance-1 (IST1) and charged multivesicular body protein-3 (CHMP3) form equivalent four-helix bundles, revealing that IST1 is a previously unrecognized ESCRT-III family member. Sodium 59-65 IST1 factor associated with ESCRT-III Homo sapiens 79-83 19525971-2 2009 Here we show that the N-terminal core domains of increased sodium tolerance-1 (IST1) and charged multivesicular body protein-3 (CHMP3) form equivalent four-helix bundles, revealing that IST1 is a previously unrecognized ESCRT-III family member. Sodium 59-65 IST1 factor associated with ESCRT-III Homo sapiens 186-190 20031595-7 2009 Coexpression of SCN5A/WT+SCN1B/WT+SCN3B/L10P resulted in an 82.6% decrease in peak sodium current density, accelerated inactivation, slowed reactivation, and a -9.6-mV shift of half-inactivation voltage compared with SCN5A/WT+SCN1B/WT+SCN3B/WT. Sodium 83-89 sodium voltage-gated channel beta subunit 1 Homo sapiens 25-30 20031595-7 2009 Coexpression of SCN5A/WT+SCN1B/WT+SCN3B/L10P resulted in an 82.6% decrease in peak sodium current density, accelerated inactivation, slowed reactivation, and a -9.6-mV shift of half-inactivation voltage compared with SCN5A/WT+SCN1B/WT+SCN3B/WT. Sodium 83-89 sodium voltage-gated channel beta subunit 3 Homo sapiens 34-39 19328786-6 2009 These results show a clear-cut involvement of the DRN 5-HT(1A) somatodendritic autoreceptors in sodium satiety signaling under basal conditions and during the consummatory phase of salt intake in sodium-depleted rats. Sodium 96-102 5-hydroxytryptamine receptor 1A Rattus norvegicus 54-61 19328786-6 2009 These results show a clear-cut involvement of the DRN 5-HT(1A) somatodendritic autoreceptors in sodium satiety signaling under basal conditions and during the consummatory phase of salt intake in sodium-depleted rats. Sodium 196-202 5-hydroxytryptamine receptor 1A Rattus norvegicus 54-61 19390537-1 2009 Secretory-type Na-K-2Cl cotransporter (NKCC1) is known to play roles in both acid and sodium excretion, and is more abundant in dehydration. Sodium 86-92 solute carrier family 12 member 2 Rattus norvegicus 39-44 19221003-6 2009 Sodium challenge was followed by a sustained reduction of all three genes examined (Cyp11b2, 20 min, -63+/-6%) which was accompanied by a significant suppression of aldosterone secretion detectable after 60 min. Sodium 0-6 cytochrome P450, family 11, subfamily b, polypeptide 2 Mus musculus 84-91 19196948-4 2009 Phosphate absorption across the brush-border membrane (BBM) of enterocytes occurs mainly via a sodium-dependent pathway, which is mediated by type IIb sodium-phosphate cotransporters (NaPi-IIb). Sodium 95-101 solute carrier family 34 member 2 Homo sapiens 184-192 19152822-3 2009 NARs for protein, sugar, vitamin A, vitamin C, and sodium exceeded one and cholesterol NAR was less than one. Sodium 51-57 asparaginyl-tRNA synthetase 1 Homo sapiens 0-4 19262497-2 2009 Gene expression of prostasin was shown to be regulated by aldosterone, which increases the rate of sodium reabsorption through ENaC. Sodium 99-105 serine protease 8 Homo sapiens 19-28 19136557-11 2009 These results demonstrate that a variant of NaV1.6 participates in the control of podosome and invadopodia formation and suggest that intracellular sodium release mediated by NaV1.6 may regulate cellular invasion of macrophages and melanoma cells. Sodium 148-154 neuron navigator 1 Homo sapiens 44-48 19136557-11 2009 These results demonstrate that a variant of NaV1.6 participates in the control of podosome and invadopodia formation and suggest that intracellular sodium release mediated by NaV1.6 may regulate cellular invasion of macrophages and melanoma cells. Sodium 148-154 neuron navigator 1 Homo sapiens 175-179 23594971-2 2012 Our study of inbred C57Bl6/J mice given a high-sodium diet showed increased ENaC expression accompanied by tubular renin activation on qRT-PCR of laser-captured tubule specimens and Western blotting of membrane proteins, despite inhibition of aldosterone. Sodium 47-53 sodium channel, nonvoltage-gated 1 alpha Mus musculus 76-80 23594971-5 2012 These effects would act to suppress sodium reabsorption via ENaC and normalize molecular mechanisms that elevate blood pressure in response to increased salt intake. Sodium 36-42 sodium channel, nonvoltage-gated 1 alpha Mus musculus 60-64 22005676-4 2011 Using a whole cell patch-clamp technique, this effect on Na(V)1.7 gene expression coincided with a reduction in tetrodotoxin-sensitive sodium current, a requirement for much larger depolarizing stimulus to initiate action potentials, and reduction in repetitive action potential discharge. Sodium 135-141 neuron navigator 1 Cavia porcellus 57-63 20959142-8 2011 A role for EGF in the regulation of ENaC-mediated sodium absorption has been proposed. Sodium 50-56 epidermal growth factor Homo sapiens 11-14 19171180-7 2009 Depletion of pro-NGF isoforms from CM produced a similar effect as the exerted by k252a, TrkA and p75(NTR) receptor inhibitors in CM-treated cells, inducing the elicitation of sodium currents. Sodium 176-182 nerve growth factor receptor Rattus norvegicus 98-115 19171180-9 2009 The difference between the results obtained with the generic inhibitor for Trk receptors and the specific inhibitors for TrkA and p75(NTR) receptors in CM-treated cells, suggested that alternative pathways could be used to regulate neurite elongation, axon specification and sodium currents in PC12 cells. Sodium 275-281 nerve growth factor receptor Rattus norvegicus 130-148 19185582-1 2009 BACKGROUND & AIMS: Hartnup amino acid transporter B(0)AT1 (SLC6A19) is the major luminal sodium-dependent neutral amino acid transporter of small intestine and kidney proximal tubule. Sodium 89-95 solute carrier family 6 member 19 Homo sapiens 50-57 19185582-1 2009 BACKGROUND & AIMS: Hartnup amino acid transporter B(0)AT1 (SLC6A19) is the major luminal sodium-dependent neutral amino acid transporter of small intestine and kidney proximal tubule. Sodium 89-95 solute carrier family 6 member 19 Homo sapiens 59-66 32075761-0 2020 Hypoxia Produces Pro-arrhythmic Late Sodium Current in Cardiac Myocytes by SUMOylation of NaV1.5 Channels. Sodium 37-43 sodium voltage-gated channel alpha subunit 5 Homo sapiens 90-96 32085432-0 2020 Biophysical Characterization of Epigallocatechin-3-Gallate Effect on the Cardiac Sodium Channel Nav1.5. Sodium 81-87 sodium voltage-gated channel alpha subunit 5 Homo sapiens 96-102 20959142-9 2011 However, several investigations have reported contradictory results indicating opposite effects of EGF and its related factors on ENaC activity and sodium transport. Sodium 148-154 epidermal growth factor Homo sapiens 99-102 31522065-6 2020 However, it was noted that, at pHs 4 and 5, the sodium present in the buffer solution interfered with the adsorption, leading to lower adsorption capacities compared to the capacity at pH 3. Sodium 48-54 prolyl 4-hydroxylase, transmembrane Homo sapiens 31-42 20959142-10 2011 Recent advances in understanding how proteins in the EGF family regulate the proliferation and sodium transport in normal and PKD epithelial cells are discussed here. Sodium 95-101 epidermal growth factor Homo sapiens 53-56 18930999-1 2009 INTRODUCTION: Mutations in the voltage-gated sodium channel SCN1A gene are the main genetic cause of Dravet syndrome (previously called severe myoclonic epilepsy of infancy or SMEI). Sodium 45-51 sodium voltage-gated channel alpha subunit 1 Homo sapiens 60-65 21697242-1 2011 Sodium reabsorption via the epithelial Na(+) channel (ENaC) in the aldosterone-sensitive distal nephron plays a central role in the regulation of body fluid volume. Sodium 0-6 sodium channel, nonvoltage-gated 1 alpha Mus musculus 28-52 19129479-1 2009 The newly described yeast endosomal sorting complexes required for transport (ESCRT) protein increased sodium tolerance-1 (Ist1p) binds the late-acting ESCRT proteins Did2p/charged MVB protein (CHMP) 1 and Vps4p and exhibits synthetic vacuolar protein sorting defects when combined with mutations in the Vta1p/LIP5-Vps60p/CHMP5 complex. Sodium 103-109 putative lipoate synthase Saccharomyces cerevisiae S288C 310-314 31833504-3 2020 Carbonylation of 1 (CO, 1 atm) gives [RuCl(CNNOMe)(CO)(PPh3)] (4) (79% yield) which cleanly reacts with Na[BArf4] and PCy3, affording the cationic trans-[Ru(CNNOMe)(CO)(PCy3)(PPh3)][BArf4] (5) (92% yield). Sodium 104-113 protein phosphatase 4 catalytic subunit Homo sapiens 55-59 31833504-3 2020 Carbonylation of 1 (CO, 1 atm) gives [RuCl(CNNOMe)(CO)(PPh3)] (4) (79% yield) which cleanly reacts with Na[BArf4] and PCy3, affording the cationic trans-[Ru(CNNOMe)(CO)(PCy3)(PPh3)][BArf4] (5) (92% yield). Sodium 104-113 protein phosphatase 4 catalytic subunit Homo sapiens 175-179 21697242-1 2011 Sodium reabsorption via the epithelial Na(+) channel (ENaC) in the aldosterone-sensitive distal nephron plays a central role in the regulation of body fluid volume. Sodium 0-6 sodium channel, nonvoltage-gated 1 alpha Mus musculus 54-58 21697242-8 2011 Inhibition of cytochrome P-450 (CYP450) with MS-PPOH activated ENaC-mediated sodium transport when cells were pretreated with AA and diclofenac. Sodium 77-83 cytochrome P450, family 21, subfamily a, polypeptide 1 Mus musculus 14-30 19129479-1 2009 The newly described yeast endosomal sorting complexes required for transport (ESCRT) protein increased sodium tolerance-1 (Ist1p) binds the late-acting ESCRT proteins Did2p/charged MVB protein (CHMP) 1 and Vps4p and exhibits synthetic vacuolar protein sorting defects when combined with mutations in the Vta1p/LIP5-Vps60p/CHMP5 complex. Sodium 103-109 Vps60p Saccharomyces cerevisiae S288C 315-321 31754830-0 2020 The functional association between the sodium/bicarbonate cotransporter (NBC) and the soluble adenylyl cyclase (sAC) modulates cardiac contractility. Sodium 39-45 adenylate cyclase 10 Rattus norvegicus 86-110 21697242-8 2011 Inhibition of cytochrome P-450 (CYP450) with MS-PPOH activated ENaC-mediated sodium transport when cells were pretreated with AA and diclofenac. Sodium 77-83 cytochrome P450, family 21, subfamily a, polypeptide 1 Mus musculus 32-38 31754830-0 2020 The functional association between the sodium/bicarbonate cotransporter (NBC) and the soluble adenylyl cyclase (sAC) modulates cardiac contractility. Sodium 39-45 adenylate cyclase 10 Rattus norvegicus 112-115 21697242-8 2011 Inhibition of cytochrome P-450 (CYP450) with MS-PPOH activated ENaC-mediated sodium transport when cells were pretreated with AA and diclofenac. Sodium 77-83 sodium channel, nonvoltage-gated 1 alpha Mus musculus 63-67 21697807-10 2011 Thus, PKCalpha and PKCbetaII, GSK3alpha and GSK3beta, and cAMP-dependent signaling pathways may have important roles in regulating proximal tubular sodium and fluid transport in Ang II-induced hypertensive rats. Sodium 148-154 phospholipase C, beta 2 Rattus norvegicus 19-28 21451595-2 2011 Previous findings have suggested that single-nucleotide polymorphisms of the cytoskeletal protein, alpha-adducin, are associated with increased membrane expression of the Na/K pump and abnormal renal sodium transport in Milan hypertensive strain (MHS) rats and in humans. Sodium 200-206 adducin 1 Rattus norvegicus 99-112 21621375-0 2011 A novel nonsense variant in Nav1.5 cofactor MOG1 eliminates its sodium current increasing effect and may increase the risk of arrhythmias. Sodium 64-70 sodium voltage-gated channel alpha subunit 5 Homo sapiens 28-34 21621375-2 2011 Overexpression of MOG1 in Nav1.5-expressing cells increases sodium current markedly. Sodium 60-66 sodium voltage-gated channel alpha subunit 5 Homo sapiens 26-32 21536988-6 2011 Chronic urocortin 2 also persistently augmented urinary sodium (day 4: 4-fold increase; P<0.001) and creatinine (1.4-fold; P<0.001) excretion and creatinine clearance (1.5-fold; P<0.01) compared with control. Sodium 56-62 urocortin-2 Ovis aries 8-19 21546577-1 2011 The putative transcription factor AF17 upregulates the transcription of the epithelial sodium channel (ENaC) genes, but whether AF17 modulates sodium homeostasis and BP is unknown. Sodium 87-93 sodium channel, nonvoltage-gated 1 alpha Mus musculus 103-107 21052805-10 2011 Fast rebound bursts due to T-type calcium current and slow rebounds due to persistent sodium current could be differentially regulated by synaptic input, and the pattern of these rebounds was further influenced by HCN current. Sodium 86-92 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 214-217 21549091-0 2011 Salt-inducible kinase 1 is present in lung alveolar epithelial cells and regulates active sodium transport. Sodium 90-96 salt inducible kinase 1 Mus musculus 0-23 21549091-1 2011 Salt-inducible kinase 1 (SIK1) in epithelial cells mediates the increases in active sodium transport (Na(+), K(+)-ATPase-mediated) in response to elevations in the intracellular concentration of sodium. Sodium 84-90 salt inducible kinase 1 Mus musculus 0-23 21549091-1 2011 Salt-inducible kinase 1 (SIK1) in epithelial cells mediates the increases in active sodium transport (Na(+), K(+)-ATPase-mediated) in response to elevations in the intracellular concentration of sodium. Sodium 84-90 salt inducible kinase 1 Mus musculus 25-29 21624334-3 2011 The epithelial sodium channel (ENaC) is a key pathway for sodium transport in epithelia, vascular endothelium, and other tissues; although the expressions of alpha and gamma ENaC mRNA were found in osteoblasts, the regulation of ENaC by estrogen in osteoblasts has not been studied. Sodium 15-21 sodium channel, nonvoltage-gated 1 alpha Mus musculus 31-35 21624334-3 2011 The epithelial sodium channel (ENaC) is a key pathway for sodium transport in epithelia, vascular endothelium, and other tissues; although the expressions of alpha and gamma ENaC mRNA were found in osteoblasts, the regulation of ENaC by estrogen in osteoblasts has not been studied. Sodium 15-21 sodium channel, nonvoltage-gated 1 alpha Mus musculus 174-178 21624334-3 2011 The epithelial sodium channel (ENaC) is a key pathway for sodium transport in epithelia, vascular endothelium, and other tissues; although the expressions of alpha and gamma ENaC mRNA were found in osteoblasts, the regulation of ENaC by estrogen in osteoblasts has not been studied. Sodium 15-21 sodium channel, nonvoltage-gated 1 alpha Mus musculus 174-178 21593315-2 2011 One of the major players in the regulation of intracellular Ca(2+) ([Ca(2+)](i)) homeostasis in neurons is the sodium/calcium exchanger (NCX), which represents the principal mechanism of Ca(2+) clearance in the synaptic sites of hippocampal neurons. Sodium 111-117 T cell leukemia, homeobox 2 Mus musculus 137-140 21572961-4 2011 Following complete Freund"s adjuvant (CFA) inflammation treatment, Na(V)1.8 and Na(V)1.9 in rat dorsal root ganglion (DRG) up-regulated mRNA and protein expressions and increased sodium current densities. Sodium 179-185 neuron navigator 1 Rattus norvegicus 67-73 21178974-2 2011 In a mouse cortical collecting duct cell line (mCCD(c11)), physiological concentrations of arginine vasopressin increased both electrogenic, amiloride-sensitive, epithelial sodium channel (ENaC)-mediated sodium transport measured by the short-circuit current (Isc) method and water flow (Jv apical to basal) measured by gravimetry with similar activation coefficient K(1/2) (6 and 12 pM, respectively). Sodium 173-179 polymerase (RNA) III (DNA directed) polypeptide K Mus musculus 52-55 21178974-2 2011 In a mouse cortical collecting duct cell line (mCCD(c11)), physiological concentrations of arginine vasopressin increased both electrogenic, amiloride-sensitive, epithelial sodium channel (ENaC)-mediated sodium transport measured by the short-circuit current (Isc) method and water flow (Jv apical to basal) measured by gravimetry with similar activation coefficient K(1/2) (6 and 12 pM, respectively). Sodium 173-179 sodium channel, nonvoltage-gated 1 alpha Mus musculus 189-193 21178974-7 2011 Around 30% of baseline and 50% of vasopressin-induced water flow is coupled to an amiloride-sensitive, ENaC-mediated, electrogenic sodium transport, whereas the remaining flow is coupled to an amiloride-insensitive, nonelectrogenic sodium transport mediated by an unknown electroneutral transporter. Sodium 131-137 sodium channel, nonvoltage-gated 1 alpha Mus musculus 103-107 21383102-1 2011 To investigate the role of the mineralocorticoid receptor (MR) in renal ENaC-mediated sodium reabsorption, we have previously used the Cre-loxP system to generate mice with principal-cell specific MR ablation (MR(AQP2Cre) mice). Sodium 86-92 nuclear receptor subfamily 3, group C, member 2 Mus musculus 59-61 21383102-7 2011 Under a low-salt diet, the induced ablation of MR at the adult stage recapitulates the renal sodium wasting observed in mice with constitutive early-onset MR ablation. Sodium 93-99 nuclear receptor subfamily 3, group C, member 2 Mus musculus 47-49 21383102-8 2011 The AQP2CreER(T2) transgene is a new tool for investigating in vivo the function of genes downstream of MR in renal ENaC-mediated sodium reabsorption by inducible somatic gene inactivation. Sodium 130-136 aquaporin 2 Mus musculus 4-8 21383102-8 2011 The AQP2CreER(T2) transgene is a new tool for investigating in vivo the function of genes downstream of MR in renal ENaC-mediated sodium reabsorption by inducible somatic gene inactivation. Sodium 130-136 nuclear receptor subfamily 3, group C, member 2 Mus musculus 104-106 21115638-0 2011 Nav1.7 mutations associated with paroxysmal extreme pain disorder, but not erythromelalgia, enhance Navbeta4 peptide-mediated resurgent sodium currents. Sodium 136-142 sodium voltage-gated channel beta subunit 4 Homo sapiens 100-108 31659116-0 2019 Gating control of the cardiac sodium channel Nav1.5 by its beta3-subunit involves distinct roles for a transmembrane glutamic acid and the extracellular domain. Sodium 30-36 sodium voltage-gated channel alpha subunit 5 Homo sapiens 45-51 31659116-0 2019 Gating control of the cardiac sodium channel Nav1.5 by its beta3-subunit involves distinct roles for a transmembrane glutamic acid and the extracellular domain. Sodium 30-36 basic helix-loop-helix family member e22 Homo sapiens 59-64 31659116-1 2019 The auxiliary beta3-subunit is an important functional regulator of the cardiac sodium channel Nav1.5, and some beta3 mutations predispose individuals to cardiac arrhythmias. Sodium 80-86 basic helix-loop-helix family member e22 Homo sapiens 14-19 31659116-1 2019 The auxiliary beta3-subunit is an important functional regulator of the cardiac sodium channel Nav1.5, and some beta3 mutations predispose individuals to cardiac arrhythmias. Sodium 80-86 sodium voltage-gated channel alpha subunit 5 Homo sapiens 95-101 31861522-8 2019 Using a PCR-based assay to evaluate mtDNA damage, we demonstrate that overexpression of hTERT in MRC-5 fibroblasts protects mtDNA from H2O2 and NaAsO2 induced damage, compared with their isogenic telomerase-negative counterparts. Sodium 144-150 telomerase reverse transcriptase Homo sapiens 88-93 31933626-6 2019 Using Western blot studies and high-resolution confocal microscopy in the prefrontal frontal cortex (PFC), our data indicate disrupted expression of different isoforms of the voltage-gated sodium channels (NaV) at the AIS, whereas other components of AIS such as ankyrin-G and fibroblast growth factor 14 (FGF14) and contactin-associated protein 1 (Caspr) in BTBR were comparable to those in wild-type control mice. Sodium 189-195 ankyrin 3, epithelial Mus musculus 263-272 31844077-3 2019 It was clarified that the high transmutation rate of about 8%/year was achieved, if the new LLFP target assemblies of 4 nuclides were loaded in the blanket region of the sodium cooled, MOX fueled fast reactor. Sodium 170-176 monooxygenase DBH like 1 Homo sapiens 185-188 18632234-2 2009 The gene encoding voltage-gated sodium channel alpha1-subunit: SCN1A analysis revealed a heterozygous de novo one-point mutation (IVS16+2 T>C) at a splice-acceptor site. Sodium 32-38 sodium voltage-gated channel alpha subunit 1 Homo sapiens 63-68 19133747-1 2009 BACKGROUND: Several plasma membrane transporters have been shown to mediate the cellular influx and/or efflux of iodothyronines, including the sodium-independent organic anion co-transporting polypeptide 1 (OATP1), the sodium taurocholate co-transporting polypeptide (NTCP), the L-type amino acid transporter 1 (LAT1) and 2 (LAT2), and the monocarboxylate transporter 8 (MCT8). Sodium 143-149 solute carrier family 16 (monocarboxylic acid transporters), member 2 Mus musculus 371-375 18795889-1 2009 COMMD {COMM [copper metabolism Murr1 (mouse U2af1-rs1 region 1)] domain-containing} proteins participate in several cellular processes, ranging from NF-kappaB (nuclear factor kappaB) regulation, copper homoeostasis, sodium transport and adaptation to hypoxia. Sodium 216-222 COMM domain containing 1 Mus musculus 31-36 18795889-1 2009 COMMD {COMM [copper metabolism Murr1 (mouse U2af1-rs1 region 1)] domain-containing} proteins participate in several cellular processes, ranging from NF-kappaB (nuclear factor kappaB) regulation, copper homoeostasis, sodium transport and adaptation to hypoxia. Sodium 216-222 COMM domain containing 1 Mus musculus 44-62 18849360-1 2009 We have uncovered a significant allosteric response of the D(2) dopamine receptor to physiologically relevant concentrations of sodium (140 mM), characterized by a sodium-enhanced binding affinity for a D(4)-selective class of agonists and antagonists. Sodium 128-134 dopamine receptor D2 Homo sapiens 59-81 18849360-1 2009 We have uncovered a significant allosteric response of the D(2) dopamine receptor to physiologically relevant concentrations of sodium (140 mM), characterized by a sodium-enhanced binding affinity for a D(4)-selective class of agonists and antagonists. Sodium 164-170 dopamine receptor D2 Homo sapiens 59-81 18849360-8 2009 Our findings demonstrate how key interactions can be modulated by occupancy at an allosteric site and are consistent with a mechanism in which sodium binding enhances the affinity of selected ligands through dynamic changes that increase accessibility of substituted benzamides and 1,4-DAP ligands to the orthosteric site and accessibility of 1,4-DAPs to V2.61(91)F. Sodium 143-149 death associated protein Homo sapiens 286-289 18802429-0 2008 Abnormal glucose metabolism in hypertensive mice with genetically interrupted gamma-melanocyte stimulating hormone signaling fed a high-sodium diet. Sodium 136-142 pro-opiomelanocortin-alpha Mus musculus 78-114 18753266-5 2008 Activation of endogenous ANG II production by sodium depletion (10 days low-sodium diet followed by furosemide, 1 mg sc) enhanced NaCl intake in NSE-AT(1A) mice compared with wild types. Sodium 46-52 enolase 2, gamma neuronal Mus musculus 145-148 18753266-6 2008 Fos immunohistochemistry, used to assess neuronal activation, demonstrated sodium depletion-enhanced activity in the anteroventral third ventricle region of the brain in NSE-AT(1A) mice compared with control animals. Sodium 75-81 enolase 2, gamma neuronal Mus musculus 170-173 22076132-4 2011 All three CA isoforms increased transport activity of NBCe1, as measured by the transport current and the rate of intracellular sodium rise in oocytes. Sodium 128-134 solute carrier family 4 member 4 L homeolog Xenopus laevis 54-59 21931830-5 2011 AtHKT1;1-dependent currents were carried by sodium ions and these currents were not observed in athkt1;1 mutant stelar cells. Sodium 44-50 high-affinity K+ transporter 1 Arabidopsis thaliana 0-6 21887217-9 2011 CONCLUSIONS: The present study shows that sodium coupled bicarbonate influx regulates intracellular and apical pH in cultured caput epididymal epithelium. Sodium 42-48 glucose-6-phosphate isomerase Rattus norvegicus 111-113 18794864-0 2008 A sodium-mediated structural switch that controls the sensitivity of Kir channels to PtdIns(4,5)P(2). Sodium 2-8 killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 4 Homo sapiens 69-72 18794864-3 2008 Using an interactive computational-experimental approach, we show that sodium sensitivity of Kir channels involves the side chains of an aspartate and a histidine located across from each other in a crucial loop in the cytosolic domain, as well as the backbone carbonyls of two more residues and a water molecule. Sodium 71-77 killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 4 Homo sapiens 93-96 31741437-4 2019 A simple model that unifies the immediate and long-term effects of SGLT2 inhibitors on kidney function is based on the assumption that diabetic hyperfiltration puts the kidney at long-term risk and evidence that hyperfiltration is an immediate response to a reduced signal for tubuloglomerular feedback, which occurs to the extent that SGLT2 activity mediates a primary increase in sodium and fluid reabsorption by the proximal tubule. Sodium 382-388 solute carrier family 5 member 2 Homo sapiens 67-72 31825310-4 2019 TCAs activate both TPC1 and TPC2 in a voltage-dependent manner, referred to as Lysosomal Na+ channel Voltage-dependent Activators (LyNa-VAs). Sodium 131-135 two pore segment channel 2 Homo sapiens 28-32 20817005-7 2010 Anomalies in the behaviour and biochemistry of BACE(-/-) mice have pointed to the role this enzyme plays in the processing of neuregulin and of voltage-gated sodium channel beta-subunit. Sodium 158-164 beta-site APP cleaving enzyme 1 Mus musculus 47-51 20947633-3 2010 To investigate the relative importance of ENaC-mediated sodium absorption in the CNT, we used Cre-lox technology to generate mice lacking alphaENaC in the aquaporin 2-expressing CNT and CD. Sodium 56-62 sodium channel, nonvoltage-gated 1 alpha Mus musculus 42-46 18365245-2 2008 Oocytes expressing the human (h) sodium-dicarboxylate cotransporter (NaDC3) showed sodium-dependent inward currents mediated by GA, 3OHGA, L: -, and D: -2OHGA. Sodium 33-39 solute carrier family 13 member 3 Homo sapiens 69-74 18586672-0 2008 NF-kappaB inhibits sodium transport via down-regulation of SGK1 in renal collecting duct principal cells. Sodium 19-25 serum/glucocorticoid regulated kinase 1 Rattus norvegicus 59-63 18784102-2 2008 Data from animal models suggest that sodium-hydrogen exchanger regulatory factor 1 (NHERF1) controls renal phosphate transport. Sodium 37-43 SLC9A3 regulator 1 Homo sapiens 84-90 18479393-1 2008 PURPOSE: Genetic abnormalities of the gene encoding alpha1 subunit of the sodium channel (SCN1A), which can be detected by direct sequencing, are present in more than 60% of patients with severe myoclonic epilepsy in infancy (SMEI) or its borderline phenotype (SMEB). Sodium 74-80 sodium voltage-gated channel alpha subunit 1 Homo sapiens 90-95 18591664-7 2008 A390V-SNTA1 expressed with SCN5A, nNOS, and PMCA4b in heterologous cells increased peak and late sodium current compared with WT-SNTA1, and the increase was partially inhibited by NOS blockers. Sodium 97-103 nitric oxide synthase 1 Homo sapiens 34-38 18591664-7 2008 A390V-SNTA1 expressed with SCN5A, nNOS, and PMCA4b in heterologous cells increased peak and late sodium current compared with WT-SNTA1, and the increase was partially inhibited by NOS blockers. Sodium 97-103 ATPase plasma membrane Ca2+ transporting 4 Homo sapiens 44-50 18591664-9 2008 We conclude that the A390V mutation disrupted binding with PMCA4b, released inhibition of nNOS, caused S-nitrosylation of SCN5A, and was associated with increased late sodium current, which is the characteristic biophysical dysfunction for sodium-channel-mediated LQTS (LQT3). Sodium 168-174 ATPase plasma membrane Ca2+ transporting 4 Homo sapiens 59-65 18591664-9 2008 We conclude that the A390V mutation disrupted binding with PMCA4b, released inhibition of nNOS, caused S-nitrosylation of SCN5A, and was associated with increased late sodium current, which is the characteristic biophysical dysfunction for sodium-channel-mediated LQTS (LQT3). Sodium 168-174 nitric oxide synthase 1 Homo sapiens 90-94 18591664-10 2008 These results establish an SNTA1-based nNOS complex attached to SCN5A as a key regulator of sodium current and suggest that SNTA1 be considered a rare LQTS-susceptibility gene. Sodium 92-98 nitric oxide synthase 1 Homo sapiens 39-43 20618077-1 2010 The sodium channel isoform Na(v)1.5 mediates sodium current, excitability, and electrical conduction in the human heart. Sodium 4-10 immunoglobulin lambda variable 2-18 Homo sapiens 27-35 20685870-6 2010 In response to 1 wk sodium restriction, VIP and NPY fibers elongated in parallel with expansion of the ZG, shown by aldosterone synthase (AS) expression, but calcitonin gene-related peptide fibers were not affected. Sodium 20-26 cytochrome P450, family 11, subfamily b, polypeptide 1 Rattus norvegicus 116-136 20495177-1 2010 Renal cytochrome P450 (CYP)-derived epoxyeicosatrienoic acids (EETs) regulate sodium transport and blood pressure. Sodium 78-84 cytochrome P450, family 21, subfamily a, polypeptide 1 Mus musculus 6-21 18957817-2 2008 Selective renal reduction of AT1R expression by intrarenal cortical infusion of antisense oligodeoxynucleotides (As-Odns) in conscious, uninephrectomized, sodium-loaded rats decreases proteinuria, normalizes the glomerular sclerosis index (GSI), increases the sodium excretion (UNaV), and modestly increases blood pressure (BP) in spontaneously hypertensive rats (SHR) but not in normotensive Wistar-Kyoto rats (WKY). Sodium 155-161 angiotensin II receptor, type 1a Rattus norvegicus 29-33 18957817-2 2008 Selective renal reduction of AT1R expression by intrarenal cortical infusion of antisense oligodeoxynucleotides (As-Odns) in conscious, uninephrectomized, sodium-loaded rats decreases proteinuria, normalizes the glomerular sclerosis index (GSI), increases the sodium excretion (UNaV), and modestly increases blood pressure (BP) in spontaneously hypertensive rats (SHR) but not in normotensive Wistar-Kyoto rats (WKY). Sodium 260-266 angiotensin II receptor, type 1a Rattus norvegicus 29-33 18668436-2 2008 hCNT1 and hCNT2 translocate pyrimidine- and purine-nucleosides, respectively, by a sodium-dependent mechanism, whereas hCNT3 shows broad substrate selectivity and the unique ability of translocating nucleosides both in a sodium- and a proton-coupled manner. Sodium 221-227 solute carrier family 28 member 3 Homo sapiens 119-124 18408010-9 2008 Telethonin was found to be expressed in the human gastrointestinal smooth muscle, co-localized with Na(v)1.5, and co-immunoprecipitated with sodium channels. Sodium 141-147 titin-cap Homo sapiens 0-10 18408010-11 2008 These results suggest a new role for telethonin, namely that telethonin is a sodium channel-interacting protein. Sodium 77-83 titin-cap Homo sapiens 37-47 18408010-11 2008 These results suggest a new role for telethonin, namely that telethonin is a sodium channel-interacting protein. Sodium 77-83 titin-cap Homo sapiens 61-71 18294202-0 2008 Balanced translocation in a patient with severe myoclonic epilepsy of infancy disrupts the sodium channel gene SCN1A. Sodium 91-97 sodium voltage-gated channel alpha subunit 1 Homo sapiens 111-116 18464934-4 2008 Here, we investigated SCN1B, which encodes the function-modifying sodium channel beta1 subunit, in 282 probands with Brugada syndrome and in 44 patients with conduction disease, none of whom had SCN5A mutations. Sodium 66-72 sodium voltage-gated channel beta subunit 1 Homo sapiens 22-27 18322024-7 2008 The decreased NHE3 expression is likely to be responsible for the reduction of sodium, bicarbonate, and fluid reabsorption in the proximal tubule consistently perceived in experimental models of PTH disorders. Sodium 79-85 solute carrier family 9 member A3 Rattus norvegicus 14-18 18550922-4 2008 BNP levels were higher in patients with HFCC (P<.0001) and correlated with New York Heart Association (NYHA) class; right atrial pressure; wedge pressure; cardiac output; levels of serum sodium, hemoglobin, urea, and tumor necrosis factor-alpha; and ejection fraction. Sodium 190-196 natriuretic peptide B Homo sapiens 0-3 18355814-11 2008 Finally, therapeutic inhibition of MEK1/2 restored electrogenic sodium absorption in CD. Sodium 64-70 mitogen activated protein kinase kinase 1 Rattus norvegicus 35-41 30739221-8 2019 The critical roles of the sodium pump alpha1 subunit (ATP1A1) in mediating the XPO1-targeted anticancer effect of bufalin in human glioma were further confirmed. Sodium 26-32 exportin 1 Homo sapiens 79-83 31262209-1 2019 SCN5A is expressed in cardiomyocytes and gastrointestinal (GI) smooth muscle cells (SMCs) as the voltage-gated mechanosensitive sodium channel NaV1.5. Sodium 128-134 sodium voltage-gated channel alpha subunit 5 Homo sapiens 0-5 31262209-1 2019 SCN5A is expressed in cardiomyocytes and gastrointestinal (GI) smooth muscle cells (SMCs) as the voltage-gated mechanosensitive sodium channel NaV1.5. Sodium 128-134 sodium voltage-gated channel alpha subunit 5 Homo sapiens 143-149 31653700-1 2019 Endoplasmic reticulum protein of 29 kDa (ERp29) is a thioredoxin-homologous endoplasmic reticulum (ER) protein that regulates the biogenesis of cystic fibrosis transmembrane conductance regulator (CFTR) and the epithelial sodium channel (ENaC). Sodium 222-228 endoplasmic reticulum protein 29 Homo sapiens 0-39 31653700-1 2019 Endoplasmic reticulum protein of 29 kDa (ERp29) is a thioredoxin-homologous endoplasmic reticulum (ER) protein that regulates the biogenesis of cystic fibrosis transmembrane conductance regulator (CFTR) and the epithelial sodium channel (ENaC). Sodium 222-228 endoplasmic reticulum protein 29 Homo sapiens 41-46 31409727-8 2019 RESULTS: In normal mice, Npt2a inhibition caused a dose-dependent increase in urinary phosphate (ED50 approximately 21 mg/kg), calcium, sodium and chloride excretion. Sodium 136-142 solute carrier family 34 (sodium phosphate), member 1 Mus musculus 25-30 31409727-12 2019 CONCLUSIONS: Npt2a inhibition causes a dose-dependent increase in phosphate, sodium and chloride excretion associated with reductions in plasma phosphate and PTH levels in normal mice and in a CKD mouse model. Sodium 77-83 solute carrier family 34 (sodium phosphate), member 1 Mus musculus 13-18 31732390-0 2019 De novo variant in SCN4A causes neonatal sodium channel myotonia with general muscle stiffness and respiratory failure. Sodium 41-47 sodium voltage-gated channel alpha subunit 4 Homo sapiens 19-24 31732390-1 2019 Variants of the skeletal muscle sodium channel gene SCN4A are associated with different neuromuscular disorders including sodium channel myotonia. Sodium 32-38 sodium voltage-gated channel alpha subunit 4 Homo sapiens 52-57 31732390-1 2019 Variants of the skeletal muscle sodium channel gene SCN4A are associated with different neuromuscular disorders including sodium channel myotonia. Sodium 122-128 sodium voltage-gated channel alpha subunit 4 Homo sapiens 52-57 31708756-7 2019 Results: NaHS (a donor of H2S) significantly alleviated cognitive impairments in the B2M-exposed rats tested by Y-maze test, NOR test and MWM test. Sodium 9-13 beta-2 microglobulin Rattus norvegicus 85-88 31708756-8 2019 Furthermore, NaHS recovered autophagic flux in the hippocampus of B2M-exposed rats, as evidenced by decreases in the ratio of autophagosome to autolysosome and the expression of p62 protein in the hippocampus. Sodium 13-17 beta-2 microglobulin Rattus norvegicus 66-69 18405837-5 2008 When expressed in Xenopus oocytes, 33 DmNa(V) variants generated sodium currents large enough for functional characterization. Sodium 65-71 paralytic Drosophila melanogaster 38-45 18398380-0 2008 Segmental regulation of sodium and water excretion by TRPV1 activation in the kidney. Sodium 24-30 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 54-59 18398380-1 2008 Our previous studies show that activation of the transient receptor potential vanilloid type 1 (TRPV1) channels by a selective agonist, capsaicin (CAP), given unilaterally into the renal pelvis leads to increases in urine flow rate (Uflow) and urinary sodium excretion (UNa) bilaterally, although the mechanisms underlying enhanced renal excretory function are unknown. Sodium 252-258 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 49-94 18398380-1 2008 Our previous studies show that activation of the transient receptor potential vanilloid type 1 (TRPV1) channels by a selective agonist, capsaicin (CAP), given unilaterally into the renal pelvis leads to increases in urine flow rate (Uflow) and urinary sodium excretion (UNa) bilaterally, although the mechanisms underlying enhanced renal excretory function are unknown. Sodium 252-258 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 96-101 18424559-13 2008 These results illuminate a previously uncharacterized role for renal IR to reduce BP and facilitate sodium and water excretion, possibly via NO production. Sodium 100-106 insulin receptor Mus musculus 69-71 31508879-11 2019 A significant association between plasma Hp concentration and 24-h sodium clearance was observed in Hp 1-1 subjects without polyuria (beta = 0.222; 95% CI 0.003-0.441; p = 0.047). Sodium 67-73 chromobox 5 Homo sapiens 100-106 31508879-13 2019 Hp 1-1 subjects demonstrated an altered ability to concentrate urine with a slower continuous excretion of sodium throughout the day. Sodium 107-113 chromobox 5 Homo sapiens 0-6 31508879-14 2019 Plasma Hp concentration of Hp 1-1 was positively correlated with 24-h sodium clearance in subjects without polyuria. Sodium 70-76 chromobox 5 Homo sapiens 27-33 31663064-0 2019 Ghrelin-Induced Sodium Reabsorption Is Mediated by PKA and Microtubule-Dependent alphaENaC Translocation in Female Rats. Sodium 16-22 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 51-54 20495177-1 2010 Renal cytochrome P450 (CYP)-derived epoxyeicosatrienoic acids (EETs) regulate sodium transport and blood pressure. Sodium 78-84 cytochrome P450, family 21, subfamily a, polypeptide 1 Mus musculus 23-26 31352823-2 2019 In the present study, we aimed to study the role of megalin in the generation of renal Ang II and sodium handling during nephrotic syndrome. Sodium 98-104 low density lipoprotein receptor-related protein 2 Mus musculus 52-59 18256274-10 2008 Because these transcriptional effects of ANG II in isolated nuclei were induced by ANG II in the absence of cell surface receptor-mediated signaling and completely blocked by losartan, we concluded that ANG II may directly stimulate nuclear AT(1a) receptors to induce transcriptional responses that are associated with tubular epithelial sodium transport, cellular growth and hypertrophy, and proinflammatory cytokines. Sodium 338-344 angiotensin II receptor, type 1a Rattus norvegicus 241-246 31352823-9 2019 Compared with control NEP25 mice, megalin KO/NEP25 mice excreted 5-fold more sodium in the urine. Sodium 77-83 low density lipoprotein receptor-related protein 2 Mus musculus 34-41 20441802-9 2010 Taken together, we show that NHA2 is a RANKL-induced plasmalemmal sodium/hydrogen exchanger in osteoclasts. Sodium 66-72 tumor necrosis factor (ligand) superfamily, member 11 Mus musculus 39-44 31352823-11 2019 These data indicate that Agt reabsorbed by proximal tubules via megalin in nephrotic syndrome is converted to Ang II, which may contribute to sodium retention and edema formation by activating NHE3 and Epithelial Na Channel. Sodium 142-148 low density lipoprotein receptor-related protein 2 Mus musculus 64-71 31253402-1 2019 Mutations in gene SCN5A, which encodes cardiac voltage-gated sodium channel Nav1.5, are associated with multiple clinical phenotypes. Sodium 61-67 sodium voltage-gated channel alpha subunit 5 Homo sapiens 18-23 31253402-1 2019 Mutations in gene SCN5A, which encodes cardiac voltage-gated sodium channel Nav1.5, are associated with multiple clinical phenotypes. Sodium 61-67 sodium voltage-gated channel alpha subunit 5 Homo sapiens 76-82 31253402-4 2019 The wild-type channel Nav1.5 and mutant Nav1.5-A1294G were expressed in the CHO-K1 and HEK293T cells and whole-cell sodium currents were recorded using the patch-clamp method. Sodium 116-122 sodium voltage-gated channel alpha subunit 5 Homo sapiens 40-46 31444371-7 2019 At baseline, hepsin-deficient mice accumulate uromodulin, along with hyperactivated NKCC2, resulting in a positive sodium balance and a better adaptation to water deprivation. Sodium 115-121 uromodulin Mus musculus 46-56 30821358-0 2019 Significant association of rare variant p.Gly8Ser in cardiac sodium channel beta4-subunit SCN4B with atrial fibrillation. Sodium 61-67 sodium voltage-gated channel beta subunit 4 Homo sapiens 90-95 30821358-3 2019 The voltage-gated cardiac sodium channel complex is responsible for the generation and conduction of the cardiac action potential, and composed of the main pore-forming alpha-subunit Nav 1.5 (encoded by the SCN5A gene) and one or more auxiliary beta-subunits, including Nav beta1 to Nav beta4 encoded by SCN1B to SCN4B, respectively. Sodium 26-32 sodium voltage-gated channel alpha subunit 5 Homo sapiens 207-212 30821358-3 2019 The voltage-gated cardiac sodium channel complex is responsible for the generation and conduction of the cardiac action potential, and composed of the main pore-forming alpha-subunit Nav 1.5 (encoded by the SCN5A gene) and one or more auxiliary beta-subunits, including Nav beta1 to Nav beta4 encoded by SCN1B to SCN4B, respectively. Sodium 26-32 sodium voltage-gated channel beta subunit 4 Homo sapiens 313-318 18045816-2 2008 The aim of this study was to examine the regulation of transepithelial sodium transport by TGF-beta1 in renal cells. Sodium 71-77 transforming growth factor, beta 1 Mus musculus 91-100 20580637-8 2010 The amplitude of the sodium current underlying the action potential was significantly decreased in GnRH neurons from young estradiol-treated animals. Sodium 21-27 gonadotropin releasing hormone 1 Mus musculus 99-103 18455018-7 2008 The proportional hazard (Cox) regression analysis showed that the risk of death increased 2.1% for each unit of donor sodium and 1.6% for each additional year of donors age over 50. Sodium 118-124 cytochrome c oxidase subunit 8A Homo sapiens 25-28 20580637-13 2010 The reduction of sodium current amplitude by estradiol suggests a negative feedback on GnRH neurons, which could lead to a downregulation of cell excitability and hormone release. Sodium 17-23 gonadotropin releasing hormone 1 Mus musculus 87-91 21468191-1 2010 When the concentration of sodium (Na(+)) in arterial plasma (P(Na)) declines sufficiently to inhibit the release of vasopressin, water will be excreted promptly when the vast majority of aquaporin 2 water channels (AQP2) have been removed from luminal membranes of late distal nephron segments. Sodium 26-32 aquaporin 2 Rattus norvegicus 187-198 18216318-3 2008 Gene array analysis revealed that these findings were associated with significant downregulation of water channels (aquaporin-1, -2, -3, and -4) and transporters of sodium, glucose, urea, and other solutes. Sodium 165-171 aquaporin 1 Rattus norvegicus 116-143 20185830-7 2010 The ion transporter SLC4A11 mediates sodium-dependent transport of borate as well as flux of sodium and hydroxyl ions in vitro. Sodium 37-43 solute carrier family 4 member 11 Homo sapiens 20-27 17688420-7 2008 BNP values were lower in the normal-sodium group compared with the low sodium group (685+/-255 compared with 425+/-125 pg/ml respectively; P<0.0001). Sodium 36-42 natriuretic peptide B Homo sapiens 0-3 17688420-10 2008 The normal-sodium group had a lower incidence of rehospitalization during follow-up and a significant decrease in plasma BNP and aldosterone levels, and PRA. Sodium 11-17 natriuretic peptide B Homo sapiens 121-124 20185830-7 2010 The ion transporter SLC4A11 mediates sodium-dependent transport of borate as well as flux of sodium and hydroxyl ions in vitro. Sodium 93-99 solute carrier family 4 member 11 Homo sapiens 20-27 20054031-3 2010 In addition to the higher accumulation of sodium ions, atsos1-1 showed inhibition of endocytosis, abnormalities in vacuolar shape and function, and changes in intracellular pH compared to the wild type in root tip cells under stress. Sodium 42-48 sodium proton exchanger, putative (NHX7) (SOS1) Arabidopsis thaliana 55-61 20038812-4 2010 We demonstrated that a paroxysmal extreme pain disorder (PEPD) mutation in the human peripheral neuronal sodium channel Nav1.7, a paramyotonia congenita (PMC) mutation in the human skeletal muscle sodium channel Nav1.4, and a long-QT3/SIDS mutation in the human cardiac sodium channel Nav1.5 all substantially increased the amplitude of resurgent sodium currents in an optimized adult rat-derived dorsal root ganglion neuronal expression system. Sodium 105-111 sodium voltage-gated channel alpha subunit 4 Homo sapiens 212-218 20038812-4 2010 We demonstrated that a paroxysmal extreme pain disorder (PEPD) mutation in the human peripheral neuronal sodium channel Nav1.7, a paramyotonia congenita (PMC) mutation in the human skeletal muscle sodium channel Nav1.4, and a long-QT3/SIDS mutation in the human cardiac sodium channel Nav1.5 all substantially increased the amplitude of resurgent sodium currents in an optimized adult rat-derived dorsal root ganglion neuronal expression system. Sodium 105-111 sodium voltage-gated channel alpha subunit 5 Homo sapiens 285-291 20553076-5 2009 IGFBP-3 levels were associated with higher intakes of milk, yogurt, fruits and vitamin C, and lower intakes of rice, energy, protein, carbohydrate, sodium and polyunsaturated fatty acids. Sodium 148-154 insulin like growth factor binding protein 3 Homo sapiens 0-7 19842663-7 2009 Replacement of azolium cations by sodium had significant effects; cytotoxicity increased in the case of the pyrazole system from 3 (A549) to the 5.5-fold (CH1). Sodium 34-40 SUN domain containing ossification factor Homo sapiens 155-158 31109455-1 2019 We have previously shown that blockade of ATP-binding cassette transporter A1 (ABCA1) with cyclosporine A (CsA) stimulates the epithelial sodium channel (ENaC) in cultured distal nephron cells. Sodium 138-144 sodium channel, nonvoltage-gated 1 alpha Mus musculus 154-158 30945431-1 2019 AIMS: Little is known about whether sodium intake is associated with the clinical effects of SGLT2 inhibitors (SGLT2is); however, SGLT2is may increase urinary sodium excretion. Sodium 36-42 solute carrier family 5 member 2 Homo sapiens 93-98 30817077-1 2019 The voltage-gated sodium channel subunit beta4 (SCN4B) regulates neuronal activity by modulating channel gating and has been implicated in ethanol consumption in rodent models and human alcoholics. Sodium 18-24 sodium voltage-gated channel beta subunit 4 Homo sapiens 48-53 30677491-1 2019 BACKGROUND: We recently reported a quantitative relationship between the degree of functional perturbation reported in the literature for 356 variants in the cardiac sodium channel gene SCN5A and the penetrance of resulting arrhythmia phenotypes. Sodium 166-172 sodium channel protein type 5 subunit alpha Cricetulus griseus 186-191 30677491-2 2019 In the course of that work, we identified multiple SCN5A variants, including R1193Q, that are common in populations but are reported in human embryonic kidney (HEK) cells to generate large late sodium current (INa-L). Sodium 194-200 sodium voltage-gated channel alpha subunit 5 Homo sapiens 51-56 33442562-0 2019 MrgprX1 Mediates Neuronal Excitability and Itch Through Tetrodotoxin-Resistant Sodium Channels. Sodium 79-85 MAS related GPR family member X1 Homo sapiens 0-7 33442562-4 2019 Instead, activation of MrgprX1 lowers the activation threshold of TTX-resistant sodium channels and induces inward sodium currents. Sodium 80-86 MAS related GPR family member X1 Homo sapiens 23-30 33442562-4 2019 Instead, activation of MrgprX1 lowers the activation threshold of TTX-resistant sodium channels and induces inward sodium currents. Sodium 115-121 MAS related GPR family member X1 Homo sapiens 23-30 33442562-7 2019 Collectively, these data suggest that activation of MrgprX1 triggers itch sensation by increasing the activity of TTX-resistant voltage-gated sodium channels. Sodium 142-148 MAS related GPR family member X1 Homo sapiens 52-59 31055186-11 2019 A high VWF:Ag/ADAMTS13:AC ratio was associated with increased white blood cell counts, together with decreased serum albumin and sodium at Pre and 1 W. CONCLUSIONS: A high VWF:Ag/ADAMTS13:AC ratio in acute-KD persisted after primary treatment in non-responders, and unbalanced substrate-to-enzyme ratio appeared to associate with vascular endothelial damage. Sodium 129-135 ADAM metallopeptidase with thrombospondin type 1 motif 13 Homo sapiens 14-22 31252520-1 2019 The epithelial sodium channel (ENaC) has a key role in modulating endothelial cell stiffness and this in turn regulates nitric oxide (NO) synthesis. Sodium 15-21 sodium channel, nonvoltage-gated 1 alpha Mus musculus 31-35 31099578-6 2019 Generally, wild-type plectasin has higher preference for sodium ions as 9ASP is mutated in other variants. Sodium 57-63 assembly factor for spindle microtubules Homo sapiens 73-76 30737311-8 2019 NMDA application evoked local calcium transients in processes of neocortical astrocytes, which were dampened upon blocking sodium/calcium exchange (NCX) with KB-R7943 or SEA0400. Sodium 123-129 T cell leukemia, homeobox 2 Mus musculus 148-151 30737311-9 2019 Mathematical computation based on our data predict that NMDA-induced sodium increases drive the NCX into reverse mode, resulting in calcium influx. Sodium 69-75 T cell leukemia, homeobox 2 Mus musculus 96-99 30772377-0 2019 UBC9 regulates cardiac sodium channel Nav1.5 ubiquitination, degradation and sodium current density. Sodium 23-29 sodium voltage-gated channel alpha subunit 5 Homo sapiens 38-44 30772377-1 2019 Voltage-gated sodium channel Nav1.5 is critical for generation and conduction of cardiac action potentials. Sodium 14-20 sodium voltage-gated channel alpha subunit 5 Homo sapiens 29-35 31000862-1 2019 Sodium-glucose co-transporter type 2 inhibitors (SGLT 2- i)are increasingly being used in the management of type 2 diabetes mellitus (T2DM). Sodium 0-6 solute carrier family 5 member 2 Homo sapiens 49-55 30598284-9 2019 This study suggests that in Purkinje fibers, TRPM4 channels may account for sodium background current (INab), and that a heterogeneous expression of TRPM4 channels in the His/Purkinje system is required for type II heart block, as seen clinically. Sodium 76-82 transient receptor potential cation channel subfamily M member 4 Homo sapiens 45-50 30475996-7 2019 The potential direct cardiovascular benefits of SGLT2 inhibitors include: augmentation of signal transducer and activator of transcription 3; inhibition of sodium hydrogen exchange; reduction of atherosclerosis; modulation of natriuretic peptides; vasodilation; modulation of sympathetic tone; and reduction of inflammation, oxidative stress, endoplasmic reticulum stress, and cardiac glucose uptake via down-regulation of SGLT1 expression. Sodium 156-162 solute carrier family 5 member 2 Homo sapiens 48-53 17993510-7 2008 The sodium activation kinetic analysis of both transporters revealed a variation in the affinity for sodium and a shift in the Hill coefficient that could be consistent with a stoichiometry of 2:1 and 1:1 sodium/nucleoside, for hCNT3 and hCNT3(C602R), respectively. Sodium 4-10 solute carrier family 28 member 3 Homo sapiens 228-233 19593208-10 2009 CONCLUSION: The CYP2C9*3 allele was associated with lower activity of the renin-angiotensin-aldosterone system in hypertensive men, which may reflect a more efficient sodium reabsorption capacity. Sodium 167-173 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 16-22 17993510-7 2008 The sodium activation kinetic analysis of both transporters revealed a variation in the affinity for sodium and a shift in the Hill coefficient that could be consistent with a stoichiometry of 2:1 and 1:1 sodium/nucleoside, for hCNT3 and hCNT3(C602R), respectively. Sodium 4-10 solute carrier family 28 member 3 Homo sapiens 238-243 17993510-7 2008 The sodium activation kinetic analysis of both transporters revealed a variation in the affinity for sodium and a shift in the Hill coefficient that could be consistent with a stoichiometry of 2:1 and 1:1 sodium/nucleoside, for hCNT3 and hCNT3(C602R), respectively. Sodium 101-107 solute carrier family 28 member 3 Homo sapiens 228-233 17993510-7 2008 The sodium activation kinetic analysis of both transporters revealed a variation in the affinity for sodium and a shift in the Hill coefficient that could be consistent with a stoichiometry of 2:1 and 1:1 sodium/nucleoside, for hCNT3 and hCNT3(C602R), respectively. Sodium 101-107 solute carrier family 28 member 3 Homo sapiens 228-233 17684771-4 2008 The isoform of the Na(+)/H(+) exchanger mediating proximal tubule sodium absorption, NHE3, is virtually absent in the neonatal rat kidney. Sodium 66-72 solute carrier family 9 member A3 Rattus norvegicus 85-89 19463845-11 2009 In isolated kidney, the PLA(2) from B. caissarum increased the perfusion pressure, renal vascular resistance, urinary flow, glomerular filtration rate, and sodium, potassium and chloride levels of excretion. Sodium 156-162 phospholipase A2 Apis mellifera 24-29 17947299-10 2008 We conclude that the interaction may be important for Na+/K+ ATPase beta1 subunit maturation; loss of this interaction may contribute to the pathology seen in Wolfram syndrome via reductions in sodium pump alpha1 and beta1 subunit expression in pancreatic beta-cells. Sodium 194-200 ATPase H+ transporting V0 subunit a1 Homo sapiens 206-222 18091753-2 2008 This study was conducted to further elucidate the role of neuronal nitric oxide synthase (nNOS) in blood pressure regulation and renin release in relation to different sodium loads. Sodium 168-174 nitric oxide synthase 1, neuronal Mus musculus 58-88 18091753-2 2008 This study was conducted to further elucidate the role of neuronal nitric oxide synthase (nNOS) in blood pressure regulation and renin release in relation to different sodium loads. Sodium 168-174 nitric oxide synthase 1, neuronal Mus musculus 90-94 18091753-7 2008 On the low sodium diet, nNOS(-/-) mice also showed increased urine flow rate and osmolar excretion, observations not made during a high sodium diet. Sodium 11-17 nitric oxide synthase 1, neuronal Mus musculus 24-28 18091753-7 2008 On the low sodium diet, nNOS(-/-) mice also showed increased urine flow rate and osmolar excretion, observations not made during a high sodium diet. Sodium 136-142 nitric oxide synthase 1, neuronal Mus musculus 24-28 18091753-8 2008 CONCLUSIONS: Our results show that nNOS is necessary for stimulation of renin in response to sodium restriction. Sodium 93-99 nitric oxide synthase 1, neuronal Mus musculus 35-39 19277862-0 2009 Enhancement of lanthanum (III) on sodium currents in acutely isolated hippocampal CA1 neurons of rat. Sodium 34-40 carbonic anhydrase 1 Rattus norvegicus 82-85 18209489-2 2008 Sodium selenite treatment exerted a profound preventive effect on apoptotic cell death, including p-P38, p-SAPK/JNK, caspases, and PARP activity, and ameliorated astrogliosis and hypomyelination, which occurs in regions of active cell death in the spinal cords of SCI rats. Sodium 0-6 mitogen activated protein kinase 14 Rattus norvegicus 100-103 19632629-10 2009 Surprisingly, co-expression of SCN5A-R34fs/60 with SCN5A-R1195H elicited a significant increase in late sodium current, whereas co-expression of SCN5A-WT with SCN5A-R34fs/60 did not. Sodium 104-110 sodium voltage-gated channel alpha subunit 5 Homo sapiens 31-36 18661333-3 2008 This ubiquitously expressed sodium/hydrogen exchanger (NHE-1) plays a central housekeeping role in all cells regulating cell volume and internal pH (pHi). Sodium 28-34 glucose-6-phosphate isomerase Homo sapiens 149-152 18090673-3 2008 Next, this review will outline the progression of data providing support for our hypothesis that an intra-renal mechanism of endothelin activation of ETB receptors stimulates NOS1 activity and nitric oxide production to promote sodium excretion. Sodium 228-234 nitric oxide synthase 1 Homo sapiens 175-179 19632629-10 2009 Surprisingly, co-expression of SCN5A-R34fs/60 with SCN5A-R1195H elicited a significant increase in late sodium current, whereas co-expression of SCN5A-WT with SCN5A-R34fs/60 did not. Sodium 104-110 sodium voltage-gated channel alpha subunit 5 Homo sapiens 51-56 19632629-10 2009 Surprisingly, co-expression of SCN5A-R34fs/60 with SCN5A-R1195H elicited a significant increase in late sodium current, whereas co-expression of SCN5A-WT with SCN5A-R34fs/60 did not. Sodium 104-110 sodium voltage-gated channel alpha subunit 5 Homo sapiens 51-56 19632629-10 2009 Surprisingly, co-expression of SCN5A-R34fs/60 with SCN5A-R1195H elicited a significant increase in late sodium current, whereas co-expression of SCN5A-WT with SCN5A-R34fs/60 did not. Sodium 104-110 sodium voltage-gated channel alpha subunit 5 Homo sapiens 51-56 17763866-0 2008 Sodium and chloride absorptive defects in the small intestine in Slc26a6 null mice. Sodium 0-6 solute carrier family 26, member 6 Mus musculus 65-72 19632629-12 2009 Unexpectedly, the 94-amino-acid fusion peptide derived from the R34fs/60 mutation accentuated the late sodium current of R1195H-containing Na(V)1.5 channels in vitro. Sodium 103-109 immunoglobulin lambda variable 2-18 Homo sapiens 139-147 17996119-8 2007 The viability of microbial cells treated with MUC7 12-mer in the presence of sodium or potassium was also determined by killing assay or flow cytometry. Sodium 77-83 mucin 7, secreted Homo sapiens 46-50 19587447-2 2009 It specifically functions to increase renal absorption of sodium from tubular fluid via regulation of the alpha subunit of the epithelial sodium channel (alphaENaC). Sodium 58-64 sodium channel, nonvoltage-gated 1 alpha Mus musculus 106-164 19587447-9 2009 These results suggest a role for Period 1 in the regulation of the renal epithelial sodium channel and more broadly implicate the circadian clock in control of sodium balance. Sodium 84-90 period circadian clock 1 Mus musculus 33-41 17954289-1 2007 BACKGROUND: The relationship between SLC12A3 mutations and actual sodium-chloride (Na-Cl) cotransporter (NCC) expression in patients with Gitelman syndrome (GS) was rarely evaluated. Sodium 66-72 solute carrier family 12 member 3 Homo sapiens 37-44 17954289-1 2007 BACKGROUND: The relationship between SLC12A3 mutations and actual sodium-chloride (Na-Cl) cotransporter (NCC) expression in patients with Gitelman syndrome (GS) was rarely evaluated. Sodium 66-72 solute carrier family 12 member 3 Homo sapiens 83-103 19563686-7 2009 CONCLUSION: These data suggest that activation of NK-1 receptor potentiates Na(v)1.8 sodium current via PKCepsilon-dependent signaling pathway, probably participating in the generation of inflammatory hyperalgesia. Sodium 85-91 tachykinin receptor 1 Rattus norvegicus 50-63 19429017-0 2009 mu-Opioid receptor-independent fashion of the suppression of sodium currents by mu-opioid analgesics in thalamic neurons. Sodium 61-67 opioid receptor mu 1 Homo sapiens 0-18 17959796-6 2007 Coexpression of Fyn with Na(V)1.2 channels decreases sodium currents by increasing the rate of inactivation and causing a negative shift in the voltage dependence of inactivation. Sodium 53-59 immunoglobulin lambda variable 2-8 Homo sapiens 25-33 17959797-3 2007 Here we have identified the amino acid residues on Na(V)1.2 channels that coordinate binding of Fyn kinase and mediate inhibition of sodium currents by enhancing fast inactivation. Sodium 133-139 immunoglobulin lambda variable 2-8 Homo sapiens 51-59 17959797-4 2007 Fyn kinase binds to a Src homology 3 (SH3)-binding motif in the second half of the intracellular loop connecting domains I and II (L(I-II)) of Na(V)1.2, and mutation of that SH3-binding motif prevents Fyn binding and Fyn enhancement of fast inactivation of sodium currents. Sodium 257-263 immunoglobulin lambda variable 2-8 Homo sapiens 143-151 17704762-6 2007 Here we show that introduction of a negatively charged amino acid at or near one of the two putative sodium-binding sites of the GABA (gamma-aminobutyric acid) transporter GAT-1 from rat brain (also called SLC6A1) renders both net flux and exchange of GABA largely chloride independent. Sodium 101-107 solute carrier family 6 member 1 Rattus norvegicus 206-212 17485228-0 2007 Abnormal expression of ENaC and SGK1 mRNA induced by dietary sodium in Dahl salt-sensitively hypertensive rats. Sodium 61-67 serum/glucocorticoid regulated kinase 1 Rattus norvegicus 32-36 19429017-6 2009 These results suggest that morphine, fentanyl and oxycodone each produce the MOR-independent suppression of sodium currents by distinct mechanisms in thalamic neurons. Sodium 108-114 opioid receptor mu 1 Homo sapiens 77-80 17485228-3 2007 In the present study, we investigated whether dietary sodium abnormally affects the expression of ENaC and SGK1 mRNA in DS rats. Sodium 54-60 serum/glucocorticoid regulated kinase 1 Rattus norvegicus 107-111 17485228-6 2007 The expression of alpha-ENaC mRNA in DS rats was abnormally increased by high sodium diet in contrast to DR rats, while it was normally increased by low sodium diet in DS rats similar to DR rats. Sodium 78-84 sodium channel epithelial 1 subunit alpha Rattus norvegicus 18-28 17485228-6 2007 The expression of alpha-ENaC mRNA in DS rats was abnormally increased by high sodium diet in contrast to DR rats, while it was normally increased by low sodium diet in DS rats similar to DR rats. Sodium 153-159 sodium channel epithelial 1 subunit alpha Rattus norvegicus 18-28 17485228-8 2007 The expression of SGK1 mRNA was elevated by high sodium diet in DS rats, but it was decreased in DR rats. Sodium 49-55 serum/glucocorticoid regulated kinase 1 Rattus norvegicus 18-22 17485228-9 2007 These observations indicate that the expression of ENaC and SGK1 mRNA is abnormally regulated by dietary sodium in salt-sensitively hypertensive rats, and that this abnormal expression would be one of the factors causing salt-sensitive hypertension. Sodium 105-111 serum/glucocorticoid regulated kinase 1 Rattus norvegicus 60-64 30382582-11 2019 Application of diethylamine nitric oxide (NO) sodium, a potent NO donor, to the cerebellar slices restored LTD in MLI/PC-Grin1 cKO mice, suggesting that NO is probably downstream to NMDARs. Sodium 46-52 glutamate receptor, ionotropic, NMDA1 (zeta 1) Mus musculus 118-126 19167409-0 2009 Differential modulation of late sodium current by protein kinase A in R1623Q mutant of LQT3. Sodium 32-38 sodium voltage-gated channel alpha subunit 5 Homo sapiens 87-91 19284629-3 2009 Initial cell depolarization is attributable to sodium influx through TRPM5 in sweet, bitter, and umami cells and an undetermined cation influx through an ion channel in sour cells expressing PKD2L1, a candidate sour taste receptor. Sodium 47-53 transient receptor potential cation channel, subfamily M, member 5 Mus musculus 69-74 19185281-0 2009 Mutations in SPINT2 cause a syndromic form of congenital sodium diarrhea. Sodium 57-63 serine peptidase inhibitor, Kunitz type 2 Homo sapiens 13-19 19133747-1 2009 BACKGROUND: Several plasma membrane transporters have been shown to mediate the cellular influx and/or efflux of iodothyronines, including the sodium-independent organic anion co-transporting polypeptide 1 (OATP1), the sodium taurocholate co-transporting polypeptide (NTCP), the L-type amino acid transporter 1 (LAT1) and 2 (LAT2), and the monocarboxylate transporter 8 (MCT8). Sodium 143-149 solute carrier family 10 (sodium/bile acid cotransporter family), member 1 Mus musculus 268-272 19133747-1 2009 BACKGROUND: Several plasma membrane transporters have been shown to mediate the cellular influx and/or efflux of iodothyronines, including the sodium-independent organic anion co-transporting polypeptide 1 (OATP1), the sodium taurocholate co-transporting polypeptide (NTCP), the L-type amino acid transporter 1 (LAT1) and 2 (LAT2), and the monocarboxylate transporter 8 (MCT8). Sodium 143-149 linker for activation of T cells family, member 2 Mus musculus 325-329 18768591-7 2008 Urinary sodium excretion reached signficantly lower values in sgk1(+/+) mice (15 +/- 5 mumol/mg crea) than in sgk1(-/-) mice (35 +/- 5 mumol/mg crea) and was associated with a significantly higher body weight gain in sgk1(+/+) compared with sgk1(-/-) mice (+6.6 +/- 0.7 vs. +4.1 +/- 0.8 g). Sodium 8-14 serum/glucocorticoid regulated kinase 1 Mus musculus 62-66 30530653-7 2018 Plants harboring alleles responsible for low root expression of HKT1;1 and consequently high leaf sodium (HKT1;1 HLS ) were migrants that have moved specifically into areas where soil sodium levels fluctuate widely due to geography and rainfall variation. Sodium 98-104 high-affinity K+ transporter 1 Arabidopsis thaliana 106-112 30530653-7 2018 Plants harboring alleles responsible for low root expression of HKT1;1 and consequently high leaf sodium (HKT1;1 HLS ) were migrants that have moved specifically into areas where soil sodium levels fluctuate widely due to geography and rainfall variation. Sodium 184-190 high-affinity K+ transporter 1 Arabidopsis thaliana 106-112 30530653-8 2018 We demonstrate that the proportion of plants harboring HKT1;1 HLS alleles correlates with soil sodium level over time, HKT1;1 HLS -harboring plants are better adapted to intermediate levels of salinity, and the HKT1;1 HLS allele clusters with high-sodium accumulator accessions worldwide. Sodium 95-101 high-affinity K+ transporter 1 Arabidopsis thaliana 55-61 30530653-8 2018 We demonstrate that the proportion of plants harboring HKT1;1 HLS alleles correlates with soil sodium level over time, HKT1;1 HLS -harboring plants are better adapted to intermediate levels of salinity, and the HKT1;1 HLS allele clusters with high-sodium accumulator accessions worldwide. Sodium 248-254 high-affinity K+ transporter 1 Arabidopsis thaliana 119-125 30530653-8 2018 We demonstrate that the proportion of plants harboring HKT1;1 HLS alleles correlates with soil sodium level over time, HKT1;1 HLS -harboring plants are better adapted to intermediate levels of salinity, and the HKT1;1 HLS allele clusters with high-sodium accumulator accessions worldwide. Sodium 248-254 high-affinity K+ transporter 1 Arabidopsis thaliana 119-125 30618807-1 2018 Background: Carriers of the E161K mutation in the SCN5A gene, encoding the NaV1.5 pore-forming alpha-subunit of the ion channel carrying the fast sodium current (INa), show sinus bradycardia and occasional exit block. Sodium 146-152 sodium voltage-gated channel alpha subunit 5 Homo sapiens 50-55 30618807-1 2018 Background: Carriers of the E161K mutation in the SCN5A gene, encoding the NaV1.5 pore-forming alpha-subunit of the ion channel carrying the fast sodium current (INa), show sinus bradycardia and occasional exit block. Sodium 146-152 sodium voltage-gated channel alpha subunit 5 Homo sapiens 75-81 30367157-3 2018 Here, we show that the MR and other members of the mineralocorticoid signalling pathway including HSP90 and FKBP4, possess anti-viral activity against HSV-1 independent of their effect on sodium transport, as shown by sodium channel inhibitors. Sodium 218-224 heat shock protein 90 alpha family class A member 1 Homo sapiens 98-103 30185469-0 2018 The Absence of the ACE N-Domain Decreases Renal Inflammation and Facilitates Sodium Excretion during Diabetic Kidney Disease. Sodium 77-83 angiotensin I converting enzyme (peptidyl-dipeptidase A) 1 Mus musculus 19-22 30185469-10 2018 CONCLUSIONS: These data indicate that increasing AcSDKP by blocking the ACE N-domain facilitates sodium excretion and ameliorates diabetic kidney disease independent of intrarenal angiotensin II regulation. Sodium 97-103 angiotensin I converting enzyme (peptidyl-dipeptidase A) 1 Mus musculus 72-75 30007527-6 2018 By increasing the distal sodium chloride and calcium ion load with chronic furosemide administration, an intrinsic compensatory defect in the DCT from Umod-/- compared to wild type mice was found manifested as sodium wasting and hypercalciuria. Sodium 25-31 uromodulin Mus musculus 151-155 30041812-6 2018 In vitro, sodium-dependent phosphate uptake was decreased in cultured vascular smooth muscle cells isolated from PiT-2 heterozygous knockout mice compared with those from wild-type mice. Sodium 10-16 solute carrier family 20, member 2 Mus musculus 113-118 29722287-8 2018 Cardioprotection by levothyroxine-sodium pretreatment is probably attributable to increased myocardial expression of heat shock protein 70 and myosin heavy chain alpha. Sodium 34-40 heat shock protein family A (Hsp70) member 1B Rattus norvegicus 117-138 29917063-9 2018 In a linear regression model, urinary sodium excretion remained significantly associated with PAI-1 values even after adjusting for age, gender, and BMI. Sodium 38-44 serpin family E member 1 Homo sapiens 94-99 30093883-6 2018 Treatment with SGLT2 inhibitors significantly decreased BP and normalized circadian rhythms of both BP and SNA, but did not change HR; this treatment was also associated with an increase in urinary sodium excretion. Sodium 198-204 solute carrier family 5 member 2 Homo sapiens 15-20 31458964-4 2018 Herein, nano P2-Na2/3(Mn0.54Ni0.13Co0.13)O2 (NCM) materials are synthesized using a modified Pechini method as a prospective high-voltage sodium storage component without any modification. Sodium 138-144 CWC22 spliceosome associated protein homolog Homo sapiens 45-48 31458964-9 2018 The obtained capacity, rate performance, and energy density along with prolonged cyclic life for the cell fabricated with the NCM-850 electrodes are some of the best reported values for sodium-ion batteries as compared to those of other p2-type sodium intercalating materials. Sodium 186-192 CWC22 spliceosome associated protein homolog Homo sapiens 126-129 31458964-9 2018 The obtained capacity, rate performance, and energy density along with prolonged cyclic life for the cell fabricated with the NCM-850 electrodes are some of the best reported values for sodium-ion batteries as compared to those of other p2-type sodium intercalating materials. Sodium 245-251 CWC22 spliceosome associated protein homolog Homo sapiens 126-129 29791744-2 2018 During studies to characterize agents that modulate Nav 1.3 function, we identified a compound that appears to exhibit both enhancement and inhibition of sodium ion conduction that appeared to be dependent on the gating state that the channel was in. Sodium 154-160 sodium voltage-gated channel alpha subunit 3 Homo sapiens 52-59 29929989-0 2018 Intestinal Mineralocorticoid Receptor Contributes to Epithelial Sodium Channel-Mediated Intestinal Sodium Absorption and Blood Pressure Regulation. Sodium 64-70 nuclear receptor subfamily 3, group C, member 2 Mus musculus 11-37 29929989-2 2018 The intestine is the sensing organ of ingested sodium; accordingly, intestinal MR is expected to have essential roles in blood pressure (BP) regulation. Sodium 47-53 nuclear receptor subfamily 3, group C, member 2 Mus musculus 79-81 29929989-4 2018 With a standard diet, fecal sodium excretion was 1.5-fold higher in IEC-MR-KO mice, with markedly decreased colonic expression of beta- and gamma-epithelial sodium channel, than in control mice. Sodium 28-34 nuclear receptor subfamily 3, group C, member 2 Mus musculus 72-74 29779889-3 2018 Importantly, alteration of fluid flow promotes proliferation of SEZ cells in an ENaC-dependent manner, eliciting sodium and calcium signals that regulate proliferation via calcium-release-activated channels and phosphorylation of ERK. Sodium 113-119 sodium channel, nonvoltage-gated 1 alpha Mus musculus 80-84 29779889-5 2018 Thus, ENaC plays a central role in regulating adult neurogenesis, and among multiple modes of ENaC function, flow-induced changes in sodium signals are critical for NSC biology. Sodium 133-139 sodium channel, nonvoltage-gated 1 alpha Mus musculus 6-10 29779889-5 2018 Thus, ENaC plays a central role in regulating adult neurogenesis, and among multiple modes of ENaC function, flow-induced changes in sodium signals are critical for NSC biology. Sodium 133-139 sodium channel, nonvoltage-gated 1 alpha Mus musculus 94-98 29521607-2 2018 CSF loss can cause severe hyponatremia, especially in the newborn and early infancy periods when dietary sodium content is relatively low. Sodium 105-111 colony stimulating factor 2 Homo sapiens 0-3 29606556-9 2018 Twenty-eight different SCN4A missense mutations (including three novel mutations) were identified in paramyotonia congenita/sodium channel myotonia, hypokalemic periodic paralysis and hyperkalemic periodic paralysis. Sodium 124-130 sodium voltage-gated channel alpha subunit 4 Homo sapiens 23-28 29575628-0 2018 Congenital sodium diarrhea and chorioretinal coloboma with optic disc coloboma in a patient with biallelic SPINT2 mutations, including p.(Tyr163Cys). Sodium 11-17 serine peptidase inhibitor, Kunitz type 2 Homo sapiens 107-113 29575628-3 2018 Mutations in the serine protease inhibitor, Kunitz-Type 2 (SPINT2) gene have been associated with congenital sodium diarrhea and additional syndromic features. Sodium 109-115 serine peptidase inhibitor, Kunitz type 2 Homo sapiens 17-57 29575628-3 2018 Mutations in the serine protease inhibitor, Kunitz-Type 2 (SPINT2) gene have been associated with congenital sodium diarrhea and additional syndromic features. Sodium 109-115 serine peptidase inhibitor, Kunitz type 2 Homo sapiens 59-65 29575628-4 2018 We present a child with congenital sodium diarrhea, cleft lip and palate, corneal erosions, optic nerve coloboma, and intermittent exotropia who was found to have biallelic mutations in SPINT2. Sodium 35-41 serine peptidase inhibitor, Kunitz type 2 Homo sapiens 186-192 29323234-6 2018 Urinary sodium excretion was increased by 94% and urine flow by 126% in Cav1-/- mice (p < 0.05). Sodium 8-14 caveolin 1, caveolae protein Mus musculus 72-76 30408810-10 2018 The serum CT-1 concentrations were positively correlated with the 24-h urinary sodium-to-potassium (Na/K) excretion ratios during both of the LS and HS diet intervention periods in SS subjects (r = 0.621, p < 0.01), but this correlation was not evident in SR subjects (r = 0.208, p = 0.107). Sodium 79-85 cardiotrophin 1 Homo sapiens 10-14 29614490-3 2018 Renal dopamine D1 receptor (D1R), regulated by G protein-coupled receptor kinase type 4 (GRK4), plays an important role in the regulation of renal sodium transport and blood pressure. Sodium 147-153 G protein-coupled receptor kinase 4 Rattus norvegicus 47-87 29614490-3 2018 Renal dopamine D1 receptor (D1R), regulated by G protein-coupled receptor kinase type 4 (GRK4), plays an important role in the regulation of renal sodium transport and blood pressure. Sodium 147-153 G protein-coupled receptor kinase 4 Rattus norvegicus 89-93 29491733-2 2018 In arabidopsis, the Ca2+ activated SOS3 interacts with SOS2 which further activates SOS1, a Na+/H+ antiporter, responsible for removing toxic sodium ions from the cells. Sodium 142-148 sodium proton exchanger, putative (NHX7) (SOS1) Arabidopsis thaliana 84-88 29491733-2 2018 In arabidopsis, the Ca2+ activated SOS3 interacts with SOS2 which further activates SOS1, a Na+/H+ antiporter, responsible for removing toxic sodium ions from the cells. Sodium 142-148 Na+/H+ exchanger 1 Arabidopsis thaliana 92-109 29997009-1 2018 INTRODUCTION: Mutations within SCN5A are found in a significant proportion (15-30%) of Brugada syndrome (BrS) cases and impair sodium transport across excitable cardiac cells that mediate ventricular contractions. Sodium 127-133 sodium voltage-gated channel alpha subunit 5 Homo sapiens 31-36 29024690-4 2018 Our objective was to determine the properties of the sodium current in iPS-CM with a mutation in SCN5A associated with Brugada syndrome. Sodium 53-59 sodium voltage-gated channel alpha subunit 5 Homo sapiens 97-102 29485643-11 2017 Negative associations were however observed between plasma AChE activity and erythrocyte sodium and magnesium levels. Sodium 89-95 acetylcholinesterase Rattus norvegicus 59-63 29311917-5 2017 In this review we analyze the structural data reported for A2AR that described for the first time the binding of mode of antagonists, including newly developed drug candidates, synthetic and endogenous agonists, sodium ions and an engineered G protein. Sodium 212-218 adenosine A2a receptor Homo sapiens 59-63 29376023-3 2017 On the basis of their sodium-dependent transport modes, ASCT2 and ATB0+ have the capacity to sustain glutamine need of cancer cells; while LAT1, which is sodium independent will have the role of providing cancer cells with some amino acids with plausible signaling roles. Sodium 22-28 solute carrier family 7 member 5 Homo sapiens 139-143 29376023-3 2017 On the basis of their sodium-dependent transport modes, ASCT2 and ATB0+ have the capacity to sustain glutamine need of cancer cells; while LAT1, which is sodium independent will have the role of providing cancer cells with some amino acids with plausible signaling roles. Sodium 154-160 solute carrier family 7 member 5 Homo sapiens 139-143 28759755-6 2017 Interestingly, SGLT2 inhibitors have been reported to reduce albuminuria in DM via an activation of renal tubuloglomerular feedback by increased macula densa sodium and chloride delivery, leading to afferent vasoconstriction and attenuated diabetes-induced renal hyperfiltration. Sodium 158-164 solute carrier family 5 member 2 Homo sapiens 15-20 29296046-3 2017 At normal levels, leptin can exert its effects on weight regulation according to white fat mass, induce sodium excretion, maintain vascular tone, and repair the myocardium. Sodium 104-110 leptin Homo sapiens 18-24 28567665-1 2017 In adulthood, an induced nephron-specific deficiency of alphaENaC (Scnn1a) resulted in pseudohypoaldosteronism type 1 (PHA-1) with sodium loss, hyperkalemia, and metabolic acidosis that is rescued through high-sodium/low-potassium (HNa+/LK+) diet. Sodium 131-137 sodium channel, nonvoltage-gated 1 alpha Mus musculus 67-73 28567665-1 2017 In adulthood, an induced nephron-specific deficiency of alphaENaC (Scnn1a) resulted in pseudohypoaldosteronism type 1 (PHA-1) with sodium loss, hyperkalemia, and metabolic acidosis that is rescued through high-sodium/low-potassium (HNa+/LK+) diet. Sodium 210-216 sodium channel, nonvoltage-gated 1 alpha Mus musculus 67-73 28957668-4 2017 NTSHSD2 neurons respond to sodium deficiency with spontaneous pacemaker-like activity-the consequence of "cardiac" HCN and Nav1.5 channels. Sodium 27-33 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 115-118 28957668-4 2017 NTSHSD2 neurons respond to sodium deficiency with spontaneous pacemaker-like activity-the consequence of "cardiac" HCN and Nav1.5 channels. Sodium 27-33 sodium voltage-gated channel alpha subunit 5 Homo sapiens 123-129 28743496-2 2017 Activation of WNK-OSR1/SPAK-NaCl cotransporter (NCC) cascade increases sodium reabsorption in the kidney, leading to pseudohypoaldosteronism type II (PHA II) characterized by salt-sensitive hypertension and hyperkalemia. Sodium 71-77 serine/threonine kinase 39 Mus musculus 23-27 29774303-1 2017 Introduction: Myotonia permanens due to Nav1.4-G1306E is a rare sodium channelopathy with potentially life-threatening respiratory complications. Sodium 64-70 sodium voltage-gated channel alpha subunit 4 Homo sapiens 40-46 28768320-4 2017 Instead, in the kidneys, SGLT2 functionally interacts with the sodium-hydrogen exchanger, which is responsible for the majority of sodium tubular reuptake following filtration. Sodium 63-69 solute carrier family 5 member 2 Homo sapiens 25-30 28768320-9 2017 Conclusions and Relevance: The benefits of SGLT2 inhibitors in heart failure may be mediated by the inhibition of sodium-hydrogen exchange rather than the effect on glucose reabsorption. Sodium 114-120 solute carrier family 5 member 2 Homo sapiens 43-48 28610554-1 2017 System xc- is a sodium-independent electroneutral transporter, comprising a catalytic subunit xCT (SLC7A11), which is involved in importing cystine. Sodium 16-22 solute carrier family 7 member 11 Homo sapiens 94-97 28610554-1 2017 System xc- is a sodium-independent electroneutral transporter, comprising a catalytic subunit xCT (SLC7A11), which is involved in importing cystine. Sodium 16-22 solute carrier family 7 member 11 Homo sapiens 99-106 28624548-5 2017 11beta-HSD2 acts as a "guardian" enzyme protecting the mineralocorticoid receptor from excess cortisol, preventing sodium and water retention in the normotensive state. Sodium 115-121 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 0-11 28516268-2 2017 In a panel of human cancer cell lines, which express the system L transporters LAT1 and LAT2, GPNA inhibits the sodium-independent influx of leucine and glutamine. Sodium 112-118 solute carrier family 7 member 5 Homo sapiens 79-83 28667491-4 2017 SGLT-2 inhibitors inhibit proximal tubular sodium and chloride reabsorption, leading to increased nephron flux throughout the distal renal tubules, most notably at the level of the macula densa. Sodium 43-49 solute carrier family 5 member 2 Homo sapiens 0-6 28492364-5 2017 Mechanistically, TCR stimulation induced rapid sodium influx in Napahyh/hyh CD4 T cells, which reduced intracellular ATP, [ATP]i. Depletion of [ATP]i inhibited mTORC2 dependent NFkappaB activation in Napahyh/hyh cells but ablation of Orai1 restored it. Sodium 47-53 T cell receptor alpha variable 6-3 Mus musculus 17-20 28492364-5 2017 Mechanistically, TCR stimulation induced rapid sodium influx in Napahyh/hyh CD4 T cells, which reduced intracellular ATP, [ATP]i. Depletion of [ATP]i inhibited mTORC2 dependent NFkappaB activation in Napahyh/hyh cells but ablation of Orai1 restored it. Sodium 47-53 ORAI calcium release-activated calcium modulator 1 Mus musculus 234-239 28492364-7 2017 Thus, non-specific sodium influx via bonafide calcium channels disrupts unexpected signaling nodes and may provide mechanistic insights into some divergent phenotypes associated with Orai1 function. Sodium 19-25 ORAI calcium release-activated calcium modulator 1 Mus musculus 183-188 28185290-14 2017 This agreement holds for both loss-of-function and gain-of-function mutations in the HCN4, SCN5A and KCNQ1 genes, underlying ion channelopathies in If , fast sodium current and slow delayed rectifier potassium current, respectively. Sodium 158-164 hyperpolarization activated cyclic nucleotide gated potassium channel 4 Homo sapiens 85-89 28196866-1 2017 There is very limited human renal sodium gradient-dependent glucose transporter protein (SGLT2) mRNA and protein expression data reported in the literature. Sodium 34-40 solute carrier family 5 member 2 Homo sapiens 89-94 28339658-0 2017 Acute cell volume regulation by Janus kinase 2-mediated sodium/hydrogen exchange activation develops at the late one-cell stage in mouse preimplantation embryos. Sodium 56-62 Janus kinase 2 Mus musculus 32-46 27878313-10 2017 Because SGLT2 reabsorbs sodium along with glucose, SGLT2 blockers are natriuretic and antihypertensive. Sodium 24-30 solute carrier family 5 member 2 Homo sapiens 8-13 27878313-10 2017 Because SGLT2 reabsorbs sodium along with glucose, SGLT2 blockers are natriuretic and antihypertensive. Sodium 24-30 solute carrier family 5 member 2 Homo sapiens 51-56 26822507-1 2017 Idiopathic basal ganglia calcification is a brain calcification disorder that has been genetically linked to autosomal dominant mutations in the sodium-dependent phosphate co-transporter, SLC20A2. Sodium 145-151 solute carrier family 20, member 2 Mus musculus 188-195 27748972-9 2017 Mlc1 overexpression reduced activity of the astrocytic sodium pump, which may underlie white matter edema followed by myelin membrane splitting. Sodium 55-61 megalencephalic leukoencephalopathy with subcortical cysts 1 homolog (human) Mus musculus 0-4 28233175-11 2017 Potential sodium binding sites in the hH3R protein were analyzed by expressing specific hH3R mutants in Sf9 cells. Sodium 10-16 histamine receptor H3 Homo sapiens 38-42 28750403-7 2017 Sodium and chloride excretion increased in HCTZ-treated pendrin KO mice, but they remained unchanged in WT or NCC KO mice. Sodium 0-6 solute carrier family 26, member 4 Mus musculus 56-63 27978521-3 2017 Although the mechanism of hyperfiltration is still unclear, there is mounting evidence that the increased reabsorption of glucose and sodium by sodium glucose transporter-2 (SGLT-2) is involved in this altered renal function. Sodium 134-140 solute carrier family 5 member 2 Homo sapiens 144-172 27978521-3 2017 Although the mechanism of hyperfiltration is still unclear, there is mounting evidence that the increased reabsorption of glucose and sodium by sodium glucose transporter-2 (SGLT-2) is involved in this altered renal function. Sodium 134-140 solute carrier family 5 member 2 Homo sapiens 174-180 28066414-0 2016 TGF-beta Affects the Differentiation of Human GM-CSF+ CD4+ T Cells in an Activation- and Sodium-Dependent Manner. Sodium 89-95 colony stimulating factor 2 Homo sapiens 46-52 28008944-6 2016 JNK and CDK5 inhibitor attenuated increases in Nav1.6 sodium currents induced by overexpression of APP. Sodium 54-60 cyclin dependent kinase 5 Homo sapiens 8-12 27694909-2 2016 The pore-forming subunit of the cardiac sodium channel Nav1.5, which is encoded by SCN5A, is the main ion channel that conducts the voltage-gated cardiac sodium current (INa) in cardiac cells. Sodium 40-46 sodium voltage-gated channel alpha subunit 5 Homo sapiens 55-61 27694909-2 2016 The pore-forming subunit of the cardiac sodium channel Nav1.5, which is encoded by SCN5A, is the main ion channel that conducts the voltage-gated cardiac sodium current (INa) in cardiac cells. Sodium 40-46 sodium voltage-gated channel alpha subunit 5 Homo sapiens 83-88 27628105-9 2016 Serum sodium appeared to significantly differ by SGLT2 inhibitor type. Sodium 6-12 solute carrier family 5 member 2 Homo sapiens 49-54 27787771-1 2016 BACKGROUND: Several drugs may lower serum sodium concentrations (NaC) in older patients. Sodium 42-48 synuclein alpha Homo sapiens 65-68 27981544-9 2016 RESULTS: HUCMSC transplantation significantly ameliorated the severity of liver fibrosis, reduced portal hypertension and sodium retention that were induced by CCl4. Sodium 122-128 C-C motif chemokine ligand 4 Homo sapiens 160-164 27865823-4 2016 Various hormones and peptides secreted from gut such as gastrin, glucocorticoids, Glucagon-like peptide-1 impact on kidney function and BP especially influencing sodium absorption from gut. Sodium 162-168 gastrin Homo sapiens 56-63 27822054-12 2016 Local inhibition of the renin-angiotensin-aldosterone system secondary to increased delivery of sodium to the juxtaglomerular apparatus during SGLT2 inhibition has also been postulated. Sodium 96-102 solute carrier family 5 member 2 Homo sapiens 143-148 27599528-1 2016 Primarily, the sodium-glucose cotransporter 2 (SGLT2) inhibitors suppress the cotransport of glucose and sodium from the tubular lumen of the proximal tubules to the blood, and excrete glucose into the urine. Sodium 15-21 solute carrier family 5 member 2 Homo sapiens 47-52 27701382-4 2016 FHF2-deficient cardiomyocytes generate action potentials upon current injection at 25 C but are unexcitable at 40 C. The absence of FHF2 accelerates the rate of closed-state and open-state sodium channel inactivation, which synergizes with temperature-dependent enhancement of inactivation rate to severely suppress cardiac sodium currents at elevated temperatures. Sodium 191-197 fibroblast growth factor 13 Mus musculus 0-4 27733495-1 2016 BACKGROUND: The basic defect in long-QT syndrome type III (LQT3) is an excessive inflow of sodium current during phase 3 of the action potential caused by mutations in the SCN5A gene. Sodium 91-97 sodium voltage-gated channel alpha subunit 5 Homo sapiens 59-63 27733495-1 2016 BACKGROUND: The basic defect in long-QT syndrome type III (LQT3) is an excessive inflow of sodium current during phase 3 of the action potential caused by mutations in the SCN5A gene. Sodium 91-97 sodium voltage-gated channel alpha subunit 5 Homo sapiens 172-177 27338702-3 2016 By using this approach, we found that basal and insulin-stimulated rates of muscle ATP synthetic flux (VATP) and plasma inorganic phosphate (Pi) were reduced by 50% in mice with diet-induced hypophosphatemia as well as in sodium-dependent Pi transporter solute carrier family 34, member 1 (NaPi2a)-knockout (NaPi2a-/-) mice compared with their wild-type littermate controls. Sodium 222-228 solute carrier family 34 (sodium phosphate), member 1 Mus musculus 290-296 27338702-3 2016 By using this approach, we found that basal and insulin-stimulated rates of muscle ATP synthetic flux (VATP) and plasma inorganic phosphate (Pi) were reduced by 50% in mice with diet-induced hypophosphatemia as well as in sodium-dependent Pi transporter solute carrier family 34, member 1 (NaPi2a)-knockout (NaPi2a-/-) mice compared with their wild-type littermate controls. Sodium 222-228 solute carrier family 34 (sodium phosphate), member 1 Mus musculus 308-314 27489371-0 2016 Effect of phenytoin on sodium conductances in rat hippocampal CA1 pyramidal neurons. Sodium 23-29 carbonic anhydrase 1 Rattus norvegicus 62-65 27080107-0 2016 Extrusion versus diffusion: mechanisms for recovery from sodium loads in mouse CA1 pyramidal neurons. Sodium 57-63 carbonic anhydrase 1 Mus musculus 79-82 27653682-3 2016 The AP threshold changes in Fmr1 KO mice are caused by increased persistent sodium current (INaP). Sodium 76-82 nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, zeta Mus musculus 92-96 26872488-2 2016 Herein, we demonstrated in cultured cells and in vivo that increased levels of extracellular Pi activated the AKT/mammalian target of rapamycin complex 1 (mTORC1) pathway by suppressing membrane-bound phosphatase and tensin homolog (PTEN) levels in a manner requiring the sodium-dependent Pi transporter PiT-1. Sodium 272-278 phosphatase and tensin homolog Homo sapiens 233-237 27384707-1 2016 Reduction of the cyclodiphosphazane [(S=)ClP(mu-NtBu)]2 (1) with sodium metal in refluxing toluene proceeds via two different pathways. Sodium 65-77 calmodulin like 3 Homo sapiens 41-44 26775567-2 2016 Paradoxically, aldosterone also induces transcription of the endothelin-1 (Edn1) gene to increase protein (ET-1) levels, which inhibits sodium reabsorption. Sodium 136-142 endothelin 1 Mus musculus 61-73 26775567-2 2016 Paradoxically, aldosterone also induces transcription of the endothelin-1 (Edn1) gene to increase protein (ET-1) levels, which inhibits sodium reabsorption. Sodium 136-142 endothelin 1 Mus musculus 75-79 26775567-2 2016 Paradoxically, aldosterone also induces transcription of the endothelin-1 (Edn1) gene to increase protein (ET-1) levels, which inhibits sodium reabsorption. Sodium 136-142 endothelin 1 Mus musculus 107-111 27335124-4 2016 Remarkably, alpha-SNAP depletion induces formation of higher-order Orai1 oligomers, which permeate significant levels of sodium via Orai1 channels. Sodium 121-127 ORAI calcium release-activated calcium modulator 1 Mus musculus 67-72 27335124-4 2016 Remarkably, alpha-SNAP depletion induces formation of higher-order Orai1 oligomers, which permeate significant levels of sodium via Orai1 channels. Sodium 121-127 ORAI calcium release-activated calcium modulator 1 Mus musculus 132-137 27335124-5 2016 Sodium permeation in alpha-SNAP-deficient cells cannot be corrected by tethering multiple Stim1 domains to Orai1 C-terminal tail, demonstrating that alpha-SNAP regulates functional assembly and calcium selectivity of Orai1 multimers independently of Stim1 levels. Sodium 0-6 ORAI calcium release-activated calcium modulator 1 Mus musculus 217-222 27123541-9 2016 In addition, SGK inhibitor gsk650394 decreased phosphorylation of Nedd4-2 and inhibited voltage-gated sodium currents. Sodium 102-108 serum/glucocorticoid regulated kinase 1 Mus musculus 13-16 27170740-10 2016 Our findings highlight the importance of ENaC function and regulation in the early part of the aldosterone-sensitive distal nephron for the maintenance of sodium balance and blood pressure control. Sodium 155-161 sodium channel, nonvoltage-gated 1 alpha Mus musculus 41-45 27389830-3 2016 The results show that the classical "transient" sodium current ([Formula: see text]) contributes mainly to the nodal action potential generation in the normal and abnormal cases for the temperature range of 20-39[Formula: see text]C, as the contribution of fast and slow potassium currents ([Formula: see text] and [Formula: see text]) to the total ionic current ([Formula: see text]) is negligible. Sodium 48-54 nodal growth differentiation factor Homo sapiens 111-116 27230697-4 2016 Adenosine A2A receptor antagonists, mixed inhibitors of sodium/calcium channels and monoamine oxidase-B have recently been found to improve motor fluctuations. Sodium 56-62 adenosine A2a receptor Homo sapiens 0-22 27124340-0 2016 5"-Substituted Amiloride Derivatives as Allosteric Modulators Binding in the Sodium Ion Pocket of the Adenosine A2A Receptor. Sodium 77-83 adenosine A2a receptor Homo sapiens 102-124 27124340-3 2016 The availability of a high-resolution X-ray crystal structure of the human adenosine A2A receptor (hA2AAR), in which the allosteric sodium ion site was elucidated, makes it an appropriate model receptor for investigating the allosteric site. Sodium 132-138 adenosine A2a receptor Homo sapiens 75-97 26961874-6 2016 Whole-cell patch clamping showed that overexpression of alphaB-crystallin significantly increased peak sodium current (INa) density, and the underlying molecular mechanism is the increased cell surface expression level of Nav1.5 via reduced internalization of cell surface Nav1.5 and ubiquitination of Nav1.5. Sodium 103-109 sodium voltage-gated channel alpha subunit 5 Homo sapiens 222-228 26786162-4 2016 Nav1.5 N-terminal domain, by itself (the 132 aa peptide) (Nter), exerts a "chaperone-like" effect that increases sodium (I(Na)) and inward rectifier potassium (I(K1)) currents by enhancing the expression of Nav1.5, Kir2.1, and Kir2.2 channels as demonstrated in Chinese hamster ovary (CHO) cells and in rat cardiomyocytes. Sodium 113-119 sodium voltage-gated channel alpha subunit 5 Homo sapiens 0-6 26786162-4 2016 Nav1.5 N-terminal domain, by itself (the 132 aa peptide) (Nter), exerts a "chaperone-like" effect that increases sodium (I(Na)) and inward rectifier potassium (I(K1)) currents by enhancing the expression of Nav1.5, Kir2.1, and Kir2.2 channels as demonstrated in Chinese hamster ovary (CHO) cells and in rat cardiomyocytes. Sodium 113-119 sodium voltage-gated channel alpha subunit 5 Homo sapiens 207-213 26951941-4 2016 We showed that the inhibitory effect of E2 on ANGII-induced water and sodium intake requires the ERK1/2 and JNK signaling pathways. Sodium 70-76 mitogen-activated protein kinase 8 Rattus norvegicus 108-111 26987067-5 2016 This includes PCSK9"s role in: trafficking of epithelial sodium channel; hepatic regeneration; pancreatic integrity and glucose homeostasis; antiviral activity; antimalarial activity; regulation of different cell signalling pathways; cortical neural differentiation; neuronal apoptosis and Alzheimer"s disease. Sodium 57-63 proprotein convertase subtilisin/kexin type 9 Homo sapiens 14-19 26667413-0 2016 Lanosterol Synthase Gene Polymorphisms and Changes in Endogenous Ouabain in the Response to Low Sodium Intake. Sodium 96-102 lanosterol synthase Homo sapiens 0-19 26538613-0 2016 Properties of an intermediate-duration inactivation process of the voltage-gated sodium conductance in rat hippocampal CA1 neurons. Sodium 81-87 carbonic anhydrase 1 Rattus norvegicus 119-122 26530729-7 2016 The high sodium level upregulated the expression of PCNA and the phosphorylation levels of JNK, ERK1/2 and p38 MAPK. Sodium 9-15 proliferating cell nuclear antigen Homo sapiens 52-56 26530729-11 2016 On the whole, our findings demonstrate that a relatively high sodium level per se directly promotes the proliferation of VSMCs through the JNK/ERK1/2/PCNA pathway. Sodium 62-68 proliferating cell nuclear antigen Homo sapiens 150-154 25502461-4 2016 In this study, we tested the effect of TRPV4 agonists (GSK1016790A and 4alpha-PDD) on voltage-gated sodium current (I Na) in hippocampal CA1 pyramidal neurons and the protein levels of alpha/beta-subunit of VGSCs in the hippocampus of mice subjected to intracerebroventricular (icv.) Sodium 100-106 transient receptor potential cation channel, subfamily V, member 4 Mus musculus 39-44 25502461-4 2016 In this study, we tested the effect of TRPV4 agonists (GSK1016790A and 4alpha-PDD) on voltage-gated sodium current (I Na) in hippocampal CA1 pyramidal neurons and the protein levels of alpha/beta-subunit of VGSCs in the hippocampus of mice subjected to intracerebroventricular (icv.) Sodium 100-106 carbonic anhydrase 1 Mus musculus 137-140 26713557-5 2016 Of these genes, 4 alter sodium currents, and the most common known genetic cause remains loss-of-function mutants in the cardiac sodium channel gene SCN5A. Sodium 24-30 sodium voltage-gated channel alpha subunit 5 Homo sapiens 149-154 26620127-3 2015 NaCT transports citrate from the blood into the cell coupled to the transport of sodium ions. Sodium 81-87 solute carrier family 13 member 5 Homo sapiens 0-4 26888838-9 2015 The electrophysiological analysis indicated that SCN5A-V411M significantly increased the peak current density ((230.8 +- 27.6)pA/pF vs. (101.2 +- 10.9)pA/pF, n=10, P<0.01) and the late sodium current ((156.6 +- 13.6)pA/pF vs. (95.9 +- 7.9)pA/pF, n=12, P<0.01) of sodium channel compared to wide type. Sodium 188-194 sodium voltage-gated channel alpha subunit 5 Homo sapiens 49-54 26609242-7 2015 SGLT2 inhibitors provide additional reductions in body weight and blood pressure due to the therapeutically induced excretion of glucose and sodium through the kidneys. Sodium 141-147 solute carrier family 5 member 2 Homo sapiens 0-5 26022185-2 2015 Most NaV1.5 mutations associated with LQT3 promote a mode of sodium channel gating in which some channels fail to inactivate, contributing to increased late sodium current (INaL), which is directly responsible for delayed repolarization and prolongation of the QT interval. Sodium 61-67 sodium voltage-gated channel alpha subunit 5 Homo sapiens 5-11 26022185-2 2015 Most NaV1.5 mutations associated with LQT3 promote a mode of sodium channel gating in which some channels fail to inactivate, contributing to increased late sodium current (INaL), which is directly responsible for delayed repolarization and prolongation of the QT interval. Sodium 61-67 sodium voltage-gated channel alpha subunit 5 Homo sapiens 38-42 26066075-1 2015 The classic role of mineralocorticoid receptor (MR) is to promote sodium transport in epithelial tissues. Sodium 66-72 nuclear receptor subfamily 3, group C, member 2 Mus musculus 20-46 26066075-1 2015 The classic role of mineralocorticoid receptor (MR) is to promote sodium transport in epithelial tissues. Sodium 66-72 nuclear receptor subfamily 3, group C, member 2 Mus musculus 48-50 26066075-2 2015 However, the MR is also expressed in a range of tissues in which its role appears unrelated to sodium transport, and under normal physiological conditions, it may be responding to cortisol (corticosterone in rodents) rather than aldosterone. Sodium 95-101 nuclear receptor subfamily 3, group C, member 2 Mus musculus 13-15 26193676-11 2015 Sodium excretion rate following increased RPP by L-NAME was markedly decreased in RGS2-/- mice and accompanied by increased translocation of ENaC to the luminal wall. Sodium 0-6 regulator of G-protein signaling 2 Mus musculus 82-86 26193676-11 2015 Sodium excretion rate following increased RPP by L-NAME was markedly decreased in RGS2-/- mice and accompanied by increased translocation of ENaC to the luminal wall. Sodium 0-6 sodium channel, nonvoltage-gated 1 alpha Mus musculus 141-145 26171609-1 2015 The gene product of SPINT 2, that encodes a transmembrane, Kunitz-type serine protease inhibitor independently designated as HAI-2 or placenta bikunin (PB), is involved in regulation of sodium absorption in human gastrointestinal track. Sodium 186-192 serine peptidase inhibitor, Kunitz type 2 Homo sapiens 20-27 26171609-1 2015 The gene product of SPINT 2, that encodes a transmembrane, Kunitz-type serine protease inhibitor independently designated as HAI-2 or placenta bikunin (PB), is involved in regulation of sodium absorption in human gastrointestinal track. Sodium 186-192 serine peptidase inhibitor, Kunitz type 2 Homo sapiens 125-130 26167459-0 2015 Epigenetics of epithelial Na(+) channel-dependent sodium uptake and blood pressure regulation. Sodium 50-56 sodium channel, nonvoltage-gated 1 alpha Mus musculus 15-39 26101954-4 2015 Voltage-gated sodium channel Nav1.3 produces tetrodotoxin-sensitive sodium currents with rapid repriming kinetics and has been shown to contribute to neuronal hyperexcitability and ectopic firing in injured neurons. Sodium 14-20 sodium voltage-gated channel alpha subunit 3 Rattus norvegicus 29-35 25898949-11 2015 Therefore, glucose stimulates NT secretion by uptake through SGLT1 and GLUT2, both causing depolarization either as a consequence of sodium-coupled uptake (SGLT1) or by closure of KATP channels (GLUT2 and SGLT1) secondary to the ATP-generating metabolism of glucose. Sodium 133-139 solute carrier family 2 member 2 Rattus norvegicus 71-76 25477470-0 2015 STE20/SPS1-related proline/alanine-rich kinase (SPAK) is critical for sodium reabsorption in isolated, perfused thick ascending limb. Sodium 70-76 serine/threonine kinase 39 Mus musculus 48-52 25473121-1 2015 Recently we identified a sodium ion binding pocket in a high-resolution structure of the human adenosine A2A receptor. Sodium 25-31 adenosine A2a receptor Homo sapiens 95-117 25391363-6 2015 Along with previous publications, our data validate a salt-induced hypertensive state in ANP(+/-) mice fed HS chow as they displayed left ventricular hypertrophy, increased systolic blood pressure, and increased urinary sodium excretion. Sodium 220-226 natriuretic peptide type A Mus musculus 89-97 25895625-8 2015 Although the precise mechanism responsible for the subsequently renal morphological and functional response in Sk offspring is incompletely known, the current data suggest that changes in renal function are conducive to excess sodium tubule reabsorption that is associated with enhanced TGF-beta1, fibronectin and collagen deposition, intrinsically related to fibrotic process, might potentiate the programming of adult hypertension. Sodium 227-233 fibronectin 1 Rattus norvegicus 298-309 27502620-0 2014 Mathematical analysis of the sodium sensitivity of the human histamine H3 receptor. Sodium 29-35 histamine receptor H3 Homo sapiens 61-82 25012170-7 2014 In summary, the presence of ACE in renal tissue facilitates angiotensin II accumulation, GFR reductions, and changes in the expression levels and post-translational modification of sodium transporters that are obligatory for sodium retention and hypertension in response to nitric oxide synthesis inhibition. Sodium 181-187 angiotensin I converting enzyme (peptidyl-dipeptidase A) 1 Mus musculus 28-31 24770793-8 2014 By contrast, PI(3,5)P2 elicited large sodium currents in hTPC2-EGFP-containing vacuoles, while NAADP had no such effect. Sodium 38-44 two pore segment channel 2 Homo sapiens 57-62 24744440-9 2014 Overexpression of Ank3 increased and depletion of Ank3 decreased ENaC-mediated sodium transport in mCCD cells. Sodium 79-85 ankyrin 3, epithelial Mus musculus 50-54 24768612-0 2014 Myotonic dystrophy type 1 mimics and exacerbates Brugada phenotype induced by Nav1.5 sodium channel loss-of-function mutation. Sodium 85-91 sodium voltage-gated channel alpha subunit 5 Homo sapiens 78-84 25098339-0 2014 Sodium binding to hH3R and hH 4R--a molecular modeling study. Sodium 0-6 histamine receptor H3 Homo sapiens 18-22 25098339-0 2014 Sodium binding to hH3R and hH 4R--a molecular modeling study. Sodium 0-6 histamine receptor H4 Homo sapiens 27-32 25098339-1 2014 Several aminergic GPCRs, e.g., the human histamine H3-receptor (hH3R) are sensitive to sodium ions. Sodium 87-93 histamine receptor H3 Homo sapiens 41-62 25098339-1 2014 Several aminergic GPCRs, e.g., the human histamine H3-receptor (hH3R) are sensitive to sodium ions. Sodium 87-93 histamine receptor H3 Homo sapiens 64-68 25098339-3 2014 Recently, in the crystallized adenosine A2A receptor (4EIY), a sodium ion was found in a pocket, coordinated by Asp52, Ser91, and three water molecules. Sodium 63-69 adenosine A2a receptor Homo sapiens 30-52 25098339-5 2014 In order to obtain a deeper insight onto the differences in sodium sensitivity between hH3R and hH4R, we performed molecular modelling studies, including molecular dynamic simulations and calculation of Gibbs energy of solvation. Sodium 60-66 histamine receptor H3 Homo sapiens 87-91 25098339-5 2014 In order to obtain a deeper insight onto the differences in sodium sensitivity between hH3R and hH4R, we performed molecular modelling studies, including molecular dynamic simulations and calculation of Gibbs energy of solvation. Sodium 60-66 histamine receptor H4 Homo sapiens 96-100 24740791-7 2014 ANG II induced threefold increases in phosphorylated MAP kinases ERK1/2 and a onefold increase in phosphorylated sodium and hydrogen exchanger 3 (NHE3) proteins, which were also blocked by losartan and megalin-siRNA. Sodium 113-119 low density lipoprotein receptor-related protein 2 Mus musculus 202-209 24760784-4 2014 The steady-state conductances of depolarizing Ih (hyperpolarization-activated cationic current), IT (low-threshold calcium current), and INaP (persistent sodium current) move the membrane potential away from the reversal potential of the leak conductances. Sodium 154-160 nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, zeta Mus musculus 137-141 24573164-2 2014 Typically, BrS mutations in SCN5A result in a reduction of sodium current with some mutations even exhibiting a dominant-negative effect on wild-type (WT) channels, thus leading to an even more prominent decrease in current amplitudes. Sodium 59-65 sodium voltage-gated channel alpha subunit 5 Homo sapiens 28-33 24602971-1 2014 Sodium-glucose co-transporter 2 (SGLT2) inhibitors represent a new class of antihyperglycemic agents that block renal sodium and glucose reabsorption and may reduce blood pressure (BP). Sodium 118-124 solute carrier family 5 member 2 Homo sapiens 0-31 24602971-1 2014 Sodium-glucose co-transporter 2 (SGLT2) inhibitors represent a new class of antihyperglycemic agents that block renal sodium and glucose reabsorption and may reduce blood pressure (BP). Sodium 118-124 solute carrier family 5 member 2 Homo sapiens 33-38 24300033-0 2014 Persistent sodium current properties in hippocampal CA1 pyramidal neurons of young and adult rats. Sodium 11-17 carbonic anhydrase 1 Rattus norvegicus 52-55 24253537-0 2014 Novel titanium-based O3-type NaTi(0.5)Ni(0.5)O2 as a cathode material for sodium ion batteries. Sodium 74-80 N-acetyltransferase 1 Homo sapiens 29-33 24253537-1 2014 O3-type NaTi(0.5)Ni(0.5)O2 is explored as a titanium-based cathode material for sodium ion batteries. Sodium 80-86 N-acetyltransferase 1 Homo sapiens 8-12 24404202-2 2014 To assess the functional modulation of Nav1.6 channels by the auxiliary beta1 subunit we expressed the rat Nav1.6 sodium channel alpha subunit by stable transformation in HEK293 cells either alone or in combination with the rat beta1 subunit and assessed the properties of the reconstituted channels by recording sodium currents using the whole-cell patch clamp technique. Sodium 114-120 neuron navigator 1 Rattus norvegicus 107-111 24404202-5 2014 Our results define modulatory effects of the beta1 subunit on the properties of rat Nav1.6-mediated sodium currents reconstituted in HEK293 cells that differ from effects measured previously in the Xenopus oocyte expression system. Sodium 100-106 neuron navigator 1 Rattus norvegicus 84-88 24154693-2 2013 Similarly, renal cytochrome P-450 (CYP)-epoxygenase-derived arachidonic acid metabolites, epoxyeicosatrienoic acids (EETs), also are antihypertensive through inhibiting sodium reabsorption and vasodilation. Sodium 169-175 cytochrome P450, family 21, subfamily a, polypeptide 1 Mus musculus 17-33 24154693-2 2013 Similarly, renal cytochrome P-450 (CYP)-epoxygenase-derived arachidonic acid metabolites, epoxyeicosatrienoic acids (EETs), also are antihypertensive through inhibiting sodium reabsorption and vasodilation. Sodium 169-175 cytochrome P450, family 21, subfamily a, polypeptide 1 Mus musculus 35-38 24339896-0 2013 Influence of the C242T polymorphism of the p22-phox gene (CYBA) on the interaction between urinary sodium excretion and blood pressure in an urban Brazilian population. Sodium 99-105 cytochrome b-245 alpha chain Homo sapiens 43-51 24339896-0 2013 Influence of the C242T polymorphism of the p22-phox gene (CYBA) on the interaction between urinary sodium excretion and blood pressure in an urban Brazilian population. Sodium 99-105 cytochrome b-245 alpha chain Homo sapiens 58-62 23974924-4 2013 Diabetes is associated with a reduction in phosphoinositide 3-kinase (PI3K) signaling, which regulates the action potential duration (APD) of individual myocytes and thus the QT interval by altering multiple ion currents, including the persistent sodium current INaP. Sodium 247-253 phosphoinositide-3-kinase regulatory subunit 1 Mus musculus 43-68 23974924-4 2013 Diabetes is associated with a reduction in phosphoinositide 3-kinase (PI3K) signaling, which regulates the action potential duration (APD) of individual myocytes and thus the QT interval by altering multiple ion currents, including the persistent sodium current INaP. Sodium 247-253 nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, zeta Mus musculus 262-266 24089410-5 2013 In contrast, KCC4 protein expression was increased by a low-sodium diet in the whole kidney and by metabolic acidosis in the renal outer medulla, specifically at the basolateral membrane of alpha-intercalated cells. Sodium 60-66 solute carrier family 12, member 7 Mus musculus 13-17 24037379-6 2013 Taken together, the dopamine transporter structure reveals the molecular basis for antidepressant action on sodium-coupled neurotransmitter symporters and elucidates critical elements of eukaryotic transporter structure and modulation by lipids, thus expanding our understanding of the mechanism and regulation of neurotransmitter uptake at chemical synapses. Sodium 108-114 Dopamine transporter Drosophila melanogaster 20-40 24266659-1 2013 The inward rectifier potassium (Kir) channel Kir4.1 plays essential roles in modulation of neurotransmission and renal sodium transport and may represent a novel drug target for temporal lobe epilepsy and hypertension. Sodium 119-125 potassium inwardly-rectifying channel, subfamily J, member 10 Rattus norvegicus 45-51 24400138-1 2013 Sodium-dependent ascorbic acid membrane transporters SLC23A1 and SLC23A2 mediate ascorbic acid (vitamin C) transport into cells. Sodium 0-6 solute carrier family 23 member 1 Homo sapiens 53-60 24194910-7 2013 Competition experiments with other amino acids and a low sodium dependency of the influx suggests that the amino acid transporters LAT1 and LAT2 are involved in the transport of L-BMAA into milk. Sodium 57-63 linker for activation of T cells family, member 2 Mus musculus 140-144 23893162-1 2013 To determine the roles of the individual S4 segments in domains I and II to activation and inactivation kinetics of sodium current (INa) in NaV1.5, we used a tethered biotin and avidin approach after a site-directed cysteine substitution was made in the second outermost Arg in each S4 (DI-R2C and DII-R2C). Sodium 116-122 sodium voltage-gated channel alpha subunit 5 Homo sapiens 140-146 23668478-1 2013 AIMS: Sodium-glucose co-transporter 2 (SGLT2) reabsorbs glucose and sodium in the renal proximal tubule. Sodium 68-74 solute carrier family 5 member 2 Homo sapiens 6-37 23668478-1 2013 AIMS: Sodium-glucose co-transporter 2 (SGLT2) reabsorbs glucose and sodium in the renal proximal tubule. Sodium 68-74 solute carrier family 5 member 2 Homo sapiens 39-44 23357618-6 2013 Recombinant rat IL-10 (200 pg/ml) not only reduced the densities of TTX-sensitive and Nav1.8 currents in control DRG neurons, but also reversed the increase of the sodium currents induced by rat recombinant TNF-alpha (100 pg/ml), as revealed by patch-clamp recordings. Sodium 164-170 interleukin 10 Rattus norvegicus 16-21 23877755-10 2013 The results indicated that DSP suppression decreased sodium current and slowed conduction velocity in cultured cells. Sodium 53-59 desmoplakin Homo sapiens 27-30 24075511-5 2013 We showed that the most highly expressed transporters, namely sodium dependent SNAT3 (Slc38a3) and SNAT5 (Slc38a5) and sodium independent neutral amino acids transporters LAT1 (Slc7a5) and LAT2 (Slc7a8), are expressed in the basolateral membrane of acinar cells. Sodium 62-68 solute carrier family 38, member 3 Mus musculus 79-84 24075511-5 2013 We showed that the most highly expressed transporters, namely sodium dependent SNAT3 (Slc38a3) and SNAT5 (Slc38a5) and sodium independent neutral amino acids transporters LAT1 (Slc7a5) and LAT2 (Slc7a8), are expressed in the basolateral membrane of acinar cells. Sodium 62-68 solute carrier family 38, member 3 Mus musculus 86-93 24075511-5 2013 We showed that the most highly expressed transporters, namely sodium dependent SNAT3 (Slc38a3) and SNAT5 (Slc38a5) and sodium independent neutral amino acids transporters LAT1 (Slc7a5) and LAT2 (Slc7a8), are expressed in the basolateral membrane of acinar cells. Sodium 62-68 linker for activation of T cells family, member 2 Mus musculus 189-193 24075511-5 2013 We showed that the most highly expressed transporters, namely sodium dependent SNAT3 (Slc38a3) and SNAT5 (Slc38a5) and sodium independent neutral amino acids transporters LAT1 (Slc7a5) and LAT2 (Slc7a8), are expressed in the basolateral membrane of acinar cells. Sodium 62-68 solute carrier family 7 (cationic amino acid transporter, y+ system), member 8 Mus musculus 195-201 23753405-1 2013 The renal outer medullary potassium channel (ROMK, KCNJ1) mediates potassium recycling and facilitates sodium reabsorption through the Na(+)/K(+)/2Cl(-) cotransporter in the loop of Henle and potassium secretion at the cortical collecting duct. Sodium 103-109 potassium inwardly-rectifying channel, subfamily J, member 1 Mus musculus 45-49 23541953-0 2013 Caveolin-3 suppresses late sodium current by inhibiting nNOS-dependent S-nitrosylation of SCN5A. Sodium 27-33 sodium voltage-gated channel alpha subunit 5 Homo sapiens 90-95 23541953-2 2013 When co-expressed with SCN5A-encoded cardiac sodium channels these mutations increased late sodium current (INa) but the mechanism was unclear. Sodium 45-51 sodium voltage-gated channel alpha subunit 5 Homo sapiens 23-28 23529167-5 2013 However, in the renal ATRAP transgenic mice compared with wild-type mice, the following took place: (1) the development of high blood pressure in response to angiotensin II infusion was significantly suppressed based on radiotelemetry, (2) the extent of daily positive sodium balance was significantly reduced during angiotensin II infusion in metabolic cage analysis, and (3) the renal Na+ -Cl- cotransporter activation and alpha-subunit of the epithelial sodium channel induction by angiotensin II infusion were inhibited. Sodium 269-275 angiotensin II, type I receptor-associated protein Mus musculus 22-27 23766534-6 2013 Moreover, excessive chloride absorption by pendrin drove parallel absorption of sodium through the epithelial sodium channel ENaC and the sodium-driven chloride/bicarbonate exchanger (Ndcbe), despite an appropriate downregulation of these sodium transporters in response to the expanded vascular volume and hypertension. Sodium 80-86 solute carrier family 26, member 4 Mus musculus 43-50 23636020-0 2013 Letter on "sodium-dependent modulation of systemic and urinary renalase expression and activity in the rat remnant kidney". Sodium 11-17 renalase, FAD-dependent amine oxidase Rattus norvegicus 63-71 23595759-4 2013 Such a finding would be of interest because of its potential impact on neuronal activity: previous studies demonstrated that BACE1-overexpressing mice exhibit excessive cleavage of Navbeta2 and reduced sodium current density, but the phenotype associated with loss of function mutations in either Navbeta-subunits or pore-forming alpha-subunits is epilepsy. Sodium 202-208 beta-site APP cleaving enzyme 1 Mus musculus 125-130 23331097-1 2013 Nitric oxide (NO) and NO synthase 1 (NOS1) maintain sodium and water homeostasis. Sodium 52-58 nitric oxide synthase 1 Rattus norvegicus 22-35 23331097-1 2013 Nitric oxide (NO) and NO synthase 1 (NOS1) maintain sodium and water homeostasis. Sodium 52-58 nitric oxide synthase 1 Rattus norvegicus 37-41 24555036-4 2013 METHODS: In this short study, we (1) compared the biophysical properties of the sodium current (I Na) generated by the mouse Na v1.5 (mNa v1.5) and human Na v1.5 (hNa v1.5) constructs that were expressed in HEK293 cells, and (2) investigated the possible alterations of the biophysical properties of the human Na v1.5 construct that was modified with specific epitopes. Sodium 80-86 sodium channel, voltage-gated, type V, alpha Mus musculus 125-132 23034715-1 2012 Insulin has long been hypothesized to cause sodium retention, potentially of enough magnitude to contribute to hypertension in obesity, metabolic syndrome, and Type II diabetes. Sodium 44-50 insulin Canis lupus familiaris 0-7 23034715-11 2012 This new evidence that insulin has a sodium-retaining effect during hyperglycemia may have implications for maintaining sodium balance in uncontrolled Type II diabetes. Sodium 37-43 insulin Canis lupus familiaris 23-30 23034715-11 2012 This new evidence that insulin has a sodium-retaining effect during hyperglycemia may have implications for maintaining sodium balance in uncontrolled Type II diabetes. Sodium 120-126 insulin Canis lupus familiaris 23-30 22957745-0 2012 Plasma Lp-PLA(2) mass and apoB-lipoproteins that carry Lp-PLA(2) decrease after sodium. Sodium 82-88 phospholipase A2 group VII Homo sapiens 56-64 22957745-2 2012 As increasing dietary sodium intake may decrease plasma apoB-containing lipoproteins, we tested whether a sodium challenge lowers plasma Lp-PLA(2) mass, as well as the levels of apoB-containing lipoprotein particles carrying Lp-PLA(2) (apoB-Lp-PLA(2) ), employing a newly developed enzyme-linked immunosorbent assay. Sodium 106-112 phospholipase A2 group VII Homo sapiens 137-146 22957745-7 2012 CONCLUSION: Both plasma Lp-PLA(2) mass levels and apoB-Lp-PLA(2) decrease in response to a short-term oral sodium challenge. Sodium 107-113 phospholipase A2 group VII Homo sapiens 24-33 22957745-7 2012 CONCLUSION: Both plasma Lp-PLA(2) mass levels and apoB-Lp-PLA(2) decrease in response to a short-term oral sodium challenge. Sodium 107-113 phospholipase A2 group VII Homo sapiens 24-32 22686466-1 2012 Renal medullary hypoxia-inducible factor (HIF)-1alpha and its target genes, such as haem oxygenase and nitric oxide synthase, have been indicated to play an important role in the regulation of sodium excretion and blood pressure. Sodium 193-199 hypoxia inducible factor 1 subunit alpha Rattus norvegicus 16-53 22686466-5 2012 It was shown that overexpression of PHD2 transgene increased PHD2 levels and decreased HIF-1alpha levels in the renal medulla, which blunted pressure natriuresis, attenuated sodium excretion, promoted sodium retention and produced salt sensitive hypertension after high salt challenge compared with rats treated with control plasmids. Sodium 174-180 egl-9 family hypoxia-inducible factor 1 Rattus norvegicus 36-40 22686466-5 2012 It was shown that overexpression of PHD2 transgene increased PHD2 levels and decreased HIF-1alpha levels in the renal medulla, which blunted pressure natriuresis, attenuated sodium excretion, promoted sodium retention and produced salt sensitive hypertension after high salt challenge compared with rats treated with control plasmids. Sodium 201-207 egl-9 family hypoxia-inducible factor 1 Rattus norvegicus 36-40 22841594-2 2012 Natural zeolites can be used as a cheap and effective method to control sodium adsorption ratio (SAR, which is a measure of the relative preponderance of sodium to calcium and magnesium) due to its high cation exchange capacity. Sodium 72-78 sarcosine dehydrogenase Homo sapiens 97-100 22841594-2 2012 Natural zeolites can be used as a cheap and effective method to control sodium adsorption ratio (SAR, which is a measure of the relative preponderance of sodium to calcium and magnesium) due to its high cation exchange capacity. Sodium 154-160 sarcosine dehydrogenase Homo sapiens 97-100 22841594-3 2012 In this study, a natural zeolite from Queensland was examined for its potential to treat CSG water to remove sodium ions to lower SAR and reduce the pH value. Sodium 109-115 sarcosine dehydrogenase Homo sapiens 130-133 22587908-8 2012 The high-sodium diet also induced Ang II, TGF-beta(1) and alpha-SMA overexpression and decreased eNOS expression in the renal cortex and medulla. Sodium 9-15 nitric oxide synthase 3 Rattus norvegicus 97-101 22592638-3 2012 We hypothesized that high sodium intake differentially regulates and shifts a balance between opposing components of the renal RAS, namely, angiotensin-converting enzyme (ACE)-ANG II-type 1 ANG II receptor (AT(1)R) vs. AT(2)-ACE2-angiotensinogen (Ang) (1-7)-Mas receptor (MasR), in obesity. Sodium 26-32 angiotensin I converting enzyme 2 Rattus norvegicus 225-229 21916933-5 2012 Amyloidogenic TTR mutations cause significant calcium influx via L-type calcium channels in neuronal cell lines, while in primary sensory neurons, TTR mediates a calcium influx via a novel mechanism of transient receptor potential melanostatin (TRPM8) and voltage-gated sodium and calcium channel activation. Sodium 270-276 transthyretin Homo sapiens 14-17 21916933-5 2012 Amyloidogenic TTR mutations cause significant calcium influx via L-type calcium channels in neuronal cell lines, while in primary sensory neurons, TTR mediates a calcium influx via a novel mechanism of transient receptor potential melanostatin (TRPM8) and voltage-gated sodium and calcium channel activation. Sodium 270-276 transthyretin Homo sapiens 147-150 22285383-1 2012 OBJECTIVES: C-type natriuretic peptide (CNP) might be an important regulator of vasodilatation, fluid and sodium balance in liver cirrhosis. Sodium 106-112 natriuretic peptide C Homo sapiens 12-38 22285383-1 2012 OBJECTIVES: C-type natriuretic peptide (CNP) might be an important regulator of vasodilatation, fluid and sodium balance in liver cirrhosis. Sodium 106-112 natriuretic peptide C Homo sapiens 40-43 22133520-7 2012 With regard to brain Fos immunoreactivity, we observed that Furosemide-sodium depletion in the PM-Na group induced a higher number of activated cells in the subfornical organ, ventral subdivision of the paraventricular nucleus and vasopressinergic neurons of the supraoptic nucleus than in the PM-Ctrol animals. Sodium 71-77 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 21-24 22293193-3 2012 Angiotensin II (AII) is a key peptide underlying sodium retention. Sodium 49-55 arginase type II Mus musculus 0-14 22293193-3 2012 Angiotensin II (AII) is a key peptide underlying sodium retention. Sodium 49-55 arginase type II Mus musculus 16-19 22383044-5 2012 Swelling-induced ROS production in NIH3T3 fibroblasts is generated by NOX4 and by increasing total ROS, by either exogenous application of H(2)O(2) or overexpressing NOX4, we demonstrate that TonEBP activity and taurine influx are regulated negatively by ROS under hypo-osmotic, low-sodium conditions, whereas the TauT mRNA level is unaffected. Sodium 283-289 nuclear factor of activated T cells 5 Mus musculus 192-198 22677781-2 2012 In many organ systems, this activity is regulated by membrane-bound sodium/calcium (Na(+)/Ca(2+)) exchangers, which include the NCX and NCKX [sodium/calcium-potassium (Na(+)/Ca(2+)-K(+)) exchanger] proteins. Sodium 68-74 T cell leukemia homeobox 2 Homo sapiens 128-131 22870192-3 2012 Na(V)1.8 underlies the vast majority of sodium currents during action potentials. Sodium 40-46 sodium voltage-gated channel alpha subunit 10 Homo sapiens 0-8 21723844-1 2011 BACKGROUND: Loss of expression of the desmosomal protein plakophilin-2 (PKP2) leads to decreased gap junction-mediated (GJ) coupling, and alters the amplitude and kinetics of sodium current in cardiac myocytes. Sodium 175-181 plakophilin 2 Rattus norvegicus 57-70 21723844-1 2011 BACKGROUND: Loss of expression of the desmosomal protein plakophilin-2 (PKP2) leads to decreased gap junction-mediated (GJ) coupling, and alters the amplitude and kinetics of sodium current in cardiac myocytes. Sodium 175-181 plakophilin 2 Rattus norvegicus 72-76 21723844-11 2011 CONCLUSION: PKP2-dependent changes in sodium current kinetics lead to slow conduction, increased propensity to functional block, and vortex shedding. Sodium 38-44 plakophilin 2 Rattus norvegicus 12-16 21908609-1 2011 Fibroblast growth factor-23 (FGF-23) inhibits sodium-dependent phosphate transport in brush border membrane vesicles derived from hormone-treated kidney slices of the mouse and in mouse proximal tubule cells by processes involving mitogen-activated protein kinase (MAPK) but not protein kinase A (PKA) or protein kinase C (PKC). Sodium 46-52 fibroblast growth factor 23 Mus musculus 0-27 21908609-1 2011 Fibroblast growth factor-23 (FGF-23) inhibits sodium-dependent phosphate transport in brush border membrane vesicles derived from hormone-treated kidney slices of the mouse and in mouse proximal tubule cells by processes involving mitogen-activated protein kinase (MAPK) but not protein kinase A (PKA) or protein kinase C (PKC). Sodium 46-52 fibroblast growth factor 23 Mus musculus 29-35 17890487-0 2007 High dietary sodium intake increases white adipose tissue mass and plasma leptin in rats. Sodium 13-19 leptin Rattus norvegicus 74-80 17685643-2 2007 By a stepwise intercalation, the sodium form of synthetic fluorinated mica (Mica) was first exchanged with the poly(oxyalkylene)-diamine salts (POA-amine) through an ionic exchange reaction and then the BSA embedment. Sodium 33-39 MHC class I polypeptide-related sequence A Homo sapiens 70-74 17685643-2 2007 By a stepwise intercalation, the sodium form of synthetic fluorinated mica (Mica) was first exchanged with the poly(oxyalkylene)-diamine salts (POA-amine) through an ionic exchange reaction and then the BSA embedment. Sodium 33-39 MHC class I polypeptide-related sequence A Homo sapiens 76-80 17522178-0 2007 Sodium currents in mesencephalic trigeminal neurons from Nav1.6 null mice. Sodium 0-6 neuron navigator 1 Mus musculus 57-61 17522178-3 2007 We found that peak transient, persistent, and resurgent sodium currents from med (Na(v)1.6(-/-)) mice were reduced by 18, 39, and 76% relative to their wild-type (Na(v)1.6(+/+)) littermates, respectively. Sodium 56-62 sodium channel, voltage-gated, type VIII, alpha Mus musculus 82-90 17591909-0 2007 Expression of the sodium-coupled monocarboxylate transporters SMCT1 (SLC5A8) and SMCT2 (SLC5A12) in retina. Sodium 18-24 solute carrier family 5 (iodide transporter), member 8 Mus musculus 69-75 17434681-0 2007 5-HT2 and 5-HT3 receptors in the lateral parabrachial nucleus mediate opposite effects on sodium intake. Sodium 90-96 5-hydroxytryptamine receptor 2A Rattus norvegicus 0-11 17434681-8 2007 Pretreatment of the LPBN with the 5-HT3 receptor antagonist, 1-methyl-N-[8-methyl-8-azabicyclo (3.2.1)-oct-3-yl]-1H-indazole-3-carboxamide (LY-278,584) abolished the effects of PBG, but LY-278,584 had no effects on sodium or water intake when injected by itself. Sodium 215-221 5-hydroxytryptamine receptor 3A Rattus norvegicus 34-48 17434681-11 2007 In contrast, activation of the 5-HT3 receptor subtype increases sodium ingestion. Sodium 64-70 5-hydroxytryptamine receptor 3A Rattus norvegicus 31-45 17276524-3 2007 Recently, it was demonstrated in rats and humans that GLP-1 can stimulate renal excretion of sodium. Sodium 93-99 glucagon like peptide 1 receptor Homo sapiens 54-59 17276524-14 2007 Functional assays demonstrated an inhibition of sodium re-absorption with GLP-1 after 3 h of incubation. Sodium 48-54 glucagon like peptide 1 receptor Homo sapiens 74-79 17276524-17 2007 Addition of GLP-1 to these cells resulted in a reduced sodium re-absorption. Sodium 55-61 glucagon like peptide 1 receptor Homo sapiens 12-17 17276524-19 2007 We conclude that GLP-1 modulates sodium homeostasis in the kidney most likely through a direct action via its GLP-1R in proximal tubular cells. Sodium 33-39 glucagon like peptide 1 receptor Homo sapiens 17-22 17395152-5 2007 Short period activation of protein kinase C (PKC) by phorbol 12-myristate, 13-acetate (PMA) and alpha-adrenergic receptor agonist, phenylephrine (PE), downregulated sodium-dependent succinate transport presumably via hNaDC-3. Sodium 165-171 solute carrier family 13 member 3 Homo sapiens 217-224 17255103-2 2007 We have identified and characterized two different sodium-coupled monocarboxylate cotransporters (SMCT) from zebrafish (Danio rerio), electrogenic (zSMCTe) and electroneutral (zSMCTn). Sodium 51-57 solute carrier family 5 member 8, like Danio rerio 148-154 17448995-0 2007 The neuronal channel NALCN contributes resting sodium permeability and is required for normal respiratory rhythm. Sodium 47-53 sodium leak channel, non-selective Mus musculus 21-26 17360470-6 2007 Importantly, PHAII-causing mutations eliminate WNK4"s inhibition of ENaC, thereby paralleling other effects of PHAII to increase sodium balance. Sodium 129-135 WNK lysine deficient protein kinase 4 Mus musculus 47-51 17347258-1 2007 The relationship between severe myoclonic epilepsy of infancy (SMEI or Dravet syndrome) and the related syndrome SMEI-borderland (SMEB) with mutations in the sodium channel alpha 1 subunit gene SCN1A is well established. Sodium 158-164 sodium voltage-gated channel alpha subunit 1 Homo sapiens 194-199 17209804-1 2007 The mammalian NHE (Na+/H+ exchanger) is a ubiquitously expressed integral membrane protein that regulates intracellular pH by removing a proton in exchange for an extracellular sodium ion. Sodium 177-183 solute carrier family 9 member C1 Homo sapiens 14-17 17209804-1 2007 The mammalian NHE (Na+/H+ exchanger) is a ubiquitously expressed integral membrane protein that regulates intracellular pH by removing a proton in exchange for an extracellular sodium ion. Sodium 177-183 solute carrier family 9 member C1 Homo sapiens 19-35 17068143-5 2007 The CSF-1-induced rise in pH(i) is not blocked by 4,4"-diisothiocyanatostilbene-2,2"-disulfonic acid, an inhibitor of HCO(3)(-) transporters but is abolished by removing extracellular sodium. Sodium 184-190 glucose-6-phosphate isomerase Homo sapiens 26-31 17060503-9 2007 In conclusion, stimulation of ETA-R plays an important contributory role to the Ang II-mediated suppression of the activation of renal mechanosensory nerves in conditions of low-sodium diet. Sodium 178-184 endothelin receptor type A Rattus norvegicus 30-35 17129991-4 2006 Missense mutations in the voltage-gated sodium channel a1 subunit gene (SCN1A) were firstly identified in patients with generalized epilepsy with febrile seizures plus additional symptoms (GEFS + ). Sodium 40-46 sodium voltage-gated channel alpha subunit 1 Homo sapiens 72-77 17082729-1 2006 OBJECTIVE: The Na-K-2Cl cotransporter (NKCC2 isoform) of the thick ascending limb of Henle"s loop (TAL) plays an important role in renal sodium handling, and the vascular isoform (NKCC1) participates in the response to vasoconstrictors. Sodium 137-143 solute carrier family 12 member 2 Rattus norvegicus 180-185 16763077-6 2006 In anesthetized rats fed high-sodium diet, renal pelvic administration of the ETBR antagonist BQ-788 reduced the afferent renal nerve activity (ARNA) response to increasing renal pelvic pressure 7.5 mmHg from 26+/-3 to 9+/-3% and the PGE2-mediated renal pelvic release of substance P from 9+/-1 to 3+/-1 pg/min. Sodium 30-36 endothelin receptor type B Rattus norvegicus 78-82 16763077-7 2006 Conversely, in rats fed low-sodium diet, renal pelvic administration of the ETAR antagonist BQ-123 enhanced the ARNA response to increased renal pelvic pressure from 9+/-2 to 23+/-6% and the PGE2-mediated renal pelvic release of substance P from 0+/-0 to 6+/-1 pg/min. Sodium 28-34 endothelin receptor type A Rattus norvegicus 76-80 16763077-8 2006 Adding the ETAR antagonist to ETBR-blocked renal pelvises restored the responsiveness of renal sensory nerves in rats fed a high-sodium diet. Sodium 129-135 endothelin receptor type A Rattus norvegicus 11-15 16763077-8 2006 Adding the ETAR antagonist to ETBR-blocked renal pelvises restored the responsiveness of renal sensory nerves in rats fed a high-sodium diet. Sodium 129-135 endothelin receptor type B Rattus norvegicus 30-34 16763077-9 2006 Adding the ETBR antagonist to ETAR-blocked pelvises suppressed the responsiveness of the renal sensory nerves in rats fed a low-sodium diet. Sodium 128-134 endothelin receptor type B Rattus norvegicus 11-15 16763077-9 2006 Adding the ETBR antagonist to ETAR-blocked pelvises suppressed the responsiveness of the renal sensory nerves in rats fed a low-sodium diet. Sodium 128-134 endothelin receptor type A Rattus norvegicus 30-34 16763077-10 2006 In conclusion, activation of ETBR and ETAR contributes to the enhanced and suppressed responsiveness of renal sensory nerves in conditions of high- and low-sodium dietary intake, respectively. Sodium 156-162 endothelin receptor type B Rattus norvegicus 29-33 16763077-10 2006 In conclusion, activation of ETBR and ETAR contributes to the enhanced and suppressed responsiveness of renal sensory nerves in conditions of high- and low-sodium dietary intake, respectively. Sodium 156-162 endothelin receptor type A Rattus norvegicus 38-42 17065438-2 2006 Here, we present the formulation and use of a computational model for SCN1A to elucidate molecular mechanisms underlying the increased persistent sodium current exhibited by the GEFS+ mutant R1648H. Sodium 146-152 sodium voltage-gated channel alpha subunit 1 Homo sapiens 70-75 16887279-0 2006 Beta-endorphin involvement in the regulatory response to body sodium overload. Sodium 62-68 pro-opiomelanocortin-alpha Mus musculus 0-14 16887279-8 2006 In summary, our results indicate that the beta-endorphinergic system may play a part in the compensatory response to sodium overload, since the absence of beta-endorphin causes an increase in systolic blood pressure, and increases median preoptic nucleus neural activity and urinary epinephrine excretion. Sodium 117-123 pro-opiomelanocortin-alpha Mus musculus 42-56 16865694-2 2006 In 30 to 70% of SMEI patients, truncating and missense mutations in the neuronal voltage-gated sodium-channel alpha-subunit gene (SCN1A) have been identified. Sodium 95-101 sodium voltage-gated channel alpha subunit 1 Homo sapiens 130-135 16908340-6 2006 Though the metal ion transport by Smf1p, the yeast homolog of DCT1, is also a protonmotive force, a slippage of sodium ions was observed. Sodium 112-118 divalent metal ion transporter SMF1 Saccharomyces cerevisiae S288C 34-39 16531080-1 2006 We have recently shown that amino acid substitutions in the membrane domain of band 3 (anion exchanger 1, SLC4A1) are associated with hereditary stomatocytosis (HSt), a red cell condition in which the cells leak sodium and potassium ions. Sodium 212-218 solute carrier family 4 member 1 (Diego blood group) Homo sapiens 106-112 16508653-2 2006 However, the definitive proof of the implication of AQP1 in solute-free water transport, sodium sieving, and ultrafiltration (UF) during peritoneal dialysis (PD) is lacking, and the effects of its deletion on the structure of the membrane are unknown. Sodium 89-95 aquaporin 1 Mus musculus 52-56 16508653-6 2006 Heterozygous Aqp1(+/-) mice showed intermediate values in sodium sieving and initial UF, whereas cumulative UF was similar to Aqp1(+/+) mice. Sodium 58-64 aquaporin 1 Mus musculus 13-17 16141358-1 2006 Angiotensin II (Ang II) activates a wide spectrum of signaling responses via the AT1 receptor (AT1R) that mediate its physiological control of blood pressure, thirst, and sodium balance and its diverse pathological actions in cardiovascular, renal, and other cell types. Sodium 171-177 angiotensin II receptor type 1 Homo sapiens 81-93 16141358-1 2006 Angiotensin II (Ang II) activates a wide spectrum of signaling responses via the AT1 receptor (AT1R) that mediate its physiological control of blood pressure, thirst, and sodium balance and its diverse pathological actions in cardiovascular, renal, and other cell types. Sodium 171-177 angiotensin II receptor type 1 Homo sapiens 95-99 16516149-1 2006 The mineralocorticoid receptor (MR) is expressed in kidney and plays a central role in the control of sodium, homeostatic fluid, and blood pressure. Sodium 102-108 nuclear receptor subfamily 3 group C member 2 Homo sapiens 4-30 16516149-1 2006 The mineralocorticoid receptor (MR) is expressed in kidney and plays a central role in the control of sodium, homeostatic fluid, and blood pressure. Sodium 102-108 nuclear receptor subfamily 3 group C member 2 Homo sapiens 32-34 16483548-1 2006 The serum- and glucocorticoid-regulated kinase-1 (SGK1) participates in the regulation of sodium homeostasis and blood pressure by mineralocorticoids. Sodium 90-96 serum/glucocorticoid regulated kinase 1 Rattus norvegicus 4-48 16483548-1 2006 The serum- and glucocorticoid-regulated kinase-1 (SGK1) participates in the regulation of sodium homeostasis and blood pressure by mineralocorticoids. Sodium 90-96 serum/glucocorticoid regulated kinase 1 Rattus norvegicus 50-54 16778331-2 2006 In AME, defective HSD11B2 enzyme activity results in overstimulation of the mineralocorticoid receptor (MR) by cortisol, causing sodium retention, hypokalemia, and salt-dependent hypertension. Sodium 129-135 nuclear receptor subfamily 3 group C member 2 Homo sapiens 76-102 16778331-2 2006 In AME, defective HSD11B2 enzyme activity results in overstimulation of the mineralocorticoid receptor (MR) by cortisol, causing sodium retention, hypokalemia, and salt-dependent hypertension. Sodium 129-135 nuclear receptor subfamily 3 group C member 2 Homo sapiens 104-106 16189294-14 2006 The decreased abundance of NHE3, NKCC2, NCC, and Na-K-ATPase may play a compensatory role in promoting sodium excretion. Sodium 103-109 solute carrier family 9 member A3 Rattus norvegicus 27-31 16195498-0 2006 Modulation by dietary sodium intake of melanocortin 3 receptor mRNA and protein abundance in the rat kidney. Sodium 22-28 melanocortin 3 receptor Rattus norvegicus 39-62 16195498-6 2006 The increase in MC3-R expression induced by dietary sodium was observed in inner medullary collecting duct (IMCD) cells isolated from the kidneys of HSD rats, suggesting that these cells were the major site of receptor expression in the medulla. Sodium 52-58 melanocortin 3 receptor Rattus norvegicus 16-21 16505253-0 2006 SLC12A3 (solute carrier family 12 member [sodium/chloride] 3) polymorphisms are associated with end-stage renal disease in diabetic nephropathy. Sodium 42-48 solute carrier family 12 member 3 Homo sapiens 0-7 16490820-2 2006 A candidate protein is the organic cation transporter novel type 2 (OCTN2) (SLC22A5), physiologically acting as a sodium-dependent transport protein for carnitine. Sodium 114-120 solute carrier family 22 member 5 Homo sapiens 27-66 16490820-2 2006 A candidate protein is the organic cation transporter novel type 2 (OCTN2) (SLC22A5), physiologically acting as a sodium-dependent transport protein for carnitine. Sodium 114-120 solute carrier family 22 member 5 Homo sapiens 68-73 16490820-2 2006 A candidate protein is the organic cation transporter novel type 2 (OCTN2) (SLC22A5), physiologically acting as a sodium-dependent transport protein for carnitine. Sodium 114-120 solute carrier family 22 member 5 Homo sapiens 76-83 16192299-9 2006 However, further isolation of background currents by recording in solutions that contained only sodium or only potassium revealed that both leptin and CCK were capable of increasing a sodium-dependent conductance or inhibiting a potassium-dependent conductance. Sodium 96-102 leptin Rattus norvegicus 140-146 16192299-9 2006 However, further isolation of background currents by recording in solutions that contained only sodium or only potassium revealed that both leptin and CCK were capable of increasing a sodium-dependent conductance or inhibiting a potassium-dependent conductance. Sodium 184-190 leptin Rattus norvegicus 140-146 16204414-2 2006 The present study is designed to investigate the function of the AT2 receptors on renal sodium excretion and AT(2) receptor expression in the cortical membranes of streptozotocin (STZ)-induced diabetic rats. Sodium 88-94 angiotensin II receptor, type 2 Rattus norvegicus 65-68 16204414-9 2006 In conclusion, our data suggest that the tubular AT2 receptors in diabetic rats are profoundly enhanced and possibly via a cGMP pathway promote sodium excretion in this model of diabetes. Sodium 144-150 angiotensin II receptor, type 2 Rattus norvegicus 49-52 16444598-0 2006 Leptin blockade attenuates sodium excretion in saline-loaded normotensive rats. Sodium 27-33 leptin Rattus norvegicus 0-6 16444598-4 2006 In the experimental group (n = 10), leptin antibody significantly decreased urinary sodium excretion and urinary flow by approximately 30% compared to the control rats (n = 10). Sodium 84-90 leptin Rattus norvegicus 36-42 16458823-1 2006 Mutations in the voltage-gated sodium channel gene SCN1A are a major cause of severe myoclonic epilepsy of infancy (Dravet syndrome) and generalized epilepsy with febrile seizures plus. Sodium 31-37 sodium voltage-gated channel alpha subunit 1 Homo sapiens 51-56 16338225-4 2006 This prompted us to test a possible involvement of NEDD4L for the development of sodium-sensitive hypertension in Dahl salt-sensitive (DS) rats and its normotensive littermate Dahl salt-resistant (DR) rats. Sodium 81-87 NEDD4 like E3 ubiquitin protein ligase Rattus norvegicus 51-57 16338225-6 2006 Then, we analyzed the expression of rat NEDD4L in the kidney of both DS and DR under high and low sodium regimens. Sodium 98-104 NEDD4 like E3 ubiquitin protein ligase Rattus norvegicus 40-46 16338225-7 2006 NEDD4L expression examined by quantitative PCR technique revealed lower expression of NEDD4L transcripts in DS rats under either diet compared to DR animals; additionally, NEDD4L expression was significantly increased with sodium loading. Sodium 223-229 NEDD4 like E3 ubiquitin protein ligase Rattus norvegicus 0-6 16338225-8 2006 Using in situ hybridization experiments, rat NEDD4L was predominantly expressed in distal nephron in a manner dependent on both sodium regimen and genetic background. Sodium 128-134 NEDD4 like E3 ubiquitin protein ligase Rattus norvegicus 45-51 16338225-10 2006 The expression of NEDD4L in distal nephron and its response to chronic sodium loading suggest that it participates in the functioning of this segment in sodium reabsorption. Sodium 71-77 NEDD4 like E3 ubiquitin protein ligase Rattus norvegicus 18-24 16338225-10 2006 The expression of NEDD4L in distal nephron and its response to chronic sodium loading suggest that it participates in the functioning of this segment in sodium reabsorption. Sodium 153-159 NEDD4 like E3 ubiquitin protein ligase Rattus norvegicus 18-24 16325765-6 2006 Coexpression of TEH subunits with Para in Xenopus oocytes showed a strong (30-fold, TEH1), medium (5- to 10-fold, TEH2 and TEH3), or no (TEH4) increase in sodium current amplitude, while TipE increased the current 20-fold. Sodium 155-161 paralytic Drosophila melanogaster 34-38 16633989-8 2006 Quantitative polymerase chain reaction (PCR) and Western blot analysis reveal that in diabetic rats compared with controls, mRNA and protein abundance was higher for type 3 sodium/hydrogen exchanger (NHE3) in proximal tubule and ascending limbs of Henle"s loop, and higher for bumetanide-sensitive sodium-potassium-2 chloride cotransporter (NKCC2) in ascending limbs of Henle"s loop. Sodium 173-179 solute carrier family 9 member A3 Rattus norvegicus 200-204 16636594-9 2006 In the erythrocytes of dehydrated infants, Na+,K+-ATPase activity was increased correlating positively with the amount of sodium administered. Sodium 122-128 dynein axonemal heavy chain 8 Homo sapiens 50-56 16785747-2 2006 The cloning and identification of sodium transporting genes and proteins like NHE3, NKCC2, ROMK, CLCNKB, NCC, and EnaC has considerably improved our understanding of renal salt handling. Sodium 34-40 potassium inwardly rectifying channel subfamily J member 1 Homo sapiens 91-95 16785747-2 2006 The cloning and identification of sodium transporting genes and proteins like NHE3, NKCC2, ROMK, CLCNKB, NCC, and EnaC has considerably improved our understanding of renal salt handling. Sodium 34-40 chloride voltage-gated channel Kb Homo sapiens 97-103 16198010-13 2005 These results suggest that LPO are implicated in sodium balance that is mediated by V1, V2, AT1 and AT2 receptors. Sodium 49-55 angiotensin II receptor type 1 Homo sapiens 92-95 16198010-13 2005 These results suggest that LPO are implicated in sodium balance that is mediated by V1, V2, AT1 and AT2 receptors. Sodium 49-55 angiotensin II receptor type 2 Homo sapiens 100-103 16216878-9 2005 These observations suggest a novel link between GILZ and regulation of epithelial sodium transport through modulation of ERK signaling and could represent an important pathway for mediating aldosterone actions in health and disease. Sodium 82-88 TSC22 domain family member 3 Homo sapiens 48-52 16465598-1 2005 The aim of this study was to investigate the basis of disturbances in sodium transport in asthma and in airway hyperresponsiveness without symptoms of asthma (asymptomatic AHR). Sodium 70-76 aryl hydrocarbon receptor Homo sapiens 172-175 16465598-4 2005 Compared with normal subjects, those with asymptomatic AHR or asthma with controlled symptoms had a twofold increase in sodium influx and Na(i). Sodium 120-126 aryl hydrocarbon receptor Homo sapiens 55-58 16087784-7 2005 These data suggest that VR1-positive sensory nerves in the kidney enhance renal excretory function, a mechanism that may be critically involved in sodium and fluid homeostasis. Sodium 147-153 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 24-27 15993839-3 2005 Here, we showed that enterocytes from heterozygous SVCT2-knockout mice had lower sodium-dependent vitamin C accumulation compared to those from the wildtype. Sodium 81-87 solute carrier family 23 (nucleobase transporters), member 2 Mus musculus 51-56 15907345-1 2005 This study provides evidence that amylin acts centrally to increase sodium excretion in the sheep. Sodium 68-74 islet amyloid polypeptide Ovis aries 34-40 15907345-3 2005 Renal sodium excretion increased by at least 3-fold after 1 h of amylin infusion by ICV (66+/-14 to 367+/-35 mmol/min) and IC (78+/-14 to 244+/-22 mmol/min) routes of administration. Sodium 6-12 islet amyloid polypeptide Ovis aries 65-71 15907345-4 2005 Amylin infusion IV caused a 1.5-fold increase in sodium excretion while IR infusion did not have a significant effect. Sodium 49-55 islet amyloid polypeptide Ovis aries 0-6 15907345-8 2005 We conclude that amylin causes changes in sodium excretion in sheep through a central, angiotensin-dependent pathway and that amylin may increase renin secretion by a direct effect on the kidney. Sodium 42-48 islet amyloid polypeptide Ovis aries 17-23 15958509-2 2005 We describe a novel mutation in a family with erythromelalgia in SCN9A, the gene that encodes the Na(v)1.7 sodium channel. Sodium 107-113 immunoglobulin lambda variable 2-23 Homo sapiens 98-106 16101565-9 2005 During ischemia and reperfusion of the myocardium, NHE activity catalyzes increased uptake of intracellular sodium. Sodium 108-114 solute carrier family 9 member C1 Homo sapiens 51-54 15956187-6 2005 Furthermore, RGZ stimulated sodium transport in primary cultures of CD cells expressing PPARgamma and not in cells lacking this receptor. Sodium 28-34 peroxisome proliferator activated receptor gamma Mus musculus 88-97 15956187-7 2005 These findings demonstrate a PPARgamma-dependent pathway in regulation of sodium transport in the CD that underlies TZD-induced fluid retention. Sodium 74-80 peroxisome proliferator activated receptor gamma Mus musculus 29-38 15718388-3 2005 In renal medulla, prostaglandins derived from cyclooxygenase-2 (COX-2) stimulate sodium and water excretion, and renal medullary COX-2 expression increases after mineralocorticoid administration. Sodium 81-87 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 46-62 15718388-3 2005 In renal medulla, prostaglandins derived from cyclooxygenase-2 (COX-2) stimulate sodium and water excretion, and renal medullary COX-2 expression increases after mineralocorticoid administration. Sodium 81-87 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 64-69 15729735-7 2005 The Ca2+-dependent BK-type channel blocker, iberiotoxin, and the general Ca2+-dependent K+ channel blocker, TEA, attenuated or eliminated the hyperpolarization produced by NGF in sodium free media. Sodium 179-185 nerve growth factor Rattus norvegicus 172-175 15809364-0 2005 Extrarenal ETB plays a significant role in controlling cardiovascular responses to high dietary sodium in rats. Sodium 96-102 endothelin receptor type B Rattus norvegicus 11-14 15919451-5 2005 Mass-spectrometric detection by an electrospray ionization chamber made the detection and quantification of the sodium adducts of CsA and its metabolites AM1, AM1c, DihydroAM1, AM19, and AM4N possible. Sodium 112-118 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 130-133 15784954-4 2005 Sodium selenite treatment of the diabetic rats significantly restored the altered activities of glutathione-S-transferase, glucose-6-phosphate dehydrogenase, and 6-phosphogluconate dehydrogenase, which are involved in the glutathione metabolism of the heart, but slightly but significantly decreased the high blood glucose level. Sodium 0-6 glucose-6-phosphate dehydrogenase Rattus norvegicus 123-156 15861042-6 2005 All of the characterized hCNT3 variants produced in oocytes retained sodium and proton dependence of uridine transport based on measurements of radioisotope flux and two-electrode voltage-clamp studies. Sodium 69-75 solute carrier family 28 member 3 Homo sapiens 25-30 15669052-2 2005 A-II functions by binding its type 1 (AT1) receptors to cause vasoconstriction and retention of sodium and fluid. Sodium 96-102 angiotensin II receptor type 1 Homo sapiens 38-41 15539403-1 2005 We previously reported that sodium restriction during pregnancy reduces plasma volume expansion and promotes intra-uterine growth restriction (IUGR) in rats while it activates the renin-angiotensin-aldosterone system (RAAS). Sodium 28-34 renin Rattus norvegicus 180-185 15644628-11 2005 Follow-up serum sodium levels in CI patients with Af were negatively correlated with BNP levels on admission. Sodium 16-22 natriuretic peptide B Homo sapiens 85-88 15486076-9 2005 Moreover, this uptake was sodium- and pH-dependent with an apparent K(m) value of 21 muM and inhibited by verapamil, which is in line with published data for recombinant OCTN2. Sodium 26-32 solute carrier family 22 member 5 Homo sapiens 170-175 15850610-11 2005 The increase of the decline in pHi elicited by preexposure to thrombin was still observed in the presence of an inhibitor of the Na+/H+ exchange or in sodium-free solutions. Sodium 151-157 glucose-6-phosphate isomerase Homo sapiens 31-34 15292048-3 2004 Physiological changes in the activity of the endogenous renin-angiotensin system were produced by alterations in dietary sodium intake. Sodium 121-127 renin Rattus norvegicus 56-61 15465873-9 2004 These results indicate that potentiation of Nav1.6 sodium currents results from faster channel activation, and that this effect is masked by slow inactivation in Nav1.2. Sodium 51-57 neuron navigator 1 Homo sapiens 44-48 15838307-11 2004 Therefore, ET antagonism might influence blood pressure by regulating the sodium balance through reducing SGK1 gene expression. Sodium 74-80 serum/glucocorticoid regulated kinase 1 Rattus norvegicus 106-110 15355121-1 2004 We have developed a united atom force field able to accurately describe the adsorption properties of linear alkanes in the sodium form of FAU-type zeolites. Sodium 123-129 FAU ubiquitin like and ribosomal protein S30 fusion Homo sapiens 138-141 15355121-3 2004 The force field reproduces the sodium positions in dehydrated FAU-type zeolites known from crystallography, and it predicts how the sodium cations redistribute when n-alkanes adsorb. Sodium 31-37 FAU ubiquitin like and ribosomal protein S30 fusion Homo sapiens 62-65 15355121-3 2004 The force field reproduces the sodium positions in dehydrated FAU-type zeolites known from crystallography, and it predicts how the sodium cations redistribute when n-alkanes adsorb. Sodium 132-138 FAU ubiquitin like and ribosomal protein S30 fusion Homo sapiens 62-65 15304091-5 2004 In comparison to normoosmotic (305 mosmol per L) controls, a 3-5-fold induction of mRNA expression for the betaine/GABA-, the sodium-dependent myoinositol- and the TAUT was observed within 6-24 h after hyperosmotic exposure (405 mosmol per L). Sodium 126-132 solute carrier family 6 member 6 Homo sapiens 164-168 15333707-1 2004 We evaluated the hypothesis that sodium-dependent vitamin C (ascorbate) transporters SVCT1 and SVCT2 (encoded by genes Slc23a1 and Slc23a2) regulate ascorbate concentrations in tissues of adult mice. Sodium 33-39 solute carrier family 23 (nucleobase transporters), member 2 Mus musculus 95-100 15333707-1 2004 We evaluated the hypothesis that sodium-dependent vitamin C (ascorbate) transporters SVCT1 and SVCT2 (encoded by genes Slc23a1 and Slc23a2) regulate ascorbate concentrations in tissues of adult mice. Sodium 33-39 solute carrier family 23 (nucleobase transporters), member 2 Mus musculus 131-138 15286788-3 2004 SLC6A19 is a sodium-dependent and chloride-independent neutral amino acid transporter, expressed predominately in kidney and intestine, with properties of system B(0). Sodium 13-19 solute carrier family 6 member 19 Homo sapiens 0-7 15238568-7 2004 In subjects with sodium excretion <190 mmol/d (median), supine heart rate, LF, and LF:HF increased and HF decreased with the number of CYP11B2 -344T alleles, and the orthostatic changes in LF, HF, and LF:HF were blunted in carriers of the AT1R 1166C allele. Sodium 17-23 angiotensin II receptor type 1 Homo sapiens 242-246 15238568-0 2004 Genetic variation in CYP11B2 and AT1R influences heart rate variability conditional on sodium excretion. Sodium 87-93 angiotensin II receptor type 1 Homo sapiens 33-37 15558947-3 2004 The data indicate that the inhibition of hK1 by sodium, potassium, calcium and magnesium is linear competitive and that divalent cations are more potent inhibitors of hK1 than univalent cations. Sodium 48-54 keratin 1 Homo sapiens 41-44 15558947-3 2004 The data indicate that the inhibition of hK1 by sodium, potassium, calcium and magnesium is linear competitive and that divalent cations are more potent inhibitors of hK1 than univalent cations. Sodium 48-54 keratin 1 Homo sapiens 167-170 15056687-0 2004 Sodium currents in subthalamic nucleus neurons from Nav1.6-null mice. Sodium 0-6 neuron navigator 1 Mus musculus 52-56 15056687-8 2004 These results show that sodium channels other than Na(v)1.6 can make resurgent sodium current much like that from Na(v)1.6 channels. Sodium 24-30 sodium channel, voltage-gated, type VIII, alpha Mus musculus 114-122 15277591-2 2004 Focus on "Sodium currents in subthalamic nucleus neurons from Nav1.6-null mice". Sodium 10-16 neuron navigator 1 Mus musculus 62-66 15213008-8 2004 Thus, it seems that the sodium intake control is performed by MnPO neurons through the stimulatory action of angiotensin II on AT1 receptors under sodium depletion, but not water deprivation or salt overload neither of ad libitum water and salt intake condition. Sodium 24-30 angiotensin II receptor, type 1a Rattus norvegicus 127-130 15213008-8 2004 Thus, it seems that the sodium intake control is performed by MnPO neurons through the stimulatory action of angiotensin II on AT1 receptors under sodium depletion, but not water deprivation or salt overload neither of ad libitum water and salt intake condition. Sodium 147-153 angiotensin II receptor, type 1a Rattus norvegicus 127-130 15031141-3 2004 In control rats (n = 15), sodium excretion rose from 2.3 +/- 0.4 to 19.4 +/- 1.8 microeq.min(-1).g kidney weight(-1) when RPP was increased from 114 +/- 1 to 156 +/- 2 mmHg. Sodium 26-32 Body weight QTL 17 Rattus norvegicus 106-115 14999052-7 2004 In contrast, Hcrt/Orx responses were strongly attenuated by lowering extracellular Ca(2+) ( approximately 20 microM) but were not inhibited by concentrations of KB-R7943 (10 microM) selective for blockade of sodium/calcium exchange. Sodium 208-214 hypocretin Mus musculus 13-17 15010500-1 2004 Previously, we demonstrated that malignant glioma cell lines have increased intracellular pH (pHi) as a result of increased activities of the type I sodium/hydrogen exchanger (NHE1). Sodium 149-155 glucose-6-phosphate isomerase Homo sapiens 94-97 15499185-1 2004 The organic cation/carnitine transporter OCTN2 transports carnitine in a sodium-dependent manner, whereas it transports organic cations sodium-independently. Sodium 73-79 solute carrier family 22 member 5 Homo sapiens 41-46 15499185-4 2004 Within TMD1-7, Q180 and Q207 of hOCTN2 are the critical amino acids for the sodium dependence, and double mutation of Q180 and Q207 resulted in minimal change in transport activity when sodium was removed from the uptake medium. Sodium 76-82 solute carrier family 22 member 5 Homo sapiens 32-38 15499185-4 2004 Within TMD1-7, Q180 and Q207 of hOCTN2 are the critical amino acids for the sodium dependence, and double mutation of Q180 and Q207 resulted in minimal change in transport activity when sodium was removed from the uptake medium. Sodium 186-192 solute carrier family 22 member 5 Homo sapiens 32-38 15499185-5 2004 We propose that sodium-dependent affinity for carnitine is dependent on sodium recognition by these critical amino acids in hOCTN2, whereas carnitine transport by OCTN2 requires functional linkage between TMD1-7 and TMD11. Sodium 16-22 solute carrier family 22 member 5 Homo sapiens 124-130 15499185-5 2004 We propose that sodium-dependent affinity for carnitine is dependent on sodium recognition by these critical amino acids in hOCTN2, whereas carnitine transport by OCTN2 requires functional linkage between TMD1-7 and TMD11. Sodium 16-22 solute carrier family 22 member 5 Homo sapiens 125-130 15087100-1 2004 Mutations in the alpha-subunit of the first neuronal sodium channel gene SCN1A have been described in isolated patients with severe myoclonic epilepsy in infancy or Dravet syndrome and in families with generalized epilepsy with febrile seizures plus. Sodium 53-59 sodium voltage-gated channel alpha subunit 1 Homo sapiens 73-78 14630715-0 2004 Transcriptional regulation of human sodium/iodide symporter gene: a role for redox factor-1. Sodium 36-42 apurinic/apyrimidinic endodeoxyribonuclease 1 Homo sapiens 77-91 14715935-6 2004 In med cells, the resurgent component of beta-PMTX-modified sodium currents could be selectively abolished by application of intracellular alkaline phosphatase, suggesting that, like in NaV1.6-expressing cells, the open-channel block of NaV1.1 and NaV1.2 subunits is regulated by constitutive phosphorylation. Sodium 60-66 neuron navigator 1 Mus musculus 186-190 14715935-6 2004 In med cells, the resurgent component of beta-PMTX-modified sodium currents could be selectively abolished by application of intracellular alkaline phosphatase, suggesting that, like in NaV1.6-expressing cells, the open-channel block of NaV1.1 and NaV1.2 subunits is regulated by constitutive phosphorylation. Sodium 60-66 sodium channel, voltage-gated, type II, alpha Mus musculus 248-254 14700507-5 2004 Heart weight, AT1 receptor mRNA in cardiac and aortic tissues, and abundance of p38MAPK were significantly increased in rats on high sodium diet. Sodium 133-139 mitogen activated protein kinase 14 Rattus norvegicus 80-87 14512271-6 2004 These results indicate that sodium loading leads to a decrease in immunoreactive CAT1 protein in the rat renal medulla, resulting in decreased l-arginine uptake capacity. Sodium 28-34 solute carrier family 7 member 1 Rattus norvegicus 81-85 14762725-4 2004 We show that both bursting activity in single pacemaker neurons and population bursting activity may be released or suppressed depending on the expression of persistent sodium ( I(Na) P) and delayed-rectifier potassium ( I(K)) currents. Sodium 169-175 NFKB inhibitor zeta Homo sapiens 178-186 15198370-1 2004 Na+,K(+)-ATPase is an ubiquitous membrane enzyme that allows the extrusion of three sodium ions from the cell and two potassium ions from the extracellular fluid. Sodium 84-90 dynein axonemal heavy chain 8 Homo sapiens 9-15 14962074-2 2004 However, the physiological role of oxytocin and possible cooperative interactions between oxytocin and AVP in sodium balance remain obscure, even though recent studies using oxytocin knockout (OTKO) mice suggested that oxytocin may contribute to the regulation of salt appetite. Sodium 110-116 arginine vasopressin Mus musculus 103-106 14962074-12 2004 These results suggest ways in which oxytocin may play a cooperative role together with AVP in the regulation of sodium balance. Sodium 112-118 arginine vasopressin Mus musculus 87-90 14675033-2 2004 The majority of patients with Gitelman syndrome carry inactivating mutations in the SLC12A3 gene encoding the sodium-chloride cotransporter located in the distal convoluted tubule. Sodium 110-116 solute carrier family 12 member 3 Homo sapiens 84-91 14675055-13 2004 These results thus provide interesting insights into potential benefits of AT1 receptor blockade in sodium-retaining states such as congestive heart failure. Sodium 100-106 angiotensin II receptor type 1 Homo sapiens 75-78 15312909-6 2004 These data are consistent with the model that Rap1 and Ras function as counteracting regulators of voltage-gated sodium current through cAMP-dependent mechanisms. Sodium 113-119 RAS-related protein 1a Mus musculus 46-50 14689368-1 2003 INTRODUCTION: Blockade of the renin-angiotensin system (RAS) by combined angiotensin-converting enzyme inhibitor and angiotensin type 1 receptor (AT(1)) antagonist treatment with reduced dietary sodium intake produces suppression of cardiac growth and regression of cardiac hypertrophy. Sodium 195-201 angiotensin II receptor, type 1a Rattus norvegicus 146-151 14634667-2 2003 Two sodium-hydrogen exchangers (NHE1 and NHE5) are expressed in spermatozoa. Sodium 4-10 solute carrier family 9 member A5 Homo sapiens 41-45 14596364-1 2003 Angiotensin II, via activation of AT1 receptors in the kidney regulates sodium/fluid homeostasis and blood pressure. Sodium 72-78 angiotensin II receptor, type 1a Rattus norvegicus 34-37 14596364-2 2003 An exaggerated action of angiotensin II mediated via activation of AT1 receptors has been implicated in the increased renal sodium retention and the resetting of the pressure natriuresis in obesity related hypertension. Sodium 124-130 angiotensin II receptor, type 1a Rattus norvegicus 67-70 12906334-0 2003 Effect of sodium alterations on hepatic cytochrome P450 3A2 and 2C11 and renal function in rats. Sodium 10-16 cytochrome P450, family 3, subfamily a, polypeptide 2 Rattus norvegicus 40-68 12906334-11 2003 Acute manipulation of daily sodium intake does alter renal function and specific hepatic CYP isoforms and should be considered when using these rat models. Sodium 28-34 cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1 Rattus norvegicus 89-92 12929469-7 2003 Simultaneous blockade of the renin-angiotensin system, with either an ACE inhibitor or an AT1 receptor blocker, makes this compensatory hyper-reninaemia ineffective and allows maximum benefit from sodium depletion. Sodium 197-203 angiotensin II receptor type 1 Homo sapiens 90-93 12742596-4 2003 SCN1A mutations alter channel inactivation, resulting in persistent inward sodium current. Sodium 75-81 sodium voltage-gated channel alpha subunit 1 Homo sapiens 0-5 15012736-11 2003 In contrast, sustained increases in renal PGE2 in both clipped and non-clipped kidneys indicate that the COX-2-mediated PGE2 contributes importantly to the failure of the sodium reabsorption in response to acute renal hypoperfusion. Sodium 171-177 cytochrome c oxidase subunit II Canis lupus familiaris 105-110 12595490-7 2003 The functional counterpart of the increased AQP1 expression was a significant increase in sodium sieving and net UF across the PM, contrasting with a lack of effect on the osmotic gradient and permeability for small solutes. Sodium 90-96 aquaporin 1 Rattus norvegicus 44-48 12600921-2 2003 Vascular superoxide level is also increased in deoxycorticosterone acetate (DOCA)-salt hypertension, which is associated with a markedly depressed plasma renin activity because of sodium retention. Sodium 180-186 renin Rattus norvegicus 154-159 12464626-2 2003 Expression of sodium-hydrogen exchanger isoform 3 (NHE3) in the intestinal and renal epithelium plays a critical role in sodium absorption and acid/base homeostasis. Sodium 14-20 solute carrier family 9 member A3 Rattus norvegicus 51-55 12507762-2 2003 Impaired sodium-dependent uptake of bile acids has been associated with diminished expression of a basolateral Na(+)/bile acid cotransporter (Ntcp), whereas sodium-independent uptake is maintained despite a down-regulation of the organic anion transporter Oatp1. Sodium 9-15 solute carrier family 10 member 1 Rattus norvegicus 142-146 12797627-2 2003 All classic physiological effects of Ang II, such as vasoconstriction, aldosterone and vasopressin release, sodium and water retention and sympathetic facilitation, are mediated by the AT1 receptor. Sodium 108-114 angiotensin II receptor type 1 Homo sapiens 185-188 12535503-7 2003 MAIN RESULTS: In 57 trials of mainly Caucasians with normal blood pressure, low sodium intake reduced SBP by -1.27 mm Hg (CI: -1.76; -0.77)(p<0.0001) and DBP by -0.54 mm Hg (CI: -0.94; -0.14) (p = 0.009) as compared to high sodium intake. Sodium 80-86 selenium binding protein 1 Homo sapiens 102-105 12535503-8 2003 In 58 trials of mainly Caucasians with elevated blood pressure, low sodium intake reduced SBP by -4.18 mm Hg (CI: -5.08; - 3.27) (p < 0.0001) and DBP by -1.98 mm Hg (CI: -2.46; -1.32) (p < 0.0001) as compared to high sodium intake. Sodium 68-74 selenium binding protein 1 Homo sapiens 90-93 12535503-11 2003 In 8 trials of blacks with normal or elevated blood pressure, low sodium intake reduced SBP by -6.44 mm Hg (CI: -9.13; -3.74) (p < 0.0001) and DBP by -1.98 mm Hg (CI: -4.75; 0.78) (p = 0.16) as compared to high sodium intake. Sodium 66-72 selenium binding protein 1 Homo sapiens 88-91 12587046-11 2002 BNP correlated with LVEDP (r = 0.50, p <0.02), SVR (r =0.49, p <0.03) and inversely with 6MWT (r =-0.60, p <0.009), LVEF (r = -0.49, p <0.004) and sodium (r = -0.36, p = 0.04). Sodium 159-165 natriuretic peptide B Homo sapiens 0-3 12393794-6 2002 The epithelial amiloride-sensitive sodium channel (ENaC), which is expressed in many sodium-reabsorbing tissues including the inner ear and is regulated by membrane-bound channel activating serine proteases (CAPs), is a potential substrate of TMPRSS3. Sodium 35-41 transmembrane protease, serine 3 Mus musculus 243-250 12356727-1 2002 In the principal cell of the renal collecting duct, vasopressin regulates the expression of a gene network responsible for sodium and water reabsorption through the regulation of the water channel and the epithelial sodium channel (ENaC). Sodium 123-129 arginine vasopressin S homeolog Xenopus laevis 52-63 12356727-4 2002 In the kidney principal cell, VIP32 may be involved in the downregulation of transepithelial sodium transport observed within a few hours after vasopressin treatment. Sodium 93-99 arginine vasopressin S homeolog Xenopus laevis 144-155 12359983-0 2002 Neuronal nitric oxide synthase and renin stimulation by sodium deprivation are dependent on the renal nerves. Sodium 56-62 renin Rattus norvegicus 35-40 12359983-10 2002 CONCLUSION: The renal nerves mediate the increase of renin and nNOS mRNA during sodium restriction, while the suppression of nNOS and renin gene expression during a sodium load is independent of the presence of the renal nerves. Sodium 80-86 renin Rattus norvegicus 53-58 12359983-11 2002 The parallel changes in renin and nNOS mRNA during different sodium intakes suggest that nNOS can be part of the complex, and still largely unclarified, macula densa mechanism of renin regulation. Sodium 61-67 renin Rattus norvegicus 179-184 12219173-5 2002 These results suggest the angiotensinergic effect of the MSA on the AT1 and AT2 receptors of the PVN in terms of water and sodium homeostasis and MAP modulation. Sodium 123-129 angiotensin II receptor, type 1a Rattus norvegicus 68-71 12219173-5 2002 These results suggest the angiotensinergic effect of the MSA on the AT1 and AT2 receptors of the PVN in terms of water and sodium homeostasis and MAP modulation. Sodium 123-129 angiotensin II receptor, type 2 Rattus norvegicus 76-79 12191963-10 2002 In conclusion, increased sodium reabsorption might be associated with a shift of NHE3 from an inactive pool to an active pool, thus contributing to sodium retention in a state of proteinuria. Sodium 25-31 solute carrier family 9 member A3 Rattus norvegicus 81-85 12191963-10 2002 In conclusion, increased sodium reabsorption might be associated with a shift of NHE3 from an inactive pool to an active pool, thus contributing to sodium retention in a state of proteinuria. Sodium 148-154 solute carrier family 9 member A3 Rattus norvegicus 81-85 21179792-6 2002 Changes of brain water contents, sodium and potassium contents were relieved by lateral ventricular injection of PACAP in the concentration of 1 x 10(-9), 1 x 10(-10) or 1 x 10(-11) mol respectively before ischemia. Sodium 33-39 adenylate cyclase activating polypeptide 1 Rattus norvegicus 113-118 11922300-6 2002 Sodium-selective membranes containing the ionophore 4-tert-butylcalix[4]arenetetraacetic acid tetraethyl ester (sodium ionophore X) and UBC- as ionic sites showed a Nernstian response for sodium and selectivity comparable to that found in analogous electrodes containing TFPB-. Sodium 0-6 ubiquitin C Homo sapiens 136-139 11866477-1 2002 The syndrome of generalized epilepsy with febrile seizure plus (GEFS+) is associated with a single point mutation on the gene SCN1B that results in a substitution of the cysteine 121 with a tryptophane in the sodium channel beta 1-subunit protein. Sodium 209-215 sodium voltage-gated channel beta subunit 1 Homo sapiens 126-131 11906319-7 2002 Plasma renin and aldosterone concentrations and ACE activity decreased with increasing dietary sodium. Sodium 95-101 renin Rattus norvegicus 7-12 11826122-7 2002 NT-3 release depends on extracellular sodium, CaM kinase II activity, and requires intact microtubules and microfilaments. Sodium 38-44 neurotrophin 3 Gallus gallus 0-4 11805851-7 2002 Plasma renin and aldosterone concentrations decreased with increasing dietary sodium intake in both Control and L-NAME-treated rats. Sodium 78-84 renin Rattus norvegicus 7-12 11752091-6 2002 The data demonstrate that VR1 receptor agonists capsaicin and resiniferatoxin lead to a sustained increase in intracellular calcium and sodium in a concentration-dependent manner, followed by cell death. Sodium 136-142 transient receptor potential cation channel subfamily V member 1 Homo sapiens 26-29 11752091-7 2002 Pretreatment with VR1 receptor antagonists capsazepine or ruthenium red block both the calcium and sodium responses to agonists, and block agonist-induced cell death in a concentration-dependent manner. Sodium 99-105 transient receptor potential cation channel subfamily V member 1 Homo sapiens 18-21 11812965-1 2002 BACKGROUND: We recently demonstrated that pancreatitis-associated ascitic fluid (PAAF) contains cytotoxic factor(s), inducing apoptosis in hepatocytes, and that PAAF induces hepatic adenosine triphosphate depletion, hepatocellular acidosis, and accumulation of hepatic intracellular sodium. Sodium 283-289 proteasomal ATPase associated factor 1 Homo sapiens 81-85 11812965-1 2002 BACKGROUND: We recently demonstrated that pancreatitis-associated ascitic fluid (PAAF) contains cytotoxic factor(s), inducing apoptosis in hepatocytes, and that PAAF induces hepatic adenosine triphosphate depletion, hepatocellular acidosis, and accumulation of hepatic intracellular sodium. Sodium 283-289 proteasomal ATPase associated factor 1 Homo sapiens 161-165 11749809-1 2001 AIM: To investigate the effects of a sea anemone toxin anthopleurin-Q (AP-Q) isolated from Anthopleura xanthogrammica on sodium current (INa) in isolated guinea pig ventricular myocytes. Sodium 121-127 alpha-internexin Cavia porcellus 137-140 11683622-10 2001 The data suggested that the sodium ion was responsible for the induction of the GTPase activity, whereas the anion modulated the enzymatic activity through destabilization of particular regions of SsEF-1alpha. Sodium 28-34 ribosomal protein S18-alanine N-acetyltransferase Saccharolobus solfataricus 197-208 11922146-0 2001 Differential modulation of sodium channel gating and persistent sodium currents by the beta1, beta2, and beta3 subunits. Sodium 27-33 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 94-110 11692154-0 2001 Altered renal sodium handling and hypertension in men carrying the glucagon receptor gene (Gly40Ser) variant. Sodium 14-20 glucagon receptor Homo sapiens 67-84 11692154-7 2001 We conclude that the Gly40Ser polymorphism of the GCGR gene is associated with higher risk of hypertension and with enhanced proximal tubular sodium reabsorption, a factor possibly contributing to hypertension in this group. Sodium 142-148 glucagon receptor Homo sapiens 50-54 11566954-8 2001 The decrease in renal AT(1A) receptor density may also lead to sodium loss and reduction of extracellular volume. Sodium 63-69 angiotensin II receptor, type 1a Rattus norvegicus 22-27 11390018-2 2001 Ligand binding to rodent pancreatic polypeptide-responding neuropeptide Y (NPY) receptors (here termed PP/NPY receptors), or to cloned Y4 or Y5 receptors, is selectively inhibited by amiloride, peptide or alkylating modulators of sodium transport. Sodium 230-236 pancreatic polypeptide Homo sapiens 25-47 11318960-6 2001 CONCLUSIONS: This study demonstrates that renal glomerular and adrenal AT1 receptors in the dog are coordinately down-regulated by dietary sodium restriction compared with sodium loading, which is distinctly different from the reciprocal regulation observed for rat AT1 receptors in these tissues. Sodium 139-145 angiotensin II receptor, type 1a Rattus norvegicus 266-269 11318960-8 2001 These findings have important implications for the regulation of the renin-angiotensin system in humans, and suggest that coordinate regulation of AT1 receptors in the adrenal and glomeruli represent a negative feedback mechanism that when functioning normally prevents fluctuations of arterial blood pressure and development of arterial hypertension in response to changes in dietary sodium. Sodium 385-391 angiotensin II receptor type 1 Homo sapiens 147-150 11352650-1 2001 The thiazide-sensitive Na-Cl cotransporter SLC12A3 displays expression restricted to distal convoluted tubule cells where it catalyzes the uptake of sodium and chloride through the apical membrane. Sodium 149-155 solute carrier family 12 member 3 Homo sapiens 43-50 11327338-2 2001 Exchange of excessive protons for sodium via the sodium proton exchanger type 1 (NHE1) is supposed to cause intracellular sodium accumulation. Sodium 34-40 sodium/hydrogen exchanger 1 Sus scrofa 81-85 11327338-2 2001 Exchange of excessive protons for sodium via the sodium proton exchanger type 1 (NHE1) is supposed to cause intracellular sodium accumulation. Sodium 49-55 sodium/hydrogen exchanger 1 Sus scrofa 81-85 11282116-2 2001 Subtype specific mu-opioid receptor binding was further characterized in the presence of sodium and guanosine nucleotides and the activity of TAPS in isolated guinea pig ileum was compared to other mu-opioid receptor-selective ligands. Sodium 89-95 mu-type opioid receptor Cavia porcellus 17-35 11357900-3 2001 This review examines the role of the renal sodium pump (sodium, potassium-ATPase, NKA) in hypertension and its integration into mechanisms of body sodium balance. Sodium 43-49 dynein axonemal heavy chain 8 Homo sapiens 74-80 11230727-3 2001 Expression of the apical sodium-dependent bile acid transporter (ASBT) and of the organic anion transporting polypeptide (OATP-A) was detected and associated with sodium-dependent and sodium-independent [(3)H]taurocholate uptake in BEC. Sodium 163-169 solute carrier organic anion transporter family member 1A2 Homo sapiens 122-128 11325073-11 2001 4) Body mass index and the ratio of sodium to potassium excretion showed significant and positive associations with SBP and DBP in multiple linear regression analyses. Sodium 36-42 selenium binding protein 1 Homo sapiens 116-119 11150020-9 2001 Increased renin in the preglomerular arterioles may activate local angiotensin production, leading to intrarenal vasoconstriction, reduced nephron blood flow, sodium and water retention, and worsening of congestive heart failure. Sodium 159-165 renin Rattus norvegicus 10-15 11269510-7 2001 Fractional sodium excretion was likewise markedly reduced by 84% in homozygous ETB-deficient rats (P<0.001 versus wild-type rats). Sodium 11-17 endothelin receptor type B Rattus norvegicus 79-82 11269510-12 2001 The much higher increase in the fractional sodium excretion in ETB-deficient rats after pharmacological blockade of the epithelial sodium channel indicates that the decreased fractional sodium excretion in ETB-deficient rats is most probably due to a lack of the inhibitory property of the ETB receptor on the epithelial sodium channel activity. Sodium 43-49 endothelin receptor type B Rattus norvegicus 63-66 11269510-12 2001 The much higher increase in the fractional sodium excretion in ETB-deficient rats after pharmacological blockade of the epithelial sodium channel indicates that the decreased fractional sodium excretion in ETB-deficient rats is most probably due to a lack of the inhibitory property of the ETB receptor on the epithelial sodium channel activity. Sodium 43-49 endothelin receptor type B Rattus norvegicus 206-209 11269510-12 2001 The much higher increase in the fractional sodium excretion in ETB-deficient rats after pharmacological blockade of the epithelial sodium channel indicates that the decreased fractional sodium excretion in ETB-deficient rats is most probably due to a lack of the inhibitory property of the ETB receptor on the epithelial sodium channel activity. Sodium 43-49 endothelin receptor type B Rattus norvegicus 206-209 11269510-12 2001 The much higher increase in the fractional sodium excretion in ETB-deficient rats after pharmacological blockade of the epithelial sodium channel indicates that the decreased fractional sodium excretion in ETB-deficient rats is most probably due to a lack of the inhibitory property of the ETB receptor on the epithelial sodium channel activity. Sodium 131-137 endothelin receptor type B Rattus norvegicus 63-66 11269510-12 2001 The much higher increase in the fractional sodium excretion in ETB-deficient rats after pharmacological blockade of the epithelial sodium channel indicates that the decreased fractional sodium excretion in ETB-deficient rats is most probably due to a lack of the inhibitory property of the ETB receptor on the epithelial sodium channel activity. Sodium 131-137 endothelin receptor type B Rattus norvegicus 206-209 11269510-12 2001 The much higher increase in the fractional sodium excretion in ETB-deficient rats after pharmacological blockade of the epithelial sodium channel indicates that the decreased fractional sodium excretion in ETB-deficient rats is most probably due to a lack of the inhibitory property of the ETB receptor on the epithelial sodium channel activity. Sodium 131-137 endothelin receptor type B Rattus norvegicus 206-209 10930410-11 2000 Overexpression of Smf1p gave rise to a significant iron uptake that was sensitive to the sodium concentrations in the medium. Sodium 89-95 divalent metal ion transporter SMF1 Saccharomyces cerevisiae S288C 18-23 10878016-6 2000 This KCC1 mRNA is substantially increased by potassium depletion but only minimally by sodium depletion. Sodium 87-93 solute carrier family 12 member 4 Rattus norvegicus 5-9 11013071-1 2000 The renin angiotensin system (RAS) is involved in blood pressure control and water/sodium metabolism. Sodium 83-89 renin Pan troglodytes 4-9 11007885-1 2000 Two TTX-resistant sodium channels, SNS and NaN, are preferentially expressed in c-type dorsal root ganglion (DRG) neurons and have been shown recently to have distinct electrophysiological signatures, SNS producing a slowly inactivating and NaN producing a persistent sodium current with a relatively hyperpolarized voltage-dependence. Sodium 18-24 sodium voltage-gated channel alpha subunit 11 Rattus norvegicus 43-46 11007885-1 2000 Two TTX-resistant sodium channels, SNS and NaN, are preferentially expressed in c-type dorsal root ganglion (DRG) neurons and have been shown recently to have distinct electrophysiological signatures, SNS producing a slowly inactivating and NaN producing a persistent sodium current with a relatively hyperpolarized voltage-dependence. Sodium 18-24 sodium voltage-gated channel alpha subunit 11 Rattus norvegicus 241-244 10998198-3 2000 The objective of this investigation was to examine the effects of growth hormone (GH), insulin-like growth factor 1 (IGF-1), progesterone (PG), and 17beta-estradiol (EST) on renal sodium/sulfate co-transport. Sodium 180-186 insulin like growth factor 1 Canis lupus familiaris 117-122 10998198-6 2000 GH (0.1 nM) significantly increased the sodium/sulfate co-transport in MDCK/NaSi-1 cells up to 35%. Sodium 40-46 solute carrier family 13 member 1 Homo sapiens 76-82 10998198-7 2000 IGF-1 induced a concentration-related stimulation of the sodium/sulfate co-transport with a maximal response observed at 1000 nM (59% increase). Sodium 57-63 insulin like growth factor 1 Canis lupus familiaris 0-5 11001057-3 2000 Here we show that expression of BNPI, a vesicle-bound transporter associated with sodium-dependent phosphate transport, results in glutamate uptake by intracellular vesicles. Sodium 82-88 solute carrier family 17 member 7 Homo sapiens 32-36 10956274-2 2000 By administering DOCA and renin, we generated a need-free sodium appetite quickly enough to permit us to monitor the activity of individual neurons in the nucleus of the solitary tract before and after its creation, permitting a more powerful within-subjects design. Sodium 58-64 renin Rattus norvegicus 26-31 10988270-2 2000 The disease is caused by homozygous or compound heterozygous inactivating mutations in the thiazide-sensitive NaCl-cotransporter gene leading to reduced renal sodium reabsorption. Sodium 159-165 solute carrier family 12 member 3 Homo sapiens 110-128 10972663-0 2000 Effects of renal denervation on the sodium excretory actions of leptin in hypertensive rats. Sodium 36-42 leptin Rattus norvegicus 64-70 10972663-3 2000 RESULTS: In the SHR with acute renal denervation (N = 8), an intravenous bolus of 1600 microg/kg of leptin produced a significant twofold to fourfold elevation in sodium excretion but did not increase natriuresis in the sham-denervated group (N = 6). Sodium 163-169 leptin Rattus norvegicus 100-106 11392162-5 2000 The patients" group was characterized by significantly higher urine excretion of NAG (N-acetyl-beta-D-glucosaminidase) (2.75 +/- 1.69 vs 1.82 +/- 1.46 p < 0.05) and a tendency to significantly higher urine fractional sodium excretion without significant difference in albumin excretion. Sodium 220-226 O-GlcNAcase Homo sapiens 81-84 18349970-0 2000 Influence of sodium impurities on arf excimer-laser-induced absorption in CaF2 crystals. Sodium 13-19 CCR4-NOT transcription complex subunit 8 Homo sapiens 74-78 11028754-12 2000 Most were reported to be free of adverse gastrointestinal effects, but it should be noted that in the healing process of gastric ulcers and in sodium-restricted states, adverse effects of selective COX-2 inhibitors could be expected. Sodium 143-149 cytochrome c oxidase II, mitochondrial Mus musculus 198-203 10954002-0 2000 Regulation by sodium intake of type 1 angiotensin II receptor mRNAs in the kidney of Sabra rats. Sodium 14-20 angiotensin II receptor, type 1a Rattus norvegicus 31-61 10954002-1 2000 OBJECTIVE: To study the relationship between the sensitivity to sodium content of the diet in terms of development of hypertension and the regulation of the expression of type 1 angiotensin II receptor subtypes by such a diet. Sodium 64-70 angiotensin II receptor, type 1a Rattus norvegicus 171-201 10954002-6 2000 The high sodium diet induced a greater fall in the plasma renin activity in the SBH/y (-95%) than in the SBN/y (-63%). Sodium 9-15 renin Rattus norvegicus 58-63 10954002-7 2000 In the cortex (C) and inner stripe (IS), the high sodium diet decreased AT1A and AT1B mRNAs in SBH/y and SBN/y, with a higher magnitude for SBH/y, than for SBN/y (C, -28 versus -20%; IS, -42 versus -20%). Sodium 50-56 angiotensin II receptor, type 1a Rattus norvegicus 72-76 10954002-9 2000 CONCLUSION: A high sodium diet significantly decreases both AT1A and AT1B gene expression in two specific zones of the rat kidney containing the target cells of angiotensin II (C and IS). Sodium 19-25 angiotensin II receptor, type 1a Rattus norvegicus 60-64 10954002-11 2000 Finally, SBH/y and SBN/y rats differ in the basal level of AT1 mRNA expression in the IS, and in the ability to modulate AT1 mRNA level under sodium intake. Sodium 142-148 angiotensin II receptor, type 1a Rattus norvegicus 121-124 10954003-0 2000 Chronic cyclooxygenase-2 inhibition blunts low sodium-stimulated renin without changing renal haemodynamics. Sodium 47-53 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 8-24 10954003-0 2000 Chronic cyclooxygenase-2 inhibition blunts low sodium-stimulated renin without changing renal haemodynamics. Sodium 47-53 renin Rattus norvegicus 65-70 10954003-1 2000 BACKGROUND: Cyclooxygenase-2 (COX-2), the inducible isoform of cyclooxygenase, is found in the macula densa of the renal cortex and is upregulated by dietary sodium restriction. Sodium 158-164 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 12-28 10954003-1 2000 BACKGROUND: Cyclooxygenase-2 (COX-2), the inducible isoform of cyclooxygenase, is found in the macula densa of the renal cortex and is upregulated by dietary sodium restriction. Sodium 158-164 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 30-35 10954003-4 2000 RESULTS: A low sodium diet (0.02% NaCl) for 14 days elevated plasma-renin activity (PRA) nine-fold, from 6.1 +/- 2.0 to 54.9 +/- 6.5 ng angiotensin I (Ang I)/ml per h (P < 0.0001). Sodium 15-21 renin Rattus norvegicus 68-73 10894787-2 2000 Steady-state succinate-evoked inward currents in hNaDC-1 were dependent on the concentrations of succinate and sodium, and on the membrane potential. Sodium 111-117 solute carrier family 13 member 2 Homo sapiens 49-56 10894787-9 2000 The hNaDC-1 may also transport sodium ions through an uncoupled leak pathway, which is sensitive to phloretin inhibition. Sodium 31-37 solute carrier family 13 member 2 Homo sapiens 4-11 10894787-10 2000 We propose a transport model for hNaDC-1 in which the binding of three sodium ions is followed by substrate binding. Sodium 71-77 solute carrier family 13 member 2 Homo sapiens 33-40 19077543-2 2008 Ranolazine, an anti-ischemic drug, has been shown to block cardiac (Na(V)1.5) late sodium current (I(Na)). Sodium 83-89 immunoglobulin lambda variable 2-18 Homo sapiens 68-76 18826309-1 2008 Sodium amalgam reduction of the bis(indenyl)zirconium dihalide complexes, (eta5-C9H5-1-iPr-3-Me)2ZrX2 (X = Cl, Br, I), yielded the corresponding end-on dinitrogen complexes, [(eta5-C9H5-1-iPr-3-Me)2Zr(NaX)]2(mu2, eta1, eta1-N2), with inclusion of 1 equiv of salt per zirconocene. Sodium 0-6 secreted phosphoprotein 1 Homo sapiens 213-217 21784133-3 2011 Neurons in both regions constitutively express the transcription factor Forkhead protein2 (FoxP2), and become c-Fos activated after prolonged sodium depletion. Sodium 142-148 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 110-115 21746791-8 2011 Furthermore, decreased sodium intake was associated with decreased cardiac extracellular signal-regulated kinase (ERK), phosphorylated ERK (pERK), and pERK/ERK ratio; increased cardiac striatin; decreased endothelial nitric oxide synthase (eNOS) and phosphorylated eNOS (peNOS), but increased peNOS/eNOS ratio; and decreased cardiac plasminogen activator inhibitor-1. Sodium 23-29 striatin Rattus norvegicus 185-193 18826309-1 2008 Sodium amalgam reduction of the bis(indenyl)zirconium dihalide complexes, (eta5-C9H5-1-iPr-3-Me)2ZrX2 (X = Cl, Br, I), yielded the corresponding end-on dinitrogen complexes, [(eta5-C9H5-1-iPr-3-Me)2Zr(NaX)]2(mu2, eta1, eta1-N2), with inclusion of 1 equiv of salt per zirconocene. Sodium 0-6 secreted phosphoprotein 1 Homo sapiens 219-223 21788423-0 2011 Inhibition of Navbeta4 peptide-mediated resurgent sodium currents in Nav1.7 channels by carbamazepine, riluzole, and anandamide. Sodium 50-56 sodium voltage-gated channel alpha subunit 9 Homo sapiens 69-75 18678869-2 2008 Since PAR2 control ion transport in several epithelia, we searched for an effect on sodium transport in the cortical thick ascending limb of Henle"s loop, a nephron segment that avidly reabsorbs NaCl, and for its signaling. Sodium 84-90 F2R like trypsin receptor 1 Rattus norvegicus 6-10 18678869-3 2008 Activation of PAR2, by either trypsin or a specific agonist peptide, increased the maximal activity of Na,K-ATPase, its apparent affinity for sodium, the sodium permeability of the paracellular pathway, and the lumen-positive transepithelial voltage, featuring increased NaCl reabsorption. Sodium 142-148 F2R like trypsin receptor 1 Rattus norvegicus 14-18 18678869-3 2008 Activation of PAR2, by either trypsin or a specific agonist peptide, increased the maximal activity of Na,K-ATPase, its apparent affinity for sodium, the sodium permeability of the paracellular pathway, and the lumen-positive transepithelial voltage, featuring increased NaCl reabsorption. Sodium 154-160 F2R like trypsin receptor 1 Rattus norvegicus 14-18 18678869-6 2008 PAR2-induced increase in paracellular sodium permeability was mediated by the same signaling cascade. Sodium 38-44 F2R like trypsin receptor 1 Rattus norvegicus 0-4 18678869-8 2008 In conclusion, PAR2 increases sodium reabsorption in rat thick ascending limb of Henle"s loop along both the transcellular and the paracellular pathway. Sodium 30-36 F2R like trypsin receptor 1 Rattus norvegicus 15-19 18678869-9 2008 PAR2 effects are mediated in part by a phospholipase C/protein kinase C/ERK1,2 cascade, which increases Na,K-ATPase maximal activity and the paracellular sodium permeability, and by a different phospholipase C-dependent, staurosporine-sensitive cascade that controls the sodium affinity of Na,K-ATPase. Sodium 154-160 F2R like trypsin receptor 1 Rattus norvegicus 0-4 18695394-3 2008 Mutations of WNK1 and WNK4 in humans cause hypertension and hyperkalemia at least partly by altering renal sodium and potassium transport. Sodium 107-113 WNK lysine deficient protein kinase 4 Homo sapiens 22-26 10894155-3 2000 The luteotrophic hormone human CG (hCG) was found to decrease the peak amplitude of the sodium current within seconds. Sodium 88-94 hypertrichosis 2 (generalised, congenital) Homo sapiens 31-33 18508966-0 2008 Characterization of the sodium/hydrogen exchanger NHA2. Sodium 24-30 solute carrier family 9 member B2 Homo sapiens 50-54 10894155-3 2000 The luteotrophic hormone human CG (hCG) was found to decrease the peak amplitude of the sodium current within seconds. Sodium 88-94 hypertrichosis 2 (generalised, congenital) Homo sapiens 35-38 18508966-10 2008 Regarding function, human NHA2 reversed the sodium/hydrogen exchanger-null phenotype when expressed in sodium/hydrogen exchanger-deficient yeast and restored the ability to defend high salinity in the presence of acidic extracellular pH. Sodium 44-50 solute carrier family 9 member B2 Homo sapiens 26-30 20641401-4 2004 One of the transporters, described as the major vehicle of large, neutral aa such as phenylalanine, leucine, and tyrosine, is known as the L system (L-type aa transporter 1; LAT1) and is independent of sodium for the transport of these aa (5). Sodium 202-208 solute carrier family 7 member 5 Homo sapiens 174-178 18785440-6 2008 Height and amount of sodium intake were positively associated with diastolic blood pressure (P=.01 and P=.02, respectively). Sodium 21-27 tumor protein, translationally-controlled 1 Homo sapiens 103-108 18177483-13 2008 We conclude that noradrenaline-induced increases in the expression of NHE-3, NBC-1, BSC-1 and aquaporin-2 are likely to play an important role in the regulation of salt and water transport by noradrenaline in the kidney and may explain, at least in part, the altered renal sodium and water handling associated with overactivation of the sympathetic system. Sodium 273-279 aquaporin 2 Rattus norvegicus 94-105 18504185-9 2008 CONCLUSIONS: Pathophysiological changes occurs in early stage of oleic acid-induced AMI, and AQP-4 mRNA expression is up-regulated on the AT II cell membrane to regulate the exchange of fluid between the alveolar space and alveolar epithelium barrier and play an important compensational role in pulmonary liquid clearance in the event of sodium transport damages in ALI. Sodium 339-345 aquaporin 4 Rattus norvegicus 93-98 18633183-10 2008 Peritubular positive staining for alpha-SMA was present in groups receiving Ang alone or Ang-Na, in a sodium concentration-dependent manner. Sodium 102-108 actin gamma 2, smooth muscle Rattus norvegicus 34-43 18633183-12 2008 Moreover, Ang II and sodium overload induced additional changes in TGF-beta1, alpha-SMA and NF-kappaB immunostanding in glomeruli, medullary tubules and renal vessels. Sodium 21-27 actin gamma 2, smooth muscle Rattus norvegicus 78-87 18277144-9 2008 SUMMARY: Mutations of WNK1 and WNK4 cause hypertension at least partly by increasing renal sodium retention. Sodium 91-97 WNK lysine deficient protein kinase 4 Homo sapiens 31-35 18252953-1 2008 Using a highly sensitive quantitative RT-PCR method for the measurement of CYP11B1 (11beta-hydroxylase) and CYP11B2 (aldosterone synthase) mRNAs, we previously demonstrated that CYP11B2 expression in the central nervous system (CNS) is subject to regulation by dietary sodium. Sodium 269-275 cytochrome P450, family 11, subfamily b, polypeptide 1 Rattus norvegicus 75-82 10830313-3 2000 TGF-beta1 induced a selective, dose- and time-dependent increase in sodium-dependent Pi transport in ATDC5 cells. Sodium 68-74 transforming growth factor, beta 1 Mus musculus 0-9 10803602-8 2000 Plasma aldosterone concentrations and plasma renin concentrations were decreased by high sodium intake. Sodium 89-95 renin Rattus norvegicus 45-50 11060730-2 2000 Extensive animal experiments have repeatedly demonstrated the efficacy of sodium-hydrogen exchange (NHE) inhibition as a potent cardioprotective approach. Sodium 74-80 solute carrier family 9 member C1 Homo sapiens 100-103 21577129-2 2011 However, the resulting total sodium signal (NaT) represents a volume-weighted average of different sodium compartments assigned to the intra- and extracellular space. Sodium 29-35 bromodomain containing 2 Homo sapiens 44-47 21577129-2 2011 However, the resulting total sodium signal (NaT) represents a volume-weighted average of different sodium compartments assigned to the intra- and extracellular space. Sodium 99-105 bromodomain containing 2 Homo sapiens 44-47 18090665-4 2008 In type B and non-A, non-B intercalated cells chloride absorption and HCO3- secretion are accomplished through the apical sodium-independent Cl-/HCO3- exchanger pendrin. Sodium 122-128 solute carrier family 26, member 4 Mus musculus 161-168 10864001-6 2000 pHi recovery from an NH4+-induced acid load was blocked by sodium removal or amiloride addition. Sodium 59-65 glucose-6-phosphate isomerase Homo sapiens 0-3 18090665-8 2008 In vitro, angiotensin II increases sodium chloride absorption in the collecting duct by increasing the driving force for pendrin-mediated chloride absorption and the epithelial sodium channel-mediated sodium absorption through greater electrogenic hydrogen secretion. Sodium 35-41 solute carrier family 26, member 4 Mus musculus 121-128 17981648-6 2008 Although the role of TMPRSS3 in the auditory system is currently not completely understood, it has been shown to regulate the activity of the ENaC sodium channel in vitro and could therefore participate in the regulation of sodium concentration in the cochlea. Sodium 147-153 transmembrane serine protease 3 Homo sapiens 21-28 12526548-4 2000 Sodium ions tend to reside within the planes of the salicylaldimine oxygens, as in Na(NO3)(MeOH).NiL4 (1), Na(NO3)(MeOH).CuL1 (2; both with unusual seven-coordinated sodium), and Na. Sodium 0-6 cullin 1 Homo sapiens 121-125 17942286-2 2007 Using different techniques, four hNKCC1 abnormalities were described in a significant proportion of hypertensives: (i) low net sodium extrusion, (ii) high unidirectional inward cotransport, (iii) low apparent affinity for internal sodium and (iv) high maximal cotransport rate. Sodium 127-133 solute carrier family 12 member 2 Homo sapiens 33-39 10775554-0 2000 Role of citrate synthase in aldosterone-mediated sodium reabsorption. Sodium 49-55 citrate synthase Rattus norvegicus 8-24 10775554-6 2000 Because renal citrate synthase activity was reduced in Wistar-Furth rats, we hypothesized that renal sodium excretory responses to mineralocorticoids would be reduced as well. Sodium 101-107 citrate synthase Rattus norvegicus 14-30 17942286-2 2007 Using different techniques, four hNKCC1 abnormalities were described in a significant proportion of hypertensives: (i) low net sodium extrusion, (ii) high unidirectional inward cotransport, (iii) low apparent affinity for internal sodium and (iv) high maximal cotransport rate. Sodium 231-237 solute carrier family 12 member 2 Homo sapiens 33-39 17931347-6 2007 Actually, the uptake of lithium (and of other toxic cations such as sodium and norspermidine) is increased in the cat2-1 mutant while K(+) levels were decreased. Sodium 68-74 cationic amino acid transporter 2 Arabidopsis thaliana 114-118 17510235-1 2007 The epithelial sodium channel (ENaC) is a key mediator of sodium transport in epithelia; however, little is known about ENaC expression in mammary epithelia. Sodium 15-21 sodium channel, nonvoltage-gated 1 alpha Mus musculus 31-35 10742094-0 2000 Mutations of SCN1A, encoding a neuronal sodium channel, in two families with GEFS+2. Sodium 40-46 sodium voltage-gated channel alpha subunit 1 Homo sapiens 13-18 17376764-6 2007 The aldosterone-induced basolateral AQP2 expression in the CCD was thus independent of hypokalemia but was dependent on the presence of sodium and aldosterone. Sodium 136-142 aquaporin 2 Rattus norvegicus 36-40 10729750-0 2000 Sodium restriction decreases AP-1 activation after nephron reduction in the rat: role in the progression of renal lesions. Sodium 0-6 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 29-33 10729750-8 2000 Sodium restriction significantly reduced the number of PCNA-stained cells in glomeruli and tubules at days 14 and 60, but not at day 7, whereas it decreased AP-1 activation at all times of the study. Sodium 0-6 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 157-161 10729750-10 2000 In conclusion, we showed that, after nephron reduction, the beneficial effect of sodium restriction was associated with a reduction of hyperplasia and AP-1 activation, but that the latter did not parallel delayed cell proliferation rate in remaining nephrons. Sodium 81-87 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 151-155 10726708-1 2000 The 11 beta-hydroxysteroid dehydrogenase type 2 (11 PHSD2) enzyme inactivates 11 betahydroxy steroids in sodium-transporting epithelia such as the kidney, thus protecting the non-selective mineralocorticoid receptor (MR) from occupation by cortisol in humans. Sodium 105-111 nuclear receptor subfamily 3 group C member 2 Homo sapiens 189-215 21605659-1 2011 The transcription factor Forkhead box protein 2 (FoxP2) is expressed in two cell groups of the brainstem that have been implicated in sodium appetite regulation: the pre-locus coeruleus (pre-LC) and parabrachial nucleus--external lateral-inner subdivision (PBel-inner). Sodium 134-140 forkhead box P2 Rattus norvegicus 25-47 21605659-1 2011 The transcription factor Forkhead box protein 2 (FoxP2) is expressed in two cell groups of the brainstem that have been implicated in sodium appetite regulation: the pre-locus coeruleus (pre-LC) and parabrachial nucleus--external lateral-inner subdivision (PBel-inner). Sodium 134-140 forkhead box P2 Rattus norvegicus 49-54 10726708-1 2000 The 11 beta-hydroxysteroid dehydrogenase type 2 (11 PHSD2) enzyme inactivates 11 betahydroxy steroids in sodium-transporting epithelia such as the kidney, thus protecting the non-selective mineralocorticoid receptor (MR) from occupation by cortisol in humans. Sodium 105-111 nuclear receptor subfamily 3 group C member 2 Homo sapiens 217-219 10731931-0 2000 Decreased osteopontin expression in the rat kidney on a sodium deficient diet. Sodium 56-62 secreted phosphoprotein 1 Rattus norvegicus 10-21 10731931-6 2000 In rats fed a normal sodium diet, OPN mRNA and protein were expressed only in the descending thin limbs of Henle"s loop (DTL) and in the papillary and pelvic surface epithelium (PSE). Sodium 21-27 secreted phosphoprotein 1 Rattus norvegicus 34-37 17376764-8 2007 The increased basolateral expression of AQP2 induced by aldosterone may play a significant role in water metabolism in conditions with increased sodium reabsorption in the CCD. Sodium 145-151 aquaporin 2 Rattus norvegicus 40-44 10731931-7 2000 In rats fed a sodium deficient diet, there was a marked decrease in OPN immunoreactivity in the DTL, but no changes in PSE. Sodium 14-20 secreted phosphoprotein 1 Rattus norvegicus 68-71 10731931-9 2000 As expected, rats fed a sodium deficient diet were associated with increased immunoreactivity for Na-K-ATPase and renin compatible with activation of the renin-angiotensin system. Sodium 24-30 renin Rattus norvegicus 114-119 21741370-2 2011 deltaENaC is distinct from the related alpha-, beta- and gammaENaC subunits, known for their role in sodium homeostasis and blood pressure control, as deltaENaC is expressed in brain neurons and activated by external protons. Sodium 101-107 sodium channel epithelial 1 subunit gamma Homo sapiens 39-66 17463181-8 2007 A number of genes involved in sodium transport were also influenced by leptin replacement. Sodium 30-36 leptin Mus musculus 71-77 21646357-2 2011 ASBT reclaims bile acids from the distal ileum via active sodium co-transport, in a multistep process, orchestrated by key residues in exofacial loop regions, as well as in membrane-spanning helices. Sodium 58-64 solute carrier family 10 member 2 Homo sapiens 0-4 10731931-9 2000 As expected, rats fed a sodium deficient diet were associated with increased immunoreactivity for Na-K-ATPase and renin compatible with activation of the renin-angiotensin system. Sodium 24-30 renin Rattus norvegicus 154-159 10731931-10 2000 These results suggest that dietary sodium may be involved in the regulation of OPN expression in the DTL of the rat kidney. Sodium 35-41 secreted phosphoprotein 1 Rattus norvegicus 79-82 17463181-12 2007 Thus leptin, an adipocyte-derived cytokine involved with satiety and energy balance, influences gallbladder bile volume, sodium, and pH as well as multiple inflammatory cytokine genes and genes related to water, sodium, chloride, and bicarbonate transport. Sodium 121-127 leptin Mus musculus 5-11 10636871-4 2000 Biochemical ATPase assays demonstrated a large sodium-independent ATPase activity at pH 6.0 for the pump carrying the TM4 substitutions, whereas the control constructs exhibited little or no activity in the absence of sodium. Sodium 47-53 tropomyosin 4 S homeolog Xenopus laevis 118-121 21593188-9 2011 The expression of FGF-10 was lower in offspring of dams on a low-sodium diet, and the expression of Pax-2 and FGF-2 was lower in offspring of dams on a high-sodium diet. Sodium 157-163 paired box 2 Homo sapiens 100-105 17463181-12 2007 Thus leptin, an adipocyte-derived cytokine involved with satiety and energy balance, influences gallbladder bile volume, sodium, and pH as well as multiple inflammatory cytokine genes and genes related to water, sodium, chloride, and bicarbonate transport. Sodium 212-218 leptin Mus musculus 5-11 10691781-4 2000 In the kidney, ANG II at the AT2 receptor stimulates a vasodilator cascade of bradykinin (BK), NO and cyclic GMP which is tonically activated only during conditions of increased ANG II, such as sodium depletion. Sodium 194-200 angiotensin II receptor type 2 Homo sapiens 29-32 17664852-2 2007 We hypothesized a priori that persons with the T allele of CYP11B2 would have elevated blood pressure levels in response to a higher sodium intake, and thus the association between the T-344C polymorphism and blood pressure would be more evident among persons with a high sodium intake than among those with a low sodium intake. Sodium 133-139 cytochrome P450 family 11 subfamily B member 2 Homo sapiens 59-66 10691781-7 2000 In the gastrointestinal tract, physiological quantities of ANG II stimulate the AT2 receptor releasing NO and cGMP leading to increased sodium and water absorption. Sodium 136-142 angiotensin II receptor type 2 Homo sapiens 80-83 10678288-2 2000 The kidney is an important site of action of Ang II AT1 receptor blockers because intrarenal Ang II not only vasoconstricts the renal vasculature but also reduces sodium excretion and suppresses the pressure natriuresis relationship. Sodium 163-169 angiotensin II receptor, type 1a Rattus norvegicus 52-55 17664852-2 2007 We hypothesized a priori that persons with the T allele of CYP11B2 would have elevated blood pressure levels in response to a higher sodium intake, and thus the association between the T-344C polymorphism and blood pressure would be more evident among persons with a high sodium intake than among those with a low sodium intake. Sodium 272-278 cytochrome P450 family 11 subfamily B member 2 Homo sapiens 59-66 10678288-9 2000 AT1 receptor blockers such as candesartan have been shown to cause significant increases in glomerular filtration rate, renal blood flow and proportionately much greater increases in sodium excretion and fractional sodium excretion. Sodium 183-189 angiotensin II receptor, type 1a Rattus norvegicus 0-3 17664852-2 2007 We hypothesized a priori that persons with the T allele of CYP11B2 would have elevated blood pressure levels in response to a higher sodium intake, and thus the association between the T-344C polymorphism and blood pressure would be more evident among persons with a high sodium intake than among those with a low sodium intake. Sodium 272-278 cytochrome P450 family 11 subfamily B member 2 Homo sapiens 59-66 10678288-9 2000 AT1 receptor blockers such as candesartan have been shown to cause significant increases in glomerular filtration rate, renal blood flow and proportionately much greater increases in sodium excretion and fractional sodium excretion. Sodium 215-221 angiotensin II receptor, type 1a Rattus norvegicus 0-3 17492130-4 2007 Our high-resolution crystal structure of apo hDPPIV revealed the presence of sodium ion and glycerol molecules at the active site. Sodium 77-83 dipeptidyl peptidase 4 Homo sapiens 45-51 10733611-3 2000 Tests carried out on sodium currents of single muscle fibres of Rana esculenta demonstrated that (-)-(S)- and (+)-(R)-Me2 were less potent than Mex in producing tonic block, but showed a higher use-dependent block. Sodium 21-27 malic enzyme 2, NAD(+)-dependent, mitochondrial Mus musculus 118-121 10733611-5 2000 (-)-(S)-Me2 reduced spontaneous discharges and after discharges better than (-)-(R)-Mex in agreement with the use-dependent block of sodium currents. Sodium 133-139 malic enzyme 2, NAD(+)-dependent, mitochondrial Mus musculus 8-11 10620200-15 2000 CONCLUSIONS: Hemodynamic and tubular factors modify renal sodium handling in AT2 receptor knockout mice and may cause hypertension. Sodium 58-64 angiotensin II receptor, type 2 Mus musculus 77-89 10619595-6 1999 Additionally, research has indicated that the AT1 receptor modulates cardiac contractility and glomerular filtration, and increases renal tubular sodium reabsorption, and cardiac and vascular hypertrophy. Sodium 146-152 angiotensin II receptor type 1 Homo sapiens 46-49 10556521-0 1999 Cloning and functional characterization of the human sodium-dependent vitamin C transporters hSVCT1 and hSVCT2. Sodium 53-59 solute carrier family 23 member 2 Homo sapiens 104-110 10504466-2 1999 Experimental evidence indicates that ultrafiltered IGF-I, HGF, and TGF-beta may contribute to increased tubular phosphate and sodium absorption, synthesis of extracellular matrix proteins, and secretion of chemokines such as monocyte chemoattractant protein-1 (MCP-1). Sodium 126-132 hepatocyte growth factor Homo sapiens 58-61 10569186-1 1999 The sodium-hydrogen exchanger isoform, NHE-3 is essential for the absorption of sodium and water from intestine. Sodium 4-10 solute carrier family 9 member A3 Rattus norvegicus 39-44 10409475-1 1999 Both atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are involved in sodium and water homoeostasis in healthy humans. Sodium 90-96 natriuretic peptide B Homo sapiens 42-67 10409475-1 1999 Both atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are involved in sodium and water homoeostasis in healthy humans. Sodium 90-96 natriuretic peptide B Homo sapiens 69-72 10391915-3 1999 The amino acid transport activity induced by the co-expression of 4F2hc and LAT-2 was sodium-independent and showed broad specificity for small and large zwitterionic amino acids, as well as bulky analogs (e.g. BCH (2-aminobicyclo-(2,2,1)-heptane-2-carboxylic acid)). Sodium 86-92 linker for activation of T cells family member 2 Homo sapiens 76-81 21809962-1 2011 Ranolazine is an agent approved for the symptomatic treatment of chronic stable angina that inhibits the late inward sodium current (I(NaL)). Sodium 117-123 N-acetylneuraminate pyruvate lyase Homo sapiens 135-138 21228110-0 2011 Chronic sodium-retaining action of insulin in diabetic dogs. Sodium 8-14 insulin Canis lupus familiaris 35-42 21228110-1 2011 Insulin-mediated sodium retention is implicated as a mechanism for hypertension in metabolic syndrome and type II diabetes. Sodium 17-23 insulin Canis lupus familiaris 0-7 21228110-3 2011 This study used a novel approach to test for a chronic sodium-retaining action of insulin in dogs, by testing the hypothesis that natriuresis in type I diabetes is dependent on the decrease in insulin, rather than being due solely to osmotic actions of hyperglycemia. Sodium 55-61 insulin Canis lupus familiaris 82-89 21148403-1 2011 Sodium absorption in the mammalian small intestine occurs predominantly by two primary pathways that include Na/H exchange (NHE3) and Na-glucose cotransport (SGLT1) on the brush border membrane (BBM) of villus cells. Sodium 0-6 solute carrier family 9 member A3 Homo sapiens 124-128 21148403-2 2011 However, whether NHE3 and SGLT1 function together to regulate intestinal sodium absorption is unknown. Sodium 73-79 solute carrier family 9 member A3 Homo sapiens 17-21 17344426-1 2007 The mineralocorticoid hormone aldosterone controls sodium reabsorption and BP largely by regulating the cell-surface expression and function of the epithelial sodium channel (ENaC) in target kidney tubules. Sodium 51-57 sodium channel, nonvoltage-gated 1 alpha Mus musculus 175-179 21108936-0 2011 FoxP2 expression defines dorsolateral pontine neurons activated by sodium deprivation. Sodium 67-73 forkhead box P2 Rattus norvegicus 0-5 17344426-7 2007 With the use of Hek293 cells, Xenopus oocytes, and mpkCCD(c14) cells as expression systems, it was shown that Usp2-45 deubiquitylates ENaC and stimulates ENaC-mediated sodium transport, an effect that is not additive to that of Sgk1. Sodium 168-174 sodium channel, nonvoltage-gated 1 alpha Mus musculus 154-158 21108936-3 2011 In each site, after rats are fed an extremely low-sodium diet for over a week, neurons increase their expression of an activity-induced transcription factor, c-Fos. Sodium 50-56 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 158-163 17344426-8 2007 A deubiquitylating enzyme that targets ENaC in vitro and thus may play a role in sodium transport regulation was identified within a series of new in vivo early aldosterone-regulated gene products. Sodium 81-87 sodium channel, nonvoltage-gated 1 alpha Mus musculus 39-43 16713241-3 2007 We report the successful use of ion metal affinity chromatography (IMAC) to purify C-terminal polyhistidine tagged human skeletal muscle voltage-gated sodium (hSkM1-HT) channels from Sf9 insect cells; hSkM1 channels were pharmacologically functional when reconstituted into liposomes and incorporated into planar bilayer lipid membranes. Sodium 151-157 sodium voltage-gated channel alpha subunit 4 Homo sapiens 159-164 16713241-3 2007 We report the successful use of ion metal affinity chromatography (IMAC) to purify C-terminal polyhistidine tagged human skeletal muscle voltage-gated sodium (hSkM1-HT) channels from Sf9 insect cells; hSkM1 channels were pharmacologically functional when reconstituted into liposomes and incorporated into planar bilayer lipid membranes. Sodium 151-157 sodium voltage-gated channel alpha subunit 4 Homo sapiens 201-206 17160176-1 2007 The reaction of the mono-diazenide core, [ReCl2(NNC6H(4)-4-OCH3)(NCCH3)(PPh3)2], with four equivalents of the sodium or potassium salts of dithiocarbamate (dtc) ligands gives neutral complexes of the formula [Re(NNC6H(4)-4-OCH3)(dtc)2(PPh3)]. Sodium 110-116 protein phosphatase 4 catalytic subunit Homo sapiens 72-76 17160176-1 2007 The reaction of the mono-diazenide core, [ReCl2(NNC6H(4)-4-OCH3)(NCCH3)(PPh3)2], with four equivalents of the sodium or potassium salts of dithiocarbamate (dtc) ligands gives neutral complexes of the formula [Re(NNC6H(4)-4-OCH3)(dtc)2(PPh3)]. Sodium 110-116 protein phosphatase 4 catalytic subunit Homo sapiens 235-239 17198989-5 2007 RESULTS: Using whole-cell voltage clamp, we found that heterologous expression of SCN5A containing the T353I mutation resulted in 74% +/- 6% less peak macroscopic sodium current when compared with wild-type channels. Sodium 163-169 sodium voltage-gated channel alpha subunit 5 Homo sapiens 82-87 17940347-1 2007 BACKGROUND/AIMS: The renal sodium glucose cotransporter (SGLT2) and the water channel aquaporin-2 (AQP2) play a critical role in tubular sodium and water reabsorption and in the regulation of extracellular fluid volume both in physiologic and pathophysiologic conditions. Sodium 27-33 aquaporin 2 Rattus norvegicus 99-103 17605181-5 2007 This paper presents the results of molecular-and-genetic and clinical analysis of diseases caused by mutations in SCN5A gene, which codes the alpha-subunit of the sodium channel Na(v)1.5. Sodium 163-169 sodium voltage-gated channel alpha subunit 5 Homo sapiens 114-119 17060380-7 2006 With the recent observation that the LQT3-associated, SCN5A-encoded cardiac sodium channel localizes in caveolae, which are known membrane microdomains whose major component in the striated muscle is caveolin-3, we hypothesized that mutations in caveolin-3 may represent a novel pathogenetic mechanism for LQTS. Sodium 76-82 sodium voltage-gated channel alpha subunit 5 Homo sapiens 37-41 17060380-7 2006 With the recent observation that the LQT3-associated, SCN5A-encoded cardiac sodium channel localizes in caveolae, which are known membrane microdomains whose major component in the striated muscle is caveolin-3, we hypothesized that mutations in caveolin-3 may represent a novel pathogenetic mechanism for LQTS. Sodium 76-82 sodium voltage-gated channel alpha subunit 5 Homo sapiens 54-59 17060380-11 2006 Electrophysiological analysis of sodium current in HEK293 cells stably expressing hNa(v)1.5 and transiently transfected with wild-type and mutant caveolin-3 demonstrated that mutant caveolin-3 results in a 2- to 3-fold increase in late sodium current compared with wild-type caveolin-3. Sodium 33-39 immunoglobulin lambda variable 2-18 Homo sapiens 82-91 17060380-12 2006 Our observations are similar to the increased late sodium current associated with LQT3-associated SCN5A mutations. Sodium 51-57 sodium voltage-gated channel alpha subunit 5 Homo sapiens 82-86 17060380-12 2006 Our observations are similar to the increased late sodium current associated with LQT3-associated SCN5A mutations. Sodium 51-57 sodium voltage-gated channel alpha subunit 5 Homo sapiens 98-103 17047456-1 2006 We investigated, during the first postnatal week, a voltage-gated sodium current (INa) transiently expressed in neonatal utricular hair cells in rats raised in hypergravity. Sodium 66-72 internexin neuronal intermediate filament protein, alpha Rattus norvegicus 82-85 21164104-9 2011 Silencing of SAP97 expression in HEK293 and rat cardiomyocytes resulted in reduced sodium current (I(Na)) measured by patch-clamp. Sodium 83-89 discs large MAGUK scaffold protein 1 Rattus norvegicus 13-18 21088669-7 2011 RESULTS: The effect of sodium intake on BP differed by genotype at the angiotensinogen, beta2-adrenergic receptor, and kallikrein loci. Sodium 23-29 adrenoceptor beta 2 Homo sapiens 88-113 21088669-7 2011 RESULTS: The effect of sodium intake on BP differed by genotype at the angiotensinogen, beta2-adrenergic receptor, and kallikrein loci. Sodium 23-29 kallikrein related peptidase 4 Homo sapiens 119-129 20926631-1 2010 Serum and glucocorticoid-regulated kinase 2 (sgk2) is 80% identical to the kinase domain of sgk1, an important mediator of mineralocorticoid-regulated sodium (Na(+)) transport in the distal nephron of the kidney. Sodium 151-157 serum/glucocorticoid regulated kinase 1 Homo sapiens 92-96 16718433-10 2006 The increased persistent sodium current and ramp current, which are consistent with upregulation of Nav1.3 within dorsal horn neurons, suggest a basis for the hyperresponsiveness of these neurons following SCI. Sodium 25-31 sodium voltage-gated channel alpha subunit 3 Rattus norvegicus 100-106 20637816-6 2010 Fos immunoreactivity in brain areas associated with sodium appetite and excretion were not influenced by diet. Sodium 52-58 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 0-3 21187047-3 2010 This brief review pictures the evolution of our knowledge regarding renal functions of pendrin, with a special emphasis to its recently identified roles in the maintenance of sodium homeostasis and blood pressure. Sodium 175-181 solute carrier family 26 member 4 Homo sapiens 87-94 20816675-0 2010 Area postrema projects to FoxP2 neurons of the pre-locus coeruleus and parabrachial nuclei: brainstem sites implicated in sodium appetite regulation. Sodium 122-128 forkhead box P2 Rattus norvegicus 26-31 20816675-5 2010 Both pontine cell groups express the transcription factor FoxP2 and become c-Fos activated following sodium depletion. Sodium 101-107 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 75-80 20849357-0 2010 Erythrocyte sodium-lithium countertransport activity is inversely correlated to adiponectin, retinol binding protein 4 and body height. Sodium 12-18 retinol binding protein 4 Homo sapiens 93-118 20580730-1 2010 The Na-K-2Cl cotransporter (NKCC2) regulates sodium transport along the thick ascending limb of Henle"s loop and is important in control of sodium balance, renal concentrating ability and renin release. Sodium 45-51 solute carrier family 12 member 1 Rattus norvegicus 28-33 20580730-1 2010 The Na-K-2Cl cotransporter (NKCC2) regulates sodium transport along the thick ascending limb of Henle"s loop and is important in control of sodium balance, renal concentrating ability and renin release. Sodium 140-146 solute carrier family 12 member 1 Rattus norvegicus 28-33 21082022-10 2010 The exclusive expression of uromodulin in the thick portion of the ascending limb of Henle suggests a putative role of this variant in hypertension through an effect on sodium homeostasis. Sodium 169-175 uromodulin Homo sapiens 28-38 20595677-7 2010 SIRT1 in the kidney is cytoprotective and participates in the regulation of BP and sodium balance. Sodium 83-89 sirtuin 1 Homo sapiens 0-5 20429018-10 2010 Such lowering of phosphate content by pho4 mutations reversed the high calcium and sodium content of pho80 mutants and prevented the iron starvation response. Sodium 83-89 phosphate-sensing transcription factor PHO4 Saccharomyces cerevisiae S288C 38-42 16873718-6 2006 ENT4-mediated nucleoside transport was adenosine selective, sodium independent and only weakly inhibited by the classical inhibitors of equilibrative nucleoside transport, dipyridamole, dilazep, and nitrobenzylthioinosine. Sodium 60-66 solute carrier family 29 member 4 Homo sapiens 0-4 16410023-4 2006 For example, zinc is a much more effective blocker of one subtype of tetrodotoxin (TTX)-insensitive sodium (Na+) channel (NaV1.5) than other Na+ channels, whereas a certain T-type calcium (Ca2+) channel subunit (CaV3.2) is particularly sensitive to zinc. Sodium 100-106 sodium voltage-gated channel alpha subunit 5 Homo sapiens 122-128 16767101-0 2006 Mutations in sodium-borate cotransporter SLC4A11 cause recessive congenital hereditary endothelial dystrophy (CHED2). Sodium 13-19 solute carrier family 4 member 11 Homo sapiens 41-48 16767101-0 2006 Mutations in sodium-borate cotransporter SLC4A11 cause recessive congenital hereditary endothelial dystrophy (CHED2). Sodium 13-19 solute carrier family 4 member 11 Homo sapiens 110-115 16613846-1 2006 Aldosterone increases sodium absorption across renal collecting duct cells primarily by increasing the apical membrane expression of ENaC, the sodium entry channel. Sodium 22-28 sodium channel, nonvoltage-gated 1 alpha Mus musculus 133-137 16613846-2 2006 Nedd4-2, a ubiquitin-protein isopeptide ligase, tags ENaC with ubiquitin for internalization and degradation, but when it is phosphorylated by the aldosterone-induced kinase, SGK1, Nedd4-2 is inhibited and apical ENaC density and sodium absorption increase. Sodium 230-236 neural precursor cell expressed, developmentally down-regulated gene 4-like Mus musculus 0-7 16613846-2 2006 Nedd4-2, a ubiquitin-protein isopeptide ligase, tags ENaC with ubiquitin for internalization and degradation, but when it is phosphorylated by the aldosterone-induced kinase, SGK1, Nedd4-2 is inhibited and apical ENaC density and sodium absorption increase. Sodium 230-236 sodium channel, nonvoltage-gated 1 alpha Mus musculus 53-57 16759088-3 2006 Because inhibition of related enzymes such as 11beta-HSD2 and 17beta-HSDs causes sodium retention and hypertension or interferes with sex steroid hormone metabolism, respectively, highly selective 11beta-HSD1 inhibitors are required for successful therapy. Sodium 81-87 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 46-57 16636192-6 2006 GRK4 As-Odns, but not scrambled oligodeoxynucleotides, increased sodium excretion and urine volume, attenuated the increase in arterial blood pressure with age, and decreased protein excretion in SHRs, effects that were not observed in WKY rats. Sodium 65-71 G protein-coupled receptor kinase 4 Rattus norvegicus 0-4 20027604-0 2010 Preserved Na(+)/H(+) exchanger isoform 3 expression and localization, but decreased NHE3 function indicate regulatory sodium transport defect in ulcerative colitis. Sodium 118-124 solute carrier family 9 member A3 Homo sapiens 84-88 20232302-9 2010 Early inflammatory markers observed in rats with acute sodium overload is associated with the imbalance between HIF-1 alpha and eNOS expression. Sodium 55-61 hypoxia inducible factor 1 subunit alpha Rattus norvegicus 112-123 20232302-9 2010 Early inflammatory markers observed in rats with acute sodium overload is associated with the imbalance between HIF-1 alpha and eNOS expression. Sodium 55-61 nitric oxide synthase 3 Rattus norvegicus 128-132 19285353-5 2010 RESULTS: Patients with elevated CA125 (n=65) had significantly lower blood pressure, body mass index, serum sodium and peak exercise oxygen consumption, while B-type natriuretic peptide levels were significantly higher. Sodium 108-114 mucin 16, cell surface associated Homo sapiens 32-37 16636192-7 2006 These studies provide direct evidence of a crucial role of renal GRK4 in the D1 receptor control of sodium excretion and blood pressure in genetic hypertension. Sodium 100-106 G protein-coupled receptor kinase 4 Rattus norvegicus 65-69 16416336-1 2006 The epithelial sodium channel (ENaC) is the major mediator of sodium transport across the apical membranes of the distal nephron, the distal colon, the respiratory tract and the ducts of exocrine glands. Sodium 15-21 sodium channel, nonvoltage-gated 1 alpha Mus musculus 31-35 16480714-7 2006 The HERG-mediated potassium and the SCN5A-mediated sodium currents, however, were only slightly reduced by estradiol at concentrations of up to 30 microM. Sodium 51-57 sodium voltage-gated channel alpha subunit 5 Homo sapiens 36-41 17106580-7 2006 To understand the mechanisms underlying this process, we studied the effect of a dominant negative form of the transcriptional silencer REST/NRSF and found that it associates to an increase in the density of sodium currents. Sodium 208-214 RE1 silencing transcription factor S homeolog Xenopus laevis 141-145 16340664-4 2006 Endothelin-1 in vitro can inhibit sodium or water transport in the collecting duct and thick ascending limb through autocrine pathways. Sodium 34-40 endothelin 1 Mus musculus 0-12 16340664-7 2006 Mice with collecting duct-specific knockout of the endothelin-1 gene have impaired sodium excretion in response to sodium loading and have hypertension which worsens with high salt intake. Sodium 83-89 endothelin 1 Mus musculus 51-63 16340664-7 2006 Mice with collecting duct-specific knockout of the endothelin-1 gene have impaired sodium excretion in response to sodium loading and have hypertension which worsens with high salt intake. Sodium 115-121 endothelin 1 Mus musculus 51-63 16340664-11 2006 SUMMARY: Medullary endothelin-1 regulates renal sodium and water transport and medullary blood flow. Sodium 48-54 endothelin 1 Mus musculus 19-31 16340664-13 2006 Medullary endothelin-1 is fundamentally important in physiologic regulation of renal sodium and water excretion and maintenance of normal systemic blood pressure. Sodium 85-91 endothelin 1 Mus musculus 10-22 16354689-8 2006 In the pyramidal cell layer of the hippocampal CA3 region, where AE3 is strongly expressed, disruption of AE3 abolished sodium-independent chloride-bicarbonate exchange. Sodium 120-126 solute carrier family 4 (anion exchanger), member 3 Mus musculus 106-109 16367778-0 2005 Effects of extracellular delta-aminolaevulinic acid on sodium currents in acutely isolated rat hippocampal CA1 neurons. Sodium 55-61 carbonic anhydrase 1 Rattus norvegicus 107-110 15956775-12 2005 These results suggest that the increased protein abundance of ENaC subunits as well as the increased apical targeting of AQP2 may contribute to renal sodium and water retention observed during the development of hypertension in SHR. Sodium 150-156 aquaporin 2 Rattus norvegicus 121-125 16179357-5 2005 Overexpression of AtNHX1 increases sodium uptake in vacuoles, which leads to increased vacuolar solute concentration and therefore higher salt tolerance in transgenic plants. Sodium 35-41 Na+/H+ exchanger 1 Arabidopsis thaliana 18-24 16002097-0 2005 G-protein beta-3 subunit gene C825 T polymorphism: influence on plasma sodium and potassium concentrations in essential hypertensive patients. Sodium 71-77 G protein subunit beta 3 Homo sapiens 0-16 19799566-1 2010 Proguanylin and prouroguanylin are the inactive precursors of guanylin and uroguanylin, natriuretic peptides involved in the regulation of sodium balance. Sodium 139-145 guanylate cyclase activator 2B Homo sapiens 19-30 16002097-10 2005 Our data demonstrate an association between the C825T polymorphism of the GNB3 and plasma sodium and potassium concentrations in EHP, as expression of an increase in NHE-1 activity, without modifications in PRA nor relationship with salt sensitivity. Sodium 90-96 G protein subunit beta 3 Homo sapiens 74-78 19913016-4 2010 For this purpose we combined the detection of a retrograde transported dye, Fluorogold (FG) injected into the LPBN with the analysis of the Fos immunocytochemistry brain pattern after sodium intake induced by sodium depletion. Sodium 184-190 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 140-143 19913016-4 2010 For this purpose we combined the detection of a retrograde transported dye, Fluorogold (FG) injected into the LPBN with the analysis of the Fos immunocytochemistry brain pattern after sodium intake induced by sodium depletion. Sodium 209-215 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 140-143 19913016-5 2010 We analyzed the Fos-FG immunoreactivity after sodium ingestion induced by peritoneal dialysis (PD). Sodium 46-52 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 16-19 20038812-4 2010 We demonstrated that a paroxysmal extreme pain disorder (PEPD) mutation in the human peripheral neuronal sodium channel Nav1.7, a paramyotonia congenita (PMC) mutation in the human skeletal muscle sodium channel Nav1.4, and a long-QT3/SIDS mutation in the human cardiac sodium channel Nav1.5 all substantially increased the amplitude of resurgent sodium currents in an optimized adult rat-derived dorsal root ganglion neuronal expression system. Sodium 197-203 sodium voltage-gated channel alpha subunit 9 Homo sapiens 120-126 20038812-4 2010 We demonstrated that a paroxysmal extreme pain disorder (PEPD) mutation in the human peripheral neuronal sodium channel Nav1.7, a paramyotonia congenita (PMC) mutation in the human skeletal muscle sodium channel Nav1.4, and a long-QT3/SIDS mutation in the human cardiac sodium channel Nav1.5 all substantially increased the amplitude of resurgent sodium currents in an optimized adult rat-derived dorsal root ganglion neuronal expression system. Sodium 197-203 iduronate 2-sulfatase Homo sapiens 235-239 20038812-4 2010 We demonstrated that a paroxysmal extreme pain disorder (PEPD) mutation in the human peripheral neuronal sodium channel Nav1.7, a paramyotonia congenita (PMC) mutation in the human skeletal muscle sodium channel Nav1.4, and a long-QT3/SIDS mutation in the human cardiac sodium channel Nav1.5 all substantially increased the amplitude of resurgent sodium currents in an optimized adult rat-derived dorsal root ganglion neuronal expression system. Sodium 197-203 sodium voltage-gated channel alpha subunit 9 Homo sapiens 120-126 20038812-4 2010 We demonstrated that a paroxysmal extreme pain disorder (PEPD) mutation in the human peripheral neuronal sodium channel Nav1.7, a paramyotonia congenita (PMC) mutation in the human skeletal muscle sodium channel Nav1.4, and a long-QT3/SIDS mutation in the human cardiac sodium channel Nav1.5 all substantially increased the amplitude of resurgent sodium currents in an optimized adult rat-derived dorsal root ganglion neuronal expression system. Sodium 197-203 iduronate 2-sulfatase Homo sapiens 235-239 20038812-4 2010 We demonstrated that a paroxysmal extreme pain disorder (PEPD) mutation in the human peripheral neuronal sodium channel Nav1.7, a paramyotonia congenita (PMC) mutation in the human skeletal muscle sodium channel Nav1.4, and a long-QT3/SIDS mutation in the human cardiac sodium channel Nav1.5 all substantially increased the amplitude of resurgent sodium currents in an optimized adult rat-derived dorsal root ganglion neuronal expression system. Sodium 197-203 sodium voltage-gated channel alpha subunit 9 Homo sapiens 120-126 20038812-4 2010 We demonstrated that a paroxysmal extreme pain disorder (PEPD) mutation in the human peripheral neuronal sodium channel Nav1.7, a paramyotonia congenita (PMC) mutation in the human skeletal muscle sodium channel Nav1.4, and a long-QT3/SIDS mutation in the human cardiac sodium channel Nav1.5 all substantially increased the amplitude of resurgent sodium currents in an optimized adult rat-derived dorsal root ganglion neuronal expression system. Sodium 197-203 iduronate 2-sulfatase Homo sapiens 235-239 20090362-0 2010 Genetic variations in the sodium balance-regulating genes ENaC, NEDD4L, NDFIP2 and USP2 influence blood pressure and hypertension. Sodium 26-32 NEDD4 like E3 ubiquitin protein ligase Homo sapiens 64-70 20090362-2 2010 Fine-tuning of renal sodium reabsorption and excretion depends on the epithelial sodium channel protein (ENaC: protein complex of SCNN1A, SCNN1B, and SCNN1G). Sodium 21-27 sodium channel epithelial 1 subunit beta Homo sapiens 138-144 20090362-2 2010 Fine-tuning of renal sodium reabsorption and excretion depends on the epithelial sodium channel protein (ENaC: protein complex of SCNN1A, SCNN1B, and SCNN1G). Sodium 21-27 sodium channel epithelial 1 subunit gamma Homo sapiens 150-156 19733634-3 2009 Results showed that the Fos immunoreactivity (Fos-ir) expression in forebrain areas such as subfornical organ (SFO), paraventricular hypothalamic nuclei (PVN), supraoptic nucleus (SON) and organum vasculosum laminae terminalis (OVLT) all increased significantly and that the levels of ANG I, ANG II and ALD also increased in plasma and forebrain in rats fed with low sodium diet. Sodium 367-373 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 24-27 19733634-3 2009 Results showed that the Fos immunoreactivity (Fos-ir) expression in forebrain areas such as subfornical organ (SFO), paraventricular hypothalamic nuclei (PVN), supraoptic nucleus (SON) and organum vasculosum laminae terminalis (OVLT) all increased significantly and that the levels of ANG I, ANG II and ALD also increased in plasma and forebrain in rats fed with low sodium diet. Sodium 367-373 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 46-49 19855135-4 2009 Mice lacking Mib1 in the renal collecting duct displayed increased urinary production, decreased urinary osmolality, progressive hydronephrosis, sodium wasting, and a severe urinary concentrating defect manifested as nephrogenic diabetes insipidus. Sodium 145-151 MIB E3 ubiquitin protein ligase 1 Mus musculus 13-17 19683029-3 2009 The aim of this study was to investigate the effects of silver nanoparticles (nano-Ag) on voltage-activated sodium currents in hippocampal CA1 neurons. Sodium 108-114 carbonic anhydrase 1 Homo sapiens 139-142 19683029-9 2009 The results suggest that nano-Ag may alter the action potential of hippocampal CA1 neurons by depressing voltage-gated sodium current. Sodium 119-125 carbonic anhydrase 1 Homo sapiens 79-82 19789746-6 2009 To demonstrate the method, we measured the second order reaction coefficient of complementary 20-mer oligonucleotides as a function of sodium ion concentration, which ranged from 0.0048 mol(-1).sec(-1) at 5 mM sodium to 0.42 mol(-1).sec(-1) at 50 mM. Sodium 135-141 secretory blood group 1, pseudogene Homo sapiens 194-200 19789746-6 2009 To demonstrate the method, we measured the second order reaction coefficient of complementary 20-mer oligonucleotides as a function of sodium ion concentration, which ranged from 0.0048 mol(-1).sec(-1) at 5 mM sodium to 0.42 mol(-1).sec(-1) at 50 mM. Sodium 135-141 secretory blood group 1, pseudogene Homo sapiens 233-239 19789746-6 2009 To demonstrate the method, we measured the second order reaction coefficient of complementary 20-mer oligonucleotides as a function of sodium ion concentration, which ranged from 0.0048 mol(-1).sec(-1) at 5 mM sodium to 0.42 mol(-1).sec(-1) at 50 mM. Sodium 210-216 secretory blood group 1, pseudogene Homo sapiens 194-200 19576736-6 2009 Diffusion of sodium ions across alpha-hemolysin channels present in a sufficiently high number in the bilayers was quantitatively and specifically determined using ion selective electrodes. Sodium 13-19 AT695_RS11870 Staphylococcus aureus 32-47 19637353-4 2009 METHODS: The transport of 3-bromopyruvate by sodium-coupled monocarboxylate transporter SMCT1 (SLC5A8), a tumor suppressor and a sodium (Na+)-coupled, electrogenic transporter for short-chain monocarboxylates, was studied using a mammalian cell expression and the Xenopus laevis oocyte expression systems. Sodium 45-51 solute carrier family 5 member 8 Homo sapiens 88-93 19637353-4 2009 METHODS: The transport of 3-bromopyruvate by sodium-coupled monocarboxylate transporter SMCT1 (SLC5A8), a tumor suppressor and a sodium (Na+)-coupled, electrogenic transporter for short-chain monocarboxylates, was studied using a mammalian cell expression and the Xenopus laevis oocyte expression systems. Sodium 45-51 solute carrier family 5 member 8 Homo sapiens 95-101 19656910-9 2009 Sirolimus treatment reduced expression of NKCC2, and this was accompanied by greater urinary excretion of sodium, potassium, and magnesium. Sodium 106-112 solute carrier family 12 member 1 Rattus norvegicus 42-47 19681639-10 2009 Within the chains the anions display the expected bridging and chelating mode of coordination; SQUID magnetometry revealed weak intermolecular spin-spin couplings of 2J = -0.2 and approximately 0 K for the sodium and potassium salts, respectively. Sodium 206-212 spindlin 1 Homo sapiens 143-147 19681639-10 2009 Within the chains the anions display the expected bridging and chelating mode of coordination; SQUID magnetometry revealed weak intermolecular spin-spin couplings of 2J = -0.2 and approximately 0 K for the sodium and potassium salts, respectively. Sodium 206-212 spindlin 1 Homo sapiens 148-152 19593737-4 2009 Several allelic variants differ in frequency among ethnic groups and heat-adapted genetic variants have a high prevalence in low latitudes and hot, wet climates which lends support to the "sodium retention" hypothesis. Sodium 189-195 alcohol dehydrogenase iron containing 1 Homo sapiens 143-146 19455355-9 2009 The isolation and characterization of a series of new missense alleles of ATPalpha in Drosophila provides the foundation for further studies of these neurological diseases and the role of sodium pump impairment in animal longevity. Sodium 188-194 Na pump alpha subunit Drosophila melanogaster 74-82 19690383-5 2009 Here we measured sodium uptake in a Xenopus oocyte expression system and found that serum and glucocorticoid-induced kinase 1 (SGK1), an aldosterone-responsive gene expressed in the DN, attenuated the inhibitory effect of WNK4 on NCC activity. Sodium 17-23 serum/glucocorticoid regulated kinase 1 L homeolog Xenopus laevis 84-125 19690383-5 2009 Here we measured sodium uptake in a Xenopus oocyte expression system and found that serum and glucocorticoid-induced kinase 1 (SGK1), an aldosterone-responsive gene expressed in the DN, attenuated the inhibitory effect of WNK4 on NCC activity. Sodium 17-23 serum/glucocorticoid regulated kinase 1 L homeolog Xenopus laevis 127-131 19505305-5 2009 We found that pharmacological blockade of protein phosphatase 1 and the mitogen-activated protein kinase p38 isoform decreased and increased tonic sodium current amplitudes, respectively, and blockade of either occluded rapid responses to acute T4 application. Sodium 147-153 mitogen-activated protein kinase 14a Danio rerio 105-108 19505305-14 2009 CONCLUSION: T4"s nongenomic regulation of sodium current occurs in different neuronal subtypes, requires the activity of specific phosphorylation pathways, and requires both integrin alphaVbeta3 and Na(v)1.6a. Sodium 42-48 neuron navigator 1a Danio rerio 199-205 15942053-0 2005 Defective PTH regulation of sodium-dependent phosphate transport in NHERF-1-/- renal proximal tubule cells and wild-type cells adapted to low-phosphate media. Sodium 28-34 solute carrier family 9 (sodium/hydrogen exchanger), member 3 regulator 1 Mus musculus 68-75 19297452-12 2009 This TGF-alpha- or EGF-induced increase in sodium current is abolished by a phosphatidylinositol 3-kinase (PI-3 kinase) inhibitor, LY294002, suggesting that PI-3 kinase is involved in the activation of sodium transport. Sodium 43-49 transforming growth factor alpha L homeolog Xenopus laevis 5-14 15898956-12 2005 CONCLUSIONS: The results improve the possibility that the severe urinary concentrating defect in AQP3 null mice may in part be caused by the decreased expression of AQP2, p-AQP2 and AQP4 in CNT and CCD, whereas the increased urinary sodium excretion may in part be accounted for by Na,K-ATPase in CCD in AQP3 null mice. Sodium 233-239 aquaporin 2 Mus musculus 165-169 19374427-1 2009 This study examines the effects of electrolytes on microcystin (MC) electrospray ionization (ESI) mass spectrometry and quantitative LC-MS-MS. Sodium replacement ions (SRI) are prominent in MC ESI spectra in protic solvents such as HPLC grade methanol. Sodium 143-149 sorcin Homo sapiens 168-171 19193725-10 2009 Inappropriately high sodium reabsorption in the thick ascending limb via NKCC2 may contribute to hypertension with insulin resistance. Sodium 21-27 solute carrier family 12 member 1 Rattus norvegicus 73-78 16129837-2 2005 In contrast, gustatory detection of salty and sour tastes may involve direct gating of sodium channels of the DEG/ENaC family by sodium and hydrogen ions, respectively. Sodium 87-93 deg Drosophila melanogaster 110-113 16039271-2 2005 Although most LQT3 mutations cause a persistent sodium current, increasing diversity in the disease mechanism is shown. Sodium 48-54 sodium voltage-gated channel alpha subunit 5 Homo sapiens 14-18 16061836-2 2005 Impaired 11beta-HSD2 activity has been suggested in patients with hypertension as well as in patients with renal disease, where it may contribute to sodium retention, oedema and hypertension. Sodium 149-155 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 9-20 16061836-13 2005 Reduced renal 11beta-HSD2 expression may lead to occupancy of the MR by glucocorticoids such as cortisol and may contribute to the increased sodium retention seen in patients with impaired renal function. Sodium 141-147 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 14-25 15975995-10 2005 Because defects at the level of IRS1 may underlie at least some forms of insulin resistance, sodium retention, facilitated by hyperinsulinemia through the IRS1-independent pathway, could be an important factor in pathogenesis of hypertension in insulin resistance. Sodium 93-99 insulin receptor substrate 1 Mus musculus 155-159 19371587-2 2009 Na(V)1.8 alpha-subunits were expressed in mammalian sensory neuron-derived ND7/23 cells, and sodium currents were recorded using whole-cell patch clamp. Sodium 93-99 sodium voltage-gated channel alpha subunit 10 Homo sapiens 0-8 19392291-1 2009 Condensates of spin-1 sodium display rich spin dynamics due to the antiferromagnetic nature of the interactions in this system. Sodium 22-28 spindlin 1 Homo sapiens 15-21 19010311-2 2009 These neurons express the enzyme 11-beta-hydroxysteroid dehydrogenase type 2 (HSD2) and are activated by sodium deprivation. Sodium 105-111 hydroxysteroid 11-beta dehydrogenase 2 Rattus norvegicus 78-82 18753604-4 2009 This study determined the effects of the estrous cycle, pregnancy, progesterone (P4), and interferon tau (IFNT) on expression of both facilitative (SLC2A1, SLC2A3, and SLC2A4) and sodium-dependent (SLC5A1 and SLC5A11) glucose transporters in ovine uterine endometria from Days 10 to 16 of the estrous cycle and Days 10 to 20 of pregnancy, as well as in conceptuses from Days 10 to 20 of pregnancy. Sodium 180-186 solute carrier family 2 member 1 Homo sapiens 148-154 18753604-4 2009 This study determined the effects of the estrous cycle, pregnancy, progesterone (P4), and interferon tau (IFNT) on expression of both facilitative (SLC2A1, SLC2A3, and SLC2A4) and sodium-dependent (SLC5A1 and SLC5A11) glucose transporters in ovine uterine endometria from Days 10 to 16 of the estrous cycle and Days 10 to 20 of pregnancy, as well as in conceptuses from Days 10 to 20 of pregnancy. Sodium 180-186 solute carrier family 2 member 3 Homo sapiens 156-162 16014723-2 2005 Thus, modulation of the sodium current produced by Nav1.6 might significantly impact axonal conduction. Sodium 24-30 neuron navigator 1 Rattus norvegicus 51-55 15757906-3 2005 Co-expression of arpAT with the heavy subunits rBAT or 4F2hc elicited a sodium-independent alanine transport activity in HeLa cells. Sodium 72-78 solute carrier family 3 member 2 Homo sapiens 55-58 15634742-0 2005 A role for ERK1/2 in EGF- and ATP-dependent regulation of amiloride-sensitive sodium absorption. Sodium 78-84 epidermal growth factor Mus musculus 21-24 15634742-1 2005 Receptor-mediated inhibition of amiloride-sensitive sodium absorption was observed in primary and immortalized murine renal collecting duct cell (mCT12) monolayers. Sodium 52-58 solute carrier family 16 (monocarboxylic acid transporters), member 12 Mus musculus 146-151 15634742-8 2005 The results of these studies demonstrate that acute inhibition of amiloride-sensitive sodium transport by extracelluar ATP and EGF involves ERK1/2 activation and suggests a role for MAP kinase signaling as a negative regulator of electrogenic sodium absorption in epithelia. Sodium 86-92 epidermal growth factor Mus musculus 127-130 15828879-1 2005 Brugada syndrome is an inherited cardiac disorder caused by mutations in the SCN5A gene encoding the cardiac sodium channel alpha-subunit, and potentially leads to ventricular fibrillation and sudden death. Sodium 109-115 sodium voltage-gated channel alpha subunit 5 Homo sapiens 77-82 15808832-11 2005 In summary, this is the first report of a dysfunctional sodium channel created by an intronic mutation giving rise to cryptic splice site activation in SCN5A in a family with the BS. Sodium 56-62 sodium voltage-gated channel alpha subunit 5 Homo sapiens 152-157 15522985-0 2005 Abnormal EGF-dependent regulation of sodium absorption in ARPKD collecting duct cells. Sodium 37-43 epidermal growth factor Mus musculus 9-12 18653620-5 2008 The principal role of SGK1 is to mediate sodium reabsorption via its actions on the epithelial sodium channel (now known as sodium channel, nonvoltage-gated 1). Sodium 41-47 serum/glucocorticoid regulated kinase 1 Homo sapiens 22-26 19037590-12 2008 In conclusion, the detrimental effects of dietary sodium on endothelial function and progression of atherosclerosis in LDLR(-/-) mice on high-fat diet are mediated by increased ROS formation mainly through uncoupled NOS and NADPH oxidase. Sodium 50-56 low density lipoprotein receptor Mus musculus 119-123 15522985-1 2005 Amiloride-sensitive sodium entry, via the epithelial sodium channel (ENaC), is the rate-limiting step for Na+ absorption in kidney collecting ducts, and epidermal growth factor (EGF) inhibits Na+ transport and ENaC expression. Sodium 20-26 sodium channel, nonvoltage-gated 1 alpha Mus musculus 69-73 15522985-1 2005 Amiloride-sensitive sodium entry, via the epithelial sodium channel (ENaC), is the rate-limiting step for Na+ absorption in kidney collecting ducts, and epidermal growth factor (EGF) inhibits Na+ transport and ENaC expression. Sodium 20-26 epidermal growth factor Mus musculus 178-181 15522985-1 2005 Amiloride-sensitive sodium entry, via the epithelial sodium channel (ENaC), is the rate-limiting step for Na+ absorption in kidney collecting ducts, and epidermal growth factor (EGF) inhibits Na+ transport and ENaC expression. Sodium 20-26 sodium channel, nonvoltage-gated 1 alpha Mus musculus 210-214 15716695-1 2005 OBJECTIVE: In both humans and rats, polymorphisms of the alpha adducin (ADD1) gene are involved in renal sodium handling, essential hypertension and some of its organ complications. Sodium 105-111 adducin 1 Rattus norvegicus 72-76 15614025-7 2004 This effect of the CYP11B2 polymorphism occurred in subjects with a higher than median urinary sodium excretion (210 mmol/day). Sodium 95-101 cytochrome P450 family 11 subfamily B member 2 Homo sapiens 19-26 15761540-5 2004 Reduced 11beta-HSD2 activity may explain the increased sodium retention in preeclampsia, renal disease and liver cirrhosis. Sodium 55-61 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 8-19 18678877-7 2008 The NMDGT motif on the partially unwound part of the transmembrane helix TM7 and the residues Asp-390 and Asp-394 on TM8 are also distinguished by their important role in substrate binding and close interaction with mediating water molecules and/or sodium ions. Sodium 249-255 tetraspanin 16 Homo sapiens 117-120 18667543-0 2008 Persistent sodium current contributes to induced voltage oscillations in locomotor-related hb9 interneurons in the mouse spinal cord. Sodium 11-17 motor neuron and pancreas homeobox 1 Mus musculus 91-94 18794864-6 2008 Furthermore, on the basis of the molecular characteristics of the coordination site, we identify and confirm experimentally a sodium-sensitive phenotype in Kir5.1. Sodium 126-132 potassium inwardly rectifying channel subfamily J member 16 Homo sapiens 156-162 18632796-13 2008 Renal medullary PGE(2) promotes renal sodium excretion via the EP2 receptor, thereby maintaining normotension in the setting of high salt intake. Sodium 38-44 prostaglandin E receptor 2 (subtype EP2) Mus musculus 63-75 18729213-1 2008 Zebrafish scn8aa sodium channels mediate the majority of sodium conductance, which is essential for the embryonic locomotor activities. Sodium 17-23 sodium channel, voltage gated, type VIII, alpha subunit a Danio rerio 10-16 15485138-0 2004 Hypoxic excitability changes and sodium currents in hippocampus CA1 neurons. Sodium 33-39 carbonic anhydrase 1 Rattus norvegicus 64-67 18577565-9 2008 Together, these data support an inhibitory action of Uts2d on renal tubule sodium and potassium reabsorption in the rat, in addition to its previously described renal haemodynamic effects. Sodium 75-81 urotensin 2B Rattus norvegicus 53-58 18591455-2 2008 In previous studies, variants in the genes for alpha-adducin (ADD1), WNK1, and NEDD4L, which all regulate renal sodium absorption, have been associated with increased BP. Sodium 112-118 NEDD4 like E3 ubiquitin protein ligase Homo sapiens 79-85 18591455-9 2008 Physiological interaction between the ADD1 and WNK1-NEDD4L pathways influences the effects of variants in these genes on sodium-related BP regulation. Sodium 121-127 NEDD4 like E3 ubiquitin protein ligase Homo sapiens 52-58 18591455-10 2008 Relatively common alleles in the ADD1, WNK1, and NEDD4L genes when present in combination may have significant effects on renal sodium handling, BP, and antihypertensive response to thiazides. Sodium 128-134 NEDD4 like E3 ubiquitin protein ligase Homo sapiens 49-55 18523430-7 2008 Oxalate stimulates the uptake of chloride, water, and sodium by the proximal tubule through the exchange of oxalate for sulfate or chloride via the solute carrier SLC26A6. Sodium 54-60 solute carrier family 26 member 6 Homo sapiens 163-170 18668439-2 2008 Sodium (Na(+))-dependent bile acid uptake from portal blood into the liver is mediated primarily by the Na(+) taurocholate co-transporting polypeptide (NTCP), while secretion across the canalicular membrane into the bile is carried out by the bile salt export pump (BSEP). Sodium 0-6 ATP binding cassette subfamily B member 11 Homo sapiens 243-264 18668439-2 2008 Sodium (Na(+))-dependent bile acid uptake from portal blood into the liver is mediated primarily by the Na(+) taurocholate co-transporting polypeptide (NTCP), while secretion across the canalicular membrane into the bile is carried out by the bile salt export pump (BSEP). Sodium 0-6 ATP binding cassette subfamily B member 11 Homo sapiens 266-270 18238849-0 2008 The role of SGK-1 in angiotensin II-mediated sodium reabsorption in human proximal tubular cells. Sodium 45-51 serum/glucocorticoid regulated kinase 1 Homo sapiens 12-17 18238849-2 2008 Serine-glucocorticoid kinase-1 (SGK-1) increases sodium-hydrogen exchanger-3 (NHE3) expression and is known to be upregulated in in vitro and in vivo models of diabetic nephropathy. Sodium 49-55 serum/glucocorticoid regulated kinase 1 Homo sapiens 0-30 18238849-2 2008 Serine-glucocorticoid kinase-1 (SGK-1) increases sodium-hydrogen exchanger-3 (NHE3) expression and is known to be upregulated in in vitro and in vivo models of diabetic nephropathy. Sodium 49-55 serum/glucocorticoid regulated kinase 1 Homo sapiens 32-37 18238849-2 2008 Serine-glucocorticoid kinase-1 (SGK-1) increases sodium-hydrogen exchanger-3 (NHE3) expression and is known to be upregulated in in vitro and in vivo models of diabetic nephropathy. Sodium 49-55 solute carrier family 9 member A3 Homo sapiens 78-82 18238849-8 2008 SGK-1 was silenced in the PTCs using small interfering RNA to determine the role of SGK-1 in mediating Ang II-induced increases in NHE3-mediated sodium uptake. Sodium 145-151 solute carrier family 9 member A3 Homo sapiens 131-135 18238849-13 2008 CONCLUSION: These data suggest that increased sodium reabsorption in renal proximal tubular cells considered to be due to Ang II in diabetes mellitus is mediated through SGK-1 expression. Sodium 46-52 serum/glucocorticoid regulated kinase 1 Homo sapiens 170-175 18192334-7 2008 During ACE inhibition, low sodium reduced both ACE and ACE2 mRNA without affecting ACE2 activity or further reducing ACE activity. Sodium 27-33 angiotensin I converting enzyme 2 Rattus norvegicus 55-59 18192334-9 2008 Plasma Ang(1-7) and Ang II balance is positively shifted towards the beneficial vasopeptide Ang(1-7) by the ACE inhibitor lisinopril, especially during a low sodium intake. Sodium 158-164 angiogenin Rattus norvegicus 7-14 18242854-1 2008 Mutations in the sodium channel genes SCN1A and SCN2A have been identified in monogenic childhood epilepsies, but SCN3A has not previously been investigated as a candidate gene for epilepsy. Sodium 17-23 sodium voltage-gated channel alpha subunit 2 Homo sapiens 48-53 17956270-0 2007 Sodium regulation of GAF domain function. Sodium 0-6 fibroblast growth factor 9 Homo sapiens 21-24 17956270-4 2007 Sodium inhibits the activity of CyaB1, CyaB2 and mammalian PDE2A in vitro through modulation of GAF domain function. Sodium 0-6 fibroblast growth factor 9 Homo sapiens 96-99 17956270-6 2007 Sodium regulation of GAF domain function has therefore been conserved since the eukaryotic/prokaryotic divergence. Sodium 0-6 fibroblast growth factor 9 Homo sapiens 21-24 17956270-7 2007 The GAF domain is the first identified protein domain to directly sense and signal changes in environmental sodium. Sodium 108-114 fibroblast growth factor 9 Homo sapiens 4-7 17726015-1 2007 Factor Xa (FXa) is a key protease of the coagulation pathway whose activity is known to be in part modulated by binding to factor Va (FVa) and sodium ions. Sodium 143-149 coagulation factor X Homo sapiens 0-9 17726015-1 2007 Factor Xa (FXa) is a key protease of the coagulation pathway whose activity is known to be in part modulated by binding to factor Va (FVa) and sodium ions. Sodium 143-149 coagulation factor X Homo sapiens 11-14 17822683-2 2007 The present experiment explored the nature of this plasticity by quantifying Fos immunoreactivity (Fos-ir) in structures implicated in the mediation of sodium appetite and in the signaling of reward. Sodium 152-158 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 77-80 17822683-2 2007 The present experiment explored the nature of this plasticity by quantifying Fos immunoreactivity (Fos-ir) in structures implicated in the mediation of sodium appetite and in the signaling of reward. Sodium 152-158 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 99-102 17567719-5 2007 Sodium intake induced by PD significantly increased the number of Fos-5-HT cells, independently of the concentration of NaCl consumed. Sodium 0-6 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 66-69 17930877-1 2007 We observe coherent spin oscillations in an antiferromagnetic spin-1 Bose-Einstein condensate of sodium. Sodium 97-103 spindlin 1 Homo sapiens 62-68 17400549-7 2007 Our results show LeuT to be a good structural model to identify amino acid residues involved in the substrate and inhibitor selectivity of eukaryotic sodium-dependent neurotransmitter and amino acid transporters. Sodium 150-156 Leucine transport, high Homo sapiens 17-21 17464434-4 2007 Consistent enhancement or a de novo production of sodium intake induced by deactivation of inhibitory nuclei (e.g., lateral parabrachial nucleus) or hormones (oxytocin, atrial natriuretic peptide), in water-deprived, extracellular-dehydrated or, contrary to tradition, intracellular-dehydrated rats, suggests that sodium appetite and thirst share more mechanisms than previously thought. Sodium 50-56 natriuretic peptide A Rattus norvegicus 169-195 15218020-5 2004 NHERF-1(-/-) cells, on the other hand, had lower rates of sodium-dependent phosphate uptake and low phosphate media did not stimulate phosphate transport. Sodium 58-64 solute carrier family 9 (sodium/hydrogen exchanger), member 3 regulator 1 Mus musculus 0-7 15316768-2 2004 Sodium-dependent vitamin C transport is mediated by two transporters, SVCT 1 and SVCT 2, encoded by SLC23A1 and SLC23A2. Sodium 0-6 solute carrier family 23 member 1 Homo sapiens 70-76 15316768-2 2004 Sodium-dependent vitamin C transport is mediated by two transporters, SVCT 1 and SVCT 2, encoded by SLC23A1 and SLC23A2. Sodium 0-6 solute carrier family 23 member 1 Homo sapiens 100-107 15283764-9 2004 This is also the case for the SLC4A8 and SLC4A10 gene products, which are sodium dependent Cl(-), HCO(3) (-) exchangers. Sodium 74-80 solute carrier family 4 member 8 Homo sapiens 30-36 15283764-9 2004 This is also the case for the SLC4A8 and SLC4A10 gene products, which are sodium dependent Cl(-), HCO(3) (-) exchangers. Sodium 74-80 solute carrier family 4 member 10 Homo sapiens 41-48 15238568-9 2004 Thus, CYP11B2 C-344T and AT1R A1166C polymorphisms affect the autonomic modulation of heart rate, but these genetic effects depend on sodium excretion. Sodium 134-140 cytochrome P450 family 11 subfamily B member 2 Homo sapiens 6-13 15314687-0 2004 Collecting duct-specific knockout of endothelin-1 causes hypertension and sodium retention. Sodium 74-80 endothelin 1 Mus musculus 37-49 17454886-1 2007 OBJECTIVE: To investigate whether the C-type natriuretic peptide (CNP) has a role in the regulation of fluid and sodium homeostasis in normal subjects and in pre-ascitic cirrhotic patients. Sodium 113-119 natriuretic peptide C Homo sapiens 38-64 17454886-1 2007 OBJECTIVE: To investigate whether the C-type natriuretic peptide (CNP) has a role in the regulation of fluid and sodium homeostasis in normal subjects and in pre-ascitic cirrhotic patients. Sodium 113-119 natriuretic peptide C Homo sapiens 66-69 17454886-2 2007 MATERIAL AND METHODS: The daily profile of CNP plasma levels was assessed by serial measurements (0700 h, 0900 h, 1800 h, 2300 h) in 10 pre-ascitic cirrhotic outpatients (age 56+/-4 years) and in 10 age-matched healthy controls (54+/-2 years) on a normal sodium diet (150 mmol/day) while carrying on their usual activities (mobile from 0700 h to 2200 h), after an equilibration period of 5 days. Sodium 255-261 natriuretic peptide C Homo sapiens 43-46 17454886-6 2007 CONCLUSIONS: CNP plasma levels appear to play a role in the water-sodium balance regulation in patients with pre-ascitic cirrhosis. Sodium 66-72 natriuretic peptide C Homo sapiens 13-16 15151999-2 2004 4F2hc/xCT elicits sodium-independent exchange of anionic L-cysteine and L-glutamate (system x(c)(-)). Sodium 18-24 solute carrier family 3 member 2 Homo sapiens 0-5 15151999-2 2004 4F2hc/xCT elicits sodium-independent exchange of anionic L-cysteine and L-glutamate (system x(c)(-)). Sodium 18-24 solute carrier family 7 member 11 Homo sapiens 6-9 15150264-1 2004 Microsomal epoxide hydrolase (mEH) plays a central role in xenobiotic metabolism as well as mediating the sodium-dependent uptake of bile acids into the liver, where these compounds regulate numerous biological processes such as cholesterol metabolism and hepatocyte signaling pathways. Sodium 106-112 epoxide hydrolase 1 Homo sapiens 0-28 15084584-1 2004 The human sodium-dependent vitamin C transporter (hSVCT1) mediates sodium-dependent cellular uptake of the essential micronutrient l-ascorbic acid (vitamin C). Sodium 10-16 solute carrier family 23 member 1 Homo sapiens 50-56 17460064-1 2007 The persistent sodium current (I(Na(P))) has been implicated in the regulation of synaptic integration, intrinsic membrane properties, and rhythm generation in many types of neurons. Sodium 15-21 catenin, beta like 1 Mus musculus 33-40 17470132-4 2007 From these prioritized candidate sodium channels, we identified 10 mutations in the SCN9A gene encoding the sodium channel protein Nav1.7. Sodium 33-39 sodium voltage-gated channel alpha subunit 9 Homo sapiens 84-89 17470132-4 2007 From these prioritized candidate sodium channels, we identified 10 mutations in the SCN9A gene encoding the sodium channel protein Nav1.7. Sodium 33-39 sodium voltage-gated channel alpha subunit 9 Homo sapiens 131-137 17470132-4 2007 From these prioritized candidate sodium channels, we identified 10 mutations in the SCN9A gene encoding the sodium channel protein Nav1.7. Sodium 108-114 sodium voltage-gated channel alpha subunit 9 Homo sapiens 84-89 17470132-4 2007 From these prioritized candidate sodium channels, we identified 10 mutations in the SCN9A gene encoding the sodium channel protein Nav1.7. Sodium 108-114 sodium voltage-gated channel alpha subunit 9 Homo sapiens 131-137 17276074-7 2007 In the cases of Ntcp- and Asbt-mediated [(3)H]-TC uptake, these were sodium-dependent and were inhibited by BAPA-6>BAPA-8>BAPA-3 and BAPA-8>BAPA-6>BAPA-3, respectively. Sodium 69-75 solute carrier family 10 member 2 Rattus norvegicus 26-30 17226797-3 2007 A subset of neurons within the nucleus tractus solitarius (NTS) shows c-Fos activation during prolonged sodium deprivation in rats. Sodium 104-110 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 70-75 17214984-0 2007 Increased dietary sodium alters Fos expression in the lamina terminalis during intravenous angiotensin II infusion. Sodium 18-24 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 32-35 17214984-1 2007 These studies examined the effects of increased dietary sodium on expression of Fos, the protein product of c-fos, in forebrain structures in the rat following intravenous infusion with angiotensin II (AngII). Sodium 56-62 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 80-83 17582287-7 2007 CONCLUSIONS: The uroguanylin G-247A polymorphism was associated with urinary volume and sodium and potassium excretions. Sodium 88-94 guanylate cyclase activator 2B Homo sapiens 17-28 17294067-4 2007 Sequence analysis indicated that the disease segregates with a novel mutation in the alpha subunit of the voltage-gated sodium channel (SCN9A or Na(v)1.7). Sodium 120-126 sodium voltage-gated channel alpha subunit 9 Homo sapiens 136-141 15147873-3 2004 RFC1- as well as MTX-1-mediated uptake of a marker substrate into suitable human and rat cell lines increased with proton concentration, was sodium-dependent at neutral pH, and inhibited by folate at acidic pH. Sodium 141-147 metaxin 1 Homo sapiens 17-22 15075188-3 2004 We hypothesized that epithelial Na channel (ENaC) subunit dysregulation may be responsible for the increased sodium retention. Sodium 109-115 sodium voltage-gated channel alpha subunit 8 Rattus norvegicus 32-42 15028779-5 2004 OCT3/Slc22a3-deficient mice show an increase in the level of ingestion of hypertonic saline under thirst and salt appetite conditions, as well as alterations of the neural response in the SFO after sodium deprivation, as monitored by Fos immunoreactivity. Sodium 198-204 solute carrier family 22 (organic cation transporter), member 3 Mus musculus 0-4 15028779-5 2004 OCT3/Slc22a3-deficient mice show an increase in the level of ingestion of hypertonic saline under thirst and salt appetite conditions, as well as alterations of the neural response in the SFO after sodium deprivation, as monitored by Fos immunoreactivity. Sodium 198-204 solute carrier family 22 (organic cation transporter), member 3 Mus musculus 5-12 14718364-3 2004 APN transcript abundance and protein abundance were approximately 2-fold greater (P<0.05; n=6) in the kidneys of Sprague-Dawley and Lewis rats ingesting 8% versus 0.3% salt diets, suggesting that increased aminopeptidase activity may contribute to decreased renal sodium uptake during adaptation to a high-salt diet. Sodium 267-273 alanyl aminopeptidase, membrane Rattus norvegicus 0-3 14742879-1 2004 In Arabidopsis thaliana, the calcium binding protein Salt Overly Sensitive3 (SOS3) interacts with and activates the protein kinase SOS2, which in turn activates the plasma membrane Na(+)/H(+) antiporter SOS1 to bring about sodium ion homeostasis and salt tolerance. Sodium 223-229 sodium proton exchanger, putative (NHX7) (SOS1) Arabidopsis thaliana 203-207 14691038-0 2004 Endothelin A receptor antagonism in experimental congestive heart failure results in augmentation of the renin-angiotensin system and sustained sodium retention. Sodium 144-150 endothelin receptor type A Canis lupus familiaris 0-21 14643012-1 2003 Sodium currents were recorded in CA1 hippocampal cells from new-born (P(4-10)) and older (P(>22)) rats, using whole-cell voltage clamp techniques. Sodium 0-6 carbonic anhydrase 1 Rattus norvegicus 33-36 14673504-8 2003 Besides, sodium selenite significantly increased cellular telomerase activity and hTERT gene expression level. Sodium 9-15 telomerase reverse transcriptase Homo sapiens 82-87 14557559-3 2003 METHODS: Using the amphotericin B perforated patch clamp method, sodium currents were recorded at 22 and 32 degrees C from the wild-type (WT) and P1158S mutant SCN4A expressed in tsA201 cells. Sodium 65-71 sodium voltage-gated channel alpha subunit 4 Homo sapiens 160-165 14534149-3 2003 In oocytes, toluene inhibited sodium currents (INa+) in a concentration-dependent manner, with an IC50 of 274 microm (confidence limits: 141-407 microm). Sodium 30-36 internexin neuronal intermediate filament protein, alpha Rattus norvegicus 47-50 14534149-11 2003 In rat cardiac myocytes, 300 microm toluene inhibited the sodium current (INa+) by 62%; this inhibition was voltage independent. Sodium 58-64 internexin neuronal intermediate filament protein, alpha Rattus norvegicus 74-77 12898089-1 2003 Tetrodotoxin-resistant (TTX-R) sodium current in small-size dorsal root ganglia (DRG) neurons is upregulated by prostaglandin E(2) and serotonin through a protein kinase A (PKA)/protein kinase (PKC) pathway, suggesting G protein modulation of one or more TTX-R channels in these neurons. Sodium 31-37 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 155-177 17568121-6 2007 The gene investigated in these examples was SNAT3, which is responsible for the cotransport of sodium predominantly with glutamine in exchange for hydrogen ions. Sodium 95-101 solute carrier family 38, member 3 Rattus norvegicus 44-49 12952927-3 2003 In cultured opossum renal epithelial cells, sFRP-4 specifically inhibited sodium-dependent phosphate transport. Sodium 74-80 secreted frizzled-related protein 4 Rattus norvegicus 44-50 16736206-2 2006 The apical dendrites of CA1 pyramidal neurons in hippocampus express a wide variety of sodium, calcium, potassium, and other voltage-gated channels. Sodium 87-93 carbonic anhydrase 1 Homo sapiens 24-27 16720863-6 2006 Interestingly, both SGK1 and GILZ appear to negatively regulate tonic inhibition of ENaC and thus use disinhibition to propagate the rapid effects of aldosterone to increase sodium reabsorption in tight epithelia. Sodium 174-180 serum/glucocorticoid regulated kinase 1 Homo sapiens 20-24 12925696-1 2003 Aldosterone controls the final sodium reabsorption and potassium secretion in the kidney by regulating the activity of the epithelial sodium channel (ENaC) in the aldosterone-sensitive distal nephron (ASDN). Sodium 31-37 sodium channel, nonvoltage-gated 1 alpha Mus musculus 150-154 16933386-10 2006 The efferent projections of the HSD2 neurons may provide new insights into the brain circuitry responsible for sodium appetite. Sodium 111-117 hydroxysteroid 11-beta dehydrogenase 2 Rattus norvegicus 32-36 12646417-2 2003 The sodium-dependent multivitamin transport (SMVT), a biotin transporter, is expressed in both cell types. Sodium 4-10 solute carrier family 5 member 6 Homo sapiens 45-49 16597605-13 2006 This impairment may involve increased sodium reabsorption via NKCC2 or ENaC, decreased glomerular filtration rate, and/or nitric oxide bioavailability. Sodium 38-44 solute carrier family 12 member 1 Rattus norvegicus 62-67 12788832-4 2003 Reduced 11 beta-HSD2 activity may explain the increased sodium retention in preeclampsia, renal disease, and liver cirrhosis. Sodium 56-62 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 8-20 16870316-0 2006 Upregulation of renal eNOS by high-sodium diet facilitates hypertension in doxorubicin-treated rats through enhanced oxidative stress. Sodium 35-41 nitric oxide synthase 3 Rattus norvegicus 22-26 16613846-7 2006 Short interfering RNA-induced knockdown of 14-3-3beta blunted the aldosterone-induced increase in alpha-ENaC expression, returned alpha-ENaC-Nedd4-2 binding toward prealdosterone levels, and blocked the aldosterone-stimulated increase in transepithelial sodium transport. Sodium 254-260 tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, beta polypeptide Mus musculus 43-53 16613846-9 2006 Our studies show that aldosterone increases the expression of 14-3-3beta, which interacts with phospho-Nedd4-2 to block its interaction with ENaC, thus enhancing sodium absorption by increasing apical membrane ENaC density. Sodium 162-168 tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, beta polypeptide Mus musculus 62-72 12788832-8 2003 At a prereceptor level, 11 beta-HSD2 plays a key role in normal physiology in the corticosteroid regulation of sodium homeostasis and pathophysiology of hypertension. Sodium 111-117 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 5-36 12611966-0 2003 Relation between bicarbonate concentration and voltage dependence of sodium currents in freshly isolated CA1 neurons of the rat. Sodium 69-75 carbonic anhydrase 1 Rattus norvegicus 105-108 16943574-2 2006 It is caused by mutations in the SCNN1B or SCNN1C gene, which truncate the cytoplasmic carboxyl terminus of the beta and gamma subunit of the epithelial sodium channel (ENaC). Sodium 153-159 sodium channel epithelial 1 subunit beta Homo sapiens 33-39 12649390-3 2003 As leptin acts on the kidney to induce natriuresis, renal leptin receptor alterations could lead to a defect in sodium excretion and hence to hypertension. Sodium 112-118 leptin receptor Rattus norvegicus 58-73 12675144-5 2003 In Xenopus oocytes, Torpedo CTL1 expression was associated with the appearance of sodium independent high-affinity choline uptake. Sodium 82-88 solute carrier family 44 (choline transporter), member 1 S homeolog Xenopus laevis 28-32 12562928-9 2003 This confirms that H1 generates the classical cardiac sodium current. Sodium 54-60 H1.5 linker histone, cluster member Homo sapiens 19-21 12388407-0 2003 Epidermal growth factor inhibits amiloride-sensitive sodium absorption in renal collecting duct cells. Sodium 53-59 epidermal growth factor Mus musculus 0-23 12566994-4 2003 gp120 induced extensive microtubule depolymerization, an 80% decrease in transepithelial resistance, and a 70% decrease in sodium-dependent glucose transport, changes closely paralleling those of HIV enteropathy. Sodium 123-129 inter-alpha-trypsin inhibitor heavy chain 4 Homo sapiens 0-5 12544440-1 2003 BACKGROUND: Genetic variability in the gene for aldosterone synthase--a key enzyme in the production of aldosterone--can affect sodium homeostasis and thereby blood pressure. Sodium 128-134 cytochrome P450 family 11 subfamily B member 2 Homo sapiens 48-68 12436245-0 2002 Autosomal recessive renal glucosuria attributable to a mutation in the sodium glucose cotransporter (SGLT2). Sodium 71-77 solute carrier family 5 member 2 Homo sapiens 101-106 12483017-6 2002 The molecular biological study revealed a common missense mutation (Arg1448Cys) at the voltage-gated sodium channel gene (SCN4A). Sodium 101-107 sodium voltage-gated channel alpha subunit 4 Homo sapiens 122-127 12441220-6 2002 However, leptin may contribute to hypertension in these women by increasing renal tubular sodium reabsorption. Sodium 90-96 leptin Homo sapiens 9-15 12393794-6 2002 The epithelial amiloride-sensitive sodium channel (ENaC), which is expressed in many sodium-reabsorbing tissues including the inner ear and is regulated by membrane-bound channel activating serine proteases (CAPs), is a potential substrate of TMPRSS3. Sodium 35-41 sodium channel, nonvoltage-gated 1 alpha Mus musculus 51-55 12376182-0 2002 Blockade by magnesium of sodium currents in acutely isolated hippocampal CA1 neurons of rat. Sodium 25-31 carbonic anhydrase 1 Rattus norvegicus 73-76 16709664-2 2006 Gain-of-expression mutations in the WNK1 gene uncouple Na(+) and K(+) balance and cause a familial disorder of diminished renal potassium excretion, excessive sodium retention, and hypertension (pseudohypoaldosteronism type II or Gordon"s syndrome). Sodium 159-165 WNK lysine deficient protein kinase 1 L homeolog Xenopus laevis 36-40 16702558-3 2006 We studied the functional effects of a mutation of sodium channel Nav1.7 associated with a neuropathic pain syndrome, erythermalgia, within sensory and sympathetic ganglion neurons, two cell types where Nav1.7 is normally expressed. Sodium 51-57 sodium voltage-gated channel alpha subunit 9 Homo sapiens 66-72 16734752-8 2006 Two-thirds of filtered sodium and water are absorbed in the renal proximal tubule, a mechanism that intimately involves the apical sodium/hydrogen ion exchanger, NHE3. Sodium 23-29 solute carrier family 9 member A3 Homo sapiens 162-166 16734752-8 2006 Two-thirds of filtered sodium and water are absorbed in the renal proximal tubule, a mechanism that intimately involves the apical sodium/hydrogen ion exchanger, NHE3. Sodium 131-137 solute carrier family 9 member A3 Homo sapiens 162-166 12218317-2 2002 Uroguanylin plays an important role in sodium transport in the gastrointestinal tract and functions as an intestinal natriuretic hormone during oral salt load. Sodium 39-45 guanylate cyclase activator 2B Rattus norvegicus 0-11 12218317-10 2002 CONCLUSION: These findings suggest that uroguanylin regulates sodium metabolism in the intestine and kidneys during oral salt load in an autocrine and paracrine manner. Sodium 62-68 guanylate cyclase activator 2B Rattus norvegicus 40-51 12181125-1 2002 DeltaKPQ, a three amino acid [lysine (K), proline (P), glutamine (Q)] deletion mutation of the human cardiac Na channel (hH1), which is one cause of long QT syndrome (LQT3), has impaired inactivation resulting in a late sodium current. Sodium 220-226 H1.5 linker histone, cluster member Homo sapiens 121-124 12193783-0 2002 Variant of SCN5A sodium channel implicated in risk of cardiac arrhythmia. Sodium 17-23 sodium voltage-gated channel alpha subunit 5 Homo sapiens 11-16 12193783-2 2002 We identified a variant of the cardiac sodium channel gene SCN5A that is associated with arrhythmia in African Americans (P = 0.000028) and linked with arrhythmia risk in an African-American family (P = 0.005). Sodium 39-45 sodium voltage-gated channel alpha subunit 5 Homo sapiens 59-64 12169661-1 2002 Na+/H+ exchanger regulatory factor (NHERF)-1 and NHERF-2, two structurally related protein adapters containing tandem PSD-95/Discs large/ZO-1 (PDZ) domains, were identified as essential factors for protein kinase A-mediated inhibition of the sodium-hydrogen exchanger, NHE3. Sodium 242-248 solute carrier family 9 (sodium/hydrogen exchanger), member 3 regulator 1 Mus musculus 36-44 12181279-3 2002 Activation of AMPARs leads to influx of sodium and calcium ions, which can increase or decrease NMDAR activity through sodium concentration-dependent cascades or a calcium-calmodulin-dependent inactivation process, respectively. Sodium 40-46 glutamate receptor, ionotropic, NMDA1 (zeta 1) Mus musculus 96-101 12181279-3 2002 Activation of AMPARs leads to influx of sodium and calcium ions, which can increase or decrease NMDAR activity through sodium concentration-dependent cascades or a calcium-calmodulin-dependent inactivation process, respectively. Sodium 119-125 glutamate receptor, ionotropic, NMDA1 (zeta 1) Mus musculus 96-101 12107065-0 2002 Influence of ANG II on cytoplasmic sodium in cultured rabbit nonpigmented ciliary epithelium. Sodium 35-41 angiogenin Oryctolagus cuniculus 13-16 12107065-5 2002 The ANG II-induced cell sodium increase and (86)Rb uptake increase were reduced by dimethylamiloride (DMA; 10 microM). Sodium 24-30 angiogenin Oryctolagus cuniculus 4-7 12015312-7 2002 In conclusion, these findings indicate that CDCA, and to a lesser extent DCA, by inhibiting 11 beta HSD2, mediate cortisol-dependent nuclear translocation and transcriptional activation of MR and are responsible at least for a part of the sodium retention and potassium excretion observed in patients with biliary obstruction. Sodium 239-245 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 92-104 16868910-7 2006 Liddle"s syndrome (or type I pseudo-hyperaldosteronism (PHA1), is characterised by a constitutive activation of the epithelial sodium channels in the distal tubule, causing an increase in sodium and chloride reabsorption. Sodium 127-133 sodium channel epithelial 1 subunit gamma Homo sapiens 56-60 12106694-10 2002 Like hNa(V)1.3 channels, hNa(V)1.6 produced sodium currents with a prominent persistent component when expressed in HEK293 cells. Sodium 44-50 sodium voltage-gated channel alpha subunit 3 Homo sapiens 5-14 12020868-0 2002 Radix paeoniae rubra suppression of sodium current in acutely dissociated rat hippocampal CA1 neurons. Sodium 36-42 carbonic anhydrase 1 Rattus norvegicus 90-93 11961006-1 2002 The serine-threonine kinase sgk1 was recently identified as a gene rapidly induced by mineralocorticoids, resulting in increased sodium transport in vitro. Sodium 129-135 serum/glucocorticoid regulated kinase 1 Mus musculus 28-32 16443209-6 2006 RESULTS: The presence of lithium heparin at 100 units/mL in blood caused a significant negative bias of 2-3 mmol/L in sodium concentration with the ABL 725, but no significant bias occurred when the corresponding plasma fraction was analyzed on the VITROS 950. Sodium 118-124 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 148-151 16107787-2 2006 Three gene products of the sodium-calcium exchanger family NCX1, NCX2, and NCX3 couple, in a bidirectional way, the movement of these ions across the cell membrane during cerebral ischemia. Sodium 27-33 solute carrier family 8 member A2 Rattus norvegicus 65-69 16609682-0 2006 Blood pressure and urinary sodium excretion in relation to the A-1984G adrenomedullin polymorphism in a Chinese population. Sodium 27-33 adrenomedullin Homo sapiens 71-85 16609682-12 2006 In conclusion, in Chinese, the ADM -1984G allele is associated with lower sodium excretion and in older subjects also with lower systolic pressure and narrower pulse pressure. Sodium 74-80 adrenomedullin Homo sapiens 31-34 16618647-1 2006 CONCLUSIONS: The fact that pseudohypoaldosteronism type 1 (PHA-1) patients with a defect in the alpha subunit of epithelial sodium channels (ENaC) in the cochlea have normal hearing suggests compensation by alternative sodium transport mechanisms. Sodium 124-130 sodium channel epithelial 1 subunit gamma Homo sapiens 27-57 16618647-1 2006 CONCLUSIONS: The fact that pseudohypoaldosteronism type 1 (PHA-1) patients with a defect in the alpha subunit of epithelial sodium channels (ENaC) in the cochlea have normal hearing suggests compensation by alternative sodium transport mechanisms. Sodium 124-130 sodium channel epithelial 1 subunit gamma Homo sapiens 59-64 16174867-1 2006 Atrial natriuretic peptide (ANP) acutely promotes water and sodium excretion, whereas subchronic effects involve water retention. Sodium 60-66 natriuretic peptide A Rattus norvegicus 0-26 16174867-1 2006 Atrial natriuretic peptide (ANP) acutely promotes water and sodium excretion, whereas subchronic effects involve water retention. Sodium 60-66 natriuretic peptide A Rattus norvegicus 28-31 16174867-8 2006 ANP infusion evoked an instant increase in renal sodium excretion, which persisted for 90 min. Sodium 49-55 natriuretic peptide A Rattus norvegicus 0-3 16462035-2 2006 We have previously demonstrated the functional expression of the neural amino acid gamma-aminobutyric acid (GABA) signaling system including betaine/GABA transporter-1 (BGT-1) with a temperature-, sodium- and chloride-dependent activity of [(3)H]GABA accumulation in cultured rat calvarial osteoblasts. Sodium 197-203 solute carrier family 6 member 12 Rattus norvegicus 141-167 16462035-2 2006 We have previously demonstrated the functional expression of the neural amino acid gamma-aminobutyric acid (GABA) signaling system including betaine/GABA transporter-1 (BGT-1) with a temperature-, sodium- and chloride-dependent activity of [(3)H]GABA accumulation in cultured rat calvarial osteoblasts. Sodium 197-203 solute carrier family 6 member 12 Rattus norvegicus 169-174 16154648-1 2006 Intraventricular injections of the tachykinin NK3 receptor (NK3-R) agonist, senktide, suppress the ingestion of hypertonic (0.5 M) NaCl by decreasing the initial lick rate and accelerating the decay in lick rate in sodium deficient rats. Sodium 215-221 tachykinin receptor 3 Rattus norvegicus 60-65 16154648-7 2006 The results show that activation of NK3-R in sodium deficient rats suppresses the intake of tastes that are classified as "salty" tasting and that the decrease in intake reflects effects on the initial lick rate, the decay in lick rate, or both. Sodium 45-51 tachykinin receptor 3 Rattus norvegicus 36-41 17183188-0 2006 Renal protective role of atrial natriuretic peptide in acute sodium overload-induced inflammatory response. Sodium 61-67 natriuretic peptide A Rattus norvegicus 25-51 17183188-8 2006 Sodium overload increased the expression of: RANTES (38.4.3 +/- 0.8 vs. 2.9 +/- 0.6%, p < 0.001), transforming-growth-factor-beta(1) (35.3 +/- 1.0 vs. 5.0 +/- 0.7%, p < 0.001), alpha-smooth muscle actin (15.6 +/- 0.7 vs. 3.1 +/- 0.3%, p < 0.001), NF-kappaB (9.4 +/- 1.3 to 2.2 +/- 0.5 cells/mm(2), p < 0.001), HIF-1alpha (38.2 +/- 1.7 to 8.4 +/- 0.8 cells/mm(2), p < 0.001) and angiotensin II (35.9 +/- 1.3 to 8.2 +/- 0.5%, p < 0.001). Sodium 0-6 C-C motif chemokine ligand 5 Rattus norvegicus 45-51 17183188-8 2006 Sodium overload increased the expression of: RANTES (38.4.3 +/- 0.8 vs. 2.9 +/- 0.6%, p < 0.001), transforming-growth-factor-beta(1) (35.3 +/- 1.0 vs. 5.0 +/- 0.7%, p < 0.001), alpha-smooth muscle actin (15.6 +/- 0.7 vs. 3.1 +/- 0.3%, p < 0.001), NF-kappaB (9.4 +/- 1.3 to 2.2 +/- 0.5 cells/mm(2), p < 0.001), HIF-1alpha (38.2 +/- 1.7 to 8.4 +/- 0.8 cells/mm(2), p < 0.001) and angiotensin II (35.9 +/- 1.3 to 8.2 +/- 0.5%, p < 0.001). Sodium 0-6 hypoxia inducible factor 1 subunit alpha Rattus norvegicus 322-332 16352918-14 2006 CONCLUSION: We noted increased NKCC2 abundance in non-edematous disease, which enhanced body fluid accumulation, likely via the sodium loading-dependent concentration of the urine. Sodium 128-134 solute carrier family 12 member 1 Rattus norvegicus 31-36 16316636-2 2005 A subset of neurons in the nucleus tractus solitarius (NTS) are uniquely sensitive to the adrenal steroid hormone aldosterone, which is critically involved in sodium homeostasis, due to their expression of the enzyme 11-beta-hydroxysteroid dehydrogenase type 2 (HSD2). Sodium 159-165 hydroxysteroid 11-beta dehydrogenase 2 Rattus norvegicus 217-260 16317684-2 2005 The two subunits of the transporter were expressed together in human small intestine, kidney, and liver, tissues that also express the apical sodium-dependent bile acid uptake transporter ASBT (SLC10A2). Sodium 142-148 solute carrier family 10 member 2 Homo sapiens 188-192 16317684-2 2005 The two subunits of the transporter were expressed together in human small intestine, kidney, and liver, tissues that also express the apical sodium-dependent bile acid uptake transporter ASBT (SLC10A2). Sodium 142-148 solute carrier family 10 member 2 Homo sapiens 194-201 15976003-11 2005 Pharmacologic inhibition of EP4 receptors in furosemide-treated WT mice with the specific antagonist ONO-AE3-208 mimicked the changes in renin mRNA expression, plasma renin concentration, diuresis, and sodium excretion seen in EP4-/- mice. Sodium 202-208 prostaglandin E receptor 4 (subtype EP4) Mus musculus 28-31 11750920-0 2002 Effect of phenytoin on sodium and calcium currents in hippocampal CA1 neurons of phenytoin-resistant kindled rats. Sodium 23-29 carbonic anhydrase 1 Rattus norvegicus 66-69 11750920-4 2002 In line with this proposal, a reduced effect of carbamazepine on sodium currents in hippocampal CA1 neurons was found in the rat kindling model of temporal lobe epilepsy (TLE), i.e. a form of epilepsy with the poorest prognosis of all epilepsy types in adult patients. Sodium 65-71 carbonic anhydrase 1 Rattus norvegicus 96-99 11754984-10 2001 On the other hand, RAMP2 mRNA expression in the kidney was suppressed by sodium intake restriction regardless of nephrectomy, while RAMP2 levels in the remnant kidney were not significantly changed by 5/6 nephrectomy. Sodium 73-79 receptor activity modifying protein 2 Rattus norvegicus 19-24 11478427-1 2001 Atrial natriuretic peptide (ANP) is an important regulator of sodium metabolism and indirectly of blood pressure. Sodium 62-68 natriuretic peptide type A Mus musculus 0-26 11518842-1 2001 BACKGROUND: The genes encoding angiotensin converting enzyme (ACE, I/D), alpha-adducin (ADD, Gly460Trp) and aldosterone synthase (AS, -344C/T) share the potential of influencing blood pressure (BP) via sodium homeostasis. Sodium 202-208 cytochrome P450 family 11 subfamily B member 2 Homo sapiens 108-128 11834205-3 2001 Uptake of pantothenic acid into PBMC was mediated by the sodium-dependent multivitamin transporter, SMVT, as judged by sodium dependency of uptake, substrate affinity and specificity, and RT-PCR of PBMC RNA. Sodium 57-63 solute carrier family 5 member 6 Homo sapiens 100-104 11510881-7 2001 Specific COMT activity in the renal cortex was reduced by 13% after isotonic sodium loading (5% of body mass) whereas renal MAO-A and MAO-B activities remained unaltered. Sodium 77-83 catechol-O-methyltransferase Rattus norvegicus 9-13 16078136-7 2005 RESULTS: In the selected clone, hASBT-mediated taurocholate permeability across hASBT-MDCK monolayers was almost 25-fold higher with sodium, than without sodium where hASBT is not functional. Sodium 133-139 solute carrier family 10 member 2 Homo sapiens 32-37 16078136-7 2005 RESULTS: In the selected clone, hASBT-mediated taurocholate permeability across hASBT-MDCK monolayers was almost 25-fold higher with sodium, than without sodium where hASBT is not functional. Sodium 133-139 solute carrier family 10 member 2 Homo sapiens 80-85 16078136-7 2005 RESULTS: In the selected clone, hASBT-mediated taurocholate permeability across hASBT-MDCK monolayers was almost 25-fold higher with sodium, than without sodium where hASBT is not functional. Sodium 133-139 solute carrier family 10 member 2 Homo sapiens 80-85 16078136-7 2005 RESULTS: In the selected clone, hASBT-mediated taurocholate permeability across hASBT-MDCK monolayers was almost 25-fold higher with sodium, than without sodium where hASBT is not functional. Sodium 154-160 solute carrier family 10 member 2 Homo sapiens 32-37 16078136-8 2005 In the presence of sodium, taurocholate and mannitol permeabilities were 23.0x10(-6) cm/sec and 2.60x10(-6) cm/s, respectively, indicating high hASBT functionality and monolayer integrity. Sodium 19-25 solute carrier family 10 member 2 Homo sapiens 144-149 16076377-0 2005 Inhibition of intestinal sodium-dependent inorganic phosphate transport by fibroblast growth factor 23. Sodium 25-31 fibroblast growth factor 23 Mus musculus 75-102 15954990-0 2005 Effects of sodium intake on plasma potassium and renin angiotensin aldosterone system in conscious dogs. Sodium 11-17 renin Canis lupus familiaris 49-54 15954990-2 2005 This study quantifies renin-angiotensin-aldosterone system activity as a function of sodium intake. Sodium 85-91 renin Canis lupus familiaris 22-27 15954990-8 2005 RESULTS: Sudden sodium intake reduction doubled plasma renin activity and angiotensin II, and tripled aldosterone on day 1 with only small non-significant additional changes on the following days. Sodium 16-22 renin Canis lupus familiaris 55-60 15954990-10 2005 With increasing sodium intake, plasma volume increased by 0.47 +/- 0.04 mL (kg body mass)(-1) (unit increase in Na intake)(-1) (P < 0.01), and plasma potassium decreased with the slope -0.038 mm [(mmol Na+ intake) (kg body mass)(-1) day(-1)](-1) (P = 0.001) while plasma renin-activity, angiotensin II, and aldosterone decreased systematically as expected. Sodium 16-22 renin Canis lupus familiaris 274-279 15954990-11 2005 CONCLUSIONS: A step reduction in sodium intake alters renin-angiotensin-aldosterone system activity on day 1 with little further change the subsequent 4 days. Sodium 33-39 renin Canis lupus familiaris 54-59 15954990-12 2005 Week-long increases in sodium intake decreases renin-angiotensin-aldosterone system activity, increases plasma volume, and decreases plasma potassium. Sodium 23-29 renin Canis lupus familiaris 47-52 15954990-13 2005 Isolated decreases in sodium intake increase aldosterone secretion via volume-mediated action on the renin-angiotensin system and via increases in plasma potassium. Sodium 22-28 renin Canis lupus familiaris 101-106 15673553-1 2005 The presence of multiple Nav1 isotypes within a neuron and the lack of specific blockers hamper identification of the in vivo roles of sodium current (INa) components, especially during embryonic stages. Sodium 135-141 zgc:65851 Danio rerio 151-154 15882550-5 2005 Variance components linkage analysis of postural SBP change was conducted using microsatellite markers on chromosome 18, and association studies were performed with a common single nucleotide polymorphism (variant 13) in the gene encoding NEDD4L, a key regulator of fine sodium reabsorption in the distal nephron. Sodium 271-277 NEDD4 like E3 ubiquitin protein ligase Homo sapiens 239-245 15882550-7 2005 Postural SBP response was associated with variant 13 of the NEDD4L in a subset of white subjects taking medications effective in treating sodium volume-dependent hypertension (alpha1-blockers, calcium channel blockers, and/or diuretics). Sodium 138-144 NEDD4 like E3 ubiquitin protein ligase Homo sapiens 60-66 15901346-9 2005 All of these findings indicate that hOat2 is a sodium-independent multi-specific organic anion/dimethyldicarboxylate exchanger. Sodium 47-53 solute carrier family 22 member 7 Homo sapiens 36-41 15780097-7 2005 Ang-(1-7) receptor blockade elicited significant decreases in glomerular filtration rate (GFR), renal plasma flow (RPF), and sodium excretion in 2K1C rats, and in salt-depleted TGR and HanSD. Sodium 125-131 angiogenin Rattus norvegicus 0-3 15780097-11 2005 In contrast, under conditions of endogenous RAS activation due to clipping of the renal artery or to sodium restriction, Ang-(1-7) serves as opponent of the vasoconstrictor actions of Ang II. Sodium 101-107 angiogenin Rattus norvegicus 121-124 15542610-4 2005 ceGAT-1 is coded by snf-11 gene, a member of the sodium-dependent neurotransmitter symporter gene family in C. elegans. Sodium 49-55 Transporter Caenorhabditis elegans 20-26 15709964-9 2005 Although intestinal and colonic sodium absorption appear to involve at least NHE2 and NHE3, future studies are necessary to more accurately define their relative contributions to sodium absorption during human digestion and in pathophysiological conditions. Sodium 32-38 solute carrier family 9 member A2 Homo sapiens 77-81 15709964-9 2005 Although intestinal and colonic sodium absorption appear to involve at least NHE2 and NHE3, future studies are necessary to more accurately define their relative contributions to sodium absorption during human digestion and in pathophysiological conditions. Sodium 32-38 solute carrier family 9 member A3 Homo sapiens 86-90 11352736-2 2001 In this study, we determined the transport stoichiometry of the retinal cone potassium-dependent Na/Ca exchanger (NCKX) expressed in sodium-loaded cultured insect cells. Sodium 133-139 solute carrier family 24 member 1 Homo sapiens 114-118 15642785-4 2005 MnSOD activity in inner zone mitochondrial fractions was enhanced by corticotrophin and by a low-sodium diet, but suppressed by betamethasone. Sodium 97-103 superoxide dismutase 2 Rattus norvegicus 0-5 11334836-12 2001 CONCLUSIONS: We conclude that KvLQT1-invalidated TG mice discriminates in vivo drugs that blocks I(Kr) from drugs that block the transient outward current, the sodium current or the calcium current. Sodium 160-166 potassium voltage-gated channel, subfamily Q, member 1 Mus musculus 30-36 16267171-5 2005 This review discusses how COMMD1 functions as a regulator of not only copper homeostasis but also sodium transport and the NF-kappaB signaling pathway. Sodium 98-104 copper metabolism domain containing 1 Canis lupus familiaris 26-32 15639021-10 2005 They have shown that, in the renal distal tubule, WNK4 inhibits sodium reabsorption and potassium secretion, via inhibition of NCC (thiazide-sensitive Na+-Cl- cotransporter) and K+ channel ROMK activity, respectively. Sodium 64-70 serine/threonine-protein kinase WNK4 Canis lupus familiaris 50-54 11417227-3 2001 The amino acid transport activity induced by the co-expression of human 4F2hc and xCT in Xenopus oocytes was sodium independent and specific for L-cystine, L-glutamate and L-aspartate. Sodium 109-115 solute carrier family 3 member 2 Homo sapiens 72-77 15572847-5 2004 From this morphologic evidence, it is proposed that beta(2)-AR activation may regulate glomerular function and thereby sodium and water balance in the nephron segments. Sodium 119-125 adrenoceptor beta 2 Homo sapiens 52-62 11417227-3 2001 The amino acid transport activity induced by the co-expression of human 4F2hc and xCT in Xenopus oocytes was sodium independent and specific for L-cystine, L-glutamate and L-aspartate. Sodium 109-115 solute carrier family 7 member 11 Homo sapiens 82-85 15338391-7 2004 In conclusion, our data show that increased sodium intake during pregnancy induces a reduction of alpha-SM-actin, fibronectin, and PCNA expression in the renal cortex tubulointerstitium and glomeruli of neonatal rats. Sodium 44-50 proliferating cell nuclear antigen Rattus norvegicus 131-135 11278387-1 2001 Treatment of Madin-Darby canine kidney (MDCK) cells with the peptide hormone angiotensin II (Ang II) results in an increase in the concentrations of cytosolic free calcium ([Ca(2+)](i)) and sodium ([Na(+)](i)) with a concomitant decrease in cytosolic free Mg(2+) concentration ([Mg(2+)](i)). Sodium 190-196 ANG Canis lupus familiaris 93-96 15651314-2 2004 Mutations of voltage-gated sodium channel genes SCN1A and SCN2A have been reported in epilepsies with a variety of phenotypes including generalized epilepsy with febrile seizures plus (GEFS +), severe myoclonic epilepsy in infancy (SMEI), intractable childhood epilepsy with generalized tonic-clonic seizures (ICEGTC), and benign familial neonatal-infantile seizures (BFNIS). Sodium 27-33 sodium voltage-gated channel alpha subunit 2 Homo sapiens 58-63 15161602-2 2004 Specifically, we show that a 2-min exposure to 0.1 and 1 nM ANG II slowed the rate of intracellular sodium accumulation in response to an increase in extracellular sodium added in the presence of gramicidin D. From these data, we show that ANG II directly stimulates Na-K-ATPase activity at rate-limiting concentrations of intracellular sodium. Sodium 100-106 angiogenin Rattus norvegicus 60-63 15161602-2 2004 Specifically, we show that a 2-min exposure to 0.1 and 1 nM ANG II slowed the rate of intracellular sodium accumulation in response to an increase in extracellular sodium added in the presence of gramicidin D. From these data, we show that ANG II directly stimulates Na-K-ATPase activity at rate-limiting concentrations of intracellular sodium. Sodium 164-170 angiogenin Rattus norvegicus 60-63 11302728-5 2001 Human AE4 shares 84% identity with the recently reported rabbit AE4, a sodium independent, Cl(-)/HCO(-)(3) exchanger located on the apical membrane of beta-intercalated kidney cells. Sodium 71-77 anion exchange protein 4 Oryctolagus cuniculus 64-67 15161602-2 2004 Specifically, we show that a 2-min exposure to 0.1 and 1 nM ANG II slowed the rate of intracellular sodium accumulation in response to an increase in extracellular sodium added in the presence of gramicidin D. From these data, we show that ANG II directly stimulates Na-K-ATPase activity at rate-limiting concentrations of intracellular sodium. Sodium 164-170 angiogenin Rattus norvegicus 60-63 15385606-0 2004 Electrophysiological properties of mutant Nav1.7 sodium channels in a painful inherited neuropathy. Sodium 49-55 sodium voltage-gated channel alpha subunit 9 Homo sapiens 42-48 11294924-5 2001 The functional consequence of a SCN4A mutation was explored by recording sodium currents from human embryonic kidney cells transiently transfected with an expression construct that was mutated to reproduce the genetic defect. Sodium 73-79 sodium voltage-gated channel alpha subunit 4 Homo sapiens 32-37 15497696-8 2004 Low sodium buffer (1 mM) resulted in 75% and 59% reductions, respectively, in GlySar (p < 0.001) and 5-ALA (p < 0.01) uptake in PEPT2+/+ mice; no differences were observed in PEPT2-/- mice. Sodium 4-10 solute carrier family 15 (H+/peptide transporter), member 2 Mus musculus 134-139 15497696-8 2004 Low sodium buffer (1 mM) resulted in 75% and 59% reductions, respectively, in GlySar (p < 0.001) and 5-ALA (p < 0.01) uptake in PEPT2+/+ mice; no differences were observed in PEPT2-/- mice. Sodium 4-10 solute carrier family 15 (H+/peptide transporter), member 2 Mus musculus 181-186 11410707-1 2001 The amiloride-sensitive epithelial sodium channel (ENaC) is the limiting step for sodium absorption in epithelial cells of the distal nephron, distal colon, airways and excretory ducts of several glands. Sodium 35-41 sodium channel, nonvoltage-gated 1 alpha Mus musculus 51-55 15005625-4 2004 Three other surface loops on FXa including 39, 60, and the sodium-binding 220 loops have been implicated to be critical for the protease interaction with the activated AT. Sodium 59-65 coagulation factor X Homo sapiens 29-32 15005625-7 2004 On the other hand, the reactivity of AT with the sodium loop mutants of FXa in the absence of the cofactor was severely impaired. Sodium 49-55 coagulation factor X Homo sapiens 72-75 10978318-6 2000 Up-regulation of ENaC-mediated sodium conductance by overnight treatment with aldosterone or by short term incubation with vasopressin dramatically increased cell surface levels of beta-ENaC without affecting alpha- or gamma-ENaC levels. Sodium 31-37 sodium channel, non voltage gated 1 beta subunit S homeolog Xenopus laevis 181-190 14736542-7 2004 Voltage-clamp experiments in transgenic myocytes revealed a peak inward sodium current (INa) followed by a slow recovery from inactivation. Sodium 72-78 internexin neuronal intermediate filament protein, alpha Mus musculus 88-91 10978318-11 2000 The selective trafficking of beta-ENaC may provide a mechanism for regulating sodium conductance in response to physiological stimuli. Sodium 78-84 sodium channel, non voltage gated 1 beta subunit S homeolog Xenopus laevis 29-38 11004014-8 2000 ANG II caused sodium retention and a sustained increase in MAP of 30-35 mmHg. Sodium 14-20 ANG Canis lupus familiaris 0-3 14593089-3 2004 These studies were designed to test the hypothesis that rosiglitazone (RGZ, PPAR-gamma agonist) may activate sodium- and water-reabsorptive processes in the kidney, possibly in response to a drop in mean arterial blood pressure (MAP), as well as directly through PPAR-gamma. Sodium 109-115 peroxisome proliferator-activated receptor gamma Rattus norvegicus 76-86 14999490-6 2004 Peak amplitudes of fast inward sodium currents (I(Na)) were increased by low MWCO-CIM fractions compared with control sera fractions. Sodium 31-37 endoplasmic reticulum lectin 1 Homo sapiens 82-85 15153749-10 2004 CONCLUSION: We were able to confirm that urinary excretion of THP is dependent on sodium intake. Sodium 82-88 uromodulin Homo sapiens 62-65 14652358-3 2003 Sodium supplementation (NaSp) produced the difference in Na+ intake. Sodium 0-6 nuclear autoantigenic sperm protein Homo sapiens 24-28 11006093-1 2000 The molecular organization of the AE2 (SLC4A2) gene, a member of the multigene family encoding sodium-independent chloride/bicarbonate anion exchangers, has previously been described in both humans and rats. Sodium 95-101 solute carrier family 4 member 2 Homo sapiens 34-37 11006093-1 2000 The molecular organization of the AE2 (SLC4A2) gene, a member of the multigene family encoding sodium-independent chloride/bicarbonate anion exchangers, has previously been described in both humans and rats. Sodium 95-101 solute carrier family 4 member 2 Homo sapiens 39-45 10864164-6 2000 CCl4 and CH3CCl3 in the presence of a stoichiometric deficiency of sodium produced only CH4 and CH3CH3 and recovered CCl4 or CH3CCl3, respectively. Sodium 67-73 C-C motif chemokine ligand 4 Homo sapiens 0-4 10864164-6 2000 CCl4 and CH3CCl3 in the presence of a stoichiometric deficiency of sodium produced only CH4 and CH3CH3 and recovered CCl4 or CH3CCl3, respectively. Sodium 67-73 C-C motif chemokine ligand 4 Homo sapiens 117-121 10961955-1 2000 BACKGROUND: Defects of the SCN5A gene encoding the cardiac sodium channel are associated with both the LQT3 subtype of long-QT syndrome and Brugada syndrome (BS). Sodium 59-65 sodium voltage-gated channel alpha subunit 5 Homo sapiens 27-32 10944223-8 2000 The results prove that SCN4A, the gene encoding the sodium channel alpha subunit of skeletal muscle is responsible for HypoPP-2 which does not differ clinically from DHPR-HypoPP. Sodium 52-58 sodium voltage-gated channel alpha subunit 4 Homo sapiens 23-28 12967595-1 2003 Intracerebroventricular (IVT) administration of adrenomedullin (AM) to conscious male hydrated rats increases urinary volume and sodium excretion. Sodium 129-135 adrenomedullin Rattus norvegicus 48-62 12824076-0 2003 Natriuretic peptide receptor A mediates renal sodium excretory responses to blood volume expansion. Sodium 46-52 natriuretic peptide receptor 1 Mus musculus 0-30 14526231-1 2003 Atrial natriuretic peptide (ANP) plays an important role in the regulation of water and sodium in the body via cyclic GMP (cGMP) pathway. Sodium 88-94 natriuretic peptide A Rattus norvegicus 0-26 10948076-11 2000 We conclude that polymorphisms in HSD11B2 and decreased 11-HSD2 activity are associated with sensitivity to sodium loading, but a functional explanation for these associations remains to be elucidated. Sodium 108-114 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 34-41 10932223-4 2000 In addition to characterizing the hormonal regulation of the mammary gland sodium/iodide symporter, we demonstrate by scintigraphy that mammary adenocarcinomas in transgenic mice bearing Ras or Neu oncogenes actively accumulate iodide by this symporter in vivo. Sodium 75-81 erb-b2 receptor tyrosine kinase 2 Mus musculus 194-197 10864945-1 2000 Sodium-dependent action potentials initiated near the soma are known to backpropagate over the dendrites of CA1 pyramidal neurons in an activity-dependent manner. Sodium 0-6 carbonic anhydrase 1 Mus musculus 108-111 10850964-11 2000 Chloride-dependent ANF-receptor binding may function as a feedback-control mechanism regulating the ANF-receptor action and, hence, renal sodium excretion. Sodium 138-144 natriuretic peptide A Bos taurus 19-22 10850964-11 2000 Chloride-dependent ANF-receptor binding may function as a feedback-control mechanism regulating the ANF-receptor action and, hence, renal sodium excretion. Sodium 138-144 natriuretic peptide A Bos taurus 100-103 10775190-2 2000 The sodium ion (Na(+)) was partly responsible for the P(4)-induced depolarizing effect but was not required for calcium influx. Sodium 4-10 solute carrier family 10 member 4 Homo sapiens 54-58 10775190-6 2000 Prior incubation of spermatozoa with 10 microM flunarizine, a Na(+) and Ca(2+) voltage-dependent channel blocker, inhibited the sodium influx induced by 10 microM P(4) by 84.6 +/- 15.4%. Sodium 128-134 solute carrier family 10 member 4 Homo sapiens 163-167 10760058-2 2000 MR is expressed in a wide variety of tissues, most notably in sodium-transporting epithelia, but also in nonepithelial cells of the cardiovascular and central nervous systems. Sodium 62-68 nuclear receptor subfamily 3, group C, member 2 Mus musculus 0-2 12954815-0 2003 Arylacetamide kappa-opioid receptor agonists produce a tonic- and use-dependent block of tetrodotoxin-sensitive and -resistant sodium currents in colon sensory neurons. Sodium 127-133 opioid receptor kappa 1 Homo sapiens 14-35 12742089-3 2003 It was demonstrated that, as in several other transporters, sodium binding and release by GAT1, GAT3 and BGT-1, the canine homolog of GAT2, resulted in the appearance of presteady-state currents. Sodium 60-66 solute carrier family 6 (neurotransmitter transporter), member 13 L homeolog Xenopus laevis 134-138 12878176-5 2003 Expression of the atrial natriuretic peptide gene was, for instance, induced in myocytes by sodium overload and further enhanced even at the heart failure stage. Sodium 92-98 natriuretic peptide A Rattus norvegicus 18-44 12804783-2 2003 Interestingly, this function was independent of the role of the antiporter in improving tolerance to sodium cations, it required the integrity of a relatively large region (from residues 800 to 948) of its carboxy-terminal moiety, and was not performed by the fission yeast homolog antiporter Sod2, which lacks a carboxy-terminal tail. Sodium 101-107 superoxide dismutase SOD2 Saccharomyces cerevisiae S288C 293-297 12804783-3 2003 Here we show that a hybrid protein composed of the Sod2 antiporter fused to the carboxy-terminal half of Nha1 strongly increased sodium tolerance, but did not allow growth at high potassium nor did rescue growth of the sit4 hal3 conditional mutant strain. Sodium 129-135 superoxide dismutase SOD2 Saccharomyces cerevisiae S288C 51-55 12697273-0 2003 Sodium ions and GTP decrease the potency of [Nphe1]N/OFQ(1-13)NH2 in blocking nociceptin/orphanin FQ receptors coupled to cyclic AMP in N1E-115 neuroblastoma cells and rat olfactory bulb. Sodium 0-6 prepronociceptin Mus musculus 51-56 12697273-3 2003 In the present study, we show that sodium ions and GTP markedly affect the potency of Nphe in blocking N/OFQ receptors coupled to cyclic AMP inhibition in different cellular systems. Sodium 35-41 prepronociceptin Mus musculus 103-108 12697273-6 2003 Similar effects of sodium ions on the potencies of Nphe and CompB were observed when the compounds were used to antagonize the N/OFQ inhibition of adenylyl cyclase activity in membranes of the external plexiform layer of the rat olfactory bulb. Sodium 19-25 prepronociceptin Mus musculus 127-132 12488247-13 2003 NaPi-IIb2 was found to be strongly voltage sensitive, with higher affinities for both sodium and phosphate than NaPi-IIb1. Sodium 86-92 solute carrier family 34 member 2b Danio rerio 0-9 12505866-9 2003 Levels of Fos-ir were highest in fluid-depleted rats that drank water and sodium. Sodium 74-80 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 10-13 12609911-8 2003 We show that the small persistent sodium current can play a key role in spontaneous CA1 activity in zero-calcium solutions. Sodium 34-40 carbonic anhydrase 1 Homo sapiens 84-87 12502589-0 2002 Mitochondria buffer sodium-dependent CA2+ influx in cultured cerebellar granule cells. Sodium 20-26 carbonic anhydrase 2 Homo sapiens 37-40 12383080-0 2002 A role for HKT1 in sodium uptake by wheat roots. Sodium 19-25 cation transporter HKT1 Triticum aestivum 11-15 12243921-3 2002 Here, we describe a clinically intermediate variant, benign familial neonatal-infantile seizures, with mutations in the sodium-channel subunit gene SCN2A. Sodium 120-126 sodium voltage-gated channel alpha subunit 2 Homo sapiens 148-153 12082097-8 2002 Collectively, these findings support the existence of a complex regulatory circuitry in the cells of the inner medullary collecting duct linking two independent cyclic GMP-generating signal transduction systems involved in regulation of urinary sodium concentration. Sodium 245-251 5'-nucleotidase, cytosolic II Homo sapiens 168-171 12188925-0 2002 Reduced natriuretic response to acute sodium loading in COMT gene deleted mice. Sodium 38-44 catechol-O-methyltransferase Mus musculus 56-60 12188925-13 2002 The results support the hypothesis that COMT has an important role in the DA-mediated regulation of renal sodium excretion. Sodium 106-112 catechol-O-methyltransferase Mus musculus 40-44 10760060-3 2000 ENaC mediates the aldosterone-dependent sodium reabsorption in the distal nephron and is involved in the regulation of blood pressure. Sodium 40-46 sodium channel, nonvoltage-gated 1 alpha Mus musculus 0-4 10760070-4 2000 In AME, compromised 11betaHSD2 enzyme activity results in overstimulation of the MR by cortisol, causing sodium retention, hypokalemia, and salt-dependent hypertension. Sodium 105-111 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 20-30 10726708-2 2000 Inhibition by xenobiotics such as liquorice or mutations in the HSD11 B2 gene, as occur in the rare monogenic hypertensive syndrome of apparent mineralocorticoid excess (AME), result in a compromised 11 betaHSD2 enzyme activity, which in turn leads to overstimulation of the MR by cortisol, sodium retention, hypokalaemia, low plasma renin and aldosterone concentrations, and hypertension. Sodium 291-297 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 64-72 12177176-2 2002 Evaluated in vitro, 264W94 dose-dependently inhibited sodium-dependent uptake of 10 micro M [(3)H]taurocholic acid (TC) by rat and monkey brush border membrane vesicles with IC(50)s of 0.24 micro M and 0.41 micro M, and had a competitive profile with K(i) of 0.2 micro M against TC in Chinese hamster ovary cells expressing human IBAT. Sodium 54-60 solute carrier family 10 member 2 Homo sapiens 330-334 10726708-11 2000 Since steroid hormones with mineralocorticoid action modulate renal sodium retention, one might hypothesize that genetic impairment of 11 beta HSD2 activity would be more prevalent in salt-sensitive as compared with salt-resistant subjects. Sodium 68-74 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 135-147 10623603-1 2000 Previously, we isolated the human AE2 (SLC4A2) gene, a member of the sodium-independent anion exchanger family. Sodium 69-75 solute carrier family 4 member 2 Homo sapiens 34-37 12067853-8 2002 The PRL effect on (32)PO(4) uptake was abolished when sodium was absent from the uptake medium. Sodium 54-60 prolactin Mus musculus 4-7 12086636-2 2002 In generalized epilepsy with febrile seizures plus, an autosomal dominant epilepsy syndrome, mutations in three genes coding for voltage-gated sodium channel alpha or beta1 subunits (SCN1A, SCN2A, SCN1B) and one GABA receptor subunit gene (GABRG2) have been identified. Sodium 143-149 gamma-aminobutyric acid type A receptor subunit gamma2 Homo sapiens 240-246 11972032-5 2002 Whole-cell patch clamp analyses of isolated ventricular myocytes from adult Scn5a(+/-) mice demonstrate a approximately 50% reduction in sodium conductance. Sodium 137-143 sodium channel, voltage-gated, type V, alpha Mus musculus 76-81 11967240-1 2002 An apical serine protease, channel-activating protease 1 (CAP1), augments sodium transport in A6 cells. Sodium 74-80 complement component 1, s subcomponent 1 Mus musculus 10-25 12522688-2 2002 By targeting the epithelial sodium channel (ENaC) for degradation, NEDD4L is a significant determinant of sodium reabsorption in the distal nephron. Sodium 28-34 NEDD4 like E3 ubiquitin protein ligase Homo sapiens 67-73 12522688-2 2002 By targeting the epithelial sodium channel (ENaC) for degradation, NEDD4L is a significant determinant of sodium reabsorption in the distal nephron. Sodium 106-112 NEDD4 like E3 ubiquitin protein ligase Homo sapiens 67-73 12522688-10 2002 Differential function of NEDD4L isoforms could prove significant in blood pressure regulation through an effect on ENaC-dependent sodium reabsorption. Sodium 130-136 NEDD4 like E3 ubiquitin protein ligase Homo sapiens 25-31 12511180-7 2002 In contrast, intrarenal inhibition of nNOS by L-SMTC did not alter GFR, RPF or RVR and elicited a marked increase in sodium excretion in TGR. Sodium 117-123 nitric oxide synthase 1 Rattus norvegicus 38-42 12511180-10 2002 In addition, the data indicate that nNOS-derived NO increases tubular sodium reabsorption in TGR and that the renal nerves play an important modulatory role in this process. Sodium 70-76 nitric oxide synthase 1 Rattus norvegicus 36-40 11551807-0 2001 The role of SGK1 in hormone-regulated sodium transport. Sodium 38-44 serum/glucocorticoid regulated kinase 1 Homo sapiens 12-16 11506985-7 2001 Intravenous infusion of ANG II after these long captopril infusions stimulated sodium intake, but intake was less than in controls not treated with captopril. Sodium 79-85 angiogenin Rattus norvegicus 24-27 11496063-6 2001 Other recent studies unravel pathways other than those activated by aldosterone and insulin that impact on SGK1 expression and/or function, and thus shed some light onto the complex network that appears to control sodium transport. Sodium 214-220 serum/glucocorticoid regulated kinase 1 Homo sapiens 107-111 10623603-1 2000 Previously, we isolated the human AE2 (SLC4A2) gene, a member of the sodium-independent anion exchanger family. Sodium 69-75 solute carrier family 4 member 2 Homo sapiens 39-45 10696530-2 2000 In the rectum and distal nephron, sodium reabsorption is mediated by the amiloride-sensitive epithelial sodium channel (ENaC). Sodium 34-40 sodium channel, nonvoltage-gated 1 alpha Mus musculus 120-124 10696530-3 2000 The ENaC-mediated sodium transport is electrogenic and creates an amiloride-sensitive transepithelial potential difference (PD). Sodium 18-24 sodium channel, nonvoltage-gated 1 alpha Mus musculus 4-8 10651854-4 2000 This problem was addressed by studying sodium currents and action potentials in acutely isolated hippocampal CA1 neurons whose number of active sodium channels was acutely changed by applying the sodium channel blocker tetrodotoxin (TTX) at different concentrations. Sodium 39-45 carbonic anhydrase 1 Cavia porcellus 109-112 11272005-3 2000 A sub-monolayer of atomic sodium, Nan, was deposited on LiF(001) at 50 K and characterized by temperature-programmed desorption, X-ray photoelectron spectroscopy, and titration with HCl. Sodium 26-32 LIF interleukin 6 family cytokine Homo sapiens 56-59 11512567-5 2001 Simple regression analysis showed that plasma AM level correlated significantly with urinary vasopressin, urine volume, urinary sodium excretion, and plasma osmolarity. Sodium 128-134 adrenomedullin Homo sapiens 46-48 11454443-5 2001 The recent visualization at the atomic level of the inhibitory site of sodium in the known target Hal2 has helped identify the interactions determining Na(+) toxicity. Sodium 71-77 3'(2'),5'-bisphosphate nucleotidase Saccharomyces cerevisiae S288C 98-102 11402167-1 2001 The SOS3 (for SALT OVERLY SENSITIVE3) calcium binding protein and SOS2 protein kinase are required for sodium and potassium ion homeostasis and salt tolerance in Arabidopsis. Sodium 103-109 Protein kinase superfamily protein Arabidopsis thaliana 66-70 11344206-2 2001 There are 2 forms of PHA1: the autosomal recessive form with symptoms persisting into adulthood, caused by mutations in the amiloride-sensitive luminal sodium channel, and the autosomal dominant or sporadic form, which shows milder symptoms that remit with age. Sodium 152-158 sodium channel epithelial 1 subunit gamma Homo sapiens 21-25 11290403-3 2001 In this work we use c-fos-like immunoreactivity to detect active areas involved in the long-term control of increased water and sodium intake due to partial aortic ligature. Sodium 128-134 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 20-25 10627583-7 2000 During the first 24 hr of NGF-treatment, PN1 sodium channels accounted for over 90% of the sodium current. Sodium 45-51 serpin family E member 2 Rattus norvegicus 41-44 10565577-0 1999 Modulation of sodium currents in rat CA1 neurons by carbamazepine and valproate after kindling epileptogenesis. Sodium 14-20 carbonic anhydrase 1 Rattus norvegicus 37-40 10565577-1 1999 PURPOSE: To determine the modulation of sodium currents in hippocampal CA1 neurons by carbamazepine (CBZ) and valproate (VPA), before and after kindling epileptogenesis. Sodium 40-46 carbonic anhydrase 1 Rattus norvegicus 71-74 10565577-2 1999 METHODS: Voltage-dependent sodium current was measured in isolated hippocampal CA1 neurons, by using the whole-cell voltage-clamp technique. Sodium 27-33 carbonic anhydrase 1 Rattus norvegicus 79-82 33867679-4 1999 However, sodium at blood concentrations near 100 mM causes only a minor change in the lifetime of CD222. Sodium 9-15 insulin like growth factor 2 receptor Homo sapiens 98-103 11323770-2 2001 MR-spectroscopy (MRS) records protons from tissue chemicals other than water, intrinsic phosphorus containing metabolites, sodium, potassium, carbon, nitrogen, and fluorine. Sodium 123-129 sterile alpha motif domain containing 11 Mus musculus 17-20 11260387-1 2001 BACKGROUND: Liver disease resulting from common bile duct ligation (CBDL) causes abnormal sodium metabolism that is manifested by resistance to the natriuretic action of atrial natriuretic peptide (ANP). Sodium 90-96 natriuretic peptide A Rattus norvegicus 170-196 11260387-1 2001 BACKGROUND: Liver disease resulting from common bile duct ligation (CBDL) causes abnormal sodium metabolism that is manifested by resistance to the natriuretic action of atrial natriuretic peptide (ANP). Sodium 90-96 natriuretic peptide A Rattus norvegicus 198-201 11260387-14 2001 This PDE5-dependent ANP resistance may represent an important contributor to the sodium retention of liver disease. Sodium 81-87 natriuretic peptide A Rattus norvegicus 20-23 10973949-2 2000 The serine protease domain of factor Xa (FXa) contains a sodium as well as a calcium-binding site. Sodium 57-63 coagulation factor X Homo sapiens 30-39 10973949-2 2000 The serine protease domain of factor Xa (FXa) contains a sodium as well as a calcium-binding site. Sodium 57-63 coagulation factor X Homo sapiens 41-44 10973949-5 2000 Sodium-bound FXa (sodium-Xa) has approximately 18-fold increased catalytic efficiency ( approximately 4.5-fold decrease in K(m) and approximately 4-fold increase in k(cat)) in hydrolyzing S-2222 (benzoyl-Ile-Glu-Gly-Arg-p-nitroanilide), and Ca(2+) further increases this k(cat) approximately 1.4-fold. Sodium 0-6 coagulation factor X Homo sapiens 13-16 1335501-2 1992 The effects of the extracellular divalent cations barium, calcium, cadmium, cobalt, magnesium, manganese, nickel and zinc and the trivalent cation lanthanum on macroscopic sodium current (INa) were characterized in enzymatically isolated single canine cardiac Purkinje cells under voltage clamp at 9-14 degrees C. 2. Sodium 172-178 internexin neuronal intermediate filament protein alpha Canis lupus familiaris 188-191 33867679-5 1999 Hence, CD222 and lifetime-based sensing can be used to measure blood levels of potassium in the presence of 130 mM sodium. Sodium 115-121 insulin like growth factor 2 receptor Homo sapiens 7-12 33867679-7 1999 For both CD222 and PBFI, the presence of blood levels of sodium increases the apparent potassium dissociation constants into the blood physiological range. Sodium 57-63 insulin like growth factor 2 receptor Homo sapiens 9-14 10516282-0 1999 Vasopressin stimulates sodium transport in A6 cells via a phosphatidylinositide 3-kinase-dependent pathway. Sodium 23-29 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta Homo sapiens 58-88 10515937-7 1999 Therefore, the salt sensitivity of a ckb1 mutant cannot be attributed to defects in the fluxes of sodium. Sodium 98-104 casein kinase 2 regulatory subunit CKB1 Saccharomyces cerevisiae S288C 37-41 10523024-2 1999 Because steroid hormones modulate renal sodium retention, we hypothesize that the activity of the 11beta-hydroxysteroid dehydrogenase type 2 (11betaHSD2) enzyme is impaired in SS subjects as compared with salt-resistant (SR) subjects. Sodium 40-46 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 98-152 1353889-2 1992 mRNA synthesized from this clone (designated GLYT1) directs the expression of sodium- and chloride-dependent, high-affinity uptake of [3H]glycine by Xenopus oocytes. Sodium 78-84 solute carrier family 6 member 9 Rattus norvegicus 45-50 1353889-7 1992 The primary structure and hydropathicity profile of GLYT1 protein reveal that this protein is a member of the sodium- and chloride-dependent superfamily of transporters that utilize neurotransmitters and related substances as substrates. Sodium 110-116 solute carrier family 6 member 9 Rattus norvegicus 52-57 1438878-11 1992 Blockade of the response in the absence of external sodium suggests that Na+/Ca2+ exchanger participates in this response. Sodium 52-58 nascent polypeptide associated complex subunit alpha 2 Homo sapiens 73-80 10457053-7 1999 Fluorescence of YO-PRO-1 was detectable within 3 s, and the uptake reached a steady rate within 10-20 s; YO-PRO-1 uptake was greatly enhanced by removing extracellular sodium. Sodium 168-174 lamin A/C Homo sapiens 19-24 1321928-2 1992 Whether ET-1 exerts a direct stimulating effect on sodium reabsorption in the renal proximal convoluted tubule, the dominant locus of sodium reabsorption in the nephron, is currently unknown. Sodium 51-57 endothelin-1 Oryctolagus cuniculus 8-12 1321928-8 1992 The data implicate ET-1 as a novel, direct and specific modulator of sodium reabsorption in the proximal tubule. Sodium 69-75 endothelin-1 Oryctolagus cuniculus 19-23 1535756-0 1992 Role of endogenous ANP in sodium excretion in rats with experimental pulmonary hypertension. Sodium 26-32 natriuretic peptide A Rattus norvegicus 19-22 1597135-0 1992 Dietary potassium supplementation and sodium restriction stimulate aldosterone synthase but not 11 beta-hydroxylase P-450 messenger ribonucleic acid accumulation in rat adrenals and require angiotensin II production. Sodium 38-44 cytochrome P450, family 11, subfamily b, polypeptide 2 Rattus norvegicus 67-87 1597135-9 1992 High potassium or low sodium diet given to rats for 1 week increased aldosterone synthase P-450 mRNA levels by approximately 5- and 6-fold, respectively. Sodium 22-28 cytochrome P450, family 11, subfamily b, polypeptide 2 Rattus norvegicus 69-89 1535825-0 1992 Central administration of atrial natriuretic peptide suppresses sodium and water intake of sheep. Sodium 64-70 natriuretic peptides A Ovis aries 26-52 1533286-0 1992 Effect of changes in sodium intake on atrial natriuretic factor (ANF) and peptides derived from the N terminus of the ANF prohormone in the rat. Sodium 21-27 natriuretic peptide A Rattus norvegicus 38-63 1312913-2 1992 Reports have suggested that the fast inward sodium current (INa) in cardiac tissues may be modulated by beta-adrenergic stimulation and that such modulation may affect conduction in the setting of myocardial ischemia and infarction. Sodium 44-50 internexin neuronal intermediate filament protein alpha Canis lupus familiaris 60-63 1318109-4 1992 Infusion of synthetic rat atrial natriuretic factor (10 micrograms/kg/h) increased fractional sodium excretion by 7.3 +/- 2.4% in control rats but only by 1.4 +/- 0.5% in adriamycin-treated rats (P less than 0.05). Sodium 94-100 natriuretic peptide A Rattus norvegicus 26-51 1315427-4 1992 Available data suggest that the mechanism of ANF-induced natriuresis involves either renal hemodynamic effects, such as the increase in glomerular filtration rate and reduction of medullary tonicity, or direct effect on sodium transport in the medullary collecting ducts. Sodium 220-226 natriuretic peptide A Rattus norvegicus 45-48 1534370-14 1992 The removal of sodium from the superfusion medium prolonged the [Ca2+]i rise in response to NMDA indicating that the Na-Ca antiporter is instrumental in reducing [Ca2+]i. Sodium 15-21 nascent polypeptide associated complex subunit alpha Rattus norvegicus 117-122 1531208-3 1992 In the rat, intraperitoneal injections of pepsanurin (0.5 ml/100 g body wt) significantly inhibited the effects of an intravenous bolus of atrial natriuretic peptide (ANP) (0.5 micrograms) on water, sodium, and potassium excretion without altering systemic blood pressure. Sodium 199-205 natriuretic peptide A Rattus norvegicus 139-165 1657196-1 1991 Sodium current (INa) inactivation kinetics in neonatal cardiac myocytes were analyzed using whole cell voltage clamp before and after acute treatments with thyroid hormone (3,5,3"-triiodo-L-thyronine, T3). Sodium 0-6 internexin neuronal intermediate filament protein alpha Homo sapiens 16-19 10457053-7 1999 Fluorescence of YO-PRO-1 was detectable within 3 s, and the uptake reached a steady rate within 10-20 s; YO-PRO-1 uptake was greatly enhanced by removing extracellular sodium. Sodium 168-174 lamin A/C Homo sapiens 108-113 10411589-3 1999 There were small but significant differences between the rat NET and the human or bovine NETs with respect to the affinities of sodium ions (greater for rat than for bovine) of the substrates norepinephrine, epinephrine, and 1-methyl-4-phenylpyridinium (greater for human than for rat), and of the inhibitor cocaine (greater for human and bovine than for rat), whereas the affinities of dopamine and of most inhibitors, including tricyclic antidepressants, showed no species differences. Sodium 128-134 solute carrier family 6 member 2 Rattus norvegicus 61-64 1681489-3 1991 Somatostatin decreases the renal plasma flow, glomerular filtration rate, osmotic and free water clearances, sodium and potassium excretion and the tubular reabsorption of phosphorus while urinary osmolality increases. Sodium 109-115 somatostatin Homo sapiens 0-12 10381586-2 1999 Modulation of cardiac sodium currents (INa) by the G protein stimulatory alpha subunit (Gsalpha) was studied using patch-clamp techniques on freshly dissociated rat ventricular myocytes. Sodium 22-28 internexin neuronal intermediate filament protein, alpha Rattus norvegicus 39-42 10396017-12 1999 In contrast, IGF-I enhances the glomerulosa secreting phenotype and diminishes that of the fasciculata/reticularis, possibly replicating the actions of angiotensin II or a low sodium diet. Sodium 176-182 insulin-like growth factor 1 Rattus norvegicus 13-18 10373702-6 1999 The rapid neuritic outgrowth was paralleled by the emergence of a fast-activating TTX-sensitive sodium current (INa), and by an increase in both K+ currents. Sodium 96-102 internexin neuronal intermediate filament protein, alpha Rattus norvegicus 112-115 1787649-3 1991 With HD, a close correlation (R2 = 0.94) was found between changes in [Na+P] and combined changes in sodium gradient and the UF rate. Sodium 101-107 catenin beta like 1 Homo sapiens 71-76 10458651-0 1999 Characterization of rabbit kidney and brain pancreatic polypeptide-binding neuropeptide Y receptors: differences with Y1 and Y2 sites in sensitivity to amiloride derivatives affecting sodium transport. Sodium 184-190 neuropeptide Y Oryctolagus cuniculus 75-89 1831599-2 1991 We investigated the effect of intracerebroventricular (icv) ANF (alpha-rat atriopeptin III) on renal sodium excretion in unilaterally nephrectomized, conscious unrestrained rats fitted with a chronic ureteral catheter. Sodium 101-107 natriuretic peptide A Rattus norvegicus 60-63 1831599-4 1991 ANF injected at doses (icv) of 1 ng (n = 6), 100 ng (n = 7), and 1 microgram (n = 7) reduced urinary sodium excretion (all values mumol/45 min, means +/- SE) from 111.6 +/- 24.4 to 83 +/- 20 (P less than 0.05), from 96.9 +/- 25.2 to 55 +/- 14 (P less than 0.01), and from 90.8 +/- 14.2 to 51 +/- 9 (P less than 0.01), respectively, whereas urinary flow rate did not change. Sodium 101-107 natriuretic peptide A Rattus norvegicus 0-3 1864303-6 1991 Our results indicate that BNP inhibits renin secretion through sodium delivery to the macula densa and effectively inhibits the tubuloglomerular feedback response that is activated by intrarenal hypertonic saline infusion. Sodium 63-69 renin Canis lupus familiaris 39-44 1709839-4 1991 The fast sodium current, INa, is characterized by fast upstroke velocity (Vmax = 400 V/sec) and slow recovery from inactivation. Sodium 9-15 internexin neuronal intermediate filament protein alpha Homo sapiens 25-28 1828456-0 1991 Role of endogenous atrial natriuretic peptide in regulating sodium excretion in spontaneously hypertensive rats. Sodium 60-66 natriuretic peptide A Rattus norvegicus 19-45 1828456-2 1991 To explore whether pathophysiological plasma levels of atrial natriuretic peptide (ANP) actually involve sodium excretion in spontaneously hypertensive rats (SHR), we examined the in vivo and ex vivo effects of ANP and an endopeptidase inhibitor, thiorphan, on urinary sodium excretion and the elimination rate of ANP. Sodium 105-111 natriuretic peptide A Rattus norvegicus 55-81 1832979-9 1991 Atrial natriuretic peptide antibody blunted markedly endothelin-induced natriuresis: urinary sodium excretion rates changed insignificantly by 18 +/- 10 and 30 +/- 14%, respectively. Sodium 93-99 natriuretic peptide A Rattus norvegicus 0-26 1832979-10 1991 Thus, endothelin infusion results in increases in plasma atrial natriuretic peptide levels, which may contribute to endothelin-induced natriuresis, providing evidence for potentially significant interactions between these peptide hormones in the regulation of sodium balance and renal vascular tone. Sodium 260-266 natriuretic peptide A Rattus norvegicus 57-83 1827646-0 1991 Age-related changes in basal and sodium-stimulated atrial and plasma atrial natriuretic factor (ANF) in the rat. Sodium 33-39 natriuretic peptide A Rattus norvegicus 69-94 1827646-0 1991 Age-related changes in basal and sodium-stimulated atrial and plasma atrial natriuretic factor (ANF) in the rat. Sodium 33-39 natriuretic peptide A Rattus norvegicus 96-99 1827646-4 1991 Age-related increases in plasma ANF concentration and left atrial ANF content (p less than .001) were present in both low- and high-sodium fed rats. Sodium 132-138 natriuretic peptide A Rattus norvegicus 32-35 1827646-4 1991 Age-related increases in plasma ANF concentration and left atrial ANF content (p less than .001) were present in both low- and high-sodium fed rats. Sodium 132-138 natriuretic peptide A Rattus norvegicus 66-69 1827646-5 1991 Significant differences in plasma and atrial ANF levels between low- and high-sodium fed rats were noted only in older adult rats, where an inverse correlation (r = -.425, p less than .05) was observed between plasma and left atrial ANF levels. Sodium 78-84 natriuretic peptide A Rattus norvegicus 45-48 10537232-1 1999 Atrial natriuretic peptide (ANP) is thought to play a role in renal regulation of salt balance by reducing tubular reabsorption of sodium and chloride. Sodium 131-137 natriuretic peptide type A Mus musculus 0-26 10537232-1 1999 Atrial natriuretic peptide (ANP) is thought to play a role in renal regulation of salt balance by reducing tubular reabsorption of sodium and chloride. Sodium 131-137 natriuretic peptide type A Mus musculus 28-31 10537232-10 1999 We conclude that the absence of endogenous ANP activity in mice on a high-salt diet subjected to acute saline infusion causes inappropriately high reabsorption of sodium and chloride in the medullary collecting duct, resulting in a relative defect in renal excretory capacity for salt. Sodium 163-169 natriuretic peptide type A Mus musculus 43-46 10334975-2 1999 Deficiency of 11beta-HSD2 results in cortisol-mediated sodium retention and hypertension, suggesting that the physiological regulation of 11beta-HSD2 in mineralocorticoid target tissues may be important in modulating sodium homoeostasis and blood pressure control. Sodium 55-61 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 14-25 10329215-1 1999 We previously reported that T3(3,3",5-triiodo-L-thyronine) acutely increases sodium currents (INa) in neonatal rat myocytes. Sodium 77-83 internexin neuronal intermediate filament protein, alpha Rattus norvegicus 94-97 10419016-5 1999 Both, increased sodium reabsorption despite low aldosterone levels in Liddle"s patients and decreased sodium reabsorption despite high aldosterone levels in PHA-1 patients, demonstrated that ENaC is an effector for aldosterone action. Sodium 16-22 sodium channel, nonvoltage-gated 1 alpha Mus musculus 191-195 10419016-5 1999 Both, increased sodium reabsorption despite low aldosterone levels in Liddle"s patients and decreased sodium reabsorption despite high aldosterone levels in PHA-1 patients, demonstrated that ENaC is an effector for aldosterone action. Sodium 102-108 sodium channel, nonvoltage-gated 1 alpha Mus musculus 191-195 10200997-10 1999 Sodium depletion increased manganese superoxide dismutase, glutathione peroxidases, and glutathione-S-transferase activities in sham-operated kidneys but not in UUO kidneys. Sodium 0-6 hematopoietic prostaglandin D synthase Rattus norvegicus 88-113 9987991-1 1999 The neutral and basic amino acid transporter (NBAT) facilitates sodium-independent transport of L-amino acids in renal and intestinal epithelial cells and has been postulated to play a similar role in neurons. Sodium 64-70 solute carrier family 3 member 1 Rattus norvegicus 46-50 10022552-7 1999 These results show that adenovirus-mediated ANF gene expression can lead to systemic biological effects in dogs, a finding of potential relevance for the treatment of cardiovascular diseases and sodium-retaining disorders. Sodium 195-201 natriuretic peptide A Canis lupus familiaris 44-47 1674517-1 1991 Five weeks of high (8%) sodium intake, resulting in a decline of plasma atrial natriuretic factor (ANF) in normotensive Wistar-Kyoto (WKY) and Wistar rats, did not affect plasma ANF in spontaneously hypertensive rats (SHR) which became severely hypertensive. Sodium 24-30 natriuretic peptide A Rattus norvegicus 72-97 1674517-1 1991 Five weeks of high (8%) sodium intake, resulting in a decline of plasma atrial natriuretic factor (ANF) in normotensive Wistar-Kyoto (WKY) and Wistar rats, did not affect plasma ANF in spontaneously hypertensive rats (SHR) which became severely hypertensive. Sodium 24-30 natriuretic peptide A Rattus norvegicus 99-102 9887087-4 1999 When expressed in Xenopus laevis oocytes, hOAT1 mediated sodium-independent uptake of p-aminohippurate (PAH) (Km = 9. Sodium 57-63 solute carrier family 22 member 6 Homo sapiens 42-47 9916797-6 1999 Our observation that OCTN2 has the ability to transport carnitine in a sodium-dependent manner prompted us to search for mutations in the gene encoding OCTN2, SLC22A5. Sodium 71-77 solute carrier family 22 (organic cation transporter), member 5 Mus musculus 21-26 9916797-6 1999 Our observation that OCTN2 has the ability to transport carnitine in a sodium-dependent manner prompted us to search for mutations in the gene encoding OCTN2, SLC22A5. Sodium 71-77 solute carrier family 22 (organic cation transporter), member 5 Mus musculus 152-157 9916797-6 1999 Our observation that OCTN2 has the ability to transport carnitine in a sodium-dependent manner prompted us to search for mutations in the gene encoding OCTN2, SLC22A5. Sodium 71-77 solute carrier family 22 (organic cation transporter), member 5 Mus musculus 159-166 9814486-7 1998 These results indicate that 11betaHSD2 colocalizes with MR in human airway epithelia and suggest that 11betaHSD2 play an important role in pulmonary mineralocorticoid activity such as sodium and fluid transport. Sodium 184-190 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 28-38 9814486-7 1998 These results indicate that 11betaHSD2 colocalizes with MR in human airway epithelia and suggest that 11betaHSD2 play an important role in pulmonary mineralocorticoid activity such as sodium and fluid transport. Sodium 184-190 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 102-112 9725828-3 1998 Cells with null alleles in both STD1 and its homologue, MTH1, manifest numerous phenotypes observed in calcineurin mutants, including sodium, lithium, manganese, and hydroxyl ion sensitivity, as well as alpha factor toxicity. Sodium 134-140 Std1p Saccharomyces cerevisiae S288C 32-36 9698304-11 1998 The unique persistent current observed for Scn8a channels is consistent with the hypothesis that this channel is responsible for distinct sodium conductances underlying repetitive firing of action potentials in Purkinje neurons. Sodium 138-144 sodium voltage-gated channel alpha subunit 8 Rattus norvegicus 43-48 9754697-7 1998 NPY levels were inversely related to calcium excretion and drinking was inversely related to circulating sodium. Sodium 105-111 neuropeptide Y Homo sapiens 0-3 9888559-5 1998 In particular, transcription of representative genes in all three categories is increased in the glomerulosa by a low sodium diet, correlated with its hypertrophy and increased aldosterone synthase. Sodium 118-124 cytochrome P450 family 11 subfamily B member 2 Homo sapiens 177-197 9761383-5 1998 Amylin significantly increased urine flow at an infusion rate resulting in a plasma concentration of approximately 52 pM, and at a concentration of approximately 193 pM, it increased sodium excretion, glomerular filtration rate and renal plasma flow. Sodium 183-189 islet amyloid polypeptide Rattus norvegicus 0-6 9660889-0 1998 Inhibition of oxidative metabolism increases persistent sodium current in rat CA1 hippocampal neurons. Sodium 56-62 carbonic anhydrase 1 Rattus norvegicus 78-81 9702906-10 1998 It is noteworthy that the proband"s ECG suggested the sodium channel-based LQT3 genotype. Sodium 54-60 sodium voltage-gated channel alpha subunit 5 Homo sapiens 75-79 9699805-1 1998 The urinary excretion levels of sodium (Na) and potassium (K) in cadmium (Cd)-exposed subjects as related with urinary beta2-microglobulin (beta2-MG) and Cd concentrations were investigated. Sodium 32-38 beta-2-microglobulin Homo sapiens 140-148 9612661-15 1998 These results suggest that there are certain mechanisms that counteract renal tubular sodium reabsorption induced by endogenous ANP under conditions of severe pacing. Sodium 86-92 natriuretic peptide A Canis lupus familiaris 128-131 9572288-3 1998 The two high-affinity sodium-dependent glial transporters [glutamate transporter 1 (GLT-1) and glutamate aspartate transporter (GLAST)] mediate the bulk of glutamate transport. Sodium 22-28 solute carrier family 1 member 3 Rattus norvegicus 95-126 9572288-3 1998 The two high-affinity sodium-dependent glial transporters [glutamate transporter 1 (GLT-1) and glutamate aspartate transporter (GLAST)] mediate the bulk of glutamate transport. Sodium 22-28 solute carrier family 1 member 3 Rattus norvegicus 128-133 9535812-0 1998 Calcium and insulin-like growth factor I stimulation of sodium-dependent phosphate transport and proliferation of cultured rat osteoblasts. Sodium 56-62 insulin-like growth factor 1 Rattus norvegicus 12-40 9501190-6 1998 Transport of beta-D-Glc-IPM and glucose by SAAT1 is apparently performed by the same mechanism because similar sodium dependence, dependence on membrane potential, electrogenicity, and phlorizin inhibition were determined for beta-D-Glc-IPM, D-glucose, and AMG. Sodium 111-117 solute carrier family 5 member 4 Homo sapiens 43-48 9521325-5 1998 Because IVF causes cardiac rhythm disturbance, we investigated whether malfunction of ion channels could cause the disorder by studying mutations in the cardiac sodium channel gene SCN5A. Sodium 161-167 sodium voltage-gated channel alpha subunit 5 Homo sapiens 181-186 9516235-14 1998 We suggest that the CA-IV isozyme might catalyze rapid equilibration of H+ and HCO3- with CO2 in the unstirred layer outside the plasma membrane, preventing local accumulation of H+ which competes with sodium for the same external Na-H exchanger binding site. Sodium 202-208 carbonic anhydrase 4 Oryctolagus cuniculus 20-25 9478930-8 1998 As in adrenals cardiac 11beta-hydroxylase and aldosterone-synthase mRNAs were independently regulated by 1 week"s treatment with either low sodium and high potassium diet (which increased aldosterone synthase mRNA level only), angiotensin II (which raised level of both mRNAs), or adrenocorticotropin (which stimulated the 11beta-hydroxylase gene exclusively). Sodium 140-146 cytochrome P450, family 11, subfamily b, polypeptide 1 Rattus norvegicus 46-66 9478930-8 1998 As in adrenals cardiac 11beta-hydroxylase and aldosterone-synthase mRNAs were independently regulated by 1 week"s treatment with either low sodium and high potassium diet (which increased aldosterone synthase mRNA level only), angiotensin II (which raised level of both mRNAs), or adrenocorticotropin (which stimulated the 11beta-hydroxylase gene exclusively). Sodium 140-146 cytochrome P450, family 11, subfamily b, polypeptide 1 Rattus norvegicus 188-208 9495547-4 1997 Heterologous expression of rNET in HEK293 cells revealed that uptake of [3H]norepinephrine is sodium- and chloride-dependent and highly sensitive to the selective norepinephrine transporter inhibitors desipramine and nisoxetine. Sodium 94-100 solute carrier family 6 member 2 Rattus norvegicus 27-31 9495547-5 1997 The cloned rNET cDNA provides the opportunity to investigate this transporter in heterologous expression systems and adds a new member to the family of sodium- and chloride-dependent neurotransmitter transporters. Sodium 152-158 solute carrier family 6 member 2 Rattus norvegicus 11-15 9525070-1 1997 The common molecular basis of hyperkalemic periodic paralysis, of paramyotonia congenita and that of myotonia fluctuans are the mutations of sodium channel SCN4A gene. Sodium 141-147 sodium voltage-gated channel alpha subunit 4 Homo sapiens 156-161 9348183-8 1997 Our study demonstrates a specific increase of AC6 but not AC5 mRNA in the zona glomerulosa of rats given a low sodium diet. Sodium 111-117 adenylate cyclase 6 Rattus norvegicus 46-49 9395171-14 1997 The data provide further support for the hypothesis that block of the late sodium current may be of value in the treatment of LQT2 as well as LQT3 and perhaps other congenital and acquired (drug-induced) forms of LQTS. Sodium 75-81 potassium voltage-gated channel subfamily H member 2 Homo sapiens 126-130 9395171-14 1997 The data provide further support for the hypothesis that block of the late sodium current may be of value in the treatment of LQT2 as well as LQT3 and perhaps other congenital and acquired (drug-induced) forms of LQTS. Sodium 75-81 sodium voltage-gated channel alpha subunit 5 Homo sapiens 142-146 9360552-8 1997 These results indicate that 11 beta HSD2 protein colocalizes with MR protein in the great majority of sodium-transporting epithelia involved in serous secretion and supports the proposal that 11 beta HSD2 is a pivotal determinant of mineralocorticoid receptor occupancy in man. Sodium 102-108 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 28-40 9360552-8 1997 These results indicate that 11 beta HSD2 protein colocalizes with MR protein in the great majority of sodium-transporting epithelia involved in serous secretion and supports the proposal that 11 beta HSD2 is a pivotal determinant of mineralocorticoid receptor occupancy in man. Sodium 102-108 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 36-40 9326675-1 1997 Aldosterone-dependent epithelial sodium transport in the distal nephron is mediated by the absorption of sodium through the highly selective, amiloride-sensitive epithelial sodium channel (ENaC) made of three homologous subunits (alpha, beta, and gamma). Sodium 33-39 sodium channel, nonvoltage-gated 1 alpha Mus musculus 142-187 9331977-0 1997 Regulation of aldosterone synthase cytochrome P450 (CYP11B2) and 11 beta-hydroxylase cytochrome P450 (CYP11B1) expression in rat adrenal zona glomerulosa cells by low sodium diet and angiotensin II receptor antagonists. Sodium 167-173 cytochrome P450, family 11, subfamily b, polypeptide 1 Rattus norvegicus 102-109 9236220-2 1997 It previously has been shown that protein kinase A (PKA) attenuates sodium current amplitude 20-50% by phosphorylating serines located in the I-II linker of the sodium channel. Sodium 68-74 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 34-50 9236220-2 1997 It previously has been shown that protein kinase A (PKA) attenuates sodium current amplitude 20-50% by phosphorylating serines located in the I-II linker of the sodium channel. Sodium 68-74 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 52-55 9276478-6 1997 Our findings support the previous observations made with rat muscle sodium channels and demonstrate that the effect of DMPK on sodium channels is isoform specific despite conservation of a putative phosphorylation site between the two isoforms. Sodium 127-133 DM1 protein kinase Rattus norvegicus 119-123 9258207-5 1997 Indomethacin reduced ANF-induced sodium excretion and creatinine clearance by 75% (P < 0.05) and 35% (P < 0.05), respectively. Sodium 33-39 natriuretic peptide A Canis lupus familiaris 21-24 9260977-10 1997 These data suggest that the exaggerated salt-induced reduction of NPR-C in the kidney of DS rats may play an important role in the pathogenesis of salt hypertension in this animal, possibly related to impaired renal sodium excretion. Sodium 216-222 natriuretic peptide receptor 3 Rattus norvegicus 66-71 9219155-9 1997 This study supports a role of endothelin in the pathogenesis of renal insufficiency after aortic cross-clamping and demonstrates that pretreatment with the dual ETA/ETB endothelin antagonist L-754,142 preserves RBF and sodium reabsorption, leading to a significant improvement in GFR. Sodium 219-225 endothelin receptor type A Canis lupus familiaris 161-164 9252942-7 1997 The efficacy of basolateral vs apical EGF on sodium and glucose transport was compared after incubation of the monolayers with 10 nmol/L of cholera toxin. Sodium 45-51 epidermal growth factor Homo sapiens 38-41 9252942-8 1997 RESULTS: EGF increased both glucose and sodium uptake and transport, and we observed a simultaneous increase in the activity of Na+/K(+)-adenosine triphosphatase (ATPase). Sodium 40-46 epidermal growth factor Homo sapiens 9-12 9153649-0 1997 Corticosteroid effects on sodium and calcium currents in acutely dissociated rat CA1 hippocampal neurons. Sodium 26-32 carbonic anhydrase 1 Rattus norvegicus 81-84 9159181-6 1997 These data indicate that the gamma (and/or gamma2) subunit participates in amiloride binding and the sensing of the extracellular sodium concentration. Sodium 130-136 tryptophanyl-tRNA synthetase 1 L homeolog Xenopus laevis 43-49 9159181-7 1997 The close homology between gamma and gamma2 will help to define the domains involved in sensing external sodium and in the structure of this important drug receptor. Sodium 105-111 tryptophanyl-tRNA synthetase 1 L homeolog Xenopus laevis 37-43 9084415-7 1997 cGMP mimicked the effect of CNP on sodium-dependent pHi recovery, but the native nucleotide was as potent as membrane-permeant analogues. Sodium 35-41 glucose-6-phosphate isomerase Rattus norvegicus 52-55 9054374-3 1997 This phenotype was confirmed in LLC-PK1 cells stably expressing the DSEL mutant receptor, where both PTH-stimulated PLC activity and sodium-dependent phosphate co-transport were essentially abolished. Sodium 133-139 dermatan sulfate epimerase-like Rattus norvegicus 68-72 9130156-3 1997 Using macropatches, the effect of PC mutations R1448C and T1313M were compared with wild-type (WT) in Xenopus oocytes coinjected with both alpha- and beta-subunits of human skeletal muscle (SkM1) sodium channels. Sodium 196-202 sodium voltage-gated channel alpha subunit 4 Homo sapiens 190-194 9124405-5 1997 ADM mediated a natriuretic action via increases in glomerular filtration rate and decreases in distal tubular sodium reabsorption, which was attenuated by renal denervation and completely abolished by prostaglandin inhibition. Sodium 110-116 adrenomedullin Canis lupus familiaris 0-3 9124424-1 1997 In conscious deoxycorticosterone acetate (DOCA) salt-hypertensive dogs, the angiotensin-converting enzyme (ACE) inhibitors captopril and imidaprilat significantly decreased mean arterial pressure (MAP) and significantly increased urine flow rate, effective renal plasma flow (ERPF), glomerular filtration rate, and urinary sodium excretion. Sodium 323-329 angiotensin I converting enzyme Canis lupus familiaris 76-105 9124424-1 1997 In conscious deoxycorticosterone acetate (DOCA) salt-hypertensive dogs, the angiotensin-converting enzyme (ACE) inhibitors captopril and imidaprilat significantly decreased mean arterial pressure (MAP) and significantly increased urine flow rate, effective renal plasma flow (ERPF), glomerular filtration rate, and urinary sodium excretion. Sodium 323-329 angiotensin I converting enzyme Canis lupus familiaris 107-110 8997353-7 1996 The stimulatory effects of dopamine, PP inhibitor, and PKA agonist persisted even when intracellular sodium was clamped by 5 microM monensin. Sodium 101-107 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 55-58 8969917-8 1996 Vit.C depletion abolished a rise of plasma aldosterone and of aldosterone secreted in vitro stimulated by sodium depletion. Sodium 106-112 vitrin Cavia porcellus 0-3 8969917-9 1996 The in vitro conversion of [3H]deoxycorticosterone to [3H]aldosterone was reduced and sodium conservation was impaired by Vit.C depletion. Sodium 86-92 vitrin Cavia porcellus 122-125 8969917-10 1996 Vit.E depletion did not abolish but significantly attenuated the rise in plasma aldosterone stimulated by sodium depletion. Sodium 106-112 vitrin Cavia porcellus 0-3 8945089-2 1996 Since the fast cardiac sodium current (INa+) is also subject to beta-receptor dependent regulation, we investigated its regulation in a model of cardiac dysfunction. Sodium 23-29 internexin neuronal intermediate filament protein, alpha Rattus norvegicus 39-42 8981664-5 1996 Although ANF increased glomerular filtration rate from 33.9 +/- 4.2 to 43.4 +/- 5.6 ml min-1 (p < 0.05) and sodium excretion from 72 +/- 22 to 567 +/- 112 mumol min-1 (p < 0.05) at normal renal perfusion pressure, ANF was without effect on glomerular filtration rate and sodium excretion during renal arterial constriction. Sodium 111-117 natriuretic peptide A Canis lupus familiaris 9-12 8981664-5 1996 Although ANF increased glomerular filtration rate from 33.9 +/- 4.2 to 43.4 +/- 5.6 ml min-1 (p < 0.05) and sodium excretion from 72 +/- 22 to 567 +/- 112 mumol min-1 (p < 0.05) at normal renal perfusion pressure, ANF was without effect on glomerular filtration rate and sodium excretion during renal arterial constriction. Sodium 277-283 natriuretic peptide A Canis lupus familiaris 9-12 8901621-0 1996 Polyunsaturated fatty acids modulate sodium and calcium currents in CA1 neurons. Sodium 37-43 carbonic anhydrase 1 Rattus norvegicus 68-71 8897021-4 1996 GH and IGF-I increase GFR in normal rats and humans, and increase phosphate and possibly sodium reabsorption in normal and diabetic subjects. Sodium 89-95 insulin-like growth factor 1 Rattus norvegicus 7-12 8819477-5 1996 Sodium and a GTP analog elicited a concentration-dependent decrease in specific binding to the CB2 receptor. Sodium 0-6 cannabinoid receptor 2 Homo sapiens 95-98 8772128-0 1996 Role of the NHE3 isoform of the Na+/H+ exchanger in sodium absorption by the rabbit gallbladder. Sodium 52-58 sodium/hydrogen exchanger 3 Oryctolagus cuniculus 12-16 8702574-4 1996 Cytoplasmic delivery of 5 microM AA augmented the voltage-activated sodium current of hSkM1 channels by 190% (+/-54 S.E., n = 7) over a 20-min period. Sodium 68-74 sodium voltage-gated channel alpha subunit 4 Homo sapiens 86-91 8702574-6 1996 Sodium currents in HEK293t cells transfected with human cardiac muscle sodium channels (hH1) were insensitive to AA treatment, and exposure to oleic acid inhibited the hH1 currents over a 20-min period by 29% (+/-13 S.E., n = 5). Sodium 0-6 H1.5 linker histone, cluster member Homo sapiens 88-91 8613987-0 1996 Effect of sodium on the energetics of thrombin-thrombomodulin interaction and its relevance for protein C hydrolysis. Sodium 10-16 thrombomodulin Homo sapiens 47-61 8613987-0 1996 Effect of sodium on the energetics of thrombin-thrombomodulin interaction and its relevance for protein C hydrolysis. Sodium 10-16 protein C, inactivator of coagulation factors Va and VIIIa Homo sapiens 96-105 8613987-2 1996 Moreover, this experimental strategy allowed us to accurately split the free energy of sodium binding into its entropic and enthalpic components for both the TM-free and TM-bound enzyme. Sodium 87-93 thrombomodulin Homo sapiens 158-160 8613987-2 1996 Moreover, this experimental strategy allowed us to accurately split the free energy of sodium binding into its entropic and enthalpic components for both the TM-free and TM-bound enzyme. Sodium 87-93 thrombomodulin Homo sapiens 170-172 8613987-3 1996 Namely, at 25 degrees C, the value of delta G of sodium binding was found equal to -2.4 kcal/mol in the absence of TM and -3.6 kcal/mol for the thrombin-TM complex. Sodium 49-55 thrombomodulin Homo sapiens 115-117 8613987-4 1996 The enthalpic contribution to the free energy of sodium binding is equal to -27 kcal/mol and -21 kcal/mol in the TM-free and TM-bound thrombin forms, respectively. Sodium 49-55 thrombomodulin Homo sapiens 113-115 8775227-9 1996 The changes in CSF sodium concentration, and to a lesser extent potassium and chloride concentrations, paralleled those of CSF osmolality. Sodium 19-25 colony stimulating factor 2 Homo sapiens 15-18 8775227-9 1996 The changes in CSF sodium concentration, and to a lesser extent potassium and chloride concentrations, paralleled those of CSF osmolality. Sodium 19-25 colony stimulating factor 2 Homo sapiens 123-126 8821477-0 1996 The kinetic parameters of sodium currents in maturing acutely isolated rat hippocampal CA1 neurones. Sodium 26-32 carbonic anhydrase 1 Rattus norvegicus 87-90 9491628-9 1996 The pHi does not decrease below 6.8 for two reasons: 1) the uptake of sodium by the non-specific cation channel and the ensuing depolarization on one hand and the decrease of the pHi on the other hand reverse the proton-moving force; 2) at low pHi the non-specific cation channel becomes permeable to protons. Sodium 70-76 glucose-6-phosphate isomerase Rattus norvegicus 4-7 9491628-9 1996 The pHi does not decrease below 6.8 for two reasons: 1) the uptake of sodium by the non-specific cation channel and the ensuing depolarization on one hand and the decrease of the pHi on the other hand reverse the proton-moving force; 2) at low pHi the non-specific cation channel becomes permeable to protons. Sodium 70-76 glucose-6-phosphate isomerase Rattus norvegicus 179-182 9491628-9 1996 The pHi does not decrease below 6.8 for two reasons: 1) the uptake of sodium by the non-specific cation channel and the ensuing depolarization on one hand and the decrease of the pHi on the other hand reverse the proton-moving force; 2) at low pHi the non-specific cation channel becomes permeable to protons. Sodium 70-76 glucose-6-phosphate isomerase Rattus norvegicus 179-182 8594880-3 1995 We demonstrate selective, modulated expression in the renal medulla of heat shock protein HSP-70 mRNA and prostaglandin synthase-1 mRNA, with the abundance of these two mRNAs regulated in vivo in concert with changes in medullary sodium and urea. Sodium 230-236 heat shock 70 kDa protein 1 Canis lupus familiaris 90-96 7558224-3 1995 Atrial natriuretic peptide increased fractional sodium excretion by 0.009 +/- 0.002, 0.042 +/- 0.005, and 0.049 +/- 0.007, respectively; urinary excretion of atrial natriuretic peptide by -0.4 +/- 0.8, 3.3 +/- 1.4, and 15.8 +/- 7.4 fmol/min; and cGMP excretion by 0.65 +/- 0.06, 1.65 +/- 0.08, and 4.88 +/- 0.85 nmol/min in one-kidney shams. Sodium 48-54 natriuretic peptide A Canis lupus familiaris 0-26 1824757-4 1991 Administration of ANP-specific antiserum significantly impaired the return to normal sodium balance as well as the augmented kaliuresis that were observed on the second day after injection of DOCA. Sodium 85-91 natriuretic peptide A Rattus norvegicus 18-21 1679103-0 1991 Effect of sodium depletion on urinary excretion of active and inactive kallikrein in glomerulonephritic patients. Sodium 10-16 kallikrein related peptidase 4 Homo sapiens 71-81 1679103-1 1991 To investigate the response of urinary active and inactive kallikrein excretion to sodium depletion in golmerulonephritic (GN) patients, we measured the excretion of urinary active and inactive kallikreins in 10 primary GN patients before and after a low sodium (17 mEq/day), constant potassium (40 mEq/day) diet. Sodium 83-89 kallikrein related peptidase 4 Homo sapiens 59-69 1679103-10 1991 These findings suggest that the renal kallikrein-kinin system of GN patients responds normally to the stimulation of sodium depletion. Sodium 117-123 kallikrein related peptidase 4 Homo sapiens 38-48 1679107-3 1991 Both doses (0.1 and 0.3 microgram/minutes/kg) of ANF administered produced a marked increase in urinary flow, sodium and potassium excretion in the SL rats. Sodium 110-116 natriuretic peptide A Rattus norvegicus 49-52 1858208-7 1991 In the total group of examinees a significant direct relationship was established between the urinary kallikrein activity and summary sodium and potassium excretion as well as between the serum kallikrein activity and chlorine clearance. Sodium 134-140 kallikrein related peptidase 4 Homo sapiens 102-112 8593294-11 1995 Our findings indicate that VIP stimulates the jejunal secretion of water, sodium, potassium and bicarbonate and that VIP does not inhibit glucose absorption when the secretion of luminal fluid is accelerated by VIP in the jejunal loop of sheep. Sodium 74-80 vasoactive intestinal peptide Ovis aries 27-30 7561631-6 1995 The response to the Met-enkephalin analogue, [D-Ala2-Met2]-enkephalinamide (DALA), was also significantly enhanced by prior sodium depletion. Sodium 124-130 proenkephalin Rattus norvegicus 24-34 8529072-6 1995 Another cAMP independent pathway of sodium transport inhibition is mediated by phospholipase C, which has several isoforms (PLC beta, PLC gamma, and PLC delta with several members in each). Sodium 36-42 heparan sulfate proteoglycan 2 Homo sapiens 124-127 8529072-6 1995 Another cAMP independent pathway of sodium transport inhibition is mediated by phospholipase C, which has several isoforms (PLC beta, PLC gamma, and PLC delta with several members in each). Sodium 36-42 heparan sulfate proteoglycan 2 Homo sapiens 134-137 8529072-6 1995 Another cAMP independent pathway of sodium transport inhibition is mediated by phospholipase C, which has several isoforms (PLC beta, PLC gamma, and PLC delta with several members in each). Sodium 36-42 heparan sulfate proteoglycan 2 Homo sapiens 134-137 7895362-1 1995 BACKGROUND: Recent studies suggest that neurohumoral mechanisms including decreased renal responses to increases in atrial natriuretic factor (ANF) play a central role in the progression from asymptomatic cardiac dysfunction to advanced congestive heart failure (CHF) with sodium retention, vasoconstriction, and reduced exercise tolerance. Sodium 273-279 natriuretic peptide A Canis lupus familiaris 116-141 1980994-6 1990 Plasma ANP levels were lower in the low-sodium animals (98 +/- 34 vs. 345 +/- 38 pg/ml). Sodium 40-46 natriuretic peptide A Rattus norvegicus 7-10 1980994-9 1990 Conversely, propranolol treatment resulted in lower plasma ANP levels in rats with high sodium intake. Sodium 88-94 natriuretic peptide A Rattus norvegicus 59-62 1980994-10 1990 The already-suppressed plasma ANP level in rats on a low-sodium diet was unaltered with beta-adrenoceptor blockade. Sodium 57-63 natriuretic peptide A Rattus norvegicus 30-33 1980994-11 1990 The results suggest that dietary sodium intake is an important determinant of the response of atrial-specific granule number and plasma ANP levels following beta-adrenoceptor blockade with propranolol. Sodium 33-39 natriuretic peptide A Rattus norvegicus 136-139 2148057-6 1990 In a separate set of experiments, ANP increased both the glomerular filtration rate (GFR) and urinary sodium excretion (UNaV), and NE decreased the renal blood flow (RBF). Sodium 102-108 natriuretic peptide A Rattus norvegicus 34-37 2148062-6 1990 The high dose of ANP increased urine flow by 43.2 +/- 7.2 microliters.min-1.100 g body wt-1 and sodium excretion by 1.76 +/- 0.56 mu eq.min-1.100 g body wt-1 but had no effect after SX. Sodium 96-102 natriuretic peptide A Rattus norvegicus 17-20 2175278-4 1990 Transcripts for microI were present at low levels in neonatal skeletal muscle and increased to maximum levels in adult tissue, paralleling the expression of tetrodotoxin (TTX)-sensitive sodium currents. Sodium 186-192 sodium voltage-gated channel alpha subunit 4 Rattus norvegicus 16-22 7895362-1 1995 BACKGROUND: Recent studies suggest that neurohumoral mechanisms including decreased renal responses to increases in atrial natriuretic factor (ANF) play a central role in the progression from asymptomatic cardiac dysfunction to advanced congestive heart failure (CHF) with sodium retention, vasoconstriction, and reduced exercise tolerance. Sodium 273-279 natriuretic peptide A Canis lupus familiaris 143-146 7720469-10 1995 These findings suggest that a major mediator of postprandial sodium and water absorption in the ileum is the Na+/H+ exchanger. Sodium 61-67 solute carrier family 9 member A1 Canis lupus familiaris 109-125 1704977-8 1990 Infusion of r-ANF alone resulted in an 11-fold increase in urinary sodium excretion. Sodium 67-73 natriuretic peptide A Rattus norvegicus 14-17 1703080-3 1990 The sodium current, INa, was investigated at reduced extracellular Na+ (30 mM) in the presence of Cd2+ to block the calcium current, ICa, and with Cs+ substituted for K+ to reduce the K+ currents, IK. Sodium 4-10 T-cell surface antigen CD2 Cavia porcellus 98-101 7776243-0 1995 Dopamine D1 receptor modulates the voltage-gated sodium current in rat striatal neurones through a protein kinase A. Sodium 49-55 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 99-115 7621606-8 1995 In normal and compensated AV fistula dogs, synthetic pro ANF 31-67 produced similar significant reductions in arterial blood pressure, right atrial pressure and elevations in urinary sodium excretion. Sodium 183-189 natriuretic peptide A Canis lupus familiaris 57-60 7799448-1 1994 We measured macroscopic sodium currents (INa) in preparations from adult rat ventricle under four different conditions (I-IV): using the cell attached configuration of the tight-seal patch clamp technique on cells isolated with either trypsin followed by collagenase (I) or with collagenase only (II), and using the loose patch technique on cells isolated with collagenase (II) as well as on multicellular preparations not subjected to enzyme treatment (IV). Sodium 24-30 internexin neuronal intermediate filament protein, alpha Rattus norvegicus 41-44 2233666-9 1990 Furthermore, the cumulative infused sodium dose correlated with cumulated urinary sodium dose, potassium dose and cumulative NAG dose (from end of operation to POD-5). Sodium 36-42 NBAS subunit of NRZ tethering complex Homo sapiens 125-128 1698247-1 1990 The involvement of sodium and chloride ions in the process of alpha-melanocyte-stimulating hormone (a-MSH) release from hypothalamic neurons was investigated using perifused rat hypothalamic slices. Sodium 19-25 proopiomelanocortin Rattus norvegicus 62-98 2166273-9 1990 In acidified cultured DCTb cells, a partial pHi recovery was induced in sodium-free media by 15 mM HCO(-3) in the presence of an outward chloride gradient. Sodium 72-78 glucose-6-phosphate isomerase Oryctolagus cuniculus 44-47 8041748-3 1994 By expression in Xenopus laevis oocytes and in mammalian cells, we have identified Glvr-1 and Ram-1 as sodium-dependent phosphate symporters. Sodium 103-109 solute carrier family 20 member 1 Homo sapiens 83-89 8041748-3 1994 By expression in Xenopus laevis oocytes and in mammalian cells, we have identified Glvr-1 and Ram-1 as sodium-dependent phosphate symporters. Sodium 103-109 solute carrier family 20 member 2 Homo sapiens 94-99 8038180-0 1994 Mutations in LIS1 (ERG6) gene confer increased sodium and lithium uptake in Saccharomyces cerevisiae. Sodium 47-53 sterol 24-C-methyltransferase Saccharomyces cerevisiae S288C 13-17 2158388-4 1990 With the initial increase in urinary sodium excretion there were increases in plasma ANP and plasma cyclic GMP, which reached maximum levels at 15 min after the end of the saline infusion. Sodium 37-43 5'-nucleotidase, cytosolic II Homo sapiens 107-110 2160492-1 1990 The aim of this study was to determine whether the renin inhibitor CP-71362 (Pfizer Central Research, Groton, Connecticut, USA) is capable of inducing sustained reductions in arterial pressure in sodium-depleted dogs and to examine the changes in renal function associated with chronic renin inhibition. Sodium 196-202 renin Canis lupus familiaris 51-56 8038180-0 1994 Mutations in LIS1 (ERG6) gene confer increased sodium and lithium uptake in Saccharomyces cerevisiae. Sodium 47-53 sterol 24-C-methyltransferase Saccharomyces cerevisiae S288C 19-23 8005599-1 1994 Eighteen German families with a history of paramyotonia congenita (PC) were characterised by genetic and mutational analysis at the SCN4A locus, which encodes the alpha-subunit of the adult skeletal muscle sodium channel. Sodium 206-212 sodium voltage-gated channel alpha subunit 4 Homo sapiens 132-137 7913828-4 1994 In vivo, in epithelial cells a low Km, NAD-dependent, 11 beta hydroxysteroid dehydrogenase (11 beta OHSD) converts B and F, but not aldo, to receptor-inactive 11-keto congeners, thus allowing aldo to occupy epithelial MR and produce sodium retention. Sodium 233-239 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 39-90 7913429-13 1994 In addition, we have shown that if GC-A and C receptor levels in the sheep are modulated by sodium, the regulation occurs beyond the level of gene transcription. Sodium 92-98 grancalcin Ovis aries 35-54 8182409-5 1994 Slow sodium correction (< 0.5 mmol l-1 h-1) in patients with chronic hyponatraemia and rapid correction (1-2 mmol l-1 h-1) to a moderately hyponatraemic level in those with an acute development are recommended. Sodium 5-11 H1.5 linker histone, cluster member Homo sapiens 42-45 8037884-1 1994 Sexually dimorphic differences in voluntary sodium intake, locomotor activity, immobility in the swim test, and aggressive behavior were found to be altered in transgenic CD-1 mice that overexpressed transforming growth factor alpha (TGF alpha). Sodium 44-50 CD1 antigen complex Mus musculus 171-175 8037884-1 1994 Sexually dimorphic differences in voluntary sodium intake, locomotor activity, immobility in the swim test, and aggressive behavior were found to be altered in transgenic CD-1 mice that overexpressed transforming growth factor alpha (TGF alpha). Sodium 44-50 transforming growth factor alpha Mus musculus 200-232 8037884-1 1994 Sexually dimorphic differences in voluntary sodium intake, locomotor activity, immobility in the swim test, and aggressive behavior were found to be altered in transgenic CD-1 mice that overexpressed transforming growth factor alpha (TGF alpha). Sodium 44-50 transforming growth factor alpha Mus musculus 234-243 8151264-8 1994 Mean (+/- SD) 24-h sodium output rose from 19 +/- 16 mmol 24 h-1 (n = 10) on oral therapy with 250 mg F to 137 +/- 85 mmol 24 h-1 (n = 8) during 80 mg h-1 and to 268 +/- 124 mmol 24 h-1 (n = 3) on the maximal dose of 160 mg h-1. Sodium 19-25 H1.5 linker histone, cluster member Homo sapiens 61-64 2191273-1 1990 The sensitivity of voltage-dependent sodium current to the sodium channel blocker tetrodotoxin (TTX) is altered by transfection of a c-Ha-ras oncogene into an excitable cell line. Sodium 37-43 Harvey rat sarcoma virus oncogene Mus musculus 133-141 2138899-7 1990 After ANP infusion there was a prompt restoration of GFR, with a large rise in urine, sodium and potassium excretion rates. Sodium 86-92 natriuretic peptide A Rattus norvegicus 6-9 2180321-5 1990 Insulin caused transient sodium and potassium retention followed by renal "escape" that was associated with increased glomerular filtration rate (12-27%). Sodium 25-31 insulin Canis lupus familiaris 0-7 8127009-1 1994 Brain myelinolysis occurs after correction of chronic hyponatremia in rats when the magnitude of increase in serum sodium (delta SNa) exceeds 20 to 25 mEq/liter/24 hr (the critical threshold for brain). Sodium 115-121 snail family transcriptional repressor 1 Rattus norvegicus 129-132 8130120-3 1993 Enhancement in receptor number or in post-receptor components responsible for alpha 1- and alpha 2-adrenergic-mediated sodium reabsorption in proximal tubule may contribute to sodium retention and an elevation in blood pressure. Sodium 119-125 adrenoceptor alpha 1D Homo sapiens 78-98 8130120-3 1993 Enhancement in receptor number or in post-receptor components responsible for alpha 1- and alpha 2-adrenergic-mediated sodium reabsorption in proximal tubule may contribute to sodium retention and an elevation in blood pressure. Sodium 176-182 adrenoceptor alpha 1D Homo sapiens 78-98 7694510-2 1993 Electrogenic sodium transport (INa) was measured in Ussing chambers by the short-circuit current (Isc) technique and identified by the diuretic amiloride or by removal of sodium from the apical medium. Sodium 13-19 internexin neuronal intermediate filament protein alpha Gallus gallus 31-34 2138423-0 1990 Renal actions of atrial natriuretic factor: modulation of effect by changes in sodium status and aldosterone. Sodium 79-85 natriuretic peptides A Ovis aries 17-42 2138426-8 1990 These results indicate that ANP plays a physiological role in the regulation of urinary water and sodium excretion after pulmonary acid injury and suggest that ANP elevated in plasma after pulmonary injury may prevent pulmonary edema with its diuretic action and/or some direct action on water movement in the lung. Sodium 98-104 natriuretic peptide A Rattus norvegicus 28-31 2138930-7 1990 In addition, reducing the hyperglycemia in DIA rats by treatment with insulin (third group) reversed the blunted urine flow and sodium excretion responses to ANF. Sodium 128-134 natriuretic peptide A Rattus norvegicus 158-161 8237425-5 1993 ANP doubled sodium excretion (61 +/- 12 to 124 +/- 30 mumol min-1, P < 0.05) while urodilatin increased sodium excretion to 269 +/- 45 mumol min-1. Sodium 12-18 natriuretic peptide A Canis lupus familiaris 0-3 8401945-0 1993 Block of voltage-dependent sodium currents by the substance P receptor antagonist (+/-)-CP-96,345 in neurones cultured from rat cortex. Sodium 27-33 tachykinin receptor 1 Rattus norvegicus 50-70 8355461-3 1993 Serum sodium levels (SNa) and serum osmolality (SOsm) markedly decreased to 119 mEq/liter and 249 mOsm/kg H2O, respectively, 48 hours after the start of dDAVP administration. Sodium 6-12 snail family transcriptional repressor 1 Rattus norvegicus 21-24 7812749-0 1993 Characterization of sodium cations in dehydrated faujasites and zeolite EMT by 23Na DOR, 2D nutation, and MAS NMR. Sodium 20-26 IL2 inducible T cell kinase Homo sapiens 72-75 7812749-4 1993 By comparison of the 23Na MAS NMR intensities of these signals with the population of the cation sites determined by XRD and by calculation of the electric field gradients, the former signal was attributed to sodium cations at the sites SI and the latter one to sodium cations at the sites SI" as well as SII in faujasite and zeolite EMT. Sodium 209-215 IL2 inducible T cell kinase Homo sapiens 334-337 8389287-0 1993 Modulation of aldosterone synthase messenger ribonucleic acid levels by dietary sodium and potassium and by adrenocorticotropin. Sodium 80-86 cytochrome P450, family 11, subfamily b, polypeptide 1 Rattus norvegicus 14-34 8330198-1 1993 In this study we examined long-lasting effects mediated by intracellular mineralocorticoid receptors (MRs) and glucocorticoid receptors (GRs) on two voltage dependent potassium conductances in CA1 pyramidal neurons, i.e. the transient current IA and the delayed rectifier, and on the inward rectifier IQ, a mixed sodium/potassium current. Sodium 313-319 carbonic anhydrase 1 Rattus norvegicus 193-196 8384266-8 1993 Thus, changes in extracellular matrix, intracellular calcium, and sodium ions, as well as extracellular trophic factors, such as nerve growth factor, thyroxine, and insulin-like growth factor II, may regulate muscle NCAM expression during embryonic development. Sodium 66-72 neural cell adhesion molecule 1 Gallus gallus 216-220 7907455-3 1993 However, later studies have shown that cholinesterase inhibitors also interact with cholinergic receptors, with sodium and potassium ion channels and effect the uptake, synthesis and release of neurotransmitters. Sodium 112-118 butyrylcholinesterase Homo sapiens 39-53 8518023-1 1993 Recombinant interleukin-2 (rIL-2) can produce impairment of renal function with hypotension, fluid retention, elevated blood urea nitrogen, oliguria and low fractional sodium excretion; these side-effects are a common cause of reduction or interruption of rIL-2 infusion. Sodium 168-174 interleukin 2 Rattus norvegicus 27-32 8469787-7 1993 The fractional reabsorption of sodium and water by the proximal nephron increased during rIL2 treatment, from 0.707 +/- 0.030 (pretreatment) to 0.793 +/- 0.043. Sodium 31-37 interleukin 2 Rattus norvegicus 89-93 8469787-10 1993 The fractional reabsorption of sodium by the distal nephron was also significantly elevated, both during and 2 days after completing rIL2 treatment. Sodium 31-37 interleukin 2 Rattus norvegicus 133-137 1286529-8 1992 These data are interpreted as indicating that antinatriuretic mechanisms, including aldosterone-dependent sodium reabsorption in the cortical collecting tubule, can counteract the effect of ANF to inhibit sodium reabsorption in the medullary duct system, thus allowing maintenance of salt balance. Sodium 205-211 natriuretic peptide type A Mus musculus 190-193 2154853-1 1990 The atrionatriuretic peptide (ANP) is released from atrial cells in response to increased extracellular fluid volume and reduces sodium absorption by the kidney, thus reducing the blood volume. Sodium 129-135 natriuretic peptide A Rattus norvegicus 30-33 2154853-2 1990 In this report, ANP suppressed the calcium and sodium currents in rat and guinea pig ventricular myocytes. Sodium 47-53 natriuretic peptide A Rattus norvegicus 16-19 2154853-4 1990 Thus, ANP may regulate the sodium channel by altering its cationic selectivity site to calcium, thereby repressing the sodium current. Sodium 27-33 natriuretic peptide A Rattus norvegicus 6-9 2137992-8 1990 However, the changes in fractional excretion of sodium (FENa) and urine flow rate (V) as a result of ANF infusion were similar in both kidneys. Sodium 48-54 natriuretic peptide A Rattus norvegicus 101-104 2153709-4 1990 Apical Na+/H+ antiporter proton flux, assayed by the effect of sodium removal (147----0 meq/liter) on pHi, was one-third the adult level for the first 2 wk and doubled in the 3rd wk of life. Sodium 63-69 glucose-6-phosphate isomerase Oryctolagus cuniculus 102-105 2137092-0 1990 Influence of sodium balance on atrial natriuretic factor in rats with one-kidney, one-clip renal hypertension. Sodium 13-19 natriuretic peptide A Rattus norvegicus 31-56 2137092-1 1990 The influence of sodium intake on the gene expression and circulating levels of atrial natriuretic factor (ANF) was investigated in unanesthetized rats with one-kidney, one-clip renal hypertension. Sodium 17-23 natriuretic peptide A Rattus norvegicus 80-105 2137092-1 1990 The influence of sodium intake on the gene expression and circulating levels of atrial natriuretic factor (ANF) was investigated in unanesthetized rats with one-kidney, one-clip renal hypertension. Sodium 17-23 natriuretic peptide A Rattus norvegicus 107-110 2137092-3 1990 Animals which had received the regular-sodium diet exhibited significantly higher ANF mRNA levels in their right and left atria than salt-restricted animals, whereas there was no significant difference in plasma ANF levels. Sodium 39-45 natriuretic peptide A Rattus norvegicus 82-85 2302330-3 1990 During the first week post-RDX, MAP decreased from 141 /+- 6 to 121 +/- 3 mm Hg (P less than .05), while sodium balance increased from 0.32 +/- 0.05 to 0.95 +/- 0.14 mEq/kg/day (P less than .05). Sodium 105-111 radixin Sus scrofa 27-30 2105821-6 1990 These results suggest that (1) in vivo microdialysis may provide a useful technique for the evaluation of neuropeptide secretion from specific brain regions and (2) there are sodium-sensitive cells in the PVN region which respond to increases in extracellular sodium, resulting in an increase in central and peripheral oxytocin secretion. Sodium 175-181 oxytocin/neurophysin I prepropeptide Homo sapiens 319-327 2142916-12 1990 Infusion of ANF into chronic renal denervated rats also reduced the blood pressure and increased the renal excretion of water and sodium. Sodium 130-136 natriuretic peptide A Rattus norvegicus 12-15 33766485-10 2021 Aldosterone and insulin both increase the activity of serum and glucocorticoid kinase 1 (SGK-1) which in turn is a major regulator of vascular and renal sodium (Na+) channel activity.The importance of SGK-1 in the pathogenesis of the CMS is highlighted by observations that gain of function mutations in SGK-1 in humans promotes hypertension, insulin resistance and obesity. Sodium 153-159 serum/glucocorticoid regulated kinase 1 Homo sapiens 54-87 33766485-10 2021 Aldosterone and insulin both increase the activity of serum and glucocorticoid kinase 1 (SGK-1) which in turn is a major regulator of vascular and renal sodium (Na+) channel activity.The importance of SGK-1 in the pathogenesis of the CMS is highlighted by observations that gain of function mutations in SGK-1 in humans promotes hypertension, insulin resistance and obesity. Sodium 153-159 serum/glucocorticoid regulated kinase 1 Homo sapiens 89-94 33766485-10 2021 Aldosterone and insulin both increase the activity of serum and glucocorticoid kinase 1 (SGK-1) which in turn is a major regulator of vascular and renal sodium (Na+) channel activity.The importance of SGK-1 in the pathogenesis of the CMS is highlighted by observations that gain of function mutations in SGK-1 in humans promotes hypertension, insulin resistance and obesity. Sodium 153-159 serum/glucocorticoid regulated kinase 1 Homo sapiens 201-206 33766485-10 2021 Aldosterone and insulin both increase the activity of serum and glucocorticoid kinase 1 (SGK-1) which in turn is a major regulator of vascular and renal sodium (Na+) channel activity.The importance of SGK-1 in the pathogenesis of the CMS is highlighted by observations that gain of function mutations in SGK-1 in humans promotes hypertension, insulin resistance and obesity. Sodium 153-159 serum/glucocorticoid regulated kinase 1 Homo sapiens 201-206 33775738-1 2021 The two voltage gated sodium channels Nav1.7 and Nav1.8 are expressed in the peripheral nervous system and involved in various pain conditions including inflammatory and neuropathic pain. Sodium 22-28 sodium voltage-gated channel alpha subunit 9 Homo sapiens 38-44 33775738-1 2021 The two voltage gated sodium channels Nav1.7 and Nav1.8 are expressed in the peripheral nervous system and involved in various pain conditions including inflammatory and neuropathic pain. Sodium 22-28 sodium voltage-gated channel alpha subunit 10 Homo sapiens 49-55 33775443-7 2021 In addition, in experimental models of hypertension, blocking IL-17A by genetic strategies, or using neutralising antibodies, lowers blood pressure by acting on the vascular wall and tubule sodium transport and reduces damage to target organs. Sodium 190-196 interleukin 17A Homo sapiens 62-68 33779092-1 2021 Research has shown mutations in the voltage-gated sodium channel gene SCN2A to be associated with developmental delays and infantile seizures in patients with early-onset epileptic encephalopathies (EOEEs). Sodium 50-56 sodium voltage-gated channel alpha subunit 2 Homo sapiens 70-75 33794341-6 2021 Enhanced AQP4 expression by osmotic challenges with sodium in KO seems to be a compensation for the loss of AQP11. Sodium 52-58 aquaporin 4 Mus musculus 9-13 33232657-3 2021 Here, we engineered the model sodium channel NaVAb with voltage-shifting mutations and the toxin-binding site of human NaV1.7, an attractive pain target. Sodium 30-36 sodium voltage-gated channel alpha subunit 9 Homo sapiens 119-125 1459985-3 1992 Methanogenesis from a number of simple substrates such as H2 + CO2, formate, methanol, methylamines, and acetate is associated with the generation of transmembrane electrochemical gradients of protons and sodium ions which serve as driving force for a number of processes such as the synthesis of ATP via an ATP synthase, reverse electron transfer, and solute uptake. Sodium 205-211 complement C2 Homo sapiens 63-66 33794518-10 2021 EG-VEGF, VEGFR2, VEGFR3, and VEGF-D can also explain the elevated blood pressure due to the dilated lymphatic system which drains excess sodium and water back into circulation. Sodium 137-143 prokineticin 1 Homo sapiens 0-7 33794518-10 2021 EG-VEGF, VEGFR2, VEGFR3, and VEGF-D can also explain the elevated blood pressure due to the dilated lymphatic system which drains excess sodium and water back into circulation. Sodium 137-143 vascular endothelial growth factor D Homo sapiens 29-35 1475406-4 1992 Sodium retention and dexamethasone have been shown to increase circulating NPY levels in animals and the expression of NPY in neuroendocrine cells. Sodium 0-6 neuropeptide Y Homo sapiens 75-78 1475406-4 1992 Sodium retention and dexamethasone have been shown to increase circulating NPY levels in animals and the expression of NPY in neuroendocrine cells. Sodium 0-6 neuropeptide Y Homo sapiens 119-122 1466501-11 1992 The concentration of sodium in CSF was slightly higher than the value in serum, and potassium concentration was lower than the value in serum. Sodium 21-27 colony stimulating factor 2 Bos taurus 31-34 25378078-1 2015 OBJECTIVE: Liddle syndrome, an autosomal dominant form of monogenic hypertension, is attributed to mutations in the genes encoding beta and gamma subunits (SCNN1B and SCNN1G) of the epithelial sodium channel (ENaC). Sodium 193-199 sodium channel epithelial 1 subunit beta Homo sapiens 156-162 25378078-1 2015 OBJECTIVE: Liddle syndrome, an autosomal dominant form of monogenic hypertension, is attributed to mutations in the genes encoding beta and gamma subunits (SCNN1B and SCNN1G) of the epithelial sodium channel (ENaC). Sodium 193-199 sodium channel epithelial 1 subunit gamma Homo sapiens 167-173 8373012-7 1993 Investigations that employ immunocytochemical methods for the detection of the early oncogene, c-fos, indicate that neurons in the lamina terminalis, as well as the SON and PVN, are activated by the composite of systemically derived signals necessary for producing thirst and sodium appetite. Sodium 276-282 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 95-100 8373012-12 1993 Investigations that employ immunocytochemical methods for the detection of the early oncogene, c-fos, indicate that neurons in the lamina terminalis, as well as the SON and PVN, are activated by the composite of systemically derived signals necessary for producing thirst and sodium appetite. Sodium 276-282 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 95-100 34750860-0 2022 Prefrontal cortex pyramidal neurons express functional Nav1.8 TTX-resistant sodium currents. Sodium 76-82 sodium voltage-gated channel alpha subunit 10 Homo sapiens 55-61 34750860-1 2022 It has been repeatedly proved that Nav1.8 TTX-resistant sodium currents are expressed in peripheral sensory neurons where they play important role in nociception. Sodium 56-62 sodium voltage-gated channel alpha subunit 10 Homo sapiens 35-41 34750860-3 2022 The aim of this study was to assess if functional Nav1.8 TTX-resistant sodium currents are expressed in prefrontal cortex pyramidal neurons. Sodium 71-77 sodium voltage-gated channel alpha subunit 10 Homo sapiens 50-56 34750860-5 2022 The TTX-resistant sodium current recorded in this study was mainly carried by the Nav1.8 sodium channel isoform because the Nav1.9 current was inhibited by the -65 mV holding potential that we used throughout the study. Sodium 18-24 sodium voltage-gated channel alpha subunit 10 Homo sapiens 82-88 34750860-5 2022 The TTX-resistant sodium current recorded in this study was mainly carried by the Nav1.8 sodium channel isoform because the Nav1.9 current was inhibited by the -65 mV holding potential that we used throughout the study. Sodium 89-95 sodium voltage-gated channel alpha subunit 10 Homo sapiens 82-88 34750860-6 2022 Moreover, the sodium current that we recorded was inhibited by treatment with the selective Nav1.8 inhibitor A-803467. Sodium 14-20 sodium voltage-gated channel alpha subunit 10 Homo sapiens 92-98 34750860-11 2022 This study suggests that the Nav1.8 TTX-resistant sodium channel is expressed not only in DRG neurons but also in cortical neurons and may be molecular target for antiepileptic drugs such as carbamazepine. Sodium 50-56 sodium voltage-gated channel alpha subunit 10 Homo sapiens 29-35 34086898-3 2021 This mutation reduced expression of cardiomyocyte sodium channel Nav1.5 via Nedd4-2 E3 ubiquitin ligase-induced ubiquitination and degradation. Sodium 50-56 NEDD4 like E3 ubiquitin protein ligase Homo sapiens 76-83 34957475-1 2021 Patients with bi-allelic loss of function mutations in the voltage-gated sodium channel Nav1.7 present with congenital insensitivity to pain (CIP), whilst low threshold mechanosensation is reportedly normal. Sodium 73-79 sodium voltage-gated channel alpha subunit 9 Homo sapiens 88-94 34958174-1 2022 Selective inhibition of certain voltage-gated sodium channels (Nav s), such as Nav 1.8, is of primary interest for pharmacological pain research and widely studied as a pharmacological target due to its contribution to repetitive firing, neuronal excitability, and pain chronification. Sodium 46-52 sodium voltage-gated channel alpha subunit 10 Homo sapiens 79-86 1482638-6 1992 Insulin-like growth factor-1 (IGF-1), which is depressed in calorie-deficient growth failure, was depressed in all the rats on the low-sodium intakes relative to ad libitum-fed controls, but did not vary in relation to dietary sodium or weight gain within those groups. Sodium 227-233 insulin-like growth factor 1 Rattus norvegicus 30-35 34312669-2 2021 Common and rare SCN10A variants are suggested to contribute to Brugada Syndrome (BrS), an inherited channelopathy resulting from genetic-determined loss-of-function in cardiac sodium channel. Sodium 176-182 sodium voltage-gated channel alpha subunit 10 Homo sapiens 16-22 1505513-7 1992 In cells overexpressing HAL1, sodium toxicity seems to be counteracted by an increased accumulation of potassium. Sodium 30-36 Hal1p Saccharomyces cerevisiae S288C 24-28 34846128-9 2021 In contrast, the D223N mutant of Kir3.4 that mimics the sodium-bound state exhibited stronger binding for PI(4,5)P2, particularly for those with 18:0-20:4 acyl chains. Sodium 56-62 potassium inwardly rectifying channel subfamily J member 5 Homo sapiens 33-39 34942149-1 2022 The mitochondrial sodium/calcium/lithium exchanger (NCLX) is an important mediator of calcium extrusion from mitochondria. Sodium 18-24 solute carrier family 8 member B1 Homo sapiens 52-56 33315536-1 2021 The voltage-gated sodium channel Nav1.8 mediates the tetrodotoxin-resistant (TTX-R) Na+ current in nociceptive primary sensory neurons, which has an important role in the transmission of painful stimuli. Sodium 18-24 sodium voltage-gated channel alpha subunit 10 Homo sapiens 33-39 34822321-0 2021 The recycling regulation of sodium-hydrogen exchanger isoform 3(NHE3) in epithelial cells. Sodium 28-34 solute carrier family 9 member A3 Homo sapiens 64-68 34822321-1 2021 As the main exchanger of electroneutral NaCl absorption, sodium-hydrogen exchanger isoform 3 (NHE3) circulates in the epithelial brush border (BB) and intracellular compartments in a multi-protein complex. Sodium 57-63 solute carrier family 9 member A3 Homo sapiens 94-98 1400063-0 1992 ACE inhibition facilitates sodium and water excretion during PEEP in conscious volume-expanded dogs. Sodium 27-33 angiotensin I converting enzyme Canis lupus familiaris 0-3 1588770-6 1992 A significant correlation between the urinary hEGF levels and creatinine clearance (r = 0.712, p less than 0.001) and an inverse correlation between urinary hEGF levels and fractional excretion of sodium (r = -0.406, p less than 0.05) was demonstrated. Sodium 197-203 epidermal growth factor Homo sapiens 157-161 34982449-5 2021 The replacement of Histidine (His) with Asparagine (Asn) at position 1568 in the topological domain of SCN9A channel protein provides new insights into the impaired excitation and inactivation patterns of sodium channels. Sodium 205-211 sodium voltage-gated channel alpha subunit 9 Homo sapiens 103-108 34741534-0 2021 The involvement of sodium in the function of the human amino acid transporter ASCT2. Sodium 19-25 solute carrier family 1 member 5 Homo sapiens 78-83 34758144-4 2021 Here we show that mepyramine directly inhibits a variety of voltage-gated sodium channels, including the Tetrodotoxin-sensitive isoforms and the main isoforms (Nav1.7, Nav1.8, and Nav1.9) of nociceptors. Sodium 74-80 sodium voltage-gated channel alpha subunit 9 Homo sapiens 160-166 34758144-4 2021 Here we show that mepyramine directly inhibits a variety of voltage-gated sodium channels, including the Tetrodotoxin-sensitive isoforms and the main isoforms (Nav1.7, Nav1.8, and Nav1.9) of nociceptors. Sodium 74-80 sodium voltage-gated channel alpha subunit 10 Homo sapiens 168-174 34880650-3 2021 NHE3 inhibition in the small intestine results in luminal sodium and water retention, leading to a general decrease in paracellular water flux and diffusional driving force, reduced intestinal sodium absorption, and increased stool sodium excretion. Sodium 58-64 solute carrier family 9 member A3 Homo sapiens 0-4 34880650-3 2021 NHE3 inhibition in the small intestine results in luminal sodium and water retention, leading to a general decrease in paracellular water flux and diffusional driving force, reduced intestinal sodium absorption, and increased stool sodium excretion. Sodium 193-199 solute carrier family 9 member A3 Homo sapiens 0-4 34880650-3 2021 NHE3 inhibition in the small intestine results in luminal sodium and water retention, leading to a general decrease in paracellular water flux and diffusional driving force, reduced intestinal sodium absorption, and increased stool sodium excretion. Sodium 232-238 solute carrier family 9 member A3 Homo sapiens 0-4 34880650-6 2021 Inhibition of intestinal NHE3 also lowers blood pressure by reducing intestinal sodium absorption. Sodium 80-86 solute carrier family 9 member A3 Homo sapiens 25-29 34884494-5 2021 The mechanism by which these drugs exert their cardioprotective effects is unknown, although recent studies have shown that cardiovascular homeostasis occurs through the interplay of the sodium-hydrogen exchangers (NHE), specifically NHE1 and NHE3, with SGLT2i. Sodium 187-193 solute carrier family 9 member A3 Homo sapiens 243-247 34782600-2 2021 Here, we elucidate the role of the sodium channel isoform NaV1.8 for CaMKIIdeltac-dependent proarrhythmia. Sodium 35-41 sodium voltage-gated channel alpha subunit 10 Homo sapiens 58-64 34755904-4 2022 Some evidence suggests that the activation of sodium-glucose cotransporter 3a (SGLT3a) induces the depolarization of ESCs to affect their function. Sodium 46-52 solute carrier family 5, member 4a Mus musculus 79-85 34601973-4 2021 The NFAT5 KO mice exhibited high BP, hypernatremia, polyuria, and low urinary sodium excretion without significant alterations in the plasma renin activity or aldosterone concentration. Sodium 78-84 nuclear factor of activated T cells 5 Mus musculus 4-9 34601973-10 2021 In conclusion, these data indicate that renal tubular NFAT5 should play an important role in regulating sodium reabsorption through epithelial sodium channel under high-salt conditions, thereby preventing salt-dependent hypertension. Sodium 104-110 nuclear factor of activated T cells 5 Mus musculus 54-59 34601973-10 2021 In conclusion, these data indicate that renal tubular NFAT5 should play an important role in regulating sodium reabsorption through epithelial sodium channel under high-salt conditions, thereby preventing salt-dependent hypertension. Sodium 143-149 nuclear factor of activated T cells 5 Mus musculus 54-59 34778257-8 2021 Further analysis revealed that renal Fgfr1/klotho/extracellular signal-regulated kinases 1/2 signaling was activated in AAV-Fgf23 mice, resulting in downregulation of sodium-phosphate cotransporter NaPi2a and NaPi2c and suppression of Cyp27b1, further supporting the bioactivity of cardiac-derived iFgf23. Sodium 167-173 klotho Mus musculus 43-49 34778257-8 2021 Further analysis revealed that renal Fgfr1/klotho/extracellular signal-regulated kinases 1/2 signaling was activated in AAV-Fgf23 mice, resulting in downregulation of sodium-phosphate cotransporter NaPi2a and NaPi2c and suppression of Cyp27b1, further supporting the bioactivity of cardiac-derived iFgf23. Sodium 167-173 fibroblast growth factor 23 Mus musculus 124-129 34089591-1 2021 BACKGROUND: We have previously shown that high salt stimulates the expression of miR-429 in the renal medulla, which induces mRNA decay of HIF prolyl-hydroxylase 2 (PHD2), an enzyme to promote the degradation of hypoxia inducible factor (HIF)-1alpha, and increases the HIF-1alpha-mediated activation of antihypertensive genes in the renal medulla, consequently promoting extra sodium excretion. Sodium 377-383 egl-9 family hypoxia-inducible factor 1 Rattus norvegicus 139-163 34988469-7 2021 We found that furosemide sensitive sodium transport (NKCC2) is only increased during late pregnancy, thiazide sensitive sodium transport (NDCBE/pendrin) is increased in all stages of pregnancy, and that benzamil sensitive sodium transport (ENaC) is increased beginning in mid-pregnancy. Sodium 35-41 solute carrier family 12 member 1 Rattus norvegicus 53-58 1309874-0 1992 The acute renal actions of angiotensin converting enzyme inhibitors in the sodium-depleted conscious primate are mediated by inhibition of the renin-angiotensin system. Sodium 75-81 renin Callithrix jacchus 143-148 1309874-1 1992 The purpose of this study was to determine if the changes in renal function acutely produced by an inhibitor of angiotensin converting enzyme (ACE) in the sodium-depleted conscious marmoset can be explained primarily by blockade of the renin-angiotensin system. Sodium 155-161 renin Callithrix jacchus 236-241 1309874-10 1992 These results demonstrate that acute administration of an ACEI affects BP and renal function in the sodium-depleted conscious primate primarily by inhibition of the renin-angiotensin system. Sodium 100-106 renin Callithrix jacchus 165-170 1722641-8 1991 This increase in pHi was not affected by amiloride but disappeared after inhibition of Na(+)-HCO3- cotransport by 4,4"-diisothiocyanostilbene-2,2"-disulfonic acid or sodium-free conditions. Sodium 166-172 glucose-6-phosphate isomerase Rattus norvegicus 17-20 1659948-1 1991 DNA from seven unrelated patients with hyperkalemic periodic paralysis (HYPP) was examined for mutations in the adult skeletal muscle sodium channel gene (SCN4A) known to be genetically linked to the disorder. Sodium 134-140 sodium voltage-gated channel alpha subunit 4 Homo sapiens 155-160 1660029-3 1991 Parts of the gene coding for the alpha-subunit of the sodium channel of the adult human skeletal muscle (SCN4A) have been localised on chromosome 17. Sodium 54-60 sodium voltage-gated channel alpha subunit 4 Homo sapiens 105-110 2065906-6 1991 Neuropeptide Y significantly increased net absorption of water, sodium, potassium, and chloride under basal conditions. Sodium 64-70 neuropeptide Y Homo sapiens 0-14 1907105-12 1991 We describe a novel method for the study of renal clearances in a small conscious primate and suggest that the renin-angiotensin system plays an important role in the control of renal function in the sodium-depleted marmoset. Sodium 200-206 renin Callithrix jacchus 111-116 34642387-5 2021 We show that the addition of 1.0% by weight of indium arsenide nanowires increases the sodium ion conductivity in the polymer to 1.50 x 10-4 Scm-1 at 40 C. In order to explain this remarkable characteristic, we propose a new transport model in which sodium ions hop between close-spaced defect sites present on the surface of the nanowires, forming an effective complex conductive percolation network. Sodium 87-93 X-C motif chemokine ligand 1 Homo sapiens 141-146 34642387-5 2021 We show that the addition of 1.0% by weight of indium arsenide nanowires increases the sodium ion conductivity in the polymer to 1.50 x 10-4 Scm-1 at 40 C. In order to explain this remarkable characteristic, we propose a new transport model in which sodium ions hop between close-spaced defect sites present on the surface of the nanowires, forming an effective complex conductive percolation network. Sodium 251-257 X-C motif chemokine ligand 1 Homo sapiens 141-146 34679015-1 2021 The voltage-gated sodium channel NaV1.7 is an important target for drug development due to its role in pain perception. Sodium 18-24 sodium voltage-gated channel alpha subunit 9 Homo sapiens 33-39 34363725-1 2021 Uromodulin, also named Tamm Horsfall protein, have been associated with renal function and sodium homeostasis regulation. Sodium 91-97 uromodulin Homo sapiens 0-10 34703889-13 2021 Conclusion: Further studies are needed for carbamazepine, sumatriptan, buprenorphine, and oral Nav1.7 sodium channel blockers, as only one study reported outcomes. Sodium 102-108 sodium voltage-gated channel alpha subunit 9 Homo sapiens 95-101 34293127-3 2021 OBJECTIVES: We hypothesized that a low-sodium DASH diet improves (lowers) biomarkers of inflammation (C-reactive protein (CRP) and soluble urokinase plasminogen activator receptor (suPAR)) and mineral metabolism (phosphorus and fibroblast growth factor-23 (FGF23)). Sodium 39-45 fibroblast growth factor 23 Homo sapiens 257-262 34293127-10 2021 FGF23 was also higher after the low-sodium DASH diet (geometric mean 35.3 pg/mL (95% CI: 33.3, 37.3 pg/mL) compared with 28.2 pg/mL (95% CI: 26.6, 29.8 pg/mL); P < 0.001). Sodium 36-42 fibroblast growth factor 23 Homo sapiens 0-5 34373125-2 2021 Paradoxically, mutations that reduce NaV1.2 sodium currents also have a similar effect. Sodium 44-50 sodium voltage-gated channel alpha subunit 2 Homo sapiens 37-43 34621749-11 2021 The dermal eGC/ED markers UEA1, VEGFR2, and vWF all associated with plasma levels of NT-proBNP and sodium (all R 2 > 0.29 and P < 0.01), except for vWF that only associated with plasma NT-proBNP. Sodium 99-105 kinase insert domain receptor Homo sapiens 32-38 34407515-0 2021 Ship in Bottle Synthesis of Yolk-Shell MnS@Hollow Carbon Spheres for Sodium Storage. Sodium 69-75 inositol polyphosphate-5-phosphatase D Homo sapiens 0-4 34407515-0 2021 Ship in Bottle Synthesis of Yolk-Shell MnS@Hollow Carbon Spheres for Sodium Storage. Sodium 69-75 glycophorin E (MNS blood group) Homo sapiens 39-42 34407515-2 2021 In this paper, we provide a new ship in bottle strategy to synthesize MnS@C sodium ion battery anode with yolk-shell nanostructure. Sodium 76-82 inositol polyphosphate-5-phosphatase D Homo sapiens 32-36 34407515-2 2021 In this paper, we provide a new ship in bottle strategy to synthesize MnS@C sodium ion battery anode with yolk-shell nanostructure. Sodium 76-82 glycophorin E (MNS blood group) Homo sapiens 70-73 34507995-1 2021 ASCT2 (SLC1A5) is a sodium-dependent neutral amino acid transporter that controls amino acid homeostasis in peripheral tissues. Sodium 20-26 solute carrier family 1 member 5 Homo sapiens 0-5 34507995-1 2021 ASCT2 (SLC1A5) is a sodium-dependent neutral amino acid transporter that controls amino acid homeostasis in peripheral tissues. Sodium 20-26 solute carrier family 1 member 5 Homo sapiens 7-13 1849364-3 1991 The present studies tested the hypothesis that the avid sodium retention and renal ANF resistance characteristic of chronic congestive heart failure (CHF) are associated with attenuated renal cGMP responses to ANF. Sodium 56-62 natriuretic peptide A Canis lupus familiaris 210-213 1849364-6 1991 In early CHF, increased sodium excretion and renal cGMP production were observed in association with increases in plasma ANF. Sodium 24-30 natriuretic peptide A Canis lupus familiaris 121-124 1849364-7 1991 Exogenous ANF administration (10 micrograms/kg iv) before CHF also produced parallel increases in sodium excretion and renal cGMP production. Sodium 98-104 natriuretic peptide A Canis lupus familiaris 10-13 1849364-10 1991 These studies suggest that 1) renal cGMP production is a useful biological marker for the renal natriuretic action of ANF; 2) endogenous ANF contributes to the maintenance of sodium excretion in early CHF via increases in renal cGMP production; and 3) the avid sodium retention and renal ANF resistance in advanced CHF are, in part, linked to attenuated renal cGMP responses to endogenous and exogenous ANF. Sodium 175-181 natriuretic peptide A Canis lupus familiaris 137-140 1849364-10 1991 These studies suggest that 1) renal cGMP production is a useful biological marker for the renal natriuretic action of ANF; 2) endogenous ANF contributes to the maintenance of sodium excretion in early CHF via increases in renal cGMP production; and 3) the avid sodium retention and renal ANF resistance in advanced CHF are, in part, linked to attenuated renal cGMP responses to endogenous and exogenous ANF. Sodium 175-181 natriuretic peptide A Canis lupus familiaris 137-140 1849364-10 1991 These studies suggest that 1) renal cGMP production is a useful biological marker for the renal natriuretic action of ANF; 2) endogenous ANF contributes to the maintenance of sodium excretion in early CHF via increases in renal cGMP production; and 3) the avid sodium retention and renal ANF resistance in advanced CHF are, in part, linked to attenuated renal cGMP responses to endogenous and exogenous ANF. Sodium 175-181 natriuretic peptide A Canis lupus familiaris 137-140 1849364-10 1991 These studies suggest that 1) renal cGMP production is a useful biological marker for the renal natriuretic action of ANF; 2) endogenous ANF contributes to the maintenance of sodium excretion in early CHF via increases in renal cGMP production; and 3) the avid sodium retention and renal ANF resistance in advanced CHF are, in part, linked to attenuated renal cGMP responses to endogenous and exogenous ANF. Sodium 261-267 natriuretic peptide A Canis lupus familiaris 137-140 1849364-10 1991 These studies suggest that 1) renal cGMP production is a useful biological marker for the renal natriuretic action of ANF; 2) endogenous ANF contributes to the maintenance of sodium excretion in early CHF via increases in renal cGMP production; and 3) the avid sodium retention and renal ANF resistance in advanced CHF are, in part, linked to attenuated renal cGMP responses to endogenous and exogenous ANF. Sodium 261-267 natriuretic peptide A Canis lupus familiaris 137-140 1849364-10 1991 These studies suggest that 1) renal cGMP production is a useful biological marker for the renal natriuretic action of ANF; 2) endogenous ANF contributes to the maintenance of sodium excretion in early CHF via increases in renal cGMP production; and 3) the avid sodium retention and renal ANF resistance in advanced CHF are, in part, linked to attenuated renal cGMP responses to endogenous and exogenous ANF. Sodium 261-267 natriuretic peptide A Canis lupus familiaris 137-140 1676328-0 1991 Central administration of somatostatin suppresses the stimulated sodium intake of sheep. Sodium 65-71 somatostatin Ovis aries 26-38 2213567-2 1990 Previous work in this laboratory has shown A-4 and A-5 to be inhibitors of the sodium-dependent, high affinity choline uptake system (SDHACU). Sodium 79-85 immunoglobulin kappa variable 2D-26 Homo sapiens 51-54 2145876-0 1990 The atrial natriuretic factor hormonal system in the regulation of sodium excretion in dogs with experimental heart failure. Sodium 67-73 natriuretic peptide A Canis lupus familiaris 4-29 2145876-1 1990 In response to a meat meal containing 125 mEq of sodium, conscious dogs (n = 5) with an arteriovenous (AV) fistula and chronic compensated heart failure exhibited temporally related increases in postprandial plasma immunoreactive atrial natriuretic factor (iANF), right atrial pressure, and sodium excretion. Sodium 49-55 natriuretic peptide A Canis lupus familiaris 230-255 2145876-2 1990 In separate experiments, two weeks of dietary sodium restriction produced similar marked stimulation of renin and aldosterone both in normal dogs (n = 5), and in AV fistula dogs (n = 5) with chronic high circulating levels of ANF. Sodium 46-52 natriuretic peptide A Canis lupus familiaris 226-229 2145876-4 1990 These results suggest that the ANF system is involved in the postprandial regulation of sodium excretion in the AV fistula dogs with compensated heart failure. Sodium 88-94 natriuretic peptide A Canis lupus familiaris 31-34 2162348-6 1990 For both fibroblasts and adipocytes, the dependence of rubidium uptake activity on sodium concentration was characterized by K0.5 values of 9.4 and 6.2 mM, respectively, which is also diagnostic for the alpha 1 subunit in vivo. Sodium 83-89 adrenoceptor alpha 1D Homo sapiens 203-210 2207632-2 1990 In this study the measurement of extracellular sodium concentration changes [( Na+]o) induced by iontophoretic application of N-methyl-D-aspartate (NMDA) and quisqualate (Quis) is used as a tool to estimate the density of functional NMDA- and Quis-receptor sites in area CA1 and dentate gyrus of rat hippocampus. Sodium 47-53 carbonic anhydrase 1 Rattus norvegicus 271-274 2141770-6 1990 However, during 2 and 4 ng.kg-1.min-1 ANP infusion for 7 days, sodium excretion averaged 37.2 +/- 10.0 and 134.8 +/- 19.0% greater, respectively, in the ANP-infused kidneys compared with the vehicle-infused kidneys but there were no changes in glomerular filtration rate or effective renal plasma flow. Sodium 63-69 natriuretic peptide A Canis lupus familiaris 38-41 2163212-1 1990 Sodium-retaining cirrhotic and chronic caval dogs with ascites show a heterogeneous natriuretic response to atrial natriuretic factor (ANF) infusions such that half will increase their urinary excretion of sodium and half will show no natriuretic response whatsoever. Sodium 0-6 natriuretic peptide A Canis lupus familiaris 108-133 34557669-2 2021 Gain-of-function mutations in sodium channel Nav1.7 produce hyperexcitability of dorsal root ganglion neurons underlying inherited erythromelalgia, a human genetic model of neuropathic pain. Sodium 30-36 sodium voltage-gated channel alpha subunit 9 Homo sapiens 45-51 2163212-1 1990 Sodium-retaining cirrhotic and chronic caval dogs with ascites show a heterogeneous natriuretic response to atrial natriuretic factor (ANF) infusions such that half will increase their urinary excretion of sodium and half will show no natriuretic response whatsoever. Sodium 0-6 natriuretic peptide A Canis lupus familiaris 135-138 2163212-1 1990 Sodium-retaining cirrhotic and chronic caval dogs with ascites show a heterogeneous natriuretic response to atrial natriuretic factor (ANF) infusions such that half will increase their urinary excretion of sodium and half will show no natriuretic response whatsoever. Sodium 206-212 natriuretic peptide A Canis lupus familiaris 108-133 2163212-1 1990 Sodium-retaining cirrhotic and chronic caval dogs with ascites show a heterogeneous natriuretic response to atrial natriuretic factor (ANF) infusions such that half will increase their urinary excretion of sodium and half will show no natriuretic response whatsoever. Sodium 206-212 natriuretic peptide A Canis lupus familiaris 135-138 2213591-15 1990 This observation suggests that in cultured Purkinje cells the sodium-hydrogen exchanger could be activated through a protein kinase C pathway only when pHi is maintained at a low physiological value by the activity of the chloride-bicarbonate exchange. Sodium 62-68 glucose-6-phosphate isomerase Rattus norvegicus 152-155 2085517-4 1990 Sodium content is controlled primarily by the renin and aldosterone systems and by sodium appetite (Denton, 1982). Sodium 0-6 renin Capra hircus 46-51 1705631-6 1990 However, the glomerular filtration rate (GFR), urine volume, and sodium excretion all increased significantly in response to intrarenal ACE inhibition. Sodium 65-71 angiotensin I converting enzyme Canis lupus familiaris 136-139 2299401-1 1990 The involvement of phospholipase A2 (PLA2) and fatty acid release in the regulation of sodium-dependent high-affinity choline uptake in rat brain was assessed in vitro through the use of the specific binding of 3H-hemicholinium-3 (3H-HCh-3). Sodium 87-93 phospholipase A2 group IB Rattus norvegicus 19-35 2299401-1 1990 The involvement of phospholipase A2 (PLA2) and fatty acid release in the regulation of sodium-dependent high-affinity choline uptake in rat brain was assessed in vitro through the use of the specific binding of 3H-hemicholinium-3 (3H-HCh-3). Sodium 87-93 phospholipase A2 group IB Rattus norvegicus 37-41 2299401-10 1990 These results support the involvement of PLA2 and subsequent fatty acid release in the increase of 3H-HCh-3 binding in cholinergic neurons and suggest that activation of PLA2 may be the penultimate step in regulating the velocity of sodium-dependent choline transport. Sodium 233-239 phospholipase A2 group IB Rattus norvegicus 41-45 2299401-10 1990 These results support the involvement of PLA2 and subsequent fatty acid release in the increase of 3H-HCh-3 binding in cholinergic neurons and suggest that activation of PLA2 may be the penultimate step in regulating the velocity of sodium-dependent choline transport. Sodium 233-239 phospholipase A2 group IB Rattus norvegicus 170-174 33942619-2 2021 Long QT syndrome type-3 (LQT3) is a congenital form of VA caused by cardiac sodium channel (INaL) SCN5A mutations that prolongs cardiac action potential (AP) and enhances INaL current. Sodium 76-82 sodium voltage-gated channel alpha subunit 5 Homo sapiens 25-29 33942619-2 2021 Long QT syndrome type-3 (LQT3) is a congenital form of VA caused by cardiac sodium channel (INaL) SCN5A mutations that prolongs cardiac action potential (AP) and enhances INaL current. Sodium 76-82 sodium voltage-gated channel alpha subunit 5 Homo sapiens 98-103 33818128-0 2021 Deletion of renal Nedd4-2 abolishes the effect of high sodium intake (HS) on Kir4.1, ENaC and NCC, and causes hypokalemia during HS. Sodium 55-61 neural precursor cell expressed, developmentally down-regulated gene 4-like Mus musculus 18-25 33818128-0 2021 Deletion of renal Nedd4-2 abolishes the effect of high sodium intake (HS) on Kir4.1, ENaC and NCC, and causes hypokalemia during HS. Sodium 55-61 sodium channel, nonvoltage-gated 1 alpha Mus musculus 85-89 33797191-1 2021 Biallelic loss-of-function (LoF) of SLC13A5 (solute carrier family 13, member 5) induced deficiency in sodium/citrate transporter (NaCT) causes autosomal recessive developmental epileptic encephalopathy 25 with hypoplastic amelogenesis imperfecta (DEE25; MIM #615905). Sodium 103-109 solute carrier family 13 member 5 Homo sapiens 36-43 33797191-1 2021 Biallelic loss-of-function (LoF) of SLC13A5 (solute carrier family 13, member 5) induced deficiency in sodium/citrate transporter (NaCT) causes autosomal recessive developmental epileptic encephalopathy 25 with hypoplastic amelogenesis imperfecta (DEE25; MIM #615905). Sodium 103-109 solute carrier family 13 member 5 Homo sapiens 45-79 33800499-2 2021 The discovery of the association between CFTR and the hyperactive epithelial sodium channel (ENaC) has raised the question of the influence of ENaC on the clinical CF phenotype. Sodium 77-83 sodium channel, nonvoltage-gated 1 alpha Mus musculus 93-97 34089516-6 2022 A very rare variant in the SCNN1G gene encoding the gamma subunit of epithelial sodium channel ENaC was also identified in one patient. Sodium 80-86 sodium channel epithelial 1 subunit gamma Homo sapiens 27-33 34079053-4 2021 Mitochondrial calcium transients are primarily determined by the balance between calcium influx, mediated by the mitochondrial calcium uniporter (MCU), and calcium efflux through the sodium/lithium/calcium exchanger (NCLX). Sodium 183-189 solute carrier family 8 member B1 Homo sapiens 217-221 34141090-1 2021 The voltage-gated sodium channel Nav1.7 continues to be a high-profile target for the treatment of various pain afflictions due to its strong human genetic validation. Sodium 18-24 sodium voltage-gated channel alpha subunit 9 Homo sapiens 33-39 9691010-1 1998 Experiments were performed to investigate vasopressin type 2 receptor (V2)-mediated renal water reabsorption and the renal expression of the vasopressin-regulated water channel aquaporin-2 (AQP-2) in cirrhotic rats with sodium retention but without ascites. Sodium 220-226 aquaporin 2 Rattus norvegicus 190-195 34045018-12 2021 In contrast, lowering sodium from high to low levels reduced NT-proBNP independently of diet (19%; 95% CI: -24% to -14%), but did not alter hs-cTnI and mildly increased hs-CRP (9%; 95% CI: 0.4% to 18%). Sodium 22-28 troponin I3, cardiac type Homo sapiens 143-147 34045018-13 2021 Combining DASH with sodium reduction lowered hs-cTnI by 20% (95% CI: -31% to -7%) and NT-proBNP by 23% (95% CI: -32% to -12%), whereas hs-CRP was not significantly changed (-7%; 95% CI: -22% to 9%) compared with the high sodium-control diet. Sodium 20-26 troponin I3, cardiac type Homo sapiens 48-52 1597860-5 1992 When selected compounds were administered intravenously to sodium-deficient rhesus monkeys at 0.3-1.2 mg/kg, they reduced plasma renin activity by 75-98%. Sodium 59-65 renin Macaca mulatta 129-134 34136107-5 2021 Both mutant RAS and activated CRAF expression is associated with formation of membrane ruffles to which they colocalize along with actin, sodium-hydrogen exchangers (NHEs) and phosphorylated myosin phosphatase (pMYPT). Sodium 138-144 v-raf-leukemia viral oncogene 1 Mus musculus 30-34 33323889-2 2021 Gain-of-function variants in the sodium channel Nav1.7 that produce DRG neuron hyperexcitability are present in 5-10% of patients with idiopathic painful SFN. Sodium 33-39 sodium voltage-gated channel alpha subunit 9 Homo sapiens 48-54 34093402-1 2021 Background: Nav1.2 encoded by the SCN2A gene is a brain-expressed voltage-gated sodium channel known to be associated with neurodevelopment disorders ranging from benign familial neonatal infantile seizures (BFIS) to developmental and epileptic encephalopathy (DEE) and autism spectrum disorder. Sodium 80-86 sodium voltage-gated channel alpha subunit 2 Homo sapiens 12-18 34093402-1 2021 Background: Nav1.2 encoded by the SCN2A gene is a brain-expressed voltage-gated sodium channel known to be associated with neurodevelopment disorders ranging from benign familial neonatal infantile seizures (BFIS) to developmental and epileptic encephalopathy (DEE) and autism spectrum disorder. Sodium 80-86 sodium voltage-gated channel alpha subunit 2 Homo sapiens 34-39 34079822-3 2021 Its intestinal counterpart, apical sodium-dependent bile acid transporter ASBT, is responsible for the reabsorption of bile acids from the intestinal lumen. Sodium 35-41 solute carrier family 10 member 2 Homo sapiens 74-78 34095364-7 2021 The functional relevance of one LBN-induced candidate gene, Scn7a, could be confirmed by an increase in the density of voltage-gated sodium (Nav) channel activated currents in hippocampal NG2+ cells. Sodium 133-139 chondroitin sulfate proteoglycan 4 Mus musculus 188-191 34792000-10 2021 Ang-(1-7) attenuated the increased urinary flow and the fractional excretion of H2O and potassium observed in GM rats but intensified the elevated excretion of sodium in these animals. Sodium 160-166 angiogenin Rattus norvegicus 0-8 35624145-3 2022 Thirteen kinases were found to activate sodium/hydrogen exchanger (NHE1) in normal hematopoietic progenitors, of which FLT3-ITD, KRASG12D, and BTK phosphorylated NHE1 maintained alkaline intracellular pH (pHi) and supported survival of AML cells. Sodium 40-46 Bruton tyrosine kinase Homo sapiens 143-146 34870751-0 2022 Proteolytic activation of the epithelial sodium channel (ENaC) by factor VII activating protease (FSAP) and its relevance for sodium retention in nephrotic mice. Sodium 41-47 sodium channel, nonvoltage-gated 1 alpha Mus musculus 57-61 34870751-0 2022 Proteolytic activation of the epithelial sodium channel (ENaC) by factor VII activating protease (FSAP) and its relevance for sodium retention in nephrotic mice. Sodium 126-132 sodium channel, nonvoltage-gated 1 alpha Mus musculus 57-61 34870751-1 2022 Proteolytic activation of the epithelial sodium channel (ENaC) by aberrantly filtered serine proteases is thought to contribute to renal sodium retention in nephrotic syndrome. Sodium 41-47 sodium channel, nonvoltage-gated 1 alpha Mus musculus 57-61 34870751-1 2022 Proteolytic activation of the epithelial sodium channel (ENaC) by aberrantly filtered serine proteases is thought to contribute to renal sodium retention in nephrotic syndrome. Sodium 137-143 sodium channel, nonvoltage-gated 1 alpha Mus musculus 57-61 34537283-3 2022 The main characteristic of ALI/ARDS is pulmonary edema, and epithelial sodium channel (ENaC) is a key factor in effective removal of excessive alveolar edematous fluid, which is essential for repairing gas exchange and minimizing damage to the peripheral tissues. Sodium 71-77 sodium channel, nonvoltage-gated 1 alpha Mus musculus 87-91 34388924-0 2022 Synergy of surface sodium and hydroxyl on NaTi2HO5 nanotubes accelerating the Pt-dominated ambient HCHO oxidation. Sodium 19-25 N-acetyltransferase 1 Homo sapiens 42-46 34913083-5 2022 COS of DP2-6 were measured as their sodium adducts at c = 10-6 M by syringe pump infusion. Sodium 36-42 transcription factor Dp-2 Homo sapiens 7-12 35613257-1 2022 Sodium-proton exchanger 3 (NHE3/SLC9A3) located in the apical membrane of renal and gastrointestinal epithelia mediates salt and fluid absorption and regulates pH homeostasis. Sodium 0-6 solute carrier family 9 member A3 Homo sapiens 27-31 35548416-5 2022 In addition to regulating the pH, the NBC is a source of sodium influx. Sodium 57-63 solute carrier family 4 (anion exchanger), member 4 Mus musculus 38-41 35387601-11 2022 Additionally, every 1 M ratio increment of sodium -to -potassium ratio was associated with a 21% increased risk of incident CKD (IRR = 1.21, 95% CI = 1.02, 1.45), p < 0.05). Sodium 43-49 insulin receptor related receptor Homo sapiens 129-132 34978207-9 2022 Dietary sodium intake was significantly associated with anti-dsDNA and complement C4 level, while dietary potassium intake was associated with complement C3 level, supporting that dietary sodium and potassium intakes might play a key role in markers related to disease activity in SLE patients. Sodium 188-194 complement C3 Homo sapiens 143-156 35101818-1 2022 Dopamine transporter mediates the neurotransmitter dopamine homeostasis in a sodium-dependent manner. Sodium 77-83 solute carrier family 6 member 3 Homo sapiens 0-20 35092938-1 2022 The sodium channel Nav1.8, encoded by SCN10A, is reported to contribute to arrhythmogenesis by inducing the late INa and thereby enhanced persistent Na+ current. Sodium 4-10 sodium voltage-gated channel alpha subunit 10 Homo sapiens 38-44 35142111-5 2022 Thus, the SnS2 @C/CNF benefits greatly in structural stability and pseudocapacitive capacity for improved lithium/sodium storage performance. Sodium 114-120 NPHS1 adhesion molecule, nephrin Homo sapiens 18-21 35142111-6 2022 As a result of these improvements, the self-standing SnS2 @C/CNF film electrodes exhibit the highly stable capacity of 964.8 and 767.6 mAh g-1 at 0.2 A g-1 , and excellent capacity retention of 87.4% and 82.4% after 1000 cycles at high current density for lithium-ion batteries and sodium-ion batteries, respectively. Sodium 282-288 NPHS1 adhesion molecule, nephrin Homo sapiens 61-64 35188110-1 2022 SCN8A gene encodes sodium channel alpha subunit Nav1.6, and its mutation is associated with Early Infantile Epileptic Encephalopathy-13 (EIEE-13). Sodium 19-25 sodium voltage-gated channel alpha subunit 8 Homo sapiens 0-5 35200683-1 2022 The voltage-gated sodium channel subtype 1.2 (NaV1.2) is instrumental in the initiation of action potentials in the nervous system, making it a natural drug target for neurological diseases. Sodium 18-24 sodium voltage-gated channel alpha subunit 2 Homo sapiens 46-52 35136380-4 2022 This case-control (100 control: 101patients) study evaluated the association of sodium channel genes SCN1A and SCN2A with drug-resistant epilepsy. Sodium 80-86 sodium voltage-gated channel alpha subunit 2 Homo sapiens 111-116 2552821-2 1989 Sodium restriction resulted in an increase in the plasma NE concentration (P less than 0.02) and decreases in MNL beta 2-AR density (P less than 0.001), affinity for antagonist (P less than 0.001), and adenylate cyclase sensitivity to isoproterenol (ANOVA, P less than 0.01). Sodium 0-6 adrenoceptor beta 2 Homo sapiens 114-123 2552821-5 1989 Our data suggest that the downregulation of MNL beta 2-AR-mediated function in humans during dietary sodium restriction is a response to the increase in plasma NE. Sodium 101-107 adrenoceptor beta 2 Homo sapiens 48-57 2532995-11 1989 In the denervated kidney ANF increased urine flow rate and sodium excretion to rates above those established following denervation alone. Sodium 59-65 natriuretic peptide A Rattus norvegicus 25-28 2533287-0 1989 Role of atrial natriuretic peptide on sodium homeostasis in experimental renal failure. Sodium 38-44 natriuretic peptide A Rattus norvegicus 8-34 2533287-1 1989 In a study of the role of atrial natriuretic peptide (ANP) in sodium homeostasis in experimental renal failure, we found that a infusion of ANP at 0.25 microgram/min for 15 min produced an increase in the glomerular filtration rate (GFR) and fractional excretion of sodium (FENa) in five-sixth nephrectomized (5/6 Nx) rats. Sodium 62-68 natriuretic peptide A Rattus norvegicus 26-52 2528922-1 1989 Effects of purified rabbit anti-rat 25-amino acid atrial natriuretic peptide (ANP) immunoglobulin G (IgG) on renal sodium excretion and glomerular filtration rate were studied in a rat model of congestive heart failure (CHF) having high circulating ANP levels. Sodium 115-121 natriuretic peptide A Rattus norvegicus 50-76 34363547-3 2022 We hypothesized the association of serum sodium level with CAL complications differs between infants and older patients with KD. Sodium 41-47 filamin binding LIM protein 1 Homo sapiens 59-62 34363547-5 2022 We performed multivariable logistic regression analyses to evaluate the association between serum sodium and CAL complications. Sodium 98-104 filamin binding LIM protein 1 Homo sapiens 109-112 34363547-6 2022 Additionally, we stratified the serum sodium distribution associated with CAL complications by infants and older patients. Sodium 38-44 filamin binding LIM protein 1 Homo sapiens 74-77 2571302-11 1989 It has also been suggested that DA1 may also decrease sodium transport by influencing other hormones, such as atrial natriuretic peptide. Sodium 54-60 immunoglobulin heavy diversity 4-11 (non-functional) Homo sapiens 32-35 2681964-3 1989 Moderate activations of the renal sympathetic nerves, which do not change renal blood flow 1) decrease sodium excretion independent of changes in angiotensin II, 2) interact with the pressure-dependent mechanism of renin release by resetting its threshold pressure and 3) modulate autoregulation by increasing the lower limits of glomerular filtration rate and renal blood flow-autoregulation. Sodium 103-109 renin Canis lupus familiaris 215-220 2512401-3 1989 Oral administration of ES-6864 at 30 mg/kg to conscious, sodium-depleted marmosets produced a significant blood pressure reduction and a significant inhibition of plasma renin activity, which persisted for 6 hours. Sodium 57-63 renin Canis lupus familiaris 170-175 2544529-5 1989 During the first hour after 3 and 10 nmol/kg atrial natriuretic factor-(99-126), the sodium loss was 161 +/- 56 and 139 +/- 42 mueq/kg/hr in vehicle-treated rats and was significantly greater (694 +/- 316 and 1,038 +/- 135 mueq/kg/hr) in rats given 100 mumol/kg SQ 29,072. Sodium 85-91 natriuretic peptide A Rattus norvegicus 45-70 2520625-0 1989 The effect of secretin on sodium ion absorption by the isolated human gallbladder. Sodium 26-32 secretin Homo sapiens 14-22 2544099-0 1989 Adrenergic control of renin during dietary sodium deprivation in conscious dogs. Sodium 43-49 renin Canis lupus familiaris 22-27 2526789-3 1989 ANP injections at the doses of 1, 5, 25 and 50 micrograms/kg increased water and sodium excretion significantly at all but the lowest dose in the controls; only the two largest doses caused clear diuresis and natriuresis in the heart failure group. Sodium 81-87 natriuretic peptide A Rattus norvegicus 0-3 34363547-10 2022 CONCLUSIONS: Serum sodium distribution associated with CAL complications differed greatly between infants and older patients. Sodium 19-25 filamin binding LIM protein 1 Homo sapiens 55-58 34778950-7 2022 The excellent clinical response to carbamazepine observed in the patients carrying the A261T variant suggests an exquisite sensitivity of KCNA1 GoF to sodium channel inhibition that should be further explored. Sodium 151-157 potassium voltage-gated channel subfamily A member 1 Homo sapiens 138-143 34642449-1 2022 Pathological activation of kidney angiotensin II (Ang II) type 1 receptor (AT1R) signaling stimulates tubular sodium transporters, including epithelial sodium channels, to increase sodium reabsorption and blood pressure. Sodium 110-116 angiotensin II, type I receptor-associated protein Mus musculus 75-79 34642449-1 2022 Pathological activation of kidney angiotensin II (Ang II) type 1 receptor (AT1R) signaling stimulates tubular sodium transporters, including epithelial sodium channels, to increase sodium reabsorption and blood pressure. Sodium 152-158 angiotensin II, type I receptor-associated protein Mus musculus 75-79 34642449-1 2022 Pathological activation of kidney angiotensin II (Ang II) type 1 receptor (AT1R) signaling stimulates tubular sodium transporters, including epithelial sodium channels, to increase sodium reabsorption and blood pressure. Sodium 181-187 angiotensin II, type I receptor-associated protein Mus musculus 75-79 34642449-5 2022 Results from genetically engineered mice with modified ATRAP expression show that ATRAP plays a key role in the regulation of renal sodium handling and the modulation of blood pressure in response to pathological stimuli and further suggest that the function of kidney tubule ATRAP may be different between distal tubules and proximal tubules, implying that ATRAP is a target of interest in hypertension. Sodium 132-138 angiotensin II, type I receptor-associated protein Mus musculus 82-87 34740720-5 2022 In vitro, both inflammatory BALF-MVs and AM-MVs decreased the expression of alpha subunit of epithelial sodium channel (alpha-ENaC), gamma-ENaC, and Na+,K+-ATPase alpha1 and beta1 in lung epithelial cells. Sodium 104-110 sodium channel, nonvoltage-gated 1 alpha Mus musculus 120-130 34726508-2 2022 However, the molecular mechanisms underlying regulating voltage-gated sodium channel (Nav1.3) has not been well understood. Sodium 70-76 sodium voltage-gated channel alpha subunit 3 Rattus norvegicus 86-92 2589637-2 1989 The volume density (Vv) of atrial granules, which contain atrial natriuretic peptide (ANP), displayed a 135%-rise in water/sodium-restricted animals. Sodium 123-129 natriuretic peptide A Rattus norvegicus 58-84 2589637-2 1989 The volume density (Vv) of atrial granules, which contain atrial natriuretic peptide (ANP), displayed a 135%-rise in water/sodium-restricted animals. Sodium 123-129 natriuretic peptide A Rattus norvegicus 86-89 2589637-6 1989 Moreover, they suggest that not only blood volume expansion, but also sodium ions can be a potent stimulating factor of ANP release. Sodium 70-76 natriuretic peptide A Rattus norvegicus 120-123 2972583-5 1988 A deficiency of hANF could lead to renal arterial vasoconstriction and avid renal sodium retention as seen in FRFC. Sodium 82-88 HESX homeobox 1 Homo sapiens 16-20 2977165-0 1988 Effect of changes in sodium balance on renin, angiotensinogen and atrial natriuretic factor messenger RNA levels in rats. Sodium 21-27 natriuretic peptide A Rattus norvegicus 66-91 2977165-9 1988 Atrial ANF mRNA levels changed slightly with different levels of sodium intake. Sodium 65-71 natriuretic peptide A Rattus norvegicus 7-10 2849771-7 1988 By 120 min after initiating the infusion in ANP-rats urinary volume and sodium excretion had declined to values not significantly different from those of baseline or control. Sodium 72-78 natriuretic peptide A Rattus norvegicus 44-47 2973246-2 1988 Volume expansion with blood from the reservoir in two steps (of 1 and 1.5% body wt, separated by 1 h, n = 5 rats) produced a mean peak increase in plasma immunoreactive ANF from 99 +/- 21 to 1,310 +/- 230 pg/ml (P less than 0.001); plasma ANF levels throughout these experiments correlated significantly with simultaneously measured urine flow (r = 0.74, P less than 0.005) and sodium excretion (r = 0.65, P less than 0.005). Sodium 378-384 natriuretic peptide A Rattus norvegicus 169-172 2458429-2 1988 In each of these cell types, test depolarizations from the holding potential (-80 or -90 mV) elicited three distinct inward currents: a sodium current (INa) and two calcium currents. Sodium 136-142 internexin neuronal intermediate filament protein alpha Homo sapiens 152-155 3284392-0 1988 Disparity between renal venous norepinephrine and renin responses to sodium depletion. Sodium 69-75 renin Canis lupus familiaris 50-55 3284392-3 1988 At this time plasma renin activity (PRA) was increased from a control level (sodium intake = 45 meq/day) of 0.34 +/- 0.08 to 1.47 +/- 0.26 ng angiotensin I (ANG I).ml-1.h-1 in association with an approximately sixfold increase in the PRA gradient across the kidneys. Sodium 77-83 renin Canis lupus familiaris 20-25 2970886-5 1988 Atrial natriuretic factor reduced collecting duct sodium reabsorption when added to amiloride or hydrochlorothiazide to 23% and to 41%, respectively, but had no additional effect when given with amiloride and hydrochlorothiazide. Sodium 50-56 natriuretic peptide A Rattus norvegicus 0-25 2966998-4 1988 ANF infusion increased the urinary flow (P less than 0.001), the urinary sodium concentration (P less than 0.001), the sodium excretion rate (P less than 0.0001), and improved the glomerular filtration rate (GFR) recovery (P less than 0.02) determined at the end of the 2-hr infusion period. Sodium 73-79 natriuretic peptide A Rattus norvegicus 0-3 2966998-4 1988 ANF infusion increased the urinary flow (P less than 0.001), the urinary sodium concentration (P less than 0.001), the sodium excretion rate (P less than 0.0001), and improved the glomerular filtration rate (GFR) recovery (P less than 0.02) determined at the end of the 2-hr infusion period. Sodium 119-125 natriuretic peptide A Rattus norvegicus 0-3 2450891-6 1988 The reduction rates of pHi induced by a peritubular bicarbonate reduction or sodium removal were attenuated by 20% by withdrawal of ambient chloride. Sodium 77-83 glucose-6-phosphate isomerase Oryctolagus cuniculus 23-26 2456399-1 1988 Block of sodium current (INa) by ethmozin (moricizine), an antiarrhythmic drug, was investigated in isolated, voltage-clamped, canine cardiac Purkinje cells. Sodium 9-15 internexin neuronal intermediate filament protein alpha Canis lupus familiaris 25-28 2962784-7 1988 Our data suggest that decrease in atrial pressure below normal results in a decline in pANF, which, acting in concert with the activated renin-angiotensin system and vasopressin, may contribute to sodium retention. Sodium 197-203 renin Canis lupus familiaris 137-142 34957250-6 2021 A novel heterozygous splicing variant c.2437-2A>C in the sodium voltage-gated channel alpha subunit 5 gene (SCN5A) and a novel heterozygous missense variant c.161A>T (p.(Asp54Val)) in the glycerol-3-phosphate dehydrogenase 1 like gene (GPD1L) were identified in these two patients with BrS-1 and possible BrS-2, respectively. Sodium 57-63 sodium voltage-gated channel alpha subunit 5 Homo sapiens 108-113 2827518-0 1988 Glomerular ANF receptor regulation during changes in sodium and water metabolism. Sodium 53-59 natriuretic peptide A Rattus norvegicus 11-14 2827518-2 1988 A decrease in plasma immunoreactive ANF (IR-ANF) was observed after 4 days of water deprivation or after 1 wk on a low-sodium diet, whereas animals offered 1% NaCl in their drinking water had elevated plasma ANF values. Sodium 119-125 natriuretic peptide A Rattus norvegicus 36-39 2827518-2 1988 A decrease in plasma immunoreactive ANF (IR-ANF) was observed after 4 days of water deprivation or after 1 wk on a low-sodium diet, whereas animals offered 1% NaCl in their drinking water had elevated plasma ANF values. Sodium 119-125 natriuretic peptide A Rattus norvegicus 44-47 2827518-2 1988 A decrease in plasma immunoreactive ANF (IR-ANF) was observed after 4 days of water deprivation or after 1 wk on a low-sodium diet, whereas animals offered 1% NaCl in their drinking water had elevated plasma ANF values. Sodium 119-125 natriuretic peptide A Rattus norvegicus 44-47 2827518-3 1988 Atrial IR-ANF was lower in water-deprived and higher in sodium-restricted rats than in their respective controls. Sodium 56-62 natriuretic peptide A Rattus norvegicus 10-13 2827518-4 1988 A low-sodium intake or water deprivation increased the density of glomerular ANF receptors, whereas the inverse occurred with a high-salt consumption. Sodium 6-12 natriuretic peptide A Rattus norvegicus 77-80 34863181-2 2021 Stimulation of epithelial sodium channel (ENaC) increases Na+ transport, which is a driving force to keep tracheal mucosa free edema fluid during tracheal injury. Sodium 26-32 sodium channel, nonvoltage-gated 1 alpha Mus musculus 42-46 34884836-0 2021 Zfhx3 Transcription Factor Represses the Expression of SCN5A Gene and Decreases Sodium Current Density (INa). Sodium 80-86 zinc finger homeobox 3 Homo sapiens 0-5 34623182-1 2021 BACKGROUND: Cardiac voltage-gated sodium channel gain-of-function prolongs repolarization in the Long-QT Syndrome Type 3 (LQT3). Sodium 34-40 sodium voltage-gated channel alpha subunit 5 Homo sapiens 122-126 34623182-4 2021 We hypothesized that elevated extracellular sodium concentration and widened perinexus synergistically prolong APD in LQT3. Sodium 44-50 sodium voltage-gated channel alpha subunit 5 Homo sapiens 118-122 34623182-16 2021 Therefore, this is the first study to provide evidence of a tractable and effective strategy to mitigate LQT3 phenotype by managing patient sodium levels and preventing cardiac edema. Sodium 140-146 sodium voltage-gated channel alpha subunit 5 Homo sapiens 105-109 34703915-8 2021 Sodium-dependent VC transporter 1 and 2 (SVCT1 and SVCT2) expressions were higher in ileum than in duodenum and jejunum (P < 0.05). Sodium 0-6 solute carrier family 23 member 1 Homo sapiens 41-46 34852780-1 2021 BACKGROUND: Non-dystrophic myotonias (NDMs) comprise muscle chloride and sodium channelopathies due to genetic defects of the CLCN1- and SCN4A-channels. Sodium 73-79 sodium voltage-gated channel alpha subunit 4 Homo sapiens 137-142 33535892-8 2021 Furthermore, both mexiletine and the common polymorphism H558R restored peak sodium current (I Na) amplitude of the mutant channel by increasing the cell surface expression of SCN5A. Sodium 77-83 sodium voltage-gated channel alpha subunit 5 Homo sapiens 176-181 34779863-8 2021 Both the mRNA and protein expression of GRK4 and its downstream target AT1R were increased in offspring of PM2.5-exposed paternal rats, which was reflected in its function because treatment with losartan, an AT1R antagonist, decreased the blood pressure and increased urine volume and sodium excretion. Sodium 285-291 G protein-coupled receptor kinase 4 Rattus norvegicus 40-44 34840533-1 2021 SLC13A4 is a sodium sulfate co-transporter, which is expressed in brains, placentas, thymes and other tissues, plays an essential role in maintaining the metabolic balance of sulfate in vivo. Sodium 13-19 solute carrier family 13 member 4 Homo sapiens 0-7 34737403-7 2021 We identified one key target for the effects of tau, the voltage gated sodium channel, which could account for the effects of tau on the action potential. Sodium 71-77 microtubule associated protein tau Homo sapiens 48-51 34737403-7 2021 We identified one key target for the effects of tau, the voltage gated sodium channel, which could account for the effects of tau on the action potential. Sodium 71-77 microtubule associated protein tau Homo sapiens 126-129 34803699-1 2021 Over 1,500 missense variants of sodium channel hNav1.5, which are reported in the ClinVar database, are associated with cardiac diseases. Sodium 32-38 sodium voltage-gated channel alpha subunit 5 Homo sapiens 47-54 34892380-3 2021 This paper aims to model a two dimensional SCN5A L812Q mutated endocardial tissue by modifying the model equations for sodium ion channel in the Ten Tusscher model for human ventricular tissue. Sodium 119-125 sodium voltage-gated channel alpha subunit 5 Homo sapiens 43-48 2829999-5 1988 The elevation in the number of binding sites for atrial natriuretic factor may serve as a compensatory mechanism acting in part to lower fluid volume and sodium levels prior to the precipitous increase in blood pressure which occurs in S/JR rats by 10 weeks of age. Sodium 154-160 natriuretic peptide A Rattus norvegicus 49-74 2465105-7 1988 Moderate increases in urine volume, sodium and chloride excretion were seen after infusion of dextran and subsequent infusion of ANF markedly enhanced these renal effects. Sodium 36-42 natriuretic peptides A Ovis aries 129-132 2964552-0 1988 Effect of sodium ion on atrial natriuretic factor release from rat hypothalamic fragments. Sodium 10-16 natriuretic peptide A Rattus norvegicus 24-49 3244802-4 1988 The temperature dependence of delta nu 1/2 in all cases leads to the conclusion that RBc (the average relaxation rate of sodium nuclei that remain bound in the coil state of DNA) tends to zero. Sodium 121-127 RNA, 7SL, cytoplasmic 263, pseudogene Homo sapiens 85-88 3690229-1 1987 The plasma sodium concentration, [Na]P, falls following major surgery and this fall is exacerbated by the administration of sodium-free or sodium-low intravenous fluids in the postoperative period. Sodium 11-17 catenin beta like 1 Homo sapiens 34-38 3690229-1 1987 The plasma sodium concentration, [Na]P, falls following major surgery and this fall is exacerbated by the administration of sodium-free or sodium-low intravenous fluids in the postoperative period. Sodium 124-130 catenin beta like 1 Homo sapiens 34-38 3690229-1 1987 The plasma sodium concentration, [Na]P, falls following major surgery and this fall is exacerbated by the administration of sodium-free or sodium-low intravenous fluids in the postoperative period. Sodium 124-130 catenin beta like 1 Homo sapiens 34-38 2954472-7 1987 The ANF-induced increases in sodium excretion were not significantly different between UNT and BEA rats at any ANF dose. Sodium 29-35 natriuretic peptide A Rattus norvegicus 4-7 2954473-11 1987 These studies suggest that atrial natriuretic factor could influence the long-term control of arterial pressure by altering renal medullary hemodynamics and promoting the elimination of sodium and water. Sodium 186-192 natriuretic peptide A Rattus norvegicus 27-52 3573987-1 1987 Sodium depletion in dogs is known to affect both the renin-angiotensin as well as the sympathetic nervous system. Sodium 0-6 renin Canis lupus familiaris 53-58 2953260-9 1987 Infusion of ANF at a dose to mimic PANF obtained during acute volume expansion resulted in a fourfold increase in the fractional excretion of sodium. Sodium 142-148 natriuretic peptide A Rattus norvegicus 12-15 2953252-0 1987 Blunted natriuresis to atrial natriuretic peptide in chronic sodium-retaining disorders. Sodium 61-67 natriuretic peptide A Rattus norvegicus 23-49 2953252-4 1987 In control animals, atrial natriuretic peptide increased absolute and fractional urine flow rate and urinary sodium excretion. Sodium 109-115 natriuretic peptide A Rattus norvegicus 20-46 3309255-9 1987 It was found that intranasal absorption of sodium insulin was not significantly different from that of zinc insulin. Sodium 43-49 LOC105613195 Ovis aries 50-57 2951600-0 1987 Atrial natriuretic peptide inhibits angiotensin-stimulated proximal tubular sodium and water reabsorption. Sodium 76-82 natriuretic peptide A Rattus norvegicus 0-26 2951600-7 1987 Thus at physiological concentrations ANP acts within the kidney to decrease proximal reabsorption by inhibition of angiotensin-stimulated sodium and water transport. Sodium 138-144 natriuretic peptide A Rattus norvegicus 37-40 3551630-5 1987 These findings indicate that in fistula dogs enhanced medullary sodium reabsorption is associated with decreased PPF and stimulation of the renin-angiotensin and adrenergic nervous system. Sodium 64-70 renin Canis lupus familiaris 140-145 3030871-5 1987 This regulatory range of pHi (= 0.7 pH units) was abolished by sodium-free Ringer"s or addition of 10(-3) M amiloride and also by 10(-4) M ouabain. Sodium 63-69 glucose-6-phosphate isomerase Oryctolagus cuniculus 25-28 3029528-0 1987 Effect of sodium ion on the affinity of naloxone for the kappa opioid receptor. Sodium 10-16 opioid receptor kappa 1 Homo sapiens 57-78 3815338-3 1987 Transport of melphalan by BALB/c 3T3 fibroblasts was mediated by the two amino acid transport systems, the DL-beta-2-aminobicyclo(2,2,1)heptane-2-carboxylic acid-sensitive sodium-independent system preferring leucine as substrate and the sodium-dependent system preferring alanine, serine, and cysteine as substrates. Sodium 172-178 hemoglobin, beta adult minor chain Mus musculus 110-116 3815338-3 1987 Transport of melphalan by BALB/c 3T3 fibroblasts was mediated by the two amino acid transport systems, the DL-beta-2-aminobicyclo(2,2,1)heptane-2-carboxylic acid-sensitive sodium-independent system preferring leucine as substrate and the sodium-dependent system preferring alanine, serine, and cysteine as substrates. Sodium 238-244 hemoglobin, beta adult minor chain Mus musculus 110-116 34481380-1 2021 The Na+/Ca2+ exchanger NCX3 is an important regulator of sodium and calcium homeostasis in oligodendrocyte lineage. Sodium 57-63 solute carrier family 8 member A3 Rattus norvegicus 23-27 2892671-18 1987 There is preliminary evidence that cyclic GMP may inhibit renin secretion and sodium transport in kidney cells. Sodium 78-84 5'-nucleotidase, cytosolic II Homo sapiens 42-45 2824688-6 1987 Presynaptic markers of glutamate neurons (glutamate levels and glutamate sodium-dependent binding) are reduced 25-80% in cortex and hippocampus of DAT brain. Sodium 73-79 solute carrier family 6 member 3 Homo sapiens 147-150 34296787-8 2021 In addition, sodium channel protein type 3 subunit alpha isoform 1 (Nav1.3) and TLR4 were identified as targets of miR-214-3p via dual-luciferase reporter assay. Sodium 13-19 sodium voltage-gated channel alpha subunit 3 Rattus norvegicus 68-74 34465632-0 2021 RCTR1 promotes alveolar fluid clearance by activating alveolar epithelial sodium channels and Na, K-ATPase in LPS-induced acute lung injury. Sodium 74-80 solute carrier family 31 member 1 Rattus norvegicus 0-5 3598850-3 1987 Calcium, magnesium, potassium, and sodium initially stimulated NAT activity, and as the cation concentration increased inhibitory activity was observed. Sodium 35-41 bromodomain containing 2 Homo sapiens 63-66 34465632-6 2021 Furthermore, RCTR1 remarkably elevated the protein expression of sodium channels and Na, K-ATPase, and the activity of Na, K-ATPase in vivo and in vitro. Sodium 65-71 solute carrier family 31 member 1 Rattus norvegicus 13-18 3025550-2 1987 Recent data have also shown that low extracellular potassium (K+) concentration or ouabain also inhibits PTH release to an extent comparable to that seen with high Ca++ and produce a marked rise in the intracellular sodium (Na+) content. Sodium 216-222 parathyroid hormone Bos taurus 105-108 34465632-9 2021 In summary, RCTR1 enhances the protein levels of sodium channels and Na, K-ATPase, and the Na, K-ATPase activity to improve AFC in ALI through ALX/cAMP/PI3K/Nedd4-2 pathway, suggesting that RCTR1 may become a therapeutic drug for ARDS/ALI. Sodium 49-55 solute carrier family 31 member 1 Rattus norvegicus 12-17 34411705-2 2021 Sodium-calcium exchanger (NCX) is a membrane antiporter that, operating in a bidirectional way, couples the exchange of Ca2+ and Na + ions in neurons and glial cells, thus controlling the intracellular homeostasis of these ions. Sodium 0-6 T cell leukemia, homeobox 2 Mus musculus 26-29 3744467-2 1986 The infusion of PAF into the renal artery at 5, 10, and 20 ng X min-1 X kg-1 body weight resulted in dose-dependent reductions in renal blood flow, glomerular filtration rate, urine volume, and urinary sodium excretion, whereas the infusion of vehicle alone in the contralateral kidney did not result in significant changes in these parameters. Sodium 202-208 PCNA clamp associated factor Rattus norvegicus 16-19 2942748-0 1986 Increase in plasma atrial natriuretic polypeptide (ANP) following sodium load in anesthetized rats. Sodium 66-72 natriuretic peptide A Rattus norvegicus 51-54 2942748-6 1986 These results suggest that sodium ions may be a stimulating factor of ANP release as well as volume expansion. Sodium 27-33 natriuretic peptide A Rattus norvegicus 70-73 3099707-9 1986 We conclude that: acute renal failure in kidney graft recipients with TRAS is frequent, but not mandatory; sodium depletion induced by diuretics enhances the fall in GFR; acute effect of captopril must be assessed in patients with TRAS before the use of this product as long term antihypertensive treatment. Sodium 107-113 Rap guanine nucleotide exchange factor 5 Homo sapiens 166-169 2941534-1 1986 Chronic infusion of atrial natriuretic factor (ANF) decreased blood pressure in two-kidney, one clip (2-K, 1C), spontaneously hypertensive rat (SHR) and one-kidney, one clip (1-K, 1C) models of experimental hypertension in the rat, but produced increased sodium excretion only in the 1-K, 1C model. Sodium 255-261 natriuretic peptide A Rattus norvegicus 20-45 2941534-1 1986 Chronic infusion of atrial natriuretic factor (ANF) decreased blood pressure in two-kidney, one clip (2-K, 1C), spontaneously hypertensive rat (SHR) and one-kidney, one clip (1-K, 1C) models of experimental hypertension in the rat, but produced increased sodium excretion only in the 1-K, 1C model. Sodium 255-261 natriuretic peptide A Rattus norvegicus 47-50 2941540-6 1986 The data available so far suggest that ANF, apart from its effect on collecting-duct permeability, interferes with several control and feedback systems involved in sodium input into the collecting-duct system. Sodium 164-170 natriuretic peptide A Rattus norvegicus 39-42 34769164-6 2021 Several brain areas control sodium appetite, including the nucleus of the solitary tract, which contains aldosterone-sensitive HSD2 neurons, and the organum vasculosum lamina terminalis (OVLT) that contains ANG II-sensitive neurons. Sodium 28-34 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 127-131 34733169-12 2021 We hypothesize that the obtained upregulation of cardiac and renal PCSK6/corin in rats with compensated CHF may represent a compensatory response aiming at maintaining normal Na+ balance, whereas the decline in these two enzymes may contribute to the pathogenesis of avid sodium retention, cardiac hypertrophy, and blunted atrial natriuretic peptide/brain natriuretic peptide actions in decompensated CHF. Sodium 272-278 corin, serine peptidase Rattus norvegicus 73-78 2937808-0 1986 Role of atrial natriuretic peptide in adaptation of sodium excretion with reduced renal mass. Sodium 52-58 natriuretic peptide A Rattus norvegicus 8-34 2948068-2 1986 After determination of basal renal function, ANF at different doses induced a dose dependent increase of glomerular filtration rate (GFR), diuresis (V), sodium (UNaV) and potassium (UKV) excretion. Sodium 153-159 natriuretic peptide A Rattus norvegicus 45-48 34343486-0 2021 Dysfunction of Cullin 3 RING E3 ubiquitin ligase causes vasoconstriction and increased sodium reabsorption in diabetes. Sodium 87-93 mitochondrial ubiquitin ligase activator of NFKB 1 Mus musculus 29-48 34615708-8 2021 HIF1alpha silencing increased betaENaC and gammaENaC expression and stimulated sodium transport. Sodium 79-85 hypoxia inducible factor 1, alpha subunit Mus musculus 0-9 2946967-9 1986 In addition, a tremendous rise in fractional excretion rates of sodium and potassium after administration of ANF was observed. Sodium 64-70 natriuretic peptide A Rattus norvegicus 109-112 34280395-0 2021 Contributions of S- and R-citalopram to the citalopram-induced modulation of the function of Nav1.5 voltage-gated sodium channels. Sodium 114-120 sodium voltage-gated channel alpha subunit 5 Homo sapiens 93-99 4073294-5 1985 Unilateral PTH infusion did cause a significant unilateral increase in sodium excretion and significant bilateral phosphaturia. Sodium 71-77 parathyroid hormone Bos taurus 11-14 34280395-4 2021 In this study, we investigated whether citalopram, escitalopram and R-citalopram had an electrophysiological effect on Nav1.5 voltage-gated sodium channel (VGSC) current and how their electrophysiological properties affected Nav1.5 VGSC. Sodium 140-146 sodium voltage-gated channel alpha subunit 5 Homo sapiens 119-125 2856728-1 1985 Intrarenal infusion of atrial natriuretic factor has been reported to increase renal blood flow and sodium excretion, and either to depress or not to affect renin release. Sodium 100-106 natriuretic peptide A Rattus norvegicus 23-48 34610204-1 2022 AIMS: To evaluate the effectiveness and safety of the novel sodium-glucose cotransporter (SGLT2) inhibitor ertugliflozin compared to placebo or other antihyperglycemic agents (AHAs) for type 2 diabetes. Sodium 60-66 solute carrier family 5 member 2 Homo sapiens 90-95 2937944-0 1985 [Chronic effects of synthetic rat atrial natriuretic factor (ANF) on blood pressure and sodium-water excretion in conscious rats]. Sodium 88-94 natriuretic peptide A Rattus norvegicus 34-59 2937944-0 1985 [Chronic effects of synthetic rat atrial natriuretic factor (ANF) on blood pressure and sodium-water excretion in conscious rats]. Sodium 88-94 natriuretic peptide A Rattus norvegicus 61-64 2933035-3 1985 Sodium ion and osmotic pressure stimulated the release of ANP in the hyperosmotic but not in the hypo-osmotic range. Sodium 0-6 natriuretic peptide A Rattus norvegicus 58-61 34671263-1 2021 The voltage-gated sodium channel Nav1.4 is a major actor in the excitability of skeletal myofibers, driving the muscle force in response to nerve stimulation. Sodium 18-24 sodium voltage-gated channel alpha subunit 4 Homo sapiens 33-39 2931997-5 1985 During continued infusion of ANF, GFR stabilized at increased levels, but sodium and water excretion continued to increase. Sodium 74-80 natriuretic peptide A Rattus norvegicus 29-32 2931997-7 1985 Infusion of a low concentration of ANF (3 ng/ml) significantly increased sodium and water excretion without changing either GFR or potassium excretion. Sodium 73-79 natriuretic peptide A Rattus norvegicus 35-38 4064378-6 1985 SST corrects sodium/volume balance in this group by using sequential intermittent hypo or hypertonic dialysate, combined with fluid removal adapted to each episode. Sodium 13-19 somatostatin Homo sapiens 0-3 34671263-2 2021 Supporting further this key role, mutations in SCN4A, the gene encoding the pore-forming alpha subunit of Nav1.4, are responsible for a clinical spectrum of human diseases ranging from muscle stiffness (sodium channel myotonia, SCM) to muscle weakness. Sodium 203-209 sodium voltage-gated channel alpha subunit 4 Homo sapiens 47-52 34671263-2 2021 Supporting further this key role, mutations in SCN4A, the gene encoding the pore-forming alpha subunit of Nav1.4, are responsible for a clinical spectrum of human diseases ranging from muscle stiffness (sodium channel myotonia, SCM) to muscle weakness. Sodium 203-209 sodium voltage-gated channel alpha subunit 4 Homo sapiens 106-112 34423678-0 2021 Experimental nephrotic syndrome leads to proteolytic activation of the epithelial sodium channel (ENaC) in the mouse kidney. Sodium 82-88 sodium channel, nonvoltage-gated 1 alpha Mus musculus 98-102 34423678-1 2021 Proteolytic activation of the renal epithelial sodium channel ENaC involves cleavage events in its alpha- and gamma-subunits and is thought to mediate sodium retention in nephrotic syndrome (NS). Sodium 47-53 sodium channel, nonvoltage-gated 1 alpha Mus musculus 62-66 34423678-1 2021 Proteolytic activation of the renal epithelial sodium channel ENaC involves cleavage events in its alpha- and gamma-subunits and is thought to mediate sodium retention in nephrotic syndrome (NS). Sodium 151-157 sodium channel, nonvoltage-gated 1 alpha Mus musculus 62-66 34461117-2 2021 In LQTS3 and BrS different mutations in the SCN5A gene lead to a gain-or a loss-of-function of the voltage-gated sodium channel Nav1.5, respectively. Sodium 113-119 sodium voltage-gated channel alpha subunit 5 Homo sapiens 44-49 34461117-2 2021 In LQTS3 and BrS different mutations in the SCN5A gene lead to a gain-or a loss-of-function of the voltage-gated sodium channel Nav1.5, respectively. Sodium 113-119 sodium voltage-gated channel alpha subunit 5 Homo sapiens 128-134 34416509-5 2021 Moreover, these compounds" selectivity was investigated on sodium channels Nav1.2, Nav1.4 and Nav1.5 and calcium channels Cav3.1-Cav3.3. Sodium 59-65 sodium voltage-gated channel alpha subunit 4 Homo sapiens 83-89 34461752-1 2021 BACKGROUND: Brugada syndrome (BrS) is associated with mutations in the cardiac sodium channel gene, SCN5A. Sodium 79-85 sodium voltage-gated channel alpha subunit 5 Homo sapiens 100-105 34520724-1 2021 The heartbeat is initiated by voltage-gated sodium channel NaV1.5, which opens rapidly and triggers the cardiac action potential; however, the structural basis for pore opening remains unknown. Sodium 44-50 sodium voltage-gated channel alpha subunit 5 Homo sapiens 59-65 34091433-0 2021 Corrigendum to "Voltage-gated sodium channel Nav1.5 promotes tumor progression and enhances chemosensitivity to 5-fluorouracil in colorectal cancer" (Canc. Sodium 30-36 sodium voltage-gated channel alpha subunit 5 Homo sapiens 45-51 34584093-0 2021 Cryo-EM structure of the sodium-driven chloride/bicarbonate exchanger NDCBE. Sodium 25-31 solute carrier family 4 member 8 Homo sapiens 70-75 34698059-6 2021 Notably, systemic delivery of renadirsen sodium promoted dystrophin exon skipping in cardiac muscle, skeletal muscle, and diaphragm, compared with AOs with the same sequence as renadirsen but conventionally modified by PMO and 2"OMePS. Sodium 41-47 dystrophin Homo sapiens 57-67 3929618-3 1985 During the AVP infusion, there were significant increases in amniotic fluid osmolality (278.8 +/- 4.9 to 302.1 +/- 4.5 mosm) and in sodium (122.7 +/- 3.3 to 135.3 +/- 3.6 meq/l) and potassium (9.7 +/- 2.6 to 13.8 +/- 1.3 meq/l) concentrations. Sodium 132-138 vasopressin-neurophysin 2-copeptin Ovis aries 11-14 2866274-13 1985 Plasma renin activity was significantly decreased after S 3341 treatment in dogs on low normal or high sodium diets. Sodium 103-109 renin Canis lupus familiaris 7-12 3926510-0 1985 Is the renal kallikrein system relevant to sodium sensitivity in patients with essential hypertension. Sodium 43-49 kallikrein related peptidase 4 Homo sapiens 13-23 3926510-9 1985 For all patients, urinary kallikrein excretion at the end of the low sodium period (123(SEM 20.3) micrograms 24 h-1) was significantly higher than at the end of the first control period (96(SEM 16.3) micrograms 24 h-1, P less than 0.01) and at the end of the high sodium period (96(SEM 23.7) micrograms 24(-1), P less than 0.01). Sodium 69-75 kallikrein related peptidase 4 Homo sapiens 26-36 3926510-9 1985 For all patients, urinary kallikrein excretion at the end of the low sodium period (123(SEM 20.3) micrograms 24 h-1) was significantly higher than at the end of the first control period (96(SEM 16.3) micrograms 24 h-1, P less than 0.01) and at the end of the high sodium period (96(SEM 23.7) micrograms 24(-1), P less than 0.01). Sodium 264-270 kallikrein related peptidase 4 Homo sapiens 26-36 3926510-10 1985 When compared with salt-insensitive patients, salt-sensitives had lower levels of urinary kallikrein excretion and a blunted kallikrein response to dietary sodium restriction and furosemide. Sodium 156-162 kallikrein related peptidase 4 Homo sapiens 125-135 2580273-1 1985 The effects of micromolar concentrations of racemic D600 on the transmembrane inward sodium current (INa) were investigated in voltage clamped, intracellularly perfused, human heart cell segments. Sodium 85-91 internexin neuronal intermediate filament protein alpha Homo sapiens 101-104 2981380-2 1985 The results proved conclusively that ANF acted directly on the kidney since urine volume and fractional excretion of sodium, potassium, chloride and calcium were elevated in a dose-related manner in the ANF-treated kidney, but were not significantly affected in the contralateral saline-infused organ. Sodium 117-123 natriuretic peptide A Rattus norvegicus 37-40 2981380-2 1985 The results proved conclusively that ANF acted directly on the kidney since urine volume and fractional excretion of sodium, potassium, chloride and calcium were elevated in a dose-related manner in the ANF-treated kidney, but were not significantly affected in the contralateral saline-infused organ. Sodium 117-123 natriuretic peptide A Rattus norvegicus 203-206 3978310-1 1985 The effects of several anticonvulsant drugs on sodium-dependent high affinity choline uptake (HACU) in mouse hippocampal synaptosomes was investigated. Sodium 47-53 high affinity choline uptake Mus musculus 94-98 4017266-0 1985 Studies on the role of intracellular sodium and calcium in the centrally mediated pressor effects of CSF [Na+], ouabain and angiotensin II in anesthetized dogs. Sodium 37-43 colony stimulating factor 2 Canis lupus familiaris 101-104 34630451-1 2021 The Salt-Overly-Sensitive (SOS) pathway controls the net uptake of sodium by roots and the xylematic transfer to shoots in vascular plants. Sodium 67-73 sodium proton exchanger, putative (NHX7) (SOS1) Arabidopsis thaliana 27-30 34630451-2 2021 SOS3/CBL4 is a core component of the SOS pathway that senses calcium signaling of salinity stress to activate and recruit the protein kinase SOS2/CIPK24 to the plasma membrane to trigger sodium efflux by the Na/H exchanger SOS1/NHX7. Sodium 187-193 sodium proton exchanger, putative (NHX7) (SOS1) Arabidopsis thaliana 37-40 34630451-2 2021 SOS3/CBL4 is a core component of the SOS pathway that senses calcium signaling of salinity stress to activate and recruit the protein kinase SOS2/CIPK24 to the plasma membrane to trigger sodium efflux by the Na/H exchanger SOS1/NHX7. Sodium 187-193 sodium proton exchanger, putative (NHX7) (SOS1) Arabidopsis thaliana 223-227 34495195-5 2021 After exposure to the aqueous extract, the highest (P<0.05) glucose concentration and the lowest (P<0.05) plasma sodium level were when the fish were exposed to the S. erecta concentration of 50 microg mL-1. Sodium 113-119 L1 cell adhesion molecule Mus musculus 202-206 34564625-3 2021 GTx1-15 is an ICK peptide that inhibits the voltage-dependent calcium channel Cav3.1 and the voltage-dependent sodium channels Nav1.3 and Nav1.7. Sodium 111-117 sodium voltage-gated channel alpha subunit 3 Homo sapiens 127-133 2981062-3 1985 Alpha MSH (8 micrograms/day) restored plasma levels of aldosterone to normal in hypophysectomized rats on the low sodium diet. Sodium 114-120 proopiomelanocortin Rattus norvegicus 0-9 4038777-3 1985 Since it has been reported that the primary site of inappropriate sodium reabsorption by the newborn kidney during saline expansion is in the distal nephron and since the atrial natriuretic factor (ANF has been reported to inhibit sodium reabsorption in this region of the nephron, results of the current study are consistent with the hypothesis that the compromised ability of the newborn to excrete a sodium load is related to a deficiency of ANF. Sodium 66-72 natriuretic peptide A Rattus norvegicus 198-201 4038777-3 1985 Since it has been reported that the primary site of inappropriate sodium reabsorption by the newborn kidney during saline expansion is in the distal nephron and since the atrial natriuretic factor (ANF has been reported to inhibit sodium reabsorption in this region of the nephron, results of the current study are consistent with the hypothesis that the compromised ability of the newborn to excrete a sodium load is related to a deficiency of ANF. Sodium 231-237 natriuretic peptide A Rattus norvegicus 171-196 4038777-3 1985 Since it has been reported that the primary site of inappropriate sodium reabsorption by the newborn kidney during saline expansion is in the distal nephron and since the atrial natriuretic factor (ANF has been reported to inhibit sodium reabsorption in this region of the nephron, results of the current study are consistent with the hypothesis that the compromised ability of the newborn to excrete a sodium load is related to a deficiency of ANF. Sodium 231-237 natriuretic peptide A Rattus norvegicus 198-201 4038777-3 1985 Since it has been reported that the primary site of inappropriate sodium reabsorption by the newborn kidney during saline expansion is in the distal nephron and since the atrial natriuretic factor (ANF has been reported to inhibit sodium reabsorption in this region of the nephron, results of the current study are consistent with the hypothesis that the compromised ability of the newborn to excrete a sodium load is related to a deficiency of ANF. Sodium 231-237 natriuretic peptide A Rattus norvegicus 171-196 4038777-3 1985 Since it has been reported that the primary site of inappropriate sodium reabsorption by the newborn kidney during saline expansion is in the distal nephron and since the atrial natriuretic factor (ANF has been reported to inhibit sodium reabsorption in this region of the nephron, results of the current study are consistent with the hypothesis that the compromised ability of the newborn to excrete a sodium load is related to a deficiency of ANF. Sodium 231-237 natriuretic peptide A Rattus norvegicus 198-201 3858700-8 1985 The above results suggest that the renal kallikrein-kinin and prostaglandin systems may play a role in sodium homeostasis during pregnancy. Sodium 103-109 kallikrein related peptidase 4 Homo sapiens 41-51 6597453-1 1984 The PGE2/PGF2 alpha balance, controlled in part by prostaglandin-9-ketoreductase, seems to be involved in the regulation of sodium excretion by the kidney. Sodium 124-130 carbonyl reductase 1 Homo sapiens 51-80 6745606-5 1984 Motilin infusion significantly reduced absorption of water, sodium, potassium, and chloride when a plasmalike electrolyte solution was perfused. Sodium 60-66 motilin Homo sapiens 0-7 6086172-11 1984 The reduced contractile response of cells grown in 1 mM extracellular potassium and ouabain (but not isoproterenol) supports the view that elevated intracellular sodium due to Na,K-ATPase inhibition mediates the positive inotropic response to low extracellular potassium and ouabain, probably via augmented transsarcolemmal sodium-calcium exchange. Sodium 162-168 ATPase Na+/K+ transporting subunit alpha 1 Gallus gallus 176-187 6086172-11 1984 The reduced contractile response of cells grown in 1 mM extracellular potassium and ouabain (but not isoproterenol) supports the view that elevated intracellular sodium due to Na,K-ATPase inhibition mediates the positive inotropic response to low extracellular potassium and ouabain, probably via augmented transsarcolemmal sodium-calcium exchange. Sodium 324-330 ATPase Na+/K+ transporting subunit alpha 1 Gallus gallus 176-187 6611473-12 1984 The calculated sodium permeabilities were for arterioles: PNa+ = 1.6 x 10(-5) cm sec(-1) and for venules: 4.6 x 10(-5) cm sec(-1). Sodium 15-21 secretory blood group 1, pseudogene Homo sapiens 81-87 27785998-1 1984 The renin-angiotensin system (RAS) is suppressed either by high sodium intake or by high levels of angiotensin II (A II). Sodium 64-70 renin Canis lupus familiaris 4-9 27785998-9 1984 Plasma renin activity increased in all groups after CEI; however, renin secretion was suppressed by much smaller rates of angiotensin II infusion in the normal and sodium loaded dogs than in the sodium depleted dogs. Sodium 164-170 renin Canis lupus familiaris 66-71 27785998-9 1984 Plasma renin activity increased in all groups after CEI; however, renin secretion was suppressed by much smaller rates of angiotensin II infusion in the normal and sodium loaded dogs than in the sodium depleted dogs. Sodium 195-201 renin Canis lupus familiaris 66-71 27785998-12 1984 Also A II infusion and high dietary sodium can have independent effects on both plasma renin activity and plasma aldosterone concentration. Sodium 36-42 renin Canis lupus familiaris 87-92 6714653-2 1984 This assay which is based on the sodium-retaining action of PRL in the hypophysectomized killifish, Fundulus heteroclitus, has proved to be rapid, sensitive (250 pg PRL per gram of fish), and specific. Sodium 33-39 prolactin Fundulus heteroclitus 60-63 6714653-2 1984 This assay which is based on the sodium-retaining action of PRL in the hypophysectomized killifish, Fundulus heteroclitus, has proved to be rapid, sensitive (250 pg PRL per gram of fish), and specific. Sodium 33-39 prolactin Fundulus heteroclitus 165-168 34251271-1 2021 The epithelial sodium channel (ENaC) constitutes the rate-limiting step for sodium absorption in the aldosterone-sensitive distal nephron (ASDN) comprising the late distal convoluted tubule (DCT2), the connecting tubule (CNT) and the collecting duct. Sodium 15-21 sodium channel, nonvoltage-gated 1 alpha Mus musculus 31-35 34251271-1 2021 The epithelial sodium channel (ENaC) constitutes the rate-limiting step for sodium absorption in the aldosterone-sensitive distal nephron (ASDN) comprising the late distal convoluted tubule (DCT2), the connecting tubule (CNT) and the collecting duct. Sodium 76-82 sodium channel, nonvoltage-gated 1 alpha Mus musculus 31-35 34133772-1 2021 Retigabine (RTG, Ezogabine, DC23129) is the first neuronal potassium channel opener in the treatment of epilepsy and exerts its effects through the activation of neuronal KCNQ2/3 potassium channels, in higher doses, acts also on sodium and voltage-gated calcium channels. Sodium 229-235 potassium voltage-gated channel subfamily Q member 2 Rattus norvegicus 171-178 34320850-3 2021 Recent genetic studies have identified potentially pathogenic gain-of-function mutations in several the pore-forming voltage-gated sodium channel alpha subunits (NaVs) in a subset of patients with SFN, but the auxiliary sodium channel beta subunits have been less implicated in the development of the disease. Sodium 131-137 RNA exonuclease 2 Homo sapiens 197-200 34320850-6 2021 Here, we provide the first evidence for the involvement of a sodium channel beta subunit mutation in the pathogenesis of SFN with no other known causes. Sodium 61-67 RNA exonuclease 2 Homo sapiens 121-124 34062068-7 2021 Among the candidate transporters mediating lithium reabsorption examined herein, the mRNA expression of only PiT2, a sodium-dependent phosphate transporter, exhibited sexual dimorphism. Sodium 117-123 solute carrier family 20 member 2 Rattus norvegicus 109-113 6541751-6 1984 However, the precise role of atrial natriuretic factor in sodium homeostasis remains to be elucidated. Sodium 58-64 natriuretic peptide A Rattus norvegicus 29-54 6355550-0 1983 The role of the renal kallikrein-kinin system in sodium metabolism in normal and low renin essential hypertension. Sodium 49-55 kallikrein related peptidase 4 Homo sapiens 22-32 6685566-7 1983 It is suggested that atrial natriuretic factor might inhibit sodium transport in nephron segments beyond the medullary thick ascending limb. Sodium 61-67 natriuretic peptide A Rattus norvegicus 21-46 6851418-7 1983 Glomerular filtration rate and renal blood flow were not affected by atrial extract, indicating that the atrial natriuretic factor (ANF) directly inhibited sodium reabsorption at the tubular level. Sodium 156-162 natriuretic peptide A Rattus norvegicus 105-130 6851418-7 1983 Glomerular filtration rate and renal blood flow were not affected by atrial extract, indicating that the atrial natriuretic factor (ANF) directly inhibited sodium reabsorption at the tubular level. Sodium 156-162 natriuretic peptide A Rattus norvegicus 132-135 6851418-12 1983 We conclude that (a) the renal response to ANF is not affected by pentobarbitone anaesthesia, (b) the renal response to ANF is dependent on the state of the extracellular fluid volume of the animal and (c) that ANF inhibits sodium reabsorption in the distal nephron. Sodium 224-230 natriuretic peptide A Rattus norvegicus 120-123 6851418-12 1983 We conclude that (a) the renal response to ANF is not affected by pentobarbitone anaesthesia, (b) the renal response to ANF is dependent on the state of the extracellular fluid volume of the animal and (c) that ANF inhibits sodium reabsorption in the distal nephron. Sodium 224-230 natriuretic peptide A Rattus norvegicus 120-123 6549759-9 1983 Dietary sodium restriction increased the excretion of total kallikrein by 30%; active kallikrein increased 82%, while inactive kallikrein excretion was found to be unchanged. Sodium 8-14 kallikrein related peptidase 4 Homo sapiens 60-70 34403567-4 2022 We recently determined multiple structures of the human sodium-dependent citrate transporter (NaCT) and the succinate/dicarboxylate transporter from Lactobacillus acidophilus (LaINDY). Sodium 56-62 solute carrier family 13 member 5 Homo sapiens 94-98 34483955-0 2021 Activation of the Thiazide-Sensitive Sodium-Chloride Cotransporter by Beta3-Adrenoreceptor in the Distal Convoluted Tubule. Sodium 37-43 adrenergic receptor, beta 3 Mus musculus 70-90 34434164-8 2021 Extending our risk analyses to a larger number of potential carriers and non-carriers using genotype imputation (n = 299 carriers and n = 7,127 non-carriers), from previously published biomarkers we also observed a higher neutrophil-to-lymphocyte ratio (NLR) and lower serum albumin and sodium levels in the heterozygous PRKN variant carriers. Sodium 287-293 parkin RBR E3 ubiquitin protein ligase Homo sapiens 321-325 34422849-1 2021 Objective: Voltage-gated sodium channel Nav1.5 encoded by the SCN5A gene plays crucial roles in cardiac electrophysiology. Sodium 25-31 sodium voltage-gated channel alpha subunit 5 Homo sapiens 62-67 34092082-1 2021 Rationale: Loss-of-function of the cardiac sodium channel NaV1.5 causes conduction slowing and arrhythmias. Sodium 43-49 sodium voltage-gated channel alpha subunit 5 Homo sapiens 58-64 34092082-2 2021 NaV1.5 is differentially distributed within subcellular domains of cardiomyocytes, with sodium current (INa) being enriched at the intercalated discs (ID). Sodium 88-94 sodium voltage-gated channel alpha subunit 5 Homo sapiens 0-6 34100980-1 2021 Within an articulately characterized family of ion channels, the voltage-gated sodium channels, exists a black sheep, SCN7A (Nax). Sodium 79-85 sodium channel protein type 7 subunit alpha Ovis aries 118-123 34368091-3 2021 The epithelial sodium channel (ENaC) is the rate-limiting step in the sodium-water transport and edema clearance in the alveolar cavity; the role of bone marrow-derived MSC-conditioned medium (BMSC-CM) in edema clearance and how miRNAs affect ENaC are still seldom known. Sodium 15-21 sodium channel, nonvoltage-gated 1 alpha Mus musculus 31-35 34368091-3 2021 The epithelial sodium channel (ENaC) is the rate-limiting step in the sodium-water transport and edema clearance in the alveolar cavity; the role of bone marrow-derived MSC-conditioned medium (BMSC-CM) in edema clearance and how miRNAs affect ENaC are still seldom known. Sodium 70-76 sodium channel, nonvoltage-gated 1 alpha Mus musculus 31-35 34193056-1 2021 BACKGROUND: Recent trials have revealed that sodium-glucose co-transporter 2 inhibitors (SGLT2-i) are effective against hyperglycemia and also reduce micro- and macro-vascular complications in patients with type 2 diabetes mellitus (T2DM). Sodium 45-51 solute carrier family 5 member 2 Homo sapiens 89-94 34204499-2 2021 The SCN5A gene, encoding for the cardiac voltage-gated sodium channel Nav1.5, accounts for ~20-30% of BrS cases and is considered clinically relevant. Sodium 55-61 sodium voltage-gated channel alpha subunit 5 Homo sapiens 4-9 34204499-2 2021 The SCN5A gene, encoding for the cardiac voltage-gated sodium channel Nav1.5, accounts for ~20-30% of BrS cases and is considered clinically relevant. Sodium 55-61 sodium voltage-gated channel alpha subunit 5 Homo sapiens 70-76 6751098-12 1982 In both sodium-replete and -deplete animals the increases in PRA were accompanied by proportional increases in the hepatic extraction of renin and increases in the hepatic clearance of renin. Sodium 8-14 renin Canis lupus familiaris 137-142 34222246-0 2021 Homocysteine Causes Endothelial Dysfunction via Inflammatory Factor-Mediated Activation of Epithelial Sodium Channel (ENaC). Sodium 102-108 sodium channel, nonvoltage-gated 1 alpha Mus musculus 118-122 6751098-12 1982 In both sodium-replete and -deplete animals the increases in PRA were accompanied by proportional increases in the hepatic extraction of renin and increases in the hepatic clearance of renin. Sodium 8-14 renin Canis lupus familiaris 185-190 6919568-1 1982 Urinary kallikrein is increased by restriction of dietary sodium and by administration of fludrocortisone, a sodium-retaining steroid. Sodium 58-64 kallikrein related peptidase 4 Homo sapiens 8-18 6919568-1 1982 Urinary kallikrein is increased by restriction of dietary sodium and by administration of fludrocortisone, a sodium-retaining steroid. Sodium 109-115 kallikrein related peptidase 4 Homo sapiens 8-18 6919568-4 1982 Sodium restriction also caused significantly higher urinary excretion of kallikrein and aldosterone. Sodium 0-6 kallikrein related peptidase 4 Homo sapiens 73-83 6919568-8 1982 It is concluded that both salivary and urinary kallikrein increased in response to restriction of sodium and that these increases were mediated by levels of sodium-retaining steroid. Sodium 98-104 kallikrein related peptidase 4 Homo sapiens 47-57 6919568-9 1982 Increased output of kallikrein in response to increased levels of sodium-retaining steroid may be a generalized response of organs that contain glandular kallikrein and can conserve sodium. Sodium 66-72 kallikrein related peptidase 4 Homo sapiens 20-30 6919568-9 1982 Increased output of kallikrein in response to increased levels of sodium-retaining steroid may be a generalized response of organs that contain glandular kallikrein and can conserve sodium. Sodium 66-72 kallikrein related peptidase 4 Homo sapiens 154-164 6919568-9 1982 Increased output of kallikrein in response to increased levels of sodium-retaining steroid may be a generalized response of organs that contain glandular kallikrein and can conserve sodium. Sodium 182-188 kallikrein related peptidase 4 Homo sapiens 20-30 34222246-2 2021 We investigated whether and how the epithelial sodium channel (ENaC), a recently identified ion channel in endothelial cells, plays a role in HHcy-induced endothelial dysfunction. Sodium 47-53 sodium channel, nonvoltage-gated 1 alpha Mus musculus 63-67 34177810-11 2021 Level of serum sodium in NDI patients with compound het AQP2 mutations was higher than non-compound het mutations. Sodium 15-21 aquaporin 2 Homo sapiens 56-60 6286000-2 1982 The stability constant for the reaction Na(+) + 5"-GMP(2-) Na(5"-GMP)(-) was found to be 2.85 +/- 0.36 M(-1) at 5 degrees C and an ionic strength of 1.1 +/- 0.1 M. Although 5"-GMP forms ordered self-structures at high concentration in the presence of sodium ions, in dilute solution and at low sodium ion concentrations the Na(+) binding is weak and typical of that for other nucleotides. Sodium 251-257 5'-nucleotidase, cytosolic II Homo sapiens 51-54 6286000-2 1982 The stability constant for the reaction Na(+) + 5"-GMP(2-) Na(5"-GMP)(-) was found to be 2.85 +/- 0.36 M(-1) at 5 degrees C and an ionic strength of 1.1 +/- 0.1 M. Although 5"-GMP forms ordered self-structures at high concentration in the presence of sodium ions, in dilute solution and at low sodium ion concentrations the Na(+) binding is weak and typical of that for other nucleotides. Sodium 251-257 5'-nucleotidase, cytosolic II Homo sapiens 65-68 6286000-2 1982 The stability constant for the reaction Na(+) + 5"-GMP(2-) Na(5"-GMP)(-) was found to be 2.85 +/- 0.36 M(-1) at 5 degrees C and an ionic strength of 1.1 +/- 0.1 M. Although 5"-GMP forms ordered self-structures at high concentration in the presence of sodium ions, in dilute solution and at low sodium ion concentrations the Na(+) binding is weak and typical of that for other nucleotides. Sodium 251-257 5'-nucleotidase, cytosolic II Homo sapiens 65-68 6286000-2 1982 The stability constant for the reaction Na(+) + 5"-GMP(2-) Na(5"-GMP)(-) was found to be 2.85 +/- 0.36 M(-1) at 5 degrees C and an ionic strength of 1.1 +/- 0.1 M. Although 5"-GMP forms ordered self-structures at high concentration in the presence of sodium ions, in dilute solution and at low sodium ion concentrations the Na(+) binding is weak and typical of that for other nucleotides. Sodium 294-300 5'-nucleotidase, cytosolic II Homo sapiens 51-54 6286000-2 1982 The stability constant for the reaction Na(+) + 5"-GMP(2-) Na(5"-GMP)(-) was found to be 2.85 +/- 0.36 M(-1) at 5 degrees C and an ionic strength of 1.1 +/- 0.1 M. Although 5"-GMP forms ordered self-structures at high concentration in the presence of sodium ions, in dilute solution and at low sodium ion concentrations the Na(+) binding is weak and typical of that for other nucleotides. Sodium 294-300 5'-nucleotidase, cytosolic II Homo sapiens 65-68 6286000-2 1982 The stability constant for the reaction Na(+) + 5"-GMP(2-) Na(5"-GMP)(-) was found to be 2.85 +/- 0.36 M(-1) at 5 degrees C and an ionic strength of 1.1 +/- 0.1 M. Although 5"-GMP forms ordered self-structures at high concentration in the presence of sodium ions, in dilute solution and at low sodium ion concentrations the Na(+) binding is weak and typical of that for other nucleotides. Sodium 294-300 5'-nucleotidase, cytosolic II Homo sapiens 65-68 34177810-13 2021 Phenotype was found to correlate with genotypes, revealed by higher level of serum sodium in patients with compound het AQP2 mutations than non-compound het mutations. Sodium 83-89 aquaporin 2 Homo sapiens 120-124 34099183-0 2021 Expression and purification of the cardiac sodium channel NaV1.5 for cryo-EM structure determination. Sodium 43-49 sodium voltage-gated channel alpha subunit 5 Homo sapiens 58-64 6289168-1 1982 The indolalkylamine alkaloid yohimbine induced two phenomenologically-different types of sodium current (INa) inhibition in the voltage-clamped frog node of Ranvier, a tonic and a phasic ("use-dependent") block. Sodium 89-95 internexin neuronal intermediate filament protein alpha Homo sapiens 105-108 7047034-4 1982 Since sodium-retaining steroids influence urinary kallikrein excretion, two patients were studied 2 and 3 months post-transplantation while receiving alternate-day prednisone. Sodium 6-12 kallikrein related peptidase 4 Homo sapiens 50-60 7018807-8 1981 Plasma renin activity and aldosterone increased during development of hypertension and remained elevated during the period of sodium restriction. Sodium 126-132 renin Canis lupus familiaris 7-12 34099183-1 2021 Voltage-gated sodium channel NaV1.5 is responsible for initiating and propagating cardiac action potentials by selectively conducting Na+ into cardiomyocytes. Sodium 14-20 sodium voltage-gated channel alpha subunit 5 Homo sapiens 29-35 35577326-4 2022 Increases in serum FGF23 levels during growth were associated with the up- and down-regulation of the renal expression of Cyp24a1 encoding vitamin D-24-hydroxylase and Slc34a3 encoding the type IIc sodium/phosphate (Na+/Pi) co-transporter, respectively, suggesting an enhancement in the FGF23-mediated bone-kidney axis from youth to adulthood. Sodium 198-204 solute carrier family 34 (sodium phosphate), member 3 Mus musculus 168-175 35545942-3 2022 Nevertheless, inflammatory cytokines whose expression is induced in the early stages of hypertension can alter renal blood flow and sodium transporter expression and activity to foster renal sodium retention. Sodium 191-197 solute carrier family 5 member 4 Homo sapiens 132-150 35603785-1 2022 Loss-of-function (LOF) variants in SCN1B, encoding the voltage-gated sodium channel beta1/beta1B subunits, are linked to neurological and cardiovascular diseases. Sodium 69-75 adrenergic receptor, alpha 1b Mus musculus 90-96 35605014-4 2022 Solute carrier family 20 member 1 (SLC20A1) is a sodium/inorganic phosphate symporter that has been proposed to be a viable prognostic marker for the luminal A and luminal B types of ER+ breast cancer. Sodium 49-55 solute carrier family 20 member 1 Homo sapiens 35-42 35569011-5 2022 In these models, sodium retention is thought to be caused by activation of the epithelial sodium channel (ENaC) in the distal nephron through aberrantly filtered serine proteases or proteasuria. Sodium 17-23 sodium channel, nonvoltage-gated 1 alpha Mus musculus 106-110 35569011-5 2022 In these models, sodium retention is thought to be caused by activation of the epithelial sodium channel (ENaC) in the distal nephron through aberrantly filtered serine proteases or proteasuria. Sodium 90-96 sodium channel, nonvoltage-gated 1 alpha Mus musculus 106-110 35567276-5 2022 Although 23 genes have been associated with the condition, only SCN5A, encoding the cardiac sodium channel, is considered clinically actionable and disease causing. Sodium 92-98 sodium voltage-gated channel alpha subunit 5 Homo sapiens 64-69 35150131-4 2022 In the present study, we found that human immortalized podocytes express messenger RNA and protein of phosphate transporters, including NaPi 2c (SLC34A3), Pit 1 (SLC20A1), and Pit 2 (SLC20A2), which are sodium-dependent and mediate intracellular phosphate (Pi) transport, and XPR1, which is responsible for extracellular Pi transport. Sodium 203-209 solute carrier family 20 member 2 Homo sapiens 183-190 35216518-7 2022 Our patch-clamp single-channel recordings from split-open distal tubule show that SCI decreased the activity of the epithelial sodium channel (ENaC). Sodium 127-133 sodium channel, nonvoltage-gated 1 alpha Mus musculus 143-147 35499203-0 2022 Bean Pod-Like SbSn/N-Doped Carbon Fibers toward a Binder Free, Free-Standing, and High-Performance Anode for Sodium-Ion Batteries. Sodium 109-115 suprabasin Homo sapiens 14-18 35499203-1 2022 Bimetallic SbSn alloy stands out among the anode materials for sodium-ion batteries (SIBs) because of its high theoretical specific capacity (752 mAh g-1 ) and good electrical conductivity. Sodium 63-69 suprabasin Homo sapiens 11-15 35490157-7 2022 Forced expression of the sodium/calcium exchanger protein SLC8A3 could rescue the myogenic defects in TET2 knockout cells. Sodium 25-31 solute carrier family 8 (sodium/calcium exchanger), member 3 Mus musculus 58-64 35490157-7 2022 Forced expression of the sodium/calcium exchanger protein SLC8A3 could rescue the myogenic defects in TET2 knockout cells. Sodium 25-31 tet methylcytosine dioxygenase 2 Mus musculus 102-106 35409028-7 2022 Actually, the most promising category seems to be sodium-glucose cotransporter (SGLT2) inhibitors. Sodium 50-56 solute carrier family 5 member 2 Homo sapiens 80-85 35229618-0 2022 Synergistic Effect of Uroguanylin and D1 Dopamine Receptors on Sodium Excretion in Hypertension. Sodium 63-69 guanylate cyclase activator 2B Rattus norvegicus 22-33 35229618-2 2022 As one of the major natriuretic hormones secreted by both the intestines and the kidney, we hypothesized that renal uroguanylin interacts with dopamine receptors to increase sodium excretion synergistically, an impaired interaction of which may be involved in the pathogenesis of hypertension. Sodium 174-180 guanylate cyclase activator 2B Rattus norvegicus 116-127 35229618-4 2022 Although subthreshold dosages of uroguanylin or fenoldopam had no effect, the coinfusion of subthreshold dosages of those reagents significantly increased sodium excretion. Sodium 155-161 guanylate cyclase activator 2B Rattus norvegicus 33-44 35229618-10 2022 Conclusions These data suggest that there is synergism between uroguanylin and D1-like receptors to increase sodium excretion. Sodium 109-115 guanylate cyclase activator 2B Rattus norvegicus 63-74 6255144-2 1980 Voltage clamp studies of the excitatory sodium current, INa, were carried out in rabbit cardiac Purkinje fibres using th two-micro-electrode technique. Sodium 40-46 LOW QUALITY PROTEIN: alpha-internexin Oryctolagus cuniculus 56-59 35131865-0 2022 The anti-diabetic drug metformin regulates voltage-gated sodium channel NaV1.7 via the ubiquitin-ligase NEDD4-2. Sodium 57-63 neural precursor cell expressed, developmentally down-regulated gene 4-like Mus musculus 104-111 6255144-5 1980 Non-uniformities in membrane potential were kept small by reducing the size of INa to less than 50 microA/cm2 of total membrane surface area through prepulse inactivation or removal of external sodium, Nao. Sodium 194-200 LOW QUALITY PROTEIN: alpha-internexin Oryctolagus cuniculus 79-82 6993655-3 1980 Plasma renin activity (PRA) during sodium depletion (12.35 +/- 3.93 ng ml-1 hr-1) was higher than during sodium repletion (1.46 +/- 0.47 ng ml-1 hr-1; P less than .05). Sodium 35-41 renin Canis lupus familiaris 7-12 6247919-2 1980 Progressive sodium depletion was associated with progressive increased in basal (pre-ACTH) plasma levels of renin, angiotensin II, aldosterone, 18-hydroxycorticosterone (18-OH-B), and 18-hydroxy-11-deoxycorticosterone (18-OH-DOC). Sodium 12-18 renin Canis lupus familiaris 108-113 35210625-2 2022 With the exception of SCN5A, encoding the cardiac sodium channel NaV1.5, susceptibility genes remain largely unknown. Sodium 50-56 sodium voltage-gated channel alpha subunit 5 Homo sapiens 22-27 35210625-2 2022 With the exception of SCN5A, encoding the cardiac sodium channel NaV1.5, susceptibility genes remain largely unknown. Sodium 50-56 sodium voltage-gated channel alpha subunit 5 Homo sapiens 65-71 35228649-4 2022 High salt intake under reduced NO production overactivated the angiotensin II-SPAK (STE20/SPS1-related proline-alanine-rich protein kinase)-NCC (sodium chloride co-transporter) pathway in the kidney, resulting in the insufficient excretion of sodium during the day and its excessive excretion at night. Sodium 243-249 serine/threonine kinase 39 Mus musculus 78-82 35216338-1 2022 The cardiac sodium ion channel (NaV1.5) is a protein with four domains (DI-DIV), each with six transmembrane segments. Sodium 12-18 sodium voltage-gated channel alpha subunit 5 Homo sapiens 32-38 35195246-5 2022 The SCN5A gene encodes the cardiac voltage-gated sodium channel (Nav1.5) and loss-of-function mutations can cause the cardiac arrhythmia Brugada syndrome. Sodium 49-55 sodium voltage-gated channel alpha subunit 5 Homo sapiens 4-9 35195246-5 2022 The SCN5A gene encodes the cardiac voltage-gated sodium channel (Nav1.5) and loss-of-function mutations can cause the cardiac arrhythmia Brugada syndrome. Sodium 49-55 sodium voltage-gated channel alpha subunit 5 Homo sapiens 65-71 35163304-1 2022 Nav1.5 is the predominant cardiac sodium channel subtype, encoded by the SCN5A gene, which is involved in the initiation and conduction of action potentials throughout the heart. Sodium 34-40 sodium voltage-gated channel alpha subunit 5 Homo sapiens 0-6 35163304-1 2022 Nav1.5 is the predominant cardiac sodium channel subtype, encoded by the SCN5A gene, which is involved in the initiation and conduction of action potentials throughout the heart. Sodium 34-40 sodium voltage-gated channel alpha subunit 5 Homo sapiens 73-78 35023666-0 2022 Apelin-13 Decreases Epithelial Sodium Channel (ENaC) Expression and Activity in Kidney Collecting Duct Cells. Sodium 31-37 sodium channel, nonvoltage-gated 1 alpha Mus musculus 47-51 35023666-5 2022 The central role of these cells in water and sodium transport is governed by AQP-2 and the epithelial sodium channel (ENaC). Sodium 45-51 aquaporin 2 Mus musculus 77-82 35023666-5 2022 The central role of these cells in water and sodium transport is governed by AQP-2 and the epithelial sodium channel (ENaC). Sodium 45-51 sodium channel, nonvoltage-gated 1 alpha Mus musculus 118-122 35023666-5 2022 The central role of these cells in water and sodium transport is governed by AQP-2 and the epithelial sodium channel (ENaC). Sodium 102-108 sodium channel, nonvoltage-gated 1 alpha Mus musculus 118-122 35069250-10 2021 Together, these data indicate low sodium delivery to the ASDN activates PGE2 synthesis and this inhibits ROMK through autocrine activation of the EP1 receptor. Sodium 34-40 potassium inwardly-rectifying channel, subfamily J, member 1 Mus musculus 105-109 2527472-0 1989 Mechanism mediating hypotensive effect of ANF in sodium-depleted dogs. Sodium 49-55 natriuretic peptide A Canis lupus familiaris 42-45 2666607-3 1989 In conscious, sodium-depleted cynomolgus monkeys both compounds produced a dose-related inhibition of plasma renin activity (PRA) at doses ranging between 0.001 and 1.0 mumol/kg, intravenously, and total inhibition was observed after the highest dose. Sodium 14-20 renin Macaca fascicularis 109-114 2666614-8 1989 In other studies comparing renin inhibition with angiotensin converting enzyme (ACE) inhibition, there was evidence for greater efficacy of ACE inhibition in conscious sodium-deficient dogs, but no evidence of any difference in one-kidney, one clip hypertensive dogs. Sodium 168-174 angiotensin I converting enzyme Canis lupus familiaris 140-143 2562838-0 1989 Palytoxin down-modulates the epidermal growth factor receptor through a sodium-dependent pathway. Sodium 72-78 epidermal growth factor receptor Mus musculus 29-61 2562838-9 1989 Furthermore, there appears to be a direct correspondence between the extent of inhibition of EGF binding by palytoxin and the rate of sodium uptake. Sodium 134-140 epidermal growth factor Mus musculus 93-96 2562838-10 1989 Finally, the palytoxin-induced inhibition of EGF binding can be mimicked by monensin, a sodium ionophore. Sodium 88-94 epidermal growth factor Mus musculus 45-48 2521433-4 1989 These changes in urinary sodium excretion were associated with significant elevations of the mean arterial pressure (MAP) from 105 +/- 5 to 111 +/- 6 mmHg and plasma atrial natriuretic factor concentrations (ANF) from 30 +/- 2 to 57 +/- 7 pg/ml beginning the 1st day of infusion. Sodium 25-31 natriuretic peptide A Canis lupus familiaris 166-191 6990795-9 1980 The results demonstrate the importance of the renin-angiotensin system as a link between the nephron and the zona glomerulosa that is essential in controlling plasma potassium concentration and excretion during changes in sodium balance. Sodium 222-228 renin Canis lupus familiaris 46-51 2521433-4 1989 These changes in urinary sodium excretion were associated with significant elevations of the mean arterial pressure (MAP) from 105 +/- 5 to 111 +/- 6 mmHg and plasma atrial natriuretic factor concentrations (ANF) from 30 +/- 2 to 57 +/- 7 pg/ml beginning the 1st day of infusion. Sodium 25-31 natriuretic peptide A Canis lupus familiaris 208-211 2567225-0 1989 The effect of T-2 toxin on active sodium transport across frog skin in the presence of ADH and amphotericin B. Sodium 34-40 alcohol dehydrogenase 1A (class I), alpha polypeptide Homo sapiens 87-90 2552203-7 1989 The rate of pHi recovery after the readdition of Na+ to a sodium-free medium exhibited saturation kinetics (half maximal rate at 28 mM). Sodium 58-64 glucose-6-phosphate isomerase Rattus norvegicus 12-15 7374918-0 1980 Dose-response relation of CSF sodium and renal sodium excretion, and its absence in homozygous Brattleboro rats. Sodium 30-36 colony stimulating factor 2 Rattus norvegicus 26-29 7374918-0 1980 Dose-response relation of CSF sodium and renal sodium excretion, and its absence in homozygous Brattleboro rats. Sodium 47-53 colony stimulating factor 2 Rattus norvegicus 26-29 2510079-3 1989 Assumption of the upright posture as well as sodium restriction increased PAI, PAII, and PRA, but UAI and UAII excretion were not altered by these manoeuvres. Sodium 45-51 serpin family E member 1 Homo sapiens 74-77 3060124-13 1988 It is concluded that pHi can influence the secretory activity of pancreatic islets, possibly via effects on potassium permeability and sodium-calcium exchange across the plasma membrane, resulting in altered mobilisation of calcium in the islet cell. Sodium 135-141 glucose-6-phosphate isomerase Rattus norvegicus 21-24 2973511-5 1988 Thus, in the conscious newborn calf, changes in plasma ANP levels and urinary water and sodium excretion during hypertonic saline infusion are compatible with the hypothesis that endogenous ANP participates, at least in part, in the immediate diuretic and natriuretic renal response induced by the sodium overload. Sodium 88-94 natriuretic peptide A Bos taurus 190-193 2973511-5 1988 Thus, in the conscious newborn calf, changes in plasma ANP levels and urinary water and sodium excretion during hypertonic saline infusion are compatible with the hypothesis that endogenous ANP participates, at least in part, in the immediate diuretic and natriuretic renal response induced by the sodium overload. Sodium 298-304 natriuretic peptide A Bos taurus 190-193 2850509-3 1988 As a result of the mainly extracellular distribution of sodium the CSF spaces are depicted by their high signal intensity while the normal parenchyma is not visible. Sodium 56-62 colony stimulating factor 2 Homo sapiens 67-70 2961275-2 1987 To evaluate this possibility we assessed, in anesthetized dogs, the net increments in fractional excretion of sodium (FENa) and lithium (FELi) produced by ANP and by the inhibition of ANG II formation with captopril. Sodium 110-116 natriuretic peptide A Canis lupus familiaris 155-158 2961282-9 1987 Plasma ANF increased from 27.2 +/- 4.8 to 47.0 +/- 7.3 pg/ml in ATX and from 27.2 +/- 7.8 to 59.0 +/- 17.9 pg/ml in S. After vagotomy, VE caused transient increases in urine flow and sodium excretion. Sodium 183-189 natriuretic peptide A Canis lupus familiaris 7-10 2442717-5 1987 All substances tested reduced the sodium current in both intact axons and axons internally perfused with CsF. Sodium 34-40 colony stimulating factor 2 Homo sapiens 105-108 3028151-4 1987 After intracellular acidification with ammonium chloride, pH regulation was inhibited with 1 mM amiloride or by omission of external sodium, consistent with a Na-H exchange mechanism. Sodium 133-139 glucose-6-phosphate isomerase Rattus norvegicus 58-60 7221288-0 1980 [Research on rectal/resorption of I 131-labeled sodium from suppositories prepared with indigenous hydrogenated fats]. Sodium 48-54 chromosome 10 open reading frame 90 Homo sapiens 112-116 6986653-4 1980 These observations establish the role of the renin-angiotensin system in the maintenance of blood pressure in the sodium-depleted state as well as in the initiation of renovascular hypertension. Sodium 114-120 renin Canis lupus familiaris 45-50 7350058-3 1980 Intestinal perfusion studies before intravenous somatostatin infusion revealed decreased water and sodium absorption and jejunal chloride secretion. Sodium 99-105 somatostatin Homo sapiens 48-60 7350058-4 1980 Somatostatin infusion for 2 hr (8 microgram/kg/hr) reversed chloride secretion to absorption and markedly enhanced water and sodium absorption. Sodium 125-131 somatostatin Homo sapiens 0-12 7390048-0 1980 Effect of pentagastrin, secretin and cholecystokinin on intestinal water and sodium absorption in the rat. Sodium 77-83 cholecystokinin Rattus norvegicus 37-52 7005052-7 1980 Manipulation of the extracellular sodium concentration indicates the existence in islet cells of a glucose-sensitive Na-Ca counter transport process conceivably responsible for active extrusion of calcium. Sodium 34-40 nascent polypeptide associated complex subunit alpha Rattus norvegicus 117-122 3028151-6 1987 In the presence of external bicarbonate, amiloride or omission of sodium slowed, but did not completely inhibit recovery from acidification, indicating that additional pHi regulation mechanisms may operate in this preparation. Sodium 66-72 glucose-6-phosphate isomerase Rattus norvegicus 168-171 3038392-8 1987 These findings show that a similar hypotensive response is induced in sodium-depleted primates after chronic inhibition of renin or converting enzyme. Sodium 70-76 renin Callithrix jacchus 123-128 2946245-9 1986 Furthermore, the results support the concept that ANF functions to increase postprandial sodium excretion following the ingestion of a high-sodium meal. Sodium 89-95 natriuretic peptide A Canis lupus familiaris 50-53 2946245-9 1986 Furthermore, the results support the concept that ANF functions to increase postprandial sodium excretion following the ingestion of a high-sodium meal. Sodium 140-146 natriuretic peptide A Canis lupus familiaris 50-53 2944396-1 1986 The purpose of the present study was to determine if acute and chronic increases in sodium intake by isotonic saline infusion are accompanied by changes in plasma concentrations of atrial natriuretic peptide (PANP). Sodium 84-90 natriuretic peptide A Canis lupus familiaris 181-207 7350175-0 1980 Relationship between urinary kallikrein and renal sodium handling during water immersion in normal man. Sodium 50-56 kallikrein related peptidase 4 Homo sapiens 29-39 6989020-6 1980 Thus, prolactin and urinary kallikrein-kinin system might also contribute to water and sodium retention in idiopathic edema, directly or indirectly through the augmentation of the action of ADH and of aldosterone. Sodium 87-93 kallikrein related peptidase 4 Homo sapiens 28-38 2428635-1 1986 The effect of ethacyzine (a diethylamine analogue of ethmozine) on the rapid inward sodium current (INa) was studied in single rat ventricular muscle cells by a patch clamp technique. Sodium 84-90 internexin neuronal intermediate filament protein, alpha Rattus norvegicus 100-103 2941368-1 1986 The present study was designed to examine the short-term and long-term effects of increased plasma levels of atrial natriuretic peptide on the glomerular filtration rate, sodium excretion, and arterial pressure. Sodium 171-177 natriuretic peptide A Canis lupus familiaris 109-135 659580-0 1978 Renin-angiotensin system inhibition in conscious sodium-depleted dogs. Sodium 49-55 renin Canis lupus familiaris 0-5 2941368-3 1986 Short-term increases in plasma levels of atrial natriuretic peptide increased the glomerular filtration rate from 53 +/- 15 to 82 +/- 16 ml/min and increased sodium excretion from 74.4 +/- 32.6 to 146.9 +/- 38.1 microEq/min. Sodium 158-164 natriuretic peptide A Canis lupus familiaris 41-67 2941371-9 1986 These results suggest that an increase in the sodium load delivered to the macula suppression of renin secretion by atrial natriuretic factor is mediated through its interactions with the two intrarenal receptor mechanisms, the renal vascular receptor and the macula densa. Sodium 46-52 natriuretic peptide A Canis lupus familiaris 116-141 2938187-2 1986 The initial free-flow response to intrarenal infusion of 5 micrograms/min of synthetic ANF into mannitol-expanded dogs resulted in an increased urine flow rate (6.81 +/- 0.88 to 9.00 +/- 1.17 ml/min, P less than 0.05) and a 40% increase in sodium excretion (496 +/- 110 to 694 +/- 166 meq/min, P less than 0.025) when compared to paired control periods. Sodium 240-246 natriuretic peptide A Canis lupus familiaris 87-90 2933267-6 1985 Fractional excretion of sodium (FE Na%) increased 3.4-fold with ANF at 100 pmol/kg per min and 1.8-fold with the 200 pmol/kg per min dose. Sodium 24-30 natriuretic peptide A Canis lupus familiaris 64-67 3996489-3 1985 Monensin, a sodium-specific ionophore, potentiated epo-stimulated erythroid growth at concentrations of 1-30 nM. Sodium 12-18 erythropoietin Mus musculus 51-54 3157329-2 1985 Infusion of a synthetic atrial natriuretic factor into conscious dogs with caval constriction and ascites at doses of 175 and 350 ng X kg-1 X min-1 for 30 min each produced striking increases (P less than 0.05) in creatinine clearance, diuresis, and kaliuresis but failed to increase urinary sodium excretion. Sodium 292-298 natriuretic peptide A Canis lupus familiaris 24-49 3157329-3 1985 Infusions of atrial natriuretic factor at these doses into conscious normal dogs, however, produced a striking increase in sodium excretion from 41 +/- 14 and 55 +/- 19 mu eq/min to 150 +/- 58 and 181 +/- 49 mu eq/min (P less than 0.05 for both values). Sodium 123-129 natriuretic peptide A Canis lupus familiaris 13-38 3157329-7 1985 These results suggest that the pattern of renal electrolyte excretion elicited in response to the acute infusion of atrial natriuretic factor is dependent, at least partially, on the preexisting status of the renal tubules to facilitate sodium reabsorption and potassium excretion. Sodium 237-243 natriuretic peptide A Canis lupus familiaris 116-141 3882483-3 1985 Sodium-free medium decreased basal pHi by 0.3 unit and prevented increases in pHi in response to both insulin and progesterone, but S6 phosphorylation occurred normally with both hormones. Sodium 0-6 insulin S homeolog Xenopus laevis 102-109 6151183-1 1984 A small and very slow inward calcium current has been identified in isolated single ventricular cells using TTX and Cd2+ to block the sodium and fast calcium currents. Sodium 134-140 CD2 molecule Homo sapiens 116-119 6383081-7 1984 A net loss of 20 meq sodium occurred during the 1st day of AVP infusion but thereafter was unchanged. Sodium 21-27 arginine vasopressin Canis lupus familiaris 59-62 6383081-9 1984 We conclude that AVP-induced changes of arterial pressure, plasma sodium concentration and osmolality, renal escape, suppression of renin activity, and most of the observed natriuresis are events normally dependent on volume expansion. Sodium 66-72 arginine vasopressin Canis lupus familiaris 17-20 6138350-1 1983 The high affinity, sodium-dependent uptake of proline by rat brain synaptosomes was inhibited by the opioid pentapeptides, Leu-enkephalin and Met-enkephalin. Sodium 19-25 proenkephalin Rattus norvegicus 127-137 207458-0 1978 [Self-association of 5"-GMP: involvement of tetrameters, and inclusion of the sodium cation in the central cavity of the tetramers]. Sodium 78-84 5'-nucleotidase, cytosolic II Homo sapiens 24-27 641142-4 1978 Acute and chronic sodium depletion increased plasma renin activity (PRA) and blunted the RVR to AII, while acute sodium repletion and chronic sodium excess plus desoxycorticosterone acetate decreased PRA and enhanced the RVR to AII. Sodium 18-24 renin Canis lupus familiaris 52-57 620492-6 1978 After several days of dietary sodium restriction both racial groups increased their urinary kallikrein activity. Sodium 30-36 kallikrein related peptidase 4 Homo sapiens 92-102 620492-8 1978 White subjects were studied for an additional 24 h period, and urinary kallikrein activity returned to pre-water load values, indicating that the excretion of a water load in sodium-depleted subjects is associated with an increase in kallikrein excretion. Sodium 175-181 kallikrein related peptidase 4 Homo sapiens 234-244 908483-3 1977 The duct cells responded to increasing doses of secretin by producing more juice with increasing outputs of bicarbonate, sodium, potassium, and chloride. Sodium 121-127 secretin Rattus norvegicus 48-56 910953-5 1977 This superimposed sodium depletion (negative sodium balance of 137 +/- 17 meq) increased plasma renin activity 3-5 times but did not change arterial pressure or heart rate. Sodium 18-24 renin Canis lupus familiaris 96-101 910953-5 1977 This superimposed sodium depletion (negative sodium balance of 137 +/- 17 meq) increased plasma renin activity 3-5 times but did not change arterial pressure or heart rate. Sodium 45-51 renin Canis lupus familiaris 96-101 765162-1 1976 Sodium excretion is correlated with kallikrein excretion in man, rabbits and rats on a free sodium and water intake, but not on a constant sodium or constant water intake. Sodium 0-6 kallikrein related peptidase 4 Homo sapiens 36-46 1248655-3 1976 Aldosterone regulates kallikrein excretion, as normal subjects show increased kallikrein excretion in response to a low sodium intake, high potassium intake, or the synthetic mineralocorticoid, fludrocortisone, whereas kallikrein excretion falls during treatment with spironolactone. Sodium 120-126 kallikrein related peptidase 4 Homo sapiens 78-88 1248655-3 1976 Aldosterone regulates kallikrein excretion, as normal subjects show increased kallikrein excretion in response to a low sodium intake, high potassium intake, or the synthetic mineralocorticoid, fludrocortisone, whereas kallikrein excretion falls during treatment with spironolactone. Sodium 120-126 kallikrein related peptidase 4 Homo sapiens 78-88 1245602-6 1976 P113 also reduced the clearance of para-aminohippurate, creatinine, sodium, and potassium, a pattern similar to that induced by A II. Sodium 68-74 signal transducer and activator of transcription 2 Homo sapiens 0-4 1019162-3 1976 Only after the combined stress of a low sodium diet and the upright position did P113 lower the blood pressure. Sodium 40-46 signal transducer and activator of transcription 2 Homo sapiens 81-85 1214279-6 1975 On the other hand, carboxypeptidases A and B, both at 1mg/ml, suppressed the sodium and potassium conductance increases with little or no change in sodium inactivation. Sodium 77-83 carboxypeptidase B1 Homo sapiens 19-44 6138350-1 1983 The high affinity, sodium-dependent uptake of proline by rat brain synaptosomes was inhibited by the opioid pentapeptides, Leu-enkephalin and Met-enkephalin. Sodium 19-25 proenkephalin Rattus norvegicus 146-156 6620395-1 1983 Effects of mexiletine on the rapid inward sodium current (INa) were studied in freshly isolated single cells of the ventricular myocardium of adult rats and in single cultured ventricular muscle cells of newborn rats. Sodium 42-48 internexin neuronal intermediate filament protein, alpha Rattus norvegicus 58-61 1200136-0 1975 Effect of parathyroid hormone secretion on sodium reabsorption by the proximal tubule. Sodium 43-49 parathyroid hormone Canis lupus familiaris 10-29 1200136-1 1975 To determine if an increase in the endogenous secretion of parathyroid hormone could decrease sodium reabsorption by the proximal tubule, the ionized calcium concentration of blood perfusing the parathyroid gland of eight unilaterally thyroid parathyroidectomized dogs (TPTX) was reduced by infusion of an isotonic sodium citrate plus sodium chloride solution into the blood supply of the parathyroid gland. Sodium 94-100 parathyroid hormone Canis lupus familiaris 59-78 1200136-6 1975 The data demonstrate that alterations in endogenous parathyroid hormone secretion can play a significant role in the regulation of sodium reabsorption by the proximal tubule. Sodium 131-137 parathyroid hormone Canis lupus familiaris 52-71 1196315-8 1975 The same intrarenal feed-back mechanism, normally adapting the glomerular blood supply to the resorptive capacity of the proximal-tubular epithelium (mediation via the juxta-glomerular apparatus), is responsible for the GFR- and RPF-raising effect of exogenous L-thyroxine in the intact kidney as well as in acute renal failure: both sodium reabsorption and sodium filtration are accelerated.--The special conditions under which L-thyroxine interferes with the pathogenetic process of acute renal failure, the latter being characterised by the critical insufficiency of tubular sodium reabsorption and therefore by preglomerular arterial constriction, is discussed on the basis of a new hypothesis concerning the thyrogenic nephrotropic effects in general. Sodium 334-340 Rap guanine nucleotide exchange factor 5 Homo sapiens 220-223 1196315-8 1975 The same intrarenal feed-back mechanism, normally adapting the glomerular blood supply to the resorptive capacity of the proximal-tubular epithelium (mediation via the juxta-glomerular apparatus), is responsible for the GFR- and RPF-raising effect of exogenous L-thyroxine in the intact kidney as well as in acute renal failure: both sodium reabsorption and sodium filtration are accelerated.--The special conditions under which L-thyroxine interferes with the pathogenetic process of acute renal failure, the latter being characterised by the critical insufficiency of tubular sodium reabsorption and therefore by preglomerular arterial constriction, is discussed on the basis of a new hypothesis concerning the thyrogenic nephrotropic effects in general. Sodium 358-364 Rap guanine nucleotide exchange factor 5 Homo sapiens 220-223 1196315-8 1975 The same intrarenal feed-back mechanism, normally adapting the glomerular blood supply to the resorptive capacity of the proximal-tubular epithelium (mediation via the juxta-glomerular apparatus), is responsible for the GFR- and RPF-raising effect of exogenous L-thyroxine in the intact kidney as well as in acute renal failure: both sodium reabsorption and sodium filtration are accelerated.--The special conditions under which L-thyroxine interferes with the pathogenetic process of acute renal failure, the latter being characterised by the critical insufficiency of tubular sodium reabsorption and therefore by preglomerular arterial constriction, is discussed on the basis of a new hypothesis concerning the thyrogenic nephrotropic effects in general. Sodium 358-364 Rap guanine nucleotide exchange factor 5 Homo sapiens 220-223 52007-1 1975 A suggestion that mania is associated with an increased membrane transport of sodium has been investigated in a double-blind trial of a specific Na-K A.T.P.ase inhibitor (digoxin) in twelve female inpatients with mania. Sodium 78-84 arylsulfatase L Homo sapiens 51-54 1213205-1 1975 In acute experiments on dogs, a negative correlation between arterial pressure and the blood renin activity was shown during hemodynamic shifts following occlusion of the carotid arteries or v. cava anterior, as well as ephedrinum or nitrite of sodium administration. Sodium 245-251 renin Canis lupus familiaris 93-98 1177375-7 1975 We propose that ethacrynic acid increases renin release through a hemodynamic mechanism triggered by afferent arteriolar dilation and inhibits renin release by greatly increasing the delivery of sodium to the distal convoluted tubules. Sodium 195-201 renin Canis lupus familiaris 42-47 1149327-5 1975 Without replacement of urinary losses, renin secretion increased at sodium deficits of 0.7-0.9 mmol.kg-1 in the presence of elevated rates of sodium and potassium excretion. Sodium 68-74 renin Canis lupus familiaris 39-44 237865-1 1975 The effect of Jorpes secretin on the urinary volume, pH, and excretion of sodium, potassium, chloride, bicarbonate, titratable acidity, ammonia and phosphate was studied in five healthy male volunteers with and without simultaneous aspiration of duodenal fluids. Sodium 74-80 secretin Homo sapiens 21-29 237865-2 1975 A three- to fourfold increase in urinary volume and sodium excretion occurred within the first 30 min after secretin injection and this was accompanied by a significant rise in urinary pH in each instance. Sodium 52-58 secretin Homo sapiens 108-116 4831818-0 1974 [Effect of insulin on sodium, potassium and glucose transport through jejunal mucosa of the dog (author"s transl)]. Sodium 22-28 insulin Canis lupus familiaris 11-18 4719217-1 1973 Using a triple-lumen tube perfusion technique in normal human subjects secretin (2U/kg/hour intravenously) was shown to reduce the absorption of sodium, potassium, and chloride in the most proximal 30 cm of jejunum but it had no effect on bicarbonate absorption. Sodium 145-151 secretin Homo sapiens 71-79 5084885-0 1972 Effects of renal arterial infusion of sodium and potassium on renin secretion in the dog. Sodium 38-44 renin Canis lupus familiaris 62-67 5039996-0 1972 The relationship between urinary kallikrein, renal function and the excretion of sodium and water. Sodium 81-87 kallikrein related peptidase 4 Homo sapiens 33-43 4263055-0 1972 Effects of incubations in low potassium and low sodium media on Na-K-ATPase activity in snake and chicken kidney slices. Sodium 48-54 ATPase Na+/K+ transporting subunit alpha 1 Gallus gallus 64-75 6655807-5 1983 The relative bioavailability of KS-R1, calculated on the basis of AUC and urinary recovery after intramuscular administration of ABPC sodium, was 23.1% to 28.9%, compared with 31.1% to 50.2% in the case of oral ABPC. Sodium 134-140 kinase suppressor of ras 1 Canis lupus familiaris 32-37 6312350-5 1983 Since the binding site labeled by [3H]naloxone in the presence of sodium may be an alternate conformation of the morphine receptor, these data provide further evidence that morphine and enkephalin receptors are allosterically coupled. Sodium 66-72 proenkephalin Rattus norvegicus 186-196 6843893-0 1983 Aspartate and glutamate induced reductions in extracellular free calcium and sodium concentration in area CA1 of "in vitro" hippocampal slices of rats. Sodium 77-83 carbonic anhydrase 1 Rattus norvegicus 106-109 5496905-0 1970 Spin-echo nuclear magnetic resonance evidence for complexing of sodium ions in muscle, brain, and kidney. Sodium 64-70 spindlin 1 Homo sapiens 0-4 5431662-7 1970 However, in every case increased renin activity persisted throughout depletion despite development of sodium retention sufficient to inhibit renin release in normal dogs. Sodium 102-108 renin Canis lupus familiaris 141-146 17796555-1 1969 Bean plants subjected to a sodium chloride concentratioz about onetenth that of seawater for 1 week suffered no damage if the calcium concentration of the nutrient solution was 1 millimole per liter or higher, but at lower calcium concentrations damage was severe and apparently due to a massive breakthrough of sodium into the leaves. Sodium 27-33 brain expressed associated with NEDD4 1 Homo sapiens 0-4 5347393-0 1969 The effect of oxytocin on sodium excretion. Sodium 26-32 oxytocin/neurophysin I prepropeptide Homo sapiens 14-22 5256995-3 1969 The relaxation rate of the bound sodium is found to be T(1B) (-1) = 222 +/- 19 sec(-1) compared to that of free sodium T(1F) (-1) = 17.5 sec(-1). Sodium 33-39 secretory blood group 1, pseudogene Homo sapiens 79-85 5256995-3 1969 The relaxation rate of the bound sodium is found to be T(1B) (-1) = 222 +/- 19 sec(-1) compared to that of free sodium T(1F) (-1) = 17.5 sec(-1). Sodium 33-39 secretory blood group 1, pseudogene Homo sapiens 137-143 4305249-2 1968 Relationship between renin secretion and plasma sodium concentration in the peritoneal dialyzed dog. Sodium 48-54 renin Canis lupus familiaris 21-26 6034114-9 1967 During secretin stimulation the sodium concentration in pancreatic tissue increases, and the potassium concentration falls.4. Sodium 32-38 secretin Homo sapiens 7-15 16655942-0 1964 Function of Bean Roots and Stems in Sodium Retention. Sodium 36-42 brain expressed associated with NEDD4 1 Homo sapiens 12-16 13696676-0 1961 [Action of oxytocin on the renal excretion of water, sodium and potassium]. Sodium 53-59 oxytocin/neurophysin I prepropeptide Homo sapiens 11-19 13525672-8 1958 Sodium extrusion was also blocked by high concentrations of 2-methyl-1,4-napthaquinone 8-sulfonic acid and by alpha-ketoglutarate, which are known to inhibit choline acetylase in vitro. Sodium 0-6 choline O-acetyltransferase Homo sapiens 158-175 19872792-21 1934 Since CO(2) and HCO(3) (-) diffuse into A and combine with KG and NaG the inward movement of potassium and sodium falls off in proportion as the concentration of KG and NaG is lessened. Sodium 107-113 NBAS subunit of NRZ tethering complex Homo sapiens 59-69 19872792-21 1934 Since CO(2) and HCO(3) (-) diffuse into A and combine with KG and NaG the inward movement of potassium and sodium falls off in proportion as the concentration of KG and NaG is lessened. Sodium 107-113 NBAS subunit of NRZ tethering complex Homo sapiens 66-69 20487923-2 1983 EDA uptake was temperature dependent and appeared to take place by both sodium dependent and sodium independent mechanisms. Sodium 72-78 ectodysplasin-A Rattus norvegicus 0-3 20487923-2 1983 EDA uptake was temperature dependent and appeared to take place by both sodium dependent and sodium independent mechanisms. Sodium 93-99 ectodysplasin-A Rattus norvegicus 0-3 20487923-6 1983 Potassium stimulated, calcium dependent release of radioactivity from brain slices labelled with [(14)C]EDA in the presence of sodium ions was observed. Sodium 127-133 ectodysplasin-A Rattus norvegicus 104-107 20487923-9 1983 Ouabain released radioactivity from slices labelled by [(14)C]EDA in the presence of sodium but not from slices labelled in the absence of sodium. Sodium 85-91 ectodysplasin-A Rattus norvegicus 62-65 6759835-6 1982 dTDAVP and AVP both produced significant increases in sodium excretion. Sodium 54-60 arginine vasopressin Canis lupus familiaris 3-6 7120122-1 1982 The effects of lidocaine on the rapid inward sodium current (INA) of rat ventricular muscle were studied with the double sucrose gap voltage clamp technique. Sodium 45-51 internexin neuronal intermediate filament protein, alpha Rattus norvegicus 61-64 6177202-0 1982 Restriction of hydrogen and sodium ion diffusion in porcine gastric mucin: a concentration dependent phenomenon. Sodium 28-34 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 60-73 6302768-2 1982 Voltage-clamp experiments were carried out, and sodium current (INa) was recorded on single rat cardiac cells perfused internally with Ca2+-free 140 mM Tris aspartate, 2 mM EGTA buffer, pH 7.3 at 20 degrees C. A voltage control microelectrode was impaled in the cell. Sodium 48-54 internexin neuronal intermediate filament protein, alpha Rattus norvegicus 64-67 6128148-11 1982 Another follower neuron exhibits a complex GSN-induced synaptic response comprising a slow potential similar to that seen in the A neuron and also a fast, probably sodium dependent, potential. Sodium 164-170 gelsolin Homo sapiens 43-46 7185867-6 1982 The PEP diet, which includes a beneficial change in fat/carbohydrate ratio, can alter lipid profiles, blood pressure, and sodium excretion, thus leading to improved health status and a decrease in cardiac risk factors. Sodium 122-128 progestagen associated endometrial protein Homo sapiens 4-7 6126824-1 1982 The effect of toxin from sea anemone Homostichantus duerdemi (HTX-1) on the inward sodium current was studied on the isolated neurons of spinal ganglia of a rat. Sodium 83-89 Zic family member 3 Homo sapiens 62-67 33901550-11 2021 Finally, recordings of hNav1.6 sodium currents indicated that Ct1a shifts the channel activation to a more negative potential and reduces the amplitude of the peak current. Sodium 31-37 sodium voltage-gated channel alpha subunit 8 Homo sapiens 23-30 7164145-2 1982 Most of the solutions made up using WHO glucose-electrolyte mix had a satisfactory sodium content (70 to 120 mmol/l) and osmolality (200 to 350 mosmoles/kg). Sodium 83-89 Mix paired-like homeobox Homo sapiens 60-63 7215782-0 1981 Stimulation of sodium transport across the teleost urinary bladder by urotensin II. Sodium 15-21 urotensin 2 Homo sapiens 70-82 33506439-5 2021 Besides its role in childbirth and lactation, recent evidences suggested a role for OXT in sodium balance. Sodium 91-97 oxytocin/neurophysin I prepropeptide Homo sapiens 84-87 33956427-2 2021 Receptor targets such as adrenergic, cannabinoid, P2X3 and P2X7, NMDA, serotonin, and sigma, as well as ion channels like the voltage-gated sodium channels Nav1.7 and Nav1.8 have been targeted to develop novel analgesics. Sodium 140-146 sodium voltage-gated channel alpha subunit 9 Homo sapiens 156-162 34045310-2 2021 We have previously shown that the epithelial sodium channel ENaC/UNC-8 triggers an activity-dependent mechanism that drives the removal of presynaptic proteins liprin-alpha/SYD-2, Synaptobrevin/SNB-1, RAB-3 and Endophilin/UNC-57 in remodeling GABAergic neurons in C. elegans (Miller-Fleming et al., 2016). Sodium 45-51 Ras-related protein Rab-3 Caenorhabditis elegans 201-206 6779837-3 1980 Different cations exert specific effects, particularly sodium, which seems to regulate in some way the diamine oxidase activity (Fig. Sodium 55-61 amine oxidase copper containing 1 Sus scrofa 103-118 474764-6 1979 We conclude that AVP produces only a transient hypervolemic hypertension; that AVP is a natriuretic agent, either directly or indirectly, both acutely and chronically; and that chronically it is a more potent controller of the plasma sodium concentration than of the total body water except in extreme cases. Sodium 234-240 arginine vasopressin Canis lupus familiaris 79-82 253374-5 1978 Higher doses (140 pmol.h-1) were significantly pressor and caused increased excretion of sodium, chloride, urea and creatinine. Sodium 89-95 H1.5 linker histone, cluster member Homo sapiens 23-26 909130-11 1977 Furthermore, the change in mean arterial pressure induced by infusion of angiotensin II analogue seemed to correlate with DBH activity change by sodium depletion. Sodium 145-151 dopamine beta-hydroxylase Homo sapiens 122-125 301179-7 1977 Accordingly, these data are interpreted to mean that the values of E(1), approximately 130 mV, represent the E(Na) of the sodium pump at the inner barrier. Sodium 122-128 small nucleolar RNA, H/ACA box 73A Homo sapiens 67-71 33823138-0 2021 A central mechanism of analgesia in mice and humans lacking the sodium channel NaV1.7. Sodium 64-70 sodium voltage-gated channel alpha subunit 9 Homo sapiens 79-85 33823138-1 2021 Deletion of SCN9A encoding the voltage-gated sodium channel NaV1.7 in humans leads to profound pain insensitivity and anosmia. Sodium 45-51 sodium voltage-gated channel alpha subunit 9 Homo sapiens 12-17 33823138-1 2021 Deletion of SCN9A encoding the voltage-gated sodium channel NaV1.7 in humans leads to profound pain insensitivity and anosmia. Sodium 45-51 sodium voltage-gated channel alpha subunit 9 Homo sapiens 60-66 33957067-1 2021 How genetic loss of the sodium channel NaV1.7 results in painlessness is puzzling. Sodium 24-30 sodium voltage-gated channel alpha subunit 9 Homo sapiens 39-45 33788378-8 2021 The sialic acids on UMOD, local pH and sodium concentration could impact the binding capacity between UMOD and cFH and thus regulate the activation of complement AP. Sodium 39-45 uromodulin Homo sapiens 102-106 33788378-8 2021 The sialic acids on UMOD, local pH and sodium concentration could impact the binding capacity between UMOD and cFH and thus regulate the activation of complement AP. Sodium 39-45 complement factor H Homo sapiens 111-114 33782571-1 2021 Evidence from human genetic pain disorders shows that voltage-gated sodium channel alpha-subtypes Nav1.7, Nav1.8 and Nav1.9 are important in the peripheral signalling of pain. Sodium 68-74 sodium voltage-gated channel alpha subunit 9 Homo sapiens 98-104 33782571-1 2021 Evidence from human genetic pain disorders shows that voltage-gated sodium channel alpha-subtypes Nav1.7, Nav1.8 and Nav1.9 are important in the peripheral signalling of pain. Sodium 68-74 sodium voltage-gated channel alpha subunit 10 Homo sapiens 106-112 33895391-0 2021 Mutations in the sodium channel genes SCN1A, SCN3A, and SCN9A in children with epilepsy with febrile seizures plus(EFS+). Sodium 17-23 sodium voltage-gated channel alpha subunit 9 Homo sapiens 56-61 33895391-5 2021 RESULTS: We identified 10 putatively causative sodium channel gene variants in 49 patients with EFS+, including 8 variants in SCN1A (R500Q appeared twice), one in SCN3A and one in SCN9A. Sodium 47-53 sodium voltage-gated channel alpha subunit 9 Homo sapiens 180-185 33910361-3 2021 Here, we investigated the cardiac expression of SCN10A and the function of a variant-sensitive intronic enhancer previously linked to the regulation of SCN5A, encoding the major essential cardiac sodium channel NaV1.5. Sodium 196-202 sodium channel, voltage-gated, type V, alpha Mus musculus 211-217 33910361-11 2021 In patch-clamp transfection experiments, expression of Scn10a-short-encoded NaV1.8-short increased NaV1.5-mediated sodium current. Sodium 115-121 sodium channel, voltage-gated, type V, alpha Mus musculus 99-105 33910361-12 2021 We propose that non-coding genetic variation modulates transcriptional regulation of Scn10a-short in cardiomyocytes that impacts on NaV1.5-mediated sodium current and heart rhythm. Sodium 148-154 sodium channel, voltage-gated, type V, alpha Mus musculus 132-138 33900854-1 2021 High-sodium-intake (HS) inhibited epithelial-sodium-channel (ENaC) in the aldosterone-sensitive-distal-nephron (ASDN) and Na+-Cl--cotransporter (NCC) by suppressing basolateral Kir4.1/Kir5.1 in the distal-convoluted-tubule (DCT) thereby increasing renal Na+ excretion but not affecting K+ excretion. Sodium 5-11 potassium inwardly-rectifying channel, subfamily J, member 16 Mus musculus 184-190 33901038-2 2021 We report a heterozygous de novo missense variant of SCN2A, the gene coding a voltage-gated sodium ion channel enriched in the axon initial segment and nodes of Ranvier of "immature" neocortical pyramidal neurons. Sodium 92-98 sodium voltage-gated channel alpha subunit 2 Homo sapiens 53-58 33967827-9 2021 The LP rats exhibited augmented Na+/K+-ATPase in the proximal segments, and NOS1 immunoreactivity in whole renal tissue was associated with sodium retention in the proximal nephron segments. Sodium 140-146 nitric oxide synthase 1 Rattus norvegicus 76-80 33880743-3 2021 TGF-beta, by internalization of the epithelial sodium channel (ENaC), suppresses the anti-oxidant system, downregulates the cystic fibrosis transmembrane conductance regulator (CFTR), and activates the plasminogen activator inhibitor 1 (PAI-1) and nuclear factor-kappa-light-chain-enhancer of activated B cells (NF-kB). Sodium 47-53 enac None 63-67 33864813-13 2021 The increased urine excretion of glucose and sodium was mediated by decreased renal SGLT2 expression due to inactivation of the IKKalpha/beta/NF-kappaB-induced inflammatory response. Sodium 45-51 solute carrier family 5 (sodium/glucose cotransporter), member 2 Mus musculus 84-89 33928121-6 2021 In addition, comparative substrate profiles of two related sodium neutral amino acid transporters known as SNAT1 and SNAT2, revealed the latter as a significant leucine accumulator. Sodium 59-65 solute carrier family 38 member 2 Homo sapiens 117-122 33921209-0 2021 NFAT5 Is Involved in GRP-Enhanced Secretion of GLP-1 by Sodium. Sodium 56-62 nuclear factor of activated T cells 5 Mus musculus 0-5 33921209-6 2021 High sodium increases cellular GLP-1 expression, while low and high sodium concentrations increase NFAT5 and GRPR expression. Sodium 68-74 nuclear factor of activated T cells 5 Mus musculus 99-104 33921209-7 2021 Silencing NFAT5 in L-cells abrogates the stimulatory effect of GRP on the high sodium-induced GLP-1 secretion and protein expression, and the sodium-induced increase in GRPR expression. Sodium 79-85 nuclear factor of activated T cells 5 Mus musculus 10-15 33921209-7 2021 Silencing NFAT5 in L-cells abrogates the stimulatory effect of GRP on the high sodium-induced GLP-1 secretion and protein expression, and the sodium-induced increase in GRPR expression. Sodium 142-148 nuclear factor of activated T cells 5 Mus musculus 10-15 33921209-8 2021 GLP-1 and gastrin decrease the expression of Na+-K+/ATPase and increase the phosphorylation of sodium/hydrogen exchanger type 3 (NHE3) in human renal proximal tubule cells (hRPTCs). Sodium 95-101 solute carrier family 9 member A3 Homo sapiens 129-133 33829730-1 2021 Pseudohypoaldosteronism type 1 (PHA1) is an autosomal-recessive disorder characterized by defective regulation of body sodium levels. Sodium 119-125 sodium channel epithelial 1 subunit gamma Homo sapiens 32-36 33824491-7 2021 Furthermore, binding of prorenin and renin to the prorenin receptor in the collecting duct evokes a number of responses, including the non-proteolytic enzymatic activation of prorenin to produce ANGI from proximal tubule-derived angiotensinogen, which is then converted into ANGII by luminal angiotensin-converting enzyme; stimulation of the epithelial sodium channel (ENaC) in principal cells; and activation of intracellular pathways linked to the upregulation of cyclooxygenase 2 and profibrotic genes. Sodium 353-359 ATPase H+ transporting accessory protein 2 Homo sapiens 50-67 33692134-3 2021 In particular, a hereditary loss-of-function mutation in NaV1.7, a sodium channel protein associated with signaling in nociceptive sensory afferents, leads to insensitivity to pain without other neurodevelopmental alterations. Sodium 67-73 sodium voltage-gated channel alpha subunit 9 Homo sapiens 57-63 33850915-4 2021 Inhibition of neprilysin increases bradykinin, natriuretic peptides and adrenomedullin levels counteract the neurohormal activation that leads to sodium retention, vasoconstriction, and cardiac remodeling. Sodium 146-152 adrenomedullin Homo sapiens 72-86 33557948-1 2021 BACKGROUND: Intoxication with Patent Blue V [sodium compound of (diethylamino-4-phenyl)(hydroxy-5-disulfo-2,4-phenyl) methanol] can lead to high levels of methemoglobin and metabolic acidosis. Sodium 45-51 hemoglobin subunit gamma 2 Homo sapiens 155-168 33297863-10 2021 Conclusions: Flecainide remains an effective inhibitor of RyR2-mediated arrhythmogenic Ca release even when cardiac sodium channels are blocked. Sodium 116-122 ryanodine receptor 2, cardiac Mus musculus 58-62 33301562-5 2021 Transgenic expression of the nonconducting TRPC6 channel reduced intracellular calcium from 331 +- 34 nM (mean +- SD) to 190 +- 27 nM (P < 0.0001) and sodium from 15 +- 1 mM to 11 +- 1 mM (P < 0.0001). Sodium 151-157 transient receptor potential cation channel, subfamily C, member 6 Mus musculus 43-48 864614-5 1977 The urinary excretion of sodium and potassium increased without change in their filtered loads during AVP infusion. Sodium 25-31 arginine vasopressin Canis lupus familiaris 102-105 33144140-9 2021 GENERAL SIGNIFICANCE: Potassium/sodium ion balance or resveratrol binding can act to regulate G4 molecular switches for controlling SGK1 gene expression, thereby presenting a new avenue for drug development. Sodium 32-38 serum/glucocorticoid regulated kinase 1 Homo sapiens 132-136 842636-2 1977 However, secretin increases renal blood flow (RBF) markedly but produces only a very slight increase in sodium excretion (UNaV). Sodium 104-110 SCT Canis lupus familiaris 9-17 32908237-8 2021 Mechanistically, NaBu inhibited the protein levels of several sodium transporters stimulated by DOCA/salt in vivo, such as betaENaC, gammaENaC, NCC, and NKCC-2. Sodium 62-68 solute carrier family 12 member 1 Rattus norvegicus 153-159 983730-0 1976 Plasma renin activity following central infusion of angiotensin II and altered CSF sodium concentration in the conscious goat. Sodium 83-89 renin Capra hircus 7-12 33432425-8 2021 These results indicate that decreased KLHL3 likely plays a role in the pathogenesis of renal sodium reabsorption in hyperglycemic conditions. Sodium 93-99 kelch-like 3 Mus musculus 38-43 983730-7 1976 The results indicate that angiotensin II and changes in sodium balance modulate renal renin release also via the central nervous system. Sodium 56-62 renin Capra hircus 86-91 937140-10 1976 The results support the concept that the Kal system would be involved in excretory functions dealing both with sodium and water excretion. Sodium 111-117 kallikrein related-peptidase 5 like Rattus norvegicus 41-44 33617802-3 2021 Therefore, meloxicam, nimesulide, piroxicam, and diclofenac were selected and the whole cell patch clamp technique was used to investigate the electrophysiological regulatory effects of them on the sodium channel hNav1.5 and potassium channel hKv11.1, which were closely associated to the biotoxicity of cardiac, and to explore the potential cardiac risk mechanism. Sodium 198-204 sodium voltage-gated channel alpha subunit 5 Homo sapiens 213-220 33392644-1 2021 SCN5A gene encodes the voltage-gated sodium channel NaV1.5 which is composed of a pore-forming alpha subunit of the channel. Sodium 37-43 sodium voltage-gated channel alpha subunit 5 Homo sapiens 0-5 32167565-6 2021 Conversely, ANP-DGD induced marked stepwise increases in urinary cGMP, urine volume and sodium excretion in HF comparable to ANP, but without accompanying vasodilatory effects. Sodium 88-94 natriuretic peptides A Ovis aries 12-15 33460646-1 2021 Mutations in genes encoding the human brain-expressed voltage-gated sodium (NaV) channels NaV1.1, NaV1.2, and NaV1.6 are associated with a variety of human diseases including epilepsy, autism spectrum disorder, familial migraine, and other neurodevelopmental disorders. Sodium 68-74 sodium voltage-gated channel alpha subunit 2 Homo sapiens 98-104 33460646-1 2021 Mutations in genes encoding the human brain-expressed voltage-gated sodium (NaV) channels NaV1.1, NaV1.2, and NaV1.6 are associated with a variety of human diseases including epilepsy, autism spectrum disorder, familial migraine, and other neurodevelopmental disorders. Sodium 68-74 sodium voltage-gated channel alpha subunit 8 Homo sapiens 110-116 33392644-1 2021 SCN5A gene encodes the voltage-gated sodium channel NaV1.5 which is composed of a pore-forming alpha subunit of the channel. Sodium 37-43 sodium voltage-gated channel alpha subunit 5 Homo sapiens 52-58 33854440-0 2021 Effects of Allicin on Late Sodium Current Caused by DeltaKPQ-SCN5A Mutation in HEK293 Cells. Sodium 27-33 sodium voltage-gated channel alpha subunit 5 Homo sapiens 61-66 33417072-6 2021 GHB is a substrate for monocarboxylate transporters, including both sodium-dependent transporters (SMCT1, 2; SLC5A8; SLC5A12) and proton-dependent transporters (MCT1-4; SLC16A1, 7, 8, and 3), which represent significant determinants of absorption, renal reabsorption, and brain and tissue uptake. Sodium 68-74 solute carrier family 5 member 8 Homo sapiens 99-104 33854440-1 2021 Aim: The aim was to study the effect of Allitridum (Allicin) on the heterologous expression of the late sodium current on the DeltaKPQ-SCN5A mutations in HEK293 cells, with a view to screening new drugs for the treatment of long QT syndrome type 3 (LQT3). Sodium 104-110 sodium voltage-gated channel alpha subunit 5 Homo sapiens 135-140 33854440-3 2021 Application of Allicin 30 muM reduced the late sodium current (I Na,L ) of the Nav1.5 channel current encoded by DeltaKPQ-SCN5A from 1.92 +- 0.12 to 0.65 +- 0.03 pA/pF (P < 0.01, n = 15), which resulted in the decrease of I Na,L /I Na,P (from 0.94% +- 0.04% to 0.32% +- 0.02%). Sodium 47-53 sodium voltage-gated channel alpha subunit 5 Homo sapiens 79-85 33854440-7 2021 Conclusion: Allicin reduced the late sodium current of DeltaKPQ-SCN5A, whose mechanism may be related to the increase of channel steady-state inactivation (SSI) and intermediate-state inactivation (ISI) by the drug, thus reducing the window current. Sodium 37-43 sodium voltage-gated channel alpha subunit 5 Homo sapiens 64-69 33720265-4 2021 Overexpression of sodium-dependent multivitamin transporters (SMVTs) in HeLa and A549 (biotin receptor positive cell lines) is explored for the selective uptake of the nanophotosensitizer through receptor mediated endocytosis (interaction between biotin and SMVT). Sodium 18-24 solute carrier family 5 member 6 Homo sapiens 62-66 33828490-6 2021 It was previously reported that reduction in cardiac sodium currents (INa), observed in HF, could be due to the increased expression of an SCN5A splice variant - E28D, which results in a truncated sodium channel (Nav1.5-G1642X). Sodium 197-203 sodium voltage-gated channel alpha subunit 5 Homo sapiens 139-144 33828490-6 2021 It was previously reported that reduction in cardiac sodium currents (INa), observed in HF, could be due to the increased expression of an SCN5A splice variant - E28D, which results in a truncated sodium channel (Nav1.5-G1642X). Sodium 197-203 sodium voltage-gated channel alpha subunit 5 Homo sapiens 213-219 33828490-12 2021 In summary, the HF-associated splice variant Nav1.5-G1642X suppresses sodium currents in heart failure patients through a mechanism involving coupled-gating with the wildtype sodium channel. Sodium 70-76 sodium voltage-gated channel alpha subunit 5 Homo sapiens 45-51 33828490-12 2021 In summary, the HF-associated splice variant Nav1.5-G1642X suppresses sodium currents in heart failure patients through a mechanism involving coupled-gating with the wildtype sodium channel. Sodium 175-181 sodium voltage-gated channel alpha subunit 5 Homo sapiens 45-51 33738792-0 2021 The impact of type III sodium-dependent phosphate transporters (Pit 1 and Pit 2) on podocyte and kidney function. Sodium 23-29 solute carrier family 20 member 1 Homo sapiens 64-69 33738792-0 2021 The impact of type III sodium-dependent phosphate transporters (Pit 1 and Pit 2) on podocyte and kidney function. Sodium 23-29 solute carrier family 20 member 2 Homo sapiens 74-79 33738792-1 2021 The sodium-dependent phosphate transporters Pit 1 and Pit 2 belong to the solute carrier 20 (SLC20) family of membrane proteins. Sodium 4-10 solute carrier family 20 member 1 Homo sapiens 44-49 33738792-1 2021 The sodium-dependent phosphate transporters Pit 1 and Pit 2 belong to the solute carrier 20 (SLC20) family of membrane proteins. Sodium 4-10 solute carrier family 20 member 2 Homo sapiens 54-59 33688765-2 2021 SIK1 has been shown to act as a mediator during the cellular adaptation to variations in intracellular sodium in a variety of cell types. Sodium 103-109 salt inducible kinase 1 Mus musculus 0-4 33675749-4 2021 Canonical ankyrin-G (AnkG) has been shown to be vital for normal cardiac function, specifically cardiac excitability, via targeting and regulation of the cardiac voltage-gated sodium channel. Sodium 176-182 ankyrin 3, epithelial Mus musculus 10-19 33442236-11 2021 Conclusion: Adenovirus-encoding sh-PBEF could reduce lung injury and repair the sodium-water transport system in rats receiving CPB, likely through reducing MAPK, ERK1/2, and Akt signaling pathways. Sodium 80-86 nicotinamide phosphoribosyltransferase Rattus norvegicus 35-39 33112610-1 2021 Variants of the SLC24A5 gene, which encodes a putative potassium-dependent sodium-calcium exchanger (NCKX5) that most likely resides in the melanosome or its precursor, affect pigmentation in both humans and zebrafish (Danio rerio). Sodium 75-81 solute carrier family 24 member 5 Homo sapiens 16-23 33112610-1 2021 Variants of the SLC24A5 gene, which encodes a putative potassium-dependent sodium-calcium exchanger (NCKX5) that most likely resides in the melanosome or its precursor, affect pigmentation in both humans and zebrafish (Danio rerio). Sodium 75-81 solute carrier family 24 member 5 Homo sapiens 101-106 33403730-2 2021 We wished to determine which factors determine peritoneal sodium losses to glucose absorption (PD Na/Gluc). Sodium 58-64 glucosylceramidase beta 3 (gene/pseudogene) Homo sapiens 101-105 33065235-0 2021 Endothelial epithelial sodium channel involves in high-fat diet-induced atherosclerosis in low-density lipoprotein receptor-deficient mice. Sodium 23-29 low density lipoprotein receptor Mus musculus 91-123 32968789-0 2020 Variant-specific changes in persistent or resurgent sodium current in SCN8A-related epilepsy patient-derived neurons. Sodium 52-58 sodium voltage-gated channel alpha subunit 8 Homo sapiens 70-75 32968789-1 2020 Missense variants in the SCN8A voltage-gated sodium channel gene are linked to early-infantile epileptic encephalopathy type 13, also known as SCN8A-related epilepsy. Sodium 45-51 sodium voltage-gated channel alpha subunit 8 Homo sapiens 25-30 32968789-1 2020 Missense variants in the SCN8A voltage-gated sodium channel gene are linked to early-infantile epileptic encephalopathy type 13, also known as SCN8A-related epilepsy. Sodium 45-51 sodium voltage-gated channel alpha subunit 8 Homo sapiens 143-148 33098508-2 2020 The influence of cotransfection with genes of wild-type, constitutively-active, and dominant-negative small G-proteins RhoA, Rac1, and Cdc2 on the parameters of sodium current and its noninactivating component (INa,late) was estimated. Sodium 161-167 transforming protein RhoA Cricetulus griseus 119-123 33098508-3 2020 Among three studied small G-proteins, only RhoA (wild-type and constitutively-active type) strongly affected sodium current reducing its peak amplitude, but not the value of INa,late. Sodium 109-115 transforming protein RhoA Cricetulus griseus 43-47 33098508-5 2020 Thus, small G-protein RhoA has potential capability for suppression of sodium current, although physiological relevance of this property has to be verified. Sodium 71-77 transforming protein RhoA Cricetulus griseus 22-26 32603808-1 2020 INTRODUCTION: Sodium voltage-gated channel alpha subunit 2 (SCN2A) gene encodes the Nav1.2 subunit of voltage-gated sodium channel in pyramidal neurons. Sodium 116-122 sodium voltage-gated channel alpha subunit 2 Homo sapiens 14-58 32603808-1 2020 INTRODUCTION: Sodium voltage-gated channel alpha subunit 2 (SCN2A) gene encodes the Nav1.2 subunit of voltage-gated sodium channel in pyramidal neurons. Sodium 116-122 sodium voltage-gated channel alpha subunit 2 Homo sapiens 60-65 32603808-1 2020 INTRODUCTION: Sodium voltage-gated channel alpha subunit 2 (SCN2A) gene encodes the Nav1.2 subunit of voltage-gated sodium channel in pyramidal neurons. Sodium 116-122 sodium voltage-gated channel alpha subunit 2 Homo sapiens 84-90 32690610-2 2020 Cch1 is homologous to the pore-forming alpha1 subunit of animal voltage-gated Ca2+ channels (VGCCs) and sodium leak channels nonselective (NALCNs), while Mid1 is a membrane-associated protein similar to the regulatory alpha2/delta subunit of VGCCs and the regulatory subunit of NALCNs. Sodium 104-110 Cch1p Saccharomyces cerevisiae S288C 0-4 32888082-1 2020 PURPOSE: This work describes a staged approach to the application of pharmacokinetic-pharmacodynamic (PK-PD) modeling in the voltage-gated sodium ion channel (NaV1.7) inhibitor drug discovery effort to address strategic questions regarding in vitro to in vivo translation of target modulation. Sodium 139-145 sodium voltage-gated channel alpha subunit 9 Homo sapiens 159-165 32445872-3 2020 Interestingly, studies in rats have demonstrated that high dietary sodium intake results in down-regulation of the ACE2 expression in kidney tissue. Sodium 67-73 angiotensin I converting enzyme 2 Rattus norvegicus 115-119 32445872-4 2020 We hypothesize that low sodium status makes kidney involvement during the course of COVID-19 infection more likely due to upregulation of membrane bound ACE2 in the kidneys. Sodium 24-30 angiotensin I converting enzyme 2 Rattus norvegicus 153-157 33675749-4 2021 Canonical ankyrin-G (AnkG) has been shown to be vital for normal cardiac function, specifically cardiac excitability, via targeting and regulation of the cardiac voltage-gated sodium channel. Sodium 176-182 ankyrin 3, epithelial Mus musculus 21-25 33450052-7 2021 EXPERIMENTAL APPROACH: Patch-clamp experiments with ultra-fast solution exchange and photolabeling-coupled electrophysiology were applied to describe the unique mechanism of riluzole on Nav1.4 sodium channels. Sodium 193-199 sodium voltage-gated channel alpha subunit 4 Homo sapiens 186-192 32878087-1 2020 The sodium/calcium exchanger (NCX) is a unique calcium transport system, generally transporting calcium ions out of the cell in exchange for sodium ions. Sodium 4-10 T cell leukemia homeobox 2 Homo sapiens 30-33 32627831-8 2020 Klotho (1.0 ng/mL) significantly decreased the late sodium current (INa-Late) and L-type calcium current (ICa-L), similar to the Akt inhibitor (10 microM). Sodium 52-58 klotho Homo sapiens 0-6 33338532-0 2021 Voltage-gated sodium channel Nav1.5 promotes tumor progression and enhances chemosensitivity to 5-fluorouracil in colorectal cancer. Sodium 14-20 sodium voltage-gated channel alpha subunit 5 Homo sapiens 29-35 33480457-18 2021 Conclusion C683R is a novel SCN5A variant resulting in a co-association of gain-of-function and loss-of-function properties of the cardiac sodium channel Nav 1.5. Sodium 139-145 sodium voltage-gated channel alpha subunit 5 Homo sapiens 28-33 33480457-18 2021 Conclusion C683R is a novel SCN5A variant resulting in a co-association of gain-of-function and loss-of-function properties of the cardiac sodium channel Nav 1.5. Sodium 139-145 sodium voltage-gated channel alpha subunit 5 Homo sapiens 154-161 33417951-10 2021 The inhibitory actions of TRPM3 agonists (300 muM PS or 30 muM CIM0216) were blocked by pretreatment with primidone (TRPM3 antagonist; 30 muM), tetrodotoxin (sodium channel blocker; 1 muM), olcegepant (CGRP receptor antagonist; 10 muM), or H89 (non-specific PKA inhibitor; 30 muM). Sodium 158-164 transient receptor potential cation channel subfamily M member 3 Homo sapiens 26-31 33063281-2 2021 Surgical injury induces the upregulation of voltage-gated sodium channel Nav1.7 in dorsal root ganglion (DRG) neurons, suggesting that Nav1.7 is involved in the development of CPSP. Sodium 58-64 sodium voltage-gated channel alpha subunit 9 Rattus norvegicus 73-79 33063281-2 2021 Surgical injury induces the upregulation of voltage-gated sodium channel Nav1.7 in dorsal root ganglion (DRG) neurons, suggesting that Nav1.7 is involved in the development of CPSP. Sodium 58-64 sodium voltage-gated channel alpha subunit 9 Rattus norvegicus 135-141 33597751-4 2021 Liver cells import citrate through the sodium-dependent citrate transporter NaCT (encoded by SLC13A5) and, as a consequence, this protein is a potential target for anti-obesity drugs. Sodium 39-45 solute carrier family 13 member 5 Homo sapiens 76-80 33597751-4 2021 Liver cells import citrate through the sodium-dependent citrate transporter NaCT (encoded by SLC13A5) and, as a consequence, this protein is a potential target for anti-obesity drugs. Sodium 39-45 solute carrier family 13 member 5 Homo sapiens 93-100 33675632-6 2021 Validation of selected candidates in an independent cohort confirmed higher expression of the pro-inflammatory mediators interleukin-8, C-X-C motif chemokine 3, endothelin receptor type A, and the voltage-gated sodium channel 1.7 in SFN compared to FMS patients.We provide a diverse keratinocyte transcriptome signature between SFN and FMS patients, which may hint towards distinct pathomechanisms of small fiber sensitization in both entities and lay the basis for advanced diagnostics. Sodium 211-217 RNA exonuclease 2 Homo sapiens 233-236 33675632-6 2021 Validation of selected candidates in an independent cohort confirmed higher expression of the pro-inflammatory mediators interleukin-8, C-X-C motif chemokine 3, endothelin receptor type A, and the voltage-gated sodium channel 1.7 in SFN compared to FMS patients.We provide a diverse keratinocyte transcriptome signature between SFN and FMS patients, which may hint towards distinct pathomechanisms of small fiber sensitization in both entities and lay the basis for advanced diagnostics. Sodium 211-217 RNA exonuclease 2 Homo sapiens 328-331 33732157-7 2021 Electrophysiological experiments were performed by means of the patch-clamp technique at human heart muscle sodium channels (hNav1.5) heterogeneously expressed in human embryonic kidney cells. Sodium 108-114 sodium voltage-gated channel alpha subunit 5 Homo sapiens 125-132 33636374-2 2021 Since voltage-gated sodium channel subtype 7 (NaV1.7) contributes to mechanical hyperalgesia in several preclinical pain models and is critical for nociceptor excitability, we explored its role in the muscle hyperalgesia exhibited by adult NLB rats. Sodium 20-26 sodium voltage-gated channel alpha subunit 9 Rattus norvegicus 46-52 33636225-0 2021 MicroRNA-96 is required to prevent allodynia by repressing voltage-gated sodium channels in spinal cord. Sodium 73-79 microRNA 96 Mus musculus 0-11 33602114-2 2021 It is caused by mutations of the SCN4 gene which encodes the sodium channel in skeletal muscles. Sodium 61-67 glucose-6-phosphatase catalytic subunit 3 Homo sapiens 33-37 32345094-2 2020 There are 2 types of glucose transporters: one is a passive glucose transporter, GLUT (SLC2A), and the other is a sodium-dependent active glucose transporter, SGLT (SLC5A). Sodium 114-120 solute carrier family 2 (facilitated glucose transporter), member 5 Mus musculus 165-170 32715162-10 2020 Perhaps the strongest evidence linking LAT1 to pain is its interactions with key voltage-gated ion channels connected to nociception, namely the voltage-gated potassium channels Kv1.1 and Kv1.2 and the voltage-gated sodium channel Nav1.7. Sodium 216-222 sodium voltage-gated channel alpha subunit 9 Homo sapiens 231-237 32164457-8 2020 SIRT1 and AMPK also act on sodium transport mechanisms to reduce intracellular sodium concentrations. Sodium 27-33 sirtuin 1 Homo sapiens 0-5 32164457-8 2020 SIRT1 and AMPK also act on sodium transport mechanisms to reduce intracellular sodium concentrations. Sodium 79-85 sirtuin 1 Homo sapiens 0-5 32421318-0 2020 Prediction and Optimization of NaV1.7 Sodium Channel Inhibitors Based on Machine Learning and Simulated Annealing. Sodium 38-44 sodium voltage-gated channel alpha subunit 9 Homo sapiens 31-37 32421318-1 2020 Objectives Although NaV1.7 sodium channel is a promising drug target for pain, traditional screening strategies for discovery of NaV1.7 inhibitors are very painstaking and time-consuming. Sodium 27-33 sodium voltage-gated channel alpha subunit 9 Homo sapiens 20-26 32571169-1 2021 ABSTRACTSThe human voltage-gated sodium channel subtype 1.7 (hNaV1.7) is an attractive target for the development of potent and selective novel analgesics. Sodium 33-39 sodium voltage-gated channel alpha subunit 9 Homo sapiens 61-68 33594919-0 2021 Effects of modulation on sodium and potassium channel currents by extremely low frequency electromagnetic fields stimulation on hippocampal CA1 pyramidal cells. Sodium 25-31 carbonic anhydrase 1 Rattus norvegicus 140-143 33577799-0 2021 Inhibition of the epithelial sodium channel (ENaC) by connexin 30 involves stimulation of clathrin-mediated endocytosis. Sodium 29-35 sodium channel, nonvoltage-gated 1 alpha Mus musculus 45-49 33577799-1 2021 Mice lacking connexin 30 (Cx30) display increased epithelial sodium channel (ENaC) activity in the distal nephron and develop salt-sensitive hypertension. Sodium 61-67 sodium channel, nonvoltage-gated 1 alpha Mus musculus 77-81 32826759-3 2021 Several voltage-gated sodium (NaV) and calcium (CaV) channels are implicated in the etiology of chronic pain, particularly NaV1.1, NaV1.3, NaV1.7-NaV1.9, CaV2.2 and CaV3.2. Sodium 22-28 sodium voltage-gated channel alpha subunit 3 Homo sapiens 131-137 33454436-1 2021 The puzzle of the multifaceted actions of sodium-glucose cotransporter type-2 inhibitors (SGLT2is) is still incomplete. Sodium 42-48 solute carrier family 5 member 2 Homo sapiens 90-95 33391024-1 2020 Cardiac voltage-gated sodium channel NaV1.5, encoded by SCN5A, is crucial for the upstroke of action potential and excitation of cardiomyocytes. Sodium 22-28 sodium voltage-gated channel alpha subunit 5 Homo sapiens 56-61 33118634-0 2020 Structure and elevator mechanism of the mammalian sodium/proton exchanger NHE9. Sodium 50-56 solute carrier family 9 member A9 Homo sapiens 74-78 33308227-0 2020 Bone marrow mesenchymal stem cells derived miRNA-130b enhances epithelial sodium channel by targeting PTEN. Sodium 74-80 phosphatase and tensin homolog Homo sapiens 102-106 33308227-2 2020 Epithelial sodium channel (ENaC) located on the apical side of alveolar type 2 epithelial (AT2) cells is the primary rate limiting segment in alveolar fluid clearance. Sodium 11-17 sodium channel, nonvoltage-gated 1 alpha Mus musculus 27-31 33364976-4 2020 As such, PCSK9 is involved in the regulation of neuronal survival and protein degradation, it affects the expression of the epithelial sodium channel (ENaC) in the kidney, it interacts with white blood cells and with cells of the vascular wall, and it modifies contractile activity of cardiomyocytes, and contributes to the regulation of cholesterol uptake in the intestine. Sodium 135-141 proprotein convertase subtilisin/kexin type 9 Homo sapiens 9-14 32595517-4 2020 The bile acid transporter apical sodium dependent bile acid transporter (ASBT) showed decreased expression in rats with TNBS colitis. Sodium 33-39 solute carrier family 10 member 2 Rattus norvegicus 73-77 32529312-5 2020 Recent research has proposed that decreased TCF4 expression can lead to the increased translation of the sodium channel Nav1.8. Sodium 105-111 sodium voltage-gated channel alpha subunit 10 Homo sapiens 120-126 32092816-7 2020 Another important function of Nedd4-2 is to regulate the activity of epithelial sodium channel (ENaC), a membrane channel which mediates the clearance of fluid from the alveolar space at birth or during pulmonary edema. Sodium 80-86 NEDD4 like E3 ubiquitin protein ligase Homo sapiens 30-37 31900739-7 2020 Consequently, the sodium reabsorption from the Na+Cl- cotransporter (NCC) in the distal convoluted tubule and possibly from pendrin in the beta-intercalated cell will increase. Sodium 18-24 solute carrier family 26 member 4 Homo sapiens 124-131 31916329-5 2020 Instead, the reduction in intraglomerular pressures may be related to an action of SGLT2 inhibitors to interfere with the activity of sodium-hydrogen exchanger isoform 3 (NHE-3), thereby inhibiting proximal tubular sodium reabsorption and promoting tubuloglomerular feedback. Sodium 134-140 solute carrier family 9 member A3 Homo sapiens 171-176 31916329-10 2020 Enhanced AMPK/SIRT1 signaling may also contribute to the action of SGLT2 inhibitors to interfere with sodium transport mechanisms. Sodium 102-108 sirtuin 1 Homo sapiens 14-19 31904424-2 2020 In the heart, the protein CASK (Calcium/CAlmodulin-dependent Serine protein Kinase) negatively regulates the main cardiac sodium channel, NaV1.5, which carries the sodium current (INa) by preventing its anterograde trafficking. Sodium 122-128 internexin neuronal intermediate filament protein alpha Homo sapiens 180-183 31904424-2 2020 In the heart, the protein CASK (Calcium/CAlmodulin-dependent Serine protein Kinase) negatively regulates the main cardiac sodium channel, NaV1.5, which carries the sodium current (INa) by preventing its anterograde trafficking. Sodium 164-170 internexin neuronal intermediate filament protein alpha Homo sapiens 180-183 32006563-10 2020 Co-Immunoprecipitation and immunoblotting were conducted to demonstrate that SAM/NaHS suppressed the assembly of CaMKII with the ASK1-MKK3-p38 signal module after cerebral I/R, which decreased the phosphorylation of p38. Sodium 81-85 mitogen-activated protein kinase kinase 3 Homo sapiens 134-138 32006563-12 2020 Taken together, the results suggested that SAM/NaHS could suppress cerebral I/R injury by downregulating p38 phosphorylation via decreasing the assembly of CaMKII with the ASK1-MKK3-p38 signal module. Sodium 47-51 mitogen-activated protein kinase kinase 3 Homo sapiens 177-181 33219051-0 2020 Sodium taste cells require Skn-1a for generation and share molecular features with sweet, umami, and bitter taste cells. Sodium 0-6 POU class 2 homeobox 3 Homo sapiens 27-33 33219051-3 2020 Here we demonstrate that sodium-taste cells distributed only in the anterior oral epithelia and involved in evoking salty taste also require Skn-1a for their generation. Sodium 25-31 POU class 2 homeobox 3 Homo sapiens 141-147 33273469-0 2020 Structure of voltage-modulated sodium-selective NALCN-FAM155A channel complex. Sodium 31-37 NALCN channel auxiliary factor 1 Mus musculus 54-61 33131149-0 2020 Relationship Between Sodium Channel Function and Clinical Phenotype in SCN5A Variants Associated with Brugada syndrome. Sodium 21-27 sodium voltage-gated channel alpha subunit 5 Homo sapiens 71-76 32898538-4 2020 Surprisingly, the imidazolium salts have more pronounced destabilization effect on highly positively charged cyt c than the corresponding sodium counterparts. Sodium 138-144 cytochrome c, somatic Equus caballus 109-114 32372952-1 2020 Based on recent findings, an increased late sodium current (INa,late) plays an important pathophysiological role in cardiac diseases, including rhythm disorders. Sodium 44-50 internexin neuronal intermediate filament protein alpha Homo sapiens 60-63 32898538-6 2020 Comparison of an effect of imidazolium and sodium salts on acidic and alkaline transitions and to thermal transition of cyt c implies a role of hydrophobic interaction between imidazolium cation and polypeptide chain. Sodium 43-49 cytochrome c, somatic Equus caballus 120-125 32750454-0 2020 Secretion of the epithelial sodium channel chaperone PCSK9 from the cortical collecting duct links sodium retention with hypercholesterolemia in nephrotic syndrome. Sodium 28-34 proprotein convertase subtilisin/kexin type 9 Mus musculus 53-58 32750454-0 2020 Secretion of the epithelial sodium channel chaperone PCSK9 from the cortical collecting duct links sodium retention with hypercholesterolemia in nephrotic syndrome. Sodium 99-105 proprotein convertase subtilisin/kexin type 9 Mus musculus 53-58 32750454-1 2020 The proprotein PCSK9 functions as a chaperone for the epithelial sodium channel in the cortical collecting duct (CCD), is highly expressed in the liver, and plays a significant role in the pathogenesis of hypercholesterolemia. Sodium 65-71 proprotein convertase subtilisin/kexin type 9 Mus musculus 15-20 32750454-8 2020 Blocking epithelial sodium channel activity with Amiloride in Rrm2b-/- mice resulted in increased expression of its chaperone PCSK9 in the CCD, followed by elevated plasma levels and worsening hypercholesterolemia. Sodium 20-26 proprotein convertase subtilisin/kexin type 9 Mus musculus 126-131 33228767-0 2020 Selective deletion of endothelial mineralocorticoid receptor protects from vascular dysfunction in sodium-restricted female mice. Sodium 99-105 nuclear receptor subfamily 3, group C, member 2 Mus musculus 34-60 33365222-1 2020 Sodium-glucose cotransporter-2 (SGLT2) inhibitors assert their role as an anti-diabetic medication by reversibly inhibiting sodium-glucose cotransporters in the renal proximal tubules and resulting in enhanced glucose excretion. Sodium 124-130 solute carrier family 5 member 2 Homo sapiens 0-30 31991212-5 2020 At physiological pH, the degree of elastin mineralization is influenced by hydrolysis and complexity of medium composition, since ionic species, as sodium, potassium, magnesium, in addition to calcium and phosphorus, interfere with the calcification process. Sodium 148-154 elastin Homo sapiens 35-42 33365222-1 2020 Sodium-glucose cotransporter-2 (SGLT2) inhibitors assert their role as an anti-diabetic medication by reversibly inhibiting sodium-glucose cotransporters in the renal proximal tubules and resulting in enhanced glucose excretion. Sodium 124-130 solute carrier family 5 member 2 Homo sapiens 32-37 33165811-7 2021 Consistent with the previous results, sodium cantharidinate treatment decreased Bcl-2 and mitochondrial cytochrome-c protein expression, as well as phosphorylation of MDM2; meanwhile, it increased the levels of cleaved-caspase-3, cleaved-caspase-9, cleaved-PARP, Bax, and phosphorylated p53, thus inducing the apoptosis of pancreatic cancer cells. Sodium 38-44 caspase 9 Homo sapiens 238-247 32619119-2 2020 The skeletal muscle sodium channelopathies are a group of inherited, non-dystrophic ion channel disorders caused by heterozygous point mutations in the SCN4A gene, leading to clinical manifestations of congenital myotonia, paramyotonia, and periodic paralysis syndromes. Sodium 20-26 sodium voltage-gated channel alpha subunit 4 Homo sapiens 152-157 32768677-1 2020 BACKGROUND: Mutations in desmosomal genes linked to arrhythmogenic cardiomyopathy are commonly associated with Wnt/beta-catenin signaling abnormalities and reduction of the sodium current density. Sodium 173-179 catenin beta 1 Homo sapiens 115-127 32768677-8 2020 Moreover, we found that upon inhibition GSK3B sodium current was restored through Wnt/beta-catenin-independent mechanism. Sodium 46-52 catenin beta 1 Homo sapiens 86-98 32768677-9 2020 CONCLUSION: We propose that alterations in GSK3B-Wnt/beta-catenin signaling pathways lead to regulation of sodium current implying its role in molecular pathogenesis of arrhythmogenic cardiomyopathy. Sodium 107-113 catenin beta 1 Homo sapiens 53-65 32768485-0 2020 Modulation of sodium-coupled choline transporter CHT function in health and disease. Sodium 14-20 solute carrier family 5 (choline transporter), member 7 Mus musculus 49-52 32768485-1 2020 The sodium-coupled high-affinity choline transporter CHT plays a critical role in acetylcholine (ACh) synthesis by taking up the substrate choline from the synaptic cleft after neurotransmitter release; this conservation mechanism is the rate-limiting step for production of ACh, thereby facilitating communication by subsequent action potentials. Sodium 4-10 solute carrier family 5 (choline transporter), member 7 Mus musculus 53-56 33230925-6 2020 Sox6 has been implicated in the regulation of renin expression and JG cell recruitment in mice during sodium depletion and dehydration. Sodium 102-108 SRY (sex determining region Y)-box 6 Mus musculus 0-4 32817119-6 2020 The dendritic fields of NST relay cells, from adult male and female mice in which the alpha-subunit of the epithelial sodium channel (ENaC) was conditionally deleted in taste bud cells throughout life, were up to 2.4x larger and more complex than that of age-matched control mice. Sodium 118-124 sodium channel, nonvoltage-gated 1 alpha Mus musculus 134-138 32817119-8 2020 Overall, our results suggest that ENaC-mediated sodium taste activity is necessary for the maintenance of dendritic fields of relay cells in the gustatory NST.Significance Statement Neural activity plays major roles in the development of sensory circuits in the mammalian brain. Sodium 48-54 sodium channel, nonvoltage-gated 1 alpha Mus musculus 34-38 33107349-2 2021 This recognition led to development of SGLT2 inhibitors that inhibit proximal renal tubular renal glucose and sodium reabsorption. Sodium 110-116 solute carrier family 5 member 2 Homo sapiens 39-44 32986953-6 2020 Ionic conductivities of lithium, sodium, and magnesium ion BISCs have reached 1.16 mS cm-1, 0.40 mS cm-1, and 0.23 mS cm-1 at 25 oC in 25 mum thick films, corresponding to areal conductance as high as 464 mS cm-2, 160 mS cm-2 and 92 mS cm-2, respectively. Sodium 33-39 chemokine (C motif) ligand 1 Mus musculus 83-90 32014250-0 2020 Transport characteristics of 5-aminosalicylic acid into colonic epithelium: Involvement of sodium-coupled monocarboxylate transporter SMCT1-mediated transport system. Sodium 91-97 sodium-coupled monocarboxylate transporter 1 Xenopus laevis 134-139 32054635-0 2020 Reduced Function of the Glutathione S-Transferase S1 Suppresses Behavioral Hyperexcitability in Drosophila Expressing Mutant Voltage-Gated Sodium Channels. Sodium 139-145 Glutathione S transferase S1 Drosophila melanogaster 24-52 33081674-4 2021 Since, SGLT2 is the low affinity, high capacity glucose transporter, it allows the co-transport of sodium and glucose through it. Sodium 99-105 solute carrier family 5 member 2 Homo sapiens 7-12 33084224-2 2020 Recent data indicate that sodium channel blockers are particularly effective monotherapy in carriers of the R222Q SCN5A variant. Sodium 26-32 sodium voltage-gated channel alpha subunit 5 Homo sapiens 114-119 33062236-1 2020 Background: Patients with type 2 diabetes mellitus (T2DM) remain at increased cardiovascular residual risk and endothelial dysfunction, even after optimizing metabolic control and treatment by sodium-glucose-2 transporter inhibitors (SGLT2-is). Sodium 193-199 solute carrier family 5 member 2 Homo sapiens 234-239 32973172-1 2020 Na+-K+-2Cl- Cotransporter (NKCC1) is a protein that aids in the active transport of sodium, potassium, and chloride ions across cell membranes. Sodium 84-90 solute carrier family 12 member 2 Homo sapiens 27-32 32569350-1 2020 Inheritable and de novo variants in the cardiac voltage-gated sodium channel, Nav1.5, are responsible for both long-QT syndrome type 3 (LQT3) and Brugada syndrome type 1 (BrS1). Sodium 62-68 sodium voltage-gated channel alpha subunit 5 Homo sapiens 78-84 32569350-4 2020 We used a series of mutants at position 1784 to show that the most common inheritable Nav1.5 variant, E1784K, alters fast inactivation through two separable mechanisms: (1) a charge-dependent interaction that increases the noninactivating current characteristic of E1784K; and (2) a hyperpolarized voltage dependence and accelerated rate of fast inactivation that decreases the peak sodium current. Sodium 383-389 sodium voltage-gated channel alpha subunit 5 Homo sapiens 86-92 32569350-9 2020 These findings provide novel mechanistic insights into how the most common inheritable arrhythmogenic mixed syndrome variant, E1784K, simultaneously decreases transient sodium currents and increases noninactivating currents, leading to both BrS1 and LQT3. Sodium 169-175 sodium voltage-gated channel alpha subunit 5 Homo sapiens 250-254 32877464-4 2020 Capture probes were designed to target nine sodium channel genes (SCN3A, SCN8A-SCN11A, and SCN1B-SCN4B). Sodium 44-50 sodium voltage-gated channel alpha subunit 3 Homo sapiens 66-71 31659629-0 2020 IL-1 promotes alpha-epithelial Sodium Channel (alpha-ENaC) expression in murine lung epithelial cells: involvement of NF-kappaB. Sodium 31-37 sodium channel, nonvoltage-gated 1 alpha Mus musculus 47-57 31659629-3 2020 Lung fluid clearance is coupled to Na+ transport via epithelial sodium channels (ENaC). Sodium 64-70 sodium channel, nonvoltage-gated 1 alpha Mus musculus 81-85 32962503-1 2020 OBJECTIVES: Normokalemic periodic paralysis (NormoKPP) of skeletal muscle is an autosomal dominant disorder caused by mutations in the gene encoding voltage-gated sodium channel protein type 4 subunit alpha (SCN4A), which leads to ion channel dysfunction. Sodium 163-169 sodium voltage-gated channel alpha subunit 4 Homo sapiens 208-213 32144488-9 2020 Furthermore, enhanced glucose reabsorption is coupled to sodium retention through the sodium-glucose cotransporter SGLT2, which induces secondary deleterious effects. Sodium 57-63 solute carrier family 5 member 2 Homo sapiens 115-120 32264956-4 2020 Loss-of-function mutations in the SCN2A gene, which encodes the voltage-gated sodium channel NaV1.2, are associated with autism rates up to 50%. Sodium 78-84 sodium voltage-gated channel alpha subunit 2 Homo sapiens 34-39 32264956-4 2020 Loss-of-function mutations in the SCN2A gene, which encodes the voltage-gated sodium channel NaV1.2, are associated with autism rates up to 50%. Sodium 78-84 sodium voltage-gated channel alpha subunit 2 Homo sapiens 93-99 31993646-1 2020 BACKGROUND: "Neuronal precursor cell expressed developmentally down-regulated 4-like" (NEDD4L) is considered a candidate gene for hypertension-both functionally and genetically-through the regulation of the ubiquitination of the epithelial sodium channel (ENaC). Sodium 240-246 NEDD4 like E3 ubiquitin protein ligase Homo sapiens 87-93 31992575-3 2020 Transgenic mice with one-half Klotho deficiency displayed a spontaneous BP increase and salt-sensitive hypertension in response to high sodium intake. Sodium 136-142 klotho Mus musculus 30-36 31642607-3 2020 The aim was to demonstrate analgesic properties of a potent selective Nav 1.7 sodium channel blocker, PF-05089771, alone and concomitantly with pregabalin in healthy subjects using a battery of human evoked pain models. Sodium 78-84 sodium voltage-gated channel alpha subunit 9 Homo sapiens 70-77 31959933-4 2020 Here we report that serotonin 2c receptor (Htr2c)-expressing neurons in the lateral parabrachial nucleus (LPBNHtr2c neurons) inhibit sodium appetite. Sodium 133-139 5-hydroxytryptamine receptor 2C Homo sapiens 43-48 31959933-4 2020 Here we report that serotonin 2c receptor (Htr2c)-expressing neurons in the lateral parabrachial nucleus (LPBNHtr2c neurons) inhibit sodium appetite. Sodium 133-139 5-hydroxytryptamine receptor 2C Homo sapiens 106-115 31959933-7 2020 Notably, the physiological role of Htr2c expressed by LPBN neurons is to disinhibit sodium appetite. Sodium 84-90 5-hydroxytryptamine receptor 2C Homo sapiens 35-40 31959933-8 2020 Our results suggest that LPBNHtr2c neurons act as a brake against sodium appetite and that their alleviation is required for the full manifestation of sodium appetite. Sodium 66-72 5-hydroxytryptamine receptor 2C Homo sapiens 25-34 31959933-8 2020 Our results suggest that LPBNHtr2c neurons act as a brake against sodium appetite and that their alleviation is required for the full manifestation of sodium appetite. Sodium 151-157 5-hydroxytryptamine receptor 2C Homo sapiens 25-34 32078054-3 2020 Recent genome studies suggested an involvement of SCN10A sodium channels (NaV1.8) in atrial electrophysiology. Sodium 57-63 sodium voltage-gated channel alpha subunit 10 Homo sapiens 50-56 32078054-3 2020 Recent genome studies suggested an involvement of SCN10A sodium channels (NaV1.8) in atrial electrophysiology. Sodium 57-63 sodium voltage-gated channel alpha subunit 10 Homo sapiens 74-80 32903469-1 2020 Background: Long QT syndrome type 3 (LQT3) is caused by gain-of-function mutations in the SCN5A gene, which encodes the alpha subunit of the cardiac voltage-gated sodium channel. Sodium 163-169 sodium voltage-gated channel alpha subunit 5 Homo sapiens 37-41 32903469-1 2020 Background: Long QT syndrome type 3 (LQT3) is caused by gain-of-function mutations in the SCN5A gene, which encodes the alpha subunit of the cardiac voltage-gated sodium channel. Sodium 163-169 sodium voltage-gated channel alpha subunit 5 Homo sapiens 90-95 32770034-0 2020 Rock inhibition promotes NaV1.5 sodium channel-dependent SW620 colon cancer cell invasiveness. Sodium 32-38 sodium voltage-gated channel alpha subunit 5 Homo sapiens 25-31 32770034-5 2020 This effect was also obtained using the other ROCK inhibitor Fasudil as well as with knocking down the expression of ROCK-1 or ROCK-2, but was prevented by the inhibition of NaV1.5 voltage-gated sodium channel activity. Sodium 195-201 sodium voltage-gated channel alpha subunit 5 Homo sapiens 174-180 32442241-0 2020 Prostaglandin E2 stimulates the epithelial sodium channel (ENaC) in cultured mouse cortical collecting duct cells in an autocrine manner. Sodium 43-49 sodium channel, nonvoltage-gated 1 alpha Mus musculus 59-63 32566918-1 2020 Compelling human genetic studies have identified the voltage-gated sodium channel NaV1.7 as a promising therapeutic target for the treatment of pain. Sodium 67-73 sodium voltage-gated channel alpha subunit 9 Homo sapiens 82-88 31885713-9 2020 Furthermore, NaHS inhibited the expression of NLRP3, ASC and cleaved caspase-1, and the production of IL-1beta and IL-18 in adipocytes treated with HG. Sodium 13-17 interleukin 18 Homo sapiens 115-120 32698182-1 2020 INTRODUCTION: Liddle syndrome (LS), an autosomal dominant and inherited monogenic hypertension syndrome caused by pathogenic mutations in the epithelial sodium channel (ENaC) genes SCNN1A, SCNN1B, and SCNN1G. Sodium 153-159 sodium channel epithelial 1 subunit beta Homo sapiens 189-195 31845513-8 2020 Additionally, it reveals a direct interaction of zinc and sodium in the priming of T cell subpopulations and shows that Zip10 and MT-1 play a significant role in those differentiation pathways. Sodium 58-64 metallothionein 1L, pseudogene Homo sapiens 130-134 31993555-6 2020 Here we show that dapagliflozin-sensitive glucose- and insulin-dependent sodium uptake stimulates somatostatin secretion by elevating the cytoplasmic Na+ concentration ([Na+]i) and promoting intracellular Ca2+-induced Ca2+ release (CICR). Sodium 73-79 somatostatin Homo sapiens 98-110 31704583-7 2020 Mechanistically, NaHS upregulated SIRT1 expression, but inhibited activation of TGF-beta1/Smad3 signaling in vivo and in vitro. Sodium 17-21 sirtuin 1 Homo sapiens 34-39 31704583-8 2020 SIRT1 inhibition by a specific inhibitor EX527 significantly attenuated or abolished the ability of NaHS to reverse the CSE-induced oxidative stress. Sodium 100-104 sirtuin 1 Homo sapiens 0-5 31704583-9 2020 SIRT1 inhibition also abolished the protection of NaHS against CSE-induced EMT. Sodium 50-54 sirtuin 1 Homo sapiens 0-5 31881011-7 2019 While SIRT1 inhibition by EX 527 or silencing by siRNA transfection significantly attenuated or abolished the ability of NaHS to reverse the CSE-induced oxidative stress, mitochondrial dysfunction and the imbalance of mitochondrial fusion and fission. Sodium 121-125 sirtuin 1 Homo sapiens 6-11 31881011-8 2019 Also, SIRT1 inhibition or silencing abolished the protection of NaHS against CSE-induced cellular senescence and apoptosis. Sodium 64-68 sirtuin 1 Homo sapiens 6-11 31857666-4 2019 One of them is located in the Dmd gene encoding dystrophin, a protein important for the function and stabilization of voltage-gated calcium (Cav1.2) and sodium (Nav1.5) channels, respectively. Sodium 153-159 sodium channel, voltage-gated, type V, alpha Mus musculus 161-167 30739221-8 2019 The critical roles of the sodium pump alpha1 subunit (ATP1A1) in mediating the XPO1-targeted anticancer effect of bufalin in human glioma were further confirmed. Sodium 26-32 ATPase Na+/K+ transporting subunit alpha 1 Homo sapiens 54-60 31795459-4 2019 The expressions of alternative oxidase (AOX) genes (mainly AOX1a), AP capacity (Valt), and AOX protein amount were clearly induced more in Kunlun14 under Cd stress, and these parameters were further enhanced by applying sodium nitroprussid (SNP, a NO donor). Sodium 220-239 acyl-CoA oxidase 1 Homo sapiens 19-38 31795459-4 2019 The expressions of alternative oxidase (AOX) genes (mainly AOX1a), AP capacity (Valt), and AOX protein amount were clearly induced more in Kunlun14 under Cd stress, and these parameters were further enhanced by applying sodium nitroprussid (SNP, a NO donor). Sodium 220-239 acyl-CoA oxidase 1 Homo sapiens 40-43 31795459-4 2019 The expressions of alternative oxidase (AOX) genes (mainly AOX1a), AP capacity (Valt), and AOX protein amount were clearly induced more in Kunlun14 under Cd stress, and these parameters were further enhanced by applying sodium nitroprussid (SNP, a NO donor). Sodium 220-239 acyl-CoA oxidase 1 Homo sapiens 59-62 32442241-3 2020 The amiloride-sensitive epithelial sodium channel (ENaC) is rate limiting for transepithelial sodium transport in the aldosterone-sensitive distal nephron. Sodium 35-41 sodium channel, nonvoltage-gated 1 alpha Mus musculus 51-55 32442241-14 2020 These data suggest that in the cortical collecting duct, locally produced and secreted PGE2 can stimulate ENaC-mediated transepithelial sodium transport. Sodium 136-142 sodium channel, nonvoltage-gated 1 alpha Mus musculus 106-110 32439321-1 2020 Salt-Overly-Sensitive (SOS) signaling module comprising the sodium-transport protein SOS1 and the regulatory proteins SOS2 and SOS3, is well known as the central salt excretion system that helps plants against salt accumulation. Sodium 60-66 sodium proton exchanger, putative (NHX7) (SOS1) Arabidopsis thaliana 85-89 32639887-1 2020 To identify potential application of GLP1-RAs (glucagon-like peptide-1 receptor agonists) and SGLT2-Is (sodium-dependent glucose cotrasnsporter-2 inhibitors) in cardiovascular medicine, we performed PubMed search until March 31, 2020 and selected placebo-controlled randomized trials (RCTs) in patients with type 2 diabetes mellitus. Sodium 104-110 solute carrier family 5 member 2 Homo sapiens 94-99 32595185-5 2020 Clinical evidence, which shows that sodium-glucose-coupled transporter [Na+/glucose co-transporter (SGLT)-2] inhibitors slowed the progression of chronic kidney disease (CKD) and reduced heart failure hospitalizations and deaths, underscores the importance of the renocardiac syndrome in heart failure development in diabetic patients. Sodium 36-42 solute carrier family 5 member 2 Homo sapiens 72-107 32624180-3 2020 We discovered a novel inhibitor, EOS789, that interacts with several sodium-dependent phosphate transporters (NaPi-IIb, PiT-1, and PiT-2) known to contribute to intestinal phosphate absorption. Sodium 69-75 solute carrier family 20 member 2 Rattus norvegicus 131-136 32981895-3 2020 In this study, we found that insulin increased the expression and function of alpha-epithelial sodium channel (alpha-ENaC) as well as phosphorylation of cofilin, a family of actin-binding proteins which disassembles actin filaments, in mouse cortical collecting duct (mpkCCDc14) cells. Sodium 95-101 sodium channel, nonvoltage-gated 1 alpha Mus musculus 111-121 32706220-8 2020 RESULTS: In patient-specific cardiomyocytes we observed both lower amplitudes of currents through sodium Nav1.5 channels and L-type calcium channels, but higher amplitude of current through transient-outward potassium channels in comparison to donor cardiomyocytes. Sodium 98-104 sodium voltage-gated channel alpha subunit 5 Homo sapiens 105-111 32680508-3 2020 We tested the hypothesis that short palate lung and nasal epithelial clone 1 (SPLUNC1)-epithelial sodium channel (ENaC) interactions at the plasma membrane are required to reduce Bcc burden in normal airways. Sodium 98-104 sodium channel, nonvoltage-gated 1 alpha Mus musculus 114-118 32251506-1 2020 The cardiac sodium channel NaV1.5, encoded by the SCN5A gene, is responsible for the fast upstroke of the action potential. Sodium 12-18 sodium voltage-gated channel alpha subunit 5 Homo sapiens 27-33 32251506-1 2020 The cardiac sodium channel NaV1.5, encoded by the SCN5A gene, is responsible for the fast upstroke of the action potential. Sodium 12-18 sodium voltage-gated channel alpha subunit 5 Homo sapiens 50-55 32251506-2 2020 Mutations in SCN5A may cause sodium channel dysfunction by decreasing peak sodium current, which slows conduction and facilitates reentry-based arrhythmias, and by enhancing late sodium current, which prolongs the action potential and sets the stage for early afterdepolarization and arrhythmias. Sodium 29-35 sodium voltage-gated channel alpha subunit 5 Homo sapiens 13-18 32251506-2 2020 Mutations in SCN5A may cause sodium channel dysfunction by decreasing peak sodium current, which slows conduction and facilitates reentry-based arrhythmias, and by enhancing late sodium current, which prolongs the action potential and sets the stage for early afterdepolarization and arrhythmias. Sodium 75-81 sodium voltage-gated channel alpha subunit 5 Homo sapiens 13-18 32251506-2 2020 Mutations in SCN5A may cause sodium channel dysfunction by decreasing peak sodium current, which slows conduction and facilitates reentry-based arrhythmias, and by enhancing late sodium current, which prolongs the action potential and sets the stage for early afterdepolarization and arrhythmias. Sodium 75-81 sodium voltage-gated channel alpha subunit 5 Homo sapiens 13-18 32251506-6 2020 We here propose a novel classification of NaV1.5 (dys)function, categorized into (1) direct ionic effects of sodium influx through NaV1.5 on membrane potential and consequent action potential generation, (2) indirect ionic effects of sodium influx on intracellular homeostasis and signalling, and (3) non-ionic effects of NaV1.5, independent of sodium influx, through interactions with macro-molecular complexes within the different micro-domains of the cardiomyocyte. Sodium 109-115 sodium voltage-gated channel alpha subunit 5 Homo sapiens 42-48 32251506-6 2020 We here propose a novel classification of NaV1.5 (dys)function, categorized into (1) direct ionic effects of sodium influx through NaV1.5 on membrane potential and consequent action potential generation, (2) indirect ionic effects of sodium influx on intracellular homeostasis and signalling, and (3) non-ionic effects of NaV1.5, independent of sodium influx, through interactions with macro-molecular complexes within the different micro-domains of the cardiomyocyte. Sodium 109-115 sodium voltage-gated channel alpha subunit 5 Homo sapiens 131-137 32251506-6 2020 We here propose a novel classification of NaV1.5 (dys)function, categorized into (1) direct ionic effects of sodium influx through NaV1.5 on membrane potential and consequent action potential generation, (2) indirect ionic effects of sodium influx on intracellular homeostasis and signalling, and (3) non-ionic effects of NaV1.5, independent of sodium influx, through interactions with macro-molecular complexes within the different micro-domains of the cardiomyocyte. Sodium 109-115 sodium voltage-gated channel alpha subunit 5 Homo sapiens 131-137 32251506-6 2020 We here propose a novel classification of NaV1.5 (dys)function, categorized into (1) direct ionic effects of sodium influx through NaV1.5 on membrane potential and consequent action potential generation, (2) indirect ionic effects of sodium influx on intracellular homeostasis and signalling, and (3) non-ionic effects of NaV1.5, independent of sodium influx, through interactions with macro-molecular complexes within the different micro-domains of the cardiomyocyte. Sodium 234-240 sodium voltage-gated channel alpha subunit 5 Homo sapiens 42-48 32251506-6 2020 We here propose a novel classification of NaV1.5 (dys)function, categorized into (1) direct ionic effects of sodium influx through NaV1.5 on membrane potential and consequent action potential generation, (2) indirect ionic effects of sodium influx on intracellular homeostasis and signalling, and (3) non-ionic effects of NaV1.5, independent of sodium influx, through interactions with macro-molecular complexes within the different micro-domains of the cardiomyocyte. Sodium 234-240 sodium voltage-gated channel alpha subunit 5 Homo sapiens 42-48 32683248-2 2020 Niacin is transported into the cells by the monocarboxylate transporters: sodium-dependent monocarboxylate transporter (SMCT1 and SMCT2) and monocarboxylate transporter (MCT1). Sodium 74-80 solute carrier family 5 (sodium/glucose cotransporter), member 12 Mus musculus 130-135 32207317-3 2020 This study aims to investigate the associations of the TAS2R38 haplotype with consumption of sodium, sugar, saturated fats, and vegetables. Sodium 93-99 taste 2 receptor member 38 Homo sapiens 55-62 31625145-1 2019 OBJECTIVE: Monoallelic de novo gain-of-function variants in the voltage-gated sodium channel SCN8A are one of the recurrent causes of severe developmental and epileptic encephalopathy (DEE). Sodium 78-84 sodium voltage-gated channel alpha subunit 8 Homo sapiens 93-98 32207317-4 2020 HYPOTHESIS: We hypothesized that, compared to people who are alanine-valine-isoleucine (AVI) homozygous for the TAS2R38 gene, those who are heterozygous or homozygous for the proline-alanine-valine (PAV) haplotype would have (a) a higher intake of sodium, sugar, and saturated fat, and (b) a lower vegetable intake. Sodium 248-254 taste 2 receptor member 38 Homo sapiens 112-119 32637473-0 2020 Dataset of electrophysiological patch-clamp recordings of the effect of the compounds deltamethrin, ATx-II and beta4-peptide on human cardiac Nav1.5 sodium channel gating properties. Sodium 149-155 sodium voltage-gated channel alpha subunit 5 Homo sapiens 142-148 32061707-1 2020 Mandatory front-of-pack (FOP) labelling was proposed in Canada to highlight foods with high contents of sugars, sodium and/or saturated fats, which would be displayed on labels along with the mandatory Nutrition Facts table and voluntary nutrition claims. Sodium 112-118 chromatin target of PRMT1 Homo sapiens 10-23 32061707-1 2020 Mandatory front-of-pack (FOP) labelling was proposed in Canada to highlight foods with high contents of sugars, sodium and/or saturated fats, which would be displayed on labels along with the mandatory Nutrition Facts table and voluntary nutrition claims. Sodium 112-118 chromatin target of PRMT1 Homo sapiens 25-28 32205118-6 2020 Using patch-clamp, we showed that safinamide reversibly inhibited sodium currents in HEK293T cells transfected with hNav1.4. Sodium 66-72 sodium voltage-gated channel alpha subunit 4 Homo sapiens 116-123 32299681-9 2020 In this condition, these knockout mice became hypokalemic due to insufficient downregulation of the epithelial sodium channel (ENaC) and the renal outer medullary potassium channel (ROMK) in the collecting system. Sodium 111-117 sodium channel, nonvoltage-gated 1 alpha Mus musculus 127-131 32152499-2 2020 Hyperfiltration mainly occurs in response to signals passed from the tubule to the glomerulus: high levels of glucose in the glomerular filtrate drive increased reabsorption of glucose and sodium by the sodium-glucose cotransporters SGLT2 and SGLT1 in the proximal tubule. Sodium 189-195 solute carrier family 5 member 2 Homo sapiens 233-238 32152499-9 2020 SGLT2 inhibitors attenuate the proximal reabsorption of sodium and glucose, normalize tubuloglomerular feedback signals and mitigate hyperfiltration. Sodium 56-62 solute carrier family 5 member 2 Homo sapiens 0-5 32400862-2 2020 Voltage-gated sodium channel Nav1.5 was reported to be highly up-regulated in various types of cancers. Sodium 14-20 sodium voltage-gated channel alpha subunit 5 Homo sapiens 29-35 31125670-0 2019 SCN5A variant R222Q generated abnormal changes in cardiac sodium current and action potentials in murine myocytes and Purkinje cells. Sodium 58-64 sodium channel, voltage-gated, type V, alpha Mus musculus 0-5 31125670-12 2019 CONCLUSION: While SCN5A R222Q increases plateau inward sodium current, action potentials were unexpectedly shortened, likely reflecting an outward gating-pore current. Sodium 55-61 sodium channel, voltage-gated, type V, alpha Mus musculus 18-23 31472005-7 2019 In addition, ClC-5 dysfunction alters expression of the sodium/proton exchanger NHE3 on the PT apical surface thus altering transcellular sodium movement and hence paracellular calcium reabsorption. Sodium 56-62 solute carrier family 9 member A3 Homo sapiens 80-84 31472005-7 2019 In addition, ClC-5 dysfunction alters expression of the sodium/proton exchanger NHE3 on the PT apical surface thus altering transcellular sodium movement and hence paracellular calcium reabsorption. Sodium 56-62 chloride voltage-gated channel 5 Homo sapiens 13-18 31681845-1 2019 Sodium channel NaV1.7 controls firing of nociceptors, and its role in human pain has been validated by genetic and functional studies. Sodium 0-6 sodium voltage-gated channel alpha subunit 9 Homo sapiens 15-21 31640159-4 2019 Density functional calculations have been used to develop a mechanistic proposal that accounts for the different behavior of CF2, requiring only one equivalent of base for successful conversion of Na[nido-B11H14]- to [closo-1-CB11H12]-, and CCl2 and CBr2, which require more. Sodium 197-212 ATPase H+ transporting accessory protein 1 Homo sapiens 125-128 31444371-7 2019 At baseline, hepsin-deficient mice accumulate uromodulin, along with hyperactivated NKCC2, resulting in a positive sodium balance and a better adaptation to water deprivation. Sodium 115-121 hepsin Mus musculus 13-19 32433667-3 2020 Our group has established the role of a novel ER chaperone ERp29 (ER protein of 29 kDa) in the biogenesis of the Epithelial Sodium Channel, ENaC. Sodium 124-130 endoplasmic reticulum protein 29 Homo sapiens 59-64 32433667-3 2020 Our group has established the role of a novel ER chaperone ERp29 (ER protein of 29 kDa) in the biogenesis of the Epithelial Sodium Channel, ENaC. Sodium 124-130 endoplasmic reticulum protein 29 Homo sapiens 66-86 32596332-8 2020 Patients in the TDF group had higher AST, hemoglobin, and serum sodium levels and lower MELD-Na score. Sodium 64-70 sex determining region Y Homo sapiens 16-19 32315024-0 2020 Ubiquitination-activating enzymes UBE1 and UBA6 regulate ubiquitination and expression of cardiac sodium channel Nav1.5. Sodium 98-104 ubiquitin like modifier activating enzyme 1 Homo sapiens 34-38 32315024-0 2020 Ubiquitination-activating enzymes UBE1 and UBA6 regulate ubiquitination and expression of cardiac sodium channel Nav1.5. Sodium 98-104 sodium voltage-gated channel alpha subunit 5 Homo sapiens 113-119 32315024-1 2020 Cardiac sodium channel Nav1.5 is associated with cardiac arrhythmias and heart failure. Sodium 8-14 sodium voltage-gated channel alpha subunit 5 Homo sapiens 23-29 32315024-5 2020 Western blot analysis and patch-clamping recordings showed that overexpression of UBE1 or UBA6 increased ubiquitination of Nav1.5 and significantly reduced Nav1.5 expression and sodium current density, and knockdown of UBE1 or UBA6 expression significantly increased Nav1.5 expression and sodium current density in HEK293/Nav1.5 cells. Sodium 178-184 ubiquitin like modifier activating enzyme 1 Homo sapiens 82-86 32407401-1 2020 Myotonia congenita and hypokalemic periodic paralysis type 2 are both rare genetic channelopathies caused by mutations in the CLCN1 gene encoding voltage-gated chloride channel CLC-1 and the SCN4A gene encoding voltage-gated sodium channel Nav1.4. Sodium 225-231 sodium voltage-gated channel alpha subunit 4 Homo sapiens 191-196 32404204-11 2020 Metformin and SGLT2 inhibitors may also differ in their ability to mitigate diabetes-related increases in intracellular sodium concentration and its adverse effects on mitochondrial functional integrity. Sodium 120-126 solute carrier family 5 member 2 Homo sapiens 14-19 32457696-4 2020 Based on gained insight using sodium-glucose transporter 2 (SGLT-2) inhibitors, herein, we propose a role for enhanced post-prandial proximal tubular sodium uptake, mediated by increased glucose-sodium co-transport, as daily filtered glucose increases, and reduced sodium uptake when glucose reabsorption diminishes. Sodium 30-36 solute carrier family 5 member 2 Homo sapiens 60-66 31074652-11 2019 These findings provide direct evidence of dietary sodium-induced endothelial cell oxidative stress and suggest that NADPH-derived reactive oxygen species contribute to sodium-induced declines in microvascular function. Sodium 168-174 2,4-dienoyl-CoA reductase 1 Homo sapiens 116-121 31109455-1 2019 We have previously shown that blockade of ATP-binding cassette transporter A1 (ABCA1) with cyclosporine A (CsA) stimulates the epithelial sodium channel (ENaC) in cultured distal nephron cells. Sodium 138-144 ATP-binding cassette, sub-family A (ABC1), member 1 Mus musculus 42-77 31109455-1 2019 We have previously shown that blockade of ATP-binding cassette transporter A1 (ABCA1) with cyclosporine A (CsA) stimulates the epithelial sodium channel (ENaC) in cultured distal nephron cells. Sodium 138-144 ATP-binding cassette, sub-family A (ABC1), member 1 Mus musculus 79-84 31098988-1 2019 Sodium-coupled monocarboxylate transporter SMCT1 (SLC5A8) mediates monocarboxylate transport in the proximal tubule of the kidney. Sodium 0-6 solute carrier family 5 member 8 Homo sapiens 43-48 31098988-1 2019 Sodium-coupled monocarboxylate transporter SMCT1 (SLC5A8) mediates monocarboxylate transport in the proximal tubule of the kidney. Sodium 0-6 solute carrier family 5 member 8 Homo sapiens 50-56 31423419-10 2019 Factor 2 characterized by high loadings for carbohydrate, animal protein, fat, cholesterol, saturated fatty acid, sodium, biotin, copper, iron, fluoride, zinc, and calcium. Sodium 114-120 transcription termination factor 2 Homo sapiens 0-8 30834459-1 2019 The voltage-gated sodium channel NaV1.7, encoded by the gene SCN9A, is located in peripheral neurons and plays an important role in epileptogenesis. Sodium 18-24 sodium voltage-gated channel alpha subunit 9 Homo sapiens 33-39 30834459-1 2019 The voltage-gated sodium channel NaV1.7, encoded by the gene SCN9A, is located in peripheral neurons and plays an important role in epileptogenesis. Sodium 18-24 sodium voltage-gated channel alpha subunit 9 Homo sapiens 61-66 31074207-1 2019 In the mammalian small intestine, sodium is primarily absorbed by Na+ /H+ exchange (NHE3) and Na-glucose cotransport (SGLT1) in the brush border membrane (BBM) of villus cells. Sodium 34-40 solute carrier family 9 member A3 Homo sapiens 84-88 32457696-4 2020 Based on gained insight using sodium-glucose transporter 2 (SGLT-2) inhibitors, herein, we propose a role for enhanced post-prandial proximal tubular sodium uptake, mediated by increased glucose-sodium co-transport, as daily filtered glucose increases, and reduced sodium uptake when glucose reabsorption diminishes. Sodium 150-156 solute carrier family 5 member 2 Homo sapiens 30-58 32457696-4 2020 Based on gained insight using sodium-glucose transporter 2 (SGLT-2) inhibitors, herein, we propose a role for enhanced post-prandial proximal tubular sodium uptake, mediated by increased glucose-sodium co-transport, as daily filtered glucose increases, and reduced sodium uptake when glucose reabsorption diminishes. Sodium 150-156 solute carrier family 5 member 2 Homo sapiens 60-66 32457696-4 2020 Based on gained insight using sodium-glucose transporter 2 (SGLT-2) inhibitors, herein, we propose a role for enhanced post-prandial proximal tubular sodium uptake, mediated by increased glucose-sodium co-transport, as daily filtered glucose increases, and reduced sodium uptake when glucose reabsorption diminishes. Sodium 150-156 solute carrier family 5 member 2 Homo sapiens 30-58 32457696-4 2020 Based on gained insight using sodium-glucose transporter 2 (SGLT-2) inhibitors, herein, we propose a role for enhanced post-prandial proximal tubular sodium uptake, mediated by increased glucose-sodium co-transport, as daily filtered glucose increases, and reduced sodium uptake when glucose reabsorption diminishes. Sodium 150-156 solute carrier family 5 member 2 Homo sapiens 60-66 32027092-3 2020 Transcriptional profiling of ion channels in the heart in a subset of patients with Brugada syndrome revealed an inverse relationship between the expression of NaX and NaV 1.5 suggesting that, in cardiac myocytes, the expression of these channels may be linked. Sodium 160-163 sodium voltage-gated channel alpha subunit 5 Homo sapiens 168-175 32027092-6 2020 Knocking down NaX expression decreased NaV 1.5 mRNA and protein and reduced the inward sodium current (INa+ ) following cell depolarization. Sodium 14-17 sodium voltage-gated channel alpha subunit 5 Homo sapiens 39-46 32027092-7 2020 When the expression of NaV 1.5 was knocked down, ~85% of the INa+ was reduced consistent with the observations that NaV 1.5 is the main voltage-gated sodium channel in cardiac muscle and that NaX likely does not directly participate in mediating the INa+ following depolarization. Sodium 150-156 sodium voltage-gated channel alpha subunit 5 Homo sapiens 23-30 32027092-7 2020 When the expression of NaV 1.5 was knocked down, ~85% of the INa+ was reduced consistent with the observations that NaV 1.5 is the main voltage-gated sodium channel in cardiac muscle and that NaX likely does not directly participate in mediating the INa+ following depolarization. Sodium 192-195 sodium voltage-gated channel alpha subunit 5 Homo sapiens 23-30 32027092-8 2020 Silencing NaV 1.5 expression led to significant upregulation of NaX mRNA. Sodium 64-67 sodium voltage-gated channel alpha subunit 5 Homo sapiens 10-17 32027092-9 2020 Similar to NaV 1.5, NaX protein levels were rapidly downregulated when the intracellular [Ca2+ ] was increased either by CaCl2 or caffeine. Sodium 20-23 sodium voltage-gated channel alpha subunit 5 Homo sapiens 11-18 32034107-7 2020 In contrast, upregulation of pendrin induced by aldosterone excess combined with a high-salt diet was scarcely affected by deletion of mineralocorticoid receptor in intercalated cells, but depended instead on hypokalemic alkalosis through the activated mineralocorticoid receptor-epithelial sodium channel cascade in principal cells. Sodium 291-297 solute carrier family 26, member 4 Mus musculus 29-36 31612502-3 2020 Here, we show that the Nav 1.5 sodium channel carries persistent inward Na+ current which depolarizes the resting Vm at the timescale of minutes. Sodium 31-37 sodium voltage-gated channel alpha subunit 5 Homo sapiens 23-30 31916038-0 2020 Sodium absorption stimulator prostasin (PRSS8) has an anti-inflammatory effect via downregulation of TLR4 signaling in inflammatory bowel disease. Sodium 0-6 protease, serine 8 (prostasin) Mus musculus 29-38 31916038-0 2020 Sodium absorption stimulator prostasin (PRSS8) has an anti-inflammatory effect via downregulation of TLR4 signaling in inflammatory bowel disease. Sodium 0-6 protease, serine 8 (prostasin) Mus musculus 40-45 31916038-1 2020 BACKGROUND: Prostasin (PRSS8) is a stimulator of epithelial sodium transport. Sodium 60-66 protease, serine 8 (prostasin) Mus musculus 12-21 31916038-1 2020 BACKGROUND: Prostasin (PRSS8) is a stimulator of epithelial sodium transport. Sodium 60-66 protease, serine 8 (prostasin) Mus musculus 23-28 32059997-1 2020 The inappropriate over-activation of the with-no-lysine kinase (WNK)-STE20/SPS1-related proline/alanine-rich kinase (SPAK)-sodium chloride cotransporter (NCC) phosphorylation cascade increases sodium reabsorption in distal kidney nephrons, resulting in salt-sensitive hypertension. Sodium 123-129 serine/threonine kinase 39 Mus musculus 117-121 32006921-9 2020 Sodium-glucose cotransporter-2 (SGLT-2) inhibitors are a novel class of antidiabetic drugs that produce glycosuric and natriuretic effects by inhibiting glucose and sodium reabsorption from the renal proximal tubules and have already shown benefits in cardiovascular outcome trials. Sodium 165-171 solute carrier family 5 member 2 Homo sapiens 0-30 32006921-9 2020 Sodium-glucose cotransporter-2 (SGLT-2) inhibitors are a novel class of antidiabetic drugs that produce glycosuric and natriuretic effects by inhibiting glucose and sodium reabsorption from the renal proximal tubules and have already shown benefits in cardiovascular outcome trials. Sodium 165-171 solute carrier family 5 member 2 Homo sapiens 32-38 32228447-0 2020 Characterization of TMC-1 in C. elegans sodium chemotaxis and sodium conditioned aversion. Sodium 40-46 Transmembrane channel-like protein 1 Caenorhabditis elegans 20-25 32228447-0 2020 Characterization of TMC-1 in C. elegans sodium chemotaxis and sodium conditioned aversion. Sodium 62-68 Transmembrane channel-like protein 1 Caenorhabditis elegans 20-25 32228447-4 2020 Transmembrane channel-like 1 (tmc-1) has been suggested to encode a sodium-sensitive channel required for sodium chemosensation in C. elegans, but its specific role remains unclear. Sodium 68-74 Transmembrane channel-like protein 1 Caenorhabditis elegans 0-28 32228447-4 2020 Transmembrane channel-like 1 (tmc-1) has been suggested to encode a sodium-sensitive channel required for sodium chemosensation in C. elegans, but its specific role remains unclear. Sodium 68-74 Transmembrane channel-like protein 1 Caenorhabditis elegans 30-35 30957627-1 2019 Background Dopamine D5 receptor (D5R) plays an important role in the maintenance of blood pressure by regulating renal sodium transport. Sodium 119-125 dopamine receptor D5 Mus musculus 11-31 32228447-4 2020 Transmembrane channel-like 1 (tmc-1) has been suggested to encode a sodium-sensitive channel required for sodium chemosensation in C. elegans, but its specific role remains unclear. Sodium 106-112 Transmembrane channel-like protein 1 Caenorhabditis elegans 0-28 32228447-4 2020 Transmembrane channel-like 1 (tmc-1) has been suggested to encode a sodium-sensitive channel required for sodium chemosensation in C. elegans, but its specific role remains unclear. Sodium 106-112 Transmembrane channel-like protein 1 Caenorhabditis elegans 30-35 32228447-5 2020 RESULTS: We report that TMC-1 is necessary for sodium attraction, but not aversion in the nematode. Sodium 47-53 Transmembrane channel-like protein 1 Caenorhabditis elegans 24-29 32228447-7 2020 In addition, we show that sodium conditioned aversion is dependent on TMC-1 and disrupts not only sodium induced attraction, but also lithium. Sodium 26-32 Transmembrane channel-like protein 1 Caenorhabditis elegans 70-75 30788598-1 2019 Increased late sodium current (late INa) is an important arrhythmogenic trigger in cardiac disease. Sodium 15-21 internexin neuronal intermediate filament protein, alpha Mus musculus 36-39 32228447-7 2020 In addition, we show that sodium conditioned aversion is dependent on TMC-1 and disrupts not only sodium induced attraction, but also lithium. Sodium 98-104 Transmembrane channel-like protein 1 Caenorhabditis elegans 70-75 32228447-8 2020 CONCLUSIONS: These findings represent the first time a role for TMC-1 has been described in sodium and lithium attraction in vivo, as well as in sodium conditioned aversion. Sodium 92-98 Transmembrane channel-like protein 1 Caenorhabditis elegans 64-69 30618807-1 2018 Background: Carriers of the E161K mutation in the SCN5A gene, encoding the NaV1.5 pore-forming alpha-subunit of the ion channel carrying the fast sodium current (INa), show sinus bradycardia and occasional exit block. Sodium 146-152 internexin neuronal intermediate filament protein alpha Homo sapiens 162-165 32228447-9 2020 Together this clarifies TMC-1"s importance in sodium hedonics and offer molecular insight into salt chemotaxis learning. Sodium 46-52 Transmembrane channel-like protein 1 Caenorhabditis elegans 24-29 31729509-3 2020 NaSr5(BO3)(SiO4)2 crystallizes in a monoclinic space group of P21/c with a 3D structure consisting of a splendid strontium 3D framework strengthened by isolated BO3 and SiO4 groups. Sodium 0-17 H3 histone pseudogene 16 Homo sapiens 62-65 30487736-10 2018 A similar TTX-insensitive current was found in early postnatal crista hair cells (P5-9) and constituted approximately one third of the total sodium current. Sodium 141-147 HLA complex P5B Homo sapiens 82-86 30365537-10 2018 The results suggest that applying 50 muM of GA3 to the development of Tifton 85 bermudagrass provides higher dry matter yield and removal of nitrogen, phosphorus, and sodium for the first crop cycle in CWs. Sodium 167-173 succinyl-CoA:glutarate-CoA transferase Homo sapiens 44-47 30102121-0 2020 Fixed-bed column system for Cd2+ uptake from aqueous solution by sodium- and thiourea-modified clinoptilolite-rich tuff. Sodium 65-71 CD2 molecule Homo sapiens 28-31 29803110-7 2018 In addition, BAs increased the expression of the Solute Carrier family 9 member A 2 (P < 0.01) that encodes a sodium hydrogen exchanger. Sodium 113-119 sodium/hydrogen exchanger 2 Capra hircus 49-83 29934352-9 2018 Using Fluoro-Gold tracing and immunohistochemistry for c-Fos and Foxp2, a marker of sodium-deprivation responsive neurons, we revealed brainstem populations of neurons that are activated by sodium depletion and project directly to the ventral tegmental area. Sodium 190-196 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 55-60 29934352-9 2018 Using Fluoro-Gold tracing and immunohistochemistry for c-Fos and Foxp2, a marker of sodium-deprivation responsive neurons, we revealed brainstem populations of neurons that are activated by sodium depletion and project directly to the ventral tegmental area. Sodium 190-196 forkhead box P2 Rattus norvegicus 65-70 31756367-5 2020 We review the evidence for an important role of sodium-coupled glucose uptake through SGLT1 for carbohydrate sensing, of free-fatty acid receptors FFAR1/FFAR4 and the monoacyl-glycerol sensing receptor GPR119 for lipid detection, of the calcium-sensing receptor CASR and GPR142 for protein sensing, and additional modulation by neurotransmitters such as somatostatin and galanin. Sodium 48-54 G protein-coupled receptor 142 Homo sapiens 271-277 31986004-2 2020 However, instability of RNA and inefficiency of RNA therapy limit the use of miR-NAs in the treatment of AIPC. Sodium 81-84 myosin regulatory light chain interacting protein Homo sapiens 77-80 29808931-1 2018 KEY POINTS: Slc4a4 (mouse) encodes at least five variants of the electrogenic sodium/bicarbonate transporter NBCe1. Sodium 78-84 solute carrier family 4 (anion exchanger), member 4 Mus musculus 12-18 29738041-10 2018 According to multivariate linear regression, GFR was independently correlated with sodium excretion (beta=0.11; p<0.001), age (beta=-0.67; p<0.001), female sex (beta=-0.20; p<0.001), and body mass index (BMI; beta=-0.09; p<0.001). Sodium 83-89 Rap guanine nucleotide exchange factor 5 Homo sapiens 45-48 30009404-4 2018 Patch clamp was used to record sodium current (INa ) in single canine RV and LV epicardial (epi) and endocardial (endo) myocytes. Sodium 31-37 internexin neuronal intermediate filament protein alpha Canis lupus familiaris 47-50 29888331-3 2018 We report a pyrolyzed polyacrylonitrile/selenium disulfide (pPAN/SeS2) composite with dramatically enhanced active material content (63 wt %) and superior performances for both lithium and sodium storage. Sodium 189-195 secernin 2 Homo sapiens 65-69 29659026-0 2018 beta1 subunit stabilises sodium channel Nav1.7 against mechanical stress. Sodium 25-31 sodium voltage-gated channel alpha subunit 9 Homo sapiens 40-46 29659026-1 2018 KEY POINTS: The voltage-gated sodium channel Nav1.7 is a key player in neuronal excitability and pain signalling. Sodium 30-36 sodium voltage-gated channel alpha subunit 9 Homo sapiens 45-51 29694688-8 2018 The highest total sodium (NaT) values (1.02 +- 0.06 arbitrary units) in the clot were observed initially, dropped to 0.69 +- 0.13 arbitrary units after one day and increased again to initial values. Sodium 18-24 bromodomain containing 2 Homo sapiens 26-29 29393394-6 2018 In contrast, the expression of protein kinase C (PKC)-gamma, one of the negative modulators for sodium currents, increased by ~1-fold. Sodium 96-102 protein kinase C, gamma Rattus norvegicus 31-59 29491733-2 2018 In arabidopsis, the Ca2+ activated SOS3 interacts with SOS2 which further activates SOS1, a Na+/H+ antiporter, responsible for removing toxic sodium ions from the cells. Sodium 142-148 Protein kinase superfamily protein Arabidopsis thaliana 55-59 28590009-0 2018 Effect of rMnSOD on Sodium Reabsorption in Renal Proximal Tubule in Ochratoxin A-Treated Rats. Sodium 20-26 superoxide dismutase 2 Rattus norvegicus 10-16 30177317-5 2018 Variants involving SCN10A, which encodes a voltage-gated sodium channel, were already associated with alterations of cardiac conduction parameters and the cardiac rhythm disorder, thereby influencing the cardiac physiology and predisposing to arrhythmia. Sodium 57-63 sodium voltage-gated channel alpha subunit 10 Homo sapiens 19-25 30387376-5 2018 We demonstrate that NPY2R+ nociceptors, CHRNA3+ "silent" nociceptors and polymodal C-fibre nociceptors express different combinations of sodium channel alpha- and beta-subunits and accordingly exhibit functionally different sodium currents. Sodium 137-143 neuropeptide Y receptor Y2 Mus musculus 20-25 31904366-13 2020 Our data suggest that renal NHERF1 expression confers salt sensitivity with aging, associated with increased expression of sodium transporters. Sodium 123-129 SLC9A3 regulator 1 Rattus norvegicus 28-34 31965133-4 2020 Surface modification of CoB and FeB significantly enhances the photocurrent density of WO3 photoanodes from 0.53 to 0.83 and 0.85 mA cm-2, respectively, in transient chronoamperometry (CA) at 1.23 V vs. RHE (VRHE) under interrupted illumination in 0.1 M Na2SO4 electrolyte (pH 7), corresponding to an increase of 1.6 relative to pristine WO3. Sodium 254-260 metabolism of cobalamin associated B Homo sapiens 24-27 31922740-3 2020 Benefitted from the uniform atomic blending of Co2+ ions in the Co-glycerate precursors, CoP NPs in situ formed in the confined space with NaH2PO2 as phosphorus source during the annealing process; meanwhile, glycerate suffered carbonization and transformed into P-doped dual carbon shells during the annealing process, including interior thin carbon coating, closely encircled CoP NP, and peripheral hollow carbon sphere loading a lot of CoP NPs. Sodium 139-146 caspase recruitment domain family member 16 Homo sapiens 89-92 28585673-6 2018 RESULTS: Hyponatremic situations through modifying the axonal Na+ channels kinetics result in the rundown of the sodium current (INa). Sodium 113-119 internexin neuronal intermediate filament protein alpha Homo sapiens 129-132 29376023-3 2017 On the basis of their sodium-dependent transport modes, ASCT2 and ATB0+ have the capacity to sustain glutamine need of cancer cells; while LAT1, which is sodium independent will have the role of providing cancer cells with some amino acids with plausible signaling roles. Sodium 22-28 solute carrier family 1 member 5 Homo sapiens 56-61 29376023-3 2017 On the basis of their sodium-dependent transport modes, ASCT2 and ATB0+ have the capacity to sustain glutamine need of cancer cells; while LAT1, which is sodium independent will have the role of providing cancer cells with some amino acids with plausible signaling roles. Sodium 22-28 solute carrier family 1 member 5 Homo sapiens 66-70 31886722-2 2020 Our results have revealed a complex set of mechanisms consisting in 1) well-known PiT1/PiT2-mediated sodium-dependent Pi transport; 2) Slc20-unrelated sodium-dependent Pi transport that is sensitive to the stilbene derivatives 4,4"-diisothiocyanatostilbene-2,2"-disulphonic acid (DIDS) and (4-acetamido-4-isothiocyanostilbene-2,2-disulfonate) (SITS); 3) a sodium-independent Pi uptake system that is competitively inhibited by sulfate, bicarbonate, and arsenate and is weakly inhibited by DIDS, SITS, and phosphonoformate; and 4) an exit pathway from the cell that is partially chloride-dependent and unrelated to the known anion-exchangers expressed in VSMC. Sodium 101-107 solute carrier family 20 member 2 Rattus norvegicus 87-91 31594563-2 2020 Herein, glutathione (GSH) calibrated dual-functional system for GSH and cadmium ions (Cd2+) detection based on fluorescence resonance energy transfer (FRET) between NH2-NaYF4:Yb,Er/NaYF4@SiO2 upconversion nanoparticles (UCNPs) and gold nanoparticles (AuNPs) is designed. Sodium 165-177 CD2 molecule Homo sapiens 86-89 31966371-2 2017 Mutations of SCN2A, the gene encoding the aII subunit of the voltage-gated sodium channel (Nav1.2), have been detected in some EOEE patients. Sodium 75-81 sodium voltage-gated channel alpha subunit 2 Homo sapiens 13-18 31966371-2 2017 Mutations of SCN2A, the gene encoding the aII subunit of the voltage-gated sodium channel (Nav1.2), have been detected in some EOEE patients. Sodium 75-81 sodium voltage-gated channel alpha subunit 2 Homo sapiens 91-97 29096595-5 2017 In distal renal tubules, FGF23 signaling activates with-no-lysine kinase 4, leading to increased renal tubular reabsorption of calcium and sodium. Sodium 139-145 fibroblast growth factor 23 Homo sapiens 25-30 32407275-2 2020 The sodium channel Nav1.7 plays a critical role in pain perception. Sodium 4-10 sodium voltage-gated channel alpha subunit 9 Rattus norvegicus 19-25 29096595-6 2017 Therefore, FGF23 is not only a phosphaturic but also a calcium- and sodium-conserving hormone, a finding that may have important implications for the pathophysiology of chronic kidney disease. Sodium 68-74 fibroblast growth factor 23 Homo sapiens 11-16 32407275-9 2020 CONCLUSION: These results indicated that the sodium channel Nav1.7 in the DRG exerted an important function in paclitaxel-induced neuropathy, which was associated with ERK phosphorylation in neurons. Sodium 45-51 sodium voltage-gated channel alpha subunit 9 Rattus norvegicus 60-66 32003683-2 2020 Of note, epithelial sodium channel (ENaC) is one of the victims of LPS-induced airway injury. Sodium 20-26 sodium channel, nonvoltage-gated 1 alpha Mus musculus 36-40 28654510-2 2017 The prime antiarrhythmic mechanisms of late INa inhibition have been suggested to be (1) suppression of intracellular calcium [Cai]-mediated rhythmic activity (through reduction in Cai secondary to the decrease in intracellular sodium [Nai]) and (2) normalization of repolarization. Sodium 228-234 internexin neuronal intermediate filament protein alpha Homo sapiens 44-47 28445205-1 2017 BACKGROUND: We have previously shown that high salt intake suppresses the expression of prolyl hydroxylase domain-containing protein 2 (PHD2), an enzyme promoting the degradation of hypoxia-inducible factor (HIF)-1alpha, and increases HIF-1alpha along with its target genes in the renal medulla, which promotes sodium excretion and regulates salt sensitivity of blood pressure. Sodium 311-317 egl-9 family hypoxia-inducible factor 1 Rattus norvegicus 88-134 28445205-1 2017 BACKGROUND: We have previously shown that high salt intake suppresses the expression of prolyl hydroxylase domain-containing protein 2 (PHD2), an enzyme promoting the degradation of hypoxia-inducible factor (HIF)-1alpha, and increases HIF-1alpha along with its target genes in the renal medulla, which promotes sodium excretion and regulates salt sensitivity of blood pressure. Sodium 311-317 egl-9 family hypoxia-inducible factor 1 Rattus norvegicus 136-140 28445205-6 2017 Our results demonstrated that inhibition of miR-429 remarkably increased the levels of PHD2, which disrupted PHD2-associated adaptive activation of HIF-1alpha-mediated gene expression in response to high salt in the renal medulla and consequently inhibited urinary sodium excretion, enhanced sodium retention in response to chronic sodium overloading, and as a result, produced a salt-sensitive hypertension. Sodium 265-271 egl-9 family hypoxia-inducible factor 1 Rattus norvegicus 87-91 31585313-1 2020 Sodium-glucose cotransporter type-2 inhibitors (SGLT2is) reduce glomerular hyperfiltration in diabetic people with early diabetic nephropathy. Sodium 0-6 solute carrier family 5 member 2 Homo sapiens 48-53 28445205-6 2017 Our results demonstrated that inhibition of miR-429 remarkably increased the levels of PHD2, which disrupted PHD2-associated adaptive activation of HIF-1alpha-mediated gene expression in response to high salt in the renal medulla and consequently inhibited urinary sodium excretion, enhanced sodium retention in response to chronic sodium overloading, and as a result, produced a salt-sensitive hypertension. Sodium 265-271 egl-9 family hypoxia-inducible factor 1 Rattus norvegicus 109-113 28445205-6 2017 Our results demonstrated that inhibition of miR-429 remarkably increased the levels of PHD2, which disrupted PHD2-associated adaptive activation of HIF-1alpha-mediated gene expression in response to high salt in the renal medulla and consequently inhibited urinary sodium excretion, enhanced sodium retention in response to chronic sodium overloading, and as a result, produced a salt-sensitive hypertension. Sodium 265-271 hypoxia inducible factor 1 subunit alpha Rattus norvegicus 148-158 28445205-6 2017 Our results demonstrated that inhibition of miR-429 remarkably increased the levels of PHD2, which disrupted PHD2-associated adaptive activation of HIF-1alpha-mediated gene expression in response to high salt in the renal medulla and consequently inhibited urinary sodium excretion, enhanced sodium retention in response to chronic sodium overloading, and as a result, produced a salt-sensitive hypertension. Sodium 292-298 egl-9 family hypoxia-inducible factor 1 Rattus norvegicus 87-91 28445205-6 2017 Our results demonstrated that inhibition of miR-429 remarkably increased the levels of PHD2, which disrupted PHD2-associated adaptive activation of HIF-1alpha-mediated gene expression in response to high salt in the renal medulla and consequently inhibited urinary sodium excretion, enhanced sodium retention in response to chronic sodium overloading, and as a result, produced a salt-sensitive hypertension. Sodium 292-298 egl-9 family hypoxia-inducible factor 1 Rattus norvegicus 109-113 28445205-6 2017 Our results demonstrated that inhibition of miR-429 remarkably increased the levels of PHD2, which disrupted PHD2-associated adaptive activation of HIF-1alpha-mediated gene expression in response to high salt in the renal medulla and consequently inhibited urinary sodium excretion, enhanced sodium retention in response to chronic sodium overloading, and as a result, produced a salt-sensitive hypertension. Sodium 292-298 hypoxia inducible factor 1 subunit alpha Rattus norvegicus 148-158 28445205-6 2017 Our results demonstrated that inhibition of miR-429 remarkably increased the levels of PHD2, which disrupted PHD2-associated adaptive activation of HIF-1alpha-mediated gene expression in response to high salt in the renal medulla and consequently inhibited urinary sodium excretion, enhanced sodium retention in response to chronic sodium overloading, and as a result, produced a salt-sensitive hypertension. Sodium 292-298 egl-9 family hypoxia-inducible factor 1 Rattus norvegicus 87-91 28445205-6 2017 Our results demonstrated that inhibition of miR-429 remarkably increased the levels of PHD2, which disrupted PHD2-associated adaptive activation of HIF-1alpha-mediated gene expression in response to high salt in the renal medulla and consequently inhibited urinary sodium excretion, enhanced sodium retention in response to chronic sodium overloading, and as a result, produced a salt-sensitive hypertension. Sodium 292-298 egl-9 family hypoxia-inducible factor 1 Rattus norvegicus 109-113 28445205-6 2017 Our results demonstrated that inhibition of miR-429 remarkably increased the levels of PHD2, which disrupted PHD2-associated adaptive activation of HIF-1alpha-mediated gene expression in response to high salt in the renal medulla and consequently inhibited urinary sodium excretion, enhanced sodium retention in response to chronic sodium overloading, and as a result, produced a salt-sensitive hypertension. Sodium 292-298 hypoxia inducible factor 1 subunit alpha Rattus norvegicus 148-158 31914696-8 2020 NaB prevented VPA toxicity, limiting cell oxidative and mitochondrial damage (ROS, malondialdehyde, SOD activity, mitochondrial bioenergetics), and restoring fatty acid oxidation (peroxisome proliferator-activated receptor alpha expression and carnitine palmitoyl-transferase activity) in HepG2 cells, primary hepatocytes, and isolated mitochondria. Sodium 0-3 peroxisome proliferator activated receptor alpha Homo sapiens 180-228 28488023-3 2017 We examined the effects of NSP4 and glucose on sodium and chloride transport in mouse small intestines and Caco-2 cells. Sodium 47-53 protease, serine 57 Mus musculus 27-31 31136002-2 2020 Disrupting hepatic bile salt uptake, by inhibition of sodium-taurocholate cotransporting polypetide (NTCP; Slc10a1) with Myrcludex B, is expected to limit bile salt flux through the liver and thereby to decrease biliary lipid excretion. Sodium 54-60 solute carrier family 10 (sodium/bile acid cotransporter family), member 1 Mus musculus 101-105 28810618-7 2017 These results suggest that sivelestat sodium hydrate improves post-traumatic KOA through HMGB1 and NF-kappaB in rats. Sodium 38-44 high mobility group box 1 Rattus norvegicus 89-94 28604836-0 2017 Elevated sodium leads to the increased expression of HSP60 and induces apoptosis in HUVECs. Sodium 9-15 heat shock protein family D (Hsp60) member 1 Homo sapiens 53-58 28594849-12 2017 Renal HS of high sodium rats showed increased sulfation (p = 0.05), increased L-selectin binding to HS (p<0,05), and a reduction of sulfation-sensitive anti-HS mAbs JM403 (p<0.001) and 10E4 (p<0.01). Sodium 17-23 selectin L Rattus norvegicus 78-88 28591637-4 2017 We confirm and extend these findings by demonstrating that glucagon pathway blockade selectively increases expression of the sodium-coupled neutral amino acid transporter Slc38a5 in a subset of highly proliferative alpha cells and that Slc38a5 controls the pancreatic response to glucagon pathway blockade; most notably, mice deficient in Slc38a5 exhibit markedly decreased alpha cell hyperplasia to glucagon pathway blockade-induced hyperaminoacidemia. Sodium 125-131 solute carrier family 38, member 5 Mus musculus 171-178 27368672-1 2017 BACKGROUND: Tenapanor (RDX5791, AZD1722), a small molecule with minimal systemic availability, is an inhibitor of the sodium/hydrogen exchanger isoform 3 (NHE3). Sodium 118-124 solute carrier family 9 member A3 Homo sapiens 155-159 28592038-12 2017 The ARR after CCT tended to decrease in EH subjects with elevated urine-sodium compared with those with normal urine-sodium. Sodium 72-78 CCT Homo sapiens 14-17 28592038-12 2017 The ARR after CCT tended to decrease in EH subjects with elevated urine-sodium compared with those with normal urine-sodium. Sodium 117-123 CCT Homo sapiens 14-17 28620319-8 2017 These changes were partly caused by downregulation of sodium current (INa) due to reduced expression of Nav1.5. Sodium 54-60 sodium channel, voltage-gated, type V, alpha Mus musculus 104-110 28492364-5 2017 Mechanistically, TCR stimulation induced rapid sodium influx in Napahyh/hyh CD4 T cells, which reduced intracellular ATP, [ATP]i. Depletion of [ATP]i inhibited mTORC2 dependent NFkappaB activation in Napahyh/hyh cells but ablation of Orai1 restored it. Sodium 47-53 CD4 antigen Mus musculus 76-79 28200110-7 2017 RESULTS: Systolic BP (SBP) response to high-sodium intervention significantly decreased with the number of minor T allele of marker rs6967221 in RAC1 (P = 4.51 x 10-4). Sodium 44-50 Rac family small GTPase 1 Homo sapiens 145-149 28200110-9 2017 Gene-based analyses revealed that RAC1 was significantly associated with SBP response to high-sodium intervention (P = 1.00 x 10-6) and diastolic BP response to low-sodium intervention (P = 9.80 x 10-4). Sodium 94-100 Rac family small GTPase 1 Homo sapiens 34-38 28200110-9 2017 Gene-based analyses revealed that RAC1 was significantly associated with SBP response to high-sodium intervention (P = 1.00 x 10-6) and diastolic BP response to low-sodium intervention (P = 9.80 x 10-4). Sodium 165-171 Rac family small GTPase 1 Homo sapiens 34-38 28431667-4 2017 However, emerging evidence suggests that GLP-1 RA can also have direct effects in the kidney, including inhibiting NHE3-dependent sodium reabsorption in the proximal tubule. Sodium 130-136 solute carrier family 9 member A3 Homo sapiens 115-119 28557567-2 2017 We recently reported that NaC contributes to amiloride-insensitive sodium transport in mouse lungs (Respiratory Physiology & Neurobiology, 2016). Sodium 67-73 NLR family, pyrin domain containing 1A Mus musculus 26-29 31136002-2 2020 Disrupting hepatic bile salt uptake, by inhibition of sodium-taurocholate cotransporting polypetide (NTCP; Slc10a1) with Myrcludex B, is expected to limit bile salt flux through the liver and thereby to decrease biliary lipid excretion. Sodium 54-60 solute carrier family 10 (sodium/bile acid cotransporter family), member 1 Mus musculus 107-114 31484910-1 2020 Mutations in the cardiac sodium channel SCN5A can cause phenotypic overlap syndrome of long QT syndrome and Brugada syndrome. Sodium 25-31 sodium voltage-gated channel alpha subunit 5 Homo sapiens 40-45 28336914-3 2017 Activation of SGK1 in the heart causes a marked increase in both the peak and late sodium currents leading to prolongation of the action potential duration and an increased propensity to arrhythmia. Sodium 83-89 serum/glucocorticoid regulated kinase 1 Homo sapiens 14-18 31958090-8 2020 NaB had profound effects on Abeta levels and on associative learning and cognitive functioning. Sodium 0-3 amyloid beta (A4) precursor protein Mus musculus 28-33 28174043-0 2017 Sodium influx through cerebral sodium-glucose transporter type 1 exacerbates the development of cerebral ischemic neuronal damage. Sodium 0-6 solute carrier family 5 (sodium/glucose cotransporter), member 1 Mus musculus 31-64 28174043-3 2017 Here we demonstrated that sodium influx through cerebral SGLT-1 exacerbates cerebral ischemic neuronal damage. Sodium 26-32 solute carrier family 5 (sodium/glucose cotransporter), member 1 Mus musculus 57-63 28174043-13 2017 Thus, sodium influx through cerebral SGLT-1 may exacerbate cerebral ischemia-induced neuronal damage. Sodium 6-12 solute carrier family 5 (sodium/glucose cotransporter), member 1 Mus musculus 37-43 28117663-4 2017 We were able to produce high-quality NMR spectra of substrate bound to microcrystalline LeuT samples and identify one set of sodium-dependent substrate-specific chemical shifts. Sodium 125-131 Leucine transport, high Homo sapiens 88-92 31958090-9 2020 A 40% reduction in brain Abeta levels and a 25% increase in fear response in both the cued and contextual testing was observed in the NaB-treated animals compared to the control group. Sodium 134-137 amyloid beta (A4) precursor protein Mus musculus 25-30 31882442-9 2020 To this end, we identified SLC13A5/sodium-coupled citrate transporter, and recent proof-of-concept studies confirm its therapeutic potential in T2D and nonalcoholic fatty liver disease. Sodium 35-41 solute carrier family 13 member 5 Homo sapiens 27-34 28164127-5 2017 The apical membrane expression, where NKCC2 is functional, may be sufficient to normalize water, potassium, sodium, and osmolytes tubular handling. Sodium 108-114 solute carrier family 12 member 1 Rattus norvegicus 38-43 28164127-8 2017 These data suggest that the upregulation in the expression of NKCC2 in apical membranes during the postobstructive phase of BUO could contribute to improving the excretion of sodium and consequently also the excretion of potassium, osmolytes, and water. Sodium 175-181 solute carrier family 12 member 1 Rattus norvegicus 62-67 28777756-2 2017 Safinamide is a drug with an innovative mechanism of action, dopaminergic and non-dopaminergic, that includes the reversible inhibition of the monoamine oxidase-B (MAO-B) enzyme and the modulation of excessive glutamate release through the use- and state-dependent blockade of the sodium channels. Sodium 281-287 monoamine oxidase B Homo sapiens 164-169 28029095-4 2016 Within 40 s, hypoxia-induced linkage of SUMO1 to the channels is complete, shifting the voltage-dependence of channel activation so that depolarizing steps evoke larger sodium currents. Sodium 169-175 small ubiquitin-like modifier 1 Rattus norvegicus 40-45 28008944-5 2016 Coexpression of APP or its intracellular domains containing a VTPEER motif with Nav1.6 sodium channels in Xenopus oocytes resulted in an increase in peak sodium currents, which was enhanced by constitutively active Go mutant and blocked by a dominant negative mutant. Sodium 87-93 sodium voltage-gated channel alpha subunit 8 Homo sapiens 80-86 27627464-3 2016 A mitochondrial Ca2+ uniporter - MCU, controls mitochondrial Ca2+ entry while a sodium/calcium transporter - NCLX shapes calcium and sodium transients by mediating sodium entry into and removing calcium from the mitochondria. Sodium 80-86 solute carrier family 8 member B1 Homo sapiens 109-113 27627464-3 2016 A mitochondrial Ca2+ uniporter - MCU, controls mitochondrial Ca2+ entry while a sodium/calcium transporter - NCLX shapes calcium and sodium transients by mediating sodium entry into and removing calcium from the mitochondria. Sodium 133-139 solute carrier family 8 member B1 Homo sapiens 109-113 27932425-8 2016 Scn2b null atria had normal levels of sodium current density compared with wild type. Sodium 38-44 sodium channel, voltage-gated, type II, beta Mus musculus 0-5 27555230-3 2016 In euvolemic anaesthetized rats, treatment with the mTOR inhibitor rapamycin increased blood pressure (121 +- 2 to 144 +- 3 mmHg; P<.05), decreased glomerular filtration rate (GFR; 1.6 +- 0.3 to 0.5 +- 0.2 mL/min; P<.05) and increased urinary sodium excretion (UNaV; 14 +- 1 to 109 +- 25 mmol/L per hour; P<.05). Sodium 249-255 mechanistic target of rapamycin kinase Rattus norvegicus 52-56 26912587-1 2016 The subthreshold activity of hippocampal CA1 pyramidal neurons is regulated by the persistent sodium current (INaP) and the h-current (Ih), carried by tetrodotoxin-sensitive sodium channels and hyperpolarization-activated cyclic-nucleotide-gated channels, respectively. Sodium 94-100 carbonic anhydrase 1 Homo sapiens 41-44 31814290-4 2020 With the addition of an appropriate amount of GO content, the compressive Young"s modulus of 2 wt% GO+PVDF-HFP (2-GPH) composite GPE is greatly enhanced by a factor of 10, reaching 2.5 GPa, which is crucial in the suppression of sodium dendrite growth. Sodium 229-235 gephyrin Homo sapiens 114-117 27713141-10 2016 In conclusion, FGF23 increased PV arrhythmogenesis through sodium and calcium dysregulation by acting protein kinase C signaling. Sodium 59-65 fibroblast growth factor 23 Homo sapiens 15-20 27685945-0 2016 Loss of Sodium/Hydrogen Exchanger NHA2 Exacerbates Obesity- and Aging-Induced Glucose Intolerance in Mice. Sodium 8-14 solute carrier family 9, subfamily B (NHA2, cation proton antiporter 2), member 2 Mus musculus 34-38 27685945-1 2016 We previously demonstrated that the sodium/hydrogen exchanger NHA2, also known as NHEDC2 or SLC9B2, is critical for insulin secretion by beta-cells. Sodium 36-42 solute carrier family 9, subfamily B (NHA2, cation proton antiporter 2), member 2 Mus musculus 62-66 27685945-1 2016 We previously demonstrated that the sodium/hydrogen exchanger NHA2, also known as NHEDC2 or SLC9B2, is critical for insulin secretion by beta-cells. Sodium 36-42 solute carrier family 9, subfamily B (NHA2, cation proton antiporter 2), member 2 Mus musculus 82-88 27685945-1 2016 We previously demonstrated that the sodium/hydrogen exchanger NHA2, also known as NHEDC2 or SLC9B2, is critical for insulin secretion by beta-cells. Sodium 36-42 solute carrier family 9, subfamily B (NHA2, cation proton antiporter 2), member 2 Mus musculus 92-98 27653682-3 2016 The AP threshold changes in Fmr1 KO mice are caused by increased persistent sodium current (INaP). Sodium 76-82 fragile X messenger ribonucleoprotein 1 Mus musculus 28-32 27477809-11 2016 Importantly, sodium selenite treatment retarded the growth of the transplanted SGC7901 cells in nude mice, with the induction of SBP1 expression, which was associated with the decrease of Nrf2 expression and the inactivation of the Wnt/beta-catenin signaling pathway. Sodium 13-19 catenin (cadherin associated protein), beta 1 Mus musculus 236-248 27118135-4 2016 However, most Central Diabetes Insipidus models also show disorders in other neurobiological systems, specifically in the secretion of oxytocin, a neurohormone involved in body sodium excretion. Sodium 177-183 oxytocin/neurophysin I prepropeptide Homo sapiens 135-143 26892914-4 2016 We focus on two well-characterized sodium-coupled symporters: the bacterial amino acid transporter LeuT, which is the prototype for the "gated pore" mechanism in the mammalian synaptic monoamine transporters, and the archaeal GltPh, which is the prototype for the "elevator" mechanism in the mammalian excitatory amino acid transporters. Sodium 35-41 Leucine transport, high Homo sapiens 99-103 27000037-9 2016 Inhibition of recombinant Nav1.5 channels was similar to that of TTX-resistant currents in cardiomyocytes but stronger as compared to inhibition of total sodium current in cardiomyocytes. Sodium 154-160 sodium channel, voltage-gated, type V, alpha Mus musculus 26-32 27067528-0 2016 Hypertension: PPARdelta: a link between sodium and glucose homeostasis. Sodium 40-46 peroxisome proliferator activated receptor delta Homo sapiens 14-23 26707235-7 2016 In sodium sensitivity experiments, a very weak inhibitory effect of Na(+) ions was observed on the binding of [(3)H]NN, resulting in an IC50 of 150.6mM. Sodium 3-9 neurotensin Rattus norvegicus 116-118 31889105-5 2019 The Dapa + NaB group gained the least total and abdominal fat from baseline. Sodium 11-14 CD36 molecule Mus musculus 58-61 31819138-0 2019 Sodium Channel Nav1.5 Controls Epithelial-to-Mesenchymal Transition and Invasiveness in Breast Cancer Cells Through its Regulation by the Salt-Inducible Kinase-1. Sodium 0-6 sodium voltage-gated channel alpha subunit 5 Homo sapiens 15-21 27410407-4 2016 RESULTS: In continuous renal replacement therapy 24-hour sessions, SAPS 3 (p = 0.022) and baseline hypernatremia (p = 0.023) were statistically significant predictors of serum sodium variations >= 8mEq/L in univariate analysis, but only hypernatremia demonstrated an independent association (beta = 0.429, p < 0.001). Sodium 176-182 protein phosphatase 6 regulatory subunit 3 Homo sapiens 67-73 27058411-10 2016 The alphaENaC mRNA levels and sodium transport were increased in SOCS-1 overexpressing MLE-12 cells exposed to IL-1beta. Sodium 30-36 suppressor of cytokine signaling 1 Mus musculus 65-71 26586904-7 2016 Corroborating, the myocardial content of SERCA-2a and phosphorylated PLB-Ser16/total PLB ratio was decreased and sodium-calcium exchanger was increased in the MPR group. Sodium 113-119 progesterone receptor membrane component 1 Rattus norvegicus 159-162 26820468-0 2016 Group V Secretory Phospholipase A2 Is Involved in Tubular Integrity and Sodium Handling in the Kidney. Sodium 72-78 phospholipase A2, group IB, pancreas Mus musculus 18-34 26447224-10 2016 Collectively, these results provide novel evidence that GLP-1 is a physiologically relevant natriuretic factor that contributes to sodium balance, in part via tonic modulation of NHE3 activity in the proximal tubule. Sodium 131-137 glucagon Rattus norvegicus 56-61 31819138-0 2019 Sodium Channel Nav1.5 Controls Epithelial-to-Mesenchymal Transition and Invasiveness in Breast Cancer Cells Through its Regulation by the Salt-Inducible Kinase-1. Sodium 0-6 salt inducible kinase 1 Homo sapiens 138-161 31819138-3 2019 NaV1.5 activity, through an entry of sodium ions, in breast cancer cells is associated with increased invasiveness, but its participation to the EMT has to be clarified. Sodium 37-43 sodium voltage-gated channel alpha subunit 5 Homo sapiens 0-6 31629603-3 2019 Here, we find that amplification occurs in the Drosophila courtship-promoting ORNs through Pickpocket 25 (PPK25), a member of the degenerin/epithelial sodium channel family (DEG/ENaC). Sodium 151-157 pickpocket 25 Drosophila melanogaster 91-104 31629603-3 2019 Here, we find that amplification occurs in the Drosophila courtship-promoting ORNs through Pickpocket 25 (PPK25), a member of the degenerin/epithelial sodium channel family (DEG/ENaC). Sodium 151-157 pickpocket 25 Drosophila melanogaster 106-111 32734228-2 2020 One possible mechanism for the protective effects of SGLT-2 inhibitor therapy might be the activation of tubuloglomerular feedback by increased outflow of sodium, chloride, and glucose to distal parts of the nephron, including the macula densa. Sodium 155-161 solute carrier family 5 member 2 Homo sapiens 53-59 26807262-1 2016 UNLABELLED: Autosomal recessive pseudohypoaldosteronism type 1 (PHA1) is a rare disorder characterized by sodium wasting, failure to thrive, hyperkalemia, hypovolemia and metabolic acidosis. Sodium 106-112 sodium channel epithelial 1 subunit gamma Homo sapiens 32-62 26807262-1 2016 UNLABELLED: Autosomal recessive pseudohypoaldosteronism type 1 (PHA1) is a rare disorder characterized by sodium wasting, failure to thrive, hyperkalemia, hypovolemia and metabolic acidosis. Sodium 106-112 sodium channel epithelial 1 subunit gamma Homo sapiens 64-68 26849427-1 2016 Safinamide (brand name Xadago , Zambon S.p.A) is a third-generation reversible MAO-B inhibitor, which also blocks sodium voltage-sensitive channels and modulates stimulated release of glutamate. Sodium 114-120 monoamine oxidase B Homo sapiens 79-84 26403564-10 2016 The effect of the V1a -AVP receptor partial agonist on PP was associated with an improvement in urine volume and urinary excretion of sodium during the first day of treatment. Sodium 134-140 arginine vasopressin receptor 1A Rattus norvegicus 18-21 26631594-7 2016 The regional heterogeneities in Ca(2+) handling cause action potential (AP) heterogeneities through sodium-calcium exchange (NCX) activation and eventually overwhelm electrical coupling of the tissue. Sodium 100-106 T cell leukemia homeobox 2 Homo sapiens 125-128 31973392-3 2015 Specifically, sodium naphthalenide (Na-NAP) is used to capture H2 S to produce anhydrous Na2 S nanocrystals and 1,4-dihydronaphthalene, which are important materials for batteries and liquid fuels, respectively. Sodium 14-34 catenin beta like 1 Homo sapiens 39-42 31973392-3 2015 Specifically, sodium naphthalenide (Na-NAP) is used to capture H2 S to produce anhydrous Na2 S nanocrystals and 1,4-dihydronaphthalene, which are important materials for batteries and liquid fuels, respectively. Sodium 89-94 catenin beta like 1 Homo sapiens 39-42 31006168-1 2019 AIM: In nephrotic syndrome, aberrantly filtered plasminogen (plg) is converted to active plasmin by tubular urokinase-type plasminogen activator (uPA) and thought to lead to sodium retention by proteolytic activation of the epithelial sodium channel (ENaC). Sodium 174-180 plasminogen activator, urokinase Mus musculus 146-149 31006168-2 2019 This concept predicts that uPA is an important factor for sodium retention and that inhibition of uPA might be protective in nephrotic syndrome. Sodium 58-64 plasminogen activator, urokinase Mus musculus 27-30 31006168-9 2019 Amiloride prevented sodium retention in nephrotic uPA-/- mice which confirmed the critical role of ENaC in sodium retention. Sodium 107-113 sodium channel, nonvoltage-gated 1 alpha Mus musculus 99-103 31423748-0 2019 Urokinase-type plasminogen activator contributes to amiloride-sensitive sodium retention in nephrotic range glomerular proteinuria in mice. Sodium 72-78 plasminogen activator, urokinase Mus musculus 0-36 31423748-8 2019 Administration of uPA targeting antibody abolished urine activation of plasminogen, attenuated sodium accumulation and prevented cleavage of gammaENaC. Sodium 95-101 plasminogen activator, urokinase Mus musculus 18-21 31617909-5 2019 Mechanistically, we show that the increased stiffening of the vascular intima in Western diet-fed female mice is accompanied by enhanced epithelial sodium channel (ENaC) activity in endothelial cells (EnNaC). Sodium 148-154 sodium channel, nonvoltage-gated 1 alpha Mus musculus 164-168 31617909-5 2019 Mechanistically, we show that the increased stiffening of the vascular intima in Western diet-fed female mice is accompanied by enhanced epithelial sodium channel (ENaC) activity in endothelial cells (EnNaC). Sodium 201-206 sodium channel, nonvoltage-gated 1 alpha Mus musculus 164-168 31617909-6 2019 Our data further indicate that: 1) estrogen signaling through estrogen receptor alpha (ERalpha) increases EnNaC activity to a larger extent in females compared to males, 2) estrogen-induced activation of EnNaC is mediated by the serum glucocorticoid inducible-kinase 1 (SGK-1), and 3) estrogen signaling stiffens endothelial cells when nitric oxide is lacking and this stiffening effect can be reduced with amiloride, an ENaC inhibitor. Sodium 106-111 estrogen receptor 1 (alpha) Mus musculus 62-85 31617909-6 2019 Our data further indicate that: 1) estrogen signaling through estrogen receptor alpha (ERalpha) increases EnNaC activity to a larger extent in females compared to males, 2) estrogen-induced activation of EnNaC is mediated by the serum glucocorticoid inducible-kinase 1 (SGK-1), and 3) estrogen signaling stiffens endothelial cells when nitric oxide is lacking and this stiffening effect can be reduced with amiloride, an ENaC inhibitor. Sodium 106-111 estrogen receptor 1 (alpha) Mus musculus 87-94 31617909-6 2019 Our data further indicate that: 1) estrogen signaling through estrogen receptor alpha (ERalpha) increases EnNaC activity to a larger extent in females compared to males, 2) estrogen-induced activation of EnNaC is mediated by the serum glucocorticoid inducible-kinase 1 (SGK-1), and 3) estrogen signaling stiffens endothelial cells when nitric oxide is lacking and this stiffening effect can be reduced with amiloride, an ENaC inhibitor. Sodium 106-111 serum/glucocorticoid regulated kinase 1 Mus musculus 229-268 31617909-6 2019 Our data further indicate that: 1) estrogen signaling through estrogen receptor alpha (ERalpha) increases EnNaC activity to a larger extent in females compared to males, 2) estrogen-induced activation of EnNaC is mediated by the serum glucocorticoid inducible-kinase 1 (SGK-1), and 3) estrogen signaling stiffens endothelial cells when nitric oxide is lacking and this stiffening effect can be reduced with amiloride, an ENaC inhibitor. Sodium 204-209 estrogen receptor 1 (alpha) Mus musculus 62-85 31617909-6 2019 Our data further indicate that: 1) estrogen signaling through estrogen receptor alpha (ERalpha) increases EnNaC activity to a larger extent in females compared to males, 2) estrogen-induced activation of EnNaC is mediated by the serum glucocorticoid inducible-kinase 1 (SGK-1), and 3) estrogen signaling stiffens endothelial cells when nitric oxide is lacking and this stiffening effect can be reduced with amiloride, an ENaC inhibitor. Sodium 204-209 estrogen receptor 1 (alpha) Mus musculus 87-94 31617909-6 2019 Our data further indicate that: 1) estrogen signaling through estrogen receptor alpha (ERalpha) increases EnNaC activity to a larger extent in females compared to males, 2) estrogen-induced activation of EnNaC is mediated by the serum glucocorticoid inducible-kinase 1 (SGK-1), and 3) estrogen signaling stiffens endothelial cells when nitric oxide is lacking and this stiffening effect can be reduced with amiloride, an ENaC inhibitor. Sodium 204-209 serum/glucocorticoid regulated kinase 1 Mus musculus 229-268 31617909-6 2019 Our data further indicate that: 1) estrogen signaling through estrogen receptor alpha (ERalpha) increases EnNaC activity to a larger extent in females compared to males, 2) estrogen-induced activation of EnNaC is mediated by the serum glucocorticoid inducible-kinase 1 (SGK-1), and 3) estrogen signaling stiffens endothelial cells when nitric oxide is lacking and this stiffening effect can be reduced with amiloride, an ENaC inhibitor. Sodium 204-209 serum/glucocorticoid regulated kinase 1 Mus musculus 270-275 31617909-6 2019 Our data further indicate that: 1) estrogen signaling through estrogen receptor alpha (ERalpha) increases EnNaC activity to a larger extent in females compared to males, 2) estrogen-induced activation of EnNaC is mediated by the serum glucocorticoid inducible-kinase 1 (SGK-1), and 3) estrogen signaling stiffens endothelial cells when nitric oxide is lacking and this stiffening effect can be reduced with amiloride, an ENaC inhibitor. Sodium 204-209 sodium channel, nonvoltage-gated 1 alpha Mus musculus 421-425 31617909-8 2019 In females, endothelial stiffening with obesity may be attributed to estrogen signaling through the ERalpha-SGK-1-EnNaC axis, thus establishing a putative therapeutic target for female obesity-related vascular stiffening. Sodium 112-119 estrogen receptor 1 (alpha) Mus musculus 100-107 31807182-9 2019 Furthermore, PTEN-knockdown decreased the expression of specific thyroid proteins (thyroglobulin, TG; thyroid peroxidase, TPO; and sodium/iodide symporter, NIS) and inhibited the iodide uptake ability of thyroid cells by downregulating PAX8, suggesting that PTEN deficiency may impair the function of thyroid cells. Sodium 131-137 phosphatase and tensin homolog Homo sapiens 13-17 31748932-0 2019 Mechanosensitivity of NaV1.5 sodium channels is regulated by specific beta-subunits. Sodium 29-35 sodium voltage-gated channel alpha subunit 5 Homo sapiens 22-28 31872561-5 2019 In the presence of RyR mutations, frequent spontaneous calcium leaks from sarcoplasmic reticulum (SR) initiated calcium waves, which upon reaching the cell periphery produced delayed afterdepolarizations (DADs) via sodium-calcium exchanger (NCX) and T-type calcium (ICaT ) channel activation. Sodium 215-221 T cell leukemia, homeobox 2 Mus musculus 241-244 31872561-5 2019 In the presence of RyR mutations, frequent spontaneous calcium leaks from sarcoplasmic reticulum (SR) initiated calcium waves, which upon reaching the cell periphery produced delayed afterdepolarizations (DADs) via sodium-calcium exchanger (NCX) and T-type calcium (ICaT ) channel activation. Sodium 215-221 catenin beta interacting protein 1 Mus musculus 266-270 31660726-3 2019 In this study, a novel poly (vinylene carbonate)-based composite polymer electrolyte (PVC-CPE) prepared by a facile in situ solidification method, is reported for the first time to realize high performances of solid-state sodium batteries at room temperature. Sodium 222-228 carboxypeptidase E Homo sapiens 90-93 31660726-7 2019 The battery delivers a high initial discharge specific capacity of 104.2 mAh g-1 with capacity retention of about 86.8% after 250 cycles at 0.2 C, and superior rate performance with discharge specific capacity of 80.2 mAh g-1 at 1 C. This study suggests that PVC-CPE is a very promising electrolyte for solid-state sodium batteries. Sodium 315-321 carboxypeptidase E Homo sapiens 263-266 31803246-12 2019 These suggest that KCNQ1 and SCN2A, genes that encode potassium and sodium channels, respectively, may serve as putative diagnostic targets for the diagnosis and prognosis of PHEO and therefore facilitate the clinical management of PHEO. Sodium 68-74 potassium voltage-gated channel subfamily Q member 1 Homo sapiens 19-24 25855080-1 2015 Na(+)/H(+) exchange by Na(+)/H(+) exchanger 3 (NHE3) is a major route of sodium absorption in the intestine and kidney. Sodium 73-79 solute carrier family 9 member A3 Homo sapiens 23-45 25855080-1 2015 Na(+)/H(+) exchange by Na(+)/H(+) exchanger 3 (NHE3) is a major route of sodium absorption in the intestine and kidney. Sodium 73-79 solute carrier family 9 member A3 Homo sapiens 47-51 25855513-1 2015 The objective of this study was to investigate how physiological, pharmacological, and pathological conditions that alter sodium reabsorption (TNa) in the proximal tubule affect oxygen consumption (QO2 ) and Na(+) transport efficiency (TNa/QO2 ). Sodium 122-128 C-type lectin domain family 3, member B Rattus norvegicus 143-146 25855513-1 2015 The objective of this study was to investigate how physiological, pharmacological, and pathological conditions that alter sodium reabsorption (TNa) in the proximal tubule affect oxygen consumption (QO2 ) and Na(+) transport efficiency (TNa/QO2 ). Sodium 122-128 C-type lectin domain family 3, member B Rattus norvegicus 236-239 25898949-11 2015 Therefore, glucose stimulates NT secretion by uptake through SGLT1 and GLUT2, both causing depolarization either as a consequence of sodium-coupled uptake (SGLT1) or by closure of KATP channels (GLUT2 and SGLT1) secondary to the ATP-generating metabolism of glucose. Sodium 133-139 solute carrier family 5 member 1 Rattus norvegicus 61-66 32009801-11 2019 The results of the osteogenic and adipogenic assay showed that 0.1 muM Na2SeO3 could significantly promote the osteogenic and adipogenic differentiation of BMSCs by upregulating the lipid factors (LPL and PPRAG) and osteogenic factors, RUNX2, COL1, and BGP, in a concentration-dependent manner. Sodium 71-78 runt related transcription factor 2 Mus musculus 236-241 32009801-11 2019 The results of the osteogenic and adipogenic assay showed that 0.1 muM Na2SeO3 could significantly promote the osteogenic and adipogenic differentiation of BMSCs by upregulating the lipid factors (LPL and PPRAG) and osteogenic factors, RUNX2, COL1, and BGP, in a concentration-dependent manner. Sodium 71-78 carcinoembryonic antigen-related cell adhesion molecule 1 Mus musculus 253-256 32009801-12 2019 Coagulation experiments in animals (mice and rats) revealed that Na2SeO3 can reduce the coagulation time of BMSCs in a concentration-dependent manner, which is related to the high expression of hematopoietic factors (SDF-1alpha, GM-CSF, IL-7, IL-8, IL-11, and SCF). Sodium 65-72 KIT ligand Rattus norvegicus 260-263 31722710-2 2019 Sodium glucose cotransporter 2 (SGLT2) inhibitors selectively inhibit kidney glucose and sodium reabsorption, and cardiovascular benefits of SGLT2 inhibitors beyond other antidiabetic drugs have been reported in type 2 diabetes mellitus (T2DM) clinical trials. Sodium 89-95 solute carrier family 5 member 2 Homo sapiens 0-30 31722710-2 2019 Sodium glucose cotransporter 2 (SGLT2) inhibitors selectively inhibit kidney glucose and sodium reabsorption, and cardiovascular benefits of SGLT2 inhibitors beyond other antidiabetic drugs have been reported in type 2 diabetes mellitus (T2DM) clinical trials. Sodium 89-95 solute carrier family 5 member 2 Homo sapiens 32-37 31618043-2 2019 The new catalytic system based on Pd/Xphos-SO3Na or Pd/MeDavephos-CF3SO3 in PEG/H2O under microwave irradiation was found to be the best conditions for this transformation. Sodium 43-48 progestagen associated endometrial protein Homo sapiens 76-79 25770927-6 2015 Moreover the same trends were seen when adding sodium metasilicate to MC3T3-E1 cultures, with more mineralisation and higher ALP levels with higher doses of silicate (25, 125 and 625 muM). Sodium 47-53 alkaline phosphatase, biomineralization associated Danio rerio 125-128 25430696-13 2015 CONCLUSIONS: RAC1 expression was associated with an increase in MR, NGAL, NF-kappaB, and HO-1 expression, suggesting that RAC1 could be a mediator of cardiovascular damage induced by sodium, and may also useful to identify subjects with different responses to salt intake. Sodium 183-189 Rac family small GTPase 1 Homo sapiens 13-17 25430696-13 2015 CONCLUSIONS: RAC1 expression was associated with an increase in MR, NGAL, NF-kappaB, and HO-1 expression, suggesting that RAC1 could be a mediator of cardiovascular damage induced by sodium, and may also useful to identify subjects with different responses to salt intake. Sodium 183-189 Rac family small GTPase 1 Homo sapiens 122-126 25753114-10 2015 Our data suggest that the sodium ion interaction of Asp90(2.50) in the allosteric pocket of MC4R is essential to its function, explaining the loss of function of the MC4RD90N mutant. Sodium 26-32 melanocortin 4 receptor Homo sapiens 92-96 25888997-13 2015 CONCLUSION: The results of the present study demonstrated that a GLP-1 analog and a DPP4 inhibitor may have beneficial effects on renal sodium and water handling. Sodium 136-142 glucagon Rattus norvegicus 65-70 24771578-4 2015 15209T>C) in mitochondrial cytochrome b gene in a 2-year-old girl with Prader-Willi syndrome with a clinical history of lactic acidosis attacks, renal sodium loss, hepatopathy, progressive cerebral atrophy, and sudden death. Sodium 154-160 mitochondrially encoded cytochrome b Homo sapiens 30-42 25428882-0 2015 Sodium entry through endothelial store-operated calcium entry channels: regulation by Orai1. Sodium 0-6 ORAI calcium release-activated calcium modulator 1 Homo sapiens 86-91 25428882-2 2015 Orai1 silencing increases sodium permeability and decreases membrane-associated calcium, although it is not known whether Orai1 is an important determinant of cytosolic sodium transitions. Sodium 26-32 ORAI calcium release-activated calcium modulator 1 Homo sapiens 0-5 25428882-3 2015 We test the hypothesis that, upon activation of store-operated calcium entry channels, Orai1 is a critical determinant of cytosolic sodium transitions. Sodium 132-138 ORAI calcium release-activated calcium modulator 1 Homo sapiens 87-92 25428882-8 2015 The magnitude of this sustained increase in cytosolic sodium was greater when experiments were conducted in low extracellular calcium and when Orai1 expression was silenced; these two interventions were not additive, suggesting a common mechanism. Sodium 54-60 ORAI calcium release-activated calcium modulator 1 Homo sapiens 143-148 25428882-10 2015 These studies demonstrate that sodium permeates activated store-operated calcium entry channels, resulting in an increase in cytosolic sodium; the magnitude of this response is determined by Orai1. Sodium 31-37 ORAI calcium release-activated calcium modulator 1 Homo sapiens 191-196 25428882-10 2015 These studies demonstrate that sodium permeates activated store-operated calcium entry channels, resulting in an increase in cytosolic sodium; the magnitude of this response is determined by Orai1. Sodium 135-141 ORAI calcium release-activated calcium modulator 1 Homo sapiens 191-196 25278093-4 2015 We hypothesized that FGF-23 reduces the capacity of dietary sodium restriction to potentiate RAAS blockade, impairing the antiproteinuric effect. Sodium 60-66 fibroblast growth factor 23 Homo sapiens 21-27 25278093-10 2015 RESULTS: Higher baseline FGF-23 level was associated with reduced antiproteinuric response to dietary sodium restriction (standardized beta=-0.46; P=0.001; model R(2)=0.71). Sodium 102-108 fibroblast growth factor 23 Homo sapiens 25-31 25278093-11 2015 For every 100-RU/mL increase in FGF-23 level, the antiproteinuric response to dietary sodium restriction was reduced by 10.6%. Sodium 86-92 fibroblast growth factor 23 Homo sapiens 32-38 25278093-12 2015 Higher baseline FGF-23 level was a determinant of more residual proteinuria during the low-sodium diet (standardized beta=0.27; P=0.003) in linear regression analysis adjusted for baseline proteinuria (model R(2)=0.71). Sodium 91-97 fibroblast growth factor 23 Homo sapiens 16-22 25278093-16 2015 CONCLUSIONS: FGF-23 levels are associated independently with impaired antiproteinuric response to sodium restriction in addition to RAAS blockade. Sodium 98-104 fibroblast growth factor 23 Homo sapiens 13-19 25428995-8 2015 In leaves of the SXD1:RNAi plants, sodium accumulation was diminished, while proline accumulation and pools of soluble antioxidants were increased. Sodium 35-41 tocopherol cyclase Solanum tuberosum 17-21 31635319-4 2019 Glutamine is absorbed via sodium-dependent glutamine co-transport (B0AT1; SLC6A19) along the brush border membrane of absorptive villus cells. Sodium 26-32 solute carrier family 6 member 19 Rattus norvegicus 67-72 25243715-0 2015 Different spatial expressions of c-Fos in the nucleus of the solitary tract following taste stimulation with sodium, potassium, and ammonium ions in rats. Sodium 109-115 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 33-38 25301528-11 2015 Lower SGK1 expression after term CD could translate into insufficient sodium and lung liquid absorption. Sodium 70-76 serum/glucocorticoid regulated kinase 1 Homo sapiens 6-10 25661325-5 2015 The focus of this paper is formal UQ of one major sub-component of cardiac EP models, the steady-state inactivation of the fast sodium current, INa. Sodium 128-134 internexin neuronal intermediate filament protein alpha Canis lupus familiaris 144-147 25260632-0 2014 Interactions between beta-2 adrenoceptor gene variation, cardiovascular control and dietary sodium in healthy young adults. Sodium 92-98 adrenoceptor beta 2 Homo sapiens 21-40 25260632-1 2014 Dietary sodium affects function of the beta-2 adrenoceptor (ADRB2). Sodium 8-14 adrenoceptor beta 2 Homo sapiens 39-58 25260632-1 2014 Dietary sodium affects function of the beta-2 adrenoceptor (ADRB2). Sodium 8-14 adrenoceptor beta 2 Homo sapiens 60-65 25260632-2 2014 We tested the hypothesis that haplotype variation in the ADRB2 gene would influence the cardiovascular and regional vasodilator responses to sympathoexcitatory manoeuvres following low, normal and high sodium diets, and ADRB2-mediated forearm vasodilation in the high sodium condition. Sodium 202-208 adrenoceptor beta 2 Homo sapiens 57-62 25260632-2 2014 We tested the hypothesis that haplotype variation in the ADRB2 gene would influence the cardiovascular and regional vasodilator responses to sympathoexcitatory manoeuvres following low, normal and high sodium diets, and ADRB2-mediated forearm vasodilation in the high sodium condition. Sodium 268-274 adrenoceptor beta 2 Homo sapiens 57-62 24684506-0 2014 Hydrogen sulfide targets EGFR Cys797/Cys798 residues to induce Na(+)/K(+)-ATPase endocytosis and inhibition in renal tubular epithelial cells and increase sodium excretion in chronic salt-loaded rats. Sodium 155-161 epidermal growth factor receptor Rattus norvegicus 25-29 31635319-4 2019 Glutamine is absorbed via sodium-dependent glutamine co-transport (B0AT1; SLC6A19) along the brush border membrane of absorptive villus cells. Sodium 26-32 solute carrier family 6 member 19 Rattus norvegicus 74-81 31635319-6 2019 Sodium-dependent 3H-glutamine uptakes were performed to measure B0AT1 activity. Sodium 0-6 solute carrier family 6 member 19 Rattus norvegicus 64-69 31635319-10 2019 Kinetic studies suggested that the mechanism of inhibition was due to decreased maximal rate of uptake (Vmax) of the B0AT1 co-transporter, corresponding to decreased B0AT1 protein expression and secondary to an inhibited sodium-gradient at the cellular level in vitro and ex vivo. Sodium 221-227 solute carrier family 6 member 19 Rattus norvegicus 117-122 31635319-10 2019 Kinetic studies suggested that the mechanism of inhibition was due to decreased maximal rate of uptake (Vmax) of the B0AT1 co-transporter, corresponding to decreased B0AT1 protein expression and secondary to an inhibited sodium-gradient at the cellular level in vitro and ex vivo. Sodium 221-227 solute carrier family 6 member 19 Rattus norvegicus 166-171 31601020-2 2019 In the kidney, HCN1, HCN2 and HCN3 are differentially expressed and contribute to the transport of sodium, potassium (K+) and ammonium into the nephrons. Sodium 99-105 hyperpolarization activated cyclic nucleotide gated potassium channel 3 Homo sapiens 30-34 31537607-3 2019 They work by blocking SGLT2 receptors, sodium-dependent glucose co-transport molecules, which in turn prevents glucose reabsorption, facilitating glucosuria, improving glycaemic control as well as a moderate degree of weight loss. Sodium 39-45 solute carrier family 5 member 2 Homo sapiens 22-27 25089378-4 2014 LAT function, determined by sodium-independent (3)H-leucine uptake, was impaired in a parallel manner. Sodium 28-34 linker for activation of T cells Rattus norvegicus 0-3 31572187-5 2019 In the current study, we found that DNA methylation, histone methylation, and estrogen receptor alpha (ERalpha) were impaired by NH4Cl and/or Na2S in F0, F1, and F2 mouse testes. Sodium 142-146 estrogen receptor 1 (alpha) Mus musculus 78-101 31572187-5 2019 In the current study, we found that DNA methylation, histone methylation, and estrogen receptor alpha (ERalpha) were impaired by NH4Cl and/or Na2S in F0, F1, and F2 mouse testes. Sodium 142-146 estrogen receptor 1 (alpha) Mus musculus 103-110 31484365-9 2019 Determination of brevetoxin affinity for Nav1.2, Nav1.4 and Nav1.5 channels showed that Nav1.5 channels had a characteristic 5-fold reduction in affinity for brevetoxin relative to the other channel isoforms, suggesting the interaction with sodium channels is specific despite the distributed binding determinants. Sodium 241-247 sodium voltage-gated channel alpha subunit 5 Homo sapiens 88-94 31222723-1 2019 BACKGROUND AND PURPOSE: We have shown that cholesterol is synthesized in the principal cells of renal cortical collecting ducts (CCD) and stimulates the epithelial sodium channels (ENaC). Sodium 164-170 sodium channel, nonvoltage-gated 1 alpha Mus musculus 181-185 31361295-1 2019 INTRODUCTION: Our previous experiments showed that the transient sodium current (INa) was abnormally increased in early ischaemia and atorvastatin could inhibit INa. Sodium 65-71 internexin neuronal intermediate filament protein, alpha Rattus norvegicus 81-84 31361295-1 2019 INTRODUCTION: Our previous experiments showed that the transient sodium current (INa) was abnormally increased in early ischaemia and atorvastatin could inhibit INa. Sodium 65-71 internexin neuronal intermediate filament protein, alpha Rattus norvegicus 161-164 31455381-0 2019 Influence of androgenic blockade with flutamide on pain behaviour and expression of the genes that encode the NaV1.7 and NaV1.8 voltage-dependent sodium channels in a rat model of postoperative pain. Sodium 146-152 sodium voltage-gated channel alpha subunit 9 Rattus norvegicus 110-116 31474871-4 2019 Following diet switch to low sodium, Nr3c1 Pax8/LC1 mice exhibit a transient but significant reduction in the activity of NCC and expression of NHE3 and NKCC2 accompanied by significant increased Spak activity. Sodium 29-35 serine/threonine kinase 39 Mus musculus 196-200 31403841-5 2019 Although multiple conditions are addressed to illustrate these concepts, the experience obtained in the study of long-QT syndrome, Brugada syndrome, and arrhythmogenic cardiomyopathy, and in the study of functions related to SCN5A (the gene coding for the alpha-subunit of the most abundant sodium channel in the heart) and PKP2 (the gene coding for the desmosomal protein plakophilin-2), as well, is discussed in more detail. Sodium 291-297 sodium voltage-gated channel alpha subunit 5 Homo sapiens 225-230 25259750-9 2014 In response to a sodium/volume challenge, wild-type and CD4(-/-) mice infused with angiotensin II retained water and sodium, whereas CD8(-/-) mice did not. Sodium 17-23 CD4 antigen Mus musculus 56-59 25259750-9 2014 In response to a sodium/volume challenge, wild-type and CD4(-/-) mice infused with angiotensin II retained water and sodium, whereas CD8(-/-) mice did not. Sodium 117-123 CD4 antigen Mus musculus 56-59 24952894-1 2014 The hydantoin transporter Mhp1 is a sodium-coupled secondary active transport protein of the nucleobase-cation-symport family and a member of the widespread 5-helix inverted repeat superfamily of transporters. Sodium 36-42 calcium voltage-gated channel subunit alpha1 A Homo sapiens 26-30 24603075-0 2014 beta-III spectrin underpins ankyrin R function in Purkinje cell dendritic trees: protein complex critical for sodium channel activity is impaired by SCA5-associated mutations. Sodium 110-116 ankyrin 1 Homo sapiens 28-37 24603075-7 2014 Moreover, a wild-type beta-III spectrin/ankyrin-R complex increases sodium channel levels and activity in cell culture, whereas mutant beta-III spectrin complexes fail to enhance sodium currents. Sodium 68-74 ankyrin 1 Homo sapiens 40-49 24722141-0 2014 Functional analysis of a missense mutation in the serine protease inhibitor SPINT2 associated with congenital sodium diarrhea. Sodium 110-116 serine protease 8 S homeolog Xenopus laevis 50-65 24722141-3 2014 A Y163C mutation in the SPINT2 gene encoding the serine protease inhibitor Hepatocyte Growth Factor Inhibitor HAI-2 is associated with a congenital sodium diarrhea. Sodium 148-154 serine protease 8 S homeolog Xenopus laevis 49-64 24190904-1 2014 BACKGROUND: In response to high salt intake, transcription factor hypoxia-inducible factor (HIF) 1alpha activates many antihypertensive genes, such as heme oxygenase 1 (HO-1) 1 and cyclooxygenase 2 (COX-2) in the renal medulla, which is an important molecular adaptation to promote extra sodium excretion. Sodium 288-294 heme oxygenase 1 Rattus norvegicus 151-167 24689065-3 2014 We tested the hypothesis that renal expression of ANP and HIF-1alpha is involved in a mechanism responding to the oxidative stress produced in the kidneys of rats chronically fed a high sodium diet. Sodium 186-192 natriuretic peptide A Rattus norvegicus 50-53 24689065-3 2014 We tested the hypothesis that renal expression of ANP and HIF-1alpha is involved in a mechanism responding to the oxidative stress produced in the kidneys of rats chronically fed a high sodium diet. Sodium 186-192 hypoxia inducible factor 1 subunit alpha Rattus norvegicus 58-68 24689065-8 2014 The administration of tempol together with the sodium overload increased the natriuresis further and prevented the elevation of blood pressure and the increased expression of ANP, TGF-beta1, and HIF-1alpha compared to their control. Sodium 47-53 natriuretic peptide A Rattus norvegicus 175-178 24689065-8 2014 The administration of tempol together with the sodium overload increased the natriuresis further and prevented the elevation of blood pressure and the increased expression of ANP, TGF-beta1, and HIF-1alpha compared to their control. Sodium 47-53 hypoxia inducible factor 1 subunit alpha Rattus norvegicus 195-205 24689065-9 2014 These findings suggest that HIF-1alpha and ANP, synthesized by the kidney, are involved in an adaptive mechanism in response to a sodium overload to prevent or attenuate the deleterious effects of the oxidative stress and the hypoxia on the development of fibrosis. Sodium 130-136 hypoxia inducible factor 1 subunit alpha Rattus norvegicus 28-38 24689065-9 2014 These findings suggest that HIF-1alpha and ANP, synthesized by the kidney, are involved in an adaptive mechanism in response to a sodium overload to prevent or attenuate the deleterious effects of the oxidative stress and the hypoxia on the development of fibrosis. Sodium 130-136 natriuretic peptide A Rattus norvegicus 43-46 23829355-4 2013 In 40-60% of aldosterone-producing adenomas there is a somatic mutation in the region of the KCNJ5 gene that codes for the selectivity filter that decreases potassium selectivity, allowing sodium to leak into the cells, thus depolarizing the membrane and initiating events that result in increased aldosterone synthesis. Sodium 189-195 potassium inwardly rectifying channel subfamily J member 5 Homo sapiens 93-98 23931032-5 2013 The present studies were designed to explore the circadian variations of plasma renin activity (RA) and urinary aldosterone-to-creatinine ratio (UA:C) in relation to blood pressure (BP), sodium (UNa, UNa,fe), and potassium (UK, UK,fe) renal handling. Sodium 187-193 renin Canis lupus familiaris 80-85 23931032-19 2013 Specifically, sodium intake was found to interact with the tonic and the phasic secretion of renin, suggesting that varying feeding time could also impact the chronobiology of the renin cascade. Sodium 14-20 renin Canis lupus familiaris 93-98 23931032-19 2013 Specifically, sodium intake was found to interact with the tonic and the phasic secretion of renin, suggesting that varying feeding time could also impact the chronobiology of the renin cascade. Sodium 14-20 renin Canis lupus familiaris 180-185 24019399-3 2013 We hypothesized that renal gastrin and dopamine receptors interact to synergistically increase sodium excretion, an impaired interaction of which may be involved in the pathogenesis of hypertension. Sodium 95-101 gastrin Rattus norvegicus 27-34 31375088-9 2019 The majority of sodium and calcium but few chloride channels showed differential expression in the song system, among them SCN8A and CACNA1E in the direct motor pathway, and CACNG4 and RYR2 in the anterior forebrain pathway. Sodium 16-22 sodium channel, voltage gated, type VIII, alpha subunit Taeniopygia guttata 123-128 23562556-6 2013 Stably transfected mSoat-HEK293 cells revealed sodium-dependent transport for dehydroepiandrosterone sulfate (DHEAS), estrone-3-sulfate, and pregnenolone sulfate (PREGS) with apparent Km values of 60.3muM, 2.1muM, and 2.5muM, respectively. Sodium 47-53 sulfotransferase family 2A member 1 Homo sapiens 110-115 31236708-14 2019 Gastrin functions as an intestinal sodium taste sensor and inhibits NHE3 activity. Sodium 35-41 gastrin Homo sapiens 0-7 24194910-7 2013 Competition experiments with other amino acids and a low sodium dependency of the influx suggests that the amino acid transporters LAT1 and LAT2 are involved in the transport of L-BMAA into milk. Sodium 57-63 solute carrier family 7 (cationic amino acid transporter, y+ system), member 5 Mus musculus 131-135 31227915-2 2019 This review aims at analyzing the effects of sodium-glucose cotransporter type 2 inhibitors (SGLT2is) on blood pressure and more especially on SNS activity in patients with T2DM. Sodium 45-51 solute carrier family 5 member 2 Homo sapiens 93-98 24048198-7 2013 Treatment with Tempol, a superoxide scavenger, attenuates the augmented sodium sensitivity in collectrin knockout mice. Sodium 72-78 collectrin, amino acid transport regulator Mus musculus 94-104 31083464-8 2019 SCN8A encodes a voltage-gated sodium channel and the missense variant was predicted deleterious by three different in silico prediction tools. Sodium 30-36 sodium voltage-gated channel alpha subunit 8 Canis lupus familiaris 0-5 24119730-9 2013 Urinary NGAL was higher (P < 0.001) in those with high versus low fractional sodium excretion, but this was only in patients with transient or intrinsic AKI (P < 0.001 in subgroups), and not in patients without AKI. Sodium 80-86 lipocalin 2 Homo sapiens 8-12 23841645-2 2013 We hypothesized that NOS1- and/or NOS2-derived NO blunts T1D-induced activation of sodium transport in the mTAL. Sodium 83-89 nitric oxide synthase 1 Rattus norvegicus 21-25 23841645-11 2013 CONCLUSION: Under normal conditions, NOS3-derived NO inhibits sodium transport in the mTAL. Sodium 62-68 nitric oxide synthase 3 Rattus norvegicus 37-41 23841645-13 2013 Inhibition of NADPH oxidase to preserve NO bioavailability reveals an inhibitory impact of NOS1- and NOS2-derived NO on sodium transport in the mTAL. Sodium 120-126 nitric oxide synthase 1 Rattus norvegicus 91-95 24075511-5 2013 We showed that the most highly expressed transporters, namely sodium dependent SNAT3 (Slc38a3) and SNAT5 (Slc38a5) and sodium independent neutral amino acids transporters LAT1 (Slc7a5) and LAT2 (Slc7a8), are expressed in the basolateral membrane of acinar cells. Sodium 62-68 solute carrier family 7 (cationic amino acid transporter, y+ system), member 5 Mus musculus 171-175 23986260-5 2013 GlyT2 function is strictly coupled to the sodium electrochemical gradient actively generated by the Na+/K+-ATPase (NKA). Sodium 42-48 glycoprotein alpha-galactosyltransferase 1 (inactive) Homo sapiens 0-5 31006312-13 2019 In patients with LQT2, pharmacological targeting of the physiological late sodium current may provide added therapeutic efficacy to beta-blocker therapy. Sodium 75-81 potassium voltage-gated channel subfamily H member 2 Homo sapiens 17-21 30961536-6 2019 By data analysis, the response pathway of post-transcriptional regulation concerning salt and water-deprivation stresses was put forward, involving preventing sodium from entering the cell, purifying of water and compensating neutral amino acids by miR-193b, miR-542-5p interaction with SLC6A19 mRNA. Sodium 159-165 sodium-dependent neutral amino acid transporter B(0)AT1 Camelus bactrianus 287-294 30726893-4 2019 In both kidney and heart tissues, phosphorylation of mTOR is significantly decreased when aldosterone levels are physiologically increased (by dietary sodium restriction), followed by a decrease in phosphorylated p70S6K1 in cardiac, but not renal, tissue. Sodium 151-157 mechanistic target of rapamycin kinase Mus musculus 53-57 30867591-1 2019 The L-type amino acid transporter 1 (LAT1; also known as SLC7A5) catalyses the cross-membrane flux of large neutral amino acids in a sodium- and pH-independent manner1-3. Sodium 133-139 solute carrier family 7 member 5 Homo sapiens 4-35 30867591-1 2019 The L-type amino acid transporter 1 (LAT1; also known as SLC7A5) catalyses the cross-membrane flux of large neutral amino acids in a sodium- and pH-independent manner1-3. Sodium 133-139 solute carrier family 7 member 5 Homo sapiens 37-41 30867591-1 2019 The L-type amino acid transporter 1 (LAT1; also known as SLC7A5) catalyses the cross-membrane flux of large neutral amino acids in a sodium- and pH-independent manner1-3. Sodium 133-139 solute carrier family 7 member 5 Homo sapiens 57-63 30824560-1 2019 OBJECTIVE: To identify the genetic and physiologic basis for recessive myasthenic congenital myopathy in 2 families, suggestive of a channelopathy involving the sodium channel gene, SCN4A. Sodium 161-167 sodium voltage-gated channel alpha subunit 4 Homo sapiens 182-187 30824560-3 2019 RESULTS: Missense mutations of the same residue in the skeletal muscle sodium channel, R1460 of NaV1.4, were identified in a family and a single patient of Finnish origin (p.R1460Q) and a proband in the United States (p.R1460W). Sodium 71-77 sodium voltage-gated channel alpha subunit 4 Homo sapiens 96-102 30499712-16 2019 The work provides further evidence that FK506-binding protein 12 is a critical component for regulating voltage-gated sodium current and in so doing has an important role in arrhythmogenic physiology, such as atrial fibrillation. Sodium 118-124 FK506 binding protein 1a Mus musculus 40-64 23650201-1 2013 In mice, homozygous deletion of the cardiac sodium channel Scn5a results in defects in cardiac morphology and embryonic death before robust sodium current can be detected. Sodium 44-50 sodium channel, voltage-gated, type V, alpha Mus musculus 59-64 23753405-1 2013 The renal outer medullary potassium channel (ROMK, KCNJ1) mediates potassium recycling and facilitates sodium reabsorption through the Na(+)/K(+)/2Cl(-) cotransporter in the loop of Henle and potassium secretion at the cortical collecting duct. Sodium 103-109 potassium inwardly-rectifying channel, subfamily J, member 1 Rattus norvegicus 51-56 30343635-1 2019 The epithelial sodium channel (ENaC) plays a pivotal role in sodium homeostasis, and the development of drugs that modulate ENaC activity is of great potential therapeutic relevance. Sodium 15-21 sodium channel, nonvoltage-gated 1 alpha Mus musculus 31-35 30343635-1 2019 The epithelial sodium channel (ENaC) plays a pivotal role in sodium homeostasis, and the development of drugs that modulate ENaC activity is of great potential therapeutic relevance. Sodium 15-21 sodium channel, nonvoltage-gated 1 alpha Mus musculus 124-128 30343635-2 2019 We screened 6100 chemicals for their ability to activate sodium permeability of ENaC. Sodium 57-63 sodium channel, nonvoltage-gated 1 alpha Mus musculus 80-84 30414954-8 2019 This is followed by reduced luminal sodium-coupled transport of L-alanine and this change may be one of the possible mechanisms involved in the early stages of Cd2+-induced nephrotoxicity. Sodium 36-42 CD2 molecule Homo sapiens 160-163 23770352-1 2013 Sodium-calcium exchange (NCX) is the major calcium (Ca) efflux mechanism of ventricular cardiomyocytes. Sodium 0-6 T cell leukemia homeobox 2 Homo sapiens 25-28 23361943-6 2013 Using sodium-dependent and sodium-free conditions, we demonstrate that the inhibition of GLUT2 was greater than SGLT1. Sodium 6-12 solute carrier family 2 member 2 Homo sapiens 89-94 23361943-6 2013 Using sodium-dependent and sodium-free conditions, we demonstrate that the inhibition of GLUT2 was greater than SGLT1. Sodium 27-33 solute carrier family 2 member 2 Homo sapiens 89-94 30701480-1 2019 Sodium-glucose co-transporter 2 (SGLT2) inhibitors are glucose-lowering drugs that reduce plasma glucose levels by inhibiting glucose and sodium reabsorption in the kidneys, thus resulting in glucosuria. Sodium 138-144 solute carrier family 5 member 2 Homo sapiens 0-31 23711064-1 2013 The neuropeptide hormone oxytocin (OXT) mediates a wide spectrum of tissue-specific actions, ranging from cell growth, cell differentiation, sodium excretion to stress responses, reproduction and complex social behaviour. Sodium 141-147 oxytocin/neurophysin I prepropeptide Homo sapiens 35-38 23604109-6 2013 The increased intracellular sodium concentration leads to a mode switch of the sodium/calcium exchanger (NCX) that now eliminates sodium from the cell and transports calcium into the cell. Sodium 28-34 T cell leukemia homeobox 2 Homo sapiens 105-108 23604109-6 2013 The increased intracellular sodium concentration leads to a mode switch of the sodium/calcium exchanger (NCX) that now eliminates sodium from the cell and transports calcium into the cell. Sodium 79-85 T cell leukemia homeobox 2 Homo sapiens 105-108 23669717-6 2013 The [Na(+)] dependence of ASCT2-associated currents indicates that the Na(+)/amino acid stoichiometry is at least 2:1, with at least one sodium ion binding to the amino acid-free apo form of the transporter. Sodium 137-143 solute carrier family 1 member 5 Homo sapiens 26-31 23641881-2 2013 Pseudohypoaldosteronism type I (PHA1) is a rare disease of mineralocorticoid resistance caused by defects in sodium transport in the distal tubule of the kidney. Sodium 109-115 sodium channel epithelial 1 subunit gamma Homo sapiens 32-36 23481497-5 2013 Studies in humans and animals have demonstrated a decrease in the expression of proximal sodium (NHE3) and water tubular transporter, aquaporin 1 (AQP1) together with higher renal expression of the Na-K-2Cl cotransporter NKCC2. Sodium 89-95 solute carrier family 9 member A3 Homo sapiens 97-101 24967239-3 2013 After ingestion of a salty meal, GN and UGN are secreted into the intestinal lumen, where they inhibit sodium absorption and induce anion and water secretion. Sodium 103-109 guanylate cyclase activator 2a (guanylin) Mus musculus 33-35 23380500-0 2013 ErbB receptors and PKC regulate PC12 neuronal-like differentiation and sodium current elicitation. Sodium 71-77 epidermal growth factor receptor Rattus norvegicus 0-4 23380500-9 2013 In summary, we demonstrated the involvement of ErbB receptors in the regulation of neurite elongation and sodium current induction in PC12 cells and propose that these processes could be initiated by ErbB receptors followed by a fine regulation of PKC signaling. Sodium 106-112 epidermal growth factor receptor Rattus norvegicus 47-51 23596386-2 2013 We have previously demonstrated that the Nav1.9 channel underlies a tetrodotoxin-resistant sodium current which modulates the excitability of enteric neurons. Sodium 91-97 sodium channel, voltage-gated, type XI, alpha Mus musculus 41-47 30701480-1 2019 Sodium-glucose co-transporter 2 (SGLT2) inhibitors are glucose-lowering drugs that reduce plasma glucose levels by inhibiting glucose and sodium reabsorption in the kidneys, thus resulting in glucosuria. Sodium 138-144 solute carrier family 5 member 2 Homo sapiens 33-38 30252533-7 2019 Instead, sodium-hydrogen exchanger type 3 levels in the proximal tubule were dramatically reduced in Epac1-/- and Epac2-/- mice. Sodium 9-15 Rap guanine nucleotide exchange factor (GEF) 4 Mus musculus 114-119 30252533-10 2019 Deletion of Epac1 and Epac2 decreases sodium-hydrogen exchanger type 3 expression in the proximal tubule, leading to polyuria and osmotic diuresis.-Cherezova, A., Tomilin, V., Buncha, V., Zaika, O., Ortiz, P. A., Mei, F., Cheng, X., Mamenko, M., Pochynyuk, O. Urinary concentrating defect in mice lacking Epac1 or Epac2. Sodium 38-44 Rap guanine nucleotide exchange factor (GEF) 4 Mus musculus 22-27 30170230-2 2019 Genetic testing identifies pathogenic variants in the sodium voltage-gated channel alpha-subunit 5 gene (SCN5A) in up to 25% of familial BrS. Sodium 54-60 sodium voltage-gated channel alpha subunit 5 Homo sapiens 105-110 31933849-11 2019 The Muller cells exhibited signs of dedifferentiation, as paired box 6 (PAX6) and SRY box 2 (SOX2) were expressed by NaIO3 stimulated Muller glia proliferation and overexpression of proliferating cell nuclear antigen (PCNA). Sodium 117-122 SRY-box transcription factor 2 Rattus norvegicus 82-91 31933849-11 2019 The Muller cells exhibited signs of dedifferentiation, as paired box 6 (PAX6) and SRY box 2 (SOX2) were expressed by NaIO3 stimulated Muller glia proliferation and overexpression of proliferating cell nuclear antigen (PCNA). Sodium 117-122 SRY-box transcription factor 2 Rattus norvegicus 93-97 30165510-1 2019 In this study the chiral selectivity of l-undecyl-leucine (und-leu) for binapthyl derivatives was examined with the use of arginine and sodium counterions at pH"s ranging from 7 to 11. Sodium 136-142 collagen type XIV alpha 1 chain Homo sapiens 42-45 30165510-3 2019 The data indicate that und-leu has significantly improved chiral selectivity toward 1,1"-binaphthyl-2,2"-diyl hydrogenphosphate (BNP) enantiomers in the presence of arginine counterions in comparison to sodium and that, at least in the case of this study, the enantiomeric form of the arginine did not appear to play a role in the chiral selectivity. Sodium 203-209 collagen type XIV alpha 1 chain Homo sapiens 23-26 30181659-2 2019 This study aimed to comprehensively examine the association between genetic variants in the cyclic guanosine monophosphate (cGMP)-dependent protein kinase (PKG/PRKG) genes and blood pressure (BP) responses to dietary sodium intervention in a Chinese population. Sodium 217-223 protein kinase cGMP-dependent 1 Homo sapiens 156-159 23541371-0 2013 Endothelin-3 expression in the subfornical organ enhances the sensitivity of Na(x), the brain sodium-level sensor, to suppress salt intake. Sodium 94-100 endothelin 3 Homo sapiens 0-12 30181659-2 2019 This study aimed to comprehensively examine the association between genetic variants in the cyclic guanosine monophosphate (cGMP)-dependent protein kinase (PKG/PRKG) genes and blood pressure (BP) responses to dietary sodium intervention in a Chinese population. Sodium 217-223 protein kinase cGMP-dependent 1 Homo sapiens 160-164 30181659-8 2019 Mean systolic BP response to low-sodium intervention significantly decreased with the number of minor T allele of marker rs10997916 in PRKG1 (P = 2.4 x 10-5). Sodium 33-39 protein kinase cGMP-dependent 1 Homo sapiens 135-140 30181659-10 2019 Gene-based analyses demonstrated that PRKG1 was significantly associated with systolic BP response to low-sodium intervention (P = 1.2 x 10-3), whereas PRKG2 was nominally significantly associated with diastolic BP responses to high-sodium intervention (P = 2.6 x 10-2). Sodium 106-112 protein kinase cGMP-dependent 1 Homo sapiens 38-43 30181659-11 2019 The current study suggested a significant association of genetic variants in the PRKG genes with variation of BP response to dietary sodium intake in Han Chinese population. Sodium 133-139 protein kinase cGMP-dependent 1 Homo sapiens 81-85 30452906-12 2019 In addition, sodium current density showed a significant decrease upon Flotillin-1/2 KD in NRCMs as compared to scrambled siRNA-transfected NRCMs. Sodium 13-19 flotillin 1 Mus musculus 71-82 31609695-1 2019 BACKGROUND: The phenotypic spectrum of the skeletal muscle voltage-gated sodium channel gene (SCN4A) mutations has been expanding dramatically with advancements in genetic testing. Sodium 73-79 sodium voltage-gated channel alpha subunit 4 Homo sapiens 94-99 30999054-1 2019 INTRODUCTION: High throughput in vitro profiling of the cardiac Nav1.5 peak sodium current (INa) is widely used in cardiac safety screening. Sodium 76-82 sodium voltage-gated channel alpha subunit 5 Homo sapiens 64-70 30339176-11 2018 In addition, CCL2 was found to enhance whole-cell TTX-sensitive sodium currents without significantly affecting the TTX-resistant sodium currents and the potassium currents. Sodium 64-70 C-C motif chemokine ligand 2 Rattus norvegicus 13-17 29136153-10 2018 They suggest that sodium influx drives reversal of NCX, triggering a massive secondary calcium elevation while promoting export of sodium. Sodium 18-24 T cell leukemia, homeobox 2 Mus musculus 51-54 29136153-10 2018 They suggest that sodium influx drives reversal of NCX, triggering a massive secondary calcium elevation while promoting export of sodium. Sodium 131-137 T cell leukemia, homeobox 2 Mus musculus 51-54 29136153-11 2018 Reported neuroprotective effects of NCX activity in stroke models might thus be related to its dampening of ischemia-induced sodium loading. Sodium 125-131 T cell leukemia, homeobox 2 Mus musculus 36-39 30328087-8 2018 This is the first study reporting that MST3, a Ste20-like kinase, exerts a conserved regulatory role in sodium homeostasis after high-salt diet and in the development of hypertension. Sodium 104-110 serine/threonine kinase 24 Homo sapiens 39-43 30328087-8 2018 This is the first study reporting that MST3, a Ste20-like kinase, exerts a conserved regulatory role in sodium homeostasis after high-salt diet and in the development of hypertension. Sodium 104-110 STE20 like kinase Homo sapiens 47-64 30425258-1 2018 The sodium channel 1.7 (Nav1.7), which is encoded by SCN9A gene, is involved in neuropathic pain. Sodium 4-10 sodium voltage-gated channel alpha subunit 9 Rattus norvegicus 24-30 30425258-1 2018 The sodium channel 1.7 (Nav1.7), which is encoded by SCN9A gene, is involved in neuropathic pain. Sodium 4-10 sodium voltage-gated channel alpha subunit 9 Rattus norvegicus 53-58 30333319-3 2018 Herein, we show that distinct IAV strains reduced the functions of the epithelial sodium channel (ENaC) and the cystic fibrosis transmembrane regulator (CFTR) in murine respiratory and alveolar epithelia in vivo, as assessed by measurements of nasal potential differences and single-cell electrophysiology. Sodium 82-88 sodium channel, nonvoltage-gated 1 alpha Mus musculus 98-102 29959186-6 2018 The results showed that EPO could promote interleukin (IL) 10 (IL-10) expression; inhibit tumor necrosis factor-alpha (TNF-alpha), IL-6, and inducible nitric oxide synthase (iNOS) expressions; reduce the fractional excretion of sodium (FENa) and plasma creatinine (CREA) and urea; and promote the recovery of water and salt handling and AQP2 expression in BUO-R rats, especially in the high dose of EPO-treated group rats. Sodium 228-234 erythropoietin Rattus norvegicus 24-27 29489063-1 2018 AIM: Recent work has demonstrated that activation of the epithelial sodium channel (ENaC) by aberrantly filtered serine proteases causes sodium retention in nephrotic syndrome. Sodium 68-74 sodium channel, nonvoltage-gated 1 alpha Mus musculus 84-88 29489063-1 2018 AIM: Recent work has demonstrated that activation of the epithelial sodium channel (ENaC) by aberrantly filtered serine proteases causes sodium retention in nephrotic syndrome. Sodium 137-143 sodium channel, nonvoltage-gated 1 alpha Mus musculus 84-88 29767557-5 2018 Serum and urinary electrolyte determinations indicated that iKsp- Pkd1-/- mice display reduced serum levels of magnesium (Mg2+), calcium (Ca2+), sodium (Na+), and phosphate (Pi) compared with control ( Pkd1+/+) mice and renal Mg2+, Ca2+, and Pi wasting. Sodium 145-151 polycystin 1, transient receptor potential channel interacting Mus musculus 66-70 30146013-6 2018 However, these cells can also mediate thiazide-sensitive sodium chloride absorption when the pendrin-dependent apical chloride influx is coupled to apical sodium influx by the sodium-driven chloride/bicarbonate exchanger. Sodium 57-63 solute carrier family 26, member 4 Mus musculus 93-100 30146013-6 2018 However, these cells can also mediate thiazide-sensitive sodium chloride absorption when the pendrin-dependent apical chloride influx is coupled to apical sodium influx by the sodium-driven chloride/bicarbonate exchanger. Sodium 155-161 solute carrier family 26, member 4 Mus musculus 93-100 29901108-4 2018 Using patch-clamp technique and RNA interference approaches, sodium currents were recorded in epithelial ovarian cancer cells, and it was confirmed that the Nav1.5 channel carried the sodium currents. Sodium 61-67 sodium voltage-gated channel alpha subunit 5 Homo sapiens 157-163 29901108-4 2018 Using patch-clamp technique and RNA interference approaches, sodium currents were recorded in epithelial ovarian cancer cells, and it was confirmed that the Nav1.5 channel carried the sodium currents. Sodium 184-190 sodium voltage-gated channel alpha subunit 5 Homo sapiens 157-163 29863287-0 2018 Persistent sodium current modulates axonal excitability in CA1 pyramidal neurons. Sodium 11-17 carbonic anhydrase 1 Mus musculus 59-62 29863287-2 2018 The mechanisms underlying spike generation in the axonal initial segment and transmitter release from presynaptic terminals have been intensely studied and revealed a role for several specific ionic conductances, including the persistent sodium current (INaP ). Sodium 238-244 nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, zeta Mus musculus 254-258 29863287-8 2018 Thus, excitability of distal CA1 pyramidal cell axons is affected by persistent sodium currents in a direction-selective manner. Sodium 80-86 carbonic anhydrase 1 Mus musculus 29-32 29563327-1 2018 Although inhibition of phosphoinositide 3-kinase (PI3K) is an emerging strategy in cancer therapy, we and others have reported that this action can also contribute to drug-induced QT prolongation and arrhythmias by increasing cardiac late sodium current (INaL). Sodium 239-245 phosphoinositide-3-kinase regulatory subunit 1 Mus musculus 23-48 29525332-3 2018 These potentially deleterious actions of DPP-4 inhibitors might not become clinically apparent if these drugs were to promote sodium excretion. Sodium 126-132 dipeptidyl peptidase 4 Homo sapiens 41-46 29861852-6 2018 In the model of multiple linear regression analysis predictor variables influencing cerebrospinal fluid Nogo-A concentrations included: diagnosis, sex, and sodium level. Sodium 156-162 reticulon 4 Homo sapiens 104-110 29861852-8 2018 In the astrocytic brain tumor group higher sodium level occurs with lower cerebrospinal fluid Nogo-A concentrations. Sodium 43-49 reticulon 4 Homo sapiens 94-100 29861852-11 2018 In the created model of multiple linear regression analysis we found, that within predictor variables influencing CSF Nogo-A concentrations were diagnosis, sex, and sodium level. Sodium 165-171 reticulon 4 Homo sapiens 118-124 29736017-4 2018 Here we report an optical transmission spectrum for the "hot Saturn" exoplanet WASP-96b obtained with the Very Large Telescope, which exhibits the complete pressure-broadened profile of the sodium absorption feature. Sodium 190-196 WASP actin nucleation promoting factor Homo sapiens 79-83 29207052-11 2018 This indicates that the previously reported tetrodotoxin-resistant sodium current was a compound product of different Nav1.5 variants. Sodium 67-73 sodium voltage-gated channel alpha subunit 5 Homo sapiens 118-124 29379505-6 2017 Expression of SGK1, a kinase involved in sodium homeostasis, increased 90 min after ingestion of 50% NaCl solution and decreased 3 weeks after HSD consumption. Sodium 41-47 serum/glucocorticoid regulated kinase 1 Mus musculus 14-18 29301520-0 2018 SGLT-2-inhibition with dapagliflozin reduces tissue sodium content: a randomised controlled trial. Sodium 52-58 solute carrier family 5 member 2 Homo sapiens 0-6 29301520-2 2018 SGLT-2 inhibition blocks the reabsorption of glucose and of sodium in the proximal tubular cells in a 1:1 fashion. Sodium 60-66 solute carrier family 5 member 2 Homo sapiens 0-6 29301520-3 2018 We hypothesized that SGLT-2 inhibition in patients with type 2 diabetes characterized by sodium retention leads to decreased tissue sodium content due to its pharmacological action. Sodium 89-95 solute carrier family 5 member 2 Homo sapiens 21-27 29301520-3 2018 We hypothesized that SGLT-2 inhibition in patients with type 2 diabetes characterized by sodium retention leads to decreased tissue sodium content due to its pharmacological action. Sodium 132-138 solute carrier family 5 member 2 Homo sapiens 21-27 29301520-12 2018 CONCLUSION: SGLT-2 inhibition with dapagliflozin resulted in a significant decrease in tissue sodium content of the skin after 6 weeks. Sodium 94-100 solute carrier family 5 member 2 Homo sapiens 12-18 29301520-13 2018 This observation point to a decrease of total sodium content in patients with type 2 diabetes prone to cardiovascular complications, that might be mitigated by SGLT-2 inhibition. Sodium 46-52 solute carrier family 5 member 2 Homo sapiens 160-166 29016751-0 2018 Cardiac effects of SGLT2 inhibitors: the sodium hypothesis. Sodium 41-47 solute carrier family 5 member 2 Homo sapiens 19-24 28837387-6 2018 We demonstrated that editing of neurofibromin results in functional remodeling of peripheral nociceptors characterized by enhancement of interactions of the tetrodotoxin-sensitive (TTX-S) Na+ voltage-gated sodium channel (NaV1.7) and the collapsin response mediator protein 2 (CRMP2). Sodium 206-212 neurofibromin 1 Rattus norvegicus 32-45 28837387-6 2018 We demonstrated that editing of neurofibromin results in functional remodeling of peripheral nociceptors characterized by enhancement of interactions of the tetrodotoxin-sensitive (TTX-S) Na+ voltage-gated sodium channel (NaV1.7) and the collapsin response mediator protein 2 (CRMP2). Sodium 206-212 sodium voltage-gated channel alpha subunit 9 Rattus norvegicus 222-228 28836327-3 2018 However, no studies have reported on a possible association between reduced MTP and serum sodium levels. Sodium 90-96 metallothionein 1B Homo sapiens 76-79 28836327-7 2018 RESULTS: Independent of classical cardiovascular risk factors, the adjusted odds ratio of reduced MTP for a 1-standard deviation increment of serum sodium (2.21 mEq/L) was 1.29 (95% confidence interval 1.10-1.52). Sodium 148-154 metallothionein 1B Homo sapiens 98-101 28836327-9 2018 CONCLUSIONS: Serum sodium level within the normal range is independently associated with reduced MTP in older Japanese men. Sodium 19-25 metallothionein 1B Homo sapiens 97-100 28754555-8 2017 Acute salt loading with 6% dietary sodium increased daytime systolic blood pressure only in male Eln+/- mice, causing a rightward shift and blunted slope of the pressure-natriuresis curve. Sodium 35-41 elastin Mus musculus 97-100 28754555-11 2017 Thus, elastin insufficiency triggers structural defects and abnormal remodeling of renal vascular signaling involving AT1R-mediated vascular mechanotransduction and renal hyperfiltration with increased blood pressure sensitivity to dietary sodium contributing to systolic hypertension. Sodium 240-246 elastin Mus musculus 6-13 28961453-1 2017 INTRODUCTION: Antithrombin resistance (ATR) prothrombinemia is an inherited thrombophilic disorder caused by missense mutations in prothrombin gene (F2) at Arg596 of the sodium-binding region. Sodium 170-176 serpin family C member 1 Homo sapiens 14-26 29084222-0 2017 AtHKT1 drives adaptation of Arabidopsis thaliana to salinity by reducing floral sodium content. Sodium 80-86 high-affinity K+ transporter 1 Arabidopsis thaliana 0-6 29084222-1 2017 Arabidopsis thaliana high-affinity potassium transporter 1 (AtHKT1) limits the root-to-shoot sodium transportation and is believed to be essential for salt tolerance in A. thaliana. Sodium 93-99 high-affinity K+ transporter 1 Arabidopsis thaliana 60-66 29084222-4 2017 Here, we report that AtHKT1 indeed drives natural variation in the salt tolerance of A. thaliana and the coastal AtHKT1, so-called weak allele, is actually hyper-functional in reducing flowers sodium content upon salt stress. Sodium 193-199 high-affinity K+ transporter 1 Arabidopsis thaliana 21-27 29084222-4 2017 Here, we report that AtHKT1 indeed drives natural variation in the salt tolerance of A. thaliana and the coastal AtHKT1, so-called weak allele, is actually hyper-functional in reducing flowers sodium content upon salt stress. Sodium 193-199 high-affinity K+ transporter 1 Arabidopsis thaliana 113-119 28993621-5 2017 The IL-1alpha/aptamer interface is composed of unusual polar and hydrophobic elements, along with an elaborate hydrogen bonding network that is mediated by sodium ion. Sodium 156-162 interleukin 1 alpha Homo sapiens 4-13 28831242-11 2017 We believe that the data presented here will enhance our understanding of the structure-property relationships of the hNav1.5 ion channel and the underlying molecular mechanisms in sodium ion permeation and drug interactions. Sodium 181-187 sodium voltage-gated channel alpha subunit 5 Homo sapiens 118-125 28160049-11 2017 The low pH prevailing at this site and the acidic pH preference of PRCP suggest a role of this enzyme in regulating AngII degradation in the collecting tubule where this peptide increases sodium reabsorption and therfore BP. Sodium 188-194 prolylcarboxypeptidase (angiotensinase C) Mus musculus 67-71 28503166-11 2017 However, phenytoin significantly decreased NaV1.3 mRNA levels under the sodium challenge with added sodium at 10 and 20 mEq/L. Sodium 72-78 sodium voltage-gated channel alpha subunit 3 Homo sapiens 43-49 28503166-11 2017 However, phenytoin significantly decreased NaV1.3 mRNA levels under the sodium challenge with added sodium at 10 and 20 mEq/L. Sodium 100-106 sodium voltage-gated channel alpha subunit 3 Homo sapiens 43-49 28423317-0 2017 Loss of Navbeta4-Mediated Regulation of Sodium Currents in Adult Purkinje Neurons Disrupts Firing and Impairs Motor Coordination and Balance. Sodium 40-46 sodium voltage-gated channel beta subunit 4 Homo sapiens 8-16 28299616-9 2017 SGLT-2 inhibitors decrease proximal tubular sodium and chloride reabsorption, leading to a reset of the tubuloglomerular feedback. Sodium 44-50 solute carrier family 5 member 2 Homo sapiens 0-6 28428931-9 2017 Insulin stimulates the proximal tubule sodium transport, which is IRS2-dependent. Sodium 39-45 insulin receptor substrate 2 Homo sapiens 66-70 28193882-4 2017 Acutely dissociated hippocampal neurons from Scn8aN1768D/+ mice showed increases in persistent sodium current (INa) density in CA1 pyramidal but not bipolar neurons. Sodium 95-101 carbonic anhydrase 1 Mus musculus 127-130 28134511-0 2017 Sulfate-Centered Sodium-Icosahedron-Templated Uranyl Peroxide Phosphate Cages with Uranyl Bridged by mu-eta1:eta2 Peroxide. Sodium 17-23 secreted phosphoprotein 1 Homo sapiens 104-108 28122427-3 2017 Familial hyperekplexia has a heterogeneous genetic background with several identified causative genes; it demonstrates both dominant and recessive inheritance in the alpha1 subunit of the glycine receptor (GLRA1), the beta subunit of the glycine receptor and the presynaptic sodium and chloride-dependent glycine transporter 2 genes. Sodium 275-281 glycine receptor alpha 1 Homo sapiens 206-211 27934887-6 2016 The GPER agonist G-1 produced a parallel and significant increase in sodium intake, while pre-treatment with GPER antagonist G15 (10 ng 0.1 mul-1) blocked the G-1 or aldosterone-induced rapid sodium intake. Sodium 69-75 G protein-coupled estrogen receptor 1 Rattus norvegicus 4-8 27934887-6 2016 The GPER agonist G-1 produced a parallel and significant increase in sodium intake, while pre-treatment with GPER antagonist G15 (10 ng 0.1 mul-1) blocked the G-1 or aldosterone-induced rapid sodium intake. Sodium 192-198 G protein-coupled estrogen receptor 1 Rattus norvegicus 109-113 27934887-8 2016 Our results confirm previous reports, and support the hypothesis that aldosterone evokes rapid sodium intake through a non-genomic mechanism involving GPER in NTS. Sodium 95-101 G protein-coupled estrogen receptor 1 Rattus norvegicus 151-155 27620667-2 2016 The guanylin peptides could be related to sodium absorption inhibition and water secretion induction and their dysfunction may be related to various pathologies such as chronic renal failure, congestive heart failure and nephrotic syndrome. Sodium 42-48 guanylate cyclase activator 2A Homo sapiens 4-12 29908537-0 2016 [The reverse effects of allitridum on sodium current decrease caused by SCN5A-F1473S mutation]. Sodium 38-44 sodium voltage-gated channel alpha subunit 5 Homo sapiens 72-77 29908537-1 2016 This study was designed to test the allitridum (All) activity in correction of sodium current decrease caused by SCN5A-F1473S mutation in HEK293 cells. Sodium 79-85 sodium voltage-gated channel alpha subunit 5 Homo sapiens 113-118 27686614-3 2016 NHE8 is important for water/sodium absorption in the intestine, and loss of NHE8 function results in mucosal injury. Sodium 28-34 solute carrier family 9 member A8 Homo sapiens 0-4 27470878-11 2016 With additional cardiorenal protection trials underway, sodium-related physiological effects of SGLT2 inhibitors and clinical correlates of natriuresis, such as the impact on blood pressure, heart failure, kidney protection, and mortality, will be a major management focus. Sodium 56-62 solute carrier family 5 member 2 Homo sapiens 96-101 27206969-7 2016 Interestingly, genetic inactivation of beta3-AR in mice was associated with significantly increased urine excretion of water, sodium, potassium, and chloride. Sodium 126-132 adrenergic receptor, beta 3 Mus musculus 39-47 26965448-10 2016 These data also demonstrate that flecainide may serve as an effective treatment for the defect in Nav 1.5 that leads to an increased sodium window current. Sodium 133-139 sodium voltage-gated channel alpha subunit 5 Homo sapiens 98-105 26916278-1 2016 The SCN5A gene encodes the alpha-subunit of the Nav1.5 ion channel protein, which is responsible for the sodium inward current (INa). Sodium 105-111 sodium voltage-gated channel alpha subunit 5 Homo sapiens 4-9 26916278-1 2016 The SCN5A gene encodes the alpha-subunit of the Nav1.5 ion channel protein, which is responsible for the sodium inward current (INa). Sodium 105-111 sodium voltage-gated channel alpha subunit 5 Homo sapiens 48-54 27197160-5 2016 The most robust and frequent inductions were of the sodium-driven bicarbonate transporters SLC4A4 and SLC4A9, which rely upon both HIF1alpha and HIF2alpha activity for their expression. Sodium 52-58 endothelial PAS domain protein 1 Homo sapiens 145-154 27112340-4 2016 We suggest that the main driver of benefit may derive from the specific effects of sodium-glucose linked transporter-2 (SGLT2) inhibition on renal sodium and glucose handling, leading to both diuresis and improvements in diabetes-related maladaptive renal arteriolar responses. Sodium 83-89 solute carrier family 5 member 2 Homo sapiens 120-125 27355484-7 2016 While exposure to 10 muM NF110, a blocker of ATP-P2X receptors mediating sodium influx, reduced [ATPe] by 48%, and swelling by 80%, incubation of cells in sodium free medium reduced swelling by 92%. Sodium 73-79 interleukin enhancer binding factor 3 Homo sapiens 25-30 27277800-5 2016 This mutation has been shown to disrupt both the sodium-current-modulatory and cell-adhesive functions of beta1 subunits expressed in heterologous systems. Sodium 49-55 hemoglobin, beta adult major chain Mus musculus 106-111 27045029-8 2016 Agtr1a(-/-) mice had decreased mesenteric artery expression of the calcium-activated potassium channel Kcnmb1, which may enhance myogenic tone and together with sodium retention, exacerbate BP responses to aldosterone/salt in Agtr1a(-/-) mice. Sodium 161-167 potassium large conductance calcium-activated channel, subfamily M, beta member 1 Mus musculus 103-109 27183948-1 2016 Neonatal Bartter syndrome (NBS) is an autosomal recessive renal tubulopathy characterized by hypokalaemic, hypochloraemic metabolic alkalosis associated with increased urinary loss of sodium, potassium, calcium and chloride. Sodium 184-190 nibrin Homo sapiens 27-30 26923164-0 2016 The type III transporters (PiT-1 and PiT-2) are the major sodium-dependent phosphate transporters in the mice and human brains. Sodium 58-64 solute carrier family 20, member 2 Mus musculus 37-42 27053360-0 2016 Sodium Intake Regulates Glucose Homeostasis through the PPARdelta/Adiponectin-Mediated SGLT2 Pathway. Sodium 0-6 adiponectin, C1Q and collagen domain containing Mus musculus 66-77 27053360-5 2016 PPARdelta activation in perirenal fat by agonist or high sodium intake inhibited renal sodium-glucose cotransporter 2 (SGLT2) function, which is mediated by increased production of adipose adiponectin. Sodium 57-63 adiponectin, C1Q and collagen domain containing Mus musculus 189-200 27053360-8 2016 Our findings provide insights into the distinctive role of the PPARdelta/adiponectin/SGLT2 pathway in the regulation of sodium and glucose homeostasis. Sodium 120-126 adiponectin, C1Q and collagen domain containing Mus musculus 73-84 26951843-12 2016 Our data suggest that 11betaHSD2-positive neurons integrate salt appetite and the blood pressure response to dietary sodium through a mineralocorticoid receptor-dependent pathway. Sodium 117-123 nuclear receptor subfamily 3, group C, member 2 Mus musculus 134-160 26951843-13 2016 Therefore, central mineralocorticoid receptor antagonism could increase compliance to low-sodium regimens and help blood pressure management in cardiovascular disease. Sodium 90-96 nuclear receptor subfamily 3, group C, member 2 Mus musculus 19-45 26786777-1 2016 The natriuretic effect of gastrin suggests a role in the coordinated regulation of sodium balance by the gastrointestinal tract and the kidney. Sodium 83-89 gastrin Homo sapiens 26-33 26862153-3 2016 Using a split-root system to simulate a non-uniform root zone salinity in Gossypium hirsutum L., we showed that the up-regulated expression of sodium efflux-related genes (SOS1, SOS2, PMA1, and PMA2) and water uptake-related genes (PIP1 and PIP2) was possibly involved in the elevated Na(+) efflux and water use in the the roots in the non-saline side. Sodium 143-149 sodium/hydrogen exchanger 8-like Gossypium hirsutum 172-176 26869332-7 2016 Two genes previously linked with GDM, pregnancy specific beta-1 glycoprotein 6 (PSG6) and placental system A sodium-dependent transporter system (SLC38A1), were significantly increased in GDM. Sodium 109-115 solute carrier family 38 member 1 Homo sapiens 146-153 26803770-5 2016 LQT3 hiPSC-CMs recapitulated pathognomonic electrophysiological features of the disease, such as an accelerated recovery from inactivation of sodium currents as well as action potential prolongation, especially at low stimulation rates. Sodium 142-148 sodium voltage-gated channel alpha subunit 5 Homo sapiens 0-4 26874564-1 2016 Primarily the sodium-glucose cotransporter 2 (SGLT2) inhibitors suppress the cotransport of glucose and sodium from the tubular lumen of proximal tubules to the blood and enhance the glucose excretion into urine. Sodium 14-20 solute carrier family 5 member 2 Homo sapiens 46-51 27010892-8 2016 A possible target is protein kinase C (PKC), and PKCepsilon is postulated increase the permeability of the membrane of the cardiac cells to sodium, resulting in delayed repolarization and prolongation of action potential. Sodium 140-146 protein kinase C epsilon Homo sapiens 39-42 27010892-8 2016 A possible target is protein kinase C (PKC), and PKCepsilon is postulated increase the permeability of the membrane of the cardiac cells to sodium, resulting in delayed repolarization and prolongation of action potential. Sodium 140-146 protein kinase C epsilon Homo sapiens 49-59 26163195-1 2016 The epithelial Na(+) channel (ENaC) is decisive for sodium reabsorption by the aldosterone-sensitive distal nephron (ASDN) of the kidney. Sodium 52-58 sodium channel, nonvoltage-gated 1 alpha Mus musculus 4-28 26163195-1 2016 The epithelial Na(+) channel (ENaC) is decisive for sodium reabsorption by the aldosterone-sensitive distal nephron (ASDN) of the kidney. Sodium 52-58 sodium channel, nonvoltage-gated 1 alpha Mus musculus 30-34 27935319-2 2016 Genetic variability in CYP11B2 gene has been associated with heterogeneous aldosterone production, which can affect sodium homeostasis and thereby regulation of blood pressure. Sodium 116-122 cytochrome P450 family 11 subfamily B member 2 Homo sapiens 23-30 26595809-1 2016 Increased sodium influx via incomplete inactivation of the major cardiac sodium channel Na(V)1.5 is correlated with an increased incidence of atrial fibrillation (AF) in humans. Sodium 10-16 immunoglobulin lambda variable 2-18 Homo sapiens 88-96 27010539-7 2016 In anesthetized mice, medullary infusion of Nlrp3 inflammasome activator, monosodium urate (MSU), induced significant decreases in sodium excretion and medullary blood flow without changes in mean arterial blood pressure and renal cortical blood flow. Sodium 78-84 NLR family, pyrin domain containing 3 Mus musculus 44-49 27010539-8 2016 Caspase-1 inhibitor, Ac-YVAD-CMK and deletion of Nlrp3 or Asc gene abolished MSU-induced decreases in renal sodium excretion and MBF. Sodium 108-114 NLR family, pyrin domain containing 3 Mus musculus 49-54 27010539-9 2016 CONCLUSION: Our results indicate that renal medullary Nlrp3 inflammasomes represent a new regulatory mechanism of renal MBF and sodium excretion which may not depend on classical inflammatory response. Sodium 128-134 NLR family, pyrin domain containing 3 Mus musculus 54-59 26565933-2 2015 The crystalline sample (NaK-D-1) of the water-soluble, mixed sodium/potassium salt of D-1 was obtained in the 14.7% yield, which has been characterized by complete elemental analysis, TG/DTA, FTIR, single-crystal X-ray structure analysis, and solution ((183)W, (31)P, (1)H and (13)C{(1)H}) NMR spectroscopy. Sodium 61-67 TANK binding kinase 1 Homo sapiens 24-27 25319728-8 2015 DAI-7-glucuronide, but not DAI-4"-glucuronide, was transported exclusively by OATP2B1 in a sodium-independent manner. Sodium 91-97 solute carrier organic anion transporter family member 2B1 Homo sapiens 78-85 26289465-8 2015 Overall, the results show opposing effects of subthreshold sodium current and Ih in regulating subthreshold behavior of CA1 neurons, with subthreshold sodium current prominent in both rat and mouse CA1 pyramidal neurons and additional regulation by Ih in rat neurons. Sodium 59-65 carbonic anhydrase 1 Rattus norvegicus 120-123 26289465-8 2015 Overall, the results show opposing effects of subthreshold sodium current and Ih in regulating subthreshold behavior of CA1 neurons, with subthreshold sodium current prominent in both rat and mouse CA1 pyramidal neurons and additional regulation by Ih in rat neurons. Sodium 151-157 carbonic anhydrase 1 Rattus norvegicus 120-123 26289465-8 2015 Overall, the results show opposing effects of subthreshold sodium current and Ih in regulating subthreshold behavior of CA1 neurons, with subthreshold sodium current prominent in both rat and mouse CA1 pyramidal neurons and additional regulation by Ih in rat neurons. Sodium 151-157 carbonic anhydrase 1 Mus musculus 198-201 26183312-1 2015 Aldosterone interacts with mineralocorticoid receptor (MR) to stimulate sodium reabsorption in renal tubules and may also affect the vasculature. Sodium 72-78 nuclear receptor subfamily 3, group C, member 2 Mus musculus 27-53 26183312-1 2015 Aldosterone interacts with mineralocorticoid receptor (MR) to stimulate sodium reabsorption in renal tubules and may also affect the vasculature. Sodium 72-78 nuclear receptor subfamily 3, group C, member 2 Mus musculus 55-57 26309024-2 2015 To study its in vivo implication in ENaC-mediated sodium absorption, we generated a knockout mouse model for CAP2/Tmprss4. Sodium 50-56 sodium channel, nonvoltage-gated 1 alpha Mus musculus 36-40 26309024-7 2015 In summary, ENaC-mediated sodium balance is not affected by lack of CAP2/Tmprss4 expression and thus, does not seem to directly control ENaC expression and activity in vivo. Sodium 26-32 sodium channel, nonvoltage-gated 1 alpha Mus musculus 12-16 26347659-3 2015 We have determined that brain Galphai2-proteins mediate natriuretic and sympathoinhibitory responses produced by acute pharmacological (exogenous central nociceptin/orphanin FQ receptor (NOP) and alpha2-adrenoceptor activation) and physiological challenges to sodium homeostasis (intravenous volume expansion and 1 M sodium load) in conscious Sprague-Dawley rats. Sodium 260-266 G protein subunit alpha i2 Rattus norvegicus 30-38 26347659-3 2015 We have determined that brain Galphai2-proteins mediate natriuretic and sympathoinhibitory responses produced by acute pharmacological (exogenous central nociceptin/orphanin FQ receptor (NOP) and alpha2-adrenoceptor activation) and physiological challenges to sodium homeostasis (intravenous volume expansion and 1 M sodium load) in conscious Sprague-Dawley rats. Sodium 317-323 G protein subunit alpha i2 Rattus norvegicus 30-38 26347659-7 2015 Collectively, our data demonstrate that brain, and likely PVN specific, Galphai2 protein pathways represent a central molecular pathway mediating sympathoinhibitory renal-nerve dependent responses evoked to maintain sodium homeostasis and a salt-resistant phenotype. Sodium 216-222 G protein subunit alpha i2 Rattus norvegicus 72-80 26182346-5 2015 The C-terminal tail of Navbeta4 is thought to mediate resurgent sodium current, an atypical current that occurs immediately following the action potential and is predicted to enhance excitability. Sodium 64-70 sodium voltage-gated channel beta subunit 4 Homo sapiens 23-31 25701775-1 2015 BACKGROUND: The human cardiac action potential in atrial and ventricular cells is initiated by a fast-activating, fast-inactivating sodium current generated by the SCN5A/Nav1.5 channel in association with its beta1/SCN1B subunit. Sodium 132-138 sodium voltage-gated channel alpha subunit 5 Homo sapiens 164-169 25701775-1 2015 BACKGROUND: The human cardiac action potential in atrial and ventricular cells is initiated by a fast-activating, fast-inactivating sodium current generated by the SCN5A/Nav1.5 channel in association with its beta1/SCN1B subunit. Sodium 132-138 sodium voltage-gated channel alpha subunit 5 Homo sapiens 170-176 25757662-11 2015 Functional analysis of variants not previously characterized (R458C, S1609L, and Q1909R in SCN5A) predominantly revealed increased transient and sustained sodium current. Sodium 155-161 sodium voltage-gated channel alpha subunit 5 Homo sapiens 91-96 25587116-9 2015 Here, we show for the first time that PRL activates sodium and chloride transport in renal epithelial cells via ENaC and ClC4. Sodium 52-58 chloride voltage-gated channel 4 Homo sapiens 121-125 25613995-3 2015 Here, we aim to highlight the recent advances made using transgenic mouse models towards the understanding of the regulation of NCC and ENaC function relevant to the control of sodium balance and blood pressure. Sodium 177-183 sodium channel, nonvoltage-gated 1 alpha Mus musculus 136-140 30364910-0 2015 Sodium Ion Effect on Separation Of Butyrylcholinesterase from Plasma by Ion-Exchange Chromatography. Sodium 0-6 butyrylcholinesterase Homo sapiens 35-56 25734516-2 2015 Although both populations express similar endogenous conductances, we have discovered that AVPV/PeN Kiss1 neurons express a subthreshold, persistent sodium current (INaP) that dramatically alters their firing activity. Sodium 149-155 nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, zeta Mus musculus 165-169 25660391-2 2015 No DM2 cases have been described with sodium channel gene (SCN4A) mutations. Sodium 38-44 sodium voltage-gated channel alpha subunit 4 Homo sapiens 59-64 25626868-6 2015 In sum, these results suggest the ability of ClCN2 to negatively regulate sodium absorption through ENaC, supporting its role as a therapeutic target for the treatment of CF. Sodium 74-80 chloride voltage-gated channel 2 Homo sapiens 45-50 24943134-1 2015 BACKGROUND: Myotonic dystrophy type 1 (DM1) generates missplicing of the SCN5A gene, encoding the cardiac sodium channel (Nav 1.5). Sodium 106-112 sodium voltage-gated channel alpha subunit 5 Homo sapiens 73-78 24943134-1 2015 BACKGROUND: Myotonic dystrophy type 1 (DM1) generates missplicing of the SCN5A gene, encoding the cardiac sodium channel (Nav 1.5). Sodium 106-112 sodium voltage-gated channel alpha subunit 5 Homo sapiens 122-129 26491696-3 2015 In insulin resistance, the IRS2 in kidney cortex is exceptionally preserved and may mediate the stimulatory effect of insulin on NBCe1 to cause hypertension in diabetes via sodium retention. Sodium 173-179 insulin receptor substrate 2 Homo sapiens 27-31 25824645-8 2015 Also, 24-hour urinary sodium excretion positively correlated with urine renalase and serum dopamine in the whole population. Sodium 22-28 renalase, FAD dependent amine oxidase Homo sapiens 72-80 26112332-10 2015 Expression of antisense miR-22 significantly attenuated the levels of liver fibrosis, portal hypertension and sodium retention caused by CCl4, possibly through upregulation of BMP7. Sodium 110-116 C-C motif chemokine ligand 4 Homo sapiens 137-141 25470017-5 2015 RECENT FINDINGS: Novel sodium-glucose cotransporter-2 (SGLT2) inhibitors reduce proximal tubular sodium reabsorption, thereby increasing distal sodium delivery to the macula densa, causing tubuloglomerular feedback, afferent vasoconstriction and decreased hyperfiltration in animals. Sodium 23-29 solute carrier family 5 member 2 Homo sapiens 55-60 25470017-5 2015 RECENT FINDINGS: Novel sodium-glucose cotransporter-2 (SGLT2) inhibitors reduce proximal tubular sodium reabsorption, thereby increasing distal sodium delivery to the macula densa, causing tubuloglomerular feedback, afferent vasoconstriction and decreased hyperfiltration in animals. Sodium 97-103 solute carrier family 5 member 2 Homo sapiens 23-53 25470017-5 2015 RECENT FINDINGS: Novel sodium-glucose cotransporter-2 (SGLT2) inhibitors reduce proximal tubular sodium reabsorption, thereby increasing distal sodium delivery to the macula densa, causing tubuloglomerular feedback, afferent vasoconstriction and decreased hyperfiltration in animals. Sodium 97-103 solute carrier family 5 member 2 Homo sapiens 55-60 26295465-0 2015 Angiotensin II Type 1 Receptor Binding Molecule ATRAP as a Possible Modulator of Renal Sodium Handling and Blood Pressure in Pathophysiology. Sodium 87-93 angiotensin II, type I receptor-associated protein Mus musculus 48-53 26295465-7 2015 The results employing genetic engineered mice with modified ATRAP expression showed that ATRAP plays a key role in the regulation of renal sodium handling and the modulation of blood pressure in response to pathological stimuli such as chronic Ang II infusion, and suggest ATRAP to be a target of interest. Sodium 139-145 angiotensin II, type I receptor-associated protein Mus musculus 60-65 26295465-7 2015 The results employing genetic engineered mice with modified ATRAP expression showed that ATRAP plays a key role in the regulation of renal sodium handling and the modulation of blood pressure in response to pathological stimuli such as chronic Ang II infusion, and suggest ATRAP to be a target of interest. Sodium 139-145 angiotensin II, type I receptor-associated protein Mus musculus 89-94 26295465-7 2015 The results employing genetic engineered mice with modified ATRAP expression showed that ATRAP plays a key role in the regulation of renal sodium handling and the modulation of blood pressure in response to pathological stimuli such as chronic Ang II infusion, and suggest ATRAP to be a target of interest. Sodium 139-145 angiotensin II, type I receptor-associated protein Mus musculus 89-94 26191411-2 2015 Inhibition of SGLT2 activity also reduces sodium reabsorption, which together with glycosuria produces a mild diuretic effect with the potential for dehydration and hyperkalemia. Sodium 42-48 solute carrier family 5 member 2 Homo sapiens 14-19 26552299-0 2015 Thrombin modulates persistent sodium current in CA1 pyramidal neurons of young and adult rat hippocampus. Sodium 30-36 carbonic anhydrase 1 Rattus norvegicus 48-51 25007170-5 2014 In addition, there is some evidence that GLP-1 receptor agonists and DPP-4 inhibitors mediate sodium excretion and diuresis to lower blood pressure. Sodium 94-100 dipeptidyl peptidase 4 Homo sapiens 69-74 25269074-10 2014 Application of PDF inhibited outward potassium or inward sodium currents, sometimes in the same neuron. Sodium 57-63 peptide deformylase, mitochondrial Homo sapiens 15-18 25086309-3 2014 Regarding sodium- and potassium-coupled Cl(-) transport (NKCC1) both up- and downregulations have been proposed. Sodium 10-16 solute carrier family 12 member 2 Homo sapiens 57-62 25141027-8 2014 Our studies in correlation of our data with others suggested that sodium may reduce the binding affinities of endogenous agonists or its analogs to CB2. Sodium 66-72 cannabinoid receptor 2 Homo sapiens 148-151 24868010-0 2014 Feedforward activation of endothelial ENaC by high sodium. Sodium 51-57 sodium channel, nonvoltage-gated 1 alpha Mus musculus 38-42 24868010-8 2014 Interestingly, in the presence of high-sodium concentrations, FAD286 increased the transcription of the MR by 69%. Sodium 39-45 nuclear receptor subfamily 3, group C, member 2 Mus musculus 104-106 24868010-9 2014 Taken together, a novel feedforward activation of EnNaC by sodium is proposed that contrasts ENaC feedback inhibition in kidney. Sodium 59-65 sodium channel, nonvoltage-gated 1 alpha Mus musculus 93-97 25010007-7 2014 This mutation is predicted to generate a truncated SCN5A protein, which could result in the loss of sodium current, a defined mechanism of SCN5A related arrhythmias. Sodium 100-106 sodium voltage-gated channel alpha subunit 5 Homo sapiens 51-56 25010007-7 2014 This mutation is predicted to generate a truncated SCN5A protein, which could result in the loss of sodium current, a defined mechanism of SCN5A related arrhythmias. Sodium 100-106 sodium voltage-gated channel alpha subunit 5 Homo sapiens 139-144 24995870-5 2014 Analysis of rare variants in genes consistent with an autosomal-recessive mode of inheritance led to identification of mutations in SLC13A5, which encodes the cytoplasmic sodium-dependent citrate carrier, notably expressed in neurons. Sodium 171-177 solute carrier family 13 member 5 Homo sapiens 132-139 24677666-10 2014 Localisation of sodium/hydrogen exchanger-3 (NHE3; SLC9A3) and aquaporins 1 and 9 (AQP1, AQP9) along the microvillus border was also consistent with ion transport and fluid reabsorption by this epithelium. Sodium 16-22 sodium/hydrogen exchanger 3 Mesocricetus auratus 51-57 24815519-3 2014 Our objectives were to investigate relationships between ascorbate concentrations in plasma, aqueous humor and lens and whether these relationships are influenced by Single Nucleotide Polymorphisms (SNPs) in sodium-dependent vitamin C transporter genes (SLC23A1 and SLC23A2). Sodium 208-214 solute carrier family 23 member 1 Homo sapiens 254-261 24777977-7 2014 Using an isoform selective inhibitor and an adenovirus expressing dominant negative protein kinase C-alpha revealed that protein kinase C-alpha in the subfornical organ was necessary to mediate elevated fluid and sodium intake in sRA mice. Sodium 213-219 steroid receptor RNA activator 1 Mus musculus 230-233 24480829-1 2014 Aldosterone promotes electrogenic sodium reabsorption through the amiloride-sensitive epithelial sodium channel (ENaC). Sodium 34-40 sodium channel, nonvoltage-gated 1 alpha Mus musculus 113-117 24480829-7 2014 However, Scnn1a(KO) mice fed a low-salt diet lost significant amounts of sodium in their feces and exhibited high plasma aldosterone and increased urinary sodium retention. Sodium 73-79 sodium channel, nonvoltage-gated 1 alpha Mus musculus 9-15 24480829-7 2014 However, Scnn1a(KO) mice fed a low-salt diet lost significant amounts of sodium in their feces and exhibited high plasma aldosterone and increased urinary sodium retention. Sodium 155-161 sodium channel, nonvoltage-gated 1 alpha Mus musculus 9-15 24480829-10 2014 Prss8(KO) mice fed a low-salt diet also exhibited sodium loss through feces and higher plasma aldosterone levels. Sodium 50-56 protease, serine 8 (prostasin) Mus musculus 0-5 24652800-7 2014 Functional analyses showed that Bmal1(lox/lox)/Ren1(d)Cre mice exhibited multiple abnormalities, including increased urine volume, changes in the circadian rhythm of urinary sodium excretion, increased GFR, and significantly reduced plasma aldosterone levels. Sodium 174-180 aryl hydrocarbon receptor nuclear translocator-like Mus musculus 32-37 24573316-0 2014 Relation between BK-alpha/beta4-mediated potassium secretion and ENaC-mediated sodium reabsorption. Sodium 79-85 sodium channel, nonvoltage-gated 1 alpha Mus musculus 65-69 24573316-2 2014 Here we determine whether BK-alpha/beta4-mediated potassium transport is dependent on epithelial sodium channel (ENaC)-mediated sodium reabsorption. Sodium 97-103 sodium channel, nonvoltage-gated 1 alpha Mus musculus 113-117 24573316-11 2014 Thus, the enhanced effect of amiloride on potassium secretion in wild-type compared to knockout mice on the alkaline diet clarify a BK- alpha/beta4-mediated potassium secretory pathway in intercalated cells driven by ENaC-mediated sodium reabsorption linked to bicarbonate secretion. Sodium 231-237 sodium channel, nonvoltage-gated 1 alpha Mus musculus 217-221 25058146-6 2014 There was a significant inverse correlation between the serum renalase level and 24-h urinary sodium excretion. Sodium 94-100 renalase, FAD dependent amine oxidase Homo sapiens 62-70 24939454-1 2014 Mutations of the skeletal muscle voltage-gated sodium channel (NaV1.4) are an established cause of several clinically distinct forms of periodic paralysis and myotonia. Sodium 47-53 sodium voltage-gated channel alpha subunit 4 Homo sapiens 63-69 24939454-7 2014 The known mutation p.Val1293Ile was found in the muscle sodium channel gene (SCN4A). Sodium 56-62 sodium voltage-gated channel alpha subunit 4 Homo sapiens 77-82 24093724-2 2014 Transepithelial sodium transport via alveolar epithelial Na(+) channels (ENaC) and Na(+),K(+)-ATPase constitutes the driving force for removal of alveolar edema fluid. Sodium 16-22 sodium channel, nonvoltage-gated 1 alpha Mus musculus 46-71 24093724-2 2014 Transepithelial sodium transport via alveolar epithelial Na(+) channels (ENaC) and Na(+),K(+)-ATPase constitutes the driving force for removal of alveolar edema fluid. Sodium 16-22 sodium channel, nonvoltage-gated 1 alpha Mus musculus 73-77 24378774-5 2014 In particular, renal ACE and locally generated angiotensin II affect the activity of several key sodium transporters and the induction of sodium and water retention resulting in the elevation of BP. Sodium 97-103 angiotensin I converting enzyme (peptidyl-dipeptidase A) 1 Mus musculus 21-24 24424281-7 2014 We also show that cultured MSC exhibit sodium currents that have characteristics of Nav1.9 channels. Sodium 39-45 neuron navigator 1 Rattus norvegicus 84-88 24142340-2 2014 Here we establish SPINT2, previously ascribed to congenital sodium diarrhea, as a second gene associated with CTE and report molecular and immunohistochemistry data in 57 CTE patients. Sodium 60-66 serine peptidase inhibitor, Kunitz type 2 Homo sapiens 18-24 24324041-6 2014 Chronic renal function curves demonstrate a leftward shift in KO mice, suggesting that the relationship between UMOD and blood pressure is affected by sodium. Sodium 151-157 uromodulin Mus musculus 112-116 24324041-11 2014 Collectively, we demonstrate that UMOD regulates sodium uptake in the thick ascending limb of the loop of Henle by modulating the effect of tumor necrosis factor-alpha on NKCC2A expression, making UMOD an important determinant of blood pressure control. Sodium 49-55 uromodulin Mus musculus 34-38 24324041-11 2014 Collectively, we demonstrate that UMOD regulates sodium uptake in the thick ascending limb of the loop of Henle by modulating the effect of tumor necrosis factor-alpha on NKCC2A expression, making UMOD an important determinant of blood pressure control. Sodium 49-55 uromodulin Mus musculus 197-201 24379189-12 2014 Removal of luminal sodium blocked pHi recovery. Sodium 19-25 glucose-6-phosphate isomerase Rattus norvegicus 34-37 24903467-6 2014 RESULTS: Bardoxolone-methyl-treated patients in the BEACON substudy had a clinically meaningful reduction in urine volume and sodium excretion at week 4 relative to baseline (p < 0.05), and a separate study revealed that decreased sodium excretion and urine output occurred in some patients with stage 4 CKD but not those with stage 3b CKD. Sodium 126-132 ubiquitin like 5 Homo sapiens 52-58 23708151-2 2014 The bioavailability of this vitamin depends upon the nutritional intake and its uptake by cells, mainly through the sodium-dependent transporters SVCT1/Svct1 and SVCT2/Svct2 (human/rat). Sodium 116-122 solute carrier family 23 member 1 Homo sapiens 146-151 23708151-2 2014 The bioavailability of this vitamin depends upon the nutritional intake and its uptake by cells, mainly through the sodium-dependent transporters SVCT1/Svct1 and SVCT2/Svct2 (human/rat). Sodium 116-122 solute carrier family 23 member 1 Homo sapiens 152-157 25097934-0 2014 [The effect of enzymatic treatment using proteases on properties of persistent sodium current in CA1 pyramidal neurons of rat hippocampus]. Sodium 79-85 carbonic anhydrase 1 Rattus norvegicus 97-100 24737232-2 2014 The other family members, beta1B, beta3, and beta4, were identified by homology and shown to modulate sodium current in heterologous systems. Sodium 102-108 eukaryotic translation elongation factor 1 beta 2 pseudogene 2 Homo sapiens 34-50 23690164-11 2013 These novel findings may provide a new unexplored link between sodium regulation and GST homeostasis. Sodium 63-69 glutathione S-transferase kappa 1 Homo sapiens 85-88 23443727-6 2013 When switching from the low- to high-sodium intervention, increases in diastolic BP (DBP) and MAP were attenuated by the COL18A1 rs2838944 minor A allele (P = 1.41x10(-4) and 1.55x10(-4), respectively). Sodium 37-43 collagen type XVIII alpha 1 chain Homo sapiens 121-128 23443727-8 2013 Ten variants from 3 independent SELE loci displayed significant genotype-sex interactions on DBP and MAP responses to low-sodium (P for interaction = 1.56x10(-3) to 1.00x10(-4)). Sodium 122-128 selectin E Homo sapiens 32-36 23499375-3 2013 Herein, SPAK knockout (KO) C57BL/6 mice exhibited significant increases in intestinal transepithelial resistance, a marked decrease in paracellular permeability to fluorescence isothiocyanate-dextran, and altered apical side tight junction sodium ion selectivity, compared with wild-type mice. Sodium 240-246 serine/threonine kinase 39 Mus musculus 8-12 23619363-7 2013 In particular, renal ACE activity is required to increase local Ang II, to stimulate sodium transport in loop of Henle and the distal nephron, and to induce hypertension. Sodium 85-91 angiotensin I converting enzyme (peptidyl-dipeptidase A) 1 Mus musculus 21-24 23327996-8 2013 Exposure to a high-sodium diet (8% NaCl) markedly reduced HR in MSH-OE mice without concomitant changes in blood pressure, suggesting improved reflex regulation of HR. Sodium 19-25 msh homeobox 1 Mus musculus 64-67 23399718-3 2013 All 3 methods consistently show a substantial health benefit for reductions in dietary sodium under each of the 3 scenarios tested. Sodium 87-93 paired box 5 Homo sapiens 0-5 23423722-7 2013 It was concluded that the extract acts by reducing the Na(+)/K(+) ATPase activity of enterocytes and consequently the sodium gradient required for sugar transport by SGLT1, which leads to down-regulation of GLUT2 and contributes to the observed anti-hyperglycemic effect. Sodium 118-124 solute carrier family 5 member 1 Rattus norvegicus 166-171 23375893-5 2013 Yet, upon first reencounter in a novel sodium-depletion state to promote mesocorticolimbic reactivity (reflected by elevated Fos activation in ventral tegmentum, nucleus accumbens, ventral pallidum, and the orbitofrontal prefrontal cortex), the learned cue was instantly transformed into an attractive and powerful motivational magnet. Sodium 39-45 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 125-128 23139220-13 2013 These data suggest that NMD enhances TTX-resistant sodium activity of colon DRG neurons, which is most likely mediated by a leftward shift of activation curve and by enhanced expression of Na(V)1.8 at protein levels, thus identifying a specific molecular mechanism underlying chronic visceral pain and sensitization in patients with IBS. Sodium 51-57 sodium voltage-gated channel alpha subunit 10 Homo sapiens 189-197 23075334-7 2013 In the kidneys, SIRT1 may inhibit renal cell apoptosis, inflammation and fibrosis, and may regulate lipid metabolism, autophagy, blood pressure and sodium balance. Sodium 148-154 sirtuin 1 Homo sapiens 16-21 23956981-0 2013 Concerted action of ANP and dopamine D1-receptor to regulate sodium homeostasis in nephrotic syndrome. Sodium 61-67 natriuretic peptide A Rattus norvegicus 20-23 23343681-8 2013 Accompanied with such increase in PRA, glomerular filtration rate (GFR), renal blood flow (RBF), urine volume (UV) and sodium excretion (UNaV) more significantly decreased in CD38(-/-) than CD38(+/+) mice. Sodium 119-125 CD38 antigen Mus musculus 175-179 22784207-0 2013 Voluntary sodium ingestion in wild-type and oxytocin knockout mice. Sodium 10-16 oxytocin Mus musculus 44-52 22784207-1 2013 Oxytocin knockout (OT KO) mice acutely consume inappropriate amounts of sodium following overnight water deprivation suggesting that oxytocinergic neurons inhibit excessive sodium ingestion (Amico JA, Morris M, Vollmer RR. Sodium 72-78 oxytocin Mus musculus 0-8 22784207-1 2013 Oxytocin knockout (OT KO) mice acutely consume inappropriate amounts of sodium following overnight water deprivation suggesting that oxytocinergic neurons inhibit excessive sodium ingestion (Amico JA, Morris M, Vollmer RR. Sodium 173-179 oxytocin Mus musculus 0-8 22784207-4 2013 This study sought to determine whether oxytocin (OT) provides long-term regulation of voluntary sodium ingestion. Sodium 96-102 oxytocin Mus musculus 39-47 22931370-8 2013 Molecular modelling analysis confirmed that the Asp409del mutant dramatically altered the conformation of the 185-189 loop and impaired binding of the loop to sodium ions (Na(+) ), diminishing the enzymatic activity of FXa. Sodium 159-165 coagulation factor X Homo sapiens 219-222 23090952-5 2013 Celf4 mutant neurons also demonstrate an increase in persistent sodium current (I(NaP)) and a hyperpolarizing shift in the voltage dependence of activation. Sodium 64-70 CUGBP, Elav-like family member 4 Mus musculus 0-5 22995823-0 2012 In silico docking reveals possible Riluzole binding sites on Nav1.6 sodium channel: implications for amyotrophic lateral sclerosis therapy. Sodium 68-74 sodium voltage-gated channel alpha subunit 8 Homo sapiens 61-67 22752520-6 2012 Moreover, we reported that beta2 adrenoceptor alters histone acetylation and further regulates sodium resorption at distal tubules via activating glucocorticoid receptor. Sodium 95-101 adrenoceptor beta 2 Homo sapiens 27-45 22764151-0 2012 Sodium current deficit and arrhythmogenesis in a murine model of plakophilin-2 haploinsufficiency. Sodium 0-6 plakophilin 2 Mus musculus 65-78 22764151-1 2012 AIMS: The shRNA-mediated loss of expression of the desmosomal protein plakophilin-2 leads to sodium current (I(Na)) dysfunction. Sodium 93-99 plakophilin 2 Mus musculus 70-83 22691875-0 2012 SGK regulation of renal sodium transport. Sodium 24-30 serum/glucocorticoid regulated kinase 1 Homo sapiens 0-3 22691875-1 2012 PURPOSE OF REVIEW: The serum and glucocorticoid regulated kinase (SGK) family of protein kinases shares similar biochemical and hormonal signaling properties; however, the SGK kinases also exhibit distinct differences in regulating renal sodium (Na(+)) transport. Sodium 238-244 serum/glucocorticoid regulated kinase 1 Homo sapiens 23-64 22691875-1 2012 PURPOSE OF REVIEW: The serum and glucocorticoid regulated kinase (SGK) family of protein kinases shares similar biochemical and hormonal signaling properties; however, the SGK kinases also exhibit distinct differences in regulating renal sodium (Na(+)) transport. Sodium 238-244 serum/glucocorticoid regulated kinase 1 Homo sapiens 66-69 22691875-1 2012 PURPOSE OF REVIEW: The serum and glucocorticoid regulated kinase (SGK) family of protein kinases shares similar biochemical and hormonal signaling properties; however, the SGK kinases also exhibit distinct differences in regulating renal sodium (Na(+)) transport. Sodium 238-244 serum/glucocorticoid regulated kinase 1 Homo sapiens 172-175 22750882-4 2012 The resulting neurons express canonical markers and functional properties of human nociceptors, including tetrodotoxin (TTX)-resistant, SCN10A-dependent sodium currents and response to nociceptive stimuli such as ATP and capsaicin. Sodium 153-159 sodium voltage-gated channel alpha subunit 10 Homo sapiens 136-142 22402471-13 2012 Flutamide by itself exerts influence over aldosterone in the absence of gonadal steroid replacement suggesting AR involvement in renal sodium handling. Sodium 135-141 androgen receptor Rattus norvegicus 111-113 22460714-1 2012 The Na(+)/H(+) exchanger-3 (NHE3) belongs to the mammalian NHE protein family and catalyzes the electro-neutral exchange of extracellular sodium for intracellular proton across cellular membranes. Sodium 138-144 solute carrier family 9 member A3 Homo sapiens 4-26 22460714-1 2012 The Na(+)/H(+) exchanger-3 (NHE3) belongs to the mammalian NHE protein family and catalyzes the electro-neutral exchange of extracellular sodium for intracellular proton across cellular membranes. Sodium 138-144 solute carrier family 9 member A3 Homo sapiens 28-32 22349312-5 2012 Overexpression of HIF-1alpha transgenes in the renal medulla enhanced the pressure natriuresis, promoted the sodium excretion and reduced sodium retention after salt overload. Sodium 109-115 hypoxia inducible factor 1 subunit alpha Rattus norvegicus 18-28 22349312-5 2012 Overexpression of HIF-1alpha transgenes in the renal medulla enhanced the pressure natriuresis, promoted the sodium excretion and reduced sodium retention after salt overload. Sodium 138-144 hypoxia inducible factor 1 subunit alpha Rattus norvegicus 18-28 22566498-6 2012 Also notable among the 273 polymorphisms was rs11649420 on chromosome 16 in the amiloride-sensitive sodium channel subunit SCNN1G involved in mediating renal sodium reabsorption and maintaining blood pressure when the renin-angiotensin system is inhibited by candesartan. Sodium 100-106 sodium channel epithelial 1 subunit gamma Homo sapiens 123-129 22370956-4 2012 We find that a high-salt diet (4% sodium) significantly reduced endothelial NOS mRNA (2.6-fold) and protein (1.5-fold) but increased nNOS mRNA (2.4-fold) and protein (1.9-fold) in the renal cortex of these animals. Sodium 34-40 nitric oxide synthase 1 Rattus norvegicus 133-137 22504846-1 2012 BACKGROUND: The renin-angiotensin (Ang) system controls blood pressure, in part, by regulating renal tubular sodium transport. Sodium 109-115 angiogenin Rattus norvegicus 16-39 22556341-1 2012 The glucocorticoid-induced leucine zipper (Tsc22d3-2) is a widely expressed dexamethasone-induced transcript that has been proposed to be important in immunity, adipogenesis, and renal sodium handling based on in vitro studies. Sodium 185-191 TSC22 domain family, member 3 Mus musculus 43-50 22556341-4 2012 Tsc22d3-2 knockout mice adapted to a sodium-deprived diet and to water deprivation conditions but developed a subtle deficiency in renal sodium and water handling. Sodium 37-43 TSC22 domain family, member 3 Mus musculus 0-7 22556341-4 2012 Tsc22d3-2 knockout mice adapted to a sodium-deprived diet and to water deprivation conditions but developed a subtle deficiency in renal sodium and water handling. Sodium 137-143 TSC22 domain family, member 3 Mus musculus 0-7 21950687-1 2012 BACKGROUND AND PURPOSE: KB-R7943 is an isothiourea derivative that is used widely as a pharmacological inhibitor of sodium-calcium exchange (NCX) in experiments on cardiac and other tissue types. Sodium 116-122 T cell leukemia homeobox 2 Homo sapiens 141-144 22315453-6 2012 Expression of the mutated KCNJ5 gene decreases plasma membrane polarization, allowing sodium and calcium influx into the cells. Sodium 86-92 potassium inwardly rectifying channel subfamily J member 5 Homo sapiens 26-31 21963429-1 2012 The serum- and glucocorticoid-inducible kinase 1 (SGK1) is known to regulate a wide variety of cellular processes, including renal sodium retention and cell survival. Sodium 131-137 serum/glucocorticoid regulated kinase 1 Homo sapiens 4-48 21963429-1 2012 The serum- and glucocorticoid-inducible kinase 1 (SGK1) is known to regulate a wide variety of cellular processes, including renal sodium retention and cell survival. Sodium 131-137 serum/glucocorticoid regulated kinase 1 Homo sapiens 50-54 22215718-2 2012 The sodium-retaining action of insulin appeared to require hyperglycemia, and it completely reversed the diabetic natriuresis and diuresis. Sodium 4-10 insulin Canis lupus familiaris 31-38 22383044-1 2012 The present work was initiated to investigate regulation of the taurine transporter TauT by reactive oxygen species (ROS) and the tonicity-responsive enhancer binding protein (TonEBP) in NIH3T3 mouse fibroblasts during acute and long-term (4 h) exposure to low-sodium/hypo-osmotic stress. Sodium 261-267 nuclear factor of activated T cells 5 Mus musculus 176-182 21993530-0 2012 Rhcg1 and NHE3b are involved in ammonium-dependent sodium uptake by zebrafish larvae acclimated to low-sodium water. Sodium 51-57 solute carrier family 9 member A3, tandem duplicate 2 Danio rerio 10-15 22150373-4 2012 In patients with PHA1, miliaria rubra-like cutaneous eruptions are suggested to occur due to obstruction of eccrine sweat glands through inflammation caused by excessive sodium excretion in sweat during hyponatremic crises. Sodium 170-176 sodium channel epithelial 1 subunit gamma Homo sapiens 17-21 22150373-6 2012 A hypothesis is proposed suggesting that sympathetic activation which provides vascular tonus during sodium excretion in sweat and salt-depletion crisis may play a role in the development of eruptions and thrombocytosis in patients with PHA1. Sodium 101-107 sodium channel epithelial 1 subunit gamma Homo sapiens 237-241 22536434-6 2012 A significant increase in SepSecS mRNA levels was observed in all of the brain tissues of chickens fed diets containing 1-5 mg/kg sodium selenite. Sodium 130-136 Sep (O-phosphoserine) tRNA:Sec (selenocysteine) tRNA synthase Gallus gallus 26-33 21983428-1 2011 We expressed rat Na(v)1.6 sodium channels in combination with the rat beta1 and beta2 auxiliary subunits in human embryonic kidney (HEK293) cells and evaluated the effects of the pyrethroid insecticides tefluthrin and deltamethrin on expressed sodium currents using the whole-cell patch clamp technique. Sodium 26-32 sodium voltage-gated channel alpha subunit 8 Homo sapiens 17-25 22438854-2 2011 Ang-(1-7) is present in the kidneys at concentrations comparable to those of Ang II and is associated with vasodilation, modulation of sodium and water transport, and stimulation of nitric oxide (NO) synthase. Sodium 135-141 angiogenin Rattus norvegicus 0-8 22087007-5 2011 The Possum mutation enhanced Na(v)1.8 sodium currents and neuronal excitability and heightened sensitivity of mutants to cold stimuli. Sodium 38-44 sodium voltage-gated channel alpha subunit 10 Homo sapiens 29-37 22087007-9 2011 Hyperactive sodium conduction via Na(v)1.8 thus leads to a complex neurobehavioral phenotype, which resembles catatonia in schizophrenic humans and tonic immobility in other mammals upon application of a discrete stimulus; no other form of mechanosensory stimulus could induce the immobility phenotype. Sodium 12-18 sodium voltage-gated channel alpha subunit 10 Homo sapiens 34-42 22105349-4 2011 We provide evidence that cortactin-cofilin binding is regulated by local pH changes at invadopodia that are mediated by the sodium-hydrogen exchanger NHE1. Sodium 124-130 cortactin Homo sapiens 25-34 22109525-4 2011 These metabolites also activate native TRPA1 and, as a consequence, reduce voltage-gated calcium and sodium currents in primary sensory neurons. Sodium 117-123 transient receptor potential cation channel, subfamily A, member 1 Mus musculus 39-44 22071811-7 2011 The effect of sodium reduction in normotensive Blacks was SBP -4.02 mmHg (95% CI:-7.37, -0.68; p=0.002), DBP -2.01 mmHg (95% CI:-4.37, 0.35; p=0.09). Sodium 14-20 DEAH-box helicase 16 Homo sapiens 105-111 22071811-9 2011 The effect of sodium reduction in hypertensive Caucasians was SBP -5.48 mmHg (95% CI: -6.53, -4.43; p<0.00001), DBP -2.75 mmHg (95% CI: -3.34, -2.17; p<0.00001). Sodium 14-20 DEAH-box helicase 16 Homo sapiens 115-121 22071811-10 2011 The effect of sodium reduction in hypertensive Blacks was SBP -6.44 mmHg (95% CI:-8.85, -4.03; p=0.00001), DBP -2.40 mmHg (95% CI:-4.68, -0.12; p=0.04). Sodium 14-20 DEAH-box helicase 16 Homo sapiens 107-113 21838571-7 2011 Nutritionally, the CAI food/beverage promotions were higher in fats, sugar, sodium and energy per 100 grams. Sodium 76-82 carbonic anhydrase 1 Homo sapiens 19-22 21670672-3 2011 RECENT FINDINGS: A variation in sodium and potassium intake or plasma aldosterone changes the number of cleaved alpha and gamma-ENaC subunits and is associated with changes in ENaC currents. Sodium 32-38 sodium channel epithelial 1 subunit gamma Homo sapiens 122-132 21677638-5 2011 Mice treated with DMHCA or TO901317, two LXR agonists that prevent atherosclerosis in ApoE or LDLR knockout mice, significantly decreased the activity of intestinal and kidney proximal tubular brush border membrane sodium gradient-dependent phosphate uptake, decreased serum phosphate, and increased urine phosphate excretion. Sodium 215-221 low density lipoprotein receptor Mus musculus 94-98 21697807-10 2011 Thus, PKCalpha and PKCbetaII, GSK3alpha and GSK3beta, and cAMP-dependent signaling pathways may have important roles in regulating proximal tubular sodium and fluid transport in Ang II-induced hypertensive rats. Sodium 148-154 protein kinase C, alpha Rattus norvegicus 6-14 21554894-5 2011 This estrogen-dependent inhibition on induced sodium appetite (approximately 50% reduction) can be correlated with changes in Fos activation observed in the organum vasculosum of the lamina terminalis (OVLT) and DRN, in response to sodium depletion. Sodium 46-52 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 126-129 21554894-5 2011 This estrogen-dependent inhibition on induced sodium appetite (approximately 50% reduction) can be correlated with changes in Fos activation observed in the organum vasculosum of the lamina terminalis (OVLT) and DRN, in response to sodium depletion. Sodium 232-238 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 126-129 21593184-5 2011 GLP-1-infused rats displayed increased urine flow, fractional excretion of sodium, potassium, and bicarbonate compared with those rats that received vehicle (1% BSA/saline). Sodium 75-81 glucagon Rattus norvegicus 0-5 21593184-11 2011 Moreover, our findings support the view that GLP-1-based agents may have a potential therapeutic use not only as antidiabetic drugs but also in hypertension and other disorders of sodium retention. Sodium 180-186 glucagon Rattus norvegicus 45-50 21746918-3 2011 Genome-wide microarrays in sodium-deficient mice or after ACTH infusion showed up-regulation of hypothalamic genes, including dopamine- and cAMP-regulated neuronal phosphoprotein 32 kDa (DARPP-32), dopamine receptors-1 and -2, alpha-2C- adrenoceptor, and striatally enriched protein tyrosine phosphatase (STEP). Sodium 27-33 adrenergic receptor, alpha 2c Mus musculus 227-249 21989446-0 2011 Expression and correlation of sodium/iodide symporter and thyroid stimulating hormone receptor in human thyroid carcinoma. Sodium 30-36 thyroid stimulating hormone receptor Homo sapiens 58-94 21546577-1 2011 The putative transcription factor AF17 upregulates the transcription of the epithelial sodium channel (ENaC) genes, but whether AF17 modulates sodium homeostasis and BP is unknown. Sodium 87-93 myeloid/lymphoid or mixed-lineage leukemia; translocated to, 6 Mus musculus 34-38 21546577-7 2011 Taken together, these data identify Af17 as a potential locus for the maintenance of sodium and BP homeostasis and suggest that a particular histone modification is directly linked to these processes. Sodium 85-91 myeloid/lymphoid or mixed-lineage leukemia; translocated to, 6 Mus musculus 36-40 21335064-8 2011 The effect of TNFalpha on BDNF expression is dependent on sodium influx through TTX-sensitive channels and on p38-mitogen-activated protein kinase. Sodium 58-64 brain-derived neurotrophic factor Rattus norvegicus 26-30 21364531-7 2011 Choline binding to a location close to the second, low-affinity sodium-binding site (Na2) of LeuT-fold transporters is facilitated by the introduced aspartate. Sodium 64-70 Leucine transport, high Homo sapiens 93-97 21069391-8 2011 We further found that exogenous supplementation of BDNF considerably reduced the aberrant phosphorylation of neurofilaments, complementing our earlier findings of restored expression of voltage gated sodium channel. Sodium 200-206 brain-derived neurotrophic factor Rattus norvegicus 51-55 21145890-9 2011 Furthermore, genetic deletion of TNF receptor 1 (TNFR-1) in mice attenuated the mechanical allodynia and prevented the increase in sodium currents in DRG neurons induced by L5-VRT. Sodium 131-137 tumor necrosis factor receptor superfamily, member 1a Mus musculus 33-47 21145890-9 2011 Furthermore, genetic deletion of TNF receptor 1 (TNFR-1) in mice attenuated the mechanical allodynia and prevented the increase in sodium currents in DRG neurons induced by L5-VRT. Sodium 131-137 tumor necrosis factor receptor superfamily, member 1a Mus musculus 49-55 21084682-1 2011 Sodium (Na(+)) ions are of primary importance for hydromineral and cardiovascular homeostasis, and the level of Na(+) in the body fluid compartments [plasma and cerebrospinal fluid (CSF)] is precisely monitored in the hypothalamus. Sodium 0-6 colony stimulating factor 2 Rattus norvegicus 182-185 21115638-0 2011 Nav1.7 mutations associated with paroxysmal extreme pain disorder, but not erythromelalgia, enhance Navbeta4 peptide-mediated resurgent sodium currents. Sodium 136-142 sodium voltage-gated channel alpha subunit 9 Homo sapiens 0-6 21253390-8 2011 RESULTS: The HO-1 mRNA and protein expression levels in kidney, 24 h total urinary volume, renal artery blood flow, serum and urine sodium concentration and Ccr were lower in cirrhotic group than in sham group (P < 0.05). Sodium 132-138 heme oxygenase 1 Rattus norvegicus 13-17 21143427-4 2011 The absorption of salt (sodium and chloride) in the small intestine is predominantly mediated via the chloride/base exchangers DRA (Down Regulated in Adenoma) (SLC26A3) and PAT1 (Putative Anion Transporter 1) (SLC26A6), and the Na(+) /H(+) exchanger NHE3 (Sodium Hydrogen Exchanger3) (SLC9A3). Sodium 24-30 solute carrier family 26, member 3 Mus musculus 127-130 21143427-4 2011 The absorption of salt (sodium and chloride) in the small intestine is predominantly mediated via the chloride/base exchangers DRA (Down Regulated in Adenoma) (SLC26A3) and PAT1 (Putative Anion Transporter 1) (SLC26A6), and the Na(+) /H(+) exchanger NHE3 (Sodium Hydrogen Exchanger3) (SLC9A3). Sodium 24-30 solute carrier family 26, member 3 Mus musculus 132-157 21143427-4 2011 The absorption of salt (sodium and chloride) in the small intestine is predominantly mediated via the chloride/base exchangers DRA (Down Regulated in Adenoma) (SLC26A3) and PAT1 (Putative Anion Transporter 1) (SLC26A6), and the Na(+) /H(+) exchanger NHE3 (Sodium Hydrogen Exchanger3) (SLC9A3). Sodium 24-30 solute carrier family 26, member 3 Mus musculus 160-167 21887366-3 2011 There are two sodium/myo-inositol transporters (SMIT1, SMIT2) that may be responsible for regulating brain inositol levels. Sodium 14-20 solute carrier family 5 (sodium/glucose cotransporter), member 11 Mus musculus 55-60 21217835-1 2010 BACKGROUND: The SCN5A encoded sodium current (I(Na)) generates the action potential (AP) upstroke and is a major determinant of AP characteristics and AP propagation in cardiac myocytes. Sodium 30-36 sodium channel protein type 5 subunit alpha Oryctolagus cuniculus 16-21 21105923-0 2010 Type-B response regulators ARR1 and ARR12 regulate expression of AtHKT1;1 and accumulation of sodium in Arabidopsis shoots. Sodium 94-100 response regulator 1 Arabidopsis thaliana 27-31 20736165-1 2010 The small intestinal BB Na(+)/H(+) antiporter NHE3 accounts for the majority of intestinal sodium and water absorption. Sodium 91-97 solute carrier family 9 member A3 Homo sapiens 46-50 20685870-0 2010 Sodium depletion increases sympathetic neurite outgrowth and expression of a novel TMEM35 gene-derived protein (TUF1) in the rat adrenal zona glomerulosa. Sodium 0-6 transmembrane protein 35A Rattus norvegicus 83-89 20685870-14 2010 Collectively, these findings suggest that TMEM35/TUF1 is a candidate for modulating neurite outgrowth in the ZG after sodium depletion. Sodium 118-124 transmembrane protein 35A Rattus norvegicus 42-48 20711351-4 2010 Remarkably, the presence of a sodium ion at this allosteric site induces a conformational change of the rotamer toggle switch Trp6.48 which locks in a conformation identical to the one found in the partially inactive state of the crystallized human beta(2) adrenergic receptor. Sodium 30-36 adrenoceptor beta 2 Homo sapiens 249-276 20441802-0 2010 Sodium/hydrogen exchanger NHA2 in osteoclasts: subcellular localization and role in vitro and in vivo. Sodium 0-6 solute carrier family 9, subfamily B (NHA2, cation proton antiporter 2), member 2 Mus musculus 26-30 20441802-9 2010 Taken together, we show that NHA2 is a RANKL-induced plasmalemmal sodium/hydrogen exchanger in osteoclasts. Sodium 66-72 solute carrier family 9, subfamily B (NHA2, cation proton antiporter 2), member 2 Mus musculus 29-33 20501887-1 2010 X-linked creatine transporter defect is caused by mutations in SLC6A8 at Xq28, which encodes the sodium-dependent creatine transporter. Sodium 97-103 solute carrier family 6 member 8 Homo sapiens 63-69 20813664-4 2010 RESULTS: The rats with acute sodium depletion exhibited significantly more numerous c-fos-positive neurons and GABA/Fos double-labeled neurons in the CeA than the control group (P<0.01, P<0.05). Sodium 29-35 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 84-89 20813664-4 2010 RESULTS: The rats with acute sodium depletion exhibited significantly more numerous c-fos-positive neurons and GABA/Fos double-labeled neurons in the CeA than the control group (P<0.01, P<0.05). Sodium 29-35 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 116-119 20376516-8 2010 CONCLUSION: Taken together, increased sodium reabsorption via the upregulation of the expression of NCC might have been responsible, at least in part, for the clinical improvement seen in an AR-PHA1 patient. Sodium 38-44 sodium channel epithelial 1 subunit gamma Homo sapiens 194-198 19962379-4 2010 The effects of reactive oxygen species on Na(V)1.5 function in whole hearts can be modeled in cultured myocytes, where oxidants shift the availability curve of I(Na) to hyperpolarized potentials, decreasing cardiac sodium current at the normal activation threshold. Sodium 215-221 sodium channel, voltage-gated, type V, alpha Mus musculus 42-50 19962379-7 2010 We now confirm that exposure to oxidants induces lipoxidative modification of Na(V)1.5 and that the selective isoketal scavengers block voltage-dependent changes in sodium current by the oxidant tert-butylhydroperoxide, both in cells heterologously expressing Na(V)1.5 and in a mouse cardiac myocyte cell line (HL-1). Sodium 165-171 sodium channel, voltage-gated, type V, alpha Mus musculus 78-86 19962379-7 2010 We now confirm that exposure to oxidants induces lipoxidative modification of Na(V)1.5 and that the selective isoketal scavengers block voltage-dependent changes in sodium current by the oxidant tert-butylhydroperoxide, both in cells heterologously expressing Na(V)1.5 and in a mouse cardiac myocyte cell line (HL-1). Sodium 165-171 sodium channel, voltage-gated, type V, alpha Mus musculus 260-268 19687166-3 2010 Sodium-hydrogen exchanger isoform 1 (NHE-1) also contributes to intracellular sodium regulation. Sodium 78-84 solute carrier family 9 member A1 Rattus norvegicus 37-42 21063096-1 2010 The serum- and glucocorticoid-regulated kinase (Sgk1) is essential for hormonal regulation of ENaC-mediated sodium transport and is involved in the transduction of growth-factor-dependent cell survival and proliferation. Sodium 108-114 serum/glucocorticoid regulated kinase 1 Homo sapiens 48-52 20038812-4 2010 We demonstrated that a paroxysmal extreme pain disorder (PEPD) mutation in the human peripheral neuronal sodium channel Nav1.7, a paramyotonia congenita (PMC) mutation in the human skeletal muscle sodium channel Nav1.4, and a long-QT3/SIDS mutation in the human cardiac sodium channel Nav1.5 all substantially increased the amplitude of resurgent sodium currents in an optimized adult rat-derived dorsal root ganglion neuronal expression system. Sodium 105-111 sodium voltage-gated channel alpha subunit 9 Homo sapiens 120-126 20038812-4 2010 We demonstrated that a paroxysmal extreme pain disorder (PEPD) mutation in the human peripheral neuronal sodium channel Nav1.7, a paramyotonia congenita (PMC) mutation in the human skeletal muscle sodium channel Nav1.4, and a long-QT3/SIDS mutation in the human cardiac sodium channel Nav1.5 all substantially increased the amplitude of resurgent sodium currents in an optimized adult rat-derived dorsal root ganglion neuronal expression system. Sodium 105-111 iduronate 2-sulfatase Homo sapiens 235-239 19770404-5 2009 DOCA/HS COMT(-/-) mice also exhibited more urinary sodium excretion (COMT(-/-) versus wild-type: 3038+/-430 versus 659+/-102 micromol/L per 24 hours; P<0.01). Sodium 51-57 catechol-O-methyltransferase Mus musculus 8-12 19556451-6 2009 Increased Na(+) uptake was paralleled by increased apical surface abundance of the sodium/hydrogen exchangers NHE2 and NHE3. Sodium 83-89 solute carrier family 9 member A2 Homo sapiens 110-114 19556451-6 2009 Increased Na(+) uptake was paralleled by increased apical surface abundance of the sodium/hydrogen exchangers NHE2 and NHE3. Sodium 83-89 solute carrier family 9 member A3 Homo sapiens 119-123 19519766-0 2009 An atypical PMR2 locus is responsible for hypersensitivity to sodium and lithium cations in the laboratory strain Saccharomyces cerevisiae CEN.PK113-7D. Sodium 62-68 Na(+)/Li(+)-exporting P-type ATPase ENA1 Saccharomyces cerevisiae S288C 12-16 19244589-0 2009 Enhanced pressor response to increased CSF sodium concentration and to central ANG I in heterozygous alpha2 Na+ -K+ -ATPase knockout mice. Sodium 43-49 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 39-42 19244589-1 2009 Intracerebroventricular (ICV) infusion of NaCl mimics the effects of a high-salt diet in salt-sensitive hypertension, raising the sodium concentration in the cerebrospinal fluid (CSF [Na]) and subsequently increasing the concentration of an endogenous ouabain-like substance (OLS) in the brain. Sodium 130-136 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 179-182 19304393-3 2009 Different mutations in the SCN9A gene causing loss of function of the voltage-gated sodium channel Nav1.7 have been reported in patients with this rare disease. Sodium 84-90 sodium voltage-gated channel alpha subunit 9 Homo sapiens 27-32 19304393-3 2009 Different mutations in the SCN9A gene causing loss of function of the voltage-gated sodium channel Nav1.7 have been reported in patients with this rare disease. Sodium 84-90 sodium voltage-gated channel alpha subunit 9 Homo sapiens 99-105 18997160-4 2009 We have recently demonstrated that Sgk-1 additionally regulates sodium reabsorption through the proximal tubular sodium hydrogen exchanger-3 (NHE3). Sodium 64-70 serum/glucocorticoid regulated kinase 1 Homo sapiens 35-40 18997160-4 2009 We have recently demonstrated that Sgk-1 additionally regulates sodium reabsorption through the proximal tubular sodium hydrogen exchanger-3 (NHE3). Sodium 64-70 solute carrier family 9 member A3 Homo sapiens 142-146 19171180-5 2009 On the other hand, specific inhibition of TrkA and p75(NTR) receptors in CM-treated cells reduced the neurite length in comparison with cells treated only with CM, although the effect over the induction of sodium currents was continuously observed. Sodium 206-212 neurotrophic receptor tyrosine kinase 1 Rattus norvegicus 42-46 19171180-7 2009 Depletion of pro-NGF isoforms from CM produced a similar effect as the exerted by k252a, TrkA and p75(NTR) receptor inhibitors in CM-treated cells, inducing the elicitation of sodium currents. Sodium 176-182 neurotrophic receptor tyrosine kinase 1 Rattus norvegicus 89-93 19073902-2 2009 Slow sodium loading may decrease plasma renin concentration (PRC) and cause natriuresis at constant mean arterial blood pressure (MAP) and glomerular filtration rate (GFR). Sodium 5-11 renin Canis lupus familiaris 40-45 19073902-3 2009 We hypothesized that in this setting, renin secretion and renin-dependent sodium excretion are controlled by via the renal nerves and therefore are eliminated or reduced by blocking the action of norepinephrine on the juxtaglomerular cells with the beta1-receptor antagonist metoprolol. Sodium 74-80 renin Canis lupus familiaris 58-63 19073902-12 2009 In conclusion, PRC depended on dietary sodium and beta1-adrenergic control as expected; however, the acute sodium-driven decrease in PRC at constant MAP and GFR was unaffected by beta1-receptor blockade demonstrating that renin may be regulated without changes in MAP, GFR, or beta1-mediated effects of norepinephrine. Sodium 107-113 renin Canis lupus familiaris 222-227 19133747-1 2009 BACKGROUND: Several plasma membrane transporters have been shown to mediate the cellular influx and/or efflux of iodothyronines, including the sodium-independent organic anion co-transporting polypeptide 1 (OATP1), the sodium taurocholate co-transporting polypeptide (NTCP), the L-type amino acid transporter 1 (LAT1) and 2 (LAT2), and the monocarboxylate transporter 8 (MCT8). Sodium 143-149 solute carrier family 7 (cationic amino acid transporter, y+ system), member 5 Mus musculus 279-310 19133747-1 2009 BACKGROUND: Several plasma membrane transporters have been shown to mediate the cellular influx and/or efflux of iodothyronines, including the sodium-independent organic anion co-transporting polypeptide 1 (OATP1), the sodium taurocholate co-transporting polypeptide (NTCP), the L-type amino acid transporter 1 (LAT1) and 2 (LAT2), and the monocarboxylate transporter 8 (MCT8). Sodium 143-149 solute carrier family 7 (cationic amino acid transporter, y+ system), member 5 Mus musculus 312-316 18823687-9 2009 KIM-1 level was decreased by using placebo/LS (1,201 +/- 388 ng/d; P = 0.04), losartan/high sodium (1,184 +/- 296 ng/d; P = 0.09), losartan/LS (921 +/- 176 ng/d; P = 0.008), losartan/high sodium plus HCT (862 +/- 151 ng/d; P = 0.008) and losartan/LS plus HCT (743 +/- 170 ng/d; P = 0.001). Sodium 92-98 hepatitis A virus cellular receptor 1 Homo sapiens 0-5 18823687-9 2009 KIM-1 level was decreased by using placebo/LS (1,201 +/- 388 ng/d; P = 0.04), losartan/high sodium (1,184 +/- 296 ng/d; P = 0.09), losartan/LS (921 +/- 176 ng/d; P = 0.008), losartan/high sodium plus HCT (862 +/- 151 ng/d; P = 0.008) and losartan/LS plus HCT (743 +/- 170 ng/d; P = 0.001). Sodium 188-194 hepatitis A virus cellular receptor 1 Homo sapiens 0-5 18823687-15 2009 CONCLUSIONS: Urinary KIM-1 level was increased in patients with nondiabetic CKD with proteinuria and decreased in parallel with proteinuria by using losartan, sodium restriction, their combination, losartan plus HCT, and the latter plus sodium restriction. Sodium 159-165 hepatitis A virus cellular receptor 1 Homo sapiens 21-26 18823687-15 2009 CONCLUSIONS: Urinary KIM-1 level was increased in patients with nondiabetic CKD with proteinuria and decreased in parallel with proteinuria by using losartan, sodium restriction, their combination, losartan plus HCT, and the latter plus sodium restriction. Sodium 237-243 hepatitis A virus cellular receptor 1 Homo sapiens 21-26 19462937-2 2009 Fibroblast Growth Factor 23 (FGF-23) is a phosphaturic peptide, secreted by the osteoblast precursors, that also inhibits renal 1-alpha-hydroxylase activitiy and tubular phosphate reabsorption by the inhibition of sodium-dependant renal phosphate transport (Na-Pi-IIa). Sodium 214-220 fibroblast growth factor 23 Homo sapiens 0-27 19462937-2 2009 Fibroblast Growth Factor 23 (FGF-23) is a phosphaturic peptide, secreted by the osteoblast precursors, that also inhibits renal 1-alpha-hydroxylase activitiy and tubular phosphate reabsorption by the inhibition of sodium-dependant renal phosphate transport (Na-Pi-IIa). Sodium 214-220 fibroblast growth factor 23 Homo sapiens 29-35 19270440-0 2009 Development of skeletal muscle sodium and potassium currents in zebrafish sofa potato mutants. Sodium 31-37 cholinergic receptor, nicotinic, delta (muscle) Danio rerio 74-85 19344080-4 2009 PHA1 is caused by mutations in genes encoding either subunits of the amiloride-sensitive epithelial sodium channel (ENaC) or mineralocorticoid receptor (MR) inherited in an autosomal recessive or dominant form, respectively. Sodium 100-106 sodium channel epithelial 1 subunit gamma Homo sapiens 0-4 18938210-8 2008 The treatment of the animal with HGF suppressed the increases in water and sodium and calcium ion contents, but not the decreases in potassium and magnesium ion contents. Sodium 75-81 hepatocyte growth factor Rattus norvegicus 33-36 19052238-2 2008 In the case of hypokalemic periodic paralysis, mutations of one of the outermost two gating charges in the S4 voltage sensor in domain II of the Na(V)1.4 alpha subunit induce gating pore current, resulting in a leak of sodium or protons through the voltage sensor that causes depolarization, sodium overload, and contractile failure correlated with low serum potassium. Sodium 219-225 sodium voltage-gated channel alpha subunit 4 Rattus norvegicus 145-153 19052238-2 2008 In the case of hypokalemic periodic paralysis, mutations of one of the outermost two gating charges in the S4 voltage sensor in domain II of the Na(V)1.4 alpha subunit induce gating pore current, resulting in a leak of sodium or protons through the voltage sensor that causes depolarization, sodium overload, and contractile failure correlated with low serum potassium. Sodium 292-298 sodium voltage-gated channel alpha subunit 4 Rattus norvegicus 145-153 18753255-1 2008 Fibroblast growth factor 23 (FGF23) is a phosphaturic factor that suppresses both sodium-dependent phosphate transport and production of 1,25-dihydroxyvitamin D [1,25(OH)(2)D] in the proximal tubule. Sodium 82-88 fibroblast growth factor 23 Mus musculus 0-27 18753255-1 2008 Fibroblast growth factor 23 (FGF23) is a phosphaturic factor that suppresses both sodium-dependent phosphate transport and production of 1,25-dihydroxyvitamin D [1,25(OH)(2)D] in the proximal tubule. Sodium 82-88 fibroblast growth factor 23 Mus musculus 29-34 18981302-2 2008 Because collectrin interacts with the soluble N-ethylmaleiamide-sensitive factor attachment protein receptor (SNARE) complexes, we investigated whether collectrin is involved in sodium handling in hypertension by vesicle trafficking of apical membrane proteins. Sodium 178-184 collectrin, amino acid transport regulator Mus musculus 152-162 18981302-10 2008 CONCLUSIONS: Upregulation of collectrin by high NaCl independent of aldosterone functionally links to the trafficking of apical membrane proteins via the SNARE complex, and collectrin may be responsible for the sodium retention in salt-sensitive hypertension. Sodium 211-217 collectrin, amino acid transport regulator Mus musculus 29-39 18981302-10 2008 CONCLUSIONS: Upregulation of collectrin by high NaCl independent of aldosterone functionally links to the trafficking of apical membrane proteins via the SNARE complex, and collectrin may be responsible for the sodium retention in salt-sensitive hypertension. Sodium 211-217 collectrin, amino acid transport regulator Mus musculus 173-183 19080182-1 2008 BACKGROUND: Few studies have explored the inward sodium current (INa) kinetics of transitional cardiomyocytes. Sodium 49-55 LOW QUALITY PROTEIN: alpha-internexin Oryctolagus cuniculus 65-68 19008644-6 2008 Most neuronal cysteine uptake is mediated by sodium-dependent excitatory amino acid transporter (EAAT) systems, known as excitatory amino acid carrier 1 (EAAC1). Sodium 45-51 solute carrier family 1 (neuronal/epithelial high affinity glutamate transporter, system Xag), member 1 Mus musculus 121-152 19008644-6 2008 Most neuronal cysteine uptake is mediated by sodium-dependent excitatory amino acid transporter (EAAT) systems, known as excitatory amino acid carrier 1 (EAAC1). Sodium 45-51 solute carrier family 1 (neuronal/epithelial high affinity glutamate transporter, system Xag), member 1 Mus musculus 154-159 18687683-5 2008 281, 16323-16332) showed that aldosterone selectively increased 14-3-3 protein isoform expression and that the association of 14-3-3beta with phospho-Nedd4-2 was required for sodium transport stimulation. Sodium 175-181 NEDD4 like E3 ubiquitin protein ligase Homo sapiens 150-157 18687683-12 2008 We conclude that the two aldosterone-induced 14-3-3 isoforms, beta and epsilon, interact with phospho-Nedd4-2 as an obligatory heterodimer, blocking its interaction with ENaC and thereby increasing apical ENaC density and sodium transport. Sodium 222-228 NEDD4 like E3 ubiquitin protein ligase Homo sapiens 102-109 18788465-11 2008 In a small-scale study, sodium loading caused more increase in the systolic blood pressure in urinary low-kallikrein group than in urinary high-kallikrein group. Sodium 24-30 kallikrein related peptidase 4 Homo sapiens 106-116 18788465-11 2008 In a small-scale study, sodium loading caused more increase in the systolic blood pressure in urinary low-kallikrein group than in urinary high-kallikrein group. Sodium 24-30 kallikrein related peptidase 4 Homo sapiens 144-154 18662720-1 2008 The "late sodium current" (I(NaL)) is a sustained component of the fast Na+ current of cardiac myocytes and neurons. Sodium 10-16 N-acetylneuraminate pyruvate lyase Homo sapiens 29-32 18598739-6 2008 However, two taste discrimination experiments showed that rats easily discriminated between sucrose and L-AP4 over a wide range of concentrations, even when the cue function of sodium associated with L-AP4 was reduced by amiloride and neutralized by adding equimolar concentrations of NaCl to sucrose. Sodium 177-183 replication initiator 1 Rattus norvegicus 202-205 18599309-3 2008 In contrast, the voltage dependence of slow inactivation was more positive for Na(v)1.6 channels, they conducted substantially larger persistent sodium currents than Na(v)1.2 channels, and they were much less sensitive to inhibition by phosphorylation by cAMP-dependent protein kinase and protein kinase C. Resurgent sodium current, a hallmark of Na(v)1.6 channels in neurons, was not observed for Na(V)1.6 expressed alone or with the auxiliary beta(4) subunit. Sodium 145-151 sodium voltage-gated channel alpha subunit 8 Homo sapiens 79-87 18599309-3 2008 In contrast, the voltage dependence of slow inactivation was more positive for Na(v)1.6 channels, they conducted substantially larger persistent sodium currents than Na(v)1.2 channels, and they were much less sensitive to inhibition by phosphorylation by cAMP-dependent protein kinase and protein kinase C. Resurgent sodium current, a hallmark of Na(v)1.6 channels in neurons, was not observed for Na(V)1.6 expressed alone or with the auxiliary beta(4) subunit. Sodium 317-323 sodium voltage-gated channel alpha subunit 8 Homo sapiens 79-87 18399542-5 2008 Compared with more common VGSCs, Na(v)1.8 and Na(v)1.9 have unusual biophysical and pharmacological properties, including persistent sodium currents and resistance to the canonical sodium channel blocker tetrodotoxin (TTX). Sodium 133-139 sodium channel, voltage-gated, type XI, alpha Mus musculus 46-54 18177483-13 2008 We conclude that noradrenaline-induced increases in the expression of NHE-3, NBC-1, BSC-1 and aquaporin-2 are likely to play an important role in the regulation of salt and water transport by noradrenaline in the kidney and may explain, at least in part, the altered renal sodium and water handling associated with overactivation of the sympathetic system. Sodium 273-279 solute carrier family 12 member 1 Rattus norvegicus 84-89 18234741-0 2008 Renal nerves and nNOS: roles in natriuresis of acute isovolumetric sodium loading in conscious rats. Sodium 67-73 nitric oxide synthase 1 Rattus norvegicus 17-21 18633183-10 2008 Peritubular positive staining for alpha-SMA was present in groups receiving Ang alone or Ang-Na, in a sodium concentration-dependent manner. Sodium 102-108 angiogenin Rattus norvegicus 76-79 18633183-10 2008 Peritubular positive staining for alpha-SMA was present in groups receiving Ang alone or Ang-Na, in a sodium concentration-dependent manner. Sodium 102-108 angiogenin Rattus norvegicus 89-92 18035354-5 2008 The effect of dehydroepiandrosterone sulphate on persistent sodium currents was also canceled by the sigma-1 receptor blockers and the sigma-1 receptor agonist could mimic the effect of dehydroepiandrosterone sulphate. Sodium 60-66 sigma non-opioid intracellular receptor 1 Rattus norvegicus 101-117 18035354-5 2008 The effect of dehydroepiandrosterone sulphate on persistent sodium currents was also canceled by the sigma-1 receptor blockers and the sigma-1 receptor agonist could mimic the effect of dehydroepiandrosterone sulphate. Sodium 60-66 sigma non-opioid intracellular receptor 1 Rattus norvegicus 135-151 18302698-11 2008 Endothelin-1 (10 nM) reduced the L-type calcium currents, transient outward currents, delayed rectifier currents, transient inward currents, and sodium-calcium exchanger currents in the PV cardiomyocytes with and without pacemaker activity. Sodium 145-151 endothelin-1 Oryctolagus cuniculus 0-12 18305244-0 2008 Pumilio binds para mRNA and requires Nanos and Brat to regulate sodium current in Drosophila motoneurons. Sodium 64-70 pumilio Drosophila melanogaster 0-7 18305244-2 2008 Our previous work has identified the translational repressor Pumilio (Pum) as a regulator of sodium current (I(Na)) and excitability in Drosophila motoneurons. Sodium 93-99 pumilio Drosophila melanogaster 61-68 18305244-2 2008 Our previous work has identified the translational repressor Pumilio (Pum) as a regulator of sodium current (I(Na)) and excitability in Drosophila motoneurons. Sodium 93-99 pumilio Drosophila melanogaster 61-64 17963868-1 2008 Atrial natriuretic factor (ANF) and dopamine (DA) are both important regulators of sodium and water transport across renal proximal tubules. Sodium 83-89 natriuretic peptide A Rattus norvegicus 0-25 17963868-1 2008 Atrial natriuretic factor (ANF) and dopamine (DA) are both important regulators of sodium and water transport across renal proximal tubules. Sodium 83-89 natriuretic peptide A Rattus norvegicus 27-30 17963868-2 2008 Many evidences suggest that some of ANF inhibitory effects on sodium and water reabsorption are mediated by dopaminergic mechanisms. Sodium 62-68 natriuretic peptide A Rattus norvegicus 36-39 17634077-1 2007 OBJECTIVE: Liddle syndrome is a rare autosomal-dominant monogenic form of hypertension caused by mutations in the C-termini of the epithelial sodium channel beta- or gamma-subunit encoded by SCNN1B and SCNN1G, respectively, and often presenting with a familial history of hypertension. Sodium 142-148 sodium channel epithelial 1 subunit beta Homo sapiens 191-197 17634077-1 2007 OBJECTIVE: Liddle syndrome is a rare autosomal-dominant monogenic form of hypertension caused by mutations in the C-termini of the epithelial sodium channel beta- or gamma-subunit encoded by SCNN1B and SCNN1G, respectively, and often presenting with a familial history of hypertension. Sodium 142-148 sodium channel epithelial 1 subunit gamma Homo sapiens 202-208 17970538-2 2007 The appropriate intake of fats, fibre, and minerals (sodium, calcium, magnesium, potassium) in their diets; may reduce the risk to develop hypertension and cardiovascular diseases, in the long-term. Sodium 53-59 chromosome 10 open reading frame 90 Homo sapiens 26-30 17491011-7 2007 We established a stable SOAT-HEK293 cell line that showed sodium-dependent transport of dehydroepiandrosterone sulfate, estrone-3-sulfate, and pregnenolone sulfate with apparent K(m) values of 28.7, 12.0, and 11.3 microm, respectively. Sodium 58-64 solute carrier family 10 member 6 Homo sapiens 24-28 17356130-1 2007 Serum and glucocorticoid regulated kinase 1 (SGK1) has been identified as a key regulatory protein that controls a diverse set of cellular processes including sodium (Na(+)) homeostasis, osmoregulation, cell survival, and cell proliferation. Sodium 159-167 serum/glucocorticoid regulated kinase 1 Homo sapiens 0-43 17356130-1 2007 Serum and glucocorticoid regulated kinase 1 (SGK1) has been identified as a key regulatory protein that controls a diverse set of cellular processes including sodium (Na(+)) homeostasis, osmoregulation, cell survival, and cell proliferation. Sodium 159-167 serum/glucocorticoid regulated kinase 1 Homo sapiens 45-49 17244820-10 2007 In high sodium conditions, coexpression with AKAP15m led to an increase of ENaC activity to levels similar to those observed under low Na+. Sodium 8-14 A-kinase anchoring protein 7 L homeolog Xenopus laevis 45-52 17709894-6 2007 The PRL effect on inositol uptake is sodium-dependent, temperature-dependent, and ouabain sensitive. Sodium 37-43 prolactin Mus musculus 4-7 16980339-8 2007 These findings and reverse transcription PCR experiments suggest that an upregulation of the expression of the cardiac sodium channel isoform Na(v)1.5 versus the skeletal muscle isoform Na(v)1.4 is responsible for the observed changes in sodium current function. Sodium 119-125 sodium channel, voltage-gated, type V, alpha Mus musculus 142-150 17317952-3 2007 Serum- and glucocorticoid-induced kinase 1 (Sgk1) is involved in epithelial sodium reabsorption by facilitating the accumulation of the epithelial sodium channel in the plasma membrane. Sodium 76-82 serum/glucocorticoid regulated kinase 1 Homo sapiens 0-42 17317952-3 2007 Serum- and glucocorticoid-induced kinase 1 (Sgk1) is involved in epithelial sodium reabsorption by facilitating the accumulation of the epithelial sodium channel in the plasma membrane. Sodium 76-82 serum/glucocorticoid regulated kinase 1 Homo sapiens 44-48 17317952-9 2007 Therefore, systematic investigation of other factors downstream of the MR involved in epithelial sodium reabsorption is warranted in patients with autosomal-dominant PHA1. Sodium 97-103 sodium channel epithelial 1 subunit gamma Homo sapiens 166-170 17164836-0 2007 IGF-1 vs insulin: respective roles in modulating sodium transport via the PI-3 kinase/Sgk1 pathway in a cortical collecting duct cell line. Sodium 49-55 serum/glucocorticoid regulated kinase 1 Homo sapiens 86-90 17145985-7 2006 Scn5a(1798insD/+) myocytes displayed a slower time course of sodium current decay without significant differences in voltage-dependence of activation and steady-state inactivation, slow inactivation, or recovery from inactivation. Sodium 61-67 sodium channel, voltage-gated, type V, alpha Mus musculus 0-5 16930592-0 2006 Sodium ingestion in oxytocin knockout mice. Sodium 0-6 oxytocin Mus musculus 20-28 16949774-2 2006 Consequently, DRSP, when combined with 17beta-estradiol (E2) as hormone replacement therapy (HRT), offsets E2-related water and sodium retention by blocking the mineralocorticoid receptor. Sodium 128-134 pinin, desmosome associated protein Homo sapiens 14-18 16935272-7 2006 This finding suggests that the HSD2 neurons are inhibited by signals directly related to saline ingestion, and not simply by the alleviation of sodium deficiency, which does not occur during mineralocorticoid administration. Sodium 144-150 hydroxysteroid 11-beta dehydrogenase 2 Rattus norvegicus 31-35 16720863-0 2006 Disinhibitory pathways for control of sodium transport: regulation of ENaC by SGK1 and GILZ. Sodium 38-44 serum/glucocorticoid regulated kinase 1 Homo sapiens 78-82 16712968-3 2006 The present studies examined expression of the immediate early gene Fos in the nucleus accumbens (NAc) as a marker of neuronal activation following the induction and expression of furosemide-induced sodium appetite. Sodium 199-205 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 68-71 16690767-2 2006 The objective of the present study was to analyze the kinetic properties of the sodium-dependent glucose transport in the jejunum and ileum of SHR and its genetic control, Wistar-Kyoto (WKY) rats, as well as the regulation of the transporter, SGLT1. Sodium 80-86 solute carrier family 5 member 1 Rattus norvegicus 243-248 16690767-8 2006 These findings demonstrate that SGLT1 is regulated at a transcriptional level in the intestine of hypertensive rats, and suggest that this transporter might participate in the dysregulation of sodium transport observed in hypertension. Sodium 193-199 solute carrier family 5 member 1 Rattus norvegicus 32-37 16934605-8 2006 To confirm the presence of ileal bile acid transporter (IBAT) gene message and function, we measured sodium-dependent bile acid uptake and IBAT-messenger RNA. Sodium 101-107 solute carrier family 10 member 2 Homo sapiens 56-60 16870316-3 2006 Since it has been demonstrated that doxorubicin binds to the reductase domain of endothelial NO synthase (eNOS) and generates superoxide in vitro, we tested our hypothesis that a high-sodium diet would upregulate the expression of eNOS and enhance oxidative stress in the kidney of doxorubicin-treated rats, resulting in a facilitation of hypertension. Sodium 184-190 nitric oxide synthase 3 Rattus norvegicus 81-104 16870316-3 2006 Since it has been demonstrated that doxorubicin binds to the reductase domain of endothelial NO synthase (eNOS) and generates superoxide in vitro, we tested our hypothesis that a high-sodium diet would upregulate the expression of eNOS and enhance oxidative stress in the kidney of doxorubicin-treated rats, resulting in a facilitation of hypertension. Sodium 184-190 nitric oxide synthase 3 Rattus norvegicus 106-110 16870316-3 2006 Since it has been demonstrated that doxorubicin binds to the reductase domain of endothelial NO synthase (eNOS) and generates superoxide in vitro, we tested our hypothesis that a high-sodium diet would upregulate the expression of eNOS and enhance oxidative stress in the kidney of doxorubicin-treated rats, resulting in a facilitation of hypertension. Sodium 184-190 nitric oxide synthase 3 Rattus norvegicus 231-235 16870316-5 2006 The expressions of eNOS protein in the renal cortex and medulla were significantly higher in high-sodium groups than in normal-sodium groups, regardless of doxorubicin treatment. Sodium 98-104 nitric oxide synthase 3 Rattus norvegicus 19-23 16870316-5 2006 The expressions of eNOS protein in the renal cortex and medulla were significantly higher in high-sodium groups than in normal-sodium groups, regardless of doxorubicin treatment. Sodium 127-133 nitric oxide synthase 3 Rattus norvegicus 19-23 16870316-9 2006 As such, doxorubicin treatment appears to contribute to the development of salt-sensitive hypertension through reductive activation of upregulated eNOS by a high-sodium diet instead of NO production. Sodium 162-168 nitric oxide synthase 3 Rattus norvegicus 147-151 16757479-3 2006 To identify putative lithium selectivity determinants, we have mutated the five GAT-1 residues corresponding to those whose side chains participate in the sodium binding sites Na1 and Na2 of the bacterial leucine-transporting homologue LeuT(Aa). Sodium 155-161 Leucine transport, high Homo sapiens 236-240 16879429-1 2006 There are three different sodium transport systems (Ena1-4p, Nha1p, Nhx1p) in Saccharomyces cerevisiae. Sodium 26-32 bifunctional K:H/Na:H antiporter NHX1 Saccharomyces cerevisiae S288C 68-73 16772565-10 2006 Concentrations of sodium and chloride, and electrical conductivity increased with increasing SCC but were higher in C than in A1 and A2. Sodium 18-24 SCC Bos taurus 93-96 16819406-2 2006 To explore the in vivo role of guanylin and uroguanylin in the regulation of sodium excretion, we used gene-targeted mice in which the uroguanylin, guanylin or the peptide receptor guanylate cyclase C gene expression had been ablated. Sodium 77-83 guanylate cyclase activator 2a (guanylin) Mus musculus 47-55 16819406-3 2006 RESULTS: Metabolic balance studies demonstrated that there was impaired excretion of a sodium load in uroguanylin (but not in guanylin or guanylate cyclase C) knockout mice. Sodium 87-93 guanylate cyclase activator 2a (guanylin) Mus musculus 105-113 16630545-1 2006 Liddle"s syndrome (excessive absorption of sodium ions) and PHA-1 (pseudohypoaldosteronism type 1) with decreased sodium absorption are caused by the mutations in the amiloride-sensitive epithelial sodium channel ENaC. Sodium 114-120 sodium channel epithelial 1 subunit gamma Homo sapiens 60-97 16641240-6 2006 Numerical simulations indicated that Kv3.3 increases the spontaneous firing rate via cooperation with resurgent sodium currents. Sodium 112-118 potassium voltage gated channel, Shaw-related subfamily, member 3 Mus musculus 37-42 16283296-7 2006 Overexpression of the GPD1 gene encoding glycerol-3-phosphate dehydrogenase, ENA1 encoding sodium ion efflux protein, and CUP1 encoding copper metallothionein conferred high salt stress tolerance to yeast cells, and our selection of candidate genes for the creation of stress-tolerant yeast strains based on the transcriptome data was validated. Sodium 91-97 glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1 Saccharomyces cerevisiae S288C 22-26 16352596-3 2006 However, pAp accumulates and 5"-3" degradation decreases in the presence of ions known to inhibit Hal2p activity, such as sodium or lithium. Sodium 122-128 3'(2'),5'-bisphosphate nucleotidase Saccharomyces cerevisiae S288C 98-103 16352596-4 2006 We have shown that yeast cells can better adapt to the presence of sodium than lithium because of their ability to reduce pAp accumulation by activating HAL2 expression in a Gcn4p-dependent response, a regulatory loop that is likely to be conserved in different yeast species. Sodium 67-73 3'(2'),5'-bisphosphate nucleotidase Saccharomyces cerevisiae S288C 153-157 16407562-8 2006 Reduced GLT-1 expression was associated with a progressive decrease in sodium-dependent glutamate transport capacity. Sodium 71-77 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 8-13 16325806-4 2005 Voltage-clamp analysis showed that human Nav1.8 generated an inward tetrodotoxin-resistant sodium current with an activating threshold around -50 mV, half maximal activation at -11+/-3 mV and a reversal potential of 67+/-4 mV. Sodium 91-97 sodium voltage-gated channel alpha subunit 10 Homo sapiens 41-47 16410671-9 2005 These data indicate that adrenomedullin stimulates prolactin release by modulating calcium influx through voltage-gated calcium channels dependently on extracellular sodium. Sodium 166-172 adrenomedullin Homo sapiens 25-39 16006562-4 2005 When expressed in Xenopus laevis oocytes, hOSCP1 mediated the high affinity transport of p-aminohippurate (PAH) (K(m) = 35.0 +/- 7.5 microm) and tetraethylammonium (K(m) = 62.3 +/- 12.2 microm) in a sodium-independent manner. Sodium 199-205 organic solute carrier partner 1 Homo sapiens 42-48 15946676-3 2005 Two of the mechanisms involved in returning the Ca(2+) concentration back to resting levels are located at the sarcolemma; the sodium/calcium exchanger (NCX) and the sarcolemmal calcium pump. Sodium 127-133 T cell leukemia homeobox 2 Homo sapiens 153-156 15716323-0 2005 Expression of the unconventional myosin Myo1c alters sodium transport in M1 collecting duct cells. Sodium 53-59 myosin IC Mus musculus 40-45 15916676-2 2005 In nephrotic syndrome, a decreased activity of 11betaHSD2 has been suggested to allow glucocorticoids to stimulate MR, thereby contributing to sodium retention. Sodium 143-149 hydroxysteroid 11-beta dehydrogenase 2 Rattus norvegicus 47-57 15893443-3 2005 Are also reported and analyzed molecular mechanisms of sodium retention in proximal tubule cells regarding intrinsic albumin toxicity upon type 3 sodium-hydrogen exchanger ionic pump and the activity of sodium-hydrogen exchanger regulatory factor protein (overfill theory): a better knowledge about the link between albumin, sodium-hydrogen exchanger type 3 (NHE3) ionic pump, sodium-hydrogen exchanger regulatory factor protein is necessary. Sodium 55-61 solute carrier family 9 member A3 Homo sapiens 359-363 15692145-1 2005 The human organic anion transporter 2 (hOAT2, SLC22A7) mediates the sodium-independent uptake of numerous drugs, including cephalosporins, salicylates, dicarboxylates, and prostaglandins, and is mainly expressed in hepatocytes. Sodium 68-74 solute carrier family 22 member 7 Homo sapiens 10-37 15692145-1 2005 The human organic anion transporter 2 (hOAT2, SLC22A7) mediates the sodium-independent uptake of numerous drugs, including cephalosporins, salicylates, dicarboxylates, and prostaglandins, and is mainly expressed in hepatocytes. Sodium 68-74 solute carrier family 22 member 7 Homo sapiens 39-44 15692145-1 2005 The human organic anion transporter 2 (hOAT2, SLC22A7) mediates the sodium-independent uptake of numerous drugs, including cephalosporins, salicylates, dicarboxylates, and prostaglandins, and is mainly expressed in hepatocytes. Sodium 68-74 solute carrier family 22 member 7 Homo sapiens 46-53 15680492-2 2005 Adrenomedullin (AM) participates in the regulation of sodium homeostasis and has renoprotective effects. Sodium 54-60 adrenomedullin Rattus norvegicus 0-14 15856982-5 2005 The logarithms of K2 and K3 for DNA-ActII mixtures, calculated for models I and II at different sodium ion concentrations, were in good agreement with predictions of the counterion condensation theory. Sodium 96-102 RBPJ pseudogene 3 Homo sapiens 18-27 15703401-7 2005 Despite the presence of Nav1.8, a tetrodotoxin-resistant sodium channel, sciatic nerve conduction was at least as sensitive to tetrodotoxin in Trembler-J nerves as in wild-type nerves. Sodium 57-63 sodium voltage-gated channel alpha subunit 10 Homo sapiens 24-30 15641067-12 2005 CONCLUSION: Our results link low-grade IL-8-mediated cartilaginous inflammation in OA to altered chondrocyte differentiation and disease progression through PiT-1 expression and sodium-dependent Pi uptake mediated by CXCR1 signaling. Sodium 178-184 C-X-C motif chemokine receptor 1 Homo sapiens 217-222 15614030-8 2004 The AT2 receptor antagonist PD 123319 and the Ang-(1-7) receptor antagonist A779 attenuated the effect of Ang-(1-7) found in rats fed with a normal or high sodium diet. Sodium 156-162 angiogenin Rattus norvegicus 106-109 15614030-11 2004 This non-competitive antagonism of Ang-(1-7) is abolished by a low sodium intake in normotensive rats, suggesting that it serves as a negative feedback towards Ang II in response to an altered sodium intake. Sodium 67-73 angiogenin Rattus norvegicus 35-38 15614030-11 2004 This non-competitive antagonism of Ang-(1-7) is abolished by a low sodium intake in normotensive rats, suggesting that it serves as a negative feedback towards Ang II in response to an altered sodium intake. Sodium 193-199 angiogenin Rattus norvegicus 35-38 15374752-0 2004 PGE2 increases the tetrodotoxin-resistant Nav1.9 sodium current in mouse DRG neurons via G-proteins. Sodium 49-55 sodium channel, voltage-gated, type XI, alpha Mus musculus 42-48 15109840-3 2004 P1 and P2, observed at lower than the glass transition temperature, were attributed to the sodium ionic migration from the interstitial positions after polarization procedure coordinated among neighboring silicate and phosphate to stabler positions. Sodium 91-97 crystallin gamma F, pseudogene Homo sapiens 0-9 15201541-1 2004 OBJECTIVES: The objectives of this study were to identify polymorphic variants within the gene coding for the sodium/hydrogen exchanger type 3 (NHE3) and to examine their relationship with hypertension and biochemical indices of sodium balance. Sodium 110-116 solute carrier family 9 member A3 Homo sapiens 144-148 15201541-9 2004 CONCLUSIONS: These results suggest a high degree of structural conservation of the NHE3 gene; however, the lack of association between these polymorphisms and blood pressure status does not necessarily eliminate the participation of this important sodium/hydrogen exchanger in the pathophysiology of essential hypertension, as we cannot exclude the existence of functionally important genetic variants in other sequences within the NEH3 gene. Sodium 248-254 solute carrier family 9 member A3 Homo sapiens 83-87 15180798-7 2004 During low-salt conditions, oxytocin reduced sodium and potassium excretion (11 +/- 2--4 +/- 2 and 93 +/- 19--42 +/- 3 micromol min(-1), respectively). Sodium 45-51 oxytocin/neurophysin I prepropeptide Homo sapiens 28-36 15075188-13 2004 The decreased abundance of NHE3, BSC-1, TSC, and Na-K-ATPase may play a compensatory role to promote sodium excretion. Sodium 101-107 solute carrier family 12 member 1 Rattus norvegicus 33-38 15134818-0 2004 Regulation of sodium transport in mammalian collecting duct cells by aldosterone-induced kinase, SGK1: structure/function studies. Sodium 14-20 serum/glucocorticoid regulated kinase 1 Homo sapiens 97-101 14742879-1 2004 In Arabidopsis thaliana, the calcium binding protein Salt Overly Sensitive3 (SOS3) interacts with and activates the protein kinase SOS2, which in turn activates the plasma membrane Na(+)/H(+) antiporter SOS1 to bring about sodium ion homeostasis and salt tolerance. Sodium 223-229 Protein kinase superfamily protein Arabidopsis thaliana 131-135 14600156-7 2004 Receptor-independent activation of NHE-1 by acute acid loading of RASM cells resulted in the rapid phosphorylation of ERK, which could be blocked by pharmacological inhibitors of NHE-1 or by isotonic replacement of sodium, closely linking the proton transport function of NHE-1 to ERK activation. Sodium 215-221 solute carrier family 9 member A1 Rattus norvegicus 35-40 14646339-1 2004 Compared to healthy adults, elevated levels of endogenous ouabain-like factor (OLF) have already been shown in the cord blood, and a role of OLF in the maintenance of high Na(+) excretion by reducing tubular sodium reabsorption during intrauterine life was suggested. Sodium 208-214 transmembrane O-mannosyltransferase targeting cadherins 1 Homo sapiens 141-144 14568996-1 2003 Gamma-melanocyte-stimulating hormone (gamma-MSH) is a natriuretic peptide derived from proopiomelanocortin (POMC) in the pituitary neurointermediate lobe (NIL); its plasma concentration in rats doubles after ingestion of a high (HSD; 8% NaCl) compared with a low sodium diet (LSD; 0.07%). Sodium 263-269 proopiomelanocortin Rattus norvegicus 108-112 12950984-7 2003 Non-hDAF kidneys also lost more sodium through urine than hDAF kidneys (173.67 +/- 14.05 mmol/l vs. 109 +/- 31 mmol/l, P < 0.05). Sodium 32-38 CD55 molecule (Cromer blood group) Homo sapiens 4-8 12773538-0 2003 Evidence for distinct sodium-, dopamine-, and cocaine-dependent conformational changes in transmembrane segments 7 and 8 of the dopamine transporter. Sodium 22-28 solute carrier family 6 member 3 Homo sapiens 128-148 12875997-3 2003 We examined the temporal expression of the sodium-dependent neuronal glutamate transporter, excitatory amino acid carrier 1 (EAAC1), in KA-induced rat epilepsy. Sodium 43-49 solute carrier family 1 member 1 Rattus norvegicus 92-123 12875997-3 2003 We examined the temporal expression of the sodium-dependent neuronal glutamate transporter, excitatory amino acid carrier 1 (EAAC1), in KA-induced rat epilepsy. Sodium 43-49 solute carrier family 1 member 1 Rattus norvegicus 125-130 12893280-1 2003 We have cloned and functionally expressed a sodium-dependent human nucleoside transporter, hCNT2, from a CNS cancer cell line U251. Sodium 44-50 solute carrier family 28 member 2 Homo sapiens 91-96 12657604-2 2003 Sodium transport across the human ocular nonpigmented and pigmented ciliary epithelial bilayer (NPE-PE) is essential for aqueous humor production, but the expression of SGK1 and ENaC subunits remain to be defined. Sodium 0-6 serum/glucocorticoid regulated kinase 1 Homo sapiens 169-173 12657604-10 2003 CONCLUSIONS: The expression of ENaCs within the NPE-PE and corticosteroid regulation of SGK1 through the GR and MR, indicate that this mechanism may be a feature of sodium transport in the human ocular ciliary epithelium. Sodium 165-171 serum/glucocorticoid regulated kinase 1 Homo sapiens 88-92 12679457-11 2003 It remains to be elucidated whether other defects or polymorphisms in genes coding for regulatory proteins participating in sodium homeostasis are a cause of the heterogeneity of the clinical manifestations in autosomal dominant PHA1. Sodium 124-130 sodium channel epithelial 1 subunit gamma Homo sapiens 229-233 12529272-6 2003 PAF at 1 nM maximally inhibited Qo(2) in both untreated and nystatin-stimulated (sodium entry into renal cell is not rate limiting) proximal tubules by approximately 20%. Sodium 81-87 PCNA clamp associated factor Rattus norvegicus 0-3 12529272-9 2003 These findings suggest that stimulation of PAF receptors on the proximal tubule decreases transcellular sodium transport by activating phospholipase A(2) and the cytochrome-P-450 monooxygenase pathways that lead to the inhibition of an ouabain-sensitive component of the basolateral Na(+)-K(+)-ATPase pump. Sodium 104-110 PCNA clamp associated factor Rattus norvegicus 43-46 12529272-10 2003 Thus PAF can activate both an arachidonate pathway-mediated suppression of proximal tubule sodium transport and a nitric oxide pathway-mediated dilatory action on renal hemodynamics that likely contributes to the natriuresis and diuresis observed in vivo. Sodium 91-97 PCNA clamp associated factor Rattus norvegicus 5-8 14580937-6 2003 Our data also indicate that OT mRNA levels evaluated by in situ hybridization significantly increased within the hypothalamic paraventricular nucleus of WT animals after induced sodium ingestion, giving support to former evidence indicating an inhibitory role for central OT in the control of sodium appetite. Sodium 178-184 oxytocin Mus musculus 28-30 14580937-6 2003 Our data also indicate that OT mRNA levels evaluated by in situ hybridization significantly increased within the hypothalamic paraventricular nucleus of WT animals after induced sodium ingestion, giving support to former evidence indicating an inhibitory role for central OT in the control of sodium appetite. Sodium 293-299 oxytocin Mus musculus 28-30 14580937-9 2003 Taken together, our data suggest that the reduced sodium ingestion observed in beta-endorphin deficient mice could be due to a higher expression of the OT gene. Sodium 50-56 oxytocin Mus musculus 152-154 12486163-6 2002 We also show, using a Drosophila S2 cell adhesion assay, that the C121W mutation disrupts beta1-beta1 homophilic cell adhesion, suggesting that the mutation may alter the ability of beta1 to mediate protein-protein interactions critical for sodium channel localization. Sodium 241-247 anon-A1 Drosophila melanogaster 90-95 12393164-3 2002 Using the endogenous connexin (Cx38) of Xenopus oocytes as a model system, we have shown that substituting choline for sodium in the bath solution eliminates the sodium current, thereby unmasking large hemichannel currents, and enabling pharmacological studies of agents that are known to modulate gap-junctional conductances. Sodium 119-125 connexin 38 S homeolog Xenopus laevis 31-35 12393164-3 2002 Using the endogenous connexin (Cx38) of Xenopus oocytes as a model system, we have shown that substituting choline for sodium in the bath solution eliminates the sodium current, thereby unmasking large hemichannel currents, and enabling pharmacological studies of agents that are known to modulate gap-junctional conductances. Sodium 162-168 connexin 38 S homeolog Xenopus laevis 31-35 12372775-2 2002 RA, ANG I, and ANG II levels increased in a manner inversely related to sodium content of the diet in both plasma and renal tissues. Sodium 72-78 angiogenin Rattus norvegicus 4-7 12149252-0 2002 Prothrombinase assembly and S1 site occupation restore the catalytic activity of FXa impaired by mutation at the sodium-binding site. Sodium 113-119 coagulation factor X Homo sapiens 0-14 12149252-0 2002 Prothrombinase assembly and S1 site occupation restore the catalytic activity of FXa impaired by mutation at the sodium-binding site. Sodium 113-119 coagulation factor X Homo sapiens 81-84 12218032-9 2002 In contrast, glutamate uptake in R. leguminosarum by the Escherichia coli GltS system did require sodium, which suggests that MctP may be proton coupled. Sodium 98-104 glutamate permease Escherichia coli 74-78 12161163-1 2002 The biliary excretion of the sodium salts of 8-(2-ethanesulfonic acid)-3-ethyl-2,7,9-trimethyl-1,10-dihydro-11H-dipyrrin-1-one (xanthosulfonic acid) and a fluorescent analogue (8-desethyl-N,N"-carbonyl-kryptopyrromethenone-8-sulfonic acid) was compared in Mrp2-deficient (TR(-)) and normal rats. Sodium 29-35 ATP binding cassette subfamily C member 2 Rattus norvegicus 256-260 12215465-6 2002 The FOS/HCTZ markedly increased urinary sodium excretion (P<0.001). Sodium 40-46 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 4-7 12169661-1 2002 Na+/H+ exchanger regulatory factor (NHERF)-1 and NHERF-2, two structurally related protein adapters containing tandem PSD-95/Discs large/ZO-1 (PDZ) domains, were identified as essential factors for protein kinase A-mediated inhibition of the sodium-hydrogen exchanger, NHE3. Sodium 242-248 discs large MAGUK scaffold protein 4 Mus musculus 118-124 12102631-13 2002 Sodium ions reverse the Ca(2+)-induced red shift of heme a and dramatically decrease the rate of Ca(2+) binding to the D485A mutant COX. Sodium 0-6 cytochrome c oxidase subunit 7A1 Bos taurus 132-135 19750747-2 2002 Angiotensin-converting enzyme (ACE) inhibitors are commonly administered when hypertension is present to decrease plasma concentrations of angiotensin II and aldosterone, which cause vasoconstriction and sodium and water retention, respectively. Sodium 204-210 angiotensin I converting enzyme Felis catus 0-29 19750747-2 2002 Angiotensin-converting enzyme (ACE) inhibitors are commonly administered when hypertension is present to decrease plasma concentrations of angiotensin II and aldosterone, which cause vasoconstriction and sodium and water retention, respectively. Sodium 204-210 angiotensin I converting enzyme Felis catus 31-34 12106694-10 2002 Like hNa(V)1.3 channels, hNa(V)1.6 produced sodium currents with a prominent persistent component when expressed in HEK293 cells. Sodium 44-50 sodium voltage-gated channel alpha subunit 8 Homo sapiens 25-34 12068067-0 2002 Potentiation of a sodium-calcium exchanger in the nuclear envelope by nuclear GM1 ganglioside. Sodium 18-24 coenzyme Q10A Mus musculus 78-81 12068067-3 2002 The present study provides evidence for a sodium-calcium exchanger in the nuclear envelope of NG108-15 neuroblastoma cells that is potently and specifically activated by GM1. Sodium 42-48 coenzyme Q10A Mus musculus 170-173 12042343-1 2002 The effects of sodium and chloride on the properties of the sodium-dependent component of the "pre-steady-state" currents of rGAT1, a GABA cotransporter of the Na(+)-Cl(-)-dependent family, were studied using heterologous oocyte expression and voltage clamp. Sodium 15-21 solute carrier family 6 member 12 Rattus norvegicus 125-130 12042343-1 2002 The effects of sodium and chloride on the properties of the sodium-dependent component of the "pre-steady-state" currents of rGAT1, a GABA cotransporter of the Na(+)-Cl(-)-dependent family, were studied using heterologous oocyte expression and voltage clamp. Sodium 60-66 solute carrier family 6 member 12 Rattus norvegicus 125-130 12115974-0 2002 Effects of age and gene dose on skeletal muscle sodium channel gating in mice deficient in myotonic dystrophy protein kinase. Sodium 48-54 dystrophia myotonica-protein kinase Mus musculus 91-124 11910309-8 2002 CONCLUSIONS: We conclude that DS rats have increased renal NKCC2 activity, thus explaining, at least in part, their genetic renal inability to excrete sodium. Sodium 151-157 solute carrier family 12 member 1 Rattus norvegicus 59-64 11906212-3 2002 Here we report that the majority of neurons in both wild-type and tipE mutant (tipE-) embryo cultures fire sodium-dependent action potentials in response to depolarizing current injection. Sodium 107-113 temperature-induced paralytic E Drosophila melanogaster 66-70 11895377-4 2002 Voltage-gated fast sodium currents (I(Na(+))) were studied in acutely isolated striatal neurons from healthy and dt(sz) hamsters in whole-cell voltage clamp recordings. Sodium 19-25 internexin neuronal intermediate filament protein alpha Homo sapiens 36-44 11792666-8 2002 The changes in Fos expression and PRA are consistent with a proposed role for ANG II in the control of the sodium appetite produced by water deprivation followed by rehydration with only water. Sodium 107-113 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 15-18 11972292-1 2002 In human heart failure (CHF), adrenomedullin (AM) counteracts vasoconstriction and sodium retention. Sodium 83-89 adrenomedullin Homo sapiens 30-44 11746424-1 2001 A previous study has shown that glutamine (Gln) uptake in C6 cells grown in a standard medium containing 2 mM Gln, is predominantly mediated by a sodium-dependent system that is inhibited by ASC system substrates alanine (Ala), serine (Ser), cysteine (Cys) and threonine (Thr), shows pH sensitivity and partial tolerance to substitution of Na+ by Li+, features compatible with system ASCT2 that is strongly expressed in cultured astrocytes. Sodium 146-152 solute carrier family 1 member 5 Homo sapiens 384-389 11641104-8 2001 The observations support an inhibitory role for OT in the control of sodium appetite in mice. Sodium 69-75 oxytocin Mus musculus 48-50 11547116-7 2001 The most interesting finding was significantly elevated sodium and chloride in 1 case 6 weeks after surgery that was associated with tap water treated with a home softening system. Sodium 56-62 nuclear RNA export factor 1 Homo sapiens 133-136 11547116-10 2001 Due to the elevated sodium content in softened tap water families should be alerted to use untreated tap water for preparing enemas. Sodium 20-26 nuclear RNA export factor 1 Homo sapiens 47-50 11547116-10 2001 Due to the elevated sodium content in softened tap water families should be alerted to use untreated tap water for preparing enemas. Sodium 20-26 nuclear RNA export factor 1 Homo sapiens 101-104 11514289-9 2001 We conclude that in the MnPO, ANG II via AT(1) receptors mediates cardiovascular responses to an acute increase in CSF sodium as well as the chronic pressor responses to high sodium intake in SHR. Sodium 119-125 angiogenin Rattus norvegicus 30-33 11514289-9 2001 We conclude that in the MnPO, ANG II via AT(1) receptors mediates cardiovascular responses to an acute increase in CSF sodium as well as the chronic pressor responses to high sodium intake in SHR. Sodium 175-181 angiogenin Rattus norvegicus 30-33 11408481-0 2001 The protein kinase Gcn2p mediates sodium toxicity in yeast. Sodium 34-40 serine/threonine-protein kinase GCN2 Saccharomyces cerevisiae S288C 19-24 11408481-7 2001 It can be postulated that sodium activation of the Gcn2p pathway has toxic effects on growth under NaCl stress and that this novel mechanism of sodium toxicity may be of general significance in eukaryotes. Sodium 26-32 serine/threonine-protein kinase GCN2 Saccharomyces cerevisiae S288C 51-56 11408481-7 2001 It can be postulated that sodium activation of the Gcn2p pathway has toxic effects on growth under NaCl stress and that this novel mechanism of sodium toxicity may be of general significance in eukaryotes. Sodium 144-150 serine/threonine-protein kinase GCN2 Saccharomyces cerevisiae S288C 51-56 11433187-1 2001 BACKGROUND: Atrial natriuretic factor (ANF)-induced increase in glomerular filtration rate (GFR) is inhibited on low sodium intake. Sodium 117-123 natriuretic peptide A Rattus norvegicus 12-37 11433187-1 2001 BACKGROUND: Atrial natriuretic factor (ANF)-induced increase in glomerular filtration rate (GFR) is inhibited on low sodium intake. Sodium 117-123 natriuretic peptide A Rattus norvegicus 39-42 11433187-2 2001 It has been shown that activation of renin-angiotensin system on low sodium intake antagonizes the biological effect of ANF by interfering in the intracellular metabolism of cGMP. Sodium 69-75 natriuretic peptide A Rattus norvegicus 120-123 11433187-3 2001 We have previously indicated that the renin-angiotensin system increases activity of Ca2+/calmodulin dependent-cyclic GMP phosphodiesterase (cGMP-PDE) in glomeruli and thereby inhibits the ANF-induced increase in GFR in low sodium-treated rats. Sodium 224-230 natriuretic peptide A Rattus norvegicus 189-192 11433187-7 2001 RESULTS: Low sodium intake inhibited ANF-dependent increase in GFR and nephrogenous cGMP excretion, whereas urinary sodium excretion did not differ appreciably in rats on either diet. Sodium 13-19 natriuretic peptide A Rattus norvegicus 37-40 11433187-8 2001 The basal and ANF-stimulated cGMP formation in isolated glomeruli was significantly inhibited in low sodium-treated rats as compared to normal sodium-treated rats. Sodium 101-107 natriuretic peptide A Rattus norvegicus 14-17 11433187-8 2001 The basal and ANF-stimulated cGMP formation in isolated glomeruli was significantly inhibited in low sodium-treated rats as compared to normal sodium-treated rats. Sodium 143-149 natriuretic peptide A Rattus norvegicus 14-17 11433187-9 2001 The inhibitory effect of low sodium intake on basal and ANF-stimulated glomerular cGMP formation was completely prevented by a selective cGMP-PDE inhibitor, zaprinast, but not affected by PKC activator, PMA, or PKC inhibitor, H-7. Sodium 29-35 natriuretic peptide A Rattus norvegicus 56-59 11433187-11 2001 CONCLUSIONS: These results demonstrate that the blunted glomerular response to ANF in rats on low sodium intake is due to decrease ability of cGMP formation in glomeruli by increasing activity of cGMP-PDE without altering activity of PKC. Sodium 98-104 natriuretic peptide A Rattus norvegicus 79-82 11302728-5 2001 Human AE4 shares 84% identity with the recently reported rabbit AE4, a sodium independent, Cl(-)/HCO(-)(3) exchanger located on the apical membrane of beta-intercalated kidney cells. Sodium 71-77 solute carrier family 4 member 9 Homo sapiens 6-9 11264302-0 2001 D1/D5 dopamine receptor activation differentially modulates rapidly inactivating and persistent sodium currents in prefrontal cortex pyramidal neurons. Sodium 96-102 dopamine receptor D5 Mus musculus 0-23 11288487-6 2001 OAT1 mediates sodium-independent, anion exchange for a variety of organic anions including p-aminohippurate, cyclic nucleotides, prostanoides, dicarboxylates, and anionic drugs including beta-lactams, non-steroidal antiinflammatory drugs, diuretics and antiviral drugs. Sodium 14-20 solute carrier family 22 member 6 Rattus norvegicus 0-4 11292079-0 2001 The low-temperature- and salt-induced RCI2A gene of Arabidopsis complements the sodium sensitivity caused by a deletion of the homologous yeast gene SNA1. Sodium 80-86 Pmp3p Saccharomyces cerevisiae S288C 149-153 11292079-7 2001 This effect is specific for sodium, since no growth defect was observed for the sna1 mutant on 1.7 M sorbitol, 1 M KCl or 0.6 M LiCl. Sodium 28-34 Pmp3p Saccharomyces cerevisiae S288C 80-84 11121535-1 2000 Previous work suggested a role for the voltage-dependent persistent sodium current, I(Na,P), in the generation of seizures and spreading depression (SD). Sodium 68-74 catenin beta like 1 Homo sapiens 86-90 11102523-3 2000 Nhx1p is thought to transport sodium ions into the prevacuole compartment in exchange for protons. Sodium 30-36 bifunctional K:H/Na:H antiporter NHX1 Saccharomyces cerevisiae S288C 0-5 11196476-5 2000 MnSOD activity was enhanced in zfr adrenal mitochondria from rats that were ACTH treated or on a low sodium diet. Sodium 101-107 superoxide dismutase 2 Rattus norvegicus 0-5 10998198-9 2000 OK cells exhibited endogenous sodium-dependent sulfate transport; significantly increased sodium/sulfate co-transport was also observed in OK cells that were preincubated with GH, IGF-1, and PG/EST, although not with EST alone. Sodium 90-96 somatotropin Canis lupus familiaris 176-178 10998093-5 2000 Replacement of 100% (and as little as 10%) sodium by NMDG or sucrose not only blocked the activity-mediated neurotrophin secretion, but itself led to a rapid and substantial increase of neurotrophin secretion. Sodium 43-49 brain derived neurotrophic factor Homo sapiens 108-120 10998093-5 2000 Replacement of 100% (and as little as 10%) sodium by NMDG or sucrose not only blocked the activity-mediated neurotrophin secretion, but itself led to a rapid and substantial increase of neurotrophin secretion. Sodium 43-49 brain derived neurotrophic factor Homo sapiens 186-198 10998093-9 2000 The importance of the present observations lies not only in the reevaluation of the involvement of sodium in activity-dependent neurotrophin secretion, but also in the demonstration that sodium replacement may initiate "side effects" that are unrelated to sodium replacement. Sodium 99-105 brain derived neurotrophic factor Homo sapiens 128-140 10878096-0 2000 Evidence for cystic fibrosis transmembrane conductance regulator-dependent sodium reabsorption in kidney, using Cftr(tm2cam) mice. Sodium 75-81 cystic fibrosis transmembrane conductance regulator Mus musculus 13-64 10860504-3 2000 The sodium-activated uptake of 30 microM [(14)C]glycocholate (GC) via the ileal (IBAT) and liver (LBAT) transporters was 30-40 times higher than GC uptake in a sodium-free background. Sodium 4-10 solute carrier family 10 member 2 Homo sapiens 81-85 10810228-2 2000 In 1992, a cDNA (rBAT) was isolated from kidney which induced high-affinity, sodium-independent uptake of cystine and dibasic amino acids when expressed in Xenopus oocytes. Sodium 77-83 bile acid CoA:amino acid N-acyltransferase Rattus norvegicus 17-21 10677232-0 2000 Sodium binding site of factor Xa: role of sodium in the prothrombinase complex. Sodium 0-6 coagulation factor X Homo sapiens 23-32 10677232-0 2000 Sodium binding site of factor Xa: role of sodium in the prothrombinase complex. Sodium 0-6 coagulation factor X Homo sapiens 56-70 10677232-0 2000 Sodium binding site of factor Xa: role of sodium in the prothrombinase complex. Sodium 42-48 coagulation factor X Homo sapiens 23-32 10688514-8 2000 In the face of plasma volume expansion associated with increased mineralo-corticoid production, the effects of reduced kallikrein synthesis at term on glomerular perfusion and reabsorption of sodium by the distal tubule may predispose to blood pressure elevation in late pregnancy. Sodium 192-198 kallikrein related peptidase 4 Homo sapiens 119-129 10711725-8 2000 Renal enzyme activity with NAD (11beta-HSD2 cofactor) was lower following a high sodium diet (P < 0.05). Sodium 81-87 hydroxysteroid 11-beta dehydrogenase 2 Rattus norvegicus 32-43 10845107-4 2000 Activation of renal receptors by uroguanylin stimulates urine flow and excretion of sodium, chloride, and potassium. Sodium 84-90 guanylate cyclase activator 2B Homo sapiens 33-44 10608847-1 1999 The serum- and glucocorticoid-induced kinase (sgk) is a serine and threonine kinase that stimulates amiloride-sensitive sodium transport in Xenopus oocytes. Sodium 120-126 serum/glucocorticoid regulated kinase 1 L homeolog Xenopus laevis 4-44 10608847-1 1999 The serum- and glucocorticoid-induced kinase (sgk) is a serine and threonine kinase that stimulates amiloride-sensitive sodium transport in Xenopus oocytes. Sodium 120-126 serum/glucocorticoid regulated kinase 1 L homeolog Xenopus laevis 46-49 10608847-2 1999 Because aldosterone induces phosphorylation on serine/threonine (Ser/Thr) residues in the carboxyl termini of beta and gamma subunits of epithelial sodium channels (ENaCs) and causes an increase in the sgk transcript in mammalian and amphibian renal epithelial cells, it seems likely that sgk mediates the action of aldosterone to stimulate sodium transport. Sodium 148-154 serum/glucocorticoid regulated kinase 1 Homo sapiens 202-205 10608847-2 1999 Because aldosterone induces phosphorylation on serine/threonine (Ser/Thr) residues in the carboxyl termini of beta and gamma subunits of epithelial sodium channels (ENaCs) and causes an increase in the sgk transcript in mammalian and amphibian renal epithelial cells, it seems likely that sgk mediates the action of aldosterone to stimulate sodium transport. Sodium 148-154 serum/glucocorticoid regulated kinase 1 Homo sapiens 289-292 10564122-5 1999 High-sodium intake caused a profound decrease of ANG II-induced aortic vasoconstriction in both Dahl R and Dahl S rats. Sodium 5-11 angiogenin Rattus norvegicus 49-52 10553907-7 1999 The neurotrophin-induced depolarization resulted from the activation of a sodium ion conductance which was reversibly blocked by K-252a, a protein kinase blocker which prefers tyrosine kinase Trk receptors. Sodium 74-80 brain derived neurotrophic factor Homo sapiens 4-16 10516298-3 1999 Using dendritic and somatic patch-pipette recordings, we show that calcium spikes are initiated in the apical dendrites of CA1 pyramidal neurons and drive bursts of sodium-dependent action potentials at the soma. Sodium 165-171 carbonic anhydrase 1 Homo sapiens 123-126 10512758-4 1999 Upon withdrawal of serum, 30 nM IGFBP-6 also decreased apoptosis (within 4 h) and increased protein content and sodium-dependent phosphate uptake (within 24 h), but less potently than IGF I. Sodium 112-118 insulin like growth factor binding protein 6 Homo sapiens 32-39 10473612-11 1999 Application of EGF-L to alphaIIAbeta1beta2 channels expressed in Xenopus oocytes potentiated expressed sodium currents without significantly altering current time course or the voltage dependence of current activation or inactivation. Sodium 103-109 epidermal growth factor L homeolog Xenopus laevis 15-20 10541475-2 1999 The amount of AAC decreased dramatically when the incubation with the first antibody was realized in the presence of ATP in a sodium-rich medium with 0.5 mM KCl. Sodium 126-132 glycine-N-acyltransferase Homo sapiens 14-17 10444563-0 1999 Pressure-dependent renin release: effects of sodium intake and changes of total body sodium. Sodium 45-51 renin Canis lupus familiaris 19-24 10444563-0 1999 Pressure-dependent renin release: effects of sodium intake and changes of total body sodium. Sodium 85-91 renin Canis lupus familiaris 19-24 10444563-1 1999 The impact of sodium intake and changes in total body sodium (TBS) for the setting of pressure-dependent renin release (PDRR) was studied in freely moving dogs. Sodium 14-20 renin Canis lupus familiaris 105-110 10444563-1 1999 The impact of sodium intake and changes in total body sodium (TBS) for the setting of pressure-dependent renin release (PDRR) was studied in freely moving dogs. Sodium 54-60 renin Canis lupus familiaris 105-110 10444581-9 1999 In conclusion, in this rat CRF model: 1) increased fractional sodium excretion is associated with altered expression of proximal tubule Na transporter expression (NHE-3, NaPi-II, and Na-K-ATPase), consistent with glomerulotubular imbalance in the face of increased single-nephron glomerular filtration rate; and 2) compensatory increases in BSC-1 and TSC expression per nephron occur in distal segments. Sodium 62-68 solute carrier family 12 member 1 Rattus norvegicus 341-346 10466463-12 1999 In the kidney, the 11beta-HSD-2 gene is regulated by sodium status but is not affected by gender or age. Sodium 53-59 hydroxysteroid 11-beta dehydrogenase 2 Rattus norvegicus 19-31 10401024-7 1999 Urinary excretions of AM and PAMP showed significant correlations with urine excretion of sodium (r = 0.39; P < 0.05 and r = 0.49; P < 0.01, respectively). Sodium 90-96 adrenomedullin Homo sapiens 29-33 10401024-8 1999 These findings suggest that AM and PAMP may have roles in the regulation of sodium in patients with CGN. Sodium 76-82 adrenomedullin Homo sapiens 35-39 10495475-5 1999 Because glucose transport across these barriers is mediated exclusively by the sodium-independent glucose transporter GLUT1, changes in endothelial glucose transport and GLUT1 abundance in the barriers of the brain and retina may have profound consequences on glucose delivery to these tissues and major implications in the development of two major diabetic complications, namely insulin-induced hypoglycemia and diabetic retinopathy. Sodium 79-85 solute carrier family 2 member 1 Homo sapiens 118-123 10495475-5 1999 Because glucose transport across these barriers is mediated exclusively by the sodium-independent glucose transporter GLUT1, changes in endothelial glucose transport and GLUT1 abundance in the barriers of the brain and retina may have profound consequences on glucose delivery to these tissues and major implications in the development of two major diabetic complications, namely insulin-induced hypoglycemia and diabetic retinopathy. Sodium 79-85 solute carrier family 2 member 1 Homo sapiens 170-175 10487329-13 1999 This implies that the mechanism of water-sodium excretion induced by NEP inhibitor is mediated by renal NO. Sodium 41-47 membrane metallo-endopeptidase Rattus norvegicus 69-72 10559906-5 1999 A negatively charged GIRK4 residue, two positions away from the most strongly interacting arginine, mediates stimulation of channel activity by sodium by strengthening channel-PtdIns(4,5)P2 interactions. Sodium 144-150 potassium inwardly rectifying channel subfamily J member 5 Homo sapiens 21-26 10447022-8 1999 Recent mutations have been described in the genes coding for the sodium/iodide symporter, thyroid peroxidase (TPO), and thyroglobulin. Sodium 65-71 thyroid peroxidase Homo sapiens 110-113 10382996-5 1999 RESULTS: A single systemic injection of Ad.RSV-ANP at a dose of 1.2x10(10) pfu results in a significant increase in urine excretion, water intake, urinary sodium and potassium excretion. Sodium 155-161 natriuretic peptide A Rattus norvegicus 47-50 10198401-0 1999 Distribution of Fos immunoreactivity in rat brain after sodium consumption induced by peritoneal dialysis. Sodium 56-62 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 16-19 10198401-1 1999 Fos immunoreactivity was used to map the neuronal population groups activated after sodium ingestion induced by peritoneal dialysis (PD) in rats. Sodium 84-90 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 0-3 10198401-3 1999 Sodium ingestion stimulated by PD produced Fos immunoreactivity within defined cells groups of the lamina terminalis and hindbrain areas such us the nucleus of the solitary tract, area postrema, and lateral parabrachial nucleus. Sodium 0-6 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 43-46 9950829-4 1999 In proximal colon, dietary sodium depletion enhanced both NHE2 and NHE3 isoform-specific Na+/H+ exchange activities, protein expression, and mRNA abundance. Sodium 27-33 solute carrier family 9 member A2 Rattus norvegicus 58-62 9950829-5 1999 In contrast, in distal colon both NHE2 and NHE3 isoform-specific Na+/H+ exchange activities, protein expression, and mRNA abundance were inhibited by sodium depletion. Sodium 150-156 solute carrier family 9 member A2 Rattus norvegicus 34-38 9989242-6 1999 The conformation of SP-A is altered by the presence of cations, especially calcium, then sodium, and to a small extent, magnesium. Sodium 89-95 pulmonary surfactant-associated protein A Bos taurus 20-24 10682066-8 1999 The higher initial osmolality in the ALB groups was partially due to the sodium content in the ALB powder. Sodium 73-79 albumin Rattus norvegicus 37-40 10682066-8 1999 The higher initial osmolality in the ALB groups was partially due to the sodium content in the ALB powder. Sodium 73-79 albumin Rattus norvegicus 95-98 10676448-4 1999 Recent studies suggest that bombesin, a peptide related to gastrin-releasing peptide, suppresses sodium appetite. Sodium 97-103 gastrin releasing peptide Homo sapiens 28-36 10676448-4 1999 Recent studies suggest that bombesin, a peptide related to gastrin-releasing peptide, suppresses sodium appetite. Sodium 97-103 gastrin releasing peptide Homo sapiens 59-84 10576591-5 1999 Results showed that a marked decrease of mean arterial pressure (MAP) and a significant increase of urine volume and urinary sodium excretion was produced in rats receiving the hANF construct due to the local expression of ANF and its secretion into plasma. Sodium 125-131 HESX homeobox 1 Homo sapiens 177-181 10576591-5 1999 Results showed that a marked decrease of mean arterial pressure (MAP) and a significant increase of urine volume and urinary sodium excretion was produced in rats receiving the hANF construct due to the local expression of ANF and its secretion into plasma. Sodium 125-131 natriuretic peptide A Rattus norvegicus 178-181 10613514-9 1999 We conclude that aquaporin-4 messenger RNA is present in a collection of structures typically involved in the regulation of water and sodium intake and that aquaporin-4 water channels could be the osmosensor mechanism responsible for detecting changes in cell volume by these cells. Sodium 134-140 aquaporin 4 Homo sapiens 17-28 9856473-0 1998 Dendritic sodium spikes are variable triggers of axonal action potentials in hippocampal CA1 pyramidal neurons. Sodium 10-16 carbonic anhydrase 1 Homo sapiens 89-92 9856473-2 1998 Here, we provide direct evidence from simultaneous dendritic and somatic patch-pipette recordings that excitatory synaptic inputs can elicit dendritic sodium spikes prior to axonal action potential initiation in hippocampal CA1 pyramidal neurons. Sodium 151-157 carbonic anhydrase 1 Homo sapiens 224-227 9839820-6 1998 The homologous relationship between rPN3 and hPN3 is defined by (i) a high level of sequence identity (ii) sodium currents that are highly resistant to tetrodotoxin (TTX) (iii) similar tissue distribution profiles and (iv) orthologous chromosomal map positions. Sodium 107-113 sodium voltage-gated channel alpha subunit 10 Homo sapiens 45-49 9734605-12 1998 TIMP-1 mRNA was undetectable in renal sections from sodium-depleted vehicle-treated animals using the in situ hybridization (ISH) technique. Sodium 52-58 TIMP metallopeptidase inhibitor 1 Rattus norvegicus 0-6 9734612-3 1998 We studied the level of rBSC1 mRNA in dehydration and cardiac failure, since sodium transport in TAL may be enhanced in both conditions in spite of the difference in extracellular fluid accumulation. Sodium 77-83 solute carrier family 12 member 1 Rattus norvegicus 24-29 9691021-3 1998 When expressed in Xenopus laevis oocytes, rNaDC-1 mediated sodium-dependent uptake of di- and tricarboxylates. Sodium 59-65 solute carrier family 13 member 2 Rattus norvegicus 42-49 9888564-4 1998 Feeding rats a low sodium diet resulted in a decrease in both PAMP and adrenomedullin binding in the zona glomerulosa. Sodium 19-25 adrenomedullin Rattus norvegicus 71-85 9888564-5 1998 Adrenomedullin specific binding was 378 fmol/mg protein in the controls and 89 fmol/mg protein following dietary sodium depletion. Sodium 113-119 adrenomedullin Rattus norvegicus 0-14 9689008-5 1998 Sodium-independent sulfate and oxalate uptake was enhanced 7.3-fold and 13.1-fold, respectively, in Sf9 cells expressing the sat-1 protein compared with cells infected with wild-type virus. Sodium 0-6 spermidine/spermine N1-acetyl transferase 1 Rattus norvegicus 125-130 9673436-9 1998 In canrenoate-treated rats, ANP infusion caused greater increases in sodium excretion (FENA from 3.05 +/- 0.71 to 7.21 +/- 0.45%; P < 0.05; n = 8) than saline infusion (FENA from 4.16 +/- 1.11 to 5.47 +/- 0.66%; n = 6), despite the hypocapnia. Sodium 69-75 natriuretic peptide A Rattus norvegicus 28-31 9681414-5 1998 ANP gene delivery caused significant increases in renal blood flow, glomerular filtration rate, sodium output, urine excretion, and urinary cGMP levels. Sodium 96-102 natriuretic peptide A Rattus norvegicus 0-3 11324528-3 1998 The results showed that all the five artemisinin-derivatives clearly inhibited the voltage-gated sodium current (INa) of the cells in a dose-dependent manner and the effect was partially reversibly. Sodium 97-103 internexin neuronal intermediate filament protein, alpha Mus musculus 131-135 9559673-1 1998 Four putative yeast transcription factors (Hal6-9p) have been identified which upon overexpression in multicopy plasmids increase sodium and lithium tolerance. Sodium 130-136 Cin5p Saccharomyces cerevisiae S288C 43-47 9706250-1 1998 Hig levels of circulating atrial natriuretic factor (ANF) have been reported in several physiopathologic conditions like hypertension, heart and renal failure, pregnancy and high sodium intake. Sodium 179-185 natriuretic peptide A Rattus norvegicus 26-51 9706250-1 1998 Hig levels of circulating atrial natriuretic factor (ANF) have been reported in several physiopathologic conditions like hypertension, heart and renal failure, pregnancy and high sodium intake. Sodium 179-185 natriuretic peptide A Rattus norvegicus 53-56 9786175-1 1998 In vivo, atrial natriuretic peptide (ANP) inhibits water and sodium absorption by the intestine. Sodium 61-67 natriuretic peptide A Rattus norvegicus 9-35 9786175-1 1998 In vivo, atrial natriuretic peptide (ANP) inhibits water and sodium absorption by the intestine. Sodium 61-67 natriuretic peptide A Rattus norvegicus 37-40 9786175-3 1998 ANP also decreases sodium absorption in the rat small intestine in vitro, but only if glucose is present on the luminal side of the tissue. Sodium 19-25 natriuretic peptide A Rattus norvegicus 0-3 9664622-6 1998 The transport activity observed following express of dEAAT in Xenopus oocytes or COS-7 cells shows a high affinity for L-glutamate, L-aspartate and D-aspartate, an absolute dependence on external sodium ions, and considerable stereoselectivity for the transport of L-glutamate over D-glutamate. Sodium 196-202 Excitatory amino acid transporter 1 Drosophila melanogaster 53-58 9363368-7 1997 In sham rats, ANP infusion at a rate of 12 micrograms/kg per h resulted in a smaller increase in the fractional excretion of sodium during hypocapnia (mean +/- SEM: 1.02 +/- 0.40%, n = 10) than normocapnia (3.95 +/- 0.64%, n = 9; P < 0.001). Sodium 125-131 natriuretic peptide A Rattus norvegicus 14-17 9363368-8 1997 The level of fractional excretion of sodium with ANP infusion during hypocapnia was not significantly different from the level in saline-infused hypocapnic sham rats (0.93 +/- 0.62%, n = 10). Sodium 37-43 natriuretic peptide A Rattus norvegicus 49-52 9363368-9 1997 In hypocapnic ADX rats (n = 11), ANP induced greater increases in the fractional excretion of sodium (5.59 +/- 1.35%) than did saline infusion (1.04 +/- 1.02%, n = 10; P < 0.002). Sodium 94-100 natriuretic peptide A Rattus norvegicus 33-36 9362332-5 1997 Infusion of PYY into rats (47 pmol x kg(-1) x min[-1]) increased mean arterial pressure (103 +/- 6 to 123 +/- 8 mmHg) and decreased renal plasma flow (13 +/- 1.8 to 8.4 +/- 2.1 ml/min) but produced no significant change in glomerular filtration rate or sodium excretion. Sodium 253-259 peptide YY Rattus norvegicus 12-15 9362332-7 1997 These results show that receptors for PYY are widely distributed in the kidney and that exogenously administered PYY causes renal vasoconstriction and may influence renal sodium excretion. Sodium 171-177 peptide YY Rattus norvegicus 38-41 9362332-7 1997 These results show that receptors for PYY are widely distributed in the kidney and that exogenously administered PYY causes renal vasoconstriction and may influence renal sodium excretion. Sodium 171-177 peptide YY Rattus norvegicus 113-116 9394167-7 1997 Intrarenal production of cyclic GMP, endothelin, and PGE2 are all disturbed in preeclampsia and may have implications in the sodium retention, hypertension, and intrarenal thrombosis and vasospasm of preeclamptic pregnancy. Sodium 125-131 5'-nucleotidase, cytosolic II Homo sapiens 32-35 9295340-0 1997 Regulation of a c-Jun amino-terminal kinase/stress-activated protein kinase cascade by a sodium-dependent signal transduction pathway. Sodium 89-95 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 16-21 9295340-9 1997 Collectively, these results demonstrate that palytoxin stimulates a sodium-dependent signaling pathway that activates the SEK1/JNK/c-Jun protein kinase cascade. Sodium 68-74 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 131-136 9324106-5 1997 Deficiency or inhibition of 11beta-HSD2 causes sodium retention and hypertension. Sodium 47-53 hydroxysteroid 11-beta dehydrogenase 2 Rattus norvegicus 28-39 9331977-4 1997 Upon sodium restriction (5 mmol Na(+)/kg of diet) of rats for 14d, the amount of the CYP11B2 mRNA in the adrenal glands was increased 8.5-fold compared to that from the rats fed a normal diet (225 mmol Na(+)/kg of diet), whereas no significant change in the CYP11B1 mRNA was observed after the dietary sodium restriction. Sodium 5-11 cytochrome P450, family 11, subfamily b, polypeptide 2 Rattus norvegicus 85-92 9331977-4 1997 Upon sodium restriction (5 mmol Na(+)/kg of diet) of rats for 14d, the amount of the CYP11B2 mRNA in the adrenal glands was increased 8.5-fold compared to that from the rats fed a normal diet (225 mmol Na(+)/kg of diet), whereas no significant change in the CYP11B1 mRNA was observed after the dietary sodium restriction. Sodium 302-308 cytochrome P450, family 11, subfamily b, polypeptide 2 Rattus norvegicus 85-92 9208128-0 1997 Modulation by low sodium intake of glomerular response to cicletanine and atrial natriuretic factor. Sodium 18-24 natriuretic peptide A Rattus norvegicus 74-99 9208128-5 1997 CIC (0.25 mg min-1 kg-1 BW) of ANF (0.5 microgram min-1 BW) alone, given in pharmacological doses, increased Cin significantly in normal sodium rats, whereas the effect of each agent was blunted in low sodium diet rats. Sodium 137-143 natriuretic peptide A Rattus norvegicus 31-34 9208128-6 1997 Pretreatment with CIC restored the increase in C(in) in response to ANF infusion in low sodium diet rats. Sodium 88-94 natriuretic peptide A Rattus norvegicus 68-71 9208128-10 1997 In normal sodium diet rats, CIC 10(-4) M or ANF 10(-6) M alone inhibited angiotensin II 10(-6) M (AII)-induced decrease in intracapillary volume reflected by the glomerular [3H]-inulin space (GIS). Sodium 10-16 natriuretic peptide A Rattus norvegicus 44-47 9208128-14 1997 CIC both alone and in combination with ANF increased nephrogenous cyclic GMP excretion and cyclic GMP accumulation in isolated glomeruli of rats on normal and low sodium diets. Sodium 163-169 natriuretic peptide A Rattus norvegicus 39-42 9208128-17 1997 These results suggest that CIC and ANF alone induce relaxation of glomeruli and a resultant increase in glomerular filtration rate in normal sodium diet rats; in contrast, these effects are blunted in the low sodium diet rats. Sodium 141-147 natriuretic peptide A Rattus norvegicus 35-38 9208128-17 1997 These results suggest that CIC and ANF alone induce relaxation of glomeruli and a resultant increase in glomerular filtration rate in normal sodium diet rats; in contrast, these effects are blunted in the low sodium diet rats. Sodium 209-215 natriuretic peptide A Rattus norvegicus 35-38 9174082-0 1997 Increased sodium appetite stimulates c-fos expression in the organum vasculosum of the lamina terminalis. Sodium 10-16 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 37-42 9176324-1 1997 The neuronal isoform of nitric oxide synthase (nNOS) exists in the renal cortex predominantly in the macula densa, suggesting that nitric oxide (NO) derived from the macula densa plays a role in feedback regulation of renin in response to altered sodium metabolism. Sodium 247-253 nitric oxide synthase 1 Rattus norvegicus 47-51 9154891-0 1997 Keratinocyte growth factor increases transalveolar sodium reabsorption in normal and injured rat lungs. Sodium 51-57 fibroblast growth factor 7 Rattus norvegicus 0-26 9160980-0 1997 c-Fos induction in the nucleus of the solitary tract of sodium-depleted rats by salt intake, peripheral bombesin, and the combination. Sodium 56-62 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 0-5 9113507-1 1997 Multiple dosing with recombinant adenoviral vectors containing the cystic fibrosis transmembrane conductance regulator (CFTR) cDNA to the nasal mucosa of cystic fibrosis (CF) transgenic mice reportedly results in only partial correction of the CF defect in chloride (Cl-) secretion without normalizing sodium (Na+) hyperabsorption, perhaps indicating inefficient gene transfer into the nasal airway epithelium in vivo. Sodium 302-308 cystic fibrosis transmembrane conductance regulator Mus musculus 67-118 9113507-1 1997 Multiple dosing with recombinant adenoviral vectors containing the cystic fibrosis transmembrane conductance regulator (CFTR) cDNA to the nasal mucosa of cystic fibrosis (CF) transgenic mice reportedly results in only partial correction of the CF defect in chloride (Cl-) secretion without normalizing sodium (Na+) hyperabsorption, perhaps indicating inefficient gene transfer into the nasal airway epithelium in vivo. Sodium 302-308 cystic fibrosis transmembrane conductance regulator Mus musculus 120-124 9083097-1 1997 The human rBAT protein elicits sodium-independent, high affinity obligatory exchange of cystine, dibasic amino acids, and some neutral amino acids in Xenopus oocytes (Chillaron, J., Estevez, R., Mora, C., Wagner, C. A., Suessbrich, H., Lang, F., Gelpi, J. L., Testar, X., Busch, A. E., Zorzano, A., and Palacin, M. (1996) J. Biol. Sodium 31-37 bile acid CoA:amino acid N-acyltransferase Rattus norvegicus 10-14 9084415-7 1997 cGMP mimicked the effect of CNP on sodium-dependent pHi recovery, but the native nucleotide was as potent as membrane-permeant analogues. Sodium 35-41 natriuretic peptide C Rattus norvegicus 28-31 9083275-6 1997 Our results indicate that renal ANP mRNA expression is enhanced in diabetic rats, and that renal-synthesized ANP as one of regulators to handle water and sodium balance in diabetic rats is worthy of further investigation. Sodium 154-160 natriuretic peptide A Rattus norvegicus 109-112 9175124-1 1997 Voltage-activated sodium currents (INa) in vestibular ganglion neurones acutely isolated from postnatal mice were investigated using the whole-cell configuration of the patch-clamp technique. Sodium 18-24 internexin neuronal intermediate filament protein, alpha Mus musculus 35-38 9134052-3 1997 D-Fructose induced a sodium-independent release of GLP-1. Sodium 21-27 glucagon Rattus norvegicus 51-56 9222405-1 1997 We determined whether ANP (atrial natriuretic peptide) concentrations, measured by radioimmunoassay, in the ANPergic cerebral regions involved in regulation of sodium intake and excretion and pituitary glad correlated with differences in sodium preference among 40 Wistar male rats (180-220 g). Sodium 160-166 natriuretic peptide A Rattus norvegicus 22-25 9222405-5 1997 The concentrations of ANP in the OB and the AP were correlated with sodium ingestion during the preceding 24 h, since an increase of ANP in these structures was associated with a reduced ingestion and vice-versa (OB: r = -0.3649, P < 0.05; AP: r = -0.3291, P < 0.05). Sodium 68-74 natriuretic peptide A Rattus norvegicus 22-25 9222405-7 1997 This suggests that differences in sodium preference among individual male rats can be related to variations of AP ANP level. Sodium 34-40 natriuretic peptide A Rattus norvegicus 114-117 9222405-9 1997 Our data suggests that the OB ANP level may play a role mainly in day-to-day variations of sodium ingestion in the individual rat. Sodium 91-97 natriuretic peptide A Rattus norvegicus 30-33 9323436-2 1997 Pretreatment with intravenous captopril (100 mg/kg) significantly inhibited the c-fos expression induced by sodium depletion in the SFO and OVLT. Sodium 108-114 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 80-85 9323436-4 1997 These results show that systemic interference with the angiotensin system of renal origin by captopril inhibited the production of Fos induced by sodium depletion in cells of the SFO and OVLT. Sodium 146-152 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 131-134 9398028-6 1997 A similar decline in reabsorption was seen with intratubular application of Ang 1-7 in a concentration of 10(-12) or 10(-10) M. In contrast, intratubular application of Ang 1-7 in a concentration of 10(-8) M increased fluid, potassium and sodium reabsorption in that nephron segment by 11, 9 and 3%, respectively. Sodium 239-245 angiogenin Rattus norvegicus 169-176 9532579-3 1997 Using patch clamp methods, we studied neurotrophin regulation of voltage-gated sodium, calcium, and potassium currents in SK-N-SH neuroblastoma cells. Sodium 79-85 brain derived neurotrophic factor Homo sapiens 38-50 9437707-1 1997 Atrial natriuretic peptide (ANP) decreases sodium absorption in small intestine of rats in vitro under sodium concentration-gradient conditions (SCG) and this effect may be mediated by the inhibition of the sodium/glucose cotransporter (SGLT). Sodium 43-49 natriuretic peptide A Rattus norvegicus 0-26 9437707-1 1997 Atrial natriuretic peptide (ANP) decreases sodium absorption in small intestine of rats in vitro under sodium concentration-gradient conditions (SCG) and this effect may be mediated by the inhibition of the sodium/glucose cotransporter (SGLT). Sodium 43-49 natriuretic peptide A Rattus norvegicus 28-31 9437707-1 1997 Atrial natriuretic peptide (ANP) decreases sodium absorption in small intestine of rats in vitro under sodium concentration-gradient conditions (SCG) and this effect may be mediated by the inhibition of the sodium/glucose cotransporter (SGLT). Sodium 103-109 natriuretic peptide A Rattus norvegicus 0-26 9437707-1 1997 Atrial natriuretic peptide (ANP) decreases sodium absorption in small intestine of rats in vitro under sodium concentration-gradient conditions (SCG) and this effect may be mediated by the inhibition of the sodium/glucose cotransporter (SGLT). Sodium 103-109 natriuretic peptide A Rattus norvegicus 28-31 8968581-1 1996 Rat skeletal muscle (Skm1) sodium channel alpha and beta 1 subunits were coexpressed in Xenopus oocytes, and resulting sodium currents were recorded from on-cell macropatches. Sodium 27-33 sodium voltage-gated channel alpha subunit 4 Rattus norvegicus 21-25 9222431-0 1996 Central interaction between atrial natriuretic peptide and angiotensin II in the control of sodium intake and excretion in female rats. Sodium 92-98 natriuretic peptide A Rattus norvegicus 28-54 8910555-10 1996 These results suggest that the cation sensitivity of the HAL2 nucleotidase is an important determinant of the inhibition of yeast growth by sodium and lithium salts. Sodium 140-146 3'(2'),5'-bisphosphate nucleotidase Saccharomyces cerevisiae S288C 57-61 8953248-2 1996 At toxic millimolar levels of sodium (Na+), HKT1 mediates low-affinity Na+ uptake while potassium (K+) uptake is blocked. Sodium 30-36 cation transporter HKT1 Triticum aestivum 44-48 8899888-5 1996 Treatments that induce sodium appetite all induce Fos along the lamina terminalis, but usually not in the SO or PVN. Sodium 23-29 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 50-53 8897973-8 1996 Furthermore, intracerebroventricular GLP-1 stimulated urinary excretion of water and sodium. Sodium 85-91 glucagon Rattus norvegicus 37-42 8915970-1 1996 Blunted volume expansion (VE) natriuresis and renal resistance to atrial natriuretic peptide (ANP) characterize states of pathological sodium retention. Sodium 135-141 natriuretic peptide A Rattus norvegicus 66-92 8915970-1 1996 Blunted volume expansion (VE) natriuresis and renal resistance to atrial natriuretic peptide (ANP) characterize states of pathological sodium retention. Sodium 135-141 natriuretic peptide A Rattus norvegicus 94-97 8915970-9 1996 These results suggest that ANP resistance in a model of abnormal sodium metabolism devoid of intrinsic renal disease may be related to increased activity of phosphodiesterase in renal target cells for ANP as well as to heightened renal nerve activity. Sodium 65-71 natriuretic peptide A Rattus norvegicus 27-30 8886404-16 1996 The TAPP-induced diuretic action, increased sodium/potassium excretion and elevated urinary cyclic GMP levels were also reversed by anti-ANF antibodies. Sodium 44-50 natriuretic peptide A Rattus norvegicus 137-140 8760235-1 1996 Resistance to the natriuretic action of atrial natriuretic peptide (ANP) is a hallmark of states of pathological sodium retention including congestive heart failure, cirrhosis of the liver, and nephrotic syndrome. Sodium 113-119 natriuretic peptide A Rattus norvegicus 40-66 8760236-1 1996 Resistance to the natriuretic action of atrial natriuretic peptide (ANP) is a hallmark of states of pathological sodium retention including congestive heart failure, cirrhosis of the liver, and nephrotic syndrome. Sodium 113-119 natriuretic peptide A Rattus norvegicus 40-66 8640238-4 1996 These two chromosomal regions harbour the genes encoding the three subunits of the human amiloride sensitive epithelial sodium channel (hENaC): SCNN1B and SCNN1G on 16p and SCNN1A on 12p. Sodium 120-126 sodium channel epithelial 1 subunit beta Homo sapiens 144-150 8640238-4 1996 These two chromosomal regions harbour the genes encoding the three subunits of the human amiloride sensitive epithelial sodium channel (hENaC): SCNN1B and SCNN1G on 16p and SCNN1A on 12p. Sodium 120-126 sodium channel epithelial 1 subunit gamma Homo sapiens 155-161 8643524-1 1996 In the fission yeast, Schizosaccharomyces pombe, tolerance to high sodium and lithium concentrations requires the functioning of the sod2, Na+/H+ antiporter. Sodium 67-73 superoxide dismutase SOD2 Saccharomyces cerevisiae S288C 133-137 8643524-6 1996 This bidirectional activity was also detected in S. cerevisiae strains expressing sod2 and expression of this gene complemented the sodium and lithium sensitivity resulting from inactivation of the ENA1/PMR2 encoded Na+-exporting ATPases. Sodium 132-138 superoxide dismutase SOD2 Saccharomyces cerevisiae S288C 82-86 8643524-6 1996 This bidirectional activity was also detected in S. cerevisiae strains expressing sod2 and expression of this gene complemented the sodium and lithium sensitivity resulting from inactivation of the ENA1/PMR2 encoded Na+-exporting ATPases. Sodium 132-138 Na(+)/Li(+)-exporting P-type ATPase ENA1 Saccharomyces cerevisiae S288C 198-202 8643524-6 1996 This bidirectional activity was also detected in S. cerevisiae strains expressing sod2 and expression of this gene complemented the sodium and lithium sensitivity resulting from inactivation of the ENA1/PMR2 encoded Na+-exporting ATPases. Sodium 132-138 Na(+)/Li(+)-exporting P-type ATPase ENA1 Saccharomyces cerevisiae S288C 203-207 8704111-7 1996 Surprisingly, the kallikrein response to changes in sodium intake was similar in all subgroups, although enzyme excretion was always at the lowest level in salt-sensitive hypertensive patients. Sodium 52-58 kallikrein related peptidase 4 Homo sapiens 18-28 9011753-4 1996 When REAAC1 was expressed in HeLa cells using a recombinant vaccinia-T7 virus expression system, a sodium dependent glutamate uptake was observed. Sodium 99-105 solute carrier family 1 member 1 Rattus norvegicus 5-11 8929628-7 1996 Patients with oxytocin resistant labour had lower intracellular potassium (p < .0006) and phosphorus (p < .02), and higher chloride (p < .05) and sodium (p < .03) compared to levels found in patients who responded to oxytocin treatment. Sodium 155-161 oxytocin/neurophysin I prepropeptide Homo sapiens 14-22 8929628-9 1996 The reduced level of potassium and phosphorus together with the high sodium and chloride levels found in patients with oxytocin resistant labour may be connected to an impairment in sodium-potassium pump and muscle dysfunction, clinically diagnosed as dystocia. Sodium 69-75 oxytocin/neurophysin I prepropeptide Homo sapiens 119-127 8742959-6 1996 Free water clearance also increased from 11.5 +/- 3.7 to 14.4 +/- 3.9 ml/min, indicating an increase in TALH reabsorption which was attributed to increased sodium and water reaching this segment. Sodium 156-162 transaldolase 1 Homo sapiens 104-108 7502075-0 1995 Sodium-driven potassium uptake by the plant potassium transporter HKT1 and mutations conferring salt tolerance. Sodium 0-6 cation transporter HKT1 Triticum aestivum 66-70 7498983-6 1995 Northern blot analysis showed that the ratio of renal AT1A to glyceraldehyde 3-phosphate dehydrogenase (GAPDH) mRNA was increased by losartan treatment, sodium restriction, or the combination of the two versus control (P < .05). Sodium 153-159 glyceraldehyde-3-phosphate dehydrogenase Rattus norvegicus 62-102 7498983-6 1995 Northern blot analysis showed that the ratio of renal AT1A to glyceraldehyde 3-phosphate dehydrogenase (GAPDH) mRNA was increased by losartan treatment, sodium restriction, or the combination of the two versus control (P < .05). Sodium 153-159 glyceraldehyde-3-phosphate dehydrogenase Rattus norvegicus 104-109 7498983-7 1995 In contrast, the ratio of adrenal AT1A to GAPDH mRNA was increased only by sodium restriction versus three other groups (P < .05). Sodium 75-81 glyceraldehyde-3-phosphate dehydrogenase Rattus norvegicus 42-47 8720036-4 1995 (2) ANP infusion significantly increased urine flow rate (UFR), creatinine clearance (CCr), fractional excretion rates of sodium (FENa) and chloride (FECl), and urinary phosphorus and magnesium (Mg) excretions in a dose-dependent manner without affecting renal plasma flow and fractional excretion rates of potassium and urea in cisplatin-treated rats. Sodium 122-128 natriuretic peptide A Rattus norvegicus 4-7 8720036-7 1995 In conclusion, the main mechanism of the increased renal responses to ANP is considered to be due to an increased delivery of sodium, fluid and ANP itself to the inner medullary collecting duct which is the major renal site of action of ANP under the condition of acute proximal tubular necrosis by cisplatin. Sodium 126-132 natriuretic peptide A Rattus norvegicus 70-73 8563696-7 1995 In conclusion, augmented kinins may play an important role in the renal water-sodium metabolism by NEP inhibition, and NO may contribute to the kinins" action on this mechanism, while ANP may not contribute to it, at least in normotensive rats. Sodium 78-84 membrane metallo-endopeptidase Rattus norvegicus 99-102 8989380-0 1995 Frequency-dependent propagation of sodium action potentials in dendrites of hippocampal CA1 pyramidal neurons. Sodium 35-41 carbonic anhydrase 1 Homo sapiens 88-91 8594540-0 1995 Calcium transients which accompany the activation of sodium current in rat ventricular myocytes at 37 degrees C: a trigger role for reverse Na-Ca exchange activated by membrane potential? Sodium 53-59 nascent polypeptide associated complex subunit alpha Rattus norvegicus 140-145 7573533-8 1995 Hypersensitivity of CRF rat to ANF, together with high plasma ANF levels and downregulation of clearance receptor, may contribute to increased sodium excretion in CRF. Sodium 143-149 natriuretic peptide A Rattus norvegicus 31-34 7573533-8 1995 Hypersensitivity of CRF rat to ANF, together with high plasma ANF levels and downregulation of clearance receptor, may contribute to increased sodium excretion in CRF. Sodium 143-149 natriuretic peptide A Rattus norvegicus 62-65 7584932-6 1995 However, ANP caused a 5-fold increase in fractional sodium excretion in both DR and DS. Sodium 52-58 natriuretic peptide A Rattus norvegicus 9-12 7584932-7 1995 ANP also increased sodium excretion, creatinine clearance, and urine flow. Sodium 19-25 natriuretic peptide A Rattus norvegicus 0-3 8869083-3 1995 ANF alone (5 micrograms/kg bolus then 0.5 micrograms/min/kg BW maintenance) increased diuresis and natriuresis to the same extend in low and normal sodium diet rats but had no GFR-increasing effect in low sodium diet rats. Sodium 148-154 natriuretic peptide A Rattus norvegicus 0-3 8869083-6 1995 The increase of nephrogenous cGMP excretion in response to ANF infusion in low sodium diet rats was markedly lower as compared to normal sodium diet rats (243.4 +/- 43.3 vs. 444.0 +/- 35.6 pmol/min, respectively, p < 0.01). Sodium 79-85 natriuretic peptide A Rattus norvegicus 59-62 8869083-6 1995 The increase of nephrogenous cGMP excretion in response to ANF infusion in low sodium diet rats was markedly lower as compared to normal sodium diet rats (243.4 +/- 43.3 vs. 444.0 +/- 35.6 pmol/min, respectively, p < 0.01). Sodium 137-143 natriuretic peptide A Rattus norvegicus 59-62 8869083-7 1995 Administration of a selective inhibitor of cGMP-phosphodiesterase activity (zaprinast) abolished the differences in ANF-stimulated nephrogenous cGMP excretion in low and normal sodium diet rats. Sodium 177-183 natriuretic peptide A Rattus norvegicus 116-119 8869083-8 1995 Basal and peak ANF (0.5 microM)-stimulated cGMP formation by isolated glomeruli was significantly lower in low than normal sodium diet rats (1.4 +/- 0.1 vs. 2.9 +/- 0.2 and 7.1 +/- 0.5 vs. 12.5 +/- 1.1 pmol/mg protein, for basal and ANF-stimulated cGMP formation, respectively; both p < 0.05). Sodium 123-129 natriuretic peptide A Rattus norvegicus 15-18 7473194-2 1995 Block by external tetraethylammonium (TEA) was examined on currents carried by potassium (K+) and sodium (Na+) through the cloned delayed rectifier K+ channel Kv2.1. Sodium 98-104 potassium voltage-gated channel subfamily B member 1 Homo sapiens 159-164 7554531-9 1995 Parallel to GFR, absolute reabsorption of sodium (TNa) andoxygen consumption (QO2) showed values of 110 +/- 16 and 5.46 +/- 0.33 mumol/min g kw in UPPBHb1-kidneys vs 83 +/- 6 and 5.09 +/- 0.27 in controls and vs 53 +/- 4 and 3.66 +/- 0.12 in UPPBHb2-kidneys. Sodium 42-48 C-type lectin domain family 3, member B Rattus norvegicus 50-53 7598718-1 1995 When the expression of a Ha-ras oncogene is triggered in NIH3T3 cells, a progressive inhibition of sodium dependent transport of anionic amino acids through system X-AG is observed. Sodium 99-105 Harvey rat sarcoma virus oncogene Mus musculus 25-31 7584920-12 1995 In conclusion, the results of the present studies demonstrate that long-term NEP inhibition with sinorphan has inhibitory effects on malignant hypertension and associated cardiac hypertrophy in young SHR-SP on a high-sodium diet. Sodium 217-223 membrane metallo-endopeptidase Rattus norvegicus 77-80 7675626-9 1995 Close correlation between the positional expression of SGLT1 protein and absorptive function suggests that transporter density is an important determinant for up-regulation of sodium-dependent glucose transport in diabetes. Sodium 176-182 solute carrier family 5 member 1 Rattus norvegicus 55-60 7737709-9 1995 Renal interstitial immunoreactive angiotensin decreased significantly to 124 +/- 37 nmol (P < .01) in response to intrarenal renin inhibition at the end of day 5 of sodium depletion. Sodium 168-174 renin Canis lupus familiaris 128-133 7733322-6 1995 These significant natriuresis and diuresis in the ADM kidney were associated with increases in glomerular filtration rate and fractional sodium excretion and with a decrease in distal tubular sodium reabsorption. Sodium 137-143 adrenomedullin Homo sapiens 50-53 7733322-6 1995 These significant natriuresis and diuresis in the ADM kidney were associated with increases in glomerular filtration rate and fractional sodium excretion and with a decrease in distal tubular sodium reabsorption. Sodium 192-198 adrenomedullin Homo sapiens 50-53 7733322-9 1995 The current study demonstrates that ADM is present in renal glomerular and tubular cells and is a potent natriuretic peptide that may play an important role in the regulation of sodium excretion. Sodium 178-184 adrenomedullin Homo sapiens 36-39 7721434-2 1995 Adrenomedullin decreased blood pressure in a dose-dependent manner (3 nmol/kg: -29 +/- 2% [SEM]; P < .01) and slightly increased the glomerular filtration rate and urinary sodium excretion (+108%; P < .05). Sodium 175-181 adrenomedullin Rattus norvegicus 0-14 7900841-2 1995 Infusions of ANF caused a significantly greater increase in urinary excretion of fluid, sodium, and potassium in virgin than in pregnant (13-15 days and 21 days) rats. Sodium 88-94 natriuretic peptide A Rattus norvegicus 13-16 7750665-13 1995 Glucose evoked sodium-dependently a sharp increase of IR-GLP-1 levels followed by a plateau release. Sodium 15-21 glucagon Rattus norvegicus 57-62 8587403-4 1995 Stimulation of ETB receptors in dogs in vivo inhibited sodium reabsorption, as ET-1 infusion in the presence of the ETA antagonist BQ123, but not the mixed ETA/ETB receptor antagonist, (+/-)SB 209670, resulted in increased sodium excretion. Sodium 55-61 endothelin receptor type B Canis lupus familiaris 15-18 8587403-4 1995 Stimulation of ETB receptors in dogs in vivo inhibited sodium reabsorption, as ET-1 infusion in the presence of the ETA antagonist BQ123, but not the mixed ETA/ETB receptor antagonist, (+/-)SB 209670, resulted in increased sodium excretion. Sodium 223-229 endothelin receptor type B Canis lupus familiaris 15-18 8587403-5 1995 Furthermore, infusion of the ETB-selective agonist Sarafotoxin S6c (S6c) resulted in an increase in sodium excretion, a response that was attenuated by infusion of RES-701. Sodium 100-106 endothelin receptor type B Canis lupus familiaris 29-32 7815350-11 1995 In conclusion, RB 105 is a new dual inhibitor of ACE and NEP able to target both blood pressure and renal sodium handling in different experimental renin-dependent and -independent models of hypertension. Sodium 106-112 membrane metallo-endopeptidase Rattus norvegicus 57-60 7991577-11 1994 The results are interpreted to mean that ascending stimulatory serotoninergic input into the ANP neuronal system in the AV3V region produces a tonic stimulation of ANP release, which augments sodium excretion and inhibits water intake. Sodium 192-198 natriuretic peptide A Rattus norvegicus 93-96 7991577-11 1994 The results are interpreted to mean that ascending stimulatory serotoninergic input into the ANP neuronal system in the AV3V region produces a tonic stimulation of ANP release, which augments sodium excretion and inhibits water intake. Sodium 192-198 natriuretic peptide A Rattus norvegicus 164-167 7961960-0 1994 A unique sodium-hydrogen exchange isoform (NHE-4) of the inner medulla of the rat kidney is induced by hyperosmolarity. Sodium 9-15 solute carrier family 9 member A4 Rattus norvegicus 43-48 7961960-7 1994 We conclude that NHE-4 is an unusual isoform of sodium-hydrogen exchangers that may play a specialized supplementary role in cell volume regulation. Sodium 48-54 solute carrier family 9 member A4 Rattus norvegicus 17-22 7799226-13 1994 Sodium currents (-305 +/- 50 pA pF-1, n = 21) were recorded in 40 mM Na+ with Ni2+ (1 mM) to block Ca2+ currents and with K+ replaced by Cs+. Sodium 0-6 PHD finger protein 12 Mus musculus 32-36 7749388-5 1994 In normotensive rats, we demonstrated that 1) inhibition of NEP potentiates the contribution of kinins to the renal water-sodium metabolism and overcomes the contribution of ANP to that metabolism, 2) nitric oxide participates in the action of kinins, and 3) changes in urinary cGMP excretion do not reflect the changes in plasma ANP, but the changes in nitric oxide, under these conditions. Sodium 122-128 membrane metallo-endopeptidase Rattus norvegicus 60-63 7749388-6 1994 On the other hand, it was also suggested that augmented ANP may contribute mainly to renal water-sodium handling by NEP inhibitor in DOCA-salt rats. Sodium 97-103 membrane metallo-endopeptidase Rattus norvegicus 116-119 8027774-5 1994 Stimulation of PKC by 1-oleoyl-2-acetyl-sn-glycerol (OAG) slows sodium current macroscopic inactivation rate by up to 70% and reduces the peak sodium current as much as 88%. Sodium 64-70 protein kinase C, gamma Rattus norvegicus 15-18 8027774-5 1994 Stimulation of PKC by 1-oleoyl-2-acetyl-sn-glycerol (OAG) slows sodium current macroscopic inactivation rate by up to 70% and reduces the peak sodium current as much as 88%. Sodium 143-149 protein kinase C, gamma Rattus norvegicus 15-18 8106444-0 1994 Overexpressed protein kinase C-delta and -epsilon subtypes in NIH 3T3 cells exhibit differential subcellular localization and differential regulation of sodium-dependent phosphate uptake. Sodium 153-159 protein kinase C, delta Mus musculus 14-49 8106444-8 1994 Zn(2+)-induced overexpression of PKC-delta- and PKC-epsilon-stimulated sodium-dependent phosphate uptake. Sodium 71-77 protein kinase C, delta Mus musculus 33-42 8301360-4 1994 However, voltage-dependent sodium (Na) current density was decreased by androgen treatment of C2 cells and was abolished, even in the absence of androgens, in C2 cells that overexpress the AR. Sodium 27-33 androgen receptor Rattus norvegicus 189-191 22133110-1 1994 Abstract In Table I of the paper Growth hormone responsive dermatosis in three dogs (New Zealand Veterinary Journal 41, 19.5-9, 1993), the units for the following biochemical tests are given in mumol/l, whereas the correct units are mmol/l: blood urea, glucose, cholesterol, calcium, inorganic phosphate, sodium and potassium. Sodium 307-313 somatotropin Canis lupus familiaris 35-49 8281946-0 1993 Formation of a functionally active sodium-translocating hybrid F1F0 ATPase in Escherichia coli by homologous recombination. Sodium 35-41 ATPase Escherichia coli 68-74 8281946-5 1993 The biochemical characterization of this hybrid ATPase revealed high sensitivity to dicyclohexylcarbodiimide as well as strong activation by the addition of sodium ions. Sodium 157-163 ATPase Escherichia coli 48-54 8372830-12 1993 The gene encoding for a cyclophilin-like protein, which is increased in sodium-retaining conditions, is upregulated in the kidneys of nephrotic rats, and the infusion of ANP further increases cyclophilin-like protein mRNA. Sodium 72-78 natriuretic peptide A Rattus norvegicus 170-173 8368393-7 1993 Tonic intrarenal and/or circulating ANG II synthesis of dogs on a normal sodium diet inhibit neurogenic stimulation of renin release, since PRA responses were enhanced after blockade of ANG II. Sodium 73-79 renin Canis lupus familiaris 119-124 9909719-0 1993 Velocity dependence of absolute cross sections for charge capture by Ar7+ from ground-state and excited-state sodium. Sodium 110-116 thyroid hormone receptor alpha Homo sapiens 69-72 8089438-13 1993 Furthermore, although during infusion of AVP sodium excretion increased, blood volumes did not change. Sodium 45-51 vasopressin-neurophysin 2-copeptin Ovis aries 41-44 8441823-5 1993 Results showed that ANF decreased bile flow and the excretion rate of sodium, potassium, chloride, bile acids, cholesterol and proteins. Sodium 70-76 natriuretic peptide A Rattus norvegicus 20-23 8386113-2 1993 The zona glomerulosa level of CYP11B2 mRNA was raised by potassium repletion or sodium restriction and was lowered by potassium depletion or by the administration of deoxycorticosterone, ACTH or dexamethasone. Sodium 80-86 cytochrome P450, family 11, subfamily b, polypeptide 2 Rattus norvegicus 30-37 7992552-6 1993 It is proposed i) that cell production of oncogenic p21ras hinders sodium-dependent transport of anionic amino acids and ii) that the transport alteration impairs the maintenance of cell levels of glutamate in ras-expressing cells. Sodium 67-73 Harvey rat sarcoma virus oncogene Mus musculus 52-58 8430772-0 1993 Tyrosine kinase regulates epithelial sodium transport in A6 cells. Sodium 37-43 TXK tyrosine kinase Homo sapiens 0-15 8382131-9 1993 Changes in fractional excretion of sodium were significantly correlated with those in plasma atrial natriuretic factor and cyclic GMP levels. Sodium 35-41 5'-nucleotidase, cytosolic II Homo sapiens 130-133 8477870-5 1993 (c) Exogenous hypophysial peptides (vasopressin, oxytocin, and alpha-, beta-, and gamma-MSH) stimulate increased potassium (and sodium) excretion. Sodium 128-134 proopiomelanocortin Rattus norvegicus 63-91 8386786-4 1993 This agonistic effect on INa is fully reversed when the holding potential is maintained depolarized above -80 mV as a result of an actual decrease in the sodium conductance and a reversal of the shifts of activation and activation curves. Sodium 154-160 internexin neuronal intermediate filament protein alpha Canis lupus familiaris 25-28 8321362-1 1993 Compared to healthy humans in most patients with cirrhosis and renal sodium and water retention, effects of atrial natriuretic peptide (ANP) on sodium and water excretion are reduced. Sodium 144-150 natriuretic peptide A Rattus norvegicus 108-134 8366986-0 1993 Effect of parathyroid-hormone-related protein on sodium-dependent phosphate transport in renal brush border membrane vesicles in rats. Sodium 49-55 parathyroid hormone-like hormone Rattus norvegicus 10-45 8413787-8 1993 In both the salt-sensitive and the salt-resistant groups a marked increase in the 24-hour urinary excretion of sodium was observed after the kallikrein treatment. Sodium 111-117 kallikrein related peptidase 4 Homo sapiens 141-151 9908925-0 1993 Spin-dependent observables in electron-sodium scattering calculated using the coupled-channel optical method. Sodium 39-45 spindlin 1 Homo sapiens 0-4 1337115-1 1992 The renal kallikrein-kinin system seems to participate in the regulation of blood pressure, control of sodium and water excretion, renal vascular resistance and renin release. Sodium 103-109 kallikrein related peptidase 4 Homo sapiens 10-20 1397781-5 1992 Active kallikrein excretion correlated directly with the reabsorption of sodium in the distal tubule. Sodium 73-79 kallikrein related peptidase 4 Homo sapiens 7-17 1397781-9 1992 The localization of kallikrein in the distal connecting tubule makes it plausible that altered sodium transport in the distal tubule may be a signal to increase generation of kallikrein. Sodium 95-101 kallikrein related peptidase 4 Homo sapiens 20-30 1397781-9 1992 The localization of kallikrein in the distal connecting tubule makes it plausible that altered sodium transport in the distal tubule may be a signal to increase generation of kallikrein. Sodium 95-101 kallikrein related peptidase 4 Homo sapiens 175-185 1400063-1 1992 Increased activity of the renin-angiotensin system may be involved in sodium and water retention during controlled mechanical ventilation (CMV) with positive end-expiratory pressure (PEEP). Sodium 70-76 renin Canis lupus familiaris 26-31 1406597-6 1992 When permanently expressed in mouse fibroblast Ltk- cells, the human clone is able to induce a saturable, time- and sodium-dependent, dopamine uptake. Sodium 116-122 leukocyte tyrosine kinase Mus musculus 47-50 1400260-2 1992 On sodium depletion and captopril administration, the rat showed a marked increase in the adrenal RnBP mRNA level and a slight decrease in the kidney RnBP mRNA level. Sodium 3-9 renin binding protein Rattus norvegicus 98-102 1534598-2 1992 Renal arterial infusion of hANF (99-126) at 50 micrograms/h increased sodium excretion from 99 +/- 30 to 334 +/- 102 (p less than 0.05) in normal animals, and from 77 +/- 31 to 354 +/- 118 mumol/min in hemorrhaged animals. Sodium 70-76 HESX homeobox 1 Homo sapiens 27-31 1659502-17 1991 4) If all the calcium-dependent sodium fluxes were Na-Ca exchange, then calcium flux through the exchanger per beat would be about sevenfold larger than that through the calcium channels. Sodium 32-38 nascent polypeptide associated complex subunit alpha Rattus norvegicus 51-56 1815136-3 1991 A series of cis- and trans-decahydroquinolines with substituents in the 2- and 5-position also exhibit structure-dependent inhibition of carbamylcholine-elicited sodium flux in PC12 cells and all of the decahydroquinolines inhibit binding of the noncompetitive blocking agent [3H]perhydrohistrionicotoxin to muscle-type nicotinic acetylcholine receptor-channels in membranes from Torpedo electroplax. Sodium 162-168 cholinergic receptor nicotinic alpha 2 subunit Rattus norvegicus 320-352 1946375-6 1991 Kinetic analysis of Na/Pi cotransport expressed by NaPi-1/complementary RNA demonstrated characteristics (sodium interaction) similar to those observed in cortical apical membranes. Sodium 106-112 sodium-dependent phosphate transport protein 1 Oryctolagus cuniculus 51-57 1720253-9 1991 Moreover, KGF stimulated sodium uptake by these cells, associated with the maximal increase of protein synthesis. Sodium 25-31 fibroblast growth factor 7 Rattus norvegicus 10-13 1755294-7 1991 A new finding that "more immature infants have higher potassium and lower sodium concentration in RBC" may suggest a potential risk of hyperkalaemia in tiny infants. Sodium 74-80 RNA, 7SL, cytoplasmic 263, pseudogene Homo sapiens 98-102 1656791-4 1991 Infusion of synthetic ANF-(99-126) (at either 10 or 50 micrograms.kg-1.h-1) resulted in a reduced fractional sodium excretion (P less than 0.05) in both compensated rats (0.7 +/- 0.2 and 7.9 +/- 1.6%) and sodium-retaining rats (0.3 +/- 0.1 and 0.5 +/- 0.1%) compared with controls (8.5 +/- 1.2 and 13.7 +/- 2.3% for low and high doses, respectively). Sodium 109-115 natriuretic peptide A Rattus norvegicus 22-25 1656791-4 1991 Infusion of synthetic ANF-(99-126) (at either 10 or 50 micrograms.kg-1.h-1) resulted in a reduced fractional sodium excretion (P less than 0.05) in both compensated rats (0.7 +/- 0.2 and 7.9 +/- 1.6%) and sodium-retaining rats (0.3 +/- 0.1 and 0.5 +/- 0.1%) compared with controls (8.5 +/- 1.2 and 13.7 +/- 2.3% for low and high doses, respectively). Sodium 205-211 natriuretic peptide A Rattus norvegicus 22-25 1804283-5 1991 After the trial period, urinary kallikrein in the active group increased from 0.9 +/- 0.4 U/24 h (normal value greater than 1.2 U/24 h) to 1.6 +/- 1 U/24 h (p less than 0.05); systolic and diastolic blood pressure decreased respectively from 154.6 +/- 13.8 mmHg to 140.3 +/- 12.5 mmHg (p less than 0.01) and from 92.5 +/- 1.5 mmHg to 86 +/- 3.9 mmHg (p less than 0.025); urinary sodium and potassium excretion increased respectively from 96.7 +/- 17 mEq/24 h to 119.1 +/- 32.3 mEq/24 h (p less than 0.05) and from 36.7 +/- 11 mEq/24 h to 43.5 +/- 12.8 mEq/24 h (p less than 0.05). Sodium 379-385 kallikrein related peptidase 4 Homo sapiens 32-42 1661876-5 1991 The voltage-gated sodium current (INa) was recorded from isolated ganglion cells under the voltage-clamp condition using a patch pipette in the whole cell configuration. Sodium 18-24 internexin neuronal intermediate filament protein alpha Homo sapiens 34-37 1883392-0 1991 GLP-1(7-36)amide-stimulated insulin secretion in rat islets is sodium-dependent. Sodium 63-69 glucagon Rattus norvegicus 0-5 1723324-5 1991 However, the maximal sodium currents (INa max) did not depend on temperature adaptation. Sodium 21-27 internexin neuronal intermediate filament protein alpha Homo sapiens 38-41 1682929-5 1991 Sodium transport in these cultured epithelia is thought to result from an increase in [Ca]i, which in turn activates calcium-sensitive potassium channels, so increasing the electrochemical gradient for sodium entry. Sodium 0-6 carbonic anhydrase 1 Homo sapiens 87-91 1682929-5 1991 Sodium transport in these cultured epithelia is thought to result from an increase in [Ca]i, which in turn activates calcium-sensitive potassium channels, so increasing the electrochemical gradient for sodium entry. Sodium 202-208 carbonic anhydrase 1 Homo sapiens 87-91 1655267-0 1991 Endogenous atrial natriuretic factor is involved in the natriuresis following sodium loading in rats with chronic heart failure. Sodium 78-84 natriuretic peptide A Rattus norvegicus 11-36 1655267-2 1991 To address this issue the potential contribution of endogenous atrial natriuretic factor in the renal excretion of a moderate oral sodium load in a rat model of chronic heart failure was studied. Sodium 131-137 natriuretic peptide A Rattus norvegicus 63-88 1655267-7 1991 Atrial natriuretic factor antibody given immediately before sodium loading reduced the natriuretic response (0-4 h period) in infarcted rats from 1270(171) to 805(76) mumol.kg-1 (p less than 0.01) but not in sham operated animals. Sodium 60-66 natriuretic peptide A Rattus norvegicus 0-25 2035653-5 1991 Intrarenal insulin infusion (0.6 mU.kg-1.min-1) for 7 days caused transient decreases in sodium excretion but no significant changes in potassium excretion. Sodium 89-95 insulin Canis lupus familiaris 11-18 2035653-8 1991 These results demonstrate that insulin causes transient decreases in sodium excretion, but chronic intrarenal hyperinsulinemia does not elevate blood pressure in normal dogs. Sodium 69-75 insulin Canis lupus familiaris 31-38 1649865-0 1991 Atrial natriuretic peptide during the elevation in blood pressure induced by sodium restriction. Sodium 77-83 natriuretic peptide A Rattus norvegicus 0-26 1882231-6 1991 In the case of tap water, the observed ranges for salinity, chloride and sodium were 0.7-1.5 ppt, and 280-750 and 140-400 mg l-1, respectively. Sodium 73-79 nuclear RNA export factor 1 Homo sapiens 15-18 1849060-1 1991 Heptanol blocks sodium current (INa) in nerve, but its effects on cardiac INa have not been well characterized. Sodium 16-22 internexin neuronal intermediate filament protein alpha Canis lupus familiaris 32-35 2019995-1 1991 A-4, A-5 and HC-3 are experimental bis tertiary and quaternary amines which have been shown to be potent inhibitors of the sodium-dependent, high affinity choline uptake system. Sodium 123-129 ATPase, H+ transporting, lysosomal V0 subunit A4 Mus musculus 0-3 1989979-3 1991 The largest mRNA induction was observed at day 7 in sodium-depleted rats for P-450(11 beta), with a 4-fold increase, followed by 2.7- and 2.0-fold increases for P-450scc and P-450c21, respectively. Sodium 52-58 cytochrome P450, family 11, subfamily a, polypeptide 1 Rattus norvegicus 161-169 1840285-1 1991 The effect of chronic sodium loading on the level of plasma atrial natriuretic peptide (ANP) and on plasma renin activity (PRA), as well as on the renal excretory function was studied. Sodium 22-28 natriuretic peptide A Rattus norvegicus 60-86 2016905-1 1991 Sodium-dependent amino acid transport of methylaminoisobutyric acid (MeAIB) in a human myelogenous leukemic cell line K562 was inhibited by 30 nM etoposide (VP-16). Sodium 0-6 host cell factor C1 Homo sapiens 157-162 1825126-4 1991 ANF infusion by itself produced a greater increase in urine flow and sodium excretion from the denervated kidney compared to the intact kidney before the administration of AVPX. Sodium 69-75 natriuretic peptide A Rattus norvegicus 0-3 1828542-13 1991 These results suggest that ANP may play a role in sodium homeostasis in rats with reduced renal mass. Sodium 50-56 natriuretic peptide A Rattus norvegicus 27-30 1834955-5 1991 The free form of ANP was inversely correlated with the daily urinary sodium excretion (r = -0.71, p less than 0.001) and plasma albumin (r = -0.83, p less than 0.001), and positively correlated with the daily urinary protein excretion (r = -0.85, p less than 0.001) in both control and nephrotic groups. Sodium 69-75 natriuretic peptide A Rattus norvegicus 17-20 1834955-6 1991 Based on these results, the preferential increase in the free form of ANP in nephrotic rats is considered to be a compensatory phenomenon induced by the decreased renal ability to eliminate sodium and water. Sodium 190-196 natriuretic peptide A Rattus norvegicus 70-73 2210806-5 1990 All SST patients on day 7 of the high sodium diet remained in the SST group on day 14. Sodium 38-44 somatostatin Homo sapiens 4-7 2210806-9 1990 The celiac, superior mesenteric, and renal arteries vasoconstricted with sodium repletion in both SST and SSC patients. Sodium 73-79 somatostatin Homo sapiens 98-101 1981788-5 1990 Compared to naive PC12 cells, K-ras infected PC12 cells had (a) higher activities of acetylcholinesterase and choline acetyltransferase, two enzymes involved in acetylcholine metabolism; (b) enhanced activity of tyrosine hydroxylase, the rate-limiting enzyme in catecholamine biosynthesis; (c) a higher, evoked norepinephrine release; and (d) similar levels of sodium-dependent uptake of both choline and norepinephrine. Sodium 361-367 KRAS proto-oncogene, GTPase Rattus norvegicus 30-35 9904490-0 1990 Spin-dependent electron-impact excitation of sodium. Sodium 45-51 spindlin 1 Homo sapiens 0-4 1975955-3 1990 The transporter encoded by GAT-1 has a high affinity for GABA, is sodium-and chloride-dependent, and is pharmacologically similar to neuronal GABA transporters. Sodium 66-72 solute carrier family 6 member 12 Rattus norvegicus 27-32 2148905-2 1990 Recent investigations in human atrial cells have also demonstrated that atrial natriuretic factor causes a voltage-dependent reduction in sodium channel activity and thus may reduce intracellular calcium via decreased activity of the sodium-calcium exchange mechanism. Sodium 138-144 natriuretic peptide A Rattus norvegicus 72-97 1964893-5 1990 In voltage clamp mode, suppress of sodium current (INa) by ethmozin could be recorded through all the physiological voltage range with slight shift of peak (INa) to the positive voltage. Sodium 35-41 internexin neuronal intermediate filament protein alpha Homo sapiens 51-54 1964893-5 1990 In voltage clamp mode, suppress of sodium current (INa) by ethmozin could be recorded through all the physiological voltage range with slight shift of peak (INa) to the positive voltage. Sodium 35-41 internexin neuronal intermediate filament protein alpha Homo sapiens 157-160 2166501-0 1990 Attenuated glomerular responses to atrial natriuretic factor in low-sodium rats is prevented by theophylline. Sodium 68-74 natriuretic peptide A Rattus norvegicus 35-60 2166501-1 1990 Atrial natriuretic factor administered in the large dose did not change glomerular filtration rate, but it was diuretic in low-sodium rats. Sodium 127-133 natriuretic peptide A Rattus norvegicus 0-25 2166501-2 1990 In response to ANF, excretion of c-GMP was decreased in low-sodium rats in comparison with normal-sodium stimulated c-GMP accumulation in isolated glomeruli was more diminished in low- than normal sodium rats. Sodium 60-66 natriuretic peptide A Rattus norvegicus 15-18 2166501-2 1990 In response to ANF, excretion of c-GMP was decreased in low-sodium rats in comparison with normal-sodium stimulated c-GMP accumulation in isolated glomeruli was more diminished in low- than normal sodium rats. Sodium 98-104 natriuretic peptide A Rattus norvegicus 15-18 2166501-2 1990 In response to ANF, excretion of c-GMP was decreased in low-sodium rats in comparison with normal-sodium stimulated c-GMP accumulation in isolated glomeruli was more diminished in low- than normal sodium rats. Sodium 98-104 natriuretic peptide A Rattus norvegicus 15-18 2166501-3 1990 These results indicate that attenuated glomerular responses to ANF in low-sodium rats might be due to increase of plasma Angiotensin II (Ang II) level, which increases intracellular Ca++ concentration. Sodium 74-80 natriuretic peptide A Rattus norvegicus 63-66 2142862-3 1990 Administration of ANF in incremental doses (5-50 micrograms.kg-1.h-1) to Inactin-anesthetized, sham-operated control rats resulted in dose-dependent increases in urine flow, sodium excretion, and glomerular filtration rate, and significant decreases in mean arterial blood pressure. Sodium 174-180 natriuretic peptide A Rattus norvegicus 18-21 2142862-5 1990 However, chronic oral treatment with the angiotensin-converting-enzyme inhibitor enalapril restored the natriuretic response of sodium-retaining rats with a-v fistula to high doses of ANF. Sodium 128-134 natriuretic peptide A Rattus norvegicus 184-187 2143001-9 1990 The present results reveal that, in ischemic brain edema, ANP may act directly on the central nervous system to inhibit brain water and sodium accumulation. Sodium 136-142 natriuretic peptide A Rattus norvegicus 58-61 2145947-4 1990 In this study, the effect of ANP on the intracranial pressure, brain water content and brain sodium concentration was studied with congenital hydrocephalus rats (HTX strain). Sodium 93-99 natriuretic peptide A Rattus norvegicus 29-32 2141422-15 1990 Finally, the kidneys of HYPOX rats are capable of increasing sodium and water output in response to large doses of exogenous ANF. Sodium 61-67 natriuretic peptide A Rattus norvegicus 125-128 2114483-4 1990 Sodium level in tap water ranged from 100 to 545.9 mg/l, with an average of 309.4 mg/l. Sodium 0-6 nuclear RNA export factor 1 Homo sapiens 16-19 2337610-7 1990 Administration of 1 U parathyroid hormone prior to study resulted in a decrease in sodium-dependent uptake by 40-50% and in pH-dependent uptake (36%) with no change in the respective Km values. Sodium 83-89 parathyroid hormone Sus scrofa 22-41 2337610-8 1990 In conclusion, the antecedent dietary phosphate intake and parathyroid hormone administration appropriately alters phosphate uptake across the brush-border membrane of all three systems, sodium-dependent and pH gradient-stimulated phosphate transport. Sodium 187-193 parathyroid hormone Sus scrofa 59-78 2140017-4 1990 ProANFs-(1-30), (31-67), (79-98), and (99-126) (ANF) increased sodium excretion by 231, 973, 167, and 1,405%, respectively. Sodium 63-69 natriuretic peptide A Rattus norvegicus 3-6 2139545-0 1990 Role of atrial natriuretic peptide in sodium balance in conscious spontaneously hypertensive rats. Sodium 38-44 natriuretic peptide A Rattus norvegicus 8-34 2139545-3 1990 The natriuretic responses to the highest dose of ANP-(99-126) (150 pmol/min) were independent of the rate of fluid infusion but were highly dependent on the sodium intake. Sodium 157-163 natriuretic peptide A Rattus norvegicus 49-52 2139545-7 1990 In conclusion, high sodium intake enhanced the renal responses to exogenous ANP-(99-126) despite increases in endogenous peptide concentrations in conscious SHR. Sodium 20-26 natriuretic peptide A Rattus norvegicus 76-79 2182970-5 1990 System ASC was studied by measuring uptake of alpha-aminoisobutyric acid (AIB) in the presence of 25 mmol/L MeAIB and 25 mmol/L 2-amino-2-norbornane carboxylic acid (BCH) to inhibit uptake by systems A and L. System L activity was defined as sodium-independent uptake of cycloleucine. Sodium 242-248 PYD and CARD domain containing Rattus norvegicus 7-10 1979267-2 1990 The role of prostaglandins and intracellular Ca2+ in regulation of active transepithelial sodium transport in frog skin were studied by examinations of effects of the calcium ionophore A23187 on short-circuit current (SCC) and intracellular voltage. Sodium 90-96 carbonic anhydrase 2 Homo sapiens 45-48 2151754-0 1990 Effect of a chronic infusion of atrial natriuretic peptide on sodium balance in normotensive and two-kidney, one-clip hypertensive rats. Sodium 62-68 natriuretic peptide A Rattus norvegicus 32-58 2151754-4 1990 Sodium excretion fell from 2,536 +/- 60 to 2,047 +/- 86 (p less than 0.001) and 2,211 +/- 96 mu Eq/24 h (p less than 0.05) by days 1 and 2 of ANP administration. Sodium 0-6 natriuretic peptide A Rattus norvegicus 142-145 2151754-5 1990 Furthermore, fractional excretion of sodium intake decreased from 99.1 +/- 1.5 to 81.1 +/- 2.9 (p less than 0.001), 84.1 +/- 2.6 (p less than 0.05) and 85.9 +/- 5.15% (p less than 0.05) by days 1, 2 and 3 of ANP infusion, respectively, returning to basal values thereafter. Sodium 37-43 natriuretic peptide A Rattus norvegicus 208-211 2151754-8 1990 These results strongly suggest that the ANP-induced decrease in MAP might be responsible for the transitory sodium retention observed in 2K-1C hypertensive rats during the administration of the peptide. Sodium 108-114 natriuretic peptide A Rattus norvegicus 40-43 1701375-2 1990 Effects of sodium loading and dehydration on ANP gene expression were investigated in rats. Sodium 11-17 natriuretic peptide A Rattus norvegicus 45-48 1701375-6 1990 Correlation with ANP-mRNA content and the plasma sodium concentration was established. Sodium 49-55 natriuretic peptide A Rattus norvegicus 17-20 2376129-7 1990 In contrast, manipulations of sodium ion concentration, including treatment with ouabain or monensin, depressed elastin production. Sodium 30-36 elastin Homo sapiens 112-119 1977411-3 1990 Somatostatin also induced a significant increase in sodium concentration and a decrease in chloride concentration in the gastric juice. Sodium 52-58 somatostatin Homo sapiens 0-12 1983007-7 1990 Intravenous infusion of atrial natriuretic factor produced hypotension, bradycardia and an increase in sodium and water excretion. Sodium 103-109 natriuretic peptide A Rattus norvegicus 24-49 2267363-3 1990 In populations studied the arterial blood pressure (CTK) was influenced by: age, sex, education, family history with regard to the circulatory system, the alcohol intake, smoking, heart action frequency the Quetelet coefficient value, triglyceride concentration and daily sodium intake. Sodium 272-278 megakaryocyte-associated tyrosine kinase Homo sapiens 52-55 33782042-7 2021 These novel fluorescent probes were able to block substrate transport in a concentration-dependent manner of NTCP, OATP1B1, OATP1B3, OATP2B1, BSEP and intestinal apical sodium-dependent bile salt transporter (ASBT). Sodium 169-175 solute carrier family 10 member 2 Homo sapiens 209-213 33774271-1 2021 The voltage-gated sodium channel Nav1.7 can be considered as a promising target for the treatment of pain. Sodium 18-24 sodium voltage-gated channel alpha subunit 9 Homo sapiens 33-39 33822013-1 2021 Clinical trials indicate that sodium-glucose co-transporter 2 inhibitors (SGLT2i) improve kidney function, yet, the molecular regulation of SGLT2 expression is incompletely understood. Sodium 30-36 solute carrier family 5 (sodium/glucose cotransporter), member 2 Mus musculus 74-79 33800499-2 2021 The discovery of the association between CFTR and the hyperactive epithelial sodium channel (ENaC) has raised the question of the influence of ENaC on the clinical CF phenotype. Sodium 77-83 cystic fibrosis transmembrane conductance regulator Mus musculus 41-45 33800031-1 2021 Gating modifier toxins (GMTs) isolated from venomous organisms such as Protoxin-II (ProTx-II) and Huwentoxin-IV (HwTx-IV) that inhibit the voltage-gated sodium channel NaV1.7 by binding to its voltage-sensing domain II (VSDII) have been extensively investigated as non-opioid analgesics. Sodium 153-159 sodium voltage-gated channel alpha subunit 9 Homo sapiens 168-174 26337786-0 2015 Sodium homeostasis is preserved in a global 11beta-hydroxysteroid dehydrogenase type 1 knockout mouse model. Sodium 0-6 hydroxysteroid 11-beta dehydrogenase 1 Mus musculus 44-86 26337786-8 2015 Any effect of renal 11betaHSD1 on sodium homeostasis is subtle. Sodium 34-40 hydroxysteroid 11-beta dehydrogenase 1 Mus musculus 20-30 26337786-18 2015 We conclude that any effect of 11betaHSD1 on renal sodium excretion is subtle. Sodium 51-57 hydroxysteroid 11-beta dehydrogenase 1 Mus musculus 31-41 34467600-1 2022 Long-chain scorpion toxin AaH-II isolated from Androctonus australis Hector can selectively inhibit mammalian voltage-gated sodium ion channel Nav 1.7 responsible for pain sensation. Sodium 124-130 sodium voltage-gated channel alpha subunit 9 Homo sapiens 143-150 34979445-15 2022 Sodium channel blockers were effective in treating seizures for some SCN8A-related disorders however may not be relevant to the mutant location. Sodium 0-6 sodium voltage-gated channel alpha subunit 8 Homo sapiens 69-74 34780780-0 2022 Probing the impact of temperature and substrates on the conformational dynamics of the Neurotransmitter:Sodium symporter LeuT. Sodium 104-110 Leucine transport, high Homo sapiens 121-125 34962430-12 2022 SIGNIFICANCE: Insulin-mediated regulation of Nedd4-2 might impact on inner ear sodium homeostasis with implications for diabetes-induced inner ear damage. Sodium 79-85 NEDD4 like E3 ubiquitin protein ligase Homo sapiens 45-52 34852210-3 2022 PON2 and PON3 are expressed in the aldosterone-sensitive distal nephron of the kidney and have been shown to negatively regulate expression of the epithelial sodium channel (ENaC), a trimeric ion channel that orchestrates salt and water homeostasis. Sodium 158-164 paraoxonase 2 Homo sapiens 0-4 34852210-3 2022 PON2 and PON3 are expressed in the aldosterone-sensitive distal nephron of the kidney and have been shown to negatively regulate expression of the epithelial sodium channel (ENaC), a trimeric ion channel that orchestrates salt and water homeostasis. Sodium 158-164 paraoxonase 3 Homo sapiens 9-13 34237339-10 2022 Chronic genetic IL-17A-driven psoriasis mouse models underlined the role of IL-17A in dermal sodium accumulation and inflammation. Sodium 93-99 interleukin 17A Mus musculus 16-22 34237339-10 2022 Chronic genetic IL-17A-driven psoriasis mouse models underlined the role of IL-17A in dermal sodium accumulation and inflammation. Sodium 93-99 interleukin 17A Mus musculus 76-82 34716231-0 2021 Hyperexcitability and pharmacological responsiveness of cortical neurons derived from human iPSCs carrying epilepsy-associated sodium channel Nav1.2-L1342P genetic variant. Sodium 127-133 sodium voltage-gated channel alpha subunit 2 Homo sapiens 142-148 34716231-2 2021 Voltage-gated sodium channel Nav1.2, encoded by gene SCN2A, is predominantly expressed in the pyramidal excitatory neurons and supports action potential firing. Sodium 14-20 sodium voltage-gated channel alpha subunit 2 Homo sapiens 29-35 34716231-2 2021 Voltage-gated sodium channel Nav1.2, encoded by gene SCN2A, is predominantly expressed in the pyramidal excitatory neurons and supports action potential firing. Sodium 14-20 sodium voltage-gated channel alpha subunit 2 Homo sapiens 53-58 34874093-2 2022 Nav1.2 is a critical voltage-gated sodium channel of the central nervous system. Sodium 35-41 sodium voltage-gated channel alpha subunit 2 Homo sapiens 0-6 34884836-0 2021 Zfhx3 Transcription Factor Represses the Expression of SCN5A Gene and Decreases Sodium Current Density (INa). Sodium 80-86 internexin neuronal intermediate filament protein alpha Homo sapiens 104-107 34856559-0 2022 Association of Genetic Variants of Klotho with BP Responses to Dietary Sodium or Potassium Intervention and Long-Term BP Progression. Sodium 71-77 klotho Homo sapiens 35-41 34856559-12 2022 CONCLUSIONS: Common variants of the KL gene might modify individual BP sensitivity to sodium or potassium and influence the long-term progression of BP, suggesting a potential role in the development of salt-sensitive hypertension. Sodium 86-92 klotho Homo sapiens 36-38 34272843-3 2021 Therefore, we studied whether creatine kinase (CK), an ATP-regenerating enzyme that enhances vascular contractility and sodium retention, could serve as a more proximate causal parameter of therapy failure than race/ancestry. Sodium 120-126 cytidine/uridine monophosphate kinase 1 Homo sapiens 30-45 34272843-3 2021 Therefore, we studied whether creatine kinase (CK), an ATP-regenerating enzyme that enhances vascular contractility and sodium retention, could serve as a more proximate causal parameter of therapy failure than race/ancestry. Sodium 120-126 cytidine/uridine monophosphate kinase 1 Homo sapiens 47-49 34852780-1 2021 BACKGROUND: Non-dystrophic myotonias (NDMs) comprise muscle chloride and sodium channelopathies due to genetic defects of the CLCN1- and SCN4A-channels. Sodium 73-79 chloride voltage-gated channel 1 Homo sapiens 126-131 33427574-2 2021 The sodium channel subtype Nav1.7 is critical for the transmission of pain-related signaling, with gain-of-function mutations in Nav1.7 resulting in various painful pathologies. Sodium 4-10 sodium voltage-gated channel alpha subunit 9 Homo sapiens 27-33 33427574-2 2021 The sodium channel subtype Nav1.7 is critical for the transmission of pain-related signaling, with gain-of-function mutations in Nav1.7 resulting in various painful pathologies. Sodium 4-10 sodium voltage-gated channel alpha subunit 9 Homo sapiens 129-135 33487118-1 2021 Mutations in the voltage-gated sodium channel Nav1.7 are linked to human pain. Sodium 31-37 sodium voltage-gated channel alpha subunit 9 Homo sapiens 46-52 34375480-9 2021 The Ang (1-7) induced increases in sodium and water excretion were impaired in the SHR group in the context of an unstimulated RAS. Sodium 35-41 angiogenin Rattus norvegicus 4-12 34847423-1 2021 SCN8A, encoding the voltage-gated sodium channel subunit NaV1.6, has been associated with a wide spectrum of neuropsychiatric disorders. Sodium 34-40 sodium voltage-gated channel alpha subunit 8 Homo sapiens 0-5 34808247-2 2022 Previously, we and others reported diffuse distribution of Nav1.2, a voltage-gated sodium channel alpha-subunit encoded by the SCN2A gene, on unmyelinated striatal projection fibers. Sodium 83-89 sodium voltage-gated channel alpha subunit 2 Homo sapiens 59-65 34808247-2 2022 Previously, we and others reported diffuse distribution of Nav1.2, a voltage-gated sodium channel alpha-subunit encoded by the SCN2A gene, on unmyelinated striatal projection fibers. Sodium 83-89 sodium voltage-gated channel alpha subunit 2 Homo sapiens 127-132 34869624-1 2021 Background: Uromodulin, also named Tamm Horsfall protein, has been associated with renal function and regulation of sodium homeostasis. Sodium 116-122 uromodulin Homo sapiens 12-22 34799533-1 2021 ABSTRACT: Mutations in the alpha subunit of voltage-gated sodium channel 1.7 (NaV1.7), encoded by SCN9A gene, play an important role in the regulation of nociception, and can lead to a wide range of clinical outcomes, ranging from extreme pain syndromes to congenital inability to experience pain. Sodium 58-64 sodium voltage-gated channel alpha subunit 9 Homo sapiens 78-84 34799533-1 2021 ABSTRACT: Mutations in the alpha subunit of voltage-gated sodium channel 1.7 (NaV1.7), encoded by SCN9A gene, play an important role in the regulation of nociception, and can lead to a wide range of clinical outcomes, ranging from extreme pain syndromes to congenital inability to experience pain. Sodium 58-64 sodium voltage-gated channel alpha subunit 9 Homo sapiens 98-103 34544834-10 2021 Physiological recordings from SST interneurons show that SCN8A mutations lead to an elevated persistent sodium current which drives initial hyperexcitability, followed by premature action potential failure due to depolarization block. Sodium 104-110 somatostatin Homo sapiens 30-33 34544834-10 2021 Physiological recordings from SST interneurons show that SCN8A mutations lead to an elevated persistent sodium current which drives initial hyperexcitability, followed by premature action potential failure due to depolarization block. Sodium 104-110 sodium voltage-gated channel alpha subunit 8 Homo sapiens 57-62 34665704-5 2021 Stimulated PG salivary sodium levels correlated with the degree of CD45+ lymphocytic cell infiltrate in the parotid glands (r=0.69, p<0.001), and even more strongly so with infiltrating CD20+ B cells (r=0.73, p<0.0001). Sodium 23-29 protein tyrosine phosphatase receptor type C Homo sapiens 67-71 34689571-1 2021 BACKGROUND: Animal models implicate FGF-23 (fibroblast growth factor-23) as a direct contributor to adverse cardiorenal interactions such as sodium avidity, diuretic resistance, and neurohormonal activation, but this has not been conclusively demonstrated in humans. Sodium 141-147 fibroblast growth factor 23 Homo sapiens 36-42 34689571-1 2021 BACKGROUND: Animal models implicate FGF-23 (fibroblast growth factor-23) as a direct contributor to adverse cardiorenal interactions such as sodium avidity, diuretic resistance, and neurohormonal activation, but this has not been conclusively demonstrated in humans. Sodium 141-147 fibroblast growth factor 23 Homo sapiens 44-71 34171450-9 2021 IL-10 was negatively associated with BUN (r = -0.39,p = 0.07), creatinine (r = -0.35, p = 0.002), sodium (r = -0.45, p = 0.03), and potassium (r = -0.68, p = 0.003). Sodium 98-104 interleukin 10 Homo sapiens 0-5 34464882-3 2021 Na+/H+ exchanger 3 (NHE3), the main exchanger of electroneutral sodium in intestinal epithelial cells, is closely associated with the occurrence of diarrhea. Sodium 64-70 solute carrier family 9 member A3 Homo sapiens 0-18 34464882-3 2021 Na+/H+ exchanger 3 (NHE3), the main exchanger of electroneutral sodium in intestinal epithelial cells, is closely associated with the occurrence of diarrhea. Sodium 64-70 solute carrier family 9 member A3 Homo sapiens 20-24 34827446-9 2021 Other potential therapeutic strategies include targeting macrophages, lipid metabolism, and Nav1.8 sodium channel in demyelinating CMT and the P2X7 receptor, which regulates calcium influx into Schwann cells, in CMT1A. Sodium 99-105 sodium voltage-gated channel alpha subunit 10 Homo sapiens 92-98 34686334-7 2021 Our data indicate that p38 regulates cell volumes through the sodium-potassium-chloride cotransporter NKCC1. Sodium 62-68 p38b MAP kinase Drosophila melanogaster 23-26 34343486-10 2021 Thus, KLHL2/RhoBTB1/KLHL3 inactivation in the aortic tissues and kidney is a result of excessive activation of neddylation in hyperglycemia and hyperinsulinemia, which affects vascular tone and sodium reabsorption. Sodium 194-200 kelch-like 2, Mayven Mus musculus 6-11 34343486-10 2021 Thus, KLHL2/RhoBTB1/KLHL3 inactivation in the aortic tissues and kidney is a result of excessive activation of neddylation in hyperglycemia and hyperinsulinemia, which affects vascular tone and sodium reabsorption. Sodium 194-200 kelch-like 3 Mus musculus 20-25 34607551-2 2022 In the last decade, various coding and noncoding sequence variations of voltage-gated sodium channels SCN2A have been identified in patients with seizures, implying their genetic base. Sodium 86-92 sodium voltage-gated channel alpha subunit 2 Homo sapiens 102-107 34746693-0 2021 SLO2.1/NALCN a sodium signaling complex that regulates uterine activity. Sodium 15-21 potassium sodium-activated channel subfamily T member 2 Homo sapiens 0-6 34416509-5 2021 Moreover, these compounds" selectivity was investigated on sodium channels Nav1.2, Nav1.4 and Nav1.5 and calcium channels Cav3.1-Cav3.3. Sodium 59-65 sodium voltage-gated channel alpha subunit 2 Homo sapiens 75-81 34223773-1 2021 PURPOSE: Liddle syndrome is a hereditary form of arterial hypertension caused by mutations in the genes coding of the epithelial sodium channel - SCNN1A, SCNN1B and SCNN1G. Sodium 129-135 sodium channel epithelial 1 subunit gamma Homo sapiens 165-171 34223773-7 2021 RESULTS: We identified a novel mutation in the beta-subunit of an epithelial sodium channel coded by the SCNN1B gene, causing the nonsense mutation in the protein sequence p.Tyr604*. Sodium 77-83 sodium channel epithelial 1 subunit beta Homo sapiens 105-111 34223773-17 2021 We found a new mutation of the SCNN1B gene which encodes the beta-subunit of the epithelial sodium channel. Sodium 92-98 sodium channel epithelial 1 subunit beta Homo sapiens 31-37 34658797-1 2021 In the late "90, Dr. Indira Raman, at the time a postdoctoral fellow with Dr. Bruce Bean, at Harvard University, identified a new type of sodium current, flowing through the channels that reopens when the membrane is repolarized. Sodium 138-144 brain expressed associated with NEDD4 1 Homo sapiens 84-88 34528656-0 2021 Ultrahigh-energy sodium ion capacitors enabled by the enhanced intercalation pseudocapacitance of self-standing Ti2Nb2O9/CNF anodes. Sodium 17-23 NPHS1 adhesion molecule, nephrin Homo sapiens 121-124 34528656-1 2021 In order to increase the capacity and improve the sluggish Na+-reaction kinetics of anodes as sodium ion capacitors (SICs), a Ti2Nb2O9/CNF self-standing film electrode comprised of Ti2Nb2O9 nanosheets and carbon nanofibers has been fabricated via electrospinning HTiNbO5 nanosheets with PAN and subsequent carbonization treatment. Sodium 94-100 NPHS1 adhesion molecule, nephrin Homo sapiens 135-138 34389319-0 2021 The insecticide deltamethrin enhances sodium channel slow inactivation of human Nav1.9, Nav1.8 and Nav1.7. Sodium 38-44 sodium voltage-gated channel alpha subunit 10 Homo sapiens 88-94 34389319-0 2021 The insecticide deltamethrin enhances sodium channel slow inactivation of human Nav1.9, Nav1.8 and Nav1.7. Sodium 38-44 sodium voltage-gated channel alpha subunit 9 Homo sapiens 99-105 34630451-2 2021 SOS3/CBL4 is a core component of the SOS pathway that senses calcium signaling of salinity stress to activate and recruit the protein kinase SOS2/CIPK24 to the plasma membrane to trigger sodium efflux by the Na/H exchanger SOS1/NHX7. Sodium 187-193 Protein kinase superfamily protein Arabidopsis thaliana 141-145 34630451-2 2021 SOS3/CBL4 is a core component of the SOS pathway that senses calcium signaling of salinity stress to activate and recruit the protein kinase SOS2/CIPK24 to the plasma membrane to trigger sodium efflux by the Na/H exchanger SOS1/NHX7. Sodium 187-193 Protein kinase superfamily protein Arabidopsis thaliana 146-152 34472363-1 2021 Background Sodium-calcium (Ca2+) exchanger isoform 1 (NCX1) is the dominant Ca2+ efflux mechanism in cardiomyocytes and is critical to maintaining Ca2+ homeostasis during excitation-contraction coupling. Sodium 11-17 solute carrier family 8 (sodium/calcium exchanger), member 1 Mus musculus 54-58 34397047-1 2021 A cyclocyanine (CC)-based organic small molecule two-photon (TP) fluorescent probe (CCNa1) was developed for mitochondrial sodium ion sensing. Sodium 123-129 cyclin A1 Mus musculus 84-89 34489488-6 2021 At 1 week after MI, cardiac sodium channel gene (Scn5a) transcript was reduced in WT but not in KO hearts, consistent with previous studies showing Scn5a inhibition by Wnt/beta-catenin signaling. Sodium 28-34 sodium channel, voltage-gated, type V, alpha Mus musculus 49-54 34489488-6 2021 At 1 week after MI, cardiac sodium channel gene (Scn5a) transcript was reduced in WT but not in KO hearts, consistent with previous studies showing Scn5a inhibition by Wnt/beta-catenin signaling. Sodium 28-34 catenin (cadherin associated protein), beta 1 Mus musculus 172-184 34564625-3 2021 GTx1-15 is an ICK peptide that inhibits the voltage-dependent calcium channel Cav3.1 and the voltage-dependent sodium channels Nav1.3 and Nav1.7. Sodium 111-117 sodium voltage-gated channel alpha subunit 9 Homo sapiens 138-144 34418703-3 2021 Molecules Nav1.6 sodium channel, Brain-derived Neurotrophic Factor, Catechol-O-methyltransferase and Guanosine Triphosphate Cyclohydrolase 1 have been involved in mechanisms that underlie pain and neurological conditions. Sodium 17-23 sodium voltage-gated channel alpha subunit 8 Homo sapiens 10-16 34481319-0 2021 Correction: Phosphorylation of a chronic pain mutation in the voltage-gated sodium channel Nav1.7 increases voltage sensitivity. Sodium 76-82 sodium voltage-gated channel alpha subunit 9 Homo sapiens 91-97 34287911-5 2021 ABSTRACT: Mutations in voltage gated sodium (NaV ) channel genes, including SCN2A (encoding NaV 1.2), are associated with diverse neurodevelopmental disorders with or without epilepsy that present clinically with varying severity, age-of-onset, and pharmacoresponsiveness. Sodium 37-43 sodium voltage-gated channel alpha subunit 2 Homo sapiens 76-81 34287911-5 2021 ABSTRACT: Mutations in voltage gated sodium (NaV ) channel genes, including SCN2A (encoding NaV 1.2), are associated with diverse neurodevelopmental disorders with or without epilepsy that present clinically with varying severity, age-of-onset, and pharmacoresponsiveness. Sodium 37-43 sodium voltage-gated channel alpha subunit 2 Homo sapiens 92-99 34471132-4 2021 The Na+ selectivity of the artificial sodium-selective ionic device reached 15 against K + , which is comparable to the biological counterpart, 523 against Ca2 + , which is nearly two orders of magnitude higher than the biological one, and 1128 against Mg2 + . Sodium 38-44 carbonic anhydrase 2 Homo sapiens 156-159 34353676-4 2021 In this review we describe the identification of a new epileptic encephalopathy caused by a de novo mutation in the SCN8A gene, which encodes for NaV1.6, a vital sodium channel in the central nervous system. Sodium 162-168 sodium voltage-gated channel alpha subunit 8 Homo sapiens 116-121 34353676-8 2021 Gain-of-function of the Nav1.6 channel predicts effectiveness of sodium channel-blocking agents in the treatment of seizures, which has been corroborated by clinical experience. Sodium 65-71 sodium voltage-gated channel alpha subunit 8 Homo sapiens 24-30 34436362-5 2021 (2) Methods and Results: We used databases ClinVar, Humsavar, gnomAD, and Ensembl to compose a dataset of pathogenic/likely pathogenic and benign variants of hCav1.2 and its 20 paralogues: voltage-gated sodium and calcium channels. Sodium 203-209 calcium voltage-gated channel subunit alpha1 C Homo sapiens 158-165 34348157-0 2021 Paradoxical hyperexcitability from NaV1.2 sodium channel loss in neocortical pyramidal cells. Sodium 42-48 sodium voltage-gated channel alpha subunit 2 Homo sapiens 35-41 34348157-1 2021 Loss-of-function variants in the gene SCN2A, which encodes the sodium channel NaV1.2, are strongly associated with autism spectrum disorder and intellectual disability. Sodium 63-69 sodium voltage-gated channel alpha subunit 2 Homo sapiens 38-43 34414225-8 2021 Additionally, the phosphorylation levels of three membrane proteins, the zinc transporter SLC39A7, the sodium-dependent neutral amino acid transporters SLC1A5 and SLC38A7, and three translation initiation factors, eukaryotic initiation factor (eIF)5B, eIF4G, and eIF3C, were positively regulated by amino acid signals. Sodium 103-109 solute carrier family 1 member 5 Homo sapiens 152-158 34288161-0 2021 Ti3 C2 Tx MXene Conductive Layers Supported Bio-Derived Fex -1 Sex /MXene/Carbonaceous Nanoribbons for High-Performance Half/Full Sodium-Ion and Potassium-Ion Batteries. Sodium 130-136 stabilin 1 Homo sapiens 56-62 34288161-2 2021 In this work, a novel Fex -1 Sex heterostructure is prepared on fungus-derived carbon matrix encapsulated by 2D Ti3 C2 Tx MXene highly conductive layers, which exhibits high specific sodium ion (Na+ ) and potassium ion (K+ ) storage capacities of 610.9 and 449.3 mAh g-1 at a current density of 0.1 A g-1 , respectively, and excellent capacity retention at high charge-discharge rates. Sodium 183-189 stabilin 1 Homo sapiens 22-28 34335171-8 2021 In addition, the wild-type (WT) and mutated p. Cys1339Arg were assessed in HEK293 cells expressing Nav1.7, and the results showed that p. Cys1339Arg almost abolished the Nav1.7 sodium current. Sodium 177-183 sodium voltage-gated channel alpha subunit 9 Homo sapiens 170-176 34237901-1 2021 The dopamine transporter utilizes the transmembrane sodium gradient to mediate reuptake of dopamine from the extracellular space. Sodium 52-58 solute carrier family 6 member 3 Homo sapiens 4-24 35577326-4 2022 Increases in serum FGF23 levels during growth were associated with the up- and down-regulation of the renal expression of Cyp24a1 encoding vitamin D-24-hydroxylase and Slc34a3 encoding the type IIc sodium/phosphate (Na+/Pi) co-transporter, respectively, suggesting an enhancement in the FGF23-mediated bone-kidney axis from youth to adulthood. Sodium 198-204 fibroblast growth factor 23 Mus musculus 19-24 35436748-1 2022 The voltage-gated sodium channel Nav1.7 is an attractive target for the treatment of pain based on the high level of target validation with genetic evidence linking Nav1.7 to pain in humans. Sodium 18-24 sodium voltage-gated channel alpha subunit 9 Homo sapiens 33-39 35436748-1 2022 The voltage-gated sodium channel Nav1.7 is an attractive target for the treatment of pain based on the high level of target validation with genetic evidence linking Nav1.7 to pain in humans. Sodium 18-24 sodium voltage-gated channel alpha subunit 9 Homo sapiens 165-171 35436748-6 2022 ABBV-318 also inhibited Nav1.8, another sodium channel isoform that is an active target for the development of new pain treatments. Sodium 40-46 sodium voltage-gated channel alpha subunit 10 Homo sapiens 24-30 35114252-4 2022 Our data demonstrates intrinsic differences between atrial and ventricular cardiac voltage-gated sodium currents (INa), leading to reduced maximum upstroke velocity of action potential and slower conduction, in left atria compared to ventricle. Sodium 97-103 internexin neuronal intermediate filament protein alpha Homo sapiens 114-117 35413129-0 2022 Non-canonical endogenous expression of voltage-gated sodium channel NaV1.7 subtype by the TE671 rhabdomyosarcoma cell line. Sodium 53-59 sodium voltage-gated channel alpha subunit 9 Homo sapiens 68-74 35413129-14 2022 Abstract figure legend Phase contrast image of undifferentiated TE671 cells and the experimental approaches used to confirm dominant expression of the NaV1.7 subtype of voltage-gated sodium channels. Sodium 183-189 sodium voltage-gated channel alpha subunit 9 Homo sapiens 151-157 35499203-0 2022 Bean Pod-Like SbSn/N-Doped Carbon Fibers toward a Binder Free, Free-Standing, and High-Performance Anode for Sodium-Ion Batteries. Sodium 109-115 brain expressed associated with NEDD4 1 Homo sapiens 0-4 35482723-2 2022 The NALCN/UNC80/UNC79 complex is a non-selective channel that allows inward flow of sodium and other cations. Sodium 84-90 Protein unc-80 Caenorhabditis elegans 10-15 35482723-2 2022 The NALCN/UNC80/UNC79 complex is a non-selective channel that allows inward flow of sodium and other cations. Sodium 84-90 Uncoordinated protein 79 Caenorhabditis elegans 16-21 35388287-8 2022 TR rats also showed a decrease in intestinal BA reabsorption due to reduced ileal sodium/bile acid cotransporter (Asbt) expression. Sodium 82-88 solute carrier family 10 member 2 Rattus norvegicus 114-118 35328671-0 2022 Description of Osmolyte Pathways in Maturing Mdx Mice Reveals Altered Levels of Taurine and Sodium/Myo-Inositol Co-Transporters. Sodium 92-98 synaptopodin 2 Mus musculus 99-102 35110381-1 2022 ATP1A1 encodes the alpha1 subunit of the sodium-potassium ATPase, an electrogenic cation pump highly expressed in the nervous system. Sodium 41-47 ATPase Na+/K+ transporting subunit alpha 1 Homo sapiens 0-6 35114589-1 2022 The isoform 2 of sodium-calcium exchanger family (NCX2) is selectively expressed in neuronal and glial cells where it participates in Ca2+-clearance following neuronal depolarization, synaptic plasticity, hippocampal-dependent learning and memory consolidation processes. Sodium 17-23 solute carrier family 8 member A2 Rattus norvegicus 50-54 35167877-1 2022 mu-Conotoxins are components of cone snail venom, well-known for their analgesic activity through potent inhibition of voltage-gated sodium channel (NaV) subtypes, including NaV1.7. Sodium 133-139 sodium voltage-gated channel alpha subunit 9 Homo sapiens 174-180 35195262-2 2022 Fibroblast Growth Factor 13 (FGF13) encodes an intracellular protein involved in microtubule stabilization and regulation of voltage-gated sodium channels (VGSCs) function. Sodium 139-145 fibroblast growth factor 13 Homo sapiens 0-27 35195262-2 2022 Fibroblast Growth Factor 13 (FGF13) encodes an intracellular protein involved in microtubule stabilization and regulation of voltage-gated sodium channels (VGSCs) function. Sodium 139-145 fibroblast growth factor 13 Homo sapiens 29-34 35115491-0 2022 Carbon-coated MoS1.5Te0.5 nanocables for efficient sodium-ion storage in non-aqueous dual-ion batteries. Sodium 51-57 MOS proto-oncogene, serine/threonine kinase Homo sapiens 14-17 35372746-4 2022 This study documents weekly sodium and chloride concentrations in municipal tap water from three municipalities within the Philadelphia metropolitan area during winter 2018-2019 (November through March). Sodium 28-34 nuclear RNA export factor 1 Homo sapiens 76-79 35061048-1 2022 Shroom is a family of related proteins linked to the actin cytoskeleton, and one of them, xShroom1, is constitutively expressed in Xenopus laevis oocytes which is required for the expression of the epithelial sodium channel (ENaC). Sodium 209-215 shroom family member 1 L homeolog Xenopus laevis 90-98 35163352-12 2022 In LECs, high sodium reduced phosphorylated NKCC1 and SPAK, an upstream activating kinase of NKCC1, and eNOS, a downstream effector of lymphatic contractility. Sodium 14-20 serine threonine kinase 39 Rattus norvegicus 54-58 35163352-12 2022 In LECs, high sodium reduced phosphorylated NKCC1 and SPAK, an upstream activating kinase of NKCC1, and eNOS, a downstream effector of lymphatic contractility. Sodium 14-20 nitric oxide synthase 3 Rattus norvegicus 104-108 35163352-14 2022 High sodium within the renal interstitium following proteinuric injury is associated with impaired renal lymphatic pumping that may, in part, involve the SPAK-NKCC1-eNOS pathway, which may contribute to sodium retention and reduce lymphatic responsiveness to furosemide. Sodium 5-11 serine threonine kinase 39 Rattus norvegicus 154-158 35163352-14 2022 High sodium within the renal interstitium following proteinuric injury is associated with impaired renal lymphatic pumping that may, in part, involve the SPAK-NKCC1-eNOS pathway, which may contribute to sodium retention and reduce lymphatic responsiveness to furosemide. Sodium 5-11 nitric oxide synthase 3 Rattus norvegicus 165-169 35163352-14 2022 High sodium within the renal interstitium following proteinuric injury is associated with impaired renal lymphatic pumping that may, in part, involve the SPAK-NKCC1-eNOS pathway, which may contribute to sodium retention and reduce lymphatic responsiveness to furosemide. Sodium 203-209 serine threonine kinase 39 Rattus norvegicus 154-158 35163352-14 2022 High sodium within the renal interstitium following proteinuric injury is associated with impaired renal lymphatic pumping that may, in part, involve the SPAK-NKCC1-eNOS pathway, which may contribute to sodium retention and reduce lymphatic responsiveness to furosemide. Sodium 203-209 nitric oxide synthase 3 Rattus norvegicus 165-169 34993764-8 2022 We further revealed that after Lrh-1 overexpression in Hu sheep granulosa cells, the expression of the pro-apoptotic gene Bax decreased significantly, while that of the anti-apoptotic gene Bcl-2 increased significantly, as well as the sodium peptide system. Sodium 235-241 nuclear receptor subfamily 5 group A member 2 Ovis aries 31-36 35041802-2 2022 This medication"s new phosphate lowering mechanism of action reduces intestinal phosphate absorption predominantly through reduction of passive paracellular phosphate flux by inhibition of the sodium/hydrogen exporter isoform 3 (NHE3). Sodium 193-199 solute carrier family 9 member A3 Homo sapiens 229-233 2532962-2 1989 Intracerebroventricular (IVT) administration of rat atrial natriuretic factor (ANF) (99-126) to conscious male hydrated rats induces a dose-dependent increase in urine and sodium excretion. Sodium 172-178 natriuretic peptide A Rattus norvegicus 52-77 2532962-2 1989 Intracerebroventricular (IVT) administration of rat atrial natriuretic factor (ANF) (99-126) to conscious male hydrated rats induces a dose-dependent increase in urine and sodium excretion. Sodium 172-178 natriuretic peptide A Rattus norvegicus 79-82 2548762-0 1989 Enkephalinase inhibition increases plasma atrial natriuretic peptide levels, glomerular filtration rate, and urinary sodium excretion in rats with reduced renal mass. Sodium 117-123 membrane metallo-endopeptidase Rattus norvegicus 0-13 2548385-4 1989 At pHo = 7.4, proton extrusion was stimulated by extracellular sodium with a K1/2 = 58 +/- 16 mM and a maximal rate of recovery of 55 +/- 7 mmol/(1 cell H2O.min). Sodium 63-69 keratin 1 Rattus norvegicus 77-86 2560911-13 1989 In rats immunized against ANP (Greenwald et al, 1988), although the ability to excrete an acute saline load was impaired, long-term sodium balance was normal, suggesting that the rats were able to compensate for the absence of ANP. Sodium 132-138 natriuretic peptide A Rattus norvegicus 26-29 2550106-4 1989 In SK-N-SH cell membranes, the ability of sodium to promote regulation of [125I]beta h-endorphin binding by GTP was mimicked by the monovalent cations lithium and potassium, but not by the divalent cations magnesium, calcium, or manganese. Sodium 42-48 hedgehog acyltransferase Homo sapiens 3-7 2570368-8 1989 These results indicate that methylxanthines can potentiate the renin response to a reduction in renal perfusion pressure most likely by directly affecting the juxtaglomerular cells; however, since increased sodium delivery to the macula densa inhibits renin release, the extent to which methylxanthines affect the renin response to renal artery hypotension depends on how vigorous the diuretic response is to a given methylxanthine. Sodium 207-213 renin Canis lupus familiaris 252-257 2570368-8 1989 These results indicate that methylxanthines can potentiate the renin response to a reduction in renal perfusion pressure most likely by directly affecting the juxtaglomerular cells; however, since increased sodium delivery to the macula densa inhibits renin release, the extent to which methylxanthines affect the renin response to renal artery hypotension depends on how vigorous the diuretic response is to a given methylxanthine. Sodium 207-213 renin Canis lupus familiaris 252-257 2533261-4 1989 In the absence of indomethacin AVP infusion induced dose-related increases in sodium output that were positively correlated with increases in mean arterial blood pressure (MAP) and plasma atrial natriuretic factor (ANF) immunoreactivity. Sodium 78-84 natriuretic peptide A Rattus norvegicus 215-218 2535285-8 1989 During increased sodium intake, plasma ANP levels increased in sham-operated controls but not in rats with heart failure. Sodium 17-23 natriuretic peptide A Rattus norvegicus 39-42 2535285-9 1989 Thus, sodium loading, as compared with cardiac insufficiency, appears to be a weak stimulus for ANP release in rats. Sodium 6-12 natriuretic peptide A Rattus norvegicus 96-99 2524397-3 1989 ANF-induced increases in sodium, chloride and volume excretion were higher, whereas changes in potassium excretion were lower in homozygous, as compared to heterozygous rats. Sodium 25-31 natriuretic peptide A Rattus norvegicus 0-3 2557757-6 1989 Sodium metabolism and renal kallikrein-kinin system: In normal subjects, fractional excretions of sodium and inorganic phosphorus which reflect the total and proximal sodium reabsorption, show significantly positive correlations for both urinary kallikrein and kinin excretions. Sodium 0-6 kallikrein related peptidase 4 Homo sapiens 246-256 2557757-6 1989 Sodium metabolism and renal kallikrein-kinin system: In normal subjects, fractional excretions of sodium and inorganic phosphorus which reflect the total and proximal sodium reabsorption, show significantly positive correlations for both urinary kallikrein and kinin excretions. Sodium 98-104 kallikrein related peptidase 4 Homo sapiens 28-38 2557757-6 1989 Sodium metabolism and renal kallikrein-kinin system: In normal subjects, fractional excretions of sodium and inorganic phosphorus which reflect the total and proximal sodium reabsorption, show significantly positive correlations for both urinary kallikrein and kinin excretions. Sodium 167-173 kallikrein related peptidase 4 Homo sapiens 28-38 2557757-10 1989 From these studies reported up to the present, it is suggested that the renal kallikrein-kinin system produced in the distal nephron in the kidney may play a role in the sodium metabolism with other renal depressor systems in addition to its own action. Sodium 170-176 kallikrein related peptidase 4 Homo sapiens 78-88 2521430-3 1989 We microdissected and perfused rat cortical collecting ducts in vitro to determine whether ANF-(1-28) can directly inhibit net sodium and fluid absorption. Sodium 127-133 natriuretic peptide A Rattus norvegicus 91-94 2521430-4 1989 ANF decreased both net sodium absorption and vasopressin-stimulated net fluid absorption by 50-90% when added to the peritubular bath solution. Sodium 23-29 natriuretic peptide A Rattus norvegicus 0-3 2521430-7 1989 If ANF has a similar action on the cortical collecting duct in vivo, it could account for a substantial part of the ANF-mediated increase in urinary sodium and water excretion. Sodium 149-155 natriuretic peptide A Rattus norvegicus 3-6 2521430-7 1989 If ANF has a similar action on the cortical collecting duct in vivo, it could account for a substantial part of the ANF-mediated increase in urinary sodium and water excretion. Sodium 149-155 natriuretic peptide A Rattus norvegicus 116-119 2567225-0 1989 The effect of T-2 toxin on active sodium transport across frog skin in the presence of ADH and amphotericin B. Sodium 34-40 solute carrier family 25 member 5 Homo sapiens 14-17 2567225-2 1989 The effect of T-2 toxin on active sodium transport across frog skin both in the presence and in the absence of stimulants of sodium transport, such as Amphotericin B and ADH, was studied using the short circuit current technique with the following results. Sodium 34-40 solute carrier family 25 member 5 Homo sapiens 14-17 2567225-4 1989 T-2 toxin produces inhibition of active sodium transport in a dose-response correlation. Sodium 40-46 solute carrier family 25 member 5 Homo sapiens 0-3 2525512-1 1989 The human atrial natriuretic factor (hANF) is a cardiovascular hormone, which promotes renal sodium secretion in response to increases in extracellular fluid volume and atrial pressure. Sodium 93-99 HESX homeobox 1 Homo sapiens 37-41 2626031-1 1989 We studied the effect of dietary sodium restriction (3 weeks) and high potassium intake (7 days) on transcriptional regulation of cytochrome P-450 cholesterol side chain cleavage (P-450 scc) and adrenodoxin (Adx) in rat adrenal glands. Sodium 33-39 cytochrome P450, family 11, subfamily a, polypeptide 1 Rattus norvegicus 180-189 2626031-4 1989 The low sodium diet provoked a 2.9-fold increase in P-450scc mRNA level in the Z-G compared to 2.1-fold in the Z-F-R, whereas Adx mRNA levels were enhanced 2.2- and 1.7-fold respectively in these two zones. Sodium 8-14 cytochrome P450, family 11, subfamily a, polypeptide 1 Rattus norvegicus 52-60 2626031-8 1989 These results thus indicate that both sodium depletion and high potassium intake in rats could act at the transcriptional level of P-450scc and Adx, two components of a rate-limiting step in steroidogenesis leading to aldosterone production. Sodium 38-44 cytochrome P450, family 11, subfamily a, polypeptide 1 Rattus norvegicus 131-139 2552202-1 1989 The characteristics of sodium currents (INa) in single frog ventricular cells were studied with the oil gap method. Sodium 23-29 internexin neuronal intermediate filament protein alpha Canis lupus familiaris 40-43 2552202-3 1989 In this preparation the threshold of INa was about -60 mV and the reversal potential was 58 mV, which is close to the value calculated by the Nernst equation for sodium ions. Sodium 162-168 internexin neuronal intermediate filament protein alpha Canis lupus familiaris 37-40 2532695-1 1989 The influence of chronic changes in sodium intake on the acute effects of atrial natriuretic peptide (ANP) on arterial pressure and fluid translocation was assessed in acutely binephrectomized rats. Sodium 36-42 natriuretic peptide A Rattus norvegicus 74-100 2532695-1 1989 The influence of chronic changes in sodium intake on the acute effects of atrial natriuretic peptide (ANP) on arterial pressure and fluid translocation was assessed in acutely binephrectomized rats. Sodium 36-42 natriuretic peptide A Rattus norvegicus 102-105 2532695-3 1989 A marked and irreversible hypotensive response to ANP was observed with the higher infusion rate in the low sodium group, whereas blood pressure did not change significantly in the other groups. Sodium 108-114 natriuretic peptide A Rattus norvegicus 50-53 2532695-5 1989 The effect of both doses of ANP on hematocrit was enhanced in the high sodium group, indicating that the fluid shift out of the intravascular compartment was magnified by high sodium intake. Sodium 71-77 natriuretic peptide A Rattus norvegicus 28-31 2532695-5 1989 The effect of both doses of ANP on hematocrit was enhanced in the high sodium group, indicating that the fluid shift out of the intravascular compartment was magnified by high sodium intake. Sodium 176-182 natriuretic peptide A Rattus norvegicus 28-31 2746999-7 1989 (4) A positive correlation was found between fractional sodium excretion and active kallikrein excretion in normal subjects, but not in diabetics. Sodium 56-62 kallikrein related peptidase 4 Homo sapiens 84-94 2746999-8 1989 The results suggest that reduction in ratio of active-to-total kallikrein by renal dysfunction might decrease sodium excretion in diabetics with nephropathy. Sodium 110-116 kallikrein related peptidase 4 Homo sapiens 63-73 2521394-3 1989 Our findings suggest that atrial natriuretic factor exerts its centrally mediated effects on sodium and water metabolism, at least in part, via a dopaminergic mechanism. Sodium 93-99 natriuretic peptide A Rattus norvegicus 26-51 2521395-1 1989 Previous studies have shown that administration of synthetic atrial natriuretic factor (ANF, 101-126) decreases sodium-dependent phosphate transport across renal brush border membrane vesicles (BBMV) in rats fed a normal or low phosphate diet. Sodium 112-118 natriuretic peptide A Rattus norvegicus 61-86 2521395-1 1989 Previous studies have shown that administration of synthetic atrial natriuretic factor (ANF, 101-126) decreases sodium-dependent phosphate transport across renal brush border membrane vesicles (BBMV) in rats fed a normal or low phosphate diet. Sodium 112-118 natriuretic peptide A Rattus norvegicus 88-91 2974246-3 1988 Because sodium restriction decreases plasma ANP levels in the setting of reduced renal mass, we also determined the effect of sodium restriction on sodium, phosphate, calcium, and magnesium excretion rates in rats with 5/6 nephrectomy (NX). Sodium 8-14 natriuretic peptide A Rattus norvegicus 44-47 2974246-7 1988 Moreover, in 5/6 NX rats on the higher sodium intake, ANP antiserum significantly reduced fractional sodium, phosphate, and calcium excretion, but was without effect on magnesium excretion. Sodium 39-45 natriuretic peptide A Rattus norvegicus 54-57 2974246-7 1988 Moreover, in 5/6 NX rats on the higher sodium intake, ANP antiserum significantly reduced fractional sodium, phosphate, and calcium excretion, but was without effect on magnesium excretion. Sodium 101-107 natriuretic peptide A Rattus norvegicus 54-57 2974246-8 1988 These data implicate endogenous ANP in promoting the adaptive increase in sodium, phosphate, calcium, but not magnesium excretion per nephron in chronic renal disease. Sodium 74-80 natriuretic peptide A Rattus norvegicus 32-35 2970230-0 1988 Effect of sodium intake on gene expression and plasma levels of ANF in rats. Sodium 10-16 natriuretic peptide A Rattus norvegicus 64-67 2970230-5 1988 After 1 wk on the high-sodium diet, ANF mRNA was increased in right atria and ventricles together with circulating ANF levels when compared with animals maintained for the same period on a low-sodium diet. Sodium 23-29 natriuretic peptide A Rattus norvegicus 36-39 2970230-5 1988 After 1 wk on the high-sodium diet, ANF mRNA was increased in right atria and ventricles together with circulating ANF levels when compared with animals maintained for the same period on a low-sodium diet. Sodium 23-29 natriuretic peptide A Rattus norvegicus 115-118 2970230-5 1988 After 1 wk on the high-sodium diet, ANF mRNA was increased in right atria and ventricles together with circulating ANF levels when compared with animals maintained for the same period on a low-sodium diet. Sodium 193-199 natriuretic peptide A Rattus norvegicus 36-39 2970230-8 1988 These data suggest that in rats, the transcription of the ANF gene and peptide release in enhanced only during short-term adaptation to dietary sodium loading. Sodium 144-150 natriuretic peptide A Rattus norvegicus 58-61 2844891-8 1988 Our data suggest that the increases and decreases in density of renal glomerular ANF receptors may play a role in the differential handling of sodium by the clipped and non-clipped kidney during the various stages of development of 2-K, 1C hypertension in the rat. Sodium 143-149 natriuretic peptide A Rattus norvegicus 81-84 2968054-6 1988 In sodium-replete rats, infusion of ANF at 45 ng.kg-1.min-1 resulted in lower plasma renin activity compared with the control noninfused group (14 +/- 4 vs. 22 +/- 2 ng ANG I.ml-1.h-1, P less than 0.05), but aldosterone secretion was not different (P greater than 0.05) between the two groups. Sodium 3-9 natriuretic peptide A Rattus norvegicus 36-39 2969319-2 1988 The relationship between plasma atrial natriuretic peptide (ANP) and body sodium was determined in rats 1 month after myocardial infarction induced by coronary artery ligation. Sodium 74-80 natriuretic peptide A Rattus norvegicus 32-58 2969319-2 1988 The relationship between plasma atrial natriuretic peptide (ANP) and body sodium was determined in rats 1 month after myocardial infarction induced by coronary artery ligation. Sodium 74-80 natriuretic peptide A Rattus norvegicus 60-63 2967139-11 1988 These findings suggest that the renal response to ANP may depend on the vascular tone before administration, and that renal nerve activity may modify the effects of ANP on renal haemodynamics and sodium excretion. Sodium 196-202 natriuretic peptide A Rattus norvegicus 165-168 3401353-5 1988 Assuming that the CSF sodium is responsible for the release of EDLS, hypertonic NaCl (2.5 M) was infused into the lateral ventricle for 30 minutes. Sodium 22-28 colony stimulating factor 2 Rattus norvegicus 18-21 2978744-8 1988 Impaired sodium and water excretion in chronic heart failure may be due partly to an attenuated renal response to ANP. Sodium 9-15 natriuretic peptide A Rattus norvegicus 114-117 2887633-0 1987 Sodium-dependent proline uptake in the rat hippocampal formation: association with ipsilateral-commissural projections of CA3 pyramidal cells. Sodium 0-6 carbonic anhydrase 3 Rattus norvegicus 122-125 3326953-0 1987 [Urinary excretion of kallikrein and prostaglandins before and after sodium deprivation and their relationships to plasma vasopressive substances]. Sodium 69-75 kallikrein related peptidase 4 Homo sapiens 22-32 3119148-1 1987 It has been shown previously in sheep that physiological increase of cerebrospinal fluid (CSF) [Na] by infusion of 0.5 M NaCl artificial CSF causes a large reduction of sodium appetite of the sodium-deplete animal. Sodium 169-175 granulocyte-macrophage colony-stimulating factor Ovis aries 69-94 3119148-1 1987 It has been shown previously in sheep that physiological increase of cerebrospinal fluid (CSF) [Na] by infusion of 0.5 M NaCl artificial CSF causes a large reduction of sodium appetite of the sodium-deplete animal. Sodium 169-175 granulocyte-macrophage colony-stimulating factor Ovis aries 90-93 3119148-1 1987 It has been shown previously in sheep that physiological increase of cerebrospinal fluid (CSF) [Na] by infusion of 0.5 M NaCl artificial CSF causes a large reduction of sodium appetite of the sodium-deplete animal. Sodium 192-198 granulocyte-macrophage colony-stimulating factor Ovis aries 69-94 3119148-1 1987 It has been shown previously in sheep that physiological increase of cerebrospinal fluid (CSF) [Na] by infusion of 0.5 M NaCl artificial CSF causes a large reduction of sodium appetite of the sodium-deplete animal. Sodium 192-198 granulocyte-macrophage colony-stimulating factor Ovis aries 90-93 3119148-2 1987 Equivalent increase of CSF osmotic pressure caused by infusion 0.7 M mannitol artificial CSF which lowers CSF [Na] causes a doubling of sodium appetite. Sodium 136-142 granulocyte-macrophage colony-stimulating factor Ovis aries 23-26 3119148-2 1987 Equivalent increase of CSF osmotic pressure caused by infusion 0.7 M mannitol artificial CSF which lowers CSF [Na] causes a doubling of sodium appetite. Sodium 136-142 granulocyte-macrophage colony-stimulating factor Ovis aries 89-92 3119148-2 1987 Equivalent increase of CSF osmotic pressure caused by infusion 0.7 M mannitol artificial CSF which lowers CSF [Na] causes a doubling of sodium appetite. Sodium 136-142 granulocyte-macrophage colony-stimulating factor Ovis aries 89-92 3119148-3 1987 The results of the experiments here show that simple dilution of CSF [Na] with isotonic mannitol CSF, as distinct from use of hypertonic 0.7 M mannitol CSF, is an equally effective strong stimulus of sodium appetite. Sodium 200-206 granulocyte-macrophage colony-stimulating factor Ovis aries 65-68 3119148-4 1987 Lowering CSF [Na] concentration stimulates salt appetite in the severely sodium-deplete as well as in the mild to moderately sodium-deplete animal, and the effect of decrease of CSF [Na] on sodium appetite is sustained over 48 h. In addition, i.c.v. Sodium 73-79 granulocyte-macrophage colony-stimulating factor Ovis aries 9-12 3119148-4 1987 Lowering CSF [Na] concentration stimulates salt appetite in the severely sodium-deplete as well as in the mild to moderately sodium-deplete animal, and the effect of decrease of CSF [Na] on sodium appetite is sustained over 48 h. In addition, i.c.v. Sodium 125-131 granulocyte-macrophage colony-stimulating factor Ovis aries 9-12 3119148-4 1987 Lowering CSF [Na] concentration stimulates salt appetite in the severely sodium-deplete as well as in the mild to moderately sodium-deplete animal, and the effect of decrease of CSF [Na] on sodium appetite is sustained over 48 h. In addition, i.c.v. Sodium 125-131 granulocyte-macrophage colony-stimulating factor Ovis aries 9-12 3119148-5 1987 infusion of angiotensin II for the preceding 22 h at a rate which is an effective stimulus of both water and sodium solution intake in the sodium-replete animal, in fact, significantly decreased the sodium appetite stimulating effect of reduction of CSF [Na] in the Na-deplete animal. Sodium 139-145 granulocyte-macrophage colony-stimulating factor Ovis aries 250-253 2822798-11 1987 These results suggest that in the rat, atrial natriuretic peptide (ANP) may be important in regulating cardiovascular homeostasis only following non-physiological alterations in sodium and volume status. Sodium 178-184 natriuretic peptide A Rattus norvegicus 39-65 3630725-3 1987 An increase of intracellular chlorine (Cl; P less than 0.001) and of sodium (Na; P less than 0.1) concentrations were found 1 and 6 weeks post-surgery. Sodium 69-75 catenin beta like 1 Homo sapiens 77-82 3037340-2 1987 The p21-induced pH change was inhibited by amiloride treatment or growth of cells in medium low in sodium, suggesting a role for the Na+/H+ antiporter. Sodium 99-105 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 4-7 2963714-8 1987 The increases in urinary sodium excretion and urine output observed when ANP was infused I.V. Sodium 25-31 natriuretic peptides A Ovis aries 73-76 2948755-0 1987 Atrial natriuretic peptide inhibits the effect of endogenous angiotensin II on plasma aldosterone in conscious sodium-depleted rats. Sodium 111-117 natriuretic peptide A Rattus norvegicus 0-26 2948755-7 1987 Since the increase in plasma aldosterone levels in sodium-depleted rats is mainly dependent on the activation of the renin-angiotensin system, we conclude that ANP may modulate the effect of endogenous as well as exogenous angiotensin II on plasma aldosterone secretion. Sodium 51-57 natriuretic peptide A Rattus norvegicus 160-163 2948089-5 1986 These results suggest that ANP is rapidly released into the circulation when sodium is loaded, however, the atrial storage of ANP remains depleted for about one week. Sodium 77-83 natriuretic peptide A Rattus norvegicus 27-30 3023376-1 1986 Sodium and potassium ion-transport adenosine triphosphatase from dog kidney was incubated with 0.4-2 mM Ca2+ at 23 degrees C for more than 2 min in the absence of monovalent inorganic cations, cooled to 0 degrees C, and phosphorylated from 1 mM Pi with 2.4 mM MgCl2. Sodium 0-6 carbonic anhydrase 2 Canis lupus familiaris 104-107 2946962-3 1986 ANP may reduce sodium reabsorption in the renal tubules, but it is also known that it increases the rate of glomerular filtration in the kidney, and relaxes preparations of smooth muscle, including one made from arteries that supply the kidney. Sodium 15-21 natriuretic peptide A Rattus norvegicus 0-3 3782468-4 1986 Kinetic analysis of the rate of bicarbonate-dependent sodium uptake as a function of sodium concentration revealed saturable stimulation with a Vmax of 2.7 nmol/mg protein per 2 s and a Km of 10.4 mM. Sodium 54-60 LOW QUALITY PROTEIN: period circadian protein homolog 2 Oryctolagus cuniculus 172-177 3782468-4 1986 Kinetic analysis of the rate of bicarbonate-dependent sodium uptake as a function of sodium concentration revealed saturable stimulation with a Vmax of 2.7 nmol/mg protein per 2 s and a Km of 10.4 mM. Sodium 85-91 LOW QUALITY PROTEIN: period circadian protein homolog 2 Oryctolagus cuniculus 172-177 3029391-5 1986 An excellent correlation exists between activity of sodium gradient-induced calcium uptake and ouabain-sensitive (Na,K)-ATPase in crude membranes of embryonic, newborn and adult hearts. Sodium 52-58 ATPase Na+/K+ transporting subunit alpha 1 Gallus gallus 114-126 3772382-1 1986 The effects of several gamma-aminobutyric acid (GABA)-ergic drugs on sodium-dependent high-affinity choline uptake (HACU) were investigated in the hippocampus. Sodium 69-75 high affinity choline uptake Mus musculus 116-120 2946239-2 1986 Intra-aortic infusions of synthetic ANF (28 amino acids) at 7.5 and 15 micrograms X kg-1 X h-1 produced dose-related increases in absolute and fractional sodium and water excretion under steady-state conditions; renal blood flow (RBF) was unchanged, whereas mean arterial pressure significantly decreased but remained within the autoregulatory range. Sodium 154-160 natriuretic peptide A Rattus norvegicus 36-39 2944396-5 1986 The increase of sodium intake from 5 to 75 meq/day produced decreases of plasma renin activity (PRA) (2.5 +/- 0.5 to 1.5 +/- 0.4 ng angiotensin I X ml-1 X h-1, P less than 0.05), plasma aldosterone concentration (PAC) (19.3 +/- 5.4 to 2.9 +/- 0.4 pg/ml, P less than 0.05), and urinary excretion of prostaglandin E2 (760 +/- 131 to 320 +/- 58 pg/min, P less than 0.05). Sodium 16-22 renin Canis lupus familiaris 80-85 3781235-1 1986 Sodium-retaining activity of chum salmon prolactin (PRL) was examined in several euryhaline teleosts. Sodium 0-6 prolactin Fundulus heteroclitus 52-55 3781235-2 1986 Chum PRL was 100 times more potent than ovine PRL in maintaining plasma sodium levels in the hypophysectomized killifish, Fundulus heteroclitus, transferred from 50% seawater to fresh water. Sodium 72-78 prolactin Fundulus heteroclitus 5-8 3015915-4 1986 The demand for sodium ion transport by the (Na+ + K+)-ATPase was modulated by activating voltage-sensitive sodium channels with veratridine or exposing cultures to low [K+]o (0.5 mM). Sodium 15-21 ATPase Na+/K+ transporting subunit alpha 1 Gallus gallus 44-60 3488538-2 1986 The aim was to study the kinetics of sodium current INa and gating current Igat over a large potential range (-92 to -12 mV) and to compare the time constants for the turning-on of INa or Igat with those for the turning-off measured at the same potential. Sodium 37-43 internexin neuronal intermediate filament protein alpha Homo sapiens 52-55 3488538-11 1986 In addition, the time constant of the turning-on of sodium activation m (tau m on) was determined, assuming INa approximately m2 (with a small initial delay) or INa approximately m3 (without an initial delay). Sodium 52-58 internexin neuronal intermediate filament protein alpha Homo sapiens 108-111 2941632-1 1986 Atrial natriuretic factor (ANF) increases sodium (Na+) and water excretion 8-10 fold on repeated administration to anesthetized rats. Sodium 42-48 natriuretic peptide A Rattus norvegicus 0-25 2941632-1 1986 Atrial natriuretic factor (ANF) increases sodium (Na+) and water excretion 8-10 fold on repeated administration to anesthetized rats. Sodium 42-48 natriuretic peptide A Rattus norvegicus 27-30 3011520-10 1986 The natriuretic effect of ANF, therefore, was not caused solely by enhanced tubular load, but included specific inhibition of duct sodium reabsorption as an essential feature of the renal response. Sodium 131-137 natriuretic peptide A Rattus norvegicus 26-29 2941371-4 1986 This fall in renin secretion was associated with significant increases (p less than 0.05) in creatinine clearance, urine flow, sodium excretion, and the filtered load of sodium. Sodium 127-133 renin Canis lupus familiaris 13-18 2941371-4 1986 This fall in renin secretion was associated with significant increases (p less than 0.05) in creatinine clearance, urine flow, sodium excretion, and the filtered load of sodium. Sodium 170-176 renin Canis lupus familiaris 13-18 2941371-9 1986 These results suggest that an increase in the sodium load delivered to the macula suppression of renin secretion by atrial natriuretic factor is mediated through its interactions with the two intrarenal receptor mechanisms, the renal vascular receptor and the macula densa. Sodium 46-52 renin Canis lupus familiaris 97-102 3013772-8 1986 Binding of atrial natriuretic factor to platelets was higher with the low-sodium diet (10.3 +/- 1.0 sites per cell) than with the high-sodium diet (7.1 +/- 0.7 sites per cell). Sodium 74-80 natriuretic peptide A Rattus norvegicus 11-36 3013772-8 1986 Binding of atrial natriuretic factor to platelets was higher with the low-sodium diet (10.3 +/- 1.0 sites per cell) than with the high-sodium diet (7.1 +/- 0.7 sites per cell). Sodium 135-141 natriuretic peptide A Rattus norvegicus 11-36 3013772-9 1986 In conclusion, human platelets bear binding sites for atrial natriuretic factor, the density of which may be modulated by sodium intake. Sodium 122-128 natriuretic peptide A Rattus norvegicus 54-79 2941612-1 1986 To examine the physiological role of atrial natriuretic factor (ANF) in the maintenance of sodium homeostasis under various conditions, we performed experiments in rats across a wide range of sodium intake, in rats with chronic renal insufficiency at extremes of sodium intake, and in rats given desoxycorticosterone acetate. Sodium 91-97 natriuretic peptide A Rattus norvegicus 37-62 2941612-1 1986 To examine the physiological role of atrial natriuretic factor (ANF) in the maintenance of sodium homeostasis under various conditions, we performed experiments in rats across a wide range of sodium intake, in rats with chronic renal insufficiency at extremes of sodium intake, and in rats given desoxycorticosterone acetate. Sodium 91-97 natriuretic peptide A Rattus norvegicus 64-67 2871836-9 1986 It is also suggested that the depression of plasma ANF may contribute to the well known post-surgery sodium retention. Sodium 101-107 natriuretic peptide A Rattus norvegicus 51-54 3513620-0 1986 Chronic effects of vasopressin on plasma renin activity in sodium-restricted dogs. Sodium 59-65 renin Canis lupus familiaris 41-46 3544725-5 1986 When urinary kallikrein excretion rate was correlated with the sodium excretion rate the relationship was found to be positive and significant as was the correlation found between urine volume and urinary kallikrein excretion rate. Sodium 63-69 kallikrein related peptidase 4 Homo sapiens 13-23 3544725-5 1986 When urinary kallikrein excretion rate was correlated with the sodium excretion rate the relationship was found to be positive and significant as was the correlation found between urine volume and urinary kallikrein excretion rate. Sodium 63-69 kallikrein related peptidase 4 Homo sapiens 205-215 3484612-4 1986 From these data was derived the working hypothesis that the value of [Ca]i during the contracture plateau is a steady-state value due to influx through a sodium-dependent mechanism and calcium uptake or efflux via a sodium-independent mechanism. Sodium 154-160 carbonic anhydrase 1 Homo sapiens 70-74 3484612-4 1986 From these data was derived the working hypothesis that the value of [Ca]i during the contracture plateau is a steady-state value due to influx through a sodium-dependent mechanism and calcium uptake or efflux via a sodium-independent mechanism. Sodium 216-222 carbonic anhydrase 1 Homo sapiens 70-74 2948059-11 1986 Some of the effects on tubular reabsorptive capacity probably result from medullary wash-out which thereby contributes to the natriuresis by potentiating the rise in the filtered load of sodium at high ANP levels. Sodium 187-193 natriuretic peptide A Rattus norvegicus 202-205 2998690-5 1985 Our data suggest that acute infusion of ANF reveals a defect of sodium and water handling in SHR. Sodium 64-70 natriuretic peptide A Rattus norvegicus 40-43 2934063-0 1985 Antisera to atrial natriuretic factor reduces urinary sodium excretion and increases plasma renin activity in rats. Sodium 54-60 natriuretic peptide A Rattus norvegicus 12-37 2934063-7 1985 The results of this study provide evidence indicating that endogenous atrial natriuretic factor plays an important role in the regulation of urinary water and sodium excretion and plasma renin activity. Sodium 159-165 natriuretic peptide A Rattus norvegicus 70-95 4079383-3 1985 Since 6-7 reduction of DOCA and 9 alpha-F-Cac substantially reduces affinity for Type II receptors but not Type I receptors, 6-dehydro-derivatives will thus bind preferentially to receptors influencing the retention of sodium (the "mineralocorticoid" or Type I receptor), and compete with mineralocorticoids for such receptors. Sodium 219-225 solute carrier family 25 member 20 Rattus norvegicus 42-45 2411531-10 1985 Similarly, both the concentration of renal CaBP and renal CaBP mRNA levels increased 4-fold in rats fed low phosphorus diets, increased 2-fold in rats fed low calcium diets, and decreased 67% in rats fed low sodium diets, providing evidence that the nutritional induction or decrease in renal CaBP is accompanied by a corresponding alteration in the concentration of its specific translatable mRNA. Sodium 208-214 hippocalcin Rattus norvegicus 43-47 2411531-10 1985 Similarly, both the concentration of renal CaBP and renal CaBP mRNA levels increased 4-fold in rats fed low phosphorus diets, increased 2-fold in rats fed low calcium diets, and decreased 67% in rats fed low sodium diets, providing evidence that the nutritional induction or decrease in renal CaBP is accompanied by a corresponding alteration in the concentration of its specific translatable mRNA. Sodium 208-214 hippocalcin Rattus norvegicus 58-62 2411531-10 1985 Similarly, both the concentration of renal CaBP and renal CaBP mRNA levels increased 4-fold in rats fed low phosphorus diets, increased 2-fold in rats fed low calcium diets, and decreased 67% in rats fed low sodium diets, providing evidence that the nutritional induction or decrease in renal CaBP is accompanied by a corresponding alteration in the concentration of its specific translatable mRNA. Sodium 208-214 hippocalcin Rattus norvegicus 58-62 2932778-4 1985 This high affinity ANP receptor site in renal cortex membrane indicated that ANP controlled the balance of water and sodium excretion due to this receptor site in the kidney. Sodium 117-123 natriuretic peptide A Rattus norvegicus 19-22 2932778-4 1985 This high affinity ANP receptor site in renal cortex membrane indicated that ANP controlled the balance of water and sodium excretion due to this receptor site in the kidney. Sodium 117-123 natriuretic peptide A Rattus norvegicus 77-80 3161343-1 1985 Atrial natriuretic factor (ANF), a family of peptides isolated from cardiac atria, has marked effects on sodium excretion. Sodium 105-111 natriuretic peptide A Rattus norvegicus 0-25 3161343-1 1985 Atrial natriuretic factor (ANF), a family of peptides isolated from cardiac atria, has marked effects on sodium excretion. Sodium 105-111 natriuretic peptide A Rattus norvegicus 27-30 2989338-0 1985 Administration of atrial natriuretic factor inhibits sodium-coupled transport in proximal tubules. Sodium 53-59 natriuretic peptide A Rattus norvegicus 18-43 3157850-0 1985 Effects of changes in water-sodium balance on levels of atrial natriuretic factor messenger RNA and peptide in rats. Sodium 28-34 natriuretic peptide A Rattus norvegicus 56-81 3157850-2 1985 Specific changes in the level of ANF mRNA relative to total atrial RNA were observed in atria from sodium restricted rats and water deprived then sodium loaded rats, demonstrating an association of change in water-sodium balance with the expression of ANF gene. Sodium 99-105 natriuretic peptide A Rattus norvegicus 33-36 3157850-2 1985 Specific changes in the level of ANF mRNA relative to total atrial RNA were observed in atria from sodium restricted rats and water deprived then sodium loaded rats, demonstrating an association of change in water-sodium balance with the expression of ANF gene. Sodium 146-152 natriuretic peptide A Rattus norvegicus 33-36 3157850-2 1985 Specific changes in the level of ANF mRNA relative to total atrial RNA were observed in atria from sodium restricted rats and water deprived then sodium loaded rats, demonstrating an association of change in water-sodium balance with the expression of ANF gene. Sodium 146-152 natriuretic peptide A Rattus norvegicus 33-36 3884237-7 1985 Overall, urinary kallikrein excretion correlated significantly with urine flow and with sodium excretion. Sodium 88-94 kallikrein related peptidase 4 Homo sapiens 17-27 3884237-8 1985 Peak kallikrein excretion occurred in the second 30 min of the infusion, and preceded maximal urine flow and sodium excretion. Sodium 109-115 kallikrein related peptidase 4 Homo sapiens 5-15 3158607-8 1985 In sodium-depleted one-kidney, one-clip rats, which became saralasin responsive, ANF administration significantly reduced blood pressure (from 184 +/- 11 to 156 +/- 12 mm Hg; n = 8), plasma aldosterone levels (from 286 +/- 41 to 179 +/- 36 ng/dl), and plasma renin activity (from 69 +/- 19 to 44 +/- 13 ng/ml/hr). Sodium 3-9 natriuretic peptide A Rattus norvegicus 81-84 3986166-3 1985 Mean cord sodium levels were significantly lower in the oxytocin (131.4, SD 3.6 mmol/l) and glucose groups (132.5, SD 3.2 mmol/l) than in the control group (135.0, SD 3.0 mmol/l). Sodium 10-16 oxytocin/neurophysin I prepropeptide Homo sapiens 56-64 3986166-5 1985 Significant negative linear correlations were seen between serum sodium and the dose of oxytocin (P less than 0.01) and log of the volume of glucose solution infused (P less than 0.001). Sodium 65-71 oxytocin/neurophysin I prepropeptide Homo sapiens 88-96 2985222-2 1985 In the absence of CEI, ANF produced rapid and significant increases in sodium, potassium, calcium, and urine excretions while blood pressure declined transiently. Sodium 71-77 natriuretic peptide A Rattus norvegicus 23-26 2985222-3 1985 In the presence of CEI, ANF enhanced the excretion of sodium and potassium but not of calcium and urine. Sodium 54-60 natriuretic peptide A Rattus norvegicus 24-27 3983902-3 1985 The hydrolysis of BzArgpNA by alpha-thrombin was less effective in the presence of sodium ions than in the presence of potassium ions. Sodium 83-89 coagulation factor II, thrombin Bos taurus 36-44 3983902-4 1985 The hydrolysis of this latter substrate by beta-thrombin was similar in the presence of either sodium ions or potassium ions. Sodium 95-101 coagulation factor II, thrombin Bos taurus 48-56 6100736-0 1984 Dietary sodium regulation of alpha 2-adrenoceptors in Sabra hypertensive (SHB) and normotensive (SBN) rats. Sodium 8-14 SH2 domain containing adaptor protein B Rattus norvegicus 74-77 6100736-3 1984 After two or five weeks of high sodium diet alpha 2-adrenoceptor density was increased in the renal cortex of SHB and SBN rats. Sodium 32-38 SH2 domain containing adaptor protein B Rattus norvegicus 110-113 6329546-15 1984 The results suggest that Na-Ca exchange mechanisms may be present in these vessels but that they only play a role under extreme conditions; under normal conditions the effect of ouabain on activated vessels seems to be primarily due to its depolarizing effect, and not to its effect on intracellular sodium. Sodium 300-306 nascent polypeptide associated complex subunit alpha Rattus norvegicus 25-30 6326267-3 1984 These data suggest that atrial natriuretic factor affects sodium excretion by the kidneys both directly and through the inhibition of aldosterone production. Sodium 58-64 natriuretic peptide A Rattus norvegicus 24-49 6376345-0 1984 Effects of sodium depletion on inactive and active renin from dog kidney and plasma. Sodium 11-17 renin Canis lupus familiaris 51-56 6376345-1 1984 The relationship of active renin and inactive renin (trypsin-activated angiotensin-I-forming enzyme) to sodium depletion was examined in renal and peripheral plasma and at the subcellular level in the kidneys of dogs. Sodium 104-110 renin Canis lupus familiaris 46-51 6376345-6 1984 Sodium depletion also caused a 20-fold increase in active renin and a twofold increase in inactive renin in peripheral plasma. Sodium 0-6 renin Canis lupus familiaris 58-63 6376345-6 1984 Sodium depletion also caused a 20-fold increase in active renin and a twofold increase in inactive renin in peripheral plasma. Sodium 0-6 renin Canis lupus familiaris 99-104 6376345-7 1984 The renal venous-arterial concentration difference of inactive renin was statistically significant in low-sodium dogs, although it was not significant in controls. Sodium 106-112 renin Canis lupus familiaris 63-68 6376345-8 1984 The ratio of inactive to active renin was 0.2 to 0.4 in plasma from low-sodium dogs, while it was 1.5 to 3 in plasma from control dogs. Sodium 72-78 renin Canis lupus familiaris 32-37 6707628-7 1984 Their transport characteristics showed they used mostly system ASC (a sodium-dependent system distinguished from A) and/or system L (sodium-independent). Sodium 70-76 PYD and CARD domain containing Rattus norvegicus 63-66 6633158-0 1983 Evidence that sodium deprivation influences vitamin D dependent rat renal calcium binding protein. Sodium 14-20 hippocalcin Rattus norvegicus 74-97 6633158-4 1983 Renal CaBP/mg protein from rats fed the low sodium diet decreased 50% from the control values. Sodium 44-50 hippocalcin Rattus norvegicus 6-10 6633158-7 1983 The decrease in renal CaBP in rats fed the low sodium diet suggests for the first time that sodium is required for vitamin D dependent distal tubular calcium transport processes. Sodium 47-53 hippocalcin Rattus norvegicus 22-26 6633158-7 1983 The decrease in renal CaBP in rats fed the low sodium diet suggests for the first time that sodium is required for vitamin D dependent distal tubular calcium transport processes. Sodium 92-98 hippocalcin Rattus norvegicus 22-26 6349389-1 1983 The effects of inhibition of the renin-angiotensin system on the decreased renal excretion of sodium and water resulting from behavioral stress (shock avoidance) were examined in conscious saline-infused (4-5 ml/min) dogs. Sodium 94-100 renin Canis lupus familiaris 33-38 6349389-7 1983 Whereas decreases in fractional sodium and water excretion were attenuated by renin-angiotensin inhibition, decreases in glomerular filtration rate and effective renal blood flow and increases in mean arterial pressure were not affected. Sodium 32-38 renin Canis lupus familiaris 78-83 6308184-0 1983 Increased sodium ion conductance through nicotinic acetylcholine receptor channels in PC12 cells exposed to nerve growth factors. Sodium 10-16 cholinergic receptor nicotinic alpha 2 subunit Rattus norvegicus 41-73 6348251-6 1983 While the bioactivity of intravenously administered sodium insulin was equal to the bioactivity of intravenously administered regular insulin, the hypoglycemic effect of subcutaneously injected sodium insulin differed from the effect of subcutaneously injected regular insulin. Sodium 52-58 insulin Canis lupus familiaris 59-66 6343378-0 1983 Inhibitory effects of sodium and other monovalent cations on purified versus membrane-bound kallikrein. Sodium 22-28 kallikrein related peptidase 4 Homo sapiens 92-102 6837735-4 1983 These data support the hypothesis that the natriuretic response to increased CSF sodium concentration in the rat is due to a pressor response and/or increased glomerular filtration rate and demonstrate that ablation of AV3V periventricular tissue blunts the natriuretic response, possibly through diminished central pressor mechanisms and/or decreased central control of glomerular filtration rate. Sodium 81-87 colony stimulating factor 2 Rattus norvegicus 77-80 6549759-0 1983 Effects of alterations in sodium and water metabolism on urinary excretion of active and inactive kallikrein in man. Sodium 26-32 kallikrein related peptidase 4 Homo sapiens 98-108 6549759-2 1983 Several previous studies have examined the response of active kallikrein excretion to alterations in sodium and water metabolism, but the response of inactive kallikrein has not been evaluated systematically. Sodium 101-107 kallikrein related peptidase 4 Homo sapiens 62-72 6549759-7 1983 We have used this technique to study the effect of alterations in sodium and water metabolism on kallikrein excretion. Sodium 66-72 kallikrein related peptidase 4 Homo sapiens 97-107 6303467-2 1983 This reduction in the amplitude of the cyclic GMP depolarization may be due to the direct effect of external Na+ concentration on dark current and an indirect effect resulting from the inactivation of a sodium-calcium exchange mechanism raising the intracellular Ca2+ concentration. Sodium 203-209 5'-nucleotidase, cytosolic II Homo sapiens 46-49 6321830-0 1983 Intracellular injection of cyclic-GMP increases sodium conductance in gecko photoreceptors. Sodium 48-54 5'-nucleotidase, cytosolic II Homo sapiens 34-37 6601226-2 1983 The increase in Na transport is due to an increase in the unidirectional influx of sodium, is amiloride sensitive and is prevented with pretreatment with indomethacin, mefanamic acid and phospholipase inhibitor, mepacrine. Sodium 83-89 LY6/PLAUR domain containing 8 Homo sapiens 187-210 7137338-5 1982 Kinetic analysis of the sodium-dependent component of alpha-methylglucoside flux into LLC-PK1 apical membrane vesicles indicates the existence of single transporter with Km congruent to 2 mM and Vmax congruent to 3 nmol.min-1.mg protein-1. Sodium 24-30 prokineticin 1 Homo sapiens 90-93 6890383-4 1982 (2) Thrombin-induced release from the platelets was dependent upon extracellular sodium ions, while no dependence was observed for the drug-induced release. Sodium 81-87 prothrombin Oryctolagus cuniculus 4-12 7049917-0 1982 Effects of chronic sodium depletion on canine brain renin and cathepsin D activities. Sodium 19-25 renin Canis lupus familiaris 52-57 7049917-2 1982 The purpose of this study was twofold: to assess the effect of sodium depletion on brain renin activity; and to assess in the same regions alterations in brain renin and cathepsin D activities. Sodium 63-69 renin Canis lupus familiaris 89-94 7049917-3 1982 Sodium depletion caused a ninefold increase in plasma renin activity, hemoconcentration, and hyponatremia. Sodium 0-6 renin Canis lupus familiaris 54-59 7049917-7 1982 These observations support the view that there is an inverse relationship between plasma and brain renin activity in chronically sodium-depleted dogs. Sodium 129-135 renin Canis lupus familiaris 99-104 7049933-6 1982 Dietary sodium restriction increases kallikrein excretion while lowering blood pressure, but the blood pressure reduction correlates with plasma volume contraction rather than the increase in kallikrein. Sodium 8-14 kallikrein related peptidase 4 Homo sapiens 37-47 6123389-2 1982 Effects of kallikrein and some autacoids on in vitro transport of valine and sodium ion. Sodium 77-83 kallikrein related peptidase 4 Homo sapiens 11-21 6274473-2 1981 The ability of plasma to stimulate G6PD was significantly greater in the hypertensive patients when they were taking their normal sodium diet than in the normotensive subjects, and was significantly correlated with blood pressure. Sodium 130-136 glucose-6-phosphate dehydrogenase Homo sapiens 35-39 6274473-3 1981 The ability of plasma to stimulate G6PD was inversely correlated with plasma renin activity in the hypertensive patients and increased with age and sodium intake in the normotensive subjects. Sodium 148-154 glucose-6-phosphate dehydrogenase Homo sapiens 35-39 6170580-0 1981 Kallikrein inhibitors decrease short-circuit current by inhibiting sodium uptake. Sodium 67-73 kallikrein related peptidase 4 Homo sapiens 0-10 7028613-1 1981 Sodium depletion, a maneuver that is accompanied by a 14-fold elevation of plasma renin activity (PRA), alters the norepinephrine concentration of the canine area postrema (AP), a circumventricular organ of the 4th ventricle known to be sensitive to circulating angiotensin II. Sodium 0-6 renin Canis lupus familiaris 82-87 7270714-1 1981 Reduction of sodium intake affects both the renin-angiotensin and sympathetic nervous systems, but the effects on the latter are less well understood. Sodium 13-19 renin Canis lupus familiaris 44-49 7246839-4 1981 Since the difference in 24-hour dietary sodium consumption was 300 milligrams between the communities, an intake of one liter of high sodium tap water represented approximately 25 per cent of the difference in total sodium intake between the two communities. Sodium 134-140 nuclear RNA export factor 1 Homo sapiens 141-144 7246839-4 1981 Since the difference in 24-hour dietary sodium consumption was 300 milligrams between the communities, an intake of one liter of high sodium tap water represented approximately 25 per cent of the difference in total sodium intake between the two communities. Sodium 134-140 nuclear RNA export factor 1 Homo sapiens 141-144 7317028-0 1981 Acetylcholinesterase: evidence that sodium ion binding at the anionic site causes inhibition of the second-order hydrolysis of acetylcholine and a decrease of its pKa as well as of deacetylation. Sodium 36-42 acetylcholinesterase Bos taurus 0-20 7291040-0 1981 alpha-MSH at physiological concentrations stimulates "late pathway" steroid products in adrenal zona glomerulosa cells from sodium restricted rats. Sodium 124-130 proopiomelanocortin Rattus norvegicus 0-9 7291040-4 1981 In contrast, in cells taken from animals subjected to dietary sodium restriction, aldosterone and 18-OH-B were significantly stimulated at 10(10) moles alpha-MSH per 1, whereas corticosterone and 18-OH-DOC were unaffected at all concentrations tested. Sodium 62-68 proopiomelanocortin Rattus norvegicus 152-161 7291040-6 1981 However, the threshold concentration at which alpha-MSH induces increased aldosterone secretion in cells from sodium depleted rats clearly falls well within the physiological range, and it is therefore likely that alpha-MSH contributes to the support of aldosterone secretion in these animals in vivo. Sodium 110-116 proopiomelanocortin Rattus norvegicus 46-55 7291040-6 1981 However, the threshold concentration at which alpha-MSH induces increased aldosterone secretion in cells from sodium depleted rats clearly falls well within the physiological range, and it is therefore likely that alpha-MSH contributes to the support of aldosterone secretion in these animals in vivo. Sodium 110-116 proopiomelanocortin Rattus norvegicus 214-223 7243627-6 1981 The fact that the release of alpha-MSH is stimulated by veratridine and inhibited by tetrodotoxin demonstrates the necessity for neuronal sodium influx for alpha-MSH release. Sodium 138-144 proopiomelanocortin Rattus norvegicus 29-38 7243627-6 1981 The fact that the release of alpha-MSH is stimulated by veratridine and inhibited by tetrodotoxin demonstrates the necessity for neuronal sodium influx for alpha-MSH release. Sodium 138-144 proopiomelanocortin Rattus norvegicus 156-165 7011046-13 1981 Prolactin increases sodium absorption fourfold but increases Isc only twofold. Sodium 20-26 prolactin Mus musculus 0-9 7011963-3 1981 Three weeks of sodium depletion supplemented with diuretics caused a 24-fold increase in plasma renin activity, hemoconcentration, and elevated serum protein concentration. Sodium 15-21 renin Canis lupus familiaris 96-101 6947954-4 1981 In the diabetic children the tubular sodium reabsorption was closely correlated to the absolute phosphate reabsorption (p less than 0.001) and to GFR (p less than 0.0001). Sodium 37-43 Rap guanine nucleotide exchange factor 5 Homo sapiens 146-149 7022537-2 1981 Systemic blood pressure was decreased and arterial plasma renin concentration increased in the sodium-loaded dogs by infusion of PGI2 (1200 ng/min). Sodium 95-101 renin Canis lupus familiaris 58-63 7022537-4 1981 In the sodium-depleted dogs systemic blood pressure was significantly decreased and arterial plasma renin concentration increased by infusions of PGI2 (300 and 1200 ng/min) and PGE2 (300 ng/min). Sodium 7-13 renin Canis lupus familiaris 100-105 6274002-9 1981 TmP/GFR was negatively correlated to fractional excretion of sodium. Sodium 61-67 Rap guanine nucleotide exchange factor 5 Homo sapiens 4-7 6801758-5 1981 Urinary sodium excretion increased only during the infusion of secretin in a dose of 0.25 CU/kg and h, whereas secretin showed no effect on the urinary outputs of water, potassium, and solutes. Sodium 8-14 secretin Homo sapiens 63-71 6903188-6 1980 Low or high dietary sodium intakes, maneuvers known to change human urinary Tos-Arg-OMe esterase excretion, change immunoreactive kallikrein to an equivalent degree. Sodium 20-26 kallikrein related peptidase 4 Homo sapiens 130-140 6999033-4 1980 The arterial plasma renin activity and concentration of norepinephrine were higher in the sodium-depleted animals than in the controls; the arterial concentration of PGE2 was equal in both groups. Sodium 90-96 renin Canis lupus familiaris 20-25 6999033-5 1980 The renal venous plasma renin activity was higher in the sodium-depleted dogs. Sodium 57-63 renin Canis lupus familiaris 24-29 6999033-9 1980 The results indicate that moderate chronic sodium depletion, in addition to enhancing the activity of the renin-angiotensin system, also increases the activity of the renal adrenergic nervous system and increases renal PGE2 synthesis. Sodium 43-49 renin Canis lupus familiaris 106-111 6255744-6 1980 Unlike cyclic AMP, cyclic GMP almost equally stimulated sodium and chloride transport from serosa to mucosa. Sodium 56-62 5'-nucleotidase, cytosolic II Homo sapiens 26-29 6255744-7 1980 Unlike cyclic AMP, cyclic GMP almost equally stimulated sodium and chloride transport from serosa to mucosa, while the effect on Isc of the two nucleotides was additive. Sodium 56-62 5'-nucleotidase, cytosolic II Homo sapiens 26-29 7459696-1 1980 The acute effects of intravenous infusions of phosphate and parathyroid hormone (PTH) upon the renal tubular handling of sodium, potassium, calcium, magnesium, and phosphate were examined in phosphate-depleted dogs using recollection micropuncture techniques. Sodium 121-127 parathyroid hormone Canis lupus familiaris 60-79 7444349-4 1980 Secretin induced a significant increase in urinary water, sodium, calcium and solute excretion, and a significant decrease in free water clearance. Sodium 58-64 secretin Homo sapiens 0-8 7444349-6 1980 This study confirms that secretin has a diuretic effect in man, and it is concluded that this effect is most likely due to impairment of sodium reabsorption in the renal tubule caused by the increase in RPF. Sodium 137-143 secretin Homo sapiens 25-33 6991148-6 1980 In addition, increased plasma renin activity produced by dopamine infusion during hemorrhage would tend to offset the expected increases in renal blood flow and sodium excretion. Sodium 161-167 renin Canis lupus familiaris 30-35 225056-8 1979 These data demonstrate an important role for aldosterone and the renin-angiotensin system in the retention of sodium and in ascites formation in dogs with thoracic caval constriction. Sodium 110-116 renin Canis lupus familiaris 65-70 392177-5 1979 However, the precise role of the renal kallikrein-kinin system in sodium and volume homeostasis and in blood pressure regulation still remains to be determined. Sodium 66-72 kallikrein related peptidase 4 Homo sapiens 39-49 392178-3 1979 In normal humans and rats the kallikrein activity of parotid saliva is inversely related to flow rate and sodium concentration. Sodium 106-112 kallikrein related peptidase 4 Homo sapiens 30-40 392178-9 1979 The enhanced sodium reabsorption in the duct system in the various forms of hypertension could be the cause as well as a consequence of the enhanced kallikrein secretion. Sodium 13-19 kallikrein related peptidase 4 Homo sapiens 149-159 114426-0 1979 Sodium ion binding to parvalbumin studied by 23Na NMR: a reply. Sodium 0-6 parvalbumin Homo sapiens 22-33 314308-1 1979 The responses of isolated frog skin to 5-hydroxytryptamine (increased active sodium transport and decreased passive chloride permeability) are diminished by incubation with the enzymes neuraminidase and N-acetylneuraminic acid aldolase but only in the absence of Ca2+ and presence of EDTA. Sodium 77-83 N-acetylneuraminate pyruvate lyase Homo sapiens 203-235 464123-3 1979 A time-control group was perfused with normal artificial CSF throughout C, E, and R. High sodium perfusion resulted in a marked natriuresis in each of nine animals and suppression of plasma renin activity. Sodium 90-96 renin Canis lupus familiaris 190-195 41090-0 1979 Stimulation by cyclic GMP of sodium efflux in barnacle muscle fibres. Sodium 29-35 5'-nucleotidase, cytosolic II Homo sapiens 22-25 232085-1 1979 Sodium depletion was induced in dogs to raise plasma renin activity (PRA) from 1.11 to 26.48 ng/ml/hr. Sodium 0-6 renin Canis lupus familiaris 53-58 220888-1 1979 The relation of the renin-angiotensin-aldosterone system to sodium retention was studied in dogs with an aortic-caval fistula and high output failure by administering orally the new converting enzyme inhibitor SQ 14225. Sodium 60-66 renin Canis lupus familiaris 20-25 216273-8 1978 Whether the decrease in sodium transport produced by cholinergic agents is the result of increased intracytoplasmic calcium levels, increased cyclic GMP levels, or a combination of both remains to be established. Sodium 24-30 5'-nucleotidase, cytosolic II Homo sapiens 149-152 728612-1 1978 Single injection of insulin (1 AU/kg) enhanced maximal glucose absorption, cardiotrast secretion and decreased sodium excretion without any changes of glomerular filtration in dogs. Sodium 111-117 insulin Canis lupus familiaris 20-27 215373-11 1978 However, other factors (possibly prostaglandins and sodium) have to be modified in order to activate the tonin--angiotensin II system. Sodium 52-58 kallikrein 1-related peptidase C2 Rattus norvegicus 105-110 745059-0 1978 The role of sodium-calcium exchange in controlling [Ca]i in smooth muscle [proceedings]. Sodium 12-18 carbonic anhydrase 1 Homo sapiens 52-56 741539-5 1978 The importance of elevated sodium levels in the proximal end of the distal tubule and its effects on renin release in kidney interstitium is stressed. Sodium 27-33 renin Canis lupus familiaris 101-106 568526-3 1978 The rate of increase of red cell sodium is therefore a measure of ouabain-sensitive sodium efflux (Eos). Sodium 33-39 EOS Homo sapiens 99-102 568526-4 1978 This estimate of Eos, when expressed as a fraction of the original red cell sodium concentration, gives a measure of the ouabain-sensitive, efflux rate constant (ERCos). Sodium 76-82 EOS Homo sapiens 17-20 744127-5 1978 These findings are compatible with the thesis that an increased distal tubular load of sodium stimulates renin release and suggest that the increased distal sodium absorption after the proximal effects of PTH may be regulated by the renin-angiotensin-aldosterone system. Sodium 87-93 renin Canis lupus familiaris 105-110 744127-5 1978 These findings are compatible with the thesis that an increased distal tubular load of sodium stimulates renin release and suggest that the increased distal sodium absorption after the proximal effects of PTH may be regulated by the renin-angiotensin-aldosterone system. Sodium 87-93 renin Canis lupus familiaris 233-238 744127-5 1978 These findings are compatible with the thesis that an increased distal tubular load of sodium stimulates renin release and suggest that the increased distal sodium absorption after the proximal effects of PTH may be regulated by the renin-angiotensin-aldosterone system. Sodium 157-163 renin Canis lupus familiaris 233-238 923807-0 1977 Sodium complexation by the calcium binding site of parvalbumin. Sodium 0-6 parvalbumin Homo sapiens 51-62 884249-4 1977 In sodium-free Ringer-Locke solution when the action potential in the smooth muscle cells of the ureter turns into a simple spike potential, an increase of Ca2+ concentration causes a marked increase of the action potential amplitude. Sodium 3-9 LOW QUALITY PROTEIN: carbonic anhydrase 2 Cavia porcellus 156-159 870226-0 1977 Role of the renin-angiotensin system in the regulation of aldosterone biosynthesis and arterial pressure during sodium deficiency. Sodium 112-118 renin Canis lupus familiaris 12-17 870226-8 1977 The precipitous fall in aldosterone secretion and arterial blood pressure during long-term infusion of angiotensin I-converting enzyme inhibitor demonstrates the importance of the renin-angiotensin system in mediating aldosterone biosynthesis during sodium deficiency and the essential role of the renin-angiotensin-aldosterone system in the regulation of arterial pressure during sodium deficiency. Sodium 250-256 renin Canis lupus familiaris 180-185 870226-8 1977 The precipitous fall in aldosterone secretion and arterial blood pressure during long-term infusion of angiotensin I-converting enzyme inhibitor demonstrates the importance of the renin-angiotensin system in mediating aldosterone biosynthesis during sodium deficiency and the essential role of the renin-angiotensin-aldosterone system in the regulation of arterial pressure during sodium deficiency. Sodium 381-387 renin Canis lupus familiaris 180-185 885607-1 1977 The effects of insulin administration via intracerebroventricular (ICV), third ventricular (TV) and intracisternal (IC) routes on the urine output and sodium excretion have been studied in mongrel dogs. Sodium 151-157 insulin Canis lupus familiaris 15-22 885607-2 1977 The central administration of insulin resulted in a significant increase in urine output and sodium excretion. Sodium 93-99 insulin Canis lupus familiaris 30-37 842668-7 1977 Thus, chronic sodium loading and DOCA administration causes renin depletion and dissociates the autoregulation of RBF and GFR. Sodium 14-20 renin Canis lupus familiaris 60-65 842675-5 1977 Continued infusion of the hyperoncotic albumin resulted in a natriuresis and a parallel fall in proximal glucose and sodium reabsorption. Sodium 117-123 albumin Rattus norvegicus 39-46 837470-0 1977 Intrarenal renin-angiotensin-sodium interdependent mechanism controlling postclamp renal artery pressure and renin release in the conscious dog with chronic one-kidney Goldblatt hypertension. Sodium 29-35 renin Canis lupus familiaris 11-16 837470-0 1977 Intrarenal renin-angiotensin-sodium interdependent mechanism controlling postclamp renal artery pressure and renin release in the conscious dog with chronic one-kidney Goldblatt hypertension. Sodium 29-35 renin Canis lupus familiaris 109-114 870268-2 1977 With intraperitoneal furosemide, mean net ultrafilrate sodium concentration increased significantly to 121.2 mE1/l while ethacrynic acid had no such effect and both drugs affected dialyzate volume very slightly. Sodium 55-61 small nucleolar RNA, H/ACA box 73a Mus musculus 109-112 191213-4 1977 Dogs on approximately equal to 5 mEq/day of sodium showed significant increases in plasma renin activity (PRA) with intrarenal infusion of the peptides, unmasking a negative feedback inhibition of renin release by angiotensin II. Sodium 44-50 renin Canis lupus familiaris 90-95 191213-4 1977 Dogs on approximately equal to 5 mEq/day of sodium showed significant increases in plasma renin activity (PRA) with intrarenal infusion of the peptides, unmasking a negative feedback inhibition of renin release by angiotensin II. Sodium 44-50 renin Canis lupus familiaris 197-202 899932-2 1977 In TPTx rats, as well as in normal rats, bovine PTH induced a decrease in net calcium, sodium, and water absorption. Sodium 87-93 parathyroid hormone Bos taurus 48-51 185095-2 1976 2) As sodium depletion progresses, the renin--angiotensin system becomes increasingly important in the maintenance of blood pressure. Sodium 6-12 renin Canis lupus familiaris 39-44 185095-6 1976 Although angiotensin II is essential for the initiation of the elevated blood pressure, the renin--angiotensin system plays a decreasing role in the maintenance of the chronic hypertension as sodium and water are retained, and plasma volume increases. Sodium 192-198 renin Canis lupus familiaris 92-97 976442-2 1976 Significant positive correlations were found between a) PGEs secreted in 24 h and sodium excreted in 24 h, b) the ratio PGEs/UnaV before and PGEs/UnaV after volume expansion and c) the ration Na/K and urinary PGEs. Sodium 82-88 prostaglandin E synthase Homo sapiens 56-60 984205-0 1976 Influence of dietary sodium on renin activity and arterial pressure during anesthesia. Sodium 21-27 renin Canis lupus familiaris 31-36 971575-2 1976 The effect of purified bovine parathyroid hormone on renal tubular reabsorption of sodium and calcium has been studied by micropuncture in intact and recently thyroparathyroidectomized dogs. Sodium 83-89 parathyroid hormone Bos taurus 30-49 971575-4 1976 Parathyroid hormone increased the rejection of sodium and calcium proportionately at the late proximal tubule in both intact and operated dogs. Sodium 47-53 parathyroid hormone Canis lupus familiaris 0-19 952282-6 1976 Urinary kallikrein concentration was significantly lower in black children than in white children (p less than 0.001) and was positively correlated with urinary creatinine and urinary potassium and inversely related to urinary sodium concentrations. Sodium 227-233 kallikrein related peptidase 4 Homo sapiens 8-18 953829-0 1976 Duodenal calcium-binding-protein (CaBP) in the sodium deficient growing rat. Sodium 47-53 hippocalcin Rattus norvegicus 9-32 953829-0 1976 Duodenal calcium-binding-protein (CaBP) in the sodium deficient growing rat. Sodium 47-53 hippocalcin Rattus norvegicus 34-38 932211-6 1976 These results suggest that the effects of hyperglycemia on renal handling of sodium and calcium may be mediated through changes in plasma insulin concentration. Sodium 77-83 insulin Canis lupus familiaris 138-145 957249-6 1976 At a sodium deficit of 0-6 m-mole.kg-1 renin release had doubled. Sodium 5-11 renin Canis lupus familiaris 39-44 957249-10 1976 Precise replacement of sodium loss with isotonic saline but without replacement of other urinary components returned renin release to control levels. Sodium 23-29 renin Canis lupus familiaris 117-122 973974-2 1976 2 On the high sodium intake when angiotensin II and plasma renin activity (PRA) were suppressed, P113 infusion (5-10 mug kg-1 min-1) caused a slight rise in BP and a marked drop in urine flow and sodium excretion, with a fall in glomerular filtration rate, and effective renal plasma flow. Sodium 14-20 signal transducer and activator of transcription 2 Homo sapiens 97-101 973974-2 1976 2 On the high sodium intake when angiotensin II and plasma renin activity (PRA) were suppressed, P113 infusion (5-10 mug kg-1 min-1) caused a slight rise in BP and a marked drop in urine flow and sodium excretion, with a fall in glomerular filtration rate, and effective renal plasma flow. Sodium 196-202 signal transducer and activator of transcription 2 Homo sapiens 97-101 973974-3 1976 3 On the low sodium intake, when angiotensin II and PRA were increased, P113 infusion (5-10 mugkg-1 min-1) caused no change in blood pressure, urine flow or sodium excretion. Sodium 13-19 signal transducer and activator of transcription 2 Homo sapiens 72-76 973974-5 1976 4 These results show firstly that angiotension II is involved in maintaning standing blood pressure during dietary sodium depletion in normal man and secondly that P113 does have agonist as well as antagonist activity in normal man, the effect depending on the level of angiotension II and sodium intake. Sodium 290-296 signal transducer and activator of transcription 2 Homo sapiens 164-168 767286-2 1976 Moreover, in response to various provocative stimuli it can: (i) increase plasma renin activity in response to low sodium intake; (ii) suppress PRA in response to high sodium intake; (iii) produce increased serum erythropoietin in response to hypoxia. Sodium 115-121 renin Canis lupus familiaris 81-86 767286-2 1976 Moreover, in response to various provocative stimuli it can: (i) increase plasma renin activity in response to low sodium intake; (ii) suppress PRA in response to high sodium intake; (iii) produce increased serum erythropoietin in response to hypoxia. Sodium 115-121 erythropoietin Canis lupus familiaris 213-227 767286-2 1976 Moreover, in response to various provocative stimuli it can: (i) increase plasma renin activity in response to low sodium intake; (ii) suppress PRA in response to high sodium intake; (iii) produce increased serum erythropoietin in response to hypoxia. Sodium 168-174 renin Canis lupus familiaris 81-86 767286-2 1976 Moreover, in response to various provocative stimuli it can: (i) increase plasma renin activity in response to low sodium intake; (ii) suppress PRA in response to high sodium intake; (iii) produce increased serum erythropoietin in response to hypoxia. Sodium 168-174 erythropoietin Canis lupus familiaris 213-227 793782-6 1976 d) Insulin decreases phosphate clearance by direct renal action, probably by enhancing the tubular reabsorption of this ion as well as of sodium. Sodium 138-144 insulin Canis lupus familiaris 3-10 33641076-0 2021 Dexmedetomidine alleviates pulmonary edema through the epithelial sodium channel (ENaC) via the PI3K/Akt/Nedd4-2 pathway in LPS-induced acute lung injury. Sodium 66-72 NEDD4 like E3 ubiquitin protein ligase Homo sapiens 105-112 33500550-0 2021 Phospho-ablation of cardiac sodium channel Nav1.5 mitigates susceptibility to atrial fibrillation and improves glucose homeostasis under conditions of diet-induced obesity. Sodium 28-34 sodium channel, voltage-gated, type V, alpha Mus musculus 43-49 33500550-3 2021 Recent studies have identified increased cardiac late sodium current (INa,L) downstream of calmodulin-dependent kinase II (CaMKII) activation as an important driver of AF susceptibility. Sodium 54-60 calcium/calmodulin-dependent protein kinase II, beta Mus musculus 91-121 33500550-3 2021 Recent studies have identified increased cardiac late sodium current (INa,L) downstream of calmodulin-dependent kinase II (CaMKII) activation as an important driver of AF susceptibility. Sodium 54-60 calcium/calmodulin-dependent protein kinase II, beta Mus musculus 123-129 33370552-1 2021 Suppression of the cardiac sodium channel NaV1.5 leads to fatal arrhythmias in ischemic heart disease (IHD). Sodium 27-33 sodium channel, voltage-gated, type V, alpha Mus musculus 42-48 33792238-1 2021 The main function of fibroblast growth factor 23 (FGF23) is the regulation of phosphate metabolism through its action on the sodium-dependent phosphate cotransporters in the proximal renal tubules. Sodium 125-131 fibroblast growth factor 23 Homo sapiens 21-48 33792238-1 2021 The main function of fibroblast growth factor 23 (FGF23) is the regulation of phosphate metabolism through its action on the sodium-dependent phosphate cotransporters in the proximal renal tubules. Sodium 125-131 fibroblast growth factor 23 Homo sapiens 50-55 33086288-4 2021 We describe a small molecule Nav1.7 inhibitor, ST-2530, that is an analog of the naturally occurring sodium channel blocker saxitoxin. Sodium 101-107 sodium voltage-gated channel alpha subunit 9 Homo sapiens 29-35 33711230-0 2021 The Effects of Sodium Ions on Ligand Binding and Conformational States of G Protein-Coupled Receptors-Insights from Mass Spectrometry. Sodium 15-21 vomeronasal 1 receptor 17 pseudogene Homo sapiens 74-101 33711230-3 2021 Here, using nanoscale electrospray ionization emitters, we establish conditions that enable mass spectrometry of two G protein-coupled receptors (GPCR) from buffers containing high concentrations of sodium ions. Sodium 199-205 vomeronasal 1 receptor 17 pseudogene Homo sapiens 117-144 33711230-3 2021 Here, using nanoscale electrospray ionization emitters, we establish conditions that enable mass spectrometry of two G protein-coupled receptors (GPCR) from buffers containing high concentrations of sodium ions. Sodium 199-205 vomeronasal 1 receptor 17 pseudogene Homo sapiens 146-150 33711230-4 2021 For the Class A GPCR, the adenosine 2A receptor, we observe ligand-induced changes to sodium binding of the receptor at the level of individual sodium ions. Sodium 86-92 vomeronasal 1 receptor 17 pseudogene Homo sapiens 16-20 33711230-4 2021 For the Class A GPCR, the adenosine 2A receptor, we observe ligand-induced changes to sodium binding of the receptor at the level of individual sodium ions. Sodium 144-150 vomeronasal 1 receptor 17 pseudogene Homo sapiens 16-20 33733301-3 2022 The descriptions of two recently described salt-losing tubulopathies, transient antenatal Bartter syndrome and HELIX syndrome, which are caused by mutations in MAGED2 and CLDN10 genes, respectively, highlight the role of new players in the modulation of sodium reabsorption the thick ascending limb. Sodium 254-260 MAGE family member D2 Homo sapiens 160-166 33692040-7 2021 She was managed by infusion of hypertonic saline and fluids for 5 days and discharged from ICU after improvement of her conscious level and normalisation of serum sodium. Sodium 163-169 Src homology 2 domain containing E Homo sapiens 0-3 33666761-3 2021 IL-17A promotes an increase in blood pressure through multiple mechanisms including inhibiting endothelial nitric oxide production, increasing reactive oxygen species formation, promoting vascular fibrosis, and enhancing renal sodium retention and glomerular injury. Sodium 227-233 interleukin 17A Homo sapiens 0-6 33296280-5 2021 First, we co-localized the transcription factor FoxP2 with the activity marker Fos to identify pre-LC neurons in sodium-deprived rats and show their distribution relative to surrounding catecholaminergic and cholinergic neurons. Sodium 113-119 forkhead box P2 Rattus norvegicus 48-53 33296280-7 2021 Using Cre-reporter mice for Pdyn, we confirmed that most of these sodium-depletion-activated neurons are dynorphinergic. Sodium 66-72 prodynorphin Mus musculus 28-32 32737897-1 2021 Sodium channel alpha two subunit (SCN2A) mutations cause difficult-to-treat early-onset epilepsy. Sodium 0-6 sodium voltage-gated channel alpha subunit 2 Homo sapiens 34-39 33388853-5 2021 SIRT1 is involved in the development of cardiomyocytes, regulation of voltage-gated cardiac sodium ion channels via deacetylation, prevention of atherosclerotic plaque formation in the cardiovascular system, protection against oxidative damage and anti-thrombotic actions. Sodium 92-98 sirtuin 1 Homo sapiens 0-5 33655725-0 2021 Sodium/glucose Co-Transporter 2 Inhibitor, Empagliflozin, Alleviated Transient Expression of SGLT2 after Myocardial Infarction. Sodium 0-6 solute carrier family 5 (sodium/glucose cotransporter), member 2 Mus musculus 93-98 33099282-11 2021 Non-COAT platelets use forward-mode NCX, thus pumping calcium out and moving sodium in, while COAT platelets rely on reverse NCX function, which pumps additional calcium into the cytosol, by extruding sodium. Sodium 77-83 T cell leukemia homeobox 2 Homo sapiens 36-39 33084880-2 2021 Uromodulin is almost exclusively expressed in the thick ascending limb of the loop of Henle (TAL) and its effect on BP appear to be mediated via the TAL sodium transporter, NKCC2. Sodium 153-159 uromodulin Homo sapiens 0-10 33189717-1 2021 The human apical sodium-dependent bile acid transporter (hASBT, SLC10A2) is the rate-limiting step of intestinal bile acid absorption in the enterohepatic circulation system of bile acids. Sodium 17-23 solute carrier family 10 member 2 Homo sapiens 57-62 33189717-1 2021 The human apical sodium-dependent bile acid transporter (hASBT, SLC10A2) is the rate-limiting step of intestinal bile acid absorption in the enterohepatic circulation system of bile acids. Sodium 17-23 solute carrier family 10 member 2 Homo sapiens 64-71 33145656-0 2021 Small G-protein RhoA is a potential inhibitor of cardiac fast sodium current. Sodium 62-68 ras homolog family member A Rattus norvegicus 16-20 33145656-8 2021 Thus, RhoA might be considered as a potential negative regulator of sodium channels cardiac isoform NaV1.5. Sodium 68-74 ras homolog family member A Rattus norvegicus 6-10 32826759-3 2021 Several voltage-gated sodium (NaV) and calcium (CaV) channels are implicated in the etiology of chronic pain, particularly NaV1.1, NaV1.3, NaV1.7-NaV1.9, CaV2.2 and CaV3.2. Sodium 22-28 sodium voltage-gated channel alpha subunit 9 Homo sapiens 139-145 33493520-0 2021 Engineering of highly potent and selective HNTX-III mutant against hNav1.7 sodium channel for treatment of pain. Sodium 75-81 sodium voltage-gated channel alpha subunit 9 Homo sapiens 67-74 33493520-1 2021 Human voltage-gated sodium channel (VGSC) Nav1.7 (hNav1.7) is involved in the generation and conduction of neuropathic and nociceptive pain signals. Sodium 20-26 sodium voltage-gated channel alpha subunit 9 Homo sapiens 42-48 33493520-1 2021 Human voltage-gated sodium channel (VGSC) Nav1.7 (hNav1.7) is involved in the generation and conduction of neuropathic and nociceptive pain signals. Sodium 20-26 sodium voltage-gated channel alpha subunit 9 Homo sapiens 50-57 33442688-2 2021 Plasmin, and other host proteases, may cleave the furin site of SARS-CoV-2 S protein and gamma subunits of epithelial sodium channels (gamma ENaC), resulting in an increment in virus infectivity and channel activity. Sodium 118-124 sodium channel epithelial 1 subunit gamma Homo sapiens 135-145 33384439-1 2020 SCNN1B encodes the beta subunit of the epithelial sodium channel ENaC. Sodium 50-56 sodium channel epithelial 1 subunit beta Homo sapiens 0-6 33851023-8 2021 Subsequent genetic testing revealed a novel mutation in SCNN1B (deletion: c.1713delC), leading to the premature termination of the sodium channel epithelial 1 subunit-beta protein and the LS phenotype. Sodium 131-137 sodium channel epithelial 1 subunit beta Homo sapiens 56-62 33344518-2 2020 We previously demonstrated that sodium/glucose cotransporter 2 inhibitors (SGLT2i"s) have direct cardiac effects on ion homeostasis, possibly through inhibition of the cardiac sodium/hydrogen exchanger (NHE-1). Sodium 32-38 solute carrier family 5 (sodium/glucose cotransporter), member 2 Mus musculus 75-80 33344518-2 2020 We previously demonstrated that sodium/glucose cotransporter 2 inhibitors (SGLT2i"s) have direct cardiac effects on ion homeostasis, possibly through inhibition of the cardiac sodium/hydrogen exchanger (NHE-1). Sodium 176-182 solute carrier family 5 (sodium/glucose cotransporter), member 2 Mus musculus 75-80 33059246-6 2020 The results showed that GRP could decrease voltage-gated sodium currents mainly by affecting the kinetics of recovery from the inactivated state. Sodium 57-63 gastrin releasing peptide Rattus norvegicus 24-27 33262327-7 2020 In vitro mouse hippocampal neurons transfected with mutant miR-873 showed less morphological complexity and enhanced sodium currents and excitatory neurotransmission compared to cells transfected with wild-type miR-873. Sodium 117-123 microRNA 873a Mus musculus 59-66 33211688-6 2020 Females were analyzed by sequencing and/or diagnostic PCR using de novo designed primers for detecting the kdr-like mutation in the voltage-gated sodium channel (L982F; TTA to TTT) (house fly kdr canonical mutation L1014F). Sodium 146-152 sodium channel protein para-like Musca domestica 107-110 33211688-6 2020 Females were analyzed by sequencing and/or diagnostic PCR using de novo designed primers for detecting the kdr-like mutation in the voltage-gated sodium channel (L982F; TTA to TTT) (house fly kdr canonical mutation L1014F). Sodium 146-152 sodium channel protein para-like Musca domestica 192-195 33165811-7 2021 Consistent with the previous results, sodium cantharidinate treatment decreased Bcl-2 and mitochondrial cytochrome-c protein expression, as well as phosphorylation of MDM2; meanwhile, it increased the levels of cleaved-caspase-3, cleaved-caspase-9, cleaved-PARP, Bax, and phosphorylated p53, thus inducing the apoptosis of pancreatic cancer cells. Sodium 38-44 MDM2 proto-oncogene Homo sapiens 167-171 32306429-2 2020 It also decreases airway epithelial sodium transport, especially through the epithelial sodium channel (ENaC) (1), which is crucial for osmosis-based fluid absorption across respiratory epithelium. Sodium 36-42 enac None 104-108 32306429-2 2020 It also decreases airway epithelial sodium transport, especially through the epithelial sodium channel (ENaC) (1), which is crucial for osmosis-based fluid absorption across respiratory epithelium. Sodium 88-94 enac None 104-108 32687732-0 2020 Dual mechanism of modulation of NaV1.8 sodium channels by ouabain. Sodium 39-45 sodium voltage-gated channel alpha subunit 10 Homo sapiens 32-38 33215440-8 2020 In the acute phase of KD, the serum level of miRNA-122 was positively correlated to CRP and NT-proBNP, while negatively correlated to the sodium level. Sodium 138-144 microRNA 122 Homo sapiens 45-54 32056381-2 2020 Twelve ion-coordinating residues are highly conserved among NCXs and distinct NCX orthologs contain two or three carboxylates, whilst sharing a common ion-exchange stoichiometry (3Na+ :1Ca2+ ). Sodium 179-182 T cell leukemia homeobox 2 Homo sapiens 60-63 33164306-1 2020 Klotho was involved in sodium reabsorption and the regulation of blood pressure. Sodium 23-29 klotho Homo sapiens 0-6 32403129-1 2020 BACKGROUND: Single nucleotide polymorphisms (SNPs) of the voltage-gated sodium channel alpha subunit gene (SCN9A) have been associated with pain in various settings. Sodium 72-78 sodium voltage-gated channel alpha subunit 9 Homo sapiens 107-112 33185386-12 2020 Whole-cell patch-clamping was applied to assess alterations in the tetrodotoxin-resistant (TTX-R) sodium current (Nav1.8) in DRGs. Sodium 98-104 sodium voltage-gated channel alpha subunit 10 Homo sapiens 114-120 32472700-5 2020 We found that the cation-pi interaction significantly decreases the total rate of removal of singlet oxygen (kT ) for the model system, i.e. (kT = 2.4 +- 0.2) x 108 M-1 sec-1 without sodium cation vs. (kT = 6.9 +- 0.7) x 107 M-1 sec-1 upon complexation of sodium cation to the crown ether. Sodium 183-189 secretory blood group 1, pseudogene Homo sapiens 229-234 32472700-5 2020 We found that the cation-pi interaction significantly decreases the total rate of removal of singlet oxygen (kT ) for the model system, i.e. (kT = 2.4 +- 0.2) x 108 M-1 sec-1 without sodium cation vs. (kT = 6.9 +- 0.7) x 107 M-1 sec-1 upon complexation of sodium cation to the crown ether. Sodium 256-262 secretory blood group 1, pseudogene Homo sapiens 169-174 32758497-3 2020 In this study, eight human sodium channel subtypes, hNav1.1- hNav1.8, were expressed in HEK293 or ND7/23 cells and tested on the chemically synthesized TsIIIA. Sodium 27-33 sodium voltage-gated channel alpha subunit 10 Homo sapiens 61-68 32758497-8 2020 Taken together, the hNav1.8 peptide inhibitor TsIIIA provides a pharmacological probe for sodium channels and a potential therapeutic agent for pain. Sodium 90-96 sodium voltage-gated channel alpha subunit 10 Homo sapiens 20-27 33194000-0 2020 Stimulation of Epithelial Sodium Channels in Endothelial Cells by Bone Morphogenetic Protein-4 Contributes to Salt-Sensitive Hypertension in Rats. Sodium 26-32 bone morphogenetic protein 4 Rattus norvegicus 66-94 33194000-2 2020 We used our unique split-open artery technique combined with protein biochemistry and in vitro measurement of vascular tone to test a hypothesis that bone morphogenetic protein 4 (BMP4) mediates high salt-induced loss of vascular relaxation by stimulating the epithelial sodium channel (ENaC) in endothelial cells. Sodium 271-277 bone morphogenetic protein 4 Rattus norvegicus 150-178 33194000-2 2020 We used our unique split-open artery technique combined with protein biochemistry and in vitro measurement of vascular tone to test a hypothesis that bone morphogenetic protein 4 (BMP4) mediates high salt-induced loss of vascular relaxation by stimulating the epithelial sodium channel (ENaC) in endothelial cells. Sodium 271-277 bone morphogenetic protein 4 Rattus norvegicus 180-184 33087732-3 2020 We apply this concept to the analysis of variants in sodium channel NaV1.7 subunit found in patients with chronic painful syndromes, by the implementation of a dedicated computational pipeline empowering different and complementary techniques including homology modeling, network theory, and machine learning. Sodium 53-59 sodium voltage-gated channel alpha subunit 9 Homo sapiens 68-74 33195194-1 2020 In stroke and other neurological diseases, Transient Receptor Potential Melastatin 4 (TRPM4) has been reported to cause oncotic cell death which is due to an excessive influx of sodium ions. Sodium 178-184 transient receptor potential cation channel, subfamily M, member 4 Rattus norvegicus 43-84 33195194-1 2020 In stroke and other neurological diseases, Transient Receptor Potential Melastatin 4 (TRPM4) has been reported to cause oncotic cell death which is due to an excessive influx of sodium ions. Sodium 178-184 transient receptor potential cation channel, subfamily M, member 4 Rattus norvegicus 86-91 33195194-2 2020 Following stroke, hypoxia condition activates TRPM4 channel, and the sodium influx via TRPM4 is further enhanced by an increased TRPM4 expression. Sodium 69-75 transient receptor potential cation channel, subfamily M, member 4 Rattus norvegicus 46-51 33195194-2 2020 Following stroke, hypoxia condition activates TRPM4 channel, and the sodium influx via TRPM4 is further enhanced by an increased TRPM4 expression. Sodium 69-75 transient receptor potential cation channel, subfamily M, member 4 Rattus norvegicus 87-92 33195194-2 2020 Following stroke, hypoxia condition activates TRPM4 channel, and the sodium influx via TRPM4 is further enhanced by an increased TRPM4 expression. Sodium 69-75 transient receptor potential cation channel, subfamily M, member 4 Rattus norvegicus 87-92 32908170-1 2020 The voltage-gated sodium channel isoform NaV1.7 is highly expressed in dorsal root ganglion neurons and is obligatory for nociceptive signal transmission. Sodium 18-24 sodium voltage-gated channel alpha subunit 9 Homo sapiens 41-47 32908170-5 2020 Here we describe the discovery and characterization of ST-2262, a NaV1.7 inhibitor that blocks the extracellular vestibule of the channel with an IC50 of 72 nM and greater than 200-fold selectivity over off-target sodium channel isoforms, NaV1.1-1.6 and NaV1.8. Sodium 214-220 sodium voltage-gated channel alpha subunit 9 Homo sapiens 66-72 32908170-8 2020 These findings establish the extracellular vestibule of the sodium channel as a viable receptor site for the design of selective ligands targeting NaV1.7. Sodium 60-66 sodium voltage-gated channel alpha subunit 9 Homo sapiens 147-153 32877464-4 2020 Capture probes were designed to target nine sodium channel genes (SCN3A, SCN8A-SCN11A, and SCN1B-SCN4B). Sodium 44-50 sodium voltage-gated channel alpha subunit 8 Homo sapiens 73-78 32755467-10 2020 Collectively, these results suggest that endogenous GLP-1R signaling exerts a physiologically relevant effect on BP control, which may be attributable, in part, to its tonic actions on the proximal tubule NHE3-mediated sodium reabsorption, intrarenal renin-angiotensin system, and insulin sensitivity. Sodium 219-225 glucagon-like peptide 1 receptor Rattus norvegicus 52-58 32506135-9 2020 Sodium supplementation decreased both plasma phosphate (from 1.10 +- 0.19 to 1.06 +- 0.21 mmol/L, P = 0.03) and FGF23 (from 114.3 [96.8-135.0] to 108.7 [92.3-128.1] RU/mL, P = 0.02). Sodium 0-6 fibroblast growth factor 23 Homo sapiens 112-117 31985858-10 2020 Of various nutrient transporters studied, only expression of SLC2A1 encoding facilitative glucose transporter GLUT1 was increased among patients, whereas RNA expression of genes encoding sodium-dependent glucose, sterol, fatty-acid, and peptide transport remained unchanged. Sodium 187-193 solute carrier family 2 member 1 Homo sapiens 61-67 32439321-1 2020 Salt-Overly-Sensitive (SOS) signaling module comprising the sodium-transport protein SOS1 and the regulatory proteins SOS2 and SOS3, is well known as the central salt excretion system that helps plants against salt accumulation. Sodium 60-66 Protein kinase superfamily protein Arabidopsis thaliana 118-122 32774568-3 2020 Sodium channel 1.7 (Nav1.7) plays a prominent role in pain perceptions, as evidenced by deletion of Nav1.7 alone leading to a complete loss of pain. Sodium 0-6 sodium voltage-gated channel alpha subunit 9 Homo sapiens 20-26 32774568-3 2020 Sodium channel 1.7 (Nav1.7) plays a prominent role in pain perceptions, as evidenced by deletion of Nav1.7 alone leading to a complete loss of pain. Sodium 0-6 sodium voltage-gated channel alpha subunit 9 Homo sapiens 100-106 32722255-0 2020 Bidirectional Modulation of the Voltage-Gated Sodium (Nav1.6) Channel by Rationally Designed Peptidomimetics. Sodium 46-52 sodium voltage-gated channel alpha subunit 8 Homo sapiens 54-60 32709000-2 2020 This study aimed to examine the interaction between dietary sodium/potassium intake, sodium-potassium ratios, and FGF5 rs16998073 and link these with increased risk for developing hypertension. Sodium 60-66 fibroblast growth factor 5 Homo sapiens 114-118 10406832-1 1999 In Dahl salt-sensitive rats on a high salt diet or normotensive rats with chronic central infusion of sodium, increased brain "ouabain" results in sympathetic hyperactivity and hypertension, possibly by activating the brain renin-angiotensin system. Sodium 102-108 renin Rattus norvegicus 224-229 10404817-8 1999 We hypothesize, however, that these polymorphisms might influence salt conservation negatively if they are present concurrently with other genetic defects of the MR or other proteins that participate in sodium homeostasis. Sodium 203-209 nuclear receptor subfamily 3 group C member 2 Homo sapiens 162-164 10559906-2 1999 As a result, PtdIns(4,5)P2 alone can activate IRK1 but not GIRKs, which require extra gating molecules such as the beta gamma subunits of G proteins or sodium ions. Sodium 152-158 potassium inwardly rectifying channel subfamily J member 2 Homo sapiens 46-50 10360950-4 1999 Replacements of Asp-373 with Ala, Glu, Asn, and Gln resulted in changes in sodium affinity and cation selectivity in NaDC-1, indicating that the carbonyl oxygen at this position may play a role in the topological organization of the cation-binding site. Sodium 75-81 solute carrier family 13 member 2L homeolog Xenopus laevis 117-123 10320342-1 1999 The Na+/dicarboxylate cotransporter (NaDC-1) couples the transport of sodium and tricarboxylic acid cycle intermediates, such as succinate and citrate. Sodium 70-76 solute carrier family 13 member 2 Homo sapiens 37-43 32709000-5 2020 Multivariable logistic regression was used to examine the relationship between dietary intake of sodium, potassium, and sodium-potassium ratios and the FGF5 rs16998073 genotypes (AA, AT, TT) and any increased risk of hypertension. Sodium 97-103 fibroblast growth factor 5 Homo sapiens 152-156 32709000-12 2020 In addition, we showed that high daily intake of sodium exerted a synergistic effect for hypertension when combined with FGF5 rs16998073 variants in both genders and that dietary sodium, potassium, and sodium-potassium ratios all interact with FGF5 rs16998073 and alter the risk of developing hypertension in carriers of either gender among Koreans. Sodium 49-55 fibroblast growth factor 5 Homo sapiens 244-248 32709000-12 2020 In addition, we showed that high daily intake of sodium exerted a synergistic effect for hypertension when combined with FGF5 rs16998073 variants in both genders and that dietary sodium, potassium, and sodium-potassium ratios all interact with FGF5 rs16998073 and alter the risk of developing hypertension in carriers of either gender among Koreans. Sodium 179-185 fibroblast growth factor 5 Homo sapiens 244-248 32709000-12 2020 In addition, we showed that high daily intake of sodium exerted a synergistic effect for hypertension when combined with FGF5 rs16998073 variants in both genders and that dietary sodium, potassium, and sodium-potassium ratios all interact with FGF5 rs16998073 and alter the risk of developing hypertension in carriers of either gender among Koreans. Sodium 179-185 fibroblast growth factor 5 Homo sapiens 244-248 32645615-9 2020 Patch clamp experiments showed that in an oxidative stress environment, GSTM3 down-regulation leads to a significant decrease of cardiac sodium channel current amplitude. Sodium 137-143 glutathione S-transferase mu 3 Homo sapiens 72-77 10196319-1 1999 We have previously reported that the accessory protein Vpr from human immunodeficiency virus type 1 forms cation-selective ion channels in planar lipid bilayers and is able to depolarize intact cultured neurons by causing an inward sodium current, resulting in cell death. Sodium 232-238 Vpr Human immunodeficiency virus 1 55-58 10436405-7 1999 EGF significantly decreased the lumen-to-bath isotope flux of sodium and chloride from 93.6+/-12.5 to 61.1+/-9.6 pmol/mm/min (n = 5, p<0.05) and from 86.6+/-10.0 to 54. Sodium 62-68 pro-epidermal growth factor Oryctolagus cuniculus 0-3 10436405-13 1999 In conclusion, EGF depolarizes transepithelial voltage by inhibiting sodium transport primarily and potassium and chloride transport secondarily. Sodium 69-75 pro-epidermal growth factor Oryctolagus cuniculus 15-18 10207057-6 1999 In addition, hal4 hal5 and trk1 trk2 mutants exhibit similar phenotypes: (i) they are deficient in potassium uptake; (ii) their growth is sensitive to a variety of toxic cations, including lithium, sodium, calcium, tetramethylammonium, hygromycin B, and low pH; and (iii) they exhibit increased uptake of methylammonium, an indicator of membrane potential. Sodium 198-204 Trk1p Saccharomyces cerevisiae S288C 27-31 32306766-1 2020 The diurnal rhythms of sodium handling and blood pressure are thought to be regulated by clock genes, such as Bmal1. Sodium 23-29 aryl hydrocarbon receptor nuclear translocator-like Rattus norvegicus 110-115 32306766-3 2020 Using a novel whole-body Bmal1 knockout rat model (Bmal1-/-), we hypothesized that time of day regulation of sodium excretion is dependent on Bmal1. Sodium 109-115 aryl hydrocarbon receptor nuclear translocator-like Rattus norvegicus 25-30 32306766-3 2020 Using a novel whole-body Bmal1 knockout rat model (Bmal1-/-), we hypothesized that time of day regulation of sodium excretion is dependent on Bmal1. Sodium 109-115 aryl hydrocarbon receptor nuclear translocator-like Rattus norvegicus 51-56 32306766-3 2020 Using a novel whole-body Bmal1 knockout rat model (Bmal1-/-), we hypothesized that time of day regulation of sodium excretion is dependent on Bmal1. Sodium 109-115 aryl hydrocarbon receptor nuclear translocator-like Rattus norvegicus 51-56 32306766-7 2020 Female Bmal1-/- rats, however, had significantly greater sodium excretion during the active versus inactive period similar to controls. Sodium 57-63 aryl hydrocarbon receptor nuclear translocator-like Rattus norvegicus 7-12 32469979-3 2020 The goal of the current study was to investigate the role of sodium-hydrogen exchanger type 1 (NHE1) in blood brain barrier (BBB) integrity during CSD events and the contributions of this antiporter on xenobiotic uptake. Sodium 61-67 solute carrier family 9 member A1 Rattus norvegicus 95-99 32462076-2 2020 The sodium-proton-exchanger subtype 3 (NHE3) is an important mediator of intestinal sodium absorption. Sodium 4-10 solute carrier family 9 member A3 Homo sapiens 39-43 32462076-2 2020 The sodium-proton-exchanger subtype 3 (NHE3) is an important mediator of intestinal sodium absorption. Sodium 84-90 solute carrier family 9 member A3 Homo sapiens 39-43 32462076-7 2020 Results: Inhibition of intestinal NHE3 by SAR increased fecal sodium excretion, resulted in marked changes in feces electrolyte concentrations and water content, reduced blood pressure and preserved atrial emptying function (active total percent emptying: SHR-ob SAR: 0.47 +- 0.05% vs. SHR-ob PLAC: 0.38 +- 0.007, p < 0.0001). Sodium 62-68 solute carrier family 9 member A3 Homo sapiens 34-38 32462076-10 2020 Conclusions: Reduction of intestinal sodium absorption and subsequent changes in feces milieu by pharmacological NHE3 inhibition in the gut preserved atrial emptying function and reduced AF susceptibility. Sodium 37-43 solute carrier family 9 member A3 Homo sapiens 113-117 32429423-1 2020 Sensory neurons respond to noxious stimuli by relaying information from the periphery to the central nervous system via action potentials driven by voltage-gated sodium channels, specifically Nav1.7 and Nav1.8. Sodium 162-168 sodium voltage-gated channel alpha subunit 9 Homo sapiens 192-198 32429423-1 2020 Sensory neurons respond to noxious stimuli by relaying information from the periphery to the central nervous system via action potentials driven by voltage-gated sodium channels, specifically Nav1.7 and Nav1.8. Sodium 162-168 sodium voltage-gated channel alpha subunit 10 Homo sapiens 203-209 32315024-0 2020 Ubiquitination-activating enzymes UBE1 and UBA6 regulate ubiquitination and expression of cardiac sodium channel Nav1.5. Sodium 98-104 ubiquitin like modifier activating enzyme 6 Homo sapiens 43-47 32409881-6 2020 RESULTS: Hs1a-FL showed specific and stable binding to the sodium channel NaV1.7, present on the surface of human and mouse nerves. Sodium 59-65 sodium voltage-gated channel alpha subunit 9 Homo sapiens 74-80 32408599-9 2020 We suppose a ceramide synthesis inhibitor (FB1) effect exerted onto the cell membrane, proven to be toxin dose-dependent and increasing sodium pump activity, with only indirect FA compositional correlations and lack of lipid peroxidation. Sodium 136-142 TCF3 fusion partner Homo sapiens 43-46 32385249-1 2020 The sodium channels Nav1.7, Nav1.8 and Nav1.9 are critical for pain perception in peripheral nociceptors. Sodium 4-10 sodium channel, voltage-gated, type XI, alpha Mus musculus 39-45 32244818-0 2020 Differential Inhibition of Human Nav1.2 Resurgent and Persistent Sodium Currents by Cannabidiol and GS967. Sodium 65-71 sodium voltage-gated channel alpha subunit 2 Homo sapiens 33-39 31815915-1 2020 Selective targeting of sodium channel subtypes Nav1.7, Nav1.8 and Nav1.9, preferentially expressed by peripheral nociceptors, represents a unique opportunity to develop analgesics devoid of central side effects. Sodium 23-29 sodium channel, voltage-gated, type XI, alpha Mus musculus 66-72 31830704-12 2020 From five d and above, group NaSe-0.60 excelled with increased specific hematological variables culminating at age 38d with increased Hct, mean corpuscular volume (MCV), and MC hemoglobin (MCH) as well as increased activities of aspartate transaminase and lactate dehydrogenase compared with the other groups. Sodium 29-33 MCH Sus scrofa 174-187 32059356-18 2020 This is observed for MnF3, NbF5, NiF2, and CuF2, which lead to high gas releases from the decomposition of NaBH4 at the lowest decomposition temperatures. Sodium 107-112 zinc finger protein 335 Homo sapiens 33-37 10435004-0 1999 Attenuation of ischemia induced increases in sodium and calcium by the aldose reductase inhibitor zopolrestat. Sodium 45-51 aldo-keto reductase family 1 member B1 Rattus norvegicus 71-87 32550491-0 2020 Calx, a sodium/calcium exchanger, may affect lifespan in Drosophila melanogaster. Sodium 8-14 Na/Ca-exchange protein Drosophila melanogaster 0-4 10072434-5 1999 A recently cloned homologue of the organic cation transporter, OCTN2, which has sodium-dependent carnitine uptake properties, was also mapped to the same locus. Sodium 80-86 solute carrier family 22 member 5 Homo sapiens 63-68 10051674-9 1999 These data suggest that sgk plays a central role in aldosterone regulation of Na+ absorption and thus in the control of extracellular fluid volume, blood pressure, and sodium homeostasis. Sodium 168-174 serum/glucocorticoid regulated kinase 1 Rattus norvegicus 24-27 10024318-0 1999 Intracellular sodium modulates the expression of angiotensin II subtype 2 receptor in PC12W cells. Sodium 14-20 angiotensin II receptor, type 2 Rattus norvegicus 49-82 10067792-0 1999 Effects of sodium depletion on the role of AT1- and alpha-adrenergic receptors in the regulation of forearm vascular tone in humans. Sodium 11-17 angiotensin II receptor type 1 Homo sapiens 43-46 9927610-8 1999 In contrast, replacement of Asp113 by Ala residue in NTR1 strongly decreases its ability to activate inositol turnover, indicating that the functionally active conformation of NTR1 is maintained by interaction of sodium ions with aspartate 113. Sodium 213-219 neurotensin receptor 1 Homo sapiens 53-57 9927610-8 1999 In contrast, replacement of Asp113 by Ala residue in NTR1 strongly decreases its ability to activate inositol turnover, indicating that the functionally active conformation of NTR1 is maintained by interaction of sodium ions with aspartate 113. Sodium 213-219 neurotensin receptor 1 Homo sapiens 176-180 10321970-2 1999 Neuronal AT1 receptors within these areas mediate the stimulatory actions of central Ang II on blood pressure, water and sodium intake, and vasopressin secretion, effects that involve the modulation of brain noradrenergic pathways. Sodium 121-127 angiotensin II receptor type 1 Homo sapiens 9-12 10024479-1 1999 Recombinant bovine cardiac sodium-calcium exchange (NCX1) in a baculovirus construct was used to infect cabbage looper larvae (Trichoplusia ni). Sodium 27-33 solute carrier family 8 member A1 Bos taurus 52-56 10463998-8 1999 CONCLUSION: Our results suggest that the lower SPC activity in both nonproteinuric and proteinuric PIH may be an early sign of abnormality in the transport of sodium and potassium across the vascular smooth-muscle cell membrane, which is responsible for the maintenance of blood pressure. Sodium 159-165 pregnancy-induced hypertension (pre-eclampsia, eclampsia, toxemia of pregnancy included) Homo sapiens 99-102 9892162-5 1999 Although the mechanisms responsible for the regulation of intratubular AngII concentrations remain to be determined, micropuncture studies have provided direct evidence that activation of intraluminal AT1 receptors by AngII exerts a substantial stimulatory influence on sodium and bicarbonate transport by both proximal and distal tubules. Sodium 270-276 angiotensin II receptor type 1 Homo sapiens 201-204 9916128-4 1999 Both could be blocked by PD or L-NAME, suggesting that the effects of sodium restriction occur via ANG II at the AT2 receptor. Sodium 70-76 angiotensin II receptor, type 2 Rattus norvegicus 113-116 9830050-1 1998 Nearly identical proteins (denoted NAA-Tr, rBAT, D2, NBAT), cloned from mammalian kidneys, induce a largely sodium-independent high-affinity transport system for cystine, basic amino acids, and some neutral amino acids in Xenopus oocytes (system b0,+-like). Sodium 108-114 solute carrier family 3 member 1 Homo sapiens 53-57 9843872-6 1998 Decreases in plasma ANG II concentrations of 23-52% were inversely related to sodium excretion. Sodium 78-84 angiogenin Homo sapiens 20-23 9822451-6 1998 Increasing sodium intake from basal (0.08%) to high (2.56% wt/dry wt in the diet) increased renal XOR activity dose-dependently from 68+/-8 to 143+/-21 microU/mg protein in the Dahl S (P<0.05) but not in Dahl salt-resistant (Dahl R) rats. Sodium 11-17 xanthine dehydrogenase Rattus norvegicus 98-101 9822451-8 1998 Sodium restriction (0.02% wt/wt) downregulated kidney XOR activity in both Dahl S and R rats by nearly 40%. Sodium 0-6 xanthine dehydrogenase Rattus norvegicus 54-57 9731751-3 1998 One of the mechanisms by which intracellular pH (pHi) is regulated is through the sodium/hydrogen exchanger, a ubiquitous membrane protein which exploits the intra- and extracellular sodium ion gradient to drive hydrogen ions out of the cell. Sodium 82-88 glucose-6-phosphate isomerase 1 Mus musculus 49-52 9731751-3 1998 One of the mechanisms by which intracellular pH (pHi) is regulated is through the sodium/hydrogen exchanger, a ubiquitous membrane protein which exploits the intra- and extracellular sodium ion gradient to drive hydrogen ions out of the cell. Sodium 183-189 glucose-6-phosphate isomerase 1 Mus musculus 49-52 9731756-0 1998 Effects of polyamines and calcium and sodium ions on smooth muscle cytoskeleton-associated phosphatidylinositol (4)-phosphate 5-kinase. Sodium 38-44 phosphatidylinositol-5-phosphate 4-kinase type 2 gamma Homo sapiens 91-134 9734597-2 1998 In this study a group of 18 unrelated and 2 related Gitelman patients, collected from six different countries have been screened for mutations in the human thiazide-sensitive sodium-chloride cotransporter (SLC12A3) gene. Sodium 175-181 solute carrier family 12 member 3 Homo sapiens 206-213 9734601-8 1998 Alpha-MSH also significantly preserved GFR and tubular sodium reabsorption in the isolated perfused ischemic kidney model. Sodium 55-61 pro-opiomelanocortin-alpha Mus musculus 0-9 9734601-12 1998 The preservation of sodium absorption ex vivo and inhibition of nitrite production in cultured MCT cells suggests that alpha-MSH inhibits tubular injury by direct tubular effects. Sodium 20-26 pro-opiomelanocortin-alpha Mus musculus 119-128 9729254-8 1998 These results indicate that AT1 receptors located in the SFO may have a role in mediating an enhanced sodium intake produced by methysergide treatment. Sodium 102-108 angiotensin II receptor type 1 Homo sapiens 28-31 9888610-7 1998 The experimental treatment resulted in a decrease and increase in Pref-1 expression in ACTH treated and low sodium diet treated rats respectively, in accordance with changes in abundance of glomerulosa cells. Sodium 108-114 delta like non-canonical Notch ligand 1 Rattus norvegicus 66-72 9644212-9 1998 The preferential increase of adrenal AT1B mRNA during a low-salt intake could be explained by the elevation of endogenous ANGII levels during sodium deficiency, suggesting that endogenous ANGII acts as an enhancer for adrenal AT1B but not for AT1A receptor gene expression via ANGII-AT1 receptors. Sodium 142-148 angiotensin II receptor, type 1a Rattus norvegicus 37-40 9707197-5 1998 RESULTS: The 11 patients with hyponatremia (serum sodium concentration of < 135 mEq/L) had much higher plasma BNP concentrations during each period than did healthy controls (P < 0.05), whereas the 7 patients with normonatremia did not show statistically higher values. Sodium 50-56 natriuretic peptide B Homo sapiens 113-116 9622142-10 1998 During DOC administration, cumulative urinary sodium excretion was lower in Bk2r-/- than in Bk2r+/+ (2.59+/-0.15 versus 3.31+/-0.22 mmol, respectively, during the first week; P<0.05). Sodium 46-52 bradykinin receptor, beta 2 Mus musculus 76-80 9630341-7 1998 In the presence of 10(-4) M PD123319, a selective non-peptide AT2 receptor antagonist, intracellular sodium levels rose from steady state by 30% (P < 0.01; n = 7) within 10 min of exposure to angiotensin II 10(-11) M. Over the subsequent 30 min steady state levels were re-established. Sodium 101-107 angiotensin II receptor, type 2 Rattus norvegicus 62-65 9630341-13 1998 These findings show that at both the high and low concentrations of angiotensin II, its modulation of intracellular sodium levels within the proximal tubule cells is mediated via the activation of AT1 receptors. Sodium 116-122 angiotensin II receptor, type 1a Rattus norvegicus 197-200 9564057-13 1998 Blood ethanol levels, decrease in sodium, and irrigant deficit were significantly lower in GnRH group. Sodium 34-40 gonadotropin releasing hormone 1 Homo sapiens 91-95 9596079-1 1998 Genetic analysis has demonstrated complete linkage between the human thiazide-sensitive sodium chloride cotransporter gene (NCCT or TSC) and Gitelman"s syndrome (GS). Sodium 88-94 solute carrier family 12 member 3 Homo sapiens 124-135 9618071-7 1998 Supportive evidence linking these biochemical changes to the loss of nerve function has come from studies in which aldose reductase inhibitors block polyol pathway activity, prevent the depletion of myo-inositol and the accumulation of sodium and preserve Na/K ATPase activity, as well as nerve function. Sodium 236-242 aldo-keto reductase family 1 member B1 Rattus norvegicus 115-131 9508819-4 1998 PTC hypertrophy (cellular protein content), DNA synthesis (thymidine incorporation) and apical sodium-hydrogen exchange (NHE) activity (ethylisopropylamiloride-sensitive apical 22Na+ uptake) were measured following 24 h incubation in media supplemented with 10 % pre- or post-nephrectomy sera obtained from these patients. Sodium 95-101 solute carrier family 9 member C1 Homo sapiens 121-124 9561804-1 1998 Recent studies indicate that the actions of arginine vasopressin (AVP) and other agonists that stimulate electrogenic sodium transport in renal epithelial A6 cells are linked to a Ca(2+)-mobilizing signal transduction mechanism that involves generation of inositol trisphosphate. Sodium 118-124 arginine vasopressin S homeolog Xenopus laevis 53-64 9561804-7 1998 Further studies showed that cyclohexyladenosine and insulin, additional agonists of sodium transport in A6 cells, also stimulated phosphorylation of MARCKS. Sodium 84-90 myristoylated alanine-rich protein kinase C substrate S homeolog Xenopus laevis 149-155 9544877-12 1998 These data also suggest that angiotensin AT2 receptors play a depressor role in the sodium-induced pressor response in this model. Sodium 84-90 angiotensin II receptor, type 2 Rattus norvegicus 41-44 9458824-4 1998 BNP infusion increased the urinary flow rate and the excretion of sodium in a dose-dependent way. Sodium 66-72 natriuretic peptide B Homo sapiens 0-3 9891757-2 1998 The Cat-1 gene encodes a sodium-independent high-affinity cationic amino acid transporter of the y+ system which is nearly undetectable in the quiescent liver. Sodium 25-31 solute carrier family 7 member 1 Rattus norvegicus 4-9 18470493-2 1998 BothD: -xylose andD: -mannose reduce the cell water content andD: -galactose does occasionally the same but onlyD: -xylose reduces significantly the intracellular sodium concentration, presumably by forming steric hindrances at the outlets of the sodium pumps at the outer surface of the cell membrane. Sodium 163-169 secretion associated Ras related GTPase 1B Homo sapiens 15-19 9421486-10 1998 On day 7, CIR-NAME rats had an increase in sodium excretion as compared with the CIR rats (sodium excretion: 2.4 versus 0.7 mmol per day, P < 0.001) and a negative sodium balance (-0.5 versus +0.8 mmol per day, P < 0.001). Sodium 43-49 corepressor interacting with RBPJ, 1 Rattus norvegicus 10-13 9421486-10 1998 On day 7, CIR-NAME rats had an increase in sodium excretion as compared with the CIR rats (sodium excretion: 2.4 versus 0.7 mmol per day, P < 0.001) and a negative sodium balance (-0.5 versus +0.8 mmol per day, P < 0.001). Sodium 91-97 corepressor interacting with RBPJ, 1 Rattus norvegicus 10-13 9421486-10 1998 On day 7, CIR-NAME rats had an increase in sodium excretion as compared with the CIR rats (sodium excretion: 2.4 versus 0.7 mmol per day, P < 0.001) and a negative sodium balance (-0.5 versus +0.8 mmol per day, P < 0.001). Sodium 91-97 corepressor interacting with RBPJ, 1 Rattus norvegicus 10-13 9519207-11 1998 These findings have also demonstrated a key role for CLCKB as a major basolateral chloride channel involved in mTAL sodium and chloride reabsorption (Figure 2). Sodium 116-122 chloride voltage-gated channel Kb Homo sapiens 53-58 9604281-5 1998 One of the three 47 residue toxins characterized, PCR2-10, enhances veratridine-dependent sodium uptake, displaying a K0.5 of 329 nM and 1354 nM in RT4-B and N1E-115 cell lines, respectively. Sodium 90-96 mannosidase, alpha, class 1A, member 2 Mus musculus 50-57 9435530-1 1997 Cyclic nucleotide-gated cation channels in skeletal muscle are responsible for insulin-activated sodium entry into this tissue (J. E. M. McGeoch and G. Guidotti. Sodium 97-103 insulin Oryctolagus cuniculus 79-86 9389507-12 1997 Based on Losartan displacement, we calculated that [125I]AII bound to AT1 and to AT2 receptors was increased in both ZG and ZFR + M cell preparations under sodium restriction. Sodium 156-162 angiotensin II receptor, type 2 Rattus norvegicus 81-84 9389507-13 1997 Results of binding studies on cell membranes were also indicative of an increasing effect of sodium restriction on AT1 and AT2 receptors binding capacity. Sodium 93-99 angiotensin II receptor, type 1a Rattus norvegicus 115-118 9389507-13 1997 Results of binding studies on cell membranes were also indicative of an increasing effect of sodium restriction on AT1 and AT2 receptors binding capacity. Sodium 93-99 angiotensin II receptor, type 2 Rattus norvegicus 123-126 9389507-14 1997 Furthermore, Northern blotting analysis revealed 3.0- and 2.5-fold increases in the level of AT1 receptor mRNA in the ZG and the ZFR + M of rats fed a low sodium diet as compared with those fed a normal diet. Sodium 155-161 angiotensin II receptor, type 1a Rattus norvegicus 93-96 9389507-15 1997 The low sodium intake resulted in a weaker increase (1.5-fold) in the level of AT2 receptor messenger RNA in the ZG, with no changes in the ZFR + M preparations. Sodium 8-14 angiotensin II receptor, type 2 Rattus norvegicus 79-82 9389507-16 1997 In conclusion, in this study complementary approaches were needed to determine the localization of AT1 and AT2 receptors in the rat adrenal, and to show the increasing effects of a low sodium regimen on the adrenal level of these receptors. Sodium 185-191 angiotensin II receptor, type 2 Rattus norvegicus 107-110 9389507-17 1997 Immunofluorescence studies revealed AT1 receptors mainly in the ZG and also in some cells of the inner adrenal cortex zones; in adrenals of rats kept on a low sodium diet the ZG was markedly enlarged, and an increased number of immunoreactive cells with AT1 receptors were observed throughout that zone; also more immunoreactive cells were present in the inner zones of the adrenal cortex. Sodium 159-165 angiotensin II receptor, type 1a Rattus norvegicus 36-39 9354703-6 1997 Sf9 cells infected with the histidine-tagged NaSi-1 or untagged NaSi-1 protein expressed sodium-dependent sulfate cotransport up to 60-fold higher compared to noninfected cells. Sodium 89-95 solute carrier family 13 member 1 Homo sapiens 45-51 9354703-6 1997 Sf9 cells infected with the histidine-tagged NaSi-1 or untagged NaSi-1 protein expressed sodium-dependent sulfate cotransport up to 60-fold higher compared to noninfected cells. Sodium 89-95 solute carrier family 13 member 1 Homo sapiens 64-70 9438176-9 1997 After 48 h of CsA incubation, the intracellular sodium concentration increased in all three different cell types; however, it stayed within the physiological range of mammalian cells. Sodium 48-54 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 14-17 9353588-4 1997 Sodium or chloride depletion decreased plasma levels of atrial natriuretic peptide, increased plasma renin activity, and induced extracellular fluid volume contraction. Sodium 0-6 renin Rattus norvegicus 101-106 9321889-6 1997 At steady states of secretion driven by hypervolemia, the administration of ANP antiserum (anti-ANP), which reduced plasma ANP concentrations by 90%, caused an immediate 30% reduction in fluid secretion rate and sodium excretion that lasted for 20-30 min. Sodium 212-218 natriuretic peptides A Oryctolagus cuniculus 76-79 9321889-6 1997 At steady states of secretion driven by hypervolemia, the administration of ANP antiserum (anti-ANP), which reduced plasma ANP concentrations by 90%, caused an immediate 30% reduction in fluid secretion rate and sodium excretion that lasted for 20-30 min. Sodium 212-218 natriuretic peptides A Oryctolagus cuniculus 96-99 9321889-6 1997 At steady states of secretion driven by hypervolemia, the administration of ANP antiserum (anti-ANP), which reduced plasma ANP concentrations by 90%, caused an immediate 30% reduction in fluid secretion rate and sodium excretion that lasted for 20-30 min. Sodium 212-218 natriuretic peptides A Oryctolagus cuniculus 96-99 9338511-4 1997 The DA1 agonist, fenoldopam, significantly increased urinary sodium excretion, but there was no increase in sodium excretion when a DA1 agonist was given together with a DA2 antagonist. Sodium 61-67 RT1 class II, locus Da Rattus norvegicus 4-7 9236205-3 1997 Coexpression of tipE with para results in elevated levels of sodium currents and accelerated current decay. Sodium 61-67 paralytic Drosophila melanogaster 26-30 9211350-11 1997 Ultimately, changes in proximal tubule AT1R expression, mediated by elevated glucose concentrations and insulin, could contribute to sodium-dependent hypertension in the setting of hyperinsulinemia and hyperglycemia. Sodium 133-139 insulin Oryctolagus cuniculus 104-111 9192691-8 1997 Conversely, jolting mice with a mutated Scn8a message demonstrates PC abnormalities in rapid, simple spike generation, linking CerIII to the persistent sodium current. Sodium 152-158 sodium channel, voltage-gated, type VIII, alpha Mus musculus 40-45 9176324-5 1997 Both renal venous renin (RR) and renin secretion rate (RSR) were elevated approximately fourfold by sodium restriction [RR = 5.8 +/- 0.8 vs. 20.5 +/- 2.7 ng angiotensin (ANG) I.ml-1.h-1; P < 0.001; RSR = 3.0 +/- 0.9 vs. 13.1 +/- 4.1 ng ANG I.h-1.min-1; P < 0.025]. Sodium 100-106 renin Rattus norvegicus 18-23 9176324-8 1997 Although selective NOS inhibition by 7-NI did not affect BP, RBF, or renin in control rats on a normal diet, chronic 7-NI reversed the stimulation of renin induced by dietary sodium restriction. Sodium 175-181 renin Rattus norvegicus 150-155 9176324-9 1997 These data suggest that nNOS-derived NO plays an important role in the macula densa during feedback stimulation of renin induced by dietary sodium restriction. Sodium 140-146 renin Rattus norvegicus 115-120 9141514-8 1997 Altogether, our results indicate a differential, tissue-specific expression of hMR mRNA isoforms, hMR beta being down-regulated in situations of positive sodium balance, independently of aldosterone levels. Sodium 154-160 mannose receptor C-type 1 Homo sapiens 79-82 9144579-0 1997 Expression of sodium-dependent purine nucleoside carrier (SPNT) mRNA correlates with nucleoside transport activity in rat liver. Sodium 14-20 solute carrier family 28 member 2 Rattus norvegicus 58-62 9144579-4 1997 We show that the hepatic mRNA levels of the putative sodium-dependent transport system SPNT correlate with the sodium-dependent uridine transport rates in plasma membrane vesicles from rat liver. Sodium 53-59 solute carrier family 28 member 2 Rattus norvegicus 87-91 9144579-4 1997 We show that the hepatic mRNA levels of the putative sodium-dependent transport system SPNT correlate with the sodium-dependent uridine transport rates in plasma membrane vesicles from rat liver. Sodium 111-117 solute carrier family 28 member 2 Rattus norvegicus 87-91 9144579-5 1997 These results suggest that the induction of the sodium-dependent nucleoside transport expressed in liver parenchymal cells involves regulation of SPNT gene expression. Sodium 48-54 solute carrier family 28 member 2 Rattus norvegicus 146-150 9095083-6 1997 The renal cytolocalization of the Ang II/AVP receptor to the outer medullary thick ascending limb tubules and inner medullary collecting ducts is consistent with the well-established AVP stimulation of sodium and water reabsorption in these tubules. Sodium 202-208 angiogenin Homo sapiens 34-37 9056693-1 1997 The study was undertaken to determine the possible effect of an aldosterone antagonist, spironolactone (SP), on red blood cell sodium-hydrogen exchange (NHE) enhancement in primary aldosteronism (PA) and essential hypertension (EH). Sodium 127-133 solute carrier family 9 member C1 Homo sapiens 153-156 9040450-1 1997 The combination of single oral doses of an angiotensin I-converting enzyme inhibitor (captopril) and a type 1 angiotensin II receptor antagonist (losartan) has additive effects on blood pressure fall and renin release in sodium-depleted normotensive subjects. Sodium 221-227 angiotensin II receptor type 1 Homo sapiens 103-133 9048337-1 1997 Low sodium intake has been demonstrated to upregulate the gene expression of the predominant renal type 1 angiotensin II (Ang II) receptor (AT1), the AT1A subtype. Sodium 4-10 angiotensin II receptor, type 1a Rattus norvegicus 99-143 9048337-1 1997 Low sodium intake has been demonstrated to upregulate the gene expression of the predominant renal type 1 angiotensin II (Ang II) receptor (AT1), the AT1A subtype. Sodium 4-10 angiotensin II receptor, type 1a Rattus norvegicus 150-154 9048337-2 1997 The study presented here tests the hypothesis that the upregulation of renal AT1 mRNA induced by sodium depletion occurs conjointly with an elevation of the AT1 receptor that modulates renal growth. Sodium 97-103 angiotensin II receptor, type 1a Rattus norvegicus 77-80 9048337-8 1997 Renal AT1 receptor binding in the rats subjected to sodium depletion plus losartan did not differ from that in control rats. Sodium 52-58 angiotensin II receptor, type 1a Rattus norvegicus 6-9 9048337-12 1997 Low sodium intake was found to increase mRNA and expression of the renal AT1 receptor but to have no effect on renal growth, suggesting that an increase in renal mass above a normal level requires the activation of multiple factors. Sodium 4-10 angiotensin II receptor, type 1a Rattus norvegicus 73-76 9071983-3 1997 The increase in sodium excretion of 42 +/- 9% during oxytocin infusion was significantly decreased by all three antagonists to 15 +/- 5% (10 ng [mercapto-proprionic acid1, D-Tyr(Et)2,Thr4,Orn8]-oxytocin/min), 13 +/- 5% (5 ng desGly9[D-Trp2,Thr4,Orn8]-dC6oxytocin/min) and 4 +/- 5% (1 ng d(CH2)5[Tyr(Me)2,Thr4,Orn8,Tyr(NH2)9]-vasotocin/min). Sodium 16-22 transient receptor potential cation channel subfamily C member 2 Rattus norvegicus 235-239 8989666-4 1997 In primary cultures of embryonic rat hippocampal progenitor cells, growth in proliferative conditions (FGF-2) was associated with low levels of sodium, calcium, N-methyl-D-aspartate (NMDA), and kainate currents compared with other growth conditions. Sodium 144-150 fibroblast growth factor 2 Rattus norvegicus 103-108 8958582-0 1996 Gene expression of central and peripheral renin-angiotensin system components upon dietary sodium intake in rats. Sodium 91-97 renin Rattus norvegicus 42-47 8958582-1 1996 The effects of dietary sodium intake on the gene expression of the renin-angiotensin system (RAS) were investigated in rat central and peripheral tissues in a single set of experiment. Sodium 23-29 renin Rattus norvegicus 67-72 8958582-3 1996 Plasma and renal renin levels were elevated in rats maintained on the low-sodium diet. Sodium 74-80 renin Rattus norvegicus 17-22 8958582-4 1996 Sodium deprivation enhanced the expression of angiotensinogen, renin, AT1A and AT1B receptor subtypes in the hypothalamus, but suppressed them in the brainstem. Sodium 0-6 renin Rattus norvegicus 63-68 8958582-4 1996 Sodium deprivation enhanced the expression of angiotensinogen, renin, AT1A and AT1B receptor subtypes in the hypothalamus, but suppressed them in the brainstem. Sodium 0-6 angiotensin II receptor, type 1a Rattus norvegicus 70-74 8958582-6 1996 Both AT1A and AT1B mRNAs changed in a similar magnitude in each tissue examined upon dietary sodium intake. Sodium 93-99 angiotensin II receptor, type 1a Rattus norvegicus 5-9 8997225-1 1996 A cyclic nucleotide-gated channel present in skeletal muscle plasma membrane has previously been identified as being responsible for insulin-activated sodium entry into muscle cells (J. E. M. McGeoch and G. Guidotti. Sodium 151-157 insulin Oryctolagus cuniculus 133-140 8945984-0 1996 Dietary sodium effects on renin and angiotensinogen gene expression in preweanling WKY and SHR. Sodium 8-14 renin Rattus norvegicus 26-31 8946005-8 1996 However, the human transporter, hNaDC-1, had a lower apparent affinity for sodium (KNa, 78 mM) than the rabbit transporter (KNa, 41 mM). Sodium 75-81 solute carrier family 13 member 2 Homo sapiens 32-39 8913751-1 1996 Previous work has shown that mutation of the gene that encodes the microtubule motor subunit kinesin heavy chain (Khc) in Drosophila inhibits neuronal sodium channel activity, action potentials and neurotransmitter secretion. Sodium 151-157 Kinesin heavy chain Drosophila melanogaster 93-112 8913751-1 1996 Previous work has shown that mutation of the gene that encodes the microtubule motor subunit kinesin heavy chain (Khc) in Drosophila inhibits neuronal sodium channel activity, action potentials and neurotransmitter secretion. Sodium 151-157 Kinesin heavy chain Drosophila melanogaster 114-117 8904632-4 1996 We conclude that angiotensin II is secreted into proximal tubular fluid and, in the anaesthetized rat, is maintained at a concentration that inhibits sodium and water transport via AT1 receptors. Sodium 150-156 angiotensin II receptor, type 1a Rattus norvegicus 181-184 8770082-1 1996 We have previously demonstrated that two isoforms (AT1A and AT1B) of the angiotensin II (ANG II) type 1 (AT1) receptor exist in the rat kidney and are differentially regulated by a low-sodium diet. Sodium 185-191 angiotensin II receptor, type 1a Rattus norvegicus 51-54 8770082-2 1996 The present experiment was designed to test the hypothesis that sodium deficiency upregulates AT1A and AT1B gene expression in the adrenal gland by activating the AT1 receptor. Sodium 64-70 angiotensin II receptor, type 1a Rattus norvegicus 94-97 8770082-8 1996 We conclude that sodium deficiency increases both AT1A and AT1B gene expression and elevates the AT1 receptor density in the adrenal gland. Sodium 17-23 angiotensin II receptor, type 1a Rattus norvegicus 50-53 8698199-8 1996 CONCLUSIONS: Endotoxin inhibits hepatocellular sodium-dependent bile salt uptake by decreasing both expression of Ntcp and activity of the Na+,K-ATPase. Sodium 47-53 solute carrier family 10 member 1 Rattus norvegicus 114-118 8765998-2 1996 Stimulation of the renin system was achieved by unilateral renal artery clipping (2-kidney/1-clip rats), treatment with the angiotensin II (ANG II) antagonist losartan (40 mg/kg), application of furosemide (12 mg x kg-1 x day-1) and a low-sodium diet (0.02% w/w Na+), which increased renin mRNA levels to 464%, 495%, 309% and 219% of those of control animals, respectively. Sodium 239-245 renin Rattus norvegicus 19-24 8636408-2 1996 In the spontaneously hypertensive rat (SHR), in spite of normal renal production of dopamine and receptor density, there is defective transduction of the D1 receptor signal in renal proximal tubules, resulting in decreased inhibition of sodium transport (Na+/H+ exchanger [NHE] and Na+/K+ATPase activity) by dopamine. Sodium 237-243 dopamine receptor D1 Mus musculus 154-165 8636408-8 1996 The cosegregation with hypertension of an impaired D1 receptor regulation of renal sodium transport and the development of elevated systolic and diastolic pressure in mice lacking one or both D1A alleles suggest a causal relationship of the D1A receptor gene with hypertension. Sodium 83-89 dopamine receptor D1 Mus musculus 51-62 8738419-6 1996 The sodium-dependent uptake of taurocholate was expressed permanently only in HPCT-1E3 cells, if the Ntcp was transfected by electroporation. Sodium 4-10 solute carrier family 10 member 1 Rattus norvegicus 101-105 8691747-3 1996 The plasma membrane of osteogenic cells is endowed with a sodium-dependent Pi transport system that is regulated by osteotropic factors such as parathyroid hormone (PTH), parathyroid hormone-related protein (PTHrP), insulin-like growth factor-1 (IGF-1), platelet-derived growth factor (PDGF) and fluoride. Sodium 58-64 parathyroid hormone like hormone Homo sapiens 171-206 8691747-3 1996 The plasma membrane of osteogenic cells is endowed with a sodium-dependent Pi transport system that is regulated by osteotropic factors such as parathyroid hormone (PTH), parathyroid hormone-related protein (PTHrP), insulin-like growth factor-1 (IGF-1), platelet-derived growth factor (PDGF) and fluoride. Sodium 58-64 parathyroid hormone like hormone Homo sapiens 208-213 8777826-17 1996 In conclusion, these findings suggest that in normal sodium-repleted man the renal, hormonal and blood pressure effects of AT1 antagonism and angiotensin-converting enzyme inhibition are not strictly similar and could be synergistic. Sodium 53-59 angiotensin II receptor type 1 Homo sapiens 123-126 8589728-2 1996 In vitro, assembly and expression of functional active sodium channels in the Xenopus oocyte is strictly dependent on alpha-ENaC--the beta and gamma subunits by themselves are unable to induce an amiloride-sensitive sodium current in this heterologous expression system (2). Sodium 55-61 sodium channel, non voltage gated 1 alpha subunit L homeolog Xenopus laevis 118-128 8929821-1 1996 OBJECTIVE: To develop methods based on enzyme activation for the analysis of sweat sodium and chloride using beta-galactosidase and alpha-amylase, respectively. Sodium 83-89 galactosidase beta 1 Homo sapiens 109-127 8815799-2 1996 Although its magnitude is < 1% of the transient sodium current, INaP has functional significance because it is activated about 10 mV negative to the transient sodium current, where few voltage-gated channels are activated and neuron input resistance is high. Sodium 51-57 NFKB inhibitor zeta Homo sapiens 67-71 8815799-2 1996 Although its magnitude is < 1% of the transient sodium current, INaP has functional significance because it is activated about 10 mV negative to the transient sodium current, where few voltage-gated channels are activated and neuron input resistance is high. Sodium 162-168 NFKB inhibitor zeta Homo sapiens 67-71 9138750-1 1996 Intracerebroventricular (IVT) administration of renin (R) to conscious male hydrated rats induces an increase in sodium excretion. Sodium 113-119 renin Rattus norvegicus 48-53 8846519-4 1995 Marked modulation of renin mRNA concentration is seen in adrenal, heart and hypothalamus in response to sodium depletion and inhibition of AII formation, as well as in models of renal and genetic hypertension in the rat. Sodium 104-110 renin Rattus norvegicus 21-26 7586282-7 1995 Plasma renin activity increased 45% (P < .05) in rats in sodium balance and 127% in sodium-retaining rats. Sodium 60-66 renin Rattus norvegicus 7-12 7586282-7 1995 Plasma renin activity increased 45% (P < .05) in rats in sodium balance and 127% in sodium-retaining rats. Sodium 87-93 renin Rattus norvegicus 7-12 8589326-6 1995 Endothelin blockade alone with either endothelin-converting enzyme inhibitor or the nonpeptide ETA and ETB receptor antagonist had little effect on blood pressure, RPF, or RVR, but increases in urinary sodium excretion and a small decline in GFR were observed with Bosentan. Sodium 202-208 endothelin receptor type A Rattus norvegicus 95-98 8718658-4 1995 In the kidney, BNP increases the glomerular filtration rate and inhibits sodium reabsorption in the distal tubule. Sodium 73-79 natriuretic peptide B Homo sapiens 15-18 8718658-7 1995 Plasma BNP levels are very low in healthy subjects, and respond modestly, although significantly to physiological stimuli such as changes in posture or sodium intake. Sodium 152-158 natriuretic peptide B Homo sapiens 7-10 8718658-10 1995 Evidence obtained by administering BNP to healthy subjects and hypertensive patients suggests that BNP, at physiological and pathophysiological plasma concentrations, markedly influences cardiovascular homeostasis, mainly due to its effects on sodium excretion and the renin-aldosterone axis. Sodium 244-250 natriuretic peptide B Homo sapiens 99-102 7543698-4 1995 In CF airway epithelia, the absence of this second function of CFTR as a cAMP-dependent regulator likely accounts for abnormal sodium transport. Sodium 127-133 CF transmembrane conductance regulator Canis lupus familiaris 63-67 7670488-5 1995 They thus permit cortisol to occupy the renal mineralocorticoid receptor and thereby cause sodium retention and hypertension. Sodium 91-97 nuclear receptor subfamily 3 group C member 2 Homo sapiens 46-72 7594440-8 1995 Rats fed a low-sodium diet showed a 37% increase in AT1a gene expression. Sodium 15-21 angiotensin II receptor, type 1a Rattus norvegicus 52-56 7795577-2 1995 However, the precise role of human BNP (hBNP) in the regulation of sodium balance and blood pressure in men is still unclarified. Sodium 67-73 natriuretic peptide B Homo sapiens 35-38 7534990-10 1995 Collectively, these data are consistent with endothelin-3 receptor activation at the secretory terminal initiating calcium entry, thereby leading to depolarization independent of sodium conductances. Sodium 179-185 endothelin 3 Rattus norvegicus 45-57 7736491-1 1995 The Na+/H+ exchanger in vascular smooth muscle cells represents a major mechanism for sodium influx and is also one of the principal mechanisms responsible for the regulation of intracellular pH (pHi). Sodium 86-92 glucose-6-phosphate isomerase Homo sapiens 196-199 7539404-6 1995 However, blocking of intracellular transport from Golgi to the endoplasmic reticulum, disassembly of actin filaments and disturbances in the intracellular sodium/calcium balance had identical effects on expression and release of the respective IL-2R. Sodium 155-161 interleukin 2 receptor subunit alpha Homo sapiens 244-249 7825650-2 1995 The proximal tubule mechanisms for the reabsorption of salt, volume, organic compounds, phosphate, and most bicarbonate reabsorption depend upon the generation and maintenance of a low intracellular sodium concentration by the basolateral membrane Na-K-ATPase pump. Sodium 199-205 dynein axonemal heavy chain 8 Homo sapiens 253-259 7829640-11 1995 The comparable effects of PTH and PTHrP on urinary phosphate, calcium, and sodium may indicate a non-cAMP-dependent pathway for these responses, although the intracellular pool of cAMP generated to either peptide, and thus the local target tissue response, could not be estimated in the present study. Sodium 75-81 parathyroid hormone like hormone Homo sapiens 34-39 7977783-0 1994 Influence of sodium diet on L-NAME effects on renin release and renal vasoconstriction. Sodium 13-19 renin Rattus norvegicus 46-51 8001038-1 1994 OBJECTIVE: The aim was to elucidate whether or not lactate modifies the fast sodium current (INa) in cardiac cells. Sodium 77-83 alpha-internexin Cavia porcellus 93-96 8001727-3 1994 Our experiments charted the development of the ionic specificity of sodium appetite aroused by sodium depletion or intracerebroventricular injection of renin. Sodium 68-74 renin Rattus norvegicus 152-157 7990088-4 1994 In INTERSALT, across centres, average sodium excretion was significantly related to slope of BP with age, such that 100 mmol lower sodium was associated with 10 mmHg lower rise in SBP over 30 years; among individuals, previous estimates of the size of relationships of sodium and potassium to BP in INTERSALT were too low because of insufficient correction for the "regression dilution" problem. Sodium 131-137 selenium binding protein 1 Homo sapiens 180-183 7990088-4 1994 In INTERSALT, across centres, average sodium excretion was significantly related to slope of BP with age, such that 100 mmol lower sodium was associated with 10 mmHg lower rise in SBP over 30 years; among individuals, previous estimates of the size of relationships of sodium and potassium to BP in INTERSALT were too low because of insufficient correction for the "regression dilution" problem. Sodium 131-137 selenium binding protein 1 Homo sapiens 180-183 7990088-5 1994 For sodium, revised corrected regression estimates, with adjustment for age and sex, were 4.3 mmHg/100 mmol for SBP and 1.8 mmHg/100 mmol for DBP. Sodium 4-10 selenium binding protein 1 Homo sapiens 112-115 8046459-1 1994 The dopamine transporter (DAT) and norepinephrine transporter (NET) terminate catecholaminergic neurotransmission at synapses by high-affinity sodium-dependent reuptake into presynaptic terminals, and are the initial sites of action for drugs of abuse and antidepressants. Sodium 143-149 solute carrier family 6 member 3 Rattus norvegicus 4-24 8046459-1 1994 The dopamine transporter (DAT) and norepinephrine transporter (NET) terminate catecholaminergic neurotransmission at synapses by high-affinity sodium-dependent reuptake into presynaptic terminals, and are the initial sites of action for drugs of abuse and antidepressants. Sodium 143-149 solute carrier family 6 member 3 Rattus norvegicus 26-29 8031857-0 1994 Short-term effect of epidermal growth factor (EGF) on sodium and glucose cotransport of isolated jejunal epithelial cells. Sodium 54-60 epidermal growth factor like 1 Rattus norvegicus 21-44 8031857-0 1994 Short-term effect of epidermal growth factor (EGF) on sodium and glucose cotransport of isolated jejunal epithelial cells. Sodium 54-60 epidermal growth factor like 1 Rattus norvegicus 46-49 8031857-1 1994 This study was undertaken to assess the short-term effects of EGF on sodium and glucose uptake, glucose metabolism and Na+/K(+)-ATPase activity in isolated enterocytes of rats. Sodium 69-75 epidermal growth factor like 1 Rattus norvegicus 62-65 8031857-2 1994 Jejunal cells exposed to EGF had a significantly greater total uptake of sodium compared to controls after 6 min. Sodium 73-79 epidermal growth factor like 1 Rattus norvegicus 25-28 8188173-1 1994 Activation of antinatriuretic systems such as the renin-angiotensin system, is of major importance in the pathogenesis of sodium retention in cirrhosis. Sodium 122-128 renin Rattus norvegicus 50-55 8188173-9 1994 These results indicate that sodium-retaining, nonascitic bile duct-ligated rats show abnormalities of the intrarenal renin angiotensin system that precede changes in plasma renin activity. Sodium 28-34 renin Rattus norvegicus 117-122 8188173-9 1994 These results indicate that sodium-retaining, nonascitic bile duct-ligated rats show abnormalities of the intrarenal renin angiotensin system that precede changes in plasma renin activity. Sodium 28-34 renin Rattus norvegicus 173-178 8197200-4 1994 Upon transient expression in HeLa cells, dSERT exhibited saturable, high-affinity, and sodium-dependent [3H]5HT uptake with estimated Km and Vmax values of approximately 500 nM and 5.2 x 10(-18) mol per cell per min, respectively. Sodium 87-93 Serotonin transporter Drosophila melanogaster 41-46 8203552-9 1994 Sodium overload aggravates the renal and systemic consequences of chronic NO inhibition by mechanisms that may include paradoxical activation of renin secretion. Sodium 0-6 renin Rattus norvegicus 145-150 8175172-11 1994 The results suggest a role for the renin-angiotensin system in the maintenance of glomerular filtration rate and sodium excretion in transgenic TGR (mRen-2)27 rats. Sodium 113-119 renin Rattus norvegicus 35-40 8175974-2 1994 Compared to placebo, BNP induced significant increases in effective renal plasma flow (para-aminohippurate clearance), glomerular filtration rate (creatinine clearance), urine flow rate, and sodium excretion without affecting blood pressure, heart rate, cardiac output (echocardiographic method), peripheral vascular resistance, PRA, plasma aldosterone, or plasma norepinephrine to any significant extent. Sodium 191-197 natriuretic peptide B Homo sapiens 21-24 8184968-6 1994 Compared with ANP alone, BNP induced an additional (50%) increase in sodium excretion (P < 0.05) and significant increases in both plasma (P < 0.001) and urine guanosine 3",5"-cyclic monophosphate (P < 0.01). Sodium 69-75 natriuretic peptide B Homo sapiens 25-28 8200490-0 1994 Intracerebroventricular injection of renin in the neonatal rat reveals a precocious sodium appetite that is dissociated from renin-aroused thirst. Sodium 84-90 renin Rattus norvegicus 37-42 8200490-3 1994 In this article we report experiments that dissociate neonatal renin-evoked sodium appetite and thirst, and establish the specificity of the appetite. Sodium 76-82 renin Rattus norvegicus 63-68 8200490-5 1994 During this developmental window, renin-evoked sodium appetite is dissociated from thirst because (a) NaCl is preferred to water, (b) the appetite develops faster than thirst, and (c) 3-day-old renin-stimulated pups will avidly lick dry NaCl. Sodium 47-53 renin Rattus norvegicus 34-39 8200490-5 1994 During this developmental window, renin-evoked sodium appetite is dissociated from thirst because (a) NaCl is preferred to water, (b) the appetite develops faster than thirst, and (c) 3-day-old renin-stimulated pups will avidly lick dry NaCl. Sodium 47-53 renin Rattus norvegicus 194-199 8160784-0 1994 pHi determines rate of sodium transport in frog skin: results of a new method to determine pHi. Sodium 23-29 glucose-6-phosphate isomerase Homo sapiens 0-3 8160784-0 1994 pHi determines rate of sodium transport in frog skin: results of a new method to determine pHi. Sodium 23-29 glucose-6-phosphate isomerase Homo sapiens 91-94 8191539-4 1994 The suppression of dehydrogenase activity allows glucocorticoids to activate the mineralocorticoid receptor, leading to classical mineralocorticoid type effects such as sodium retention and potassium excretion. Sodium 169-175 nuclear receptor subfamily 3 group C member 2 Homo sapiens 81-107 8297180-14 1994 ANF may be involved in the pathogenesis of the renal and water and sodium metabolic disturbances present in this disease. Sodium 67-73 natriuretic peptides A Oryctolagus cuniculus 0-3 8156651-8 1994 Sodium excretion from denervated kidneys rose by 7.49 +/- 3.11 mumol/min in response to ANP (approximately 55%, P < 0.05) compared to 0.84 +/- 0.59 mumol/min (approximately 28%, NS) in innervated kidneys. Sodium 0-6 natriuretic peptides A Oryctolagus cuniculus 88-91 8156651-11 1994 Fractional sodium excretion increased significantly in denervated kidneys in response to ANP (median 2.3% to median 3.0%, P < 0.05). Sodium 11-17 natriuretic peptides A Oryctolagus cuniculus 89-92 7506698-1 1994 Activation of the renin-angiotensin system by sodium deficiency is associated with reciprocal changes in the expression of angiotensin II receptors in adrenal glomerulosa and vascular smooth muscle cells. Sodium 46-52 renin Rattus norvegicus 18-23 7506698-4 1994 These results are consistent with previous findings on the effects of altered dietary sodium on the renin-angiotensin system. Sodium 86-92 renin Rattus norvegicus 100-105 7506698-5 1994 The expression of AT1A and AT1B receptor subtype mRNAs was determined by quantitative reverse transcriptase-polymerase chain reaction during changes in sodium intake. Sodium 152-158 angiotensin II receptor, type 1a Rattus norvegicus 18-22 7506698-7 1994 Conversely, high sodium diet increased the expression of AT1A receptors by 155% in the brain compared with low sodium intake. Sodium 17-23 angiotensin II receptor, type 1a Rattus norvegicus 57-61 7506698-7 1994 Conversely, high sodium diet increased the expression of AT1A receptors by 155% in the brain compared with low sodium intake. Sodium 111-117 angiotensin II receptor, type 1a Rattus norvegicus 57-61 8158336-0 1993 Protein excretion and renal adaptation of transgenic mRen2 rats to changing oral sodium loads. Sodium 81-87 renin 2 tandem duplication of Ren1 Mus musculus 53-58 8263040-7 1993 The 1 alpha,25-dihydroxyvitamin D3-induced increments in osteocalcin and osteopontin mRNA levels were abolished in sodium-free medium. Sodium 115-121 secreted phosphoprotein 1 Rattus norvegicus 73-84 8264144-9 1993 Plasma Lp(a) correlated directly with ANP (P < 0.01) and indirectly with urinary sodium excretion (P < 0.05). Sodium 84-90 lipoprotein(a) Homo sapiens 7-12 21244916-2 1993 Among them, its ability to regulate smooth muscle cell contractility and growth, as well as sodium and water homeostasis, making Ang II a major hormone of the cardiovascular system. Sodium 92-98 angiogenin Homo sapiens 129-132 8327470-1 1993 We have isolated two cDNA clones, NaPi-2 and NaPi-3, by screening rat kidney cortex and human kidney cortex cDNA libraries, respectively, for expression of sodium-dependent phosphate transport in Xenopus laevis oocytes. Sodium 156-162 solute carrier family 34 member 1 Homo sapiens 45-51 8498591-7 1993 These findings suggest that the delayed response of the renin-angiotensin-aldosterone system has a major role in the impaired renal and systemic adaptation to dietary sodium removal in senescent rats. Sodium 167-173 renin Rattus norvegicus 56-61 8456103-2 1993 Intracerebroventricular administration of renin reduces urine volume and increases sodium excretion and water intake in conscious, male, hydrated rats. Sodium 83-89 renin Rattus norvegicus 42-47 8384480-0 1993 The carboxy terminus of sodium and potassium ion transporting ATPase is located on the cytoplasmic surface of the membrane. Sodium 24-30 AT695_RS06370 Staphylococcus aureus 62-68 1307720-3 1992 After a long-term stimulation of renin synthesis and secretion by sodium depletion and captopril treatment the relative proportion of active renins I and II in granules significantly increased, while that of active renin III decreased. Sodium 66-72 renin Rattus norvegicus 33-38 1482638-0 1992 Plasma renin activity as a marker for growth failure due to sodium deficiency in young rats. Sodium 60-66 renin Rattus norvegicus 7-12 1396304-3 1992 Sodium depletion also has been shown to increase renal renin messenger RNA levels. Sodium 0-6 renin Rattus norvegicus 55-60 1396304-8 1992 At physiological (2.5 mM) extracellular calcium concentration, the amount of renin secreted per cell was approximately 2-fold greater (P < 0.05) when cells from enalapril-treated rats were compared to controls and sodium depletion increased both the number of renin-secreting cells and the amount of renin secreted by approximately 35% (P < 0.05). Sodium 217-223 renin Rattus norvegicus 77-82 1396304-11 1992 In contrast, sodium depletion increased renin secretion equally by both mechanisms. Sodium 13-19 renin Rattus norvegicus 40-45 1733312-0 1992 Adaptation to sodium restriction in renin-immunized spontaneously hypertensive and normotensive rats. Sodium 14-20 renin Rattus norvegicus 36-41 1733312-1 1992 The influence of active immunization against renin on the systemic and renal adaptation to abrupt suppression of dietary sodium was assessed in spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats. Sodium 121-127 renin Rattus norvegicus 45-50 1727635-6 1992 Similarly, culture in sodium-free medium, which blocks transport from endosomes to lysosomes, increased asialo-TfR resialylation by 40%, arguing that lysosomes do not lie on the transport pathway. Sodium 22-28 transferrin receptor Homo sapiens 111-114 1540848-2 1992 The response of rats with AV3V damage to sodium depletion was retarded and the excess sodium intake that is induced by pICV renin was absent, but their daily need-free sodium intake and the sodium intake that is induced by DOCA were essentially normal. Sodium 86-92 renin Rattus norvegicus 124-129 1540848-2 1992 The response of rats with AV3V damage to sodium depletion was retarded and the excess sodium intake that is induced by pICV renin was absent, but their daily need-free sodium intake and the sodium intake that is induced by DOCA were essentially normal. Sodium 86-92 renin Rattus norvegicus 124-129 1540848-2 1992 The response of rats with AV3V damage to sodium depletion was retarded and the excess sodium intake that is induced by pICV renin was absent, but their daily need-free sodium intake and the sodium intake that is induced by DOCA were essentially normal. Sodium 86-92 renin Rattus norvegicus 124-129 1352743-2 1992 It has also been shown that in addition to the changes in renal hemodynamics, the natriuretic response produced by exogenously administered DA and DA1 receptor agonists appears to be due to alterations in renal tubular sodium transport mechanisms. Sodium 219-225 RT1 class II, locus Da Rattus norvegicus 147-150 1338636-3 1992 The hypercalcemic effect of PTHrP is due to an increase in both bone resorption and renal calcium reabsorption, the latter through a sodium-independent mechanism. Sodium 133-139 parathyroid hormone like hormone Homo sapiens 28-33 1403810-6 1992 The rabbits maintained on the high sodium diet had a significantly lower basal plasma VIP level (P less than 0.025), a lower metabolic clearance rate (MCR) of the peptide (P less than 0.025) and a lower secretion rate (P less than 0.005), compared with the normal control animals. Sodium 35-41 VIP peptides Oryctolagus cuniculus 86-89 1403810-11 1992 These results confirm that VIP metabolism is affected by high dietary intake of sodium, as well as a low sodium intake, adding further support to the hypothesis that VIP may be involved in sodium homeostasis. Sodium 80-86 VIP peptides Oryctolagus cuniculus 27-30 1403810-11 1992 These results confirm that VIP metabolism is affected by high dietary intake of sodium, as well as a low sodium intake, adding further support to the hypothesis that VIP may be involved in sodium homeostasis. Sodium 105-111 VIP peptides Oryctolagus cuniculus 27-30 1403810-11 1992 These results confirm that VIP metabolism is affected by high dietary intake of sodium, as well as a low sodium intake, adding further support to the hypothesis that VIP may be involved in sodium homeostasis. Sodium 105-111 VIP peptides Oryctolagus cuniculus 27-30 1410435-1 1992 The atrial natriuretic factor (ANF) as an osmoregulatory hormone causes a reduction of extracellular fluid volume primarily through stimulation of renal and extrarenal water and sodium elimination. Sodium 178-184 natriuretic peptides A Oryctolagus cuniculus 4-29 1410435-1 1992 The atrial natriuretic factor (ANF) as an osmoregulatory hormone causes a reduction of extracellular fluid volume primarily through stimulation of renal and extrarenal water and sodium elimination. Sodium 178-184 natriuretic peptides A Oryctolagus cuniculus 31-34 1928340-1 1991 In rats, plasma renin activity (PRA) increases sharply, reaching a plateau within hours of sodium restriction. Sodium 91-97 renin Rattus norvegicus 16-21 1961256-3 1991 The activity of the renin-angiotensin system was modulated by varying of the nutritional sodium load prior to the experiments. Sodium 89-95 renin Rattus norvegicus 20-25 34425903-1 2021 BACKGROUND: Genetic variants in the voltage-gated sodium channels SCN1A, SCN2A, SCN3A, and SCN8A are leading causes of epilepsy, developmental delay, and autism spectrum disorder. Sodium 50-56 sodium voltage-gated channel alpha subunit 1 Homo sapiens 66-71 34395179-3 2021 Our multi-approach study, based on the combination of structural experimental data and quantum-chemical DFT calculations, led to identify a sequestration site for sodium, potassium and chloride ions within the central cavity of both the SARS-CoV-1 and SARS-CoV-2 spike proteins. Sodium 163-169 surface glycoprotein Severe acute respiratory syndrome coronavirus 2 263-268 34314052-7 2021 4-Benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione (TDZD-8), the glycogen synthase kinase-3beta inhibitor, ameliorated renal injury under I/R, activated autophagy and markedly increased expression of AQPs and sodium transporters in the kidney, which was associated with improved urine output and creatinine clearance in rats. Sodium 208-214 glycogen synthase kinase 3 beta Rattus norvegicus 64-94 34314446-0 2021 Modeling NaV1.1/SCN1A sodium channel mutations in a microcircuit with realistic ion concentration dynamics suggests differential GABAergic mechanisms leading to hyperexcitability in epilepsy and hemiplegic migraine. Sodium 22-28 sodium voltage-gated channel alpha subunit 1 Homo sapiens 9-15 34314446-0 2021 Modeling NaV1.1/SCN1A sodium channel mutations in a microcircuit with realistic ion concentration dynamics suggests differential GABAergic mechanisms leading to hyperexcitability in epilepsy and hemiplegic migraine. Sodium 22-28 sodium voltage-gated channel alpha subunit 1 Homo sapiens 16-21 34314446-1 2021 Loss of function mutations of SCN1A, the gene coding for the voltage-gated sodium channel NaV1.1, cause different types of epilepsy, whereas gain of function mutations cause sporadic and familial hemiplegic migraine type 3 (FHM-3). Sodium 75-81 sodium voltage-gated channel alpha subunit 1 Homo sapiens 30-35 34314446-1 2021 Loss of function mutations of SCN1A, the gene coding for the voltage-gated sodium channel NaV1.1, cause different types of epilepsy, whereas gain of function mutations cause sporadic and familial hemiplegic migraine type 3 (FHM-3). Sodium 75-81 sodium voltage-gated channel alpha subunit 1 Homo sapiens 90-96 34314446-4 2021 We modeled FHM-3 mutations by increasing the persistent sodium current in the interneuron and epileptogenic mutations by decreasing the sodium conductance in the interneuron. Sodium 56-62 sodium voltage-gated channel alpha subunit 1 Homo sapiens 11-16 34314446-4 2021 We modeled FHM-3 mutations by increasing the persistent sodium current in the interneuron and epileptogenic mutations by decreasing the sodium conductance in the interneuron. Sodium 136-142 sodium voltage-gated channel alpha subunit 1 Homo sapiens 11-16 34174751-1 2021 BACKGROUND: Variants in SCN1A gene, encoding the voltage-gated sodium channel Nav1.1, are associated with distinct epilepsy syndromes ranging from the relatively benign genetic epilepsy with febrile seizures plus (GEFS+) to Dravet syndrome, a severe developmental and epileptic encephalopathy (DEE). Sodium 63-69 sodium voltage-gated channel alpha subunit 1 Homo sapiens 24-29 34174751-1 2021 BACKGROUND: Variants in SCN1A gene, encoding the voltage-gated sodium channel Nav1.1, are associated with distinct epilepsy syndromes ranging from the relatively benign genetic epilepsy with febrile seizures plus (GEFS+) to Dravet syndrome, a severe developmental and epileptic encephalopathy (DEE). Sodium 63-69 sodium voltage-gated channel alpha subunit 1 Homo sapiens 78-84 34132028-11 2021 Spearman correlation analysis indicated that urinary sodium excretion positively correlated with urinary protein excretion (r = .178, p .001), SBP (r = .109, p = .002), and DBP (r = .086, p = .015). Sodium 53-59 selenium binding protein 1 Homo sapiens 145-148 34132028-12 2021 After adjusting for age, gender, BMI, eGFR, urinary protein excretion, and history of taking antihypertensive drug, multivariate linear regression demonstrated that higher level of urinary sodium excretion associated with increased level of SBP, DBP, and MAP (beta = 0.020, p = .049; beta = 0.015, p = .040; beta = 0.016, p = .025, respectively). Sodium 189-195 selenium binding protein 1 Homo sapiens 241-244 34222704-1 2021 Gain-of-function mutations in voltage-gated sodium channels (NaV1.7, NaV1.8, and NaV1.9) are known causes of inherited pain disorders. Sodium 44-50 sodium voltage-gated channel alpha subunit 11 Homo sapiens 81-87 34206182-0 2021 Differential Effect of Three Macrolide Antibiotics on Cardiac Pathology and Electrophysiology in a Myocardial Infarction Rat Model: Influence on Sodium Nav1.5 Channel Expression. Sodium 145-151 sodium voltage-gated channel alpha subunit 5 Rattus norvegicus 152-158 34514191-1 2021 The overactivation of the mineralocorticoid receptor (MR) in animal models of chronic kidney disease (CKD) increases sodium retention and hypertension and provokes inflammation and fibrosis in the kidneys, blood vessels, and the heart; these processes play an important role in the progression of cardiorenal disease. Sodium 117-123 nuclear receptor subfamily 3 group C member 2 Homo sapiens 26-52 34514191-1 2021 The overactivation of the mineralocorticoid receptor (MR) in animal models of chronic kidney disease (CKD) increases sodium retention and hypertension and provokes inflammation and fibrosis in the kidneys, blood vessels, and the heart; these processes play an important role in the progression of cardiorenal disease. Sodium 117-123 nuclear receptor subfamily 3 group C member 2 Homo sapiens 54-56 34814506-7 2021 24 h urinary sodium was negatively correlated with age, female, junior high school education or above, and annual family income (P<0.05), and positively correlated with perceived salty taste, BMI and SBP (P<0.05). Sodium 13-19 selenium binding protein 1 Homo sapiens 200-203 34814506-9 2021 The sodium-potassium ratio was negatively correlated with age, female and junior high school education or above annual family income (P<0.05), and positively correlated with perceived salty taste, SBP and eating out 3-5 d/week (P<0.05). Sodium 4-10 selenium binding protein 1 Homo sapiens 197-200 34179047-2 2021 We aimed to evaluate renal tubular sodium (Na+) or potassium (K+) associated transporters expression from uEVs and kidney tissues in patients with Gitelman syndrome (GS) caused by inactivating mutations in SLC12A3. Sodium 35-41 solute carrier family 12 member 3 Homo sapiens 206-213 35301122-3 2022 SCN2A encodes the voltage-gated sodium channel NaV1.2. Sodium 32-38 sodium channel, voltage-gated, type II, alpha Mus musculus 0-5 35301122-3 2022 SCN2A encodes the voltage-gated sodium channel NaV1.2. Sodium 32-38 sodium channel, voltage-gated, type II, alpha Mus musculus 47-53 35466690-0 2022 SGLT2 inhibition effect on salt-induced hypertension, RAAS, and sodium transport in Dahl SS rats. Sodium 64-70 solute carrier family 5 member 2 Rattus norvegicus 0-5 35466690-3 2022 The goal of this study was to determine whether SGLT2 inhibition alters blood pressure and kidney function via affecting the Renin-Angiotensin-Aldosterone System (RAAS) and sodium channels/transporters along the nephron in Dahl Salt-Sensitive (SS) rats, a model of salt-induced hypertension. Sodium 173-179 solute carrier family 5 member 2 Rattus norvegicus 48-53 35593512-0 2022 Detection of pyrethroid resistance mutations and intron variants in the voltage-gated sodium channel of Aedes (Stegomyia) aegypti and Aedes (Stegomyia) albopictus mosquitoes from Lao People"s Democratic Republic. Sodium 86-92 interleukin 4 induced 1 Homo sapiens 179-182 35586119-3 2022 First of all, we used the Kaplan-Meier curves and multivariable Cox regression analyses to measure the relationship between serum sodium levels and 1-year and 3-year mortality for critically ill patients with comorbid COPD. Sodium 130-136 cytochrome c oxidase subunit 8A Homo sapiens 64-67 35532068-2 2022 Cullin 3 (CUL3) targets with-no-lysine kinase 4 (WNK4), a kinase that activates the Na-Cl cotransporter (NCC) the main pathway for sodium reabsorption in the distal convoluted tubule (DCT). Sodium 131-137 cullin 3 Mus musculus 0-8 35532068-2 2022 Cullin 3 (CUL3) targets with-no-lysine kinase 4 (WNK4), a kinase that activates the Na-Cl cotransporter (NCC) the main pathway for sodium reabsorption in the distal convoluted tubule (DCT). Sodium 131-137 cullin 3 Mus musculus 10-14 35532068-2 2022 Cullin 3 (CUL3) targets with-no-lysine kinase 4 (WNK4), a kinase that activates the Na-Cl cotransporter (NCC) the main pathway for sodium reabsorption in the distal convoluted tubule (DCT). Sodium 131-137 WNK lysine deficient protein kinase 4 Mus musculus 49-53 35563590-0 2022 Small Extracellular Vesicles Containing miR-34c Derived from Bone Marrow Mesenchymal Stem Cells Regulates Epithelial Sodium Channel via Targeting MARCKS. Sodium 117-123 microRNA 34c Mus musculus 40-47 35625812-1 2022 Mutations in SCN1A gene, encoding the voltage-gated sodium channel (VGSC) NaV1.1, are widely recognized as a leading cause of genetic febrile seizures (FS), due to the decrease in the Na+ current density, mainly affecting the inhibitory neuronal transmission. Sodium 52-58 sodium voltage-gated channel alpha subunit 1 Homo sapiens 13-18 35625812-1 2022 Mutations in SCN1A gene, encoding the voltage-gated sodium channel (VGSC) NaV1.1, are widely recognized as a leading cause of genetic febrile seizures (FS), due to the decrease in the Na+ current density, mainly affecting the inhibitory neuronal transmission. Sodium 52-58 sodium voltage-gated channel alpha subunit 1 Homo sapiens 74-80 35353937-7 2022 In the presence of Abeta oligomers, knockdown of Nav1.6 reduces intracellular calcium overload by suppressing reverse sodium-calcium exchange channel, consequently increasing inactive NFAT1 (the nuclear factor of activated T cells) levels and thus reducing BACE1 transcription. Sodium 118-124 sodium channel, voltage-gated, type VIII, alpha Mus musculus 49-55 35304594-10 2022 Together, these results suggest that HIF activation promotes sodium excretion through upregulation of COX2 in the renal medulla and therefore maintains sodium homeostasis in the body. Sodium 61-67 prostaglandin-endoperoxide synthase 2 Mus musculus 102-106 35304594-10 2022 Together, these results suggest that HIF activation promotes sodium excretion through upregulation of COX2 in the renal medulla and therefore maintains sodium homeostasis in the body. Sodium 152-158 prostaglandin-endoperoxide synthase 2 Mus musculus 102-106 35285452-2 2022 We hypothesized that sodium-glucose cotransporter 2 (SGLT2) inhibition and angiotensin II type 1 receptor (AT1R) blockade can synergistically reduce renal sodium reabsorption by beneficially effects on these transporters, leading to lower BP and ameliorating renal and cardiac damage. Sodium 155-161 solute carrier family 5 member 2 Rattus norvegicus 21-51 35285452-2 2022 We hypothesized that sodium-glucose cotransporter 2 (SGLT2) inhibition and angiotensin II type 1 receptor (AT1R) blockade can synergistically reduce renal sodium reabsorption by beneficially effects on these transporters, leading to lower BP and ameliorating renal and cardiac damage. Sodium 155-161 solute carrier family 5 member 2 Rattus norvegicus 53-58 35285452-7 2022 CONCLUSION: Inhibition of SGLT2 in combination with an angiotensin II receptor blocker effectively improved BP salt sensitivity by reducing renal expression levels of sodium transporters including NHE3 and NKCC2, which eventually led to improvement of BP salt sensitivity and cardiorenal protection. Sodium 167-173 solute carrier family 5 member 2 Rattus norvegicus 26-31 35285452-7 2022 CONCLUSION: Inhibition of SGLT2 in combination with an angiotensin II receptor blocker effectively improved BP salt sensitivity by reducing renal expression levels of sodium transporters including NHE3 and NKCC2, which eventually led to improvement of BP salt sensitivity and cardiorenal protection. Sodium 167-173 solute carrier family 9 member A3 Rattus norvegicus 197-201 35235155-0 2022 Molecular characterization of alpha subunit 1 of sodium pump (ATP1A1) gene in Camelus dromedarius: its differential tissue expression potentially interprets the role in osmoregulation. Sodium 49-55 sodium/potassium-transporting ATPase subunit alpha-1 Camelus dromedarius 62-68 35235155-5 2022 Here is the first to resolve the full-length of alpha-1 subunit of sodium pump (ATP1A1) gene with its differential expression in dromedary tissues. Sodium 67-73 sodium/potassium-transporting ATPase subunit alpha-1 Camelus dromedarius 80-86 32719824-7 2020 After whole exome sequencing revealed a potentially pathogenic SCN9A-A3734G variant, sodium channel blockers were tried. Sodium 85-91 sodium voltage-gated channel alpha subunit 9 Homo sapiens 63-68 35050553-0 2022 Optimizing the electrolyte systems for Na3(VO1-xPO4)2F1+2x (0<=x<=1) cathode and understanding their interfacial chemistries towards high-rate sodium-ion batteries. Sodium 143-149 exportin 4 Homo sapiens 47-51 31928904-0 2020 Differential excitatory vs inhibitory SCN expression at single cell level regulates brain sodium channel function in neurodevelopmental disorders. Sodium 90-96 sorcin Homo sapiens 38-41 35417922-0 2022 Cellular and behavioral effects of altered NaV1.2 sodium channel ion permeability in Scn2aK1422E mice. Sodium 50-56 sodium channel, voltage-gated, type II, alpha Mus musculus 43-49 35417922-1 2022 Genetic variants in SCN2A, encoding the NaV1.2 voltage-gated sodium channel, are associated with a range of neurodevelopmental disorders with overlapping phenotypes. Sodium 61-67 sodium channel, voltage-gated, type II, alpha Mus musculus 20-25 31734278-0 2020 Elevated ocular pressure reduces voltage-gated sodium channel NaV1.2 protein expression in retinal ganglion cell axons. Sodium 47-53 sodium voltage-gated channel alpha subunit 2 Homo sapiens 62-68 35417922-1 2022 Genetic variants in SCN2A, encoding the NaV1.2 voltage-gated sodium channel, are associated with a range of neurodevelopmental disorders with overlapping phenotypes. Sodium 61-67 sodium channel, voltage-gated, type II, alpha Mus musculus 40-46 35414300-1 2022 Dravet syndrome is a severe developmental and epileptic encephalopathy mostly caused by heterozygous mutation of the SCN1A gene encoding the voltage-gated sodium channel alpha subunit Nav1.1. Sodium 155-161 sodium voltage-gated channel alpha subunit 1 Homo sapiens 117-122 35359575-2 2022 A number of in-frame deletion variants in an epilepsy-associated gene SCN1A, encoding voltage gated sodium channel alpha unit 1.1 (Nav1.1), have been reported in public database. Sodium 100-106 sodium voltage-gated channel alpha subunit 1 Homo sapiens 70-75 35359575-2 2022 A number of in-frame deletion variants in an epilepsy-associated gene SCN1A, encoding voltage gated sodium channel alpha unit 1.1 (Nav1.1), have been reported in public database. Sodium 100-106 sodium voltage-gated channel alpha subunit 1 Homo sapiens 131-137 32420800-4 2020 Functional significance of novel SCN9A mutations was assessed in HEK293 cells expressing Nav1.7, the results showed that p.Arg99His significantly decreased current density and reduced total Nav1.7 protein levels, whereas p.Trp917Gly almost abolished Nav1.7 sodium current without affecting its protein expression. Sodium 257-263 sodium voltage-gated channel alpha subunit 9 Homo sapiens 33-38 35272527-1 2022 BACKGROUND: Health literacy (HL) and health numeracy (HN), the ability to interpret and act on quantitative health information, are important for hypertension self-management such as limiting sodium intake. Sodium 192-198 lipase C, hepatic type Homo sapiens 29-31 31935735-8 2020 Kisspeptin neuron-specific Ca2+ oscillations were dependent on voltage-gated sodium channels and regulated by endoplasmic reticulum-dependent Ca2+ homeostasis. Sodium 77-83 KiSS-1 metastasis-suppressor Mus musculus 0-10 35104250-2 2022 We previously discovered that GRP170 regulates the degradation and assembly of the epithelial sodium channel (ENaC), which reabsorbs sodium in the distal nephron and thereby regulates salt-water homeostasis and blood pressure. Sodium 94-100 hypoxia up-regulated 1 Mus musculus 30-36 35104250-2 2022 We previously discovered that GRP170 regulates the degradation and assembly of the epithelial sodium channel (ENaC), which reabsorbs sodium in the distal nephron and thereby regulates salt-water homeostasis and blood pressure. Sodium 133-139 hypoxia up-regulated 1 Mus musculus 30-36 35165201-0 2022 NPRL2 Inhibition of mTORC1 Controls Sodium Channel Expression and Brain Amino Acid Homeostasis. Sodium 36-42 CREB regulated transcription coactivator 1 Mus musculus 20-26 31550727-8 2020 Moreover, NaHS markedly increased the expression of hippocampal BDNF in FA-exposed rats. Sodium 10-14 brain-derived neurotrophic factor Rattus norvegicus 64-68 35165201-7 2022 Targeted deletion of NPRL2 in primary neurons increases the expression of sodium channel Scn1A, whereas treatment with the pharmacological mTORC1 inhibitor called rapamycin prevents Scn1A upregulation. Sodium 74-80 sodium voltage-gated channel alpha subunit 1 Homo sapiens 89-94 35165201-7 2022 Targeted deletion of NPRL2 in primary neurons increases the expression of sodium channel Scn1A, whereas treatment with the pharmacological mTORC1 inhibitor called rapamycin prevents Scn1A upregulation. Sodium 74-80 CREB regulated transcription coactivator 1 Mus musculus 139-145 35165201-8 2022 These studies demonstrate a novel role of NPRL2 and mTORC1 signaling in the regulation of sodium channels, which can contribute to seizures and early lethality.Significance StatementNPRL2 is a requisite subunit of the epilepsy-linked GATOR1 complex that functions as a negative regulator of mTORC1 kinase when intracellular amino acids are limited. Sodium 90-96 CREB regulated transcription coactivator 1 Mus musculus 52-58 35165201-8 2022 These studies demonstrate a novel role of NPRL2 and mTORC1 signaling in the regulation of sodium channels, which can contribute to seizures and early lethality.Significance StatementNPRL2 is a requisite subunit of the epilepsy-linked GATOR1 complex that functions as a negative regulator of mTORC1 kinase when intracellular amino acids are limited. Sodium 90-96 CREB regulated transcription coactivator 1 Mus musculus 291-297 31888677-8 2019 DRG neurons expressing the CRMP2-K374A mutant also exhibited total sodium current increases after exposure to TNF-alpha, indicating that these effects were independent of SUMOylation of CRMP2. Sodium 67-73 dihydropyrimidinase-like 2 Rattus norvegicus 27-32 35165201-12 2022 These data reveal an unanticipated link between intracellular amino acid signaling by NPRL2 and a novel mTORC1-dependent regulation of sodium-channel expression in epilepsy. Sodium 135-141 CREB regulated transcription coactivator 1 Mus musculus 104-110 31701738-6 2019 More importantly, BF-1 affords high sensitivity for monitoring Sec stimulated by Na2SeO3 in tumor-bearing mice. Sodium 81-88 forkhead box G1 Mus musculus 18-22 31811815-5 2019 In this study, we observed that interleukin-1beta (IL-1beta)-induced MMP-9 secretion in pericytes increased BBB permeability to sodium fluorescein (Na-F) by damaging the disruption of VE-cadherin, occludin, claudin-5, and zonula occludin-1 (ZO-1). Sodium 148-152 matrix metallopeptidase 9 Homo sapiens 69-74 35083300-2 2021 This study aimed to investigate the molecular mechanism underlying the regulation of IL-2 and the sodium channel current of sodium voltage-gated channel beta subunit 3 (SCN3B) by miR-190a-5p in the progression of CAs. Sodium 98-104 sodium voltage-gated channel beta subunit 3 Homo sapiens 124-167 35083300-2 2021 This study aimed to investigate the molecular mechanism underlying the regulation of IL-2 and the sodium channel current of sodium voltage-gated channel beta subunit 3 (SCN3B) by miR-190a-5p in the progression of CAs. Sodium 98-104 sodium voltage-gated channel beta subunit 3 Homo sapiens 169-174 31553875-2 2019 The key step was an addition of difluorocarbene (:CF2) to electron-rich bicyclo[1.1.0]butanes by the CF3TMS/NaI system. Sodium 108-111 ATPase H+ transporting accessory protein 1 Homo sapiens 50-53 35083300-4 2021 Luciferase reporter assay, quantitative real-time-PCR, and whole-cell patch-clamp experiments confirmed the downregulation of IL-2 by miR-190a-5p and influence of the latter on the sodium current of SCN3B. Sodium 181-187 sodium voltage-gated channel beta subunit 3 Homo sapiens 199-204 35083300-5 2021 Overall, miR-190a-5p suppressed the increase in SCN3B sodium current caused by endogenous IL-2, whereas miR-190a-5p inhibitor significantly reversed this effect. Sodium 54-60 sodium voltage-gated channel beta subunit 3 Homo sapiens 48-53 34857709-4 2022 METHODS: The SPA Project is a multicenter, observational, cross-sectional, cohort study investigating healthy children, aged 5-8 years as to sodium and fluid intake by means of urinary sodium and creatinine from multiple samples taken in different days in order to characterize them in lower/higher sodium and lower/higher fluid intake. Sodium 141-147 surfactant protein A1 Homo sapiens 13-16 34857709-4 2022 METHODS: The SPA Project is a multicenter, observational, cross-sectional, cohort study investigating healthy children, aged 5-8 years as to sodium and fluid intake by means of urinary sodium and creatinine from multiple samples taken in different days in order to characterize them in lower/higher sodium and lower/higher fluid intake. Sodium 185-191 surfactant protein A1 Homo sapiens 13-16 34857709-4 2022 METHODS: The SPA Project is a multicenter, observational, cross-sectional, cohort study investigating healthy children, aged 5-8 years as to sodium and fluid intake by means of urinary sodium and creatinine from multiple samples taken in different days in order to characterize them in lower/higher sodium and lower/higher fluid intake. Sodium 299-305 surfactant protein A1 Homo sapiens 13-16 31703480-5 2019 After 150 d, the results showed a significant increase in testicular cytokines levels including of IL-17A, IL-6, IFN-gamma and TNF-alpha in NaF and EAO groups compared with control group. Sodium 140-143 interleukin 17A Mus musculus 99-105 2556473-8 1989 The IL-1-induced rise in pHi is both sodium dependent and amiloride sensitive, indicative of activation of the Na+/H+ antiport. Sodium 37-43 interleukin 1 complex Mus musculus 4-8 2556473-8 1989 The IL-1-induced rise in pHi is both sodium dependent and amiloride sensitive, indicative of activation of the Na+/H+ antiport. Sodium 37-43 glucose-6-phosphate isomerase 1 Mus musculus 25-28 31703480-7 2019 In addition, findings showed that in NaF and EAO groups, macrophages and T cells both significantly secreted IL-17A, and the protein and mRNA levels of cytokines (IL-6 and TGF-beta) were significantly increased. Sodium 37-40 interleukin 17A Mus musculus 109-115 31423748-2 2019 The study was designed to test the hypothesis that nephrotic proteinuria in mice after conditional deletion of podocin leads to urokinase-dependent, amiloride-sensitive plasmin-mediated sodium and water retention. Sodium 186-192 nephrosis 2, podocin Mus musculus 111-118 31423748-5 2019 RESULTS: Twelve days after deletion, podocin-deficient mice developed significant protein and albuminuria associated with increased body wt, ascites, sodium accumulation and suppressed plasma renin. Sodium 150-156 nephrosis 2, podocin Mus musculus 37-44 2531741-1 1989 Sodium-translocating ATPase in the fermentative bacterium Streptococcus faecalis exchanges sodium for potassium ions. Sodium 91-97 ATPase Enterococcus faecalis 21-27 31904120-1 2019 Variants in the SCN2A gene, encoding the voltage-gated sodium channel NaV 1.2, cause a variety of neuropsychiatric syndromes with different severity ranging from self-limiting epilepsies with early onset to developmental and epileptic encephalopathy with early or late onset and intellectual disability (ID), as well as ID or autism without seizures. Sodium 55-61 sodium voltage-gated channel alpha subunit 2 Homo sapiens 16-21 2531741-4 1989 The sodium ATPase is induced when cells are grown on media rich in sodium, particularly under conditions that limit the generation of a proton potential or block the constitutive sodium proton antiporter, indicating that an increase in the cytoplasmic sodium level serves as the signal. Sodium 4-10 ATPase Enterococcus faecalis 11-17 2531741-4 1989 The sodium ATPase is induced when cells are grown on media rich in sodium, particularly under conditions that limit the generation of a proton potential or block the constitutive sodium proton antiporter, indicating that an increase in the cytoplasmic sodium level serves as the signal. Sodium 67-73 ATPase Enterococcus faecalis 11-17 2531741-6 1989 The sodium ATPase may have evolved to cope with a sodium-rich environment under conditions that limit the magnitude of the proton potential. Sodium 4-10 ATPase Enterococcus faecalis 11-17 2574187-2 1989 To determine a mechanism of the decreased effect of DA-1 agonists on sodium transport, DA-1 receptors in renal proximal convoluted tubule (PCT) were studied by radioligand binding and by adenylate cyclase (AC) determinations. Sodium 69-75 RT1 class II, locus Da Rattus norvegicus 52-56 31904120-1 2019 Variants in the SCN2A gene, encoding the voltage-gated sodium channel NaV 1.2, cause a variety of neuropsychiatric syndromes with different severity ranging from self-limiting epilepsies with early onset to developmental and epileptic encephalopathy with early or late onset and intellectual disability (ID), as well as ID or autism without seizures. Sodium 55-61 sodium voltage-gated channel alpha subunit 2 Homo sapiens 70-77 31755034-9 2019 Low-sodium intake was associated with lower levels of Hb (P = .027), lower TNF-alpha (P = .011), and lower IL-10 (P = .029). Sodium 4-10 interleukin 10 Homo sapiens 107-112 2621618-7 1989 In the anaesthetized rabbit study portal and systemic VIP levels had both increased significantly from control values by 5 min after the sodium load in the low salt diet group (P less than 0.025, portal: P less than 0.05, systemic). Sodium 137-143 VIP peptides Oryctolagus cuniculus 54-57 2621618-10 1989 In the conscious rabbits an increase in systemic VIP levels was observed in the group on a low salt diet after a gastric but not a portal sodium load. Sodium 138-144 VIP peptides Oryctolagus cuniculus 49-52 2621618-12 1989 We conclude that VIP is released in response to gastric sodium loads in rabbits on low salt diets and that hepatic metabolism of VIP is reduced in this group. Sodium 56-62 VIP peptides Oryctolagus cuniculus 17-20 31805638-3 2019 The voltage-gated sodium channel Nav1.7 is predominantly expressed in peripheral sensory neurons and is responsible for the rising phase of action potentials, thereby mediating nociceptive conduction. Sodium 18-24 sodium voltage-gated channel alpha subunit 9 Homo sapiens 33-39 2904771-7 1988 Interestingly, IAP pretreatment alone caused increased urine flow rate and enhanced excretion of sodium and chloride without affecting potassium excretion or renal hemodynamics in vitro. Sodium 97-103 Cd47 molecule Rattus norvegicus 15-18 30312430-0 2019 Fibroblast growth factor 23 is associated with fractional excretion of sodium in patients with chronic kidney disease. Sodium 71-77 fibroblast growth factor 23 Homo sapiens 0-27 3074734-0 1988 Sodium appetite: species and strain differences and role of renin-angiotensin-aldosterone system. Sodium 0-6 renin Rattus norvegicus 60-65 3241258-4 1988 The urinary sodium to potassium ratio was significantly and positively correlated with SBP and DBP in both males and females. Sodium 12-18 selenium binding protein 1 Homo sapiens 87-90 3241258-5 1988 Urinary sodium was weakly and positively correlated with SBP only in the north. Sodium 8-14 selenium binding protein 1 Homo sapiens 57-60 30312430-1 2019 BACKGROUND: Recent studies suggest that the phosphaturic hormone fibroblast growth factor 23 (FGF23) is involved in regulation of renal sodium excretion and blood pressure. Sodium 136-142 fibroblast growth factor 23 Homo sapiens 65-92 30312430-1 2019 BACKGROUND: Recent studies suggest that the phosphaturic hormone fibroblast growth factor 23 (FGF23) is involved in regulation of renal sodium excretion and blood pressure. Sodium 136-142 fibroblast growth factor 23 Homo sapiens 94-99 30312430-3 2019 However, clinical data on the association between FGF23 and renal sodium regulation is lacking. Sodium 66-72 fibroblast growth factor 23 Homo sapiens 50-55 3046823-12 1988 In CCl4 rats included in protocol B, there was a close chronological relationship between the activation of the renin-aldosterone system, as estimated by urinary aldosterone excretion, the onset of sodium retention and the increase in urinary excretion of 6-keto-PGF1 alpha and TXB2. Sodium 198-204 renin Rattus norvegicus 112-117 30312430-4 2019 Herein, we investigated the associations of FGF23 with renal sodium handling and blood pressure in non-dialysis CKD patients. Sodium 61-67 fibroblast growth factor 23 Homo sapiens 44-49 30312430-7 2019 The association between FGF23 and renal sodium handling was explored by multivariate regression analysis. Sodium 40-46 fibroblast growth factor 23 Homo sapiens 24-29 2970225-0 1988 Sodium balance effects on renin, angiotensinogen, and atrial natriuretic polypeptide mRNA levels. Sodium 0-6 renin Rattus norvegicus 26-31 30312430-9 2019 In univariate analysis, FGF23 was positively associated with FENa (Spearman"s rho = 0.47; P < 0.001) and systolic blood pressure (rho = 0.17, P < 0.05), but not with plasma sodium, 24-h urinary sodium excretion or mean arterial blood pressure. Sodium 173-179 fibroblast growth factor 23 Homo sapiens 24-29 2970225-4 1988 In the high-sodium state, plasma renin concentration (PRC), renal renin concentration (RRC), and renal renin mRNA decreased by 88, 90, and 75%, respectively. Sodium 12-18 renin Rattus norvegicus 33-38 30312430-9 2019 In univariate analysis, FGF23 was positively associated with FENa (Spearman"s rho = 0.47; P < 0.001) and systolic blood pressure (rho = 0.17, P < 0.05), but not with plasma sodium, 24-h urinary sodium excretion or mean arterial blood pressure. Sodium 194-200 fibroblast growth factor 23 Homo sapiens 24-29 2970225-4 1988 In the high-sodium state, plasma renin concentration (PRC), renal renin concentration (RRC), and renal renin mRNA decreased by 88, 90, and 75%, respectively. Sodium 12-18 renin Rattus norvegicus 66-71 2970225-4 1988 In the high-sodium state, plasma renin concentration (PRC), renal renin concentration (RRC), and renal renin mRNA decreased by 88, 90, and 75%, respectively. Sodium 12-18 renin Rattus norvegicus 66-71 31795454-9 2019 Furthermore, NaIO3 enhanced mRNA expression of antioxidant enzymes such as glucose-6-phosphate dehydrogenase (G6PDH), catalase (CAT), and glutathione S-reductase (GSR) in the control shRNA expressing RPE cells, but not in hPTX3 shRNA expressing RPE cells. Sodium 13-18 glucose-6-phosphate dehydrogenase Homo sapiens 75-108 2970225-5 1988 In the low-sodium state, PRC, RRC, and renin mRNA increased 17-fold, 2.5-fold, and 4.5-fold, respectively. Sodium 11-17 renin Rattus norvegicus 39-44 2970225-10 1988 These results demonstrate that sodium intake affects the expression of the renin and angiotensinogen genes and slightly alters the expression of ANP gene. Sodium 31-37 renin Rattus norvegicus 75-80 31795454-9 2019 Furthermore, NaIO3 enhanced mRNA expression of antioxidant enzymes such as glucose-6-phosphate dehydrogenase (G6PDH), catalase (CAT), and glutathione S-reductase (GSR) in the control shRNA expressing RPE cells, but not in hPTX3 shRNA expressing RPE cells. Sodium 13-18 glucose-6-phosphate dehydrogenase Homo sapiens 110-115 2976315-0 1988 [Effect of sodium and calcium intake on blood pressure, plasma calmodulin and erythrocyte ATPase activities]. Sodium 11-17 dynein axonemal heavy chain 8 Homo sapiens 90-96 31647222-6 2019 To address this unmet clinical need, we explored the expression of voltage-gated sodium channel Nav1.7 as an intraoperative marker for the peripheral nervous system. Sodium 81-87 sodium voltage-gated channel alpha subunit 9 Homo sapiens 96-102 3347270-2 1988 Sodium-dependent Cl-HCO3 exchange is the dominant mechanism of pHi regulation in the invertebrate cells examined, and also occurs in mammalian cells. Sodium 0-6 glucose-6-phosphate isomerase Homo sapiens 63-66 3348423-4 1988 Plasma renin concentration was suppressed in the sodium-loaded controls. Sodium 49-55 renin Rattus norvegicus 7-12 2977978-1 1988 Prolonged (12-day) sodium deprivation strikingly raised both basal plasma aldosterone concentration (PAC) (114%) and plasma renin activity (PRA) (200%), and lowered ANF blood level (-30%). Sodium 19-25 renin Rattus norvegicus 124-129 2821820-5 1987 The kinetic basis for the inhibitory effect of acidic pHi was examined by comparing the kinetic parameters of activation of ouabain-sensitive sodium efflux by intracellular Na+ (Na+i) and extracellular K+ (K+o) at normal pHi with those at acidic pHi. Sodium 142-148 glucose-6-phosphate isomerase Homo sapiens 54-57 3816077-6 1987 We conclude that the actions of VIP on intrarenal blood vessels and renal tubules are direct, leading to increases in renal vascular resistance and fractional sodium excretion. Sodium 159-165 VIP peptides Oryctolagus cuniculus 32-35 3112407-1 1987 Sodium-calcium exchange has been suggested to play a pivotal role in the regulation of cytosolic free calcium (Caf) by epithelial cells. Sodium 0-6 lysine acetyltransferase 2B Homo sapiens 111-114 3112407-7 1987 While medium sodium substitution increased Caf, prolonged treatment with ouabain had no effect on Caf despite a clear increase in cell sodium content. Sodium 13-19 lysine acetyltransferase 2B Homo sapiens 43-46 2942044-4 1986 min-1 significantly decreased aldosterone secretion by 32% and plasma renin activity by 55% in rats that had been maintained on a normal-sodium diet. Sodium 137-143 renin Rattus norvegicus 70-75 2942044-5 1986 Similar reductions in aldosterone secretion and plasma renin activity were observed in hyperreninemic rats after chronic sodium restriction. Sodium 121-127 renin Rattus norvegicus 55-60 3524919-0 1986 Effect of sodium intake and sodium delivery to the macula densa on renal renin content and juxtaglomerular apparatus morphology. Sodium 28-34 renin Rattus norvegicus 73-78 3524919-9 1986 Increased sodium in the diet and increased delivery of NaCl to the macula densa decreased the proportion of renin present in the inactive form and decreased the proportion of crystalline cores. Sodium 10-16 renin Rattus norvegicus 108-113 3524919-10 1986 These coincidental alterations suggest that crystalline cores contain inactive renin and suggest that the delivery of sodium to the macula densa activates renin. Sodium 118-124 renin Rattus norvegicus 155-160 6323425-10 1984 The results suggest that sodium ion regulates TRH binding by interacting with a site on the receptor, while guanyl nucleotides regulate TRH binding indirectly. Sodium 25-31 thyrotropin releasing hormone Rattus norvegicus 46-49 6585142-1 1984 The rate of sodium-lithium countertransport (SLC flux) across red cell membranes has been reported to be elevated in hypertensive persons and their relatives as compared to normotensive individuals without family histories of hypertension. Sodium 12-18 C-C motif chemokine ligand 21 Homo sapiens 45-48 6362959-6 1984 Although the plasma renin concentration of recipients on a low sodium diet fell below that of unilaterally nephrectomized controls on a low sodium diet, it was higher than that of recipients on a normal diet. Sodium 63-69 renin Rattus norvegicus 20-25 6362959-6 1984 Although the plasma renin concentration of recipients on a low sodium diet fell below that of unilaterally nephrectomized controls on a low sodium diet, it was higher than that of recipients on a normal diet. Sodium 140-146 renin Rattus norvegicus 20-25 6373592-3 1984 Changes in sodium diet induced changes in adrenal capsular renin concentration (high Na 2.21 +/- 0.34, normal Na 4.34 +/- 0.53, low Na 13.19 +/- 1.67 ng AI/mg protein/hr). Sodium 11-17 renin Rattus norvegicus 59-64 6373592-7 1984 Sodium loading or dexamethasone treatment prior to nephrectomy blunted the rise in adrenal renin (nephrectomy + dexamethasone = 27.64 +/- 4.33 ng AI/mg protein/hr; nephrectomy + NaCl = 38.70 +/- 5.82 ng AI/mg protein/hr). Sodium 0-6 renin Rattus norvegicus 91-96 6206557-0 1984 The inhibition of rat renin in sodium depleted and renal hypertensive rats. Sodium 31-37 renin Rattus norvegicus 22-27 6206557-2 1984 Studies were undertaken in order to demonstrate the role of the renin-angiotensin system for blood pressure homeostasis in sodium depleted and renal hypertensive (acute and chronic) rats. Sodium 123-129 renin Rattus norvegicus 64-69 6348199-3 1983 Control sodium-deprived rats showed increased plasma renin activities, increased peripheral aldosterone concentrations and reduced urinary sodium excretion; they maintained positive sodium balance and the zona glomerulosa of the adrenal cortex hypertrophied. Sodium 8-14 renin Rattus norvegicus 53-58 6311248-0 1983 Topological localization of proteolytic sites of sodium and potassium ion stimulated adenosinetriphosphatase. Sodium 49-55 ATPase Na+/K+ transporting subunit beta 1 Homo sapiens 85-108 6348088-12 1983 Whether calculated per unit tubule length or protein content, insulin binding is highest in the thick ascending limb and the distal convoluted tubule, the same nephron sites where a regulatory role in sodium transport has been postulated for this hormone. Sodium 201-207 insulin Oryctolagus cuniculus 62-69 6882356-1 1983 Cathepsin D inactivated aldolase at pH values between 4.2 and 5.2; the chloride, sulphate or iodide, but not citrate or acetate, salts of sodium or potassium accelerated the rate of inactivation. Sodium 138-144 cathepsin D Homo sapiens 0-11 6195492-10 1983 In the animals kept on a low-sodium diet, both types of renin granules were increased. Sodium 29-35 renin Rattus norvegicus 56-61 6188649-2 1983 It was 10-15 times more potent than ovine PRL in sodium-retaining activity for juvenile rainbow trout adapted to 50% seawater. Sodium 49-55 prolactin Oncorhynchus mykiss 42-45 1145199-3 1975 However, even after 15 weeks of hypertension, following sodium depletion by either diuretics or a low sodium diet, the animals again became renin dependent as readministration of the inhibitor induced a significant fall in blood pressure. Sodium 102-108 renin Rattus norvegicus 140-145 1155613-3 1975 Increasing the medium sodium concentration (50-144 meq/liter) linearly decreased the rate of renin secretion. Sodium 22-28 renin Rattus norvegicus 93-98 1155613-6 1975 Considered with previous observations, these results suggest that renin secretionis controlled by some function of sodium on the lumenal boder of the macula densa cells. Sodium 115-121 renin Rattus norvegicus 66-71 168058-5 1975 However, the direct effects of sodium and potassium upon renin release were not conspicuous. Sodium 31-37 renin Rattus norvegicus 57-62 1133791-31 1975 This, together with the release observed with increased sodium concentration at constant osmolarity, suggests a dependence of renin release upon the mechanism controlling the volume of the juxtaglomerular cell or its organelles. Sodium 56-62 renin Rattus norvegicus 126-131 1167491-14 1975 The initial sodium retention could be a factor in the early rise of blood pressure and could account for the delay in the rise of peripheral plasma renin activity. Sodium 12-18 renin Rattus norvegicus 148-153 1167491-15 1975 The subsequent loss of the retained sodium and potassium during the development of severe hypertension could have facilitated the rise in peripheral plasma renin activity, but did not initiate this rise. Sodium 36-42 renin Rattus norvegicus 156-161 1153044-1 1975 Rats were kept for 4 weeks on a dietary regimen with a low or high sodium intake to increase or reduce, respectively, the renin activity of the kidneys and plasma. Sodium 67-73 renin Rattus norvegicus 122-127 1153045-1 1975 Renin secretion has been hypothesized to be inversely related to the tubular sodium concentration or load. Sodium 77-83 renin Rattus norvegicus 0-5 1153045-2 1975 Using rat kidney cortex slices, in vitro renin secretion was measured as a function of sodium concentration of the medium. Sodium 87-93 renin Rattus norvegicus 41-46 1153045-3 1975 We found, as have many others, that renin secretion increases with increasing medium sodium concentration. Sodium 85-91 renin Rattus norvegicus 36-41 1153045-4 1975 However, in the presence of 10(-3) M ouabain, renin secretion decreased with increasing medium sodium concentration. Sodium 95-101 renin Rattus norvegicus 46-51 4279917-0 1974 Sodium transport by phospholipid vesicles containing purified sodium and potassium ion-activated adenosine triphosphatase. Sodium 0-6 ATPase Na+/K+ transporting subunit beta 1 Homo sapiens 97-121 4436432-12 1974 However, after 8 days of sodium deprivation, both PRA and renal renin content of calcium-loaded animals were significantly lower than the respective values in pair-fed controls (P < 0.005). Sodium 25-31 renin Rattus norvegicus 64-69 4445170-0 1974 Effects of dietary sodium on renin content during renal hypertrophy in uninephrectomized rats. Sodium 19-25 renin Rattus norvegicus 29-34 4370497-0 1974 The renin-angiotensin system and aldosterone secretion during sodium depletion in the rat. Sodium 62-68 renin Rattus norvegicus 4-9 4795631-0 1973 Effects of exogenous renin and sodium load on renin activity in unilaterally nephrectomized rats. Sodium 31-37 renin Rattus norvegicus 46-51 5024038-5 1972 Fractional proximal reabsorption of sodium as assessed from proximal tubular fluid to plasma ratios of inulin ([TF/P](IN)) was found to be decreased by 28% (P < 0.001) in the hypothyroid rats. Sodium 36-42 dynein light chain LC8-type 1 Rattus norvegicus 115-121 4330653-0 1971 Effect of growth hormone on the aldosterone secretory response to sodium restriction in corticotrophin-maintained hypophysectomized nephrectomized rats. Sodium 66-72 gonadotropin releasing hormone receptor Rattus norvegicus 10-24 4943532-0 1971 [Effects of restriction, depletion and overload of sodium on plasma renin and juxta-glomerular index of the rat]. Sodium 51-57 renin Rattus norvegicus 68-73 4256160-0 1971 Electron-microscopic histochemical examination of potassium-sodium-dependent myocardial ATP-ase activity. Sodium 60-66 dynein axonemal heavy chain 8 Homo sapiens 88-95 4319969-3 1970 With less consistency, the highest sodium intake employed (52 mEq Na(+)/100 g food) tended to induce potassium depletion.In accordance with previous reports, sodium deprivation induced significant increases in plasma renin activity. Sodium 35-41 renin Rattus norvegicus 217-222 4319969-3 1970 With less consistency, the highest sodium intake employed (52 mEq Na(+)/100 g food) tended to induce potassium depletion.In accordance with previous reports, sodium deprivation induced significant increases in plasma renin activity. Sodium 158-164 renin Rattus norvegicus 217-222 4319969-6 1970 The highest serum renin levels of all occurred in the potassium-depleted animals and the usual renin response to sodium deprivation was virtually abolished in the presence of a high potassium diet. Sodium 113-119 renin Rattus norvegicus 95-100 4190502-0 1970 Variations of plasma kininogen content due to high sodium intake in rats. Sodium 51-57 kininogen 2-like 1 Rattus norvegicus 21-30 4322443-0 1970 The effect of the renin-angiotensin system on mucosal water and sodium transfer in everted sacs of rat jejunum. Sodium 64-70 renin Rattus norvegicus 18-23 4322443-9 1970 It is suggested that the renin-angiotensin system may be involved in the maintenance of sodium homoeostasis by a direct action on sodium transporting mechanisms. Sodium 88-94 renin Rattus norvegicus 25-30 4322443-9 1970 It is suggested that the renin-angiotensin system may be involved in the maintenance of sodium homoeostasis by a direct action on sodium transporting mechanisms. Sodium 130-136 renin Rattus norvegicus 25-30 4248677-0 1970 (Na plus minus K plus)-ATPase from the frog bladder and its relationship to sodium transport. Sodium 76-82 dynein axonemal heavy chain 8 Homo sapiens 23-29 19873649-6 1969 When starved sodium-poor red cells are poisoned with iodoacetamide, loaded with phosphate, and incubated in high-sodium potassium-free media, the ouabain-sensitive efflux of potassium appears to be accompanied by the reversal of the entire ATPase system. Sodium 13-19 dynein axonemal heavy chain 8 Homo sapiens 240-246 4236484-0 1968 The effects of pharmacologic agents on myocardial sodium (Na+) and potassium (K+) stimulated ATPase. Sodium 50-56 dynein axonemal heavy chain 8 Homo sapiens 93-99 4228075-4 1967 As it is known that the ouabain-sensitive ATPase in fragmented ghosts requires both sodium and potassium ions, these results show that the ATPase is activated by potassium externally and by sodium internally, and suggest that the ions activating the ATPase are the ions that are transported.2. Sodium 84-90 dynein axonemal heavy chain 8 Homo sapiens 42-48 4228075-4 1967 As it is known that the ouabain-sensitive ATPase in fragmented ghosts requires both sodium and potassium ions, these results show that the ATPase is activated by potassium externally and by sodium internally, and suggest that the ions activating the ATPase are the ions that are transported.2. Sodium 84-90 dynein axonemal heavy chain 8 Homo sapiens 139-145 4228075-4 1967 As it is known that the ouabain-sensitive ATPase in fragmented ghosts requires both sodium and potassium ions, these results show that the ATPase is activated by potassium externally and by sodium internally, and suggest that the ions activating the ATPase are the ions that are transported.2. Sodium 84-90 dynein axonemal heavy chain 8 Homo sapiens 139-145 4228075-4 1967 As it is known that the ouabain-sensitive ATPase in fragmented ghosts requires both sodium and potassium ions, these results show that the ATPase is activated by potassium externally and by sodium internally, and suggest that the ions activating the ATPase are the ions that are transported.2. Sodium 190-196 dynein axonemal heavy chain 8 Homo sapiens 42-48 4228075-4 1967 As it is known that the ouabain-sensitive ATPase in fragmented ghosts requires both sodium and potassium ions, these results show that the ATPase is activated by potassium externally and by sodium internally, and suggest that the ions activating the ATPase are the ions that are transported.2. Sodium 190-196 dynein axonemal heavy chain 8 Homo sapiens 139-145 4228075-4 1967 As it is known that the ouabain-sensitive ATPase in fragmented ghosts requires both sodium and potassium ions, these results show that the ATPase is activated by potassium externally and by sodium internally, and suggest that the ions activating the ATPase are the ions that are transported.2. Sodium 190-196 dynein axonemal heavy chain 8 Homo sapiens 139-145 6051803-8 1967 The ability to carry out sodium:sodium exchange can be restored by replacing most of the internal sodium with potassium or by preparing the cells so that they contain much more orthophosphate (P(i)) than ATP.6. Sodium 25-31 mitochondrially encoded ATP synthase 6 Homo sapiens 204-209 6051803-8 1967 The ability to carry out sodium:sodium exchange can be restored by replacing most of the internal sodium with potassium or by preparing the cells so that they contain much more orthophosphate (P(i)) than ATP.6. Sodium 32-38 mitochondrially encoded ATP synthase 6 Homo sapiens 204-209 6051803-8 1967 The ability to carry out sodium:sodium exchange can be restored by replacing most of the internal sodium with potassium or by preparing the cells so that they contain much more orthophosphate (P(i)) than ATP.6. Sodium 32-38 mitochondrially encoded ATP synthase 6 Homo sapiens 204-209 4378052-2 1967 An adenosine triphosphatase system activated by sodium and potassium is present in high activity in the cochlear membranes (tegmentum vasculosum and stria vascularis). Sodium 48-54 ATPase Na+/K+ transporting subunit beta 1 Homo sapiens 3-27 4378052-4 1967 Since the microphonic potential depends on the high concentration of potassium ions in the endolymph, our findings strongly suggest the operation of an adenosine triphosphatase cation pump system activated by sodium and potassium, in the generation of cochlear cation gradients. Sodium 209-215 ATPase Na+/K+ transporting subunit beta 1 Homo sapiens 152-176 4289490-0 1967 Extraction and bioassay of renin from kidneys of sodium depleted and sodium-loaded rats. Sodium 49-55 renin Rattus norvegicus 27-32 4289490-0 1967 Extraction and bioassay of renin from kidneys of sodium depleted and sodium-loaded rats. Sodium 69-75 renin Rattus norvegicus 27-32 4862768-0 1967 The distribution of sodium, chloride and fluid in the body of young infants with increased intake of NaC1. Sodium 20-26 nucleus accumbens associated 1 Homo sapiens 101-105 4296201-2 1967 Relationship of ATP-ase to the active transport of sodium and potassium ions. Sodium 51-57 dynein axonemal heavy chain 8 Homo sapiens 16-23 14163532-0 1964 SPECIES DIFFERENCES IN THE EFFECT OF SODIUM AND POTASSIUM IONS ON THE ATPASE OF ERYTHROCYTE MEMBRANES. Sodium 37-43 dynein axonemal heavy chain 8 Homo sapiens 70-76 14067092-0 1963 THE ROLE OF SODIUM IONS IN THE ACTIVATION OF ELECTROPHORUS ELECTRIC ORGAN ADENOSINE TRIPHOSPHATASE. Sodium 12-18 ATPase Na+/K+ transporting subunit beta 1 Homo sapiens 74-98 33901312-0 2021 Homozygous SCN1B variants causing early infantile epileptic encephalopathy 52 affect voltage-gated sodium channel function. Sodium 99-105 sodium voltage-gated channel beta subunit 1 Homo sapiens 11-16 33968186-5 2021 The present review aimed to determine whether activated CaMKII induces early afterdepolarizations and delayed afterdepolarizations that result in VA by regulating sodium, potassium and calcium ions. Sodium 163-169 calcium/calmodulin dependent protein kinase II gamma Homo sapiens 56-62 34015169-9 2021 The inhibitory effects of TRPM8 agonists were mimicked by calcitonin gene-related peptide (CGRP), and were blocked by KRP2579 (a TRPM8 antagonist), tetrodotoxin (a sodium channel blocker), olcegepant (BIBN, a CGRP receptor antagonist), SQ22536 (an adenylate cyclase antagonist), or H89 (a nonspecific cAMP-dependent protein kinase A inhibitor). Sodium 164-170 transient receptor potential cation channel subfamily M member 8 Homo sapiens 26-31 33982289-13 2021 Both Fhf1 (p.Arg52His) and Scn8a (p.Asn1768Asp) missense mutations enhance sodium channel Nav 1.6 currents and induce SUDEP with bradycardia in mice, suggesting an FHF1/Nav 1.6 functional axis underlying altered brain sodium channel gating in epileptic encephalopathy. Sodium 75-81 fibroblast growth factor 12 Mus musculus 5-9 33982289-13 2021 Both Fhf1 (p.Arg52His) and Scn8a (p.Asn1768Asp) missense mutations enhance sodium channel Nav 1.6 currents and induce SUDEP with bradycardia in mice, suggesting an FHF1/Nav 1.6 functional axis underlying altered brain sodium channel gating in epileptic encephalopathy. Sodium 75-81 sodium channel, voltage-gated, type VIII, alpha Mus musculus 27-32 33982289-13 2021 Both Fhf1 (p.Arg52His) and Scn8a (p.Asn1768Asp) missense mutations enhance sodium channel Nav 1.6 currents and induce SUDEP with bradycardia in mice, suggesting an FHF1/Nav 1.6 functional axis underlying altered brain sodium channel gating in epileptic encephalopathy. Sodium 75-81 sodium channel, voltage-gated, type VIII, alpha Mus musculus 90-97 33982289-13 2021 Both Fhf1 (p.Arg52His) and Scn8a (p.Asn1768Asp) missense mutations enhance sodium channel Nav 1.6 currents and induce SUDEP with bradycardia in mice, suggesting an FHF1/Nav 1.6 functional axis underlying altered brain sodium channel gating in epileptic encephalopathy. Sodium 218-224 fibroblast growth factor 12 Mus musculus 5-9 33982289-13 2021 Both Fhf1 (p.Arg52His) and Scn8a (p.Asn1768Asp) missense mutations enhance sodium channel Nav 1.6 currents and induce SUDEP with bradycardia in mice, suggesting an FHF1/Nav 1.6 functional axis underlying altered brain sodium channel gating in epileptic encephalopathy. Sodium 218-224 sodium channel, voltage-gated, type VIII, alpha Mus musculus 27-32 34046503-1 2021 Gitelman syndrome (GS) is an autosomal recessive inherited salt-losing renal tubular disease, which is caused by a pathogenic mutation of SLC12A3 encoding thiazide-sensitive Na-Cl cotransporter, which leads to disturbance of sodium and chlorine reabsorption in renal distal convoluted tubules, resulting in phenotypes such as hypovolemia, renin angiotensin aldosterone system (RAAS) activation, hypokalemia, and metabolic alkalosis. Sodium 225-231 solute carrier family 12 member 3 Homo sapiens 138-145 33882231-2 2021 In this work, mica was ultrasonically exfoliated into a single-layered nanomaterial after thermal activation, acidification, sodium replacement, and cetyltrimethylammonium bromide (CTAB) intercalation and then modified with ureido-pyrimidinone (UPy)-based PEG chains. Sodium 125-131 MHC class I polypeptide-related sequence A Homo sapiens 14-18 33515676-0 2021 ALDH2 deficiency induces atrial fibrillation through dysregulated cardiac sodium channel and mitochondrial bioenergetics: a multi-omics analysis. Sodium 74-80 aldehyde dehydrogenase 2 family member Homo sapiens 0-5 33482339-4 2021 As a neutral amino acid (AA), the transport of DL-Met is facilitated by multiple apical sodium-dependent/-independent high-/low-affinity transporters such as ASCT2, B0AT1 and rBAT/b0,+AT. Sodium 88-94 solute carrier family 6 member 19 Homo sapiens 165-170 33882940-9 2021 We presume that dysfunction of the ss2AdR also leads to an insufficient stimulation of the Na+/K+-ATPase causing sodium overload which reverses the transport direction of the sodium-calcium exchanger (NCX) to import calcium instead of exporting it as is also known from the ischemia-reperfusion paradigm. Sodium 113-119 solute carrier family 24 member 3 Homo sapiens 175-199 33872482-11 2021 The intake of vitamin C (APC=-3.2, p<0.05) and sodium (APC=-2.3, p<0.05) significantly decreased. Sodium 47-53 APC regulator of WNT signaling pathway 2 Homo sapiens 55-61 33889010-0 2021 Rosuvastatin Enhances Alveolar Fluid Clearance in Lipopolysaccharide-Induced Acute Lung Injury by Activating the Expression of Sodium Channel and Na,K-ATPase via the PI3K/AKT/Nedd4-2 Pathway. Sodium 127-133 NEDD4 like E3 ubiquitin protein ligase Rattus norvegicus 175-182 33994037-6 2022 Ucn-2 levels were positively associated with peripheral edemas (P = 0.022), hepatomegaly (P = 0.007) and sodium retention score (rho = 0.37, P = 0.001) and inversely correlated with inferior vena cava collapse at inspiration (rho = -0.37, P = 0.001). Sodium 105-111 urocortin 2 Homo sapiens 0-5 33369088-0 2021 Generation and basic characterization of a gene-trap knockout mouse model of Scn2a with a substantial reduction of voltage-gated sodium channel Nav 1.2 expression. Sodium 129-135 sodium channel, voltage-gated, type II, alpha Mus musculus 77-82 33411695-1 2021 BACKGROUND: Loss-of-function variants in SCN1B, encoding voltage-gated sodium channel beta1 subunits, are linked to human diseases with high risk of sudden death, including epileptic encephalopathy and cardiac arrhythmia. Sodium 71-77 sodium voltage-gated channel beta subunit 1 Homo sapiens 41-46 33411695-8 2021 These results provide important new insights into the mechanism of SCN1B-linked channelopathies, adding RIP-excitation coupling to the multi-functionality of sodium channel beta1 subunits. Sodium 158-164 sodium voltage-gated channel beta subunit 1 Homo sapiens 67-72 33307167-2 2021 The antioxidant ascorbate (the reduced form of vitamin C) is concentrated in CNS neurons through a sodium-dependent transporter named SVCT2 and participates in several CNS processes, for instance, the regulation of glutamate receptors functioning and the synthesis of neuromodulators. Sodium 99-105 solute carrier family 23 member 2 Homo sapiens 134-139 33390050-10 2021 We determined (1) whether NCC activity was greater in sodium-sensitive versus sodium-resistant participants and correlated with sodium sensitivity and (2) time course and magnitude of potassium-induced natriuresis following 35 mmol KCl directly compared with 50 mg HCTZ. Sodium 54-60 solute carrier family 12 member 3 Homo sapiens 26-29 33390050-10 2021 We determined (1) whether NCC activity was greater in sodium-sensitive versus sodium-resistant participants and correlated with sodium sensitivity and (2) time course and magnitude of potassium-induced natriuresis following 35 mmol KCl directly compared with 50 mg HCTZ. Sodium 78-84 solute carrier family 12 member 3 Homo sapiens 26-29 33390050-10 2021 We determined (1) whether NCC activity was greater in sodium-sensitive versus sodium-resistant participants and correlated with sodium sensitivity and (2) time course and magnitude of potassium-induced natriuresis following 35 mmol KCl directly compared with 50 mg HCTZ. Sodium 78-84 solute carrier family 12 member 3 Homo sapiens 26-29 32467588-1 2021 The mineralocorticoid receptor (MR) plays a central role in sodium homoeostasis by transducing the response to aldosterone in the distal nephron and other sodium transporting epithelia. Sodium 60-66 nuclear receptor subfamily 3 group C member 2 Homo sapiens 4-30 32467588-1 2021 The mineralocorticoid receptor (MR) plays a central role in sodium homoeostasis by transducing the response to aldosterone in the distal nephron and other sodium transporting epithelia. Sodium 60-66 nuclear receptor subfamily 3 group C member 2 Homo sapiens 32-34 32467588-1 2021 The mineralocorticoid receptor (MR) plays a central role in sodium homoeostasis by transducing the response to aldosterone in the distal nephron and other sodium transporting epithelia. Sodium 155-161 nuclear receptor subfamily 3 group C member 2 Homo sapiens 4-30 32467588-1 2021 The mineralocorticoid receptor (MR) plays a central role in sodium homoeostasis by transducing the response to aldosterone in the distal nephron and other sodium transporting epithelia. Sodium 155-161 nuclear receptor subfamily 3 group C member 2 Homo sapiens 32-34 32956652-0 2021 The sodium/proton exchanger NHA2 regulates blood pressure through a WNK4-NCC dependent pathway in the kidney. Sodium 4-10 WNK lysine deficient protein kinase 4 Mus musculus 68-72 33070283-4 2021 Besides, we explore how sodium consumption enhances the expression of transient receptor potential channel 3 (TrpC3) mRNA and facilitates the release of calcium inside immune cell groups, together with elevated blood pressure in essential hypertensive patients. Sodium 24-30 transient receptor potential cation channel subfamily C member 3 Homo sapiens 70-108 33070283-4 2021 Besides, we explore how sodium consumption enhances the expression of transient receptor potential channel 3 (TrpC3) mRNA and facilitates the release of calcium inside immune cell groups, together with elevated blood pressure in essential hypertensive patients. Sodium 24-30 transient receptor potential cation channel subfamily C member 3 Homo sapiens 110-115 32868747-8 2021 Furthermore, Foxo1 interacted with voltage gated sodium Nav1.7 channels and increased the Nav1.7 current density by accelerating activation rather than by changing the expression of Nav1.7 in dorsal root ganglia neurons. Sodium 49-55 forkhead box O1 Rattus norvegicus 13-18 33166587-0 2021 BLOCKADE OF ERK1/2 ACTIVATION WITH U0126 OR PEP7 REDUCES SODIUM APPETITE AND ANGIOTENSIN II-INDUCED PRESSOR RESPONSES IN SPONTANEOUSLY HYPERTENSIVE RATS. Sodium 57-63 mitogen activated protein kinase 3 Rattus norvegicus 12-18 33166587-2 2021 In normotensive rats, angiotensin II (ANG II)-induced sodium intake is blocked by the inactivation of p42/44 mitogen-activated protein kinase, also known as extracellular signal-regulated protein kinase1/2 (ERK1/2). Sodium 54-60 mitogen activated protein kinase 3 Rattus norvegicus 207-213 33166587-3 2021 Here we investigated if inhibition of ERK1/2 pathway centrally would change sodium appetite and intracerebroventricular (icv) ANG II-induced pressor response in SHRs. Sodium 76-82 mitogen activated protein kinase 3 Rattus norvegicus 38-44 33166587-10 2021 Therefore, the present results suggest that central AT1 receptor-mediated ERK1/2 activation is part of the mechanisms involved in sodium appetite and ANG II-induced pressor response in SHRs. Sodium 130-136 mitogen activated protein kinase 3 Rattus norvegicus 74-80 33499384-1 2021 Na+/H+ exchange factor-1 (NHERF1), a multidomain PDZ scaffolding phosphoprotein, is required for the type II sodium-dependent phosphate cotransporter (NPT2A)-mediated renal phosphate absorption. Sodium 109-115 SLC9A3 regulator 1 Homo sapiens 26-32 33478555-9 2021 Our study shows that the endocytic complex composed of Numb, Nedd4-2 and Eps15, is necessary for non-SUMOylated CRMP2-mediated internalization of sodium channels in vivo. Sodium 146-152 epidermal growth factor receptor pathway substrate 15 Mus musculus 73-78 33492304-0 2021 Effect of Parathyroid Hormone on Intestinal Mucosal Sodium Dependent Phosphorus Transporter. Sodium 52-58 parathyroid hormone Mus musculus 10-29 33492304-4 2021 Based on these clinical phenomena, we hypothesized that high levels of parathyroid hormone (PTH) might inhibit intestinal phosphorus absorption which mediated by sodium-dependent phosphorus transporters. Sodium 162-168 parathyroid hormone Mus musculus 71-90 34032155-1 2021 Primary carnitine deficiency (PCD) is a rare autosomal recessive disorder caused by loss of function mutations in the solute carrier family 22 member 5 (SLC22A5) gene that encodes a high-affinity sodium-ion-dependent organic cation transporter protein (OCTN2). Sodium 196-202 solute carrier family 22 member 5 Homo sapiens 118-151 34032155-1 2021 Primary carnitine deficiency (PCD) is a rare autosomal recessive disorder caused by loss of function mutations in the solute carrier family 22 member 5 (SLC22A5) gene that encodes a high-affinity sodium-ion-dependent organic cation transporter protein (OCTN2). Sodium 196-202 solute carrier family 22 member 5 Homo sapiens 153-160 34032155-1 2021 Primary carnitine deficiency (PCD) is a rare autosomal recessive disorder caused by loss of function mutations in the solute carrier family 22 member 5 (SLC22A5) gene that encodes a high-affinity sodium-ion-dependent organic cation transporter protein (OCTN2). Sodium 196-202 solute carrier family 22 member 5 Homo sapiens 253-258 32879980-1 2021 BACKGROUND: Phosphate is absorbed in the small intestine via passive flow and active transport.NaPi-IIb, a type II sodium-dependent phosphate transporter, is considered to mediate active phosphate transport in rodents. Sodium 115-121 solute carrier family 34 member 2 Rattus norvegicus 95-103 33189882-4 2021 De novo loss-of-function mutations in the voltage-gated sodium channel SCN1A are the main cause of DS, while genetic epilepsy with febrile seizures plus (GEFS+), also characterized by early-life FSs and afebrile epilepsy, is typically caused by inherited mutations that alter the biophysical properties of SCN1A. Sodium 56-62 sodium voltage-gated channel alpha subunit 1 Homo sapiens 71-76 33189882-4 2021 De novo loss-of-function mutations in the voltage-gated sodium channel SCN1A are the main cause of DS, while genetic epilepsy with febrile seizures plus (GEFS+), also characterized by early-life FSs and afebrile epilepsy, is typically caused by inherited mutations that alter the biophysical properties of SCN1A. Sodium 56-62 sodium voltage-gated channel alpha subunit 1 Homo sapiens 306-311 33518649-11 2021 Therefore, it was suggested that urine sodium concentration may be useful as a predictor of body weight and BNP decrease after TLV induction. Sodium 39-45 natriuretic peptide B Homo sapiens 108-111 33093176-4 2020 We investigated the effect of LITAF on the voltage-gated sodium channel Nav1.5, which is critical for cardiac depolarization. Sodium 57-63 lipopolysaccharide-induced TNF factor Danio rerio 30-35 33093176-5 2020 We show that overexpressed LITAF resulted in a significant increase in the density of Nav1.5-generated voltage-gated sodium current I Na and Nav1.5 surface protein levels in rabbit cardiomyocytes and in HEK cells stably expressing Nav1.5. Sodium 117-123 lipopolysaccharide-induced TNF factor Danio rerio 27-32 33376789-0 2020 Low-Temperature Multielement Fusible Alloy-Based Molten Sodium Batteries for Grid-Scale Energy Storage. Sodium 56-62 GRB2 related adaptor protein 2 Homo sapiens 77-81 33376789-7 2020 The proof-of-concept molten sodium battery enabled by the Bi-Pb-Sn fusible alloy not only circumvents the use of costly Ga and In elements but also delivers attractive performance at 100 C, holding great promise for grid-scale energy storage. Sodium 28-34 GRB2 related adaptor protein 2 Homo sapiens 217-221 32072437-12 2020 CONCLUSIONS: In the SBS situation, Teduglutide not only maximizes small intestinal mucosal hypertrophy but also partially restores small intestinal epithelial function through an altered distribution of claudin-10, facilitating sodium recirculation for Na-coupled glucose transport and water absorption. Sodium 228-234 claudin 10 Mus musculus 203-213 33118157-7 2020 Interestingly, when sodC- cells were treated with 5-(N,N-Dimethyl) amiloride hydrochloride (EIPA), an inhibitor of sodium proton exchanger (NHE), both the structure and the function of the CV improved. Sodium 115-121 solute carrier family 9 member C1 Homo sapiens 140-143 33110213-4 2020 Voltage-gated sodium (NaV) channels drive neuronal excitability and three subtypes - NaV1.7, NaV1.8 and NaV1.9 - are preferentially expressed in the peripheral nervous system, suggesting that their inhibition might treat pain while avoiding central and cardiac adverse effects. Sodium 14-20 sodium voltage-gated channel alpha subunit 11 Homo sapiens 104-110 33078551-0 2020 Salvianic Acid A Sodium Promotes the Recovery of Motor Function After Spinal Cord Injury in Rats by Reducing Microglia Inflammation through Regulating MIP2/Vdac1/Ndufa12 Signaling Axis. Sodium 17-23 C-X-C motif chemokine ligand 2 Rattus norvegicus 151-155 33078551-0 2020 Salvianic Acid A Sodium Promotes the Recovery of Motor Function After Spinal Cord Injury in Rats by Reducing Microglia Inflammation through Regulating MIP2/Vdac1/Ndufa12 Signaling Axis. Sodium 17-23 NADH:ubiquinone oxidoreductase subunit A12 Rattus norvegicus 162-169 33370868-1 2020 Here, we described the generation of human induced pluripotent stem cell lines (hiPSCs) from fibroblasts isolated by punch biopsies of two siblings carrying inherited mutation (c.434 T > C) in the SCN1A gene, encoding for the neuronal voltage gated sodium channel NaV1.1. Sodium 249-255 sodium voltage-gated channel alpha subunit 1 Homo sapiens 197-202 25905305-1 2000 Aldosterone promotes active sodium transport and excretion of potassium via the mineralocorticoid receptor (MR) and the resultant activation of specific amiloride-sensitive sodium channels (ENaC) and the Na-K ATP ase pump in the target tissues. Sodium 28-34 nuclear receptor subfamily 3 group C member 2 Homo sapiens 80-106 25905305-1 2000 Aldosterone promotes active sodium transport and excretion of potassium via the mineralocorticoid receptor (MR) and the resultant activation of specific amiloride-sensitive sodium channels (ENaC) and the Na-K ATP ase pump in the target tissues. Sodium 28-34 nuclear receptor subfamily 3 group C member 2 Homo sapiens 108-110 33228183-4 2020 We observed that the upregulated expression of cardiac gene markers (NKX2-5, MYH6, TNNT2, and DES) and cardiac ion channel genes (sodium, calcium, the potassium) also the increased levels of Connexin 43 and Nkx2.5 proteins. Sodium 130-136 gap junction protein alpha 1 Homo sapiens 191-202 33156304-6 2020 Aided by the advanced electron/ion transfer kinetics and structure stability, the SnS2-based electrode exhibits desired lithium/sodium storage performance and unprecedented long-term cycling stability (capacity retention of 74.7% after 1000 cycles at 2 A g-1 for LIBs and 102% after 200 cycles at 500 mA g-1 for SIBs). Sodium 128-134 sodium voltage-gated channel alpha subunit 11 Homo sapiens 82-86 33203861-0 2020 Structure of the human sodium leak channel NALCN in complex with FAM155A. Sodium 23-29 sodium leak channel, non-selective Homo sapiens 43-48 33203861-1 2020 NALCN, a sodium leak channel expressed mainly in the central nervous system, is responsible for the resting Na+ permeability that controls neuronal excitability. Sodium 9-15 sodium leak channel, non-selective Homo sapiens 0-5 32387251-2 2020 Mutations in CAV3 have caused an LQT3-like accentuation in late sodium current, INa (Nav1.5). Sodium 64-70 caveolin 3 Homo sapiens 13-17 33176139-4 2020 We show that leptin activates the sodium leak channel (NALCN), thereby depolarizing a subset of glutamatergic (VGluT2) LepRb NTS neurons expressing galanin. Sodium 34-40 sodium leak channel, non-selective Mus musculus 55-60 31803246-12 2019 These suggest that KCNQ1 and SCN2A, genes that encode potassium and sodium channels, respectively, may serve as putative diagnostic targets for the diagnosis and prognosis of PHEO and therefore facilitate the clinical management of PHEO. Sodium 68-74 sodium voltage-gated channel alpha subunit 2 Homo sapiens 29-34 32009801-12 2019 Coagulation experiments in animals (mice and rats) revealed that Na2SeO3 can reduce the coagulation time of BMSCs in a concentration-dependent manner, which is related to the high expression of hematopoietic factors (SDF-1alpha, GM-CSF, IL-7, IL-8, IL-11, and SCF). Sodium 65-72 colony stimulating factor 2 Rattus norvegicus 229-235 32009801-12 2019 Coagulation experiments in animals (mice and rats) revealed that Na2SeO3 can reduce the coagulation time of BMSCs in a concentration-dependent manner, which is related to the high expression of hematopoietic factors (SDF-1alpha, GM-CSF, IL-7, IL-8, IL-11, and SCF). Sodium 65-72 interleukin 7 Rattus norvegicus 237-241 31828140-4 2019 In addition, this study also aims to determine the active ingredients of H. sabdariffa (Hib) that interact with sodium-glucose cotransporter-1 (SGLT-1) so that it can increase GLP-1 secretion in the ileum and interact with GLP-1 receptors (GLP-1R) in the pancreas. Sodium 112-118 solute carrier family 5 member 1 Rattus norvegicus 144-150 33113884-7 2020 Maintenance of chlorophyll content and root growth under high salt in the prt6 mutant was linked with the restricted accumulation of sodium ions (Na+) in shoots and roots of the mutant genotype. Sodium 133-139 proteolysis 6 Arabidopsis thaliana 74-78 33066406-1 2020 The human L-type amino acid transporters LAT1 and LAT2 mediate the transport of amino acids and amino acid derivatives across plasma membranes in a sodium-independent, obligatory antiport mode. Sodium 148-154 linker for activation of T cells family member 2 Homo sapiens 50-54 32840624-8 2020 Two suggestive loci were replicated in additional samples: for sodium excretion, rs12094702 near zinc finger SWIM-type containing 5 (ZSWIM5) was replicated in the Asian ancestry sample reaching Bonferroni-corrected significance (P = 0.007), and for potassium excretion rs34473523 near sodium leak channel (NALCN) was associated at a nominal P value with potassium excretion both in European (P = 0.043) and African (P = 0.043) ancestry cohorts. Sodium 63-69 zinc finger SWIM-type containing 5 Homo sapiens 97-131 32840624-8 2020 Two suggestive loci were replicated in additional samples: for sodium excretion, rs12094702 near zinc finger SWIM-type containing 5 (ZSWIM5) was replicated in the Asian ancestry sample reaching Bonferroni-corrected significance (P = 0.007), and for potassium excretion rs34473523 near sodium leak channel (NALCN) was associated at a nominal P value with potassium excretion both in European (P = 0.043) and African (P = 0.043) ancestry cohorts. Sodium 63-69 zinc finger SWIM-type containing 5 Homo sapiens 133-139 32840624-8 2020 Two suggestive loci were replicated in additional samples: for sodium excretion, rs12094702 near zinc finger SWIM-type containing 5 (ZSWIM5) was replicated in the Asian ancestry sample reaching Bonferroni-corrected significance (P = 0.007), and for potassium excretion rs34473523 near sodium leak channel (NALCN) was associated at a nominal P value with potassium excretion both in European (P = 0.043) and African (P = 0.043) ancestry cohorts. Sodium 285-291 zinc finger SWIM-type containing 5 Homo sapiens 97-131 32840624-8 2020 Two suggestive loci were replicated in additional samples: for sodium excretion, rs12094702 near zinc finger SWIM-type containing 5 (ZSWIM5) was replicated in the Asian ancestry sample reaching Bonferroni-corrected significance (P = 0.007), and for potassium excretion rs34473523 near sodium leak channel (NALCN) was associated at a nominal P value with potassium excretion both in European (P = 0.043) and African (P = 0.043) ancestry cohorts. Sodium 285-291 zinc finger SWIM-type containing 5 Homo sapiens 133-139 32897040-7 2020 Of the 57 patients, one patient without small-fibre pathology and 2 patients with small-fibre pathology had rare variants of voltage-gated sodium channels, namely SCN11A, SCN9A, and SCN1A variants. Sodium 139-145 sodium voltage-gated channel alpha subunit 11 Homo sapiens 163-169 32897040-7 2020 Of the 57 patients, one patient without small-fibre pathology and 2 patients with small-fibre pathology had rare variants of voltage-gated sodium channels, namely SCN11A, SCN9A, and SCN1A variants. Sodium 139-145 sodium voltage-gated channel alpha subunit 1 Homo sapiens 182-187 32893499-0 2020 Anchoring SnS2 on TiC/C Backbone to Promote Sodium Ion Storage by Phosphate Ion Doping. Sodium 44-50 sodium voltage-gated channel alpha subunit 11 Homo sapiens 10-14 32893499-1 2020 Tin disulfide (SnS2 ) shows promising properties toward sodium ion storage with high capacity, but its cycle life and high rate capability are still undermined as a result of poor reaction kinetics and unstable structure. Sodium 56-62 sodium voltage-gated channel alpha subunit 11 Homo sapiens 15-19 32687659-3 2020 Persistently increased activity of G protein-coupled receptor kinase 4 (GRK4), caused by increased expression or genetic variants (eg, GRKgamma142V), impairs the ability of the kidney to excrete a sodium load, in part, by impairing renal dopamine D1 receptor function through persistent phosphorylation. Sodium 197-203 dopamine receptor D1 Mus musculus 238-258 31828140-4 2019 In addition, this study also aims to determine the active ingredients of H. sabdariffa (Hib) that interact with sodium-glucose cotransporter-1 (SGLT-1) so that it can increase GLP-1 secretion in the ileum and interact with GLP-1 receptors (GLP-1R) in the pancreas. Sodium 112-118 glucagon Rattus norvegicus 176-181 31584578-2 2019 The molar addition of anions, such as TBAF-, TBAOH-, TBACN- and TBAAcO-, induced a significant red shift in the charge transfer band (Deltalambda = 73 nm, from 337 nm to 410 nm), in agreement with visible "naked eye" detectable colorimetric activities; in addition, soaked-in-L paper strips were prepared, which could significantly discriminate cyanide (KCN) and hydroxide (NaOH) ions dissolved in tap water via the litmus test method. Sodium 374-378 nuclear RNA export factor 1 Homo sapiens 398-401 33084603-0 2020 Lack of functional wolframin causes drop in plasmalemmal sodium-calcium exchanger type 1 expression at early stage in rat model of Wolfram syndrome. Sodium 57-63 wolframin ER transmembrane glycoprotein Rattus norvegicus 19-28 32611770-0 2020 CaMKII enhances voltage-gated sodium channel Nav1.6 activity and neuronal excitability. Sodium 30-36 calcium/calmodulin dependent protein kinase II gamma Homo sapiens 0-6 31655555-3 2019 The cause of Liddle syndrome is missense or frameshift mutations in SCNN1A, SCNN1B, or SCNN1G genes that encode epithelial sodium channel subunits. Sodium 123-129 sodium channel epithelial 1 subunit beta Homo sapiens 76-82 31655555-3 2019 The cause of Liddle syndrome is missense or frameshift mutations in SCNN1A, SCNN1B, or SCNN1G genes that encode epithelial sodium channel subunits. Sodium 123-129 sodium channel epithelial 1 subunit gamma Homo sapiens 87-93 31709262-1 2019 The human SLC1A5 commonly known as ASCT2 is a sodium-dependent neutral amino acid antiporter involved in transmembrane traffic of glutamine that is exchanged through the cell membrane with smaller amino acids such as serine or threonine. Sodium 46-52 solute carrier family 1 member 5 Homo sapiens 10-16 32618095-1 2020 NALCN encodes a sodium ion leak channel expressed in the nervous system that conducts a persistent influx of sodium ions to facilitate action potential formation. Sodium 16-22 sodium leak channel, non-selective Homo sapiens 0-5 32618095-1 2020 NALCN encodes a sodium ion leak channel expressed in the nervous system that conducts a persistent influx of sodium ions to facilitate action potential formation. Sodium 109-115 sodium leak channel, non-selective Homo sapiens 0-5 32588437-2 2020 TCAP is shown to modulate alpha-subunit of the human cardiac sodium channel (hNav 1.5) by direct interactions. Sodium 61-67 titin-cap Homo sapiens 0-4 31709262-1 2019 The human SLC1A5 commonly known as ASCT2 is a sodium-dependent neutral amino acid antiporter involved in transmembrane traffic of glutamine that is exchanged through the cell membrane with smaller amino acids such as serine or threonine. Sodium 46-52 solute carrier family 1 member 5 Homo sapiens 35-40 31601020-2 2019 In the kidney, HCN1, HCN2 and HCN3 are differentially expressed and contribute to the transport of sodium, potassium (K+) and ammonium into the nephrons. Sodium 99-105 hyperpolarization activated cyclic nucleotide gated potassium channel 1 Homo sapiens 15-19 31564962-3 2019 The genesis and propagation of action potentials is dependent on voltage-gated sodium channels, in particular, Nav1.7, Nav1.8 and Nav1.9. Sodium 79-85 sodium voltage-gated channel alpha subunit 9 Homo sapiens 111-117 31564962-3 2019 The genesis and propagation of action potentials is dependent on voltage-gated sodium channels, in particular, Nav1.7, Nav1.8 and Nav1.9. Sodium 79-85 sodium voltage-gated channel alpha subunit 10 Homo sapiens 119-125 31481024-11 2019 For short durations, the effect cancels out due to a reduction of the transient TTX resistant sodium current (Nav1.8). Sodium 94-100 sodium voltage-gated channel alpha subunit 10 Homo sapiens 110-116 31172810-9 2019 Nicotine induced premature hypertension, renal expression of the sodium-potassium chloride cotransporter (NKCC2), increases in renal sodium retention, and infiltration of CD161a+/CD68+ macrophages into the renal medulla. Sodium 65-71 solute carrier family 12 member 1 Rattus norvegicus 106-111 31172810-14 2019 Noteworthy findings include the prevention of nicotine-mediated hypertension following successful immune ablation of CD161a+ immune cells and the necessary role these cells play in the overexpression of the sodium-potassium-chloride cotransporter (NKCC2) in the renal medulla and renal sodium retention. Sodium 207-213 solute carrier family 12 member 1 Rattus norvegicus 248-253 31172810-14 2019 Noteworthy findings include the prevention of nicotine-mediated hypertension following successful immune ablation of CD161a+ immune cells and the necessary role these cells play in the overexpression of the sodium-potassium-chloride cotransporter (NKCC2) in the renal medulla and renal sodium retention. Sodium 286-292 solute carrier family 12 member 1 Rattus norvegicus 248-253 30600495-5 2019 Results demonstrated that high-level silicon induced cell viability to decrease; LC3-II, p62, and apoptosis-related proteins were up-regulated after exposure to high-dose silicon (sodium metasilicate concentration more than 1 mM). Sodium 180-186 nucleoporin 62 Homo sapiens 89-92 31565882-1 2019 BACKGROUND: Striatin and caveolin-1 (cav-1) are scaffolding/regulating proteins that are associated with salt-sensitive high blood pressure and promote renal sodium and water reabsorption, respectively. Sodium 158-164 striatin Rattus norvegicus 12-20 31598168-0 2019 The voltage-gated sodium channel Nav1.7 associated with endometrial cancer. Sodium 18-24 sodium voltage-gated channel alpha subunit 9 Homo sapiens 33-39 31598168-10 2019 Conclusion: These results establish a relationship between voltage-gated sodium channel protein and endometrial cancer, and suggest that Nav1.7 is a potential prognostic biomarker and could serve as a novel therapeutic target for endometrial cancer. Sodium 73-79 sodium voltage-gated channel alpha subunit 9 Homo sapiens 137-143 31361119-5 2019 The superior sodium/potassium storage performance of the OC/SeS2 composite electrodes stems from their rational chemical structure design, including high electrical conductivity of the N-doped organic carbon network and chemical binding with SeS2 molecules. Sodium 13-19 secernin 2 Homo sapiens 60-64 31361119-6 2019 As a result, the OC/SeS2 cathode delivers a reversible capacity of 416 mAh g-1 after 700 cycles for sodium-ion batteries and 216 mAh g-1 after 500 cycles for potassium-ion batteries at 0.5 A g-1, respectively. Sodium 100-106 secernin 2 Homo sapiens 20-24 31186137-5 2019 The change in cilia morphology was associated with aberrant localization of ankyrin G (AnkG) and voltage-gated sodium channel 1.2 (Nav1.2). Sodium 111-117 sodium voltage-gated channel alpha subunit 2 Homo sapiens 131-137 32751086-5 2020 Moreover, serum vitamin C level also is dependent on genetic factors, such as SLC23A1 and SLC23A2 genes, encoding sodium-dependent vitamin C transporters and GSTM1, GSTP1 and GSTT1 genes which encode glutathione S-transferases. Sodium 114-120 solute carrier family 23 member 2 Homo sapiens 90-97 32618303-6 2020 Here we report a set of multiscale-calculations performed on the mTPC1, a ligand- and voltage-gated sodium selective channel. Sodium 100-106 two pore channel 1 Mus musculus 65-70 32618303-8 2020 Moreover, from the reconstructed free energy obtained from enhanced simulations, we have calculated the macroscopic conductance of sodium ions through the mTPC1, which we compared with measured single-channel conductance values. Sodium 131-137 two pore channel 1 Mus musculus 155-160 32686994-3 2021 Sodium channels particularly Nav1.7, Nav1.8, Nav 1.9 are key stake holders in the peripheral neuropathy, activation of these sodium channels might lead to genesis and propagation. Sodium 0-6 sodium voltage-gated channel alpha subunit 11 Homo sapiens 45-52 32686994-3 2021 Sodium channels particularly Nav1.7, Nav1.8, Nav 1.9 are key stake holders in the peripheral neuropathy, activation of these sodium channels might lead to genesis and propagation. Sodium 125-131 sodium voltage-gated channel alpha subunit 11 Homo sapiens 45-52 32909725-4 2020 These findings are consistent with abnormally increased renal sodium reabsorption, possibly caused by increased angiotensin II activity secondary to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-induced downregulation of angiotensin-converting enzyme 2 (ACE2) receptors. Sodium 62-68 angiotensin converting enzyme 2 Homo sapiens 236-267 32909725-4 2020 These findings are consistent with abnormally increased renal sodium reabsorption, possibly caused by increased angiotensin II activity secondary to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-induced downregulation of angiotensin-converting enzyme 2 (ACE2) receptors. Sodium 62-68 angiotensin converting enzyme 2 Homo sapiens 269-273 32532910-0 2020 Successful utilisation of epidural analgesia for perioperative pain management in a child with sodium voltage-gated channel alpha subunit (SCN1A) gene mutation. Sodium 95-101 sodium voltage-gated channel alpha subunit 1 Homo sapiens 139-144 32532910-1 2020 Sodium voltage-gated channel alpha subunit (SCN1A) gene mutation is a rare disorder with a large spectrum of clinical presentations. Sodium 0-6 sodium voltage-gated channel alpha subunit 1 Homo sapiens 44-49 31402610-1 2019 OBJECTIVE: Pathogenic variants in SCN8A, encoding the voltage-gated sodium (Na+) channel alpha subunit Nav1.6, is a known cause of epilepsy. Sodium 68-74 sodium voltage-gated channel alpha subunit 8 Homo sapiens 34-39 31236708-13 2019 Na/H exchanger isoform 3 (NHE3) increases BP by stimulating the intestinal absorption of sodium. Sodium 89-95 solute carrier family 9 member A3 Homo sapiens 0-24 31236708-13 2019 Na/H exchanger isoform 3 (NHE3) increases BP by stimulating the intestinal absorption of sodium. Sodium 89-95 solute carrier family 9 member A3 Homo sapiens 26-30 30765103-1 2019 Mutations in the SLC34A3 gene, encoding the sodium/phosphate cotransporter 2C (NPTIIc), induce decreased renal phosphate reabsorption, hypophosphatemia, decreased fibroblast growth factor 23 and parathyroid hormone, and increased 1,25-dihydroxyvitamin D (1,25[OH]2D) levels. Sodium 44-50 fibroblast growth factor 23 Homo sapiens 163-190 30100257-1 2019 BACKGROUND: The epithelial sodium channel ENaC consists of three subunits encoded by Scnn1a, Scnn1b, and Scnn1g and increased sodium absorption through this channel is hypothesized to lead to mucus dehydration and accumulation in cystic fibrosis (CF) patients. Sodium 27-33 sodium channel epithelial 1 subunit beta Homo sapiens 93-99 30100257-1 2019 BACKGROUND: The epithelial sodium channel ENaC consists of three subunits encoded by Scnn1a, Scnn1b, and Scnn1g and increased sodium absorption through this channel is hypothesized to lead to mucus dehydration and accumulation in cystic fibrosis (CF) patients. Sodium 27-33 sodium channel epithelial 1 subunit gamma Homo sapiens 105-111 30871604-10 2019 Network analysis by STITCH database 5.0 showed that SRPN23 interacted with sodium and calcium ions, suggesting that SRPN23 might be involved in insecticide resistance. Sodium 75-81 antichymotrypsin-2 Aedes aegypti 52-58 30871604-10 2019 Network analysis by STITCH database 5.0 showed that SRPN23 interacted with sodium and calcium ions, suggesting that SRPN23 might be involved in insecticide resistance. Sodium 75-81 antichymotrypsin-2 Aedes aegypti 116-122 30520694-17 2019 Both hormones require PAK4 activation to stimulate sodium-potassium adenosine triphosphatase activity. Sodium 51-57 p21 (RAC1) activated kinase 4 Rattus norvegicus 22-26 30745171-2 2019 Patients with PKD are generally advised to restrict their dietary sodium intake. Sodium 66-72 protein kinase D1 Homo sapiens 14-17 30172029-12 2019 CONCLUSION: This CACNA1C-E1115K variant destroyed the LTCC"s calcium selectivity and instead converted the mutant channel into a channel with a marked increase in sodium-mediated inward currents and potassium-mediated outward currents. Sodium 163-169 calcium voltage-gated channel subunit alpha1 C Homo sapiens 17-24 30193854-2 2019 Late sodium current (INa,L) is enhanced in HF and promotes Ca2+ overload; however, mechanisms underlying an antiarrhythmic effect of INa,L blockade in HF remain unclear. Sodium 5-11 internexin neuronal intermediate filament protein alpha Canis lupus familiaris 21-24 31933849-11 2019 The Muller cells exhibited signs of dedifferentiation, as paired box 6 (PAX6) and SRY box 2 (SOX2) were expressed by NaIO3 stimulated Muller glia proliferation and overexpression of proliferating cell nuclear antigen (PCNA). Sodium 117-122 proliferating cell nuclear antigen Rattus norvegicus 182-216 31933849-11 2019 The Muller cells exhibited signs of dedifferentiation, as paired box 6 (PAX6) and SRY box 2 (SOX2) were expressed by NaIO3 stimulated Muller glia proliferation and overexpression of proliferating cell nuclear antigen (PCNA). Sodium 117-122 proliferating cell nuclear antigen Rattus norvegicus 218-222 30055194-4 2019 In contrast to NET, DAT and SERT, OCT3 has higher capacity and lower affinity for substrates, is sodium-independent, and is multi-specific, with the capacity to transport norepinephrine, dopamine, serotonin and histamine. Sodium 97-103 OCTN3 Homo sapiens 34-38 30334255-10 2019 In the present study, we show that the sodium-activated, high-conductance, potassium leak channel, SLO2.1, is expressed and active at the resting membrane potential in MSMCs. Sodium 39-45 potassium sodium-activated channel subfamily T member 2 Homo sapiens 99-105 30999054-1 2019 INTRODUCTION: High throughput in vitro profiling of the cardiac Nav1.5 peak sodium current (INa) is widely used in cardiac safety screening. Sodium 76-82 internexin neuronal intermediate filament protein alpha Homo sapiens 92-95 29729938-0 2018 Solute carrier family 9, subfamily A, member 3 (SLC9A3)/sodium-hydrogen exchanger member 3 (NHE3) dysregulation and dilated intercellular spaces in patients with eosinophilic esophagitis. Sodium 56-62 solute carrier family 9 member A3 Homo sapiens 92-96 30251687-5 2018 Overexpression of dominant-negative mutant SAR1A (T39N or H79G) or SAR1B (T39N or H79G) significantly reduces the expression level of Nav1.5 on cell surface, and decreases the peak sodium current density (INa) in HEK/Nav1.5 cells and neonatal rat cardiomyocytes. Sodium 181-187 secretion associated, Ras related GTPase 1B Rattus norvegicus 67-72 30371314-1 2018 Background The sodium channel, Nav1.5, encoded by SCN 5A, undergoes developmentally regulated splicing from inclusion of exon 6A in the fetal heart to exon 6B in adults. Sodium 15-21 sodium channel, voltage-gated, type V, alpha Mus musculus 31-37 30371314-1 2018 Background The sodium channel, Nav1.5, encoded by SCN 5A, undergoes developmentally regulated splicing from inclusion of exon 6A in the fetal heart to exon 6B in adults. Sodium 15-21 sodium channel, voltage-gated, type V, alpha Mus musculus 50-56 29793215-1 2018 Studies on human genetics have implicated the voltage-gated sodium channel Nav1.7 as an appealing target for the treatment of pain. Sodium 60-66 sodium voltage-gated channel alpha subunit 9 Homo sapiens 75-81 29748250-1 2018 INTRODUCTION: Loss of the cystic fibrosis transmembrane conductance regulator in cystic fibrosis (CF) leads to hyperabsorption of sodium and fluid from the airway due to upregulation of the epithelial sodium channel (ENaC). Sodium 130-136 cystic fibrosis transmembrane conductance regulator Mus musculus 26-77 29952605-5 2018 An elevation of Fos-like immunoreactivity in Ox neurons was observed in fluid-depleted rats that were allowed to ingest water and sodium. Sodium 130-136 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 16-19 29859980-2 2018 Slack activity is enhanced by interaction with the Fragile-X-Mental-Retardation-Protein (FMRP) and loss of FMRP leads to decreased sodium-activated potassium currents in medial nucleus of the trapezoid body neurons of the Fmr1-knockout (KO) mouse representing a mouse model of the human Fragile-X-Syndrome (FXS) and autism. Sodium 131-137 potassium channel, subfamily T, member 1 Mus musculus 0-5 29859980-2 2018 Slack activity is enhanced by interaction with the Fragile-X-Mental-Retardation-Protein (FMRP) and loss of FMRP leads to decreased sodium-activated potassium currents in medial nucleus of the trapezoid body neurons of the Fmr1-knockout (KO) mouse representing a mouse model of the human Fragile-X-Syndrome (FXS) and autism. Sodium 131-137 fragile X messenger ribonucleoprotein 1 Mus musculus 89-93 29859980-2 2018 Slack activity is enhanced by interaction with the Fragile-X-Mental-Retardation-Protein (FMRP) and loss of FMRP leads to decreased sodium-activated potassium currents in medial nucleus of the trapezoid body neurons of the Fmr1-knockout (KO) mouse representing a mouse model of the human Fragile-X-Syndrome (FXS) and autism. Sodium 131-137 fragile X messenger ribonucleoprotein 1 Mus musculus 107-111 29859980-2 2018 Slack activity is enhanced by interaction with the Fragile-X-Mental-Retardation-Protein (FMRP) and loss of FMRP leads to decreased sodium-activated potassium currents in medial nucleus of the trapezoid body neurons of the Fmr1-knockout (KO) mouse representing a mouse model of the human Fragile-X-Syndrome (FXS) and autism. Sodium 131-137 fragile X messenger ribonucleoprotein 1 Mus musculus 222-226 29658892-7 2018 MAIN RESULTS: The experimental results show that the system is able to detect sodium levels in the bone as low as 16 microg Na g-1 dry bone with an effective dose to the body of about 27 microSv. Sodium 78-84 growth differentiation factor 15 Homo sapiens 124-130 29757959-7 2018 In the SCNN1G gene, six SNPs (rs4073291, rs12934362, rs7404408, rs4494543, rs5735, and rs6497657) were significantly different in 24-h urinary sodium excretion according to gene variants. Sodium 143-149 sodium channel epithelial 1 subunit gamma Homo sapiens 7-13 29757959-9 2018 Our finding indicated that 24-h urinary sodium excretions were different according to variants of the SCNN1G gene in large samples. Sodium 40-46 sodium channel epithelial 1 subunit gamma Homo sapiens 102-108 29362499-9 2018 Modeling the degree of sodium loss delivers maximum melt temperatures between 3290 and 3490 K. Our results imply that natural lighting strikes may be an important agent of syn-eruptive morphological and chemical processing of volcanic ash. Sodium 23-29 synemin Homo sapiens 172-175 30081699-4 2018 Using a rational design strategy, we identified a heptamer peptide harboring CRMP2"s SUMO motif that disrupted the CRMP2-Ubc9 interaction, inhibited CRMP2 SUMOylation, inhibited NaV1.7 membrane trafficking, and specifically inhibited NaV1.7 sodium influx in sensory neurons. Sodium 241-247 sodium voltage-gated channel alpha subunit 9 Homo sapiens 178-184 29424299-8 2018 The other two families are the SMR, which are the smallest drug efflux proteins known, and the MATE family, whose pumps can also resort to the sodium gradient as an energy source. Sodium 143-149 LY6/PLAUR domain containing 4 Homo sapiens 31-34 28993502-1 2018 The bone-derived hormone fibroblast growth factor-23 (FGF-23) activates complexes composed of FGF receptors (FGFRs), including FGFR1, and alpha-Klotho in the kidney distal tubule (DT), leading to increased sodium retention and hypertension. Sodium 206-212 fibroblast growth factor 23 Mus musculus 25-52 28993502-1 2018 The bone-derived hormone fibroblast growth factor-23 (FGF-23) activates complexes composed of FGF receptors (FGFRs), including FGFR1, and alpha-Klotho in the kidney distal tubule (DT), leading to increased sodium retention and hypertension. Sodium 206-212 fibroblast growth factor 23 Mus musculus 54-60 29069584-5 2017 DCs activated by excess sodium produce increased interleukin-1beta (IL-1beta) and promote T cell production of cytokines IL-17A and interferon gamma (IFN-gamma). Sodium 24-30 interleukin 17A Mus musculus 121-127 29038209-2 2017 Activation of the sodium-hydrogen exchanger in the heart and vasculature (NHE1 isoform) and the kidneys (NHE3 isoform) may serve as a common mechanism that links both disorders and may underlie their interplay. Sodium 18-24 solute carrier family 9 member A3 Homo sapiens 105-109 29033564-0 2017 Delivery of sodium morrhuate to hemangioma endothelial cells using immunoliposomes conjugated with anti-VEGFR2/KDR antibody. Sodium 12-18 kinase insert domain receptor Homo sapiens 104-110 29033564-0 2017 Delivery of sodium morrhuate to hemangioma endothelial cells using immunoliposomes conjugated with anti-VEGFR2/KDR antibody. Sodium 12-18 kinase insert domain receptor Homo sapiens 111-114 28495802-1 2017 Na+/H+ exchanger NHE3 mediates the majority of intestinal and renal electroneutral sodium absorption. Sodium 83-89 solute carrier family 9 member A3 Homo sapiens 17-21 28506883-10 2017 Our findings indicate the involvement of NKA-SRc-Kinase-Ras-Raf-ERK1/2 pathway in the downregulation of NHE3 by cardiotonic steroids in the renal proximal tubule, promoting a reduction of proximal sodium reabsorption and natriuresis. Sodium 197-203 SRC proto-oncogene, non-receptor tyrosine kinase Rattus norvegicus 45-48 28298361-3 2017 Results showed the CCK gene to be expressed intensely in the inner medulla and moderately in the inner stripe of the outer medulla, with the expression in the latter being enhanced by high sodium intake. Sodium 189-195 cholecystokinin Mus musculus 19-22 27622885-6 2017 In distal renal tubules, FGF23 augments calcium and sodium reabsorption by increasing the apical membrane expression of the epithelial calcium channel TRPV5 and of the sodium-chloride cotransporter NCC through a Klotho dependent activation of with-no-lysine kinase-4 (WNK4). Sodium 52-58 fibroblast growth factor 23 Homo sapiens 25-30 28283543-2 2017 KCNQ2/3 channel activity is augmented in vivo by phosphatidylinositol 4,5-bisphosphate (PIP2), which is generated from myo-inositol, an osmolyte transported into cells by sodium-dependent myo-inositol transporters (SMITs). Sodium 171-177 potassium voltage-gated channel subfamily Q member 2 Homo sapiens 0-5 28272791-0 2017 SNAT3-mediated glutamine transport in perisynaptic astrocytes in situ is regulated by intracellular sodium. Sodium 100-106 solute carrier family 38, member 3 Rattus norvegicus 0-5 28244495-1 2017 OBJECTIVES: Tenapanor is a first-in-class, small-molecule inhibitor of the gastrointestinal sodium/hydrogen exchanger NHE3. Sodium 92-98 solute carrier family 9 member A3 Homo sapiens 118-122 28126464-8 2017 When renorenal reflex is induced, NHE3 exchanger activity appears to be decreased, resulting in decreased sodium and water reabsorption in the contralateral kidney. Sodium 106-112 solute carrier family 9 member A3 Homo sapiens 34-38 27909897-0 2017 NHA2 is expressed in distal nephron and regulated by dietary sodium. Sodium 61-67 solute carrier family 9, subfamily B (NHA2, cation proton antiporter 2), member 2 Mus musculus 0-4 27909897-7 2017 We propose a model in which NHA2 plays a dual role in salt reabsorption or secretion, depending on the coupling ion (sodium or protons). Sodium 117-123 solute carrier family 9, subfamily B (NHA2, cation proton antiporter 2), member 2 Mus musculus 28-32 28094030-1 2017 Glucocorticoid induced leucine zipper protein (GILZ) is an aldosterone-regulated protein that controls sodium transport in cultured kidney epithelial cells. Sodium 103-109 TSC22 domain family, member 3 Mus musculus 0-45 28094030-1 2017 Glucocorticoid induced leucine zipper protein (GILZ) is an aldosterone-regulated protein that controls sodium transport in cultured kidney epithelial cells. Sodium 103-109 TSC22 domain family, member 3 Mus musculus 47-51 28094030-4 2017 Here we provide evidence supporting a role for GILZ in modulating the balance of renal sodium and potassium excretion by regulating the sodium-chloride cotransporter (NCC) activity in the distal nephron. Sodium 87-93 TSC22 domain family, member 3 Mus musculus 47-51 28094030-11 2017 Thus, GILZ promotes potassium secretion by inhibiting NCC and enhancing distal sodium delivery to the epithelial sodium channel. Sodium 79-85 TSC22 domain family, member 3 Mus musculus 6-10 28388946-11 2017 CONCLUSIONS: Taken together the data suggests that the two regulatory proteins, in conjunction with ALS, have overlapping but distinct functions in BCAA synthesis, and also play a role in pathways unrelated to BCAA synthesis such as sodium-ion homeostasis, extending to broader aspects of patterning and development. Sodium 233-239 chlorsulfuron/imidazolinone resistant 1 Arabidopsis thaliana 100-103 27898524-5 2017 Greater uromodulin excretion is associated with markers of volume overload such as fractional excretion of uric acid, sodium and chloride, indicating a possible role in salt and water retention. Sodium 118-124 uromodulin Homo sapiens 8-18 28222136-4 2017 Here we utilize a recently developed parsimonious ionic current model with only two currents-a sodium current that activates rapidly upon depolarization INa and a time-independent inwardly rectifying repolarization current IK-which reproduces many experimentally measured action potential waveforms. Sodium 95-101 internexin neuronal intermediate filament protein alpha Homo sapiens 153-156 27707705-1 2016 The goal of this study was to investigate water and solute transport, with a focus on sodium transport (TNa) and metabolism along individual nephron segments under differing physiological and pathophysiological conditions. Sodium 86-92 C-type lectin domain family 3, member B Rattus norvegicus 104-107 27627464-4 2016 The functional interplay between TRPV1, MCU and NCLX, in controlling the cytosolic and mitochondrial calcium and sodium transients and subsequently the nociceptive excitability, is poorly understood. Sodium 113-119 solute carrier family 8 member B1 Homo sapiens 48-52 27627464-6 2016 We show that the propagation of the TRPV1-induced cytosolic calcium and sodium fluxes into mitochondria is dependent on coordinated activity of NCLX and MCU. Sodium 72-78 solute carrier family 8 member B1 Homo sapiens 144-148 27421685-10 2016 ClC-K2-/- mice showed an increased renal sodium excretion and compromised salt conservation during a salt-restricted diet. Sodium 41-47 chloride channel, voltage-sensitive Kb Mus musculus 0-6 27440715-9 2016 Pretreatment with the cystathionine-gamma-lyase inhibitor d/l-propargylglycine (PAG) decreased hypoxic inhibition of sodium transport by H441 monolayers, whereas inhibition of cystathionine-beta-synthase (with aminooxy-acetic acid; AOAA) or 3-mercaptopyruvate sulfurtransferase (with aspartate) had no effect. Sodium 117-123 cystathionine gamma-lyase Homo sapiens 22-47 27496104-9 2016 Our results demonstrate a novel NaV1.6 mutation in TN, and show that this mutation potentiates transient and resurgent sodium currents and leads to increased excitability in TRG neurons. Sodium 119-125 sodium voltage-gated channel alpha subunit 8 Homo sapiens 32-38 27102282-1 2016 BACKGROUND: The natriuretic effect of uroguanylin (UGN) involves reduction of proximal tubule (PT) sodium reabsorption. Sodium 99-105 guanylate cyclase activator 2B Sus scrofa 38-49 27102282-1 2016 BACKGROUND: The natriuretic effect of uroguanylin (UGN) involves reduction of proximal tubule (PT) sodium reabsorption. Sodium 99-105 guanylate cyclase activator 2B Sus scrofa 51-54 27102282-8 2016 CONCLUSIONS: These results suggest that the molecular mechanism of action of UGN on sodium reabsorption in PT cells is more complex than previously thought. Sodium 84-90 guanylate cyclase activator 2B Sus scrofa 77-80 27102282-10 2016 GENERAL SIGNIFICANCE: The current results expand our understanding of the signal transduction pathways involved in the overall effect of UGN on renal sodium excretion. Sodium 150-156 guanylate cyclase activator 2B Sus scrofa 137-140 27197160-5 2016 The most robust and frequent inductions were of the sodium-driven bicarbonate transporters SLC4A4 and SLC4A9, which rely upon both HIF1alpha and HIF2alpha activity for their expression. Sodium 52-58 solute carrier family 4 member 9 Homo sapiens 102-108 27219044-6 2016 FGF-23 also inhibits angiotensin-converting enzyme 2 expression and increases sodium reabsorption in the kidney, leading to hypertension and left ventricular hypertrophy. Sodium 78-84 fibroblast growth factor 23 Homo sapiens 0-6 27595821-1 2016 Mice with a knockout of the sodium-calcium exchanger 2 (NCX2) gene were statistically significantly more successful than wild-type controls in the solution of two cognitive tasks, the test for the capacity to extrapolate the direction of the stimulus movement and the "puzzle-box" test for the capacity to find a hidden route to safe environment, which were based on food and aversive motivations, respectively. Sodium 28-34 solute carrier family 8 (sodium/calcium exchanger), member 2 Mus musculus 56-60 27141060-10 2016 These studies provide a mechanistic link by which IL-17A modulates renal sodium transport and suggest that IL-17A inhibition may improve renal function in hypertension and other autoimmune disorders. Sodium 73-79 interleukin 17A Mus musculus 50-56 27445847-5 2016 Oxidative modulation, in particular site specific carbonylation of the Na/K-ATPase alpha1 subunit, is a critical step in proximal tubular Na/K-ATPase signaling and decreased transcellular sodium transport leading to increases in urinary sodium excretion. Sodium 188-194 ATPase Na+/K+ transporting subunit alpha 1 Homo sapiens 71-97 27445847-5 2016 Oxidative modulation, in particular site specific carbonylation of the Na/K-ATPase alpha1 subunit, is a critical step in proximal tubular Na/K-ATPase signaling and decreased transcellular sodium transport leading to increases in urinary sodium excretion. Sodium 237-243 ATPase Na+/K+ transporting subunit alpha 1 Homo sapiens 71-97 26864938-3 2016 FGF23 is purported to have direct (off-target) effects in the myocardium, as well as canonical effects on FGF receptor/alpha-klotho receptor complexes in the kidney to activate the renin-angiotensin-aldosterone system, modulate soluble alpha-klotho levels, and increase sodium retention, to cause left ventricular hypertrophy (LVH). Sodium 270-276 fibroblast growth factor 23 Homo sapiens 0-5 26928804-3 2016 Castration of Cyp1b1(+/+) mice or Cyp1b1(-/-) gene disruption minimized the angiotensin II-induced increase in water consumption, urine output, proteinuria, and sodium excretion and decreases in urine osmolality. Sodium 161-167 cytochrome P450, family 1, subfamily b, polypeptide 1 Mus musculus 14-20 26928804-3 2016 Castration of Cyp1b1(+/+) mice or Cyp1b1(-/-) gene disruption minimized the angiotensin II-induced increase in water consumption, urine output, proteinuria, and sodium excretion and decreases in urine osmolality. Sodium 161-167 cytochrome P450, family 1, subfamily b, polypeptide 1 Mus musculus 34-40 26850381-5 2016 A realistic model for the mechanism of the exchanger"s allosteric regulation should not only address this property, but also it should explain the distinctive behavior of Drosophila melanogaster"s sodium/calcium exchanger, CALX, for which Ca(2+) -binding to CBD1 inhibits Ca(2+) exchange. Sodium 197-203 Na/Ca-exchange protein Drosophila melanogaster 223-227 27053360-0 2016 Sodium Intake Regulates Glucose Homeostasis through the PPARdelta/Adiponectin-Mediated SGLT2 Pathway. Sodium 0-6 solute carrier family 5 (sodium/glucose cotransporter), member 2 Mus musculus 87-92 27053360-5 2016 PPARdelta activation in perirenal fat by agonist or high sodium intake inhibited renal sodium-glucose cotransporter 2 (SGLT2) function, which is mediated by increased production of adipose adiponectin. Sodium 57-63 solute carrier family 5 (sodium/glucose cotransporter), member 2 Mus musculus 87-117 27053360-5 2016 PPARdelta activation in perirenal fat by agonist or high sodium intake inhibited renal sodium-glucose cotransporter 2 (SGLT2) function, which is mediated by increased production of adipose adiponectin. Sodium 57-63 solute carrier family 5 (sodium/glucose cotransporter), member 2 Mus musculus 119-124 27053360-8 2016 Our findings provide insights into the distinctive role of the PPARdelta/adiponectin/SGLT2 pathway in the regulation of sodium and glucose homeostasis. Sodium 120-126 solute carrier family 5 (sodium/glucose cotransporter), member 2 Mus musculus 85-90 27063795-3 2016 Using RNA sequencing, here we identify novel splicing alterations in DM heart samples, including a switch from adult exon 6B towards fetal exon 6A in the cardiac sodium channel, SCN5A. Sodium 162-168 sodium channel, voltage-gated, type V, alpha Mus musculus 178-183 26598320-1 2016 BACKGROUND: Several mammalian species display distinct biophysical properties between atrial and ventricular voltage-gated sodium current (INa); however, the potential mechanism behind this phenomenon is unknown. Sodium 123-129 internexin neuronal intermediate filament protein alpha Homo sapiens 139-142 26376860-5 2016 Using a syndrome of inappropriate secretion of antidiuretic hormone rat model, we show here that sustained reduction of serum sodium ion concentration induced gait disturbances; facilitated the extinction of a contextual fear memory; caused cognitive impairment in a novel object recognition test; and impaired long-term potentiation at hippocampal CA3-CA1 synapses. Sodium 126-132 carbonic anhydrase 3 Rattus norvegicus 349-356 31565540-6 2016 Maturation of the intestine was assessed by measuring luminal bile acids, jejunal sucrase, serum corticosterone, and mRNA expression of ileal Apical Sodium-Dependent Bile Acid Transporter (ASBT). Sodium 149-155 solute carrier family 10 member 2 Rattus norvegicus 189-193 26798387-4 2016 Wild-type and single nucleotide polymorphisms were expressed in human embryonic kidney cells, and the peak sodium current (INa ) was analyzed using the whole-cell patch-clamp technique. Sodium 107-113 internexin neuronal intermediate filament protein alpha Homo sapiens 123-126 27635187-3 2016 Our data showed that high sodium treatment significantly increased alpha-, beta-, and gamma-ENaC expression levels in HUVECs. Sodium 26-32 sodium channel epithelial 1 subunit gamma Homo sapiens 86-96 27635280-1 2016 Considering the key role of renal dopamine in tubular sodium handling, we hypothesized that c-type natriuretic peptide (CNP) and Ang-(1-7) may regulate renal dopamine availability in tubular cells, contributing to Na(+), K(+)-ATPase inhibition. Sodium 54-60 natriuretic peptide C Homo sapiens 92-118 27635280-1 2016 Considering the key role of renal dopamine in tubular sodium handling, we hypothesized that c-type natriuretic peptide (CNP) and Ang-(1-7) may regulate renal dopamine availability in tubular cells, contributing to Na(+), K(+)-ATPase inhibition. Sodium 54-60 natriuretic peptide C Homo sapiens 120-123 25319728-6 2015 DAI monosulfates were transported by the carriers NTCP and SOAT in a sodium-dependent manner, while OAT4-HEK293 cells revealed a partly sodium-dependent transport for these compounds. Sodium 69-75 solute carrier family 10 member 6 Homo sapiens 59-63 26523501-4 2015 In a mouse model of dextran-sulfate-sodium-induced typhlitis and colitis, development of intestinal pathology was associated with increases in neutrophils and CD11b(+) myeloid cells and a decrease in CD45R(+) B cells, similar to those observed in old Terc(-/-) mice. Sodium 36-42 integrin subunit alpha M Homo sapiens 159-164 26523501-4 2015 In a mouse model of dextran-sulfate-sodium-induced typhlitis and colitis, development of intestinal pathology was associated with increases in neutrophils and CD11b(+) myeloid cells and a decrease in CD45R(+) B cells, similar to those observed in old Terc(-/-) mice. Sodium 36-42 protein tyrosine phosphatase receptor type C Homo sapiens 200-205 26361848-2 2015 This channel predominates the cardiac sodium current, INa, which underlies the fast upstroke of the cardiac action potential. Sodium 38-44 internexin neuronal intermediate filament protein alpha Homo sapiens 54-57 26358773-0 2015 Reduced sodium/proton exchanger NHE3 activity causes congenital sodium diarrhea. Sodium 8-14 solute carrier family 9 member A3 Homo sapiens 32-36 26200947-10 2015 In vitro studies in AKI-primed CD4(+) T cells indicated that angiotensin II and extracellular sodium enhanced, and losartan inhibited, IL-17 expression. Sodium 94-100 Cd4 molecule Rattus norvegicus 31-34 26197202-6 2015 Pharmacologic inhibition of apically expressed gut NHE3 offers the potential of reducing sodium absorption and fluid overload independent of kidney function and with better safety than systemic drugs. Sodium 89-95 solute carrier family 9 member A3 Homo sapiens 51-55 26197202-7 2015 Two small-molecule inhibitors of NHE3 (tenapanor and SAR218034) with minimal systemic exposure reduce urinary sodium and increase stool sodium in a dose-dependent manner in rodents, with similar results observed with tenapanor in humans. Sodium 110-116 solute carrier family 9 member A3 Homo sapiens 33-37 26197202-7 2015 Two small-molecule inhibitors of NHE3 (tenapanor and SAR218034) with minimal systemic exposure reduce urinary sodium and increase stool sodium in a dose-dependent manner in rodents, with similar results observed with tenapanor in humans. Sodium 136-142 solute carrier family 9 member A3 Homo sapiens 33-37 26197202-10 2015 SUMMARY: Pharmacologic inhibition of gut NHE3 may be a viable strategy for managing sodium load in patients with CKD or with sodium-sensitive hypertension in general. Sodium 84-90 solute carrier family 9 member A3 Homo sapiens 41-45 26197202-10 2015 SUMMARY: Pharmacologic inhibition of gut NHE3 may be a viable strategy for managing sodium load in patients with CKD or with sodium-sensitive hypertension in general. Sodium 125-131 solute carrier family 9 member A3 Homo sapiens 41-45 26041446-1 2015 Two-thirds of sodium filtered by the renal glomerulus is reabsorbed from the proximal tubule via a sodium/proton exchanger isoform 3 (NHE3)-dependent mechanism. Sodium 14-20 solute carrier family 9 member A3 Homo sapiens 134-138 26041446-2 2015 Since sodium and bicarbonate reabsorption are coupled, we postulated that the molecules involved in their reabsorption [NHE3 and carbonic anhydrase II (CAII)] might physically and functionally interact. Sodium 6-12 solute carrier family 9 member A3 Homo sapiens 120-124 26041446-2 2015 Since sodium and bicarbonate reabsorption are coupled, we postulated that the molecules involved in their reabsorption [NHE3 and carbonic anhydrase II (CAII)] might physically and functionally interact. Sodium 6-12 carbonic anhydrase 2 Homo sapiens 129-150 26041446-2 2015 Since sodium and bicarbonate reabsorption are coupled, we postulated that the molecules involved in their reabsorption [NHE3 and carbonic anhydrase II (CAII)] might physically and functionally interact. Sodium 6-12 carbonic anhydrase 2 Homo sapiens 152-156 26115271-4 2015 Changes on dEB were obtained by changing the levels of sodium and chloride with calcium chloride, calcium carbonate, and sodium bicarbonate. Sodium 55-61 DebC Drosophila melanogaster 11-14 25168165-1 2015 BACKGROUND: To characterize regional kidney sodium response by MRI following NKCC2 inhibition. Sodium 44-50 solute carrier family 12 member 1 Rattus norvegicus 77-82 25168165-9 2015 CONCLUSION: The pharmacological effects in terms of regional kidney sodium signal changes induced by NKCC2 inhibition are region-specific and highly predictable. Sodium 68-74 solute carrier family 12 member 1 Rattus norvegicus 101-106 25614660-6 2015 Long-term salt exposure resulted in the highest sodium and the lowest potassium concentration in the shoots of npr1-5 mutant in comparison with the wild type and nudt7 mutant. Sodium 48-54 regulatory protein (NPR1) Arabidopsis thaliana 111-117 25734516-2 2015 Although both populations express similar endogenous conductances, we have discovered that AVPV/PeN Kiss1 neurons express a subthreshold, persistent sodium current (INaP) that dramatically alters their firing activity. Sodium 149-155 KiSS-1 metastasis-suppressor Mus musculus 100-105 25011570-1 2015 The objective of this study was to investigate the contributions of a sodium-dependent concentrative nucleoside transporter (CNT) 1 and an equilibrative nucleoside transporter (ENT) 1 to ribavirin uptake in human hepatocytes. Sodium 70-76 solute carrier family 28 member 1 Homo sapiens 101-131 25011570-1 2015 The objective of this study was to investigate the contributions of a sodium-dependent concentrative nucleoside transporter (CNT) 1 and an equilibrative nucleoside transporter (ENT) 1 to ribavirin uptake in human hepatocytes. Sodium 70-76 solute carrier family 28 member 1 Homo sapiens 101-124 26138081-5 2015 Sixty patients (38 +- 15 ml/min of GFR) presented 4.14 +- 1.71 g/24 h of urinary sodium excretion. Sodium 81-87 Rap guanine nucleotide exchange factor 5 Homo sapiens 35-38 26612332-1 2015 Tubular transport of sodium (TNa+) and chloride (TCl-) is decreased in patients with chronic kidney disease. Sodium 21-27 ras homolog family member J Homo sapiens 49-52 24380493-6 2015 Sodium current was detected in a small number of cells overexpressing BMP9, not in the BMP13-transfected cells or the control cells. Sodium 0-6 growth differentiation factor 2 Mus musculus 70-74 25613158-8 2015 RESULTS: Liver fibrosis, portal hypertension and sodium retention that were developed by CCl4, were all significantly alleviated by MSCs transplantation, which decreased TGFbeta1 levels and increased BMP7 levels in the injured liver. Sodium 49-55 chemokine (C-C motif) ligand 4 Mus musculus 89-93 25354179-1 2015 The cardiac late sodium current (INa,L) has been in the focus of research in the recent decade. Sodium 17-23 internexin neuronal intermediate filament protein alpha Homo sapiens 33-36 26065434-4 2015 NHE3 participates in the uptake of sodium ions and water from the intestinal lumen. Sodium 35-41 solute carrier family 9 member A3 Homo sapiens 0-4 25218934-0 2014 Functional asymmetry of bidirectional Ca2+-movements in an archaeal sodium-calcium exchanger (NCX_Mj). Sodium 68-74 T cell leukemia homeobox 2 Homo sapiens 94-97 25102326-0 2014 Persistent sodium currents contribute to Abeta1-42-induced hyperexcitation of hippocampal CA1 pyramidal neurons. Sodium 11-17 carbonic anhydrase 1 Homo sapiens 90-93 25063810-0 2014 The second sodium site in the dopamine transporter controls cation permeation and is regulated by chloride. Sodium 11-17 solute carrier family 6 (neurotransmitter transporter), member 3 S homeolog Xenopus laevis 30-50 28834665-1 2014 Large and growing body of data suggest that an increased late sodium current (INa,late ) can have a significant pathophysiological role in heart failure and other heart diseases. Sodium 62-68 internexin neuronal intermediate filament protein alpha Homo sapiens 78-81 24704193-3 2014 In response to 2.0M NaCl injections, mice had increased plasma sodium concentrations which were associated with a blunted rise in CORT subsequent to restraint challenge relative to 0.15M NaCl injected controls. Sodium 63-69 cortistatin Mus musculus 130-134 24911152-6 2014 Computational simulations and uptake experiments suggested that the disrupted function of the DAT-Asp421Asn mutant is the result of compromised sodium binding, in agreement with Asp421 coordinating sodium at the second sodium site. Sodium 144-150 solute carrier family 6 member 3 Homo sapiens 94-97 24911152-6 2014 Computational simulations and uptake experiments suggested that the disrupted function of the DAT-Asp421Asn mutant is the result of compromised sodium binding, in agreement with Asp421 coordinating sodium at the second sodium site. Sodium 198-204 solute carrier family 6 member 3 Homo sapiens 94-97 24911152-6 2014 Computational simulations and uptake experiments suggested that the disrupted function of the DAT-Asp421Asn mutant is the result of compromised sodium binding, in agreement with Asp421 coordinating sodium at the second sodium site. Sodium 198-204 solute carrier family 6 member 3 Homo sapiens 94-97 24753048-9 2014 Extracellular sodium (Na(+) e) replacement was used to evaluate sodium gradient requirements for DAT transport functions. Sodium 64-70 solute carrier family 6 member 3 Homo sapiens 97-100 24823874-4 2014 The d-C exhibits about three times volume expansion of the c-C after full sodiation or potassiation, thus suggesting a much higher storage capacity of Na or K ions in d-C than c-C. For the bilayer CNF-based electrode, a steady sodium capacity of 245 mAh/g is measured with a Coulombic efficiency approaching 98% after a few initial cycles. Sodium 227-233 NPHS1 adhesion molecule, nephrin Homo sapiens 197-200 24598462-0 2014 5-HT neurons of the area postrema become c-Fos-activated after increases in plasma sodium levels and transmit interoceptive information to the nucleus accumbens. Sodium 83-89 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 41-46 24598462-2 2014 Tryptophan hydroxylase (Tryp-OH, synthetic enzyme-producing 5-HT) immunoreactive neurons in the AP of rats become c-Fos-activated following conditions in which plasma sodium levels are elevated; these include intraperitoneal injections of hypertonic saline and sodium repletion. Sodium 167-173 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 114-119 24598462-2 2014 Tryptophan hydroxylase (Tryp-OH, synthetic enzyme-producing 5-HT) immunoreactive neurons in the AP of rats become c-Fos-activated following conditions in which plasma sodium levels are elevated; these include intraperitoneal injections of hypertonic saline and sodium repletion. Sodium 261-267 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 114-119 24549959-13 2014 Thus, the hyperexcitability of MRGPRA3+ and MRGPRD+ neurons, brought about in part by enhanced sodium currents, may contribute to the spontaneous itch- and pain-related behaviours accompanying contact hypersensitivity and/or other inflammatory diseases in humans. Sodium 95-101 MAS-related GPR, member A3 Mus musculus 31-38 24549959-13 2014 Thus, the hyperexcitability of MRGPRA3+ and MRGPRD+ neurons, brought about in part by enhanced sodium currents, may contribute to the spontaneous itch- and pain-related behaviours accompanying contact hypersensitivity and/or other inflammatory diseases in humans. Sodium 95-101 MAS related GPR family member D Homo sapiens 44-50 24623760-5 2014 We also show that CREB3L1 mRNA levels correlate with AVP transcription level in SONs and PVNs following sodium depletion, and as a consequence of diurnal rhythm in the suprachiasmatic nucleus. Sodium 104-110 cAMP responsive element binding protein 3-like 1 Rattus norvegicus 18-25 24381176-7 2014 In rats with chronic low or high sodium intakes, the low-sodium diet was associated with significantly higher plasma aldosterone, MR mRNA and protein expression, and c-Fos immunoreactivity within labeled preautonomic neurons. Sodium 57-63 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 166-171 24337990-9 2014 Denuder-fitted PM1 sampler can serve as a useful sampling tool in estimating the true values for nitrate, ammonium, potassium, sodium and WSOC present in the ambient PM. Sodium 127-133 transmembrane protein 11 Homo sapiens 15-18 24489810-2 2014 OBJECTIVE: We sought to determine whether sodium current (INa) reduction in the structurally normal heart unmasks a regionally heterogeneous substrate for the induction of sustained arrhythmia by premature ventricular contractions (PVCs). Sodium 42-48 LOW QUALITY PROTEIN: alpha-internexin Oryctolagus cuniculus 58-61 24190904-1 2014 BACKGROUND: In response to high salt intake, transcription factor hypoxia-inducible factor (HIF) 1alpha activates many antihypertensive genes, such as heme oxygenase 1 (HO-1) 1 and cyclooxygenase 2 (COX-2) in the renal medulla, which is an important molecular adaptation to promote extra sodium excretion. Sodium 288-294 hypoxia inducible factor 1 subunit alpha Rattus norvegicus 66-103 24583915-3 2014 Two explanations exist for this dip: (1) electrotonic interaction between regions of depolarization and hyperpolarization; and (2) the sodium-calcium exchange (NCX) current. Sodium 135-141 T cell leukemia homeobox 2 Homo sapiens 160-163 24219001-6 2014 In this review, we will focus on the effect of the newly appreciated cardiotonic steroids (CTS)-Na/K-ATPase signaling on RPT-mediated sodium handling by coordinated regulation of the Na/K-ATPase and sodium/proton exchanger isoform 3 (NHE3). Sodium 134-140 solute carrier family 9 member A3 Homo sapiens 234-238 24247822-3 2014 SIRT1 may also participate in the regulation of blood pressure by sodium handling and by decreasing the responsiveness for angiotensin II. Sodium 66-72 sirtuin 1 Homo sapiens 0-5 24248457-5 2014 Somatic mutations of the selectivity filter of the Kir3.4 channel in APA results in loss of selectivity for K(+) and entry of sodium, resulting in membrane depolarization, calcium mobilization, increased CYP11B2 expression, and hyperaldosteronism. Sodium 126-132 potassium inwardly rectifying channel subfamily J member 5 Homo sapiens 51-57 23570675-2 2013 They are reported to be supportive in preventing arteriosclerosis and diabetes and a previous study could demonstrate an inhibitory potential on sodium-dependent glucose transport (SGLT1) in oocytes und mouse intestinal everted rings (Schulze et al., 2012, Genes Nutr. Sodium 145-151 solute carrier family 5 (sodium/glucose cotransporter), member 1 Mus musculus 181-186 23665214-4 2013 CNTF induces a decrease in the sodium current and an increase in resting potential as in sodium inversion potential. Sodium 31-37 ciliary neurotrophic factor Homo sapiens 0-4 23641004-5 2013 The bound anion and the nearby sodium ion in the Na1 site organize a connection between their coordinating residues and the extracellular gate of LeuT through a continuous H-bond network. Sodium 31-37 Leucine transport, high Homo sapiens 146-150 23362203-0 2013 Mechanistic aspects of sodium-binding sites in LeuT-like fold symporters. Sodium 23-29 Leucine transport, high Homo sapiens 47-51 23362203-6 2013 Here, we review the structural, functional, and biophysical validation of sodium-binding sites in four different LeuT-like fold transporters. Sodium 74-80 Leucine transport, high Homo sapiens 113-117 32497506-4 2020 (2020) report that the epithelial sodium channel ENaC, which serves as the salty receptor, is co-expressed with the voltage-activated ATP release channel CALHM1/3 in a subset of taste cells and that these cells mediate amiloride-sensitive salty taste. Sodium 34-40 calcium homeostasis modulator 1 Homo sapiens 154-162 31797525-11 2020 The expression of Ki67 and c-Myc protein was increased in tissues treated with 50 muM NaF and the expression of Fibronectin and Vimentin in the 50 muM NaF treated tissues was stimulated. Sodium 86-89 MYC proto-oncogene, bHLH transcription factor Rattus norvegicus 27-32 31797525-11 2020 The expression of Ki67 and c-Myc protein was increased in tissues treated with 50 muM NaF and the expression of Fibronectin and Vimentin in the 50 muM NaF treated tissues was stimulated. Sodium 86-89 vimentin Rattus norvegicus 128-136 31797525-11 2020 The expression of Ki67 and c-Myc protein was increased in tissues treated with 50 muM NaF and the expression of Fibronectin and Vimentin in the 50 muM NaF treated tissues was stimulated. Sodium 151-154 MYC proto-oncogene, bHLH transcription factor Rattus norvegicus 27-32 31797525-11 2020 The expression of Ki67 and c-Myc protein was increased in tissues treated with 50 muM NaF and the expression of Fibronectin and Vimentin in the 50 muM NaF treated tissues was stimulated. Sodium 151-154 vimentin Rattus norvegicus 128-136 32112796-8 2020 Intestinal tissues and derived enteroids from MYO5B(P663L) piglets had reduced apical levels and diffuse sub-apical levels of NHE3 and SGLT1, which regulate transport of sodium, glucose, and water, compared with tissues from control piglets. Sodium 170-176 myosin VB Homo sapiens 46-51 32325152-7 2020 For instance, we show that the sodium channel Scn7a and the cation channel Trpm7 are expressed in fibroblasts but not in cardiomyocytes, which underscores the importance of investigating the endogenous cell host prior to functional studies. Sodium 31-37 sodium voltage-gated channel alpha subunit 7 Rattus norvegicus 46-51 32462850-10 2020 CONCLUSION: The sodium sensitive dye ANG-2 is a sensitive and useful probe for determination changes in Na+ content and concentration both in single cells and subcellular microparticles. Sodium 16-22 angiopoietin 2 Homo sapiens 37-42 32565909-11 2020 In addition, the expression of sodium channel protein type 5 subunit alpha (SCN5A) and beta-2 adrenergic receptor (ADRB2) was downregulated, while muscarinic acetylcholine receptor M2 (CHRM2) was upregulated in the WXKL group (P < 0.05). Sodium 31-37 sodium voltage-gated channel alpha subunit 5 Sus scrofa 76-81 32443836-3 2020 Recently, the PKP2 p.S183N mutation was found in a patient affected by Brugada syndrome (BS), an inherited arrhythmic channelopathy most commonly caused by sodium channel gene mutations. Sodium 156-162 plakophilin 2 Homo sapiens 14-18 32431610-5 2020 Recent cryo-electron microscopy structures of human KCNQ1 and hERG, along with the rat homolog of SCN5A and other mammalian sodium channels, provide atomic-level insight into the structure and function of these proteins that advance our understanding of their distinct functions in the cardiac action potential, as well as the molecular basis of LQTS. Sodium 124-130 sodium voltage-gated channel alpha subunit 5 Rattus norvegicus 98-103 32259613-7 2020 The Low-sodium, High-fiber, DASH, Low-fat, Low-protein and Vegan dietary approach were significantly more effective in reducing SBP compared to a control diet. Sodium 8-14 selenium binding protein 1 Homo sapiens 128-131 32259613-9 2020 The Low-sodium and High fiber diets had the greatest lowering effect on SBP and DBP in T2D patients. Sodium 8-14 selenium binding protein 1 Homo sapiens 72-75 32259613-11 2020 The High-fiber and Low-sodium diets had the greatest lowering effect on SBP and DBP in T2D. Sodium 23-29 selenium binding protein 1 Homo sapiens 72-75 31904424-0 2020 Distinct Calcium/CAlmodulin-dependent Serine protein Kinase domains control cardiac sodium channel membrane expression and focal adhesion anchoring. Sodium 84-90 calcium/calmodulin dependent serine protein kinase Homo sapiens 9-59 31904424-2 2020 In the heart, the protein CASK (Calcium/CAlmodulin-dependent Serine protein Kinase) negatively regulates the main cardiac sodium channel, NaV1.5, which carries the sodium current (INa) by preventing its anterograde trafficking. Sodium 122-128 calcium/calmodulin dependent serine protein kinase Homo sapiens 26-30 31904424-2 2020 In the heart, the protein CASK (Calcium/CAlmodulin-dependent Serine protein Kinase) negatively regulates the main cardiac sodium channel, NaV1.5, which carries the sodium current (INa) by preventing its anterograde trafficking. Sodium 122-128 calcium/calmodulin dependent serine protein kinase Homo sapiens 32-82 32161114-0 2020 S-Palmitoylation of the sodium channel Nav1.6 regulates its activity and neuronal excitability. Sodium 24-30 neuron navigator 1 Homo sapiens 39-43 31420581-8 2020 QR showed that the consumption of sodium was positively associated with SBP (P10) and DBP (P10) in males, and positively associated with DBP (P80-P90) alone in females. Sodium 34-40 coilin Homo sapiens 142-145 32130622-1 2020 Mammalian Na+/H+ exchanger type I isoform (NHE1) is a ubiquitously expressed membrane protein that regulates intracellular pH (pHi) by removing one intracellular proton in exchange for one extracellular sodium ion. Sodium 203-209 glucose-6-phosphate isomerase Homo sapiens 127-130 32032636-12 2020 We also found that NaHS enhanced the Warburg effect and upregulated leptin expression in the substantia nigra of 6-OHDA-exposed rats. Sodium 19-23 leptin Rattus norvegicus 68-74 32494638-1 2020 The sodium leak channel (NALCN) is essential for survival in mammals: NALCN mutations are life-threatening in humans and knockout is lethal in mice. Sodium 4-10 sodium leak channel, non-selective Homo sapiens 25-30 32494638-1 2020 The sodium leak channel (NALCN) is essential for survival in mammals: NALCN mutations are life-threatening in humans and knockout is lethal in mice. Sodium 4-10 sodium leak channel, non-selective Homo sapiens 70-75 32129084-0 2020 Adenosine A2B receptor activation stimulates alveolar fluid clearance through alveolar epithelial sodium channel via cAMP pathway in endotoxin-induced lung injury. Sodium 98-104 adenosine A2B receptor Rattus norvegicus 0-22 31758704-8 2020 KEY RESULTS: compared with WT mice, SKI mice had higher BP, lower urine volume and sodium excretion, upregulated endoplasmic reticulum (ER) stress markers and soluble epoxide hydrolase (sEH), and downregulated dopamine D1 receptor (D1R) in renal cortex and cells from renal proximal tubule (RPT). Sodium 83-89 ski sarcoma viral oncogene homolog (avian) Mus musculus 36-39 31911180-3 2020 Exposure of pancreatic tumor cells to [neratinib + sodium valproate] initially reduced the expression and phosphorylation of ERBB family receptors, c-MET and c-KIT. Sodium 51-57 erb-b2 receptor tyrosine kinase 3 Homo sapiens 125-129 32092287-12 2020 The differential protein localisation of Cldn2 in the RPE during the day-night cycle suggest that Cldn2 may facilitate paracellular water and sodium transport during the day. Sodium 142-148 claudin 2 Mus musculus 41-46 32092287-12 2020 The differential protein localisation of Cldn2 in the RPE during the day-night cycle suggest that Cldn2 may facilitate paracellular water and sodium transport during the day. Sodium 142-148 claudin 2 Mus musculus 98-103 31605437-0 2020 Mutations in the Scn8a DIIS4 voltage sensor reveal new distinctions among hypomorphic and null Nav 1.6 sodium channels. Sodium 103-109 sodium channel, voltage-gated, type VIII, alpha Mus musculus 17-22 31605437-0 2020 Mutations in the Scn8a DIIS4 voltage sensor reveal new distinctions among hypomorphic and null Nav 1.6 sodium channels. Sodium 103-109 neuron navigator 1 Mus musculus 95-100 31771816-7 2020 Moreover, NaHS inhibited CS-induced phosphorylation of ERK, JNK and p38 MAPK in vivo and in vitro, and treatment with their inhibitors reversed CSE-induced ZO-1 expression and inflammation in A549 cells. Sodium 10-14 mitogen-activated protein kinase 14 Mus musculus 68-76 32273850-6 2020 Rather, the enhanced CAP in Trpv1-/- optic nerve was associated with increased expression of the voltage-gated sodium channel subunit 1.6 (NaV1.6) in longer nodes of Ranvier within RGC axons, rendering Trpv1-/- optic nerve relatively insensitive to NaV1.6 antagonism via 4,9-anhydrotetrodotoxin. Sodium 111-117 transient receptor potential cation channel subfamily V member 1 Homo sapiens 28-33 32273850-6 2020 Rather, the enhanced CAP in Trpv1-/- optic nerve was associated with increased expression of the voltage-gated sodium channel subunit 1.6 (NaV1.6) in longer nodes of Ranvier within RGC axons, rendering Trpv1-/- optic nerve relatively insensitive to NaV1.6 antagonism via 4,9-anhydrotetrodotoxin. Sodium 111-117 neuron navigator 1 Homo sapiens 139-143 32059758-6 2020 We show a polymorph-dependent differential synaptic redistribution of alpha3-Na+/K+-ATPase, GluA2 subunit containing alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors, and GluN2B-subunit containing N-methyl-D-aspartate receptors, but not GluA1 subunit containing alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid and metabotropic glutamate receptor 5 receptors. Sodium 70-79 glutamate receptor, ionotropic, AMPA1 (alpha 1) Mus musculus 255-260 32256445-1 2020 The hypoglycaemic target of empagliflozin (EMP), as a novel inhibitor of sodium-glucose cotransporter (SGLT2), is clear. Sodium 73-79 solute carrier family 5 member 2 Rattus norvegicus 103-108 31984791-2 2020 NHERF1 is involved in the regulation of the sodium hydrogen exchanger 3 (NHE3), the sodium dependent phosphate transporter 2a (Npt2a), and the sodium potassium ATPase through its ability to scaffold these transporters to the plasma membrane, allowing regulation of these protein complexes with their associated hormone receptors. Sodium 44-50 SLC9A3 regulator 1 Homo sapiens 0-6 31943325-1 2020 OBJECTIVE: SCN8A encephalopathy is a developmental and epileptic encephalopathy (DEE) caused by de novo gain-of-function mutations of sodium channel Nav 1.6 that result in neuronal hyperactivity. Sodium 134-140 sodium channel, voltage-gated, type VIII, alpha Mus musculus 11-16 32292933-10 2020 Meanwhile, sodium-dependent neutral amino acids transporter type 2 (ASCT2) and beta-casein were up-regulated by VAL (173% in ASCT2, 238% in and 218% in beta-casein) (p < 0.05). Sodium 11-17 solute carrier family 1 member 5 Bos taurus 68-73 32292933-10 2020 Meanwhile, sodium-dependent neutral amino acids transporter type 2 (ASCT2) and beta-casein were up-regulated by VAL (173% in ASCT2, 238% in and 218% in beta-casein) (p < 0.05). Sodium 11-17 solute carrier family 1 member 5 Bos taurus 125-130 31735414-3 2020 Benefiting from the structural advantages and multimetallic compositions, the as-prepared PtCoRu NAs displayed remarkably enhanced electrocatalytic performance for the HER in 1.0 M KOH, with a low overpotential (eta, 22 mV) to drive 10 mA cm-2, small Tafel slope (46 mV dec-1), and high exchange current density (j0, 3.30 mA cm-2) during the long-term electrolysis. Sodium 97-100 endothelin receptor type A Homo sapiens 52-55 31735414-3 2020 Benefiting from the structural advantages and multimetallic compositions, the as-prepared PtCoRu NAs displayed remarkably enhanced electrocatalytic performance for the HER in 1.0 M KOH, with a low overpotential (eta, 22 mV) to drive 10 mA cm-2, small Tafel slope (46 mV dec-1), and high exchange current density (j0, 3.30 mA cm-2) during the long-term electrolysis. Sodium 97-100 deleted in esophageal cancer 1 Homo sapiens 270-275 31902005-0 2020 Molecular characterization and distribution of the voltage-gated sodium channel, Para, in the brain of the grasshopper and vinegar fly. Sodium 65-71 paralytic Drosophila melanogaster 81-85 31902005-1 2020 Voltage-gated sodium (NaV) channels, encoded by the gene para, play a critical role in the rapid processing and propagation of visual information related to collision avoidance behaviors. Sodium 14-20 paralytic Drosophila melanogaster 57-61 31902005-1 2020 Voltage-gated sodium (NaV) channels, encoded by the gene para, play a critical role in the rapid processing and propagation of visual information related to collision avoidance behaviors. Sodium 22-25 paralytic Drosophila melanogaster 57-61 31755124-2 2020 Common variants in the sodium channel gene, SCN1A, are associated with febrile seizures and rare pathogenic variants in SCN1A cause the severe developmental and epileptic encephalopathy Dravet Syndrome. Sodium 23-29 sodium voltage-gated channel alpha subunit 1 Homo sapiens 44-49 31755124-2 2020 Common variants in the sodium channel gene, SCN1A, are associated with febrile seizures and rare pathogenic variants in SCN1A cause the severe developmental and epileptic encephalopathy Dravet Syndrome. Sodium 23-29 sodium voltage-gated channel alpha subunit 1 Homo sapiens 120-125 32031527-6 2020 Here, we report a patient with a severe phenotype of Mowat-Wilson syndrome, associated with a novel heterozygous de novo frame-shift variant in the ZEB2 gene, as well as an additional novel heterozygous missense variant in the SCN1A gene, the mutation of which is known to affect NaV1.1-mediated sodium current in GABAergic interneurons. Sodium 296-302 sodium voltage-gated channel alpha subunit 1 Homo sapiens 227-232 31786370-1 2020 Over 1250 mutations in SCN1A, the Nav1.1 voltage-gated sodium channel gene, are associated with seizure disorders including GEFS+. Sodium 55-61 sodium voltage-gated channel alpha subunit 1 Homo sapiens 23-28 31822564-1 2020 Genetic and functional studies have confirmed an important role for the voltage-gated sodium channel Nav1.9 in human pain disorders. Sodium 86-92 sodium voltage-gated channel alpha subunit 11 Homo sapiens 101-107 31979418-8 2020 Exposure of the thyroid to NaI modulates 15 cellular pathways, most of which are also affected by ICM treatment (including the elF4 and P706SK cell signaling pathway and INSR identified as an upstream activator in both treatments). Sodium 27-30 insulin receptor Homo sapiens 170-174 31963573-8 2020 Superoxide dismutase and catalase hindered the effects of NaHS, and this sensitivity was partially dependent on the production of reactive oxygen species (ROS). Sodium 58-62 LOC100174793 Xenopus laevis 25-33 31963411-7 2020 For sodium ion battery, a high capacity (~522 mAh g-1) can be achieved at 5 A g-1 after 200 cycles for SnS2-x microflowers. Sodium 4-10 sodium voltage-gated channel alpha subunit 11 Homo sapiens 103-107 31677787-1 2020 BACKGROUND: Voltage-gated sodium channels Nav1.x mediate the rising phase of action potential in excitable cells. Sodium 26-32 neuron navigator 1 Homo sapiens 42-46 31668811-10 2020 Electrophysiological experiments showed that the AaHIV toxin activates Nav1.6 channel, suggesting that this sodium channel subtype is implicated in the proliferation of DU145 prostate cancer cells. Sodium 108-114 neuron navigator 1 Homo sapiens 71-75 31970162-6 2019 These compounds could reduce the intracellular sodium overload to improve mitochondrial energetics and oxidative defense in the heart through binding with NHE and/or SMIT1. Sodium 47-53 solute carrier family 9 member C1 Homo sapiens 155-158 31970162-6 2019 These compounds could reduce the intracellular sodium overload to improve mitochondrial energetics and oxidative defense in the heart through binding with NHE and/or SMIT1. Sodium 47-53 solute carrier family 5 member 3 Homo sapiens 166-171 31815998-0 2020 Cobalt-doping SnS2 nanosheets towards high-performance anodes for sodium ion batteries. Sodium 66-72 sodium voltage-gated channel alpha subunit 11 Homo sapiens 14-18 31815998-1 2020 Layered SnS2 is considered as a promising anode candidate for sodium-ion batteries yet suffers from low initial coulombic efficiency, limited specific capacity and rate capability. Sodium 62-68 sodium voltage-gated channel alpha subunit 11 Homo sapiens 8-12 31906971-1 2020 BACKGROUND: Genetic disruption of slc4a10, which encodes the sodium-dependent chloride/bicarbonate exchanger Ncbe, leads to a major decrease in Na+-dependent HCO3- import into choroid plexus epithelial cells in mice and to a marked reduction in brain intraventricular fluid volume. Sodium 61-67 solute carrier family 4, sodium bicarbonate cotransporter-like, member 10 Mus musculus 34-41 31678597-3 2020 Since Na+ current (INa) through voltage-dependent Na+ channels (NaV) is a major mechanism for excitability, the present study investigated the pharmacological characteristics and mechanisms of the action of 4TERP on INa through NaV. Sodium 228-231 peroxisomal trans-2-enoyl-CoA reductase Rattus norvegicus 208-212 31678597-8 2020 4TERP also altered voltage sensitivity of the steady state activation of NaV. Sodium 73-76 peroxisomal trans-2-enoyl-CoA reductase Rattus norvegicus 1-5 31815328-4 2020 The Fe2 [(2,3,9,10,16,17,23,24-octahydroxy phthalocyaninato)Cu] MOF composited with I2 (Fe2 -O8 -PcCu/I2 ) serves as a cathode for a Na-I2 battery exhibiting a stable specific capacity of 150 mAh g-1 after 3200 cycles and outperforming the state-of-the-art cathodes for Na-I2 batteries. Sodium 133-138 lysine acetyltransferase 8 Homo sapiens 64-67 31815328-4 2020 The Fe2 [(2,3,9,10,16,17,23,24-octahydroxy phthalocyaninato)Cu] MOF composited with I2 (Fe2 -O8 -PcCu/I2 ) serves as a cathode for a Na-I2 battery exhibiting a stable specific capacity of 150 mAh g-1 after 3200 cycles and outperforming the state-of-the-art cathodes for Na-I2 batteries. Sodium 270-275 lysine acetyltransferase 8 Homo sapiens 64-67 31940611-5 2020 Cox proportional hazards regression model was used to investigate the relationship between baseline serum sodium levels and infection-related mortality. Sodium 106-112 cytochrome c oxidase subunit 8A Homo sapiens 0-3 31835299-14 2019 In addition, endogenous JA acted as a positive regulator for the transportation of sodium ions from the roots to the shoots because the mutant opr7opr8 had a higher level of sodium in the roots but a significantly lower level in the shoots than WT. Sodium 83-89 12-oxophytodienoate reductase7 Zea mays 143-151 31835299-14 2019 In addition, endogenous JA acted as a positive regulator for the transportation of sodium ions from the roots to the shoots because the mutant opr7opr8 had a higher level of sodium in the roots but a significantly lower level in the shoots than WT. Sodium 174-180 12-oxophytodienoate reductase7 Zea mays 143-151 31709768-1 2019 OBJECTIVE: Patients with Early Infantile Epileptic Encephalopathy (EIEE) 52 have inherited, homozygous variants in the gene SCN1B, encoding the voltage-gated sodium channel (VGSC) beta1 and beta1B non-pore-forming subunits. Sodium 158-164 sodium voltage-gated channel beta subunit 1 Homo sapiens 124-129 31709768-8 2019 Biochemical and electrophysiological analyses of the SCN1B variant expressed in heterologous cells showed cell surface expression of the mutant beta1 subunit, similar to wild-type (WT), but with loss of normal beta1-mediated modification of human Nav 1.1-generated sodium current, suggesting that SCN1B-p.Arg85Cys is a loss-of-function (LOF) variant. Sodium 265-271 sodium voltage-gated channel beta subunit 1 Homo sapiens 53-58 31445158-1 2019 Dravet syndrome (DS) is an early onset refractory epilepsy typically caused by de novo heterozygous variants in SCN1A encoding the alpha-subunit of the neuronal sodium channel Nav1.1. Sodium 161-167 sodium voltage-gated channel alpha subunit 1 Homo sapiens 112-117 31852640-12 2019 Compared with those in BCNI group, the rats in BCNI+NaHS group had significantly decreased expressions of caspase-3 and Bax proteins (P < 0.05) with significantly enhanced Bcl-2 protein expression and an increased Bcl-2/Bax ratio (P < 0.05). Sodium 52-56 caspase 3 Rattus norvegicus 106-115 31730442-0 2019 Late sodium current blocker GS967 inhibits persistent currents induced by familial hemiplegic migraine type 3 mutations of the SCN1A gene. Sodium 5-11 sodium voltage-gated channel alpha subunit 1 Homo sapiens 127-132 31647642-4 2019 The integration of ultra-low-temperature sensitive Tm3+ ions and room-temperature sensitive Er3+ ions in an ultra-small alpha-NaYbF4:Tm3+@CaF2@NaYF4:Yb3+/Er3+@CaF2 core/multi-shell nanoparticle (~15 nm) as dual-mode upconverting luminescent nanoprobe enables the broad-range temperature detection from 10K to 295K. Sodium 126-132 CCR4-NOT transcription complex subunit 8 Homo sapiens 138-142 31647642-4 2019 The integration of ultra-low-temperature sensitive Tm3+ ions and room-temperature sensitive Er3+ ions in an ultra-small alpha-NaYbF4:Tm3+@CaF2@NaYF4:Yb3+/Er3+@CaF2 core/multi-shell nanoparticle (~15 nm) as dual-mode upconverting luminescent nanoprobe enables the broad-range temperature detection from 10K to 295K. Sodium 126-132 CCR4-NOT transcription complex subunit 8 Homo sapiens 159-163 31647642-5 2019 This structure induces ~14 times NIR emission and ~6-fold green UC luminescence output in comparison with alpha-NaYbF4:Tm3+ core and alpha-NaYbF4:Tm3+@CaF2@NaYF4:Yb3+/Er3+ core/shell/shell nanoparticles. Sodium 133-145 CCR4-NOT transcription complex subunit 8 Homo sapiens 151-155 31718537-8 2019 In this way we attested the implication of some voltage-gated sodium (SCN1A, SCN2A, SCN4A, SCN4B, SCN5A, SCN9A) and potassium (KCNQ2, KCNH2) channels in cardiovascular diseases, epilepsies, febrile seizures, headache disorders, neuromuscular, neurodegenerative diseases or neurobehavioral manifestations. Sodium 62-68 sodium voltage-gated channel alpha subunit 1 Homo sapiens 70-75 31853224-10 2019 Nuclear NF-kappaB p65, MAPK p38, JNK, and ERK were all activated by cyclic strain, but inhibited by the ER stress inhibitor 4-PBA or NaHS. Sodium 133-137 mitogen activated protein kinase 14 Rattus norvegicus 28-31 31622441-0 2019 In silico assessment of human Calprotectin subunits (S100A8/A9) in presence of sodium and calcium ions using Molecular Dynamics simulation approach. Sodium 79-85 S100 calcium binding protein A8 Homo sapiens 53-62 31680960-10 2019 Our findings indicated that the phosphorylated activation of Akt played a role in the proliferation of HaCat cells upon long-term, low-dose NaAsO2 exposure through the phosphorylative regulation of its downstream cell cycle regulating factors of GSK-3beta/cyclin D1, p21 and p27, which could induce the promotion of cell cycle progression from G1 to S/G2M phase. Sodium 140-146 glycogen synthase kinase 3 beta Homo sapiens 246-255 31680960-10 2019 Our findings indicated that the phosphorylated activation of Akt played a role in the proliferation of HaCat cells upon long-term, low-dose NaAsO2 exposure through the phosphorylative regulation of its downstream cell cycle regulating factors of GSK-3beta/cyclin D1, p21 and p27, which could induce the promotion of cell cycle progression from G1 to S/G2M phase. Sodium 140-146 cyclin D1 Homo sapiens 256-265 31680960-10 2019 Our findings indicated that the phosphorylated activation of Akt played a role in the proliferation of HaCat cells upon long-term, low-dose NaAsO2 exposure through the phosphorylative regulation of its downstream cell cycle regulating factors of GSK-3beta/cyclin D1, p21 and p27, which could induce the promotion of cell cycle progression from G1 to S/G2M phase. Sodium 140-146 transcription elongation factor A like 1 Homo sapiens 267-270 31601786-1 2019 The sodium leak channel NALCN is a key player in establishing the resting membrane potential (RMP) in neurons and transduces changes in extracellular Ca2+ concentration ([Ca2+]e) into increased neuronal excitability as the downstream effector of calcium-sensing receptor (CaSR). Sodium 4-10 sodium leak channel, non-selective Homo sapiens 24-29 31542800-0 2019 Pharmacological inhibition of the ideal apical sodium-dependent bile acid transporter ASBT ameliorates cholestatic liver disease in mice. Sodium 47-53 solute carrier family 10, member 2 Mus musculus 86-90 31626691-6 2019 Results: The study demonstrated that NaHS suppressed ERK 1/2 pathway activity similarly to PD98059 in retinas of experimental glaucoma rats, while PD98059 also similarly suppressed glial activation, NF-kappaB pathway, NADPH oxidase, and TNF-alpha production. Sodium 37-41 mitogen activated protein kinase 3 Rattus norvegicus 53-60 31338984-7 2019 In vivo, oral administration of quercetin in dextran-sulfate-sodium-induced colitis induces miR-369-3p expression. Sodium 61-67 microRNA 369 Homo sapiens 92-102 31256750-1 2019 Background: IVS5-91G>A (rs3812718) polymorphism of the sodium voltage-gated channel alpha subunit 1 (SCN1A) gene has been associated with inadequate responsiveness to common antiepileptic drugs which act as sodium channel blockers. Sodium 55-61 sodium voltage-gated channel alpha subunit 1 Homo sapiens 101-106 31257654-4 2019 Here we compared acl5 with a mutant of spermine synthase, spms, in terms of abiotic stress tolerance and found that acl5 was much more sensitive to sodium than the wild-type and spms. Sodium 148-154 S-adenosyl-L-methionine-dependent methyltransferases superfamily protein Arabidopsis thaliana 116-120 31611777-5 2019 Within the AIS, the percentage of Na v 1.6 voltage-gated sodium channels remained highly consistent, regardless of cell size or other AIS properties. Sodium 57-63 sodium channel, voltage-gated, type VIII, alpha Mus musculus 34-42 30980862-1 2019 Angiotensin II type I receptor (AT1R) is a critical player in regulating vasoconstriction, blood pressure, sodium retention. Sodium 107-113 angiotensin II receptor type 1 Homo sapiens 32-36 31285285-1 2019 BACKGROUND: Gitelman syndrome is a salt-losing tubulopathy caused by mutations in the SLC12A3 gene, which encodes the thiazide-sensitive sodium-chloride cotransporter. Sodium 137-143 solute carrier family 12 member 3 Homo sapiens 86-93 30623373-12 2019 PPAR-gamma attenuated pilocarpine-induced seizure severity, neuronal loss, BBB damage, and sodium currents in hippocampal neurons. Sodium 91-97 peroxisome proliferator activated receptor gamma Mus musculus 0-10 31168066-1 2019 Over the past 25 years, successive cloning of SLC34A1, SLC34A2 and SLC34A3, which encode the sodium-dependent inorganic phosphate (Pi) cotransport proteins 2a-2c, has facilitated the identification of molecular mechanisms that underlie the regulation of renal and intestinal Pi transport. Sodium 93-99 solute carrier family 34 member 1 Homo sapiens 46-53 31168066-1 2019 Over the past 25 years, successive cloning of SLC34A1, SLC34A2 and SLC34A3, which encode the sodium-dependent inorganic phosphate (Pi) cotransport proteins 2a-2c, has facilitated the identification of molecular mechanisms that underlie the regulation of renal and intestinal Pi transport. Sodium 93-99 solute carrier family 34 member 2 Homo sapiens 55-62 31362426-1 2019 One of the most intriguing findings highlighted from G protein-coupled receptor (GPCR) crystallography is the presence, in many members of class A, of a partially hydrated sodium ion in the middle of the seven transmembrane helices (7TM) bundle. Sodium 172-178 endothelin receptor type A Homo sapiens 53-79 31362426-1 2019 One of the most intriguing findings highlighted from G protein-coupled receptor (GPCR) crystallography is the presence, in many members of class A, of a partially hydrated sodium ion in the middle of the seven transmembrane helices (7TM) bundle. Sodium 172-178 endothelin receptor type A Homo sapiens 81-85 31362426-2 2019 In particular, the human adenosine A2A receptor (A2A AR) is the first GPCR in which a monovalent sodium ion was crystallized in a distal site from the canonical orthosteric one, corroborating, from a structural point of view, its role as a negative allosteric modulator. Sodium 97-103 endothelin receptor type A Homo sapiens 70-74 30885820-1 2019 Nav1.1 and Nav1.2 are the voltage-gated sodium channel alpha subunit1 and 2, encoded by the genes of SCN1A and SCN2A. Sodium 40-46 sodium voltage-gated channel alpha subunit 1 Homo sapiens 0-6 30885820-1 2019 Nav1.1 and Nav1.2 are the voltage-gated sodium channel alpha subunit1 and 2, encoded by the genes of SCN1A and SCN2A. Sodium 40-46 sodium voltage-gated channel alpha subunit 2 Rattus norvegicus 11-17 30885820-1 2019 Nav1.1 and Nav1.2 are the voltage-gated sodium channel alpha subunit1 and 2, encoded by the genes of SCN1A and SCN2A. Sodium 40-46 sodium voltage-gated channel alpha subunit 2 Rattus norvegicus 111-116 31244775-14 2019 Furthermore, CPS decreased protein expression of Kallikrein and COX-2, both involved in sodium handling. Sodium 88-94 cytochrome c oxidase II, mitochondrial Rattus norvegicus 64-69 31030607-0 2019 The Dopamine D1 Receptor and Angiotensin II Type-2 Receptor are Required for Inhibition of Sodium Transport Through a Protein Phosphatase 2A Pathway. Sodium 91-97 angiotensin II receptor type 2 Homo sapiens 29-59 31030607-1 2019 Activation of the renal D1R (dopamine D1-like receptor) or AT2R (angiotensin II type-2 receptor), individually or both, simultaneously, is necessary in the normal regulation of renal sodium (Na+) transport and blood pressure. Sodium 183-189 angiotensin II receptor type 2 Homo sapiens 59-63 31030607-1 2019 Activation of the renal D1R (dopamine D1-like receptor) or AT2R (angiotensin II type-2 receptor), individually or both, simultaneously, is necessary in the normal regulation of renal sodium (Na+) transport and blood pressure. Sodium 183-189 angiotensin II receptor type 2 Homo sapiens 65-95 31218164-6 2019 Using Sanger sequencing, Gly947Arg (2839G>A) in the sodium-potassium (Na+/K+)-ATPasealpha3 subunit gene (ATP1A3) was confirmed from her blood sample. Sodium 55-61 ATPase Na+/K+ transporting subunit alpha 3 Homo sapiens 108-114 30790705-0 2019 Maternal high-sodium intake affects the offspring" vascular renin-angiotensin system promoting endothelial dysfunction in rats. Sodium 14-20 renin Rattus norvegicus 60-65 30790705-13 2019 Our results also suggest that vascular angiotensin II is the main mediator of high sodium-programmed endothelial dysfunction, promoting COX-2 expression and oxidative stress. Sodium 83-89 cytochrome c oxidase II, mitochondrial Rattus norvegicus 136-141 30785716-0 2019 Fabrication of SnS2/Mn2SnS4/Carbon Heterostructures for Sodium-Ion Batteries with High Initial Coulombic Efficiency and Cycling Stability. Sodium 56-62 sodium voltage-gated channel alpha subunit 11 Homo sapiens 15-19 30785716-1 2019 SnS2 has been extensive studied as an anode material for sodium storage owing to its high theoretical specific capacity, whereas the unsatisfied initial Coulombic efficiency (ICE) caused by the partial irreversible conversion reaction during the charge/discharge process is one of the critical issues that hamper its practical applications. Sodium 57-63 sodium voltage-gated channel alpha subunit 11 Homo sapiens 0-4 30785716-2 2019 Hence, heterostructured SnS2/Mn2SnS4/carbon nanoboxes (SMS/C NBs) have been developed by a facial wet-chemical method and utilized as the anode material of sodium ion batteries. Sodium 156-162 sodium voltage-gated channel alpha subunit 11 Homo sapiens 24-28 30445423-0 2019 SPINT2 (HAI-2) missense variants identified in congenital sodium diarrhea/tufting enteropathy affect the ability of HAI-2 to inhibit prostasin but not matriptase. Sodium 58-64 serine protease 8 Homo sapiens 133-142 30595123-4 2019 Several studies have found that the mTORC2 pathway is involved in the regulation of renal tubular sodium and potassium transport, but its role in hypertension has remained largely unexplored. Sodium 98-104 CREB regulated transcription coactivator 2 Mus musculus 36-42 30595123-8 2019 The results indicate that mTORC2 and the related downstream associated pathways play an important role in regulation of sodium balance and arterial pressure regulation in salt-sensitive rats. Sodium 120-126 CREB regulated transcription coactivator 2 Mus musculus 26-32 30588629-6 2019 Initial studies demonstrated that LQT9-associated Cav3 mutations, F97C and S141R, increase late sodium current as a potential mechanism to prolong action potential duration (APD) and cause LQT9. Sodium 96-102 caveolin 3 Homo sapiens 34-38 30588629-6 2019 Initial studies demonstrated that LQT9-associated Cav3 mutations, F97C and S141R, increase late sodium current as a potential mechanism to prolong action potential duration (APD) and cause LQT9. Sodium 96-102 caveolin 3 Homo sapiens 50-54 30588629-6 2019 Initial studies demonstrated that LQT9-associated Cav3 mutations, F97C and S141R, increase late sodium current as a potential mechanism to prolong action potential duration (APD) and cause LQT9. Sodium 96-102 caveolin 3 Homo sapiens 189-193 30675762-0 2019 Synergistical Coupling Interconnected ZnS/SnS2 Nanoboxes with Polypyrrole-Derived N/S Dual-Doped Carbon for Boosting High-Performance Sodium Storage. Sodium 134-140 sodium voltage-gated channel alpha subunit 11 Homo sapiens 42-46 30559144-4 2019 RESULTS: Low sodium intake stimulated basolateral Kir4.1/Kir5.1 activity, increased basolateral K+ conductance, and hyperpolarized the membrane. Sodium 13-19 potassium inwardly-rectifying channel, subfamily J, member 10 Mus musculus 50-56 30559144-7 2019 Thus, elevated NCC activity induced by low sodium intake was associated with upregulation of Kir4.1/Kir5.1 activity in the DCT, whereas inhibition of NCC activity by high sodium intake was associated with diminished Kir4.1/Kir5.1 activity. Sodium 43-49 potassium inwardly-rectifying channel, subfamily J, member 10 Mus musculus 93-99 30559144-7 2019 Thus, elevated NCC activity induced by low sodium intake was associated with upregulation of Kir4.1/Kir5.1 activity in the DCT, whereas inhibition of NCC activity by high sodium intake was associated with diminished Kir4.1/Kir5.1 activity. Sodium 171-177 potassium inwardly-rectifying channel, subfamily J, member 10 Mus musculus 216-222 30559144-9 2019 Further, Kir4.1 deletion not only abolished basolateral K+ conductance and depolarized the DCT membrane, but also abrogated the stimulating effects induced by low sodium intake on basolateral K+ conductance and hyperpolarization. Sodium 163-169 potassium inwardly-rectifying channel, subfamily J, member 10 Mus musculus 9-15 30559144-11 2019 CONCLUSIONS: Stimulation of Kir4.1/Kir5.1 by low intake of dietary sodium is essential for NCC upregulation, and inhibition of Kir4.1/Kir5.1 induced by high sodium intake is a key step for downregulation of NCC. Sodium 67-73 potassium inwardly-rectifying channel, subfamily J, member 10 Mus musculus 28-34 30559144-11 2019 CONCLUSIONS: Stimulation of Kir4.1/Kir5.1 by low intake of dietary sodium is essential for NCC upregulation, and inhibition of Kir4.1/Kir5.1 induced by high sodium intake is a key step for downregulation of NCC. Sodium 157-163 potassium inwardly-rectifying channel, subfamily J, member 10 Mus musculus 28-34 30559144-11 2019 CONCLUSIONS: Stimulation of Kir4.1/Kir5.1 by low intake of dietary sodium is essential for NCC upregulation, and inhibition of Kir4.1/Kir5.1 induced by high sodium intake is a key step for downregulation of NCC. Sodium 157-163 potassium inwardly-rectifying channel, subfamily J, member 10 Mus musculus 127-133 30508412-4 2019 The present results are the first to demonstrate that PKC/p38 MAPK signaling is involved in ANGII-induced water and sodium intake and oxytocin (OT) secretion in OVX rats. Sodium 116-122 mitogen activated protein kinase 14 Rattus norvegicus 58-61 30508412-4 2019 The present results are the first to demonstrate that PKC/p38 MAPK signaling is involved in ANGII-induced water and sodium intake and oxytocin (OT) secretion in OVX rats. Sodium 116-122 mitogen activated protein kinase 3 Rattus norvegicus 62-66 30681965-4 2019 OBJECTIVE: The MI-BP app aims to reduce health disparities related to HTN in the community by employing a user-centered intervention focused on self-BP monitoring, physical activity, reduced sodium intake, and medication adherence. Sodium 191-197 nicotinamide riboside kinase 2 Homo sapiens 15-20 30681965-10 2019 We seek to determine the effect of MI-BP on BP for 1 year (using BP control and mean systolic BP as coprimary outcomes and physical activity, sodium intake, and medication adherence as secondary outcomes) compared with usual care controls. Sodium 142-148 nicotinamide riboside kinase 2 Homo sapiens 35-40 30380007-1 2019 The mineralocorticoid receptor (MR) is indispensable for survival through its critical role in maintaining blood pressure in response to sodium scarcity or bleeding. Sodium 137-143 nuclear receptor subfamily 3 group C member 2 Homo sapiens 4-30 30380007-1 2019 The mineralocorticoid receptor (MR) is indispensable for survival through its critical role in maintaining blood pressure in response to sodium scarcity or bleeding. Sodium 137-143 nuclear receptor subfamily 3 group C member 2 Homo sapiens 32-34 30052308-0 2019 DUOX1-mediated hydrogen peroxide release regulates sodium transport in H441 bronchiolar epithelial cells. Sodium 51-57 dual oxidase 1 Homo sapiens 0-5 30052308-3 2019 We therefore ask the question whether DUOX1 expression and production of submillimolar amounts of H2 O2 is instrumental for the sodium channel upregulation observed in H441 cells. Sodium 128-134 dual oxidase 1 Homo sapiens 38-43 30052308-10 2019 CONCLUSION: Our observations suggest that tonic production of H2 O2 by DUOX1 participates in maintaining the level of vectorial sodium transport by lung epithelial cells. Sodium 128-134 dual oxidase 1 Homo sapiens 71-76 30285481-2 2019 Humans obtain vitamin C from dietary sources via intestinal absorption, a process that involves the sodium-dependent vitamin C transporters-1 and -2 (SVCT1 and SVCT2). Sodium 100-106 solute carrier family 23 member 2 Homo sapiens 160-165 31269481-10 2019 CONCLUSIONS: Our study identifies uPLG-PL abundance as an independent influencing factor of edema in adult NS patients, and supports the conclusion that plasmin-dependent ENaC activation is an important pathophysiological mechanism of sodium retention and edema formation in humans with NS. Sodium 235-241 plasminogen Homo sapiens 153-160 31269481-0 2019 Association of Urinary Plasminogen-Plasmin with Edema and Epithelial Sodium Channel Activation in Patients with Nephrotic Syndrome. Sodium 69-75 plasminogen Homo sapiens 23-30 31269481-1 2019 BACKGROUND: Previous animal experiments and small human studies suggest that urinary plasmin can activate the epithelial sodium channel (ENaC) and contribute to sodium retention in nephrotic syndrome (NS), but this however is not well studied in clinical settings, and its relevance to edema formation is not well characterized in humans. Sodium 121-127 plasminogen Homo sapiens 85-92 31269481-1 2019 BACKGROUND: Previous animal experiments and small human studies suggest that urinary plasmin can activate the epithelial sodium channel (ENaC) and contribute to sodium retention in nephrotic syndrome (NS), but this however is not well studied in clinical settings, and its relevance to edema formation is not well characterized in humans. Sodium 161-167 plasminogen Homo sapiens 85-92 30071192-1 2019 The mammalian Na+/H+ exchanger isoform 1 (NHE1) is an integral membrane protein that regulates intracellular pH (pHi) by removing a single intracellular proton in exchange for one extracellular sodium ion. Sodium 194-200 glucose-6-phosphate isomerase Homo sapiens 113-116 31671420-11 2019 AQP1, but not AQP2, was suppressed in the contralateral kidney, resulting in significant increase in urinary flow rate and sodium excretion. Sodium 123-129 aquaporin 1 Rattus norvegicus 0-4 29982819-2 2019 Aldosterone stimulates the collecting duct mineralocorticoid receptor (MR) to upregulate the epithelial sodium channel (ENaC) and stimulate electrogenic sodium reabsorption, with secretion of potassium and protons. Sodium 104-110 nuclear receptor subfamily 3 group C member 2 Homo sapiens 43-69 29982819-2 2019 Aldosterone stimulates the collecting duct mineralocorticoid receptor (MR) to upregulate the epithelial sodium channel (ENaC) and stimulate electrogenic sodium reabsorption, with secretion of potassium and protons. Sodium 104-110 nuclear receptor subfamily 3 group C member 2 Homo sapiens 71-73 29982819-2 2019 Aldosterone stimulates the collecting duct mineralocorticoid receptor (MR) to upregulate the epithelial sodium channel (ENaC) and stimulate electrogenic sodium reabsorption, with secretion of potassium and protons. Sodium 153-159 nuclear receptor subfamily 3 group C member 2 Homo sapiens 43-69 29982819-2 2019 Aldosterone stimulates the collecting duct mineralocorticoid receptor (MR) to upregulate the epithelial sodium channel (ENaC) and stimulate electrogenic sodium reabsorption, with secretion of potassium and protons. Sodium 153-159 nuclear receptor subfamily 3 group C member 2 Homo sapiens 71-73 31415908-2 2019 The aim of this study was to determine whether glucagon-like peptide receptor agonists (GLP-1 RAs), used as antihyperglycemic agents for type 2 diabetes (T2DM) management, may reduce salt cravings as they are known to reduce hedonic feeding behavior and are involved in sodium homeostasis by increasing renal sodium excretion. Sodium 270-276 glucagon like peptide 1 receptor Homo sapiens 88-93 31415908-2 2019 The aim of this study was to determine whether glucagon-like peptide receptor agonists (GLP-1 RAs), used as antihyperglycemic agents for type 2 diabetes (T2DM) management, may reduce salt cravings as they are known to reduce hedonic feeding behavior and are involved in sodium homeostasis by increasing renal sodium excretion. Sodium 309-315 glucagon like peptide 1 receptor Homo sapiens 88-93 30153324-10 2018 Further study revealed that 9-phenanthrol modulated the gating properties of cardiac sodium channels and dose-dependently inhibited INaL and peak sodium current (INaP ) in VMs with an IC50 of 18 and 71.5 muM respectively. Sodium 85-91 NFKB inhibitor zeta Homo sapiens 162-166 30354807-10 2018 Therefore, RMIC COX-2 expression plays a crucial role in renal handling water and sodium homeostasis, preventing salt-sensitive hypertension and maintaining structural integrity of papilla. Sodium 82-88 prostaglandin-endoperoxide synthase 2 Mus musculus 16-21 29582401-2 2018 TRPV4 is now recognized as a polymodal ionotropic receptor: it is a broadly expressed, nonselective cation channel (permeable to calcium, potassium, magnesium, and sodium) that plays an important role in a multitude of physiological processes. Sodium 164-170 transient receptor potential cation channel subfamily V member 4 Homo sapiens 0-5 29923768-10 2018 These data demonstrate that chronic inhibition of intrarenal GR activity significantly reduces alphaENaC-dependent sodium retention, resulting in a negative cumulative sodium balance, thereby ameliorating angiotensin II-induced hypertension in rats. Sodium 115-121 growth hormone secretagogue receptor Rattus norvegicus 61-63 29923768-10 2018 These data demonstrate that chronic inhibition of intrarenal GR activity significantly reduces alphaENaC-dependent sodium retention, resulting in a negative cumulative sodium balance, thereby ameliorating angiotensin II-induced hypertension in rats. Sodium 168-174 growth hormone secretagogue receptor Rattus norvegicus 61-63 30170187-6 2018 Interestingly, prior injection of gamma-aminobutyric acid type A (GABAA) receptor antagonist, bicuculline (4.0 nmol/0.5 mul) into the CeA region partially reversed the deficit of sodium intake induced by alpha,beta-methylene ATP. Sodium 179-185 carcinoembryonic antigen gene family 4 Rattus norvegicus 134-137 30170187-7 2018 These results suggest that purinergic receptors in the CeA are involved in the control of sodium intake in the sodium-depleted rats and this negative modulation may be, at least partly, mediated by the GABAA receptor. Sodium 90-96 carcinoembryonic antigen gene family 4 Rattus norvegicus 55-58 30170187-7 2018 These results suggest that purinergic receptors in the CeA are involved in the control of sodium intake in the sodium-depleted rats and this negative modulation may be, at least partly, mediated by the GABAA receptor. Sodium 111-117 carcinoembryonic antigen gene family 4 Rattus norvegicus 55-58 30377123-8 2018 CONCLUSIONS: The regulation of sodium intake by aldosterone is subjected to descending facilitatory modulation by the bilateral CeA, and CeA integrity is essential for aldosterone to execute the nongenomic effect in regulating rapid sodium intake. Sodium 31-37 carcinoembryonic antigen gene family 4 Rattus norvegicus 128-131 30377123-8 2018 CONCLUSIONS: The regulation of sodium intake by aldosterone is subjected to descending facilitatory modulation by the bilateral CeA, and CeA integrity is essential for aldosterone to execute the nongenomic effect in regulating rapid sodium intake. Sodium 233-239 carcinoembryonic antigen gene family 4 Rattus norvegicus 137-140 30231858-1 2018 BACKGROUND: Liver cirrhosis is characterized by avid sodium retention where the activation of the renin angiotensin aldosterone system (RAAS) is considered to be the hallmark of the sodium retaining mechanisms. Sodium 182-188 renin Rattus norvegicus 98-103 30231508-1 2018 The mineralocorticoid receptor (MR) was first identified as a blood pressure regulator, modulating renal sodium handling in response to its principal ligand aldosterone. Sodium 105-111 nuclear receptor subfamily 3 group C member 2 Homo sapiens 32-34 29537313-0 2018 Predicted effect of circadian clock modulation of NHE3 of a proximal tubule cell on sodium transport. Sodium 84-90 solute carrier family 9 member A3 Rattus norvegicus 50-54 29870060-2 2018 The synaptic activation of mGluR5-mediated calcium signalling causes a significant increase in persistent sodium current (INa,P ) in the dendrites. Sodium 106-112 glutamate receptor, ionotropic, kainate 1 Mus musculus 27-33 30012693-7 2018 In addition, we discovered that V1R are spontaneously active during SNA and can already generate several intrinsic activity patterns including repetitive-spiking and sodium-dependent plateau potential that rely on the presence of persistent sodium currents (INap). Sodium 166-172 NFKB inhibitor zeta Homo sapiens 258-262 30012693-7 2018 In addition, we discovered that V1R are spontaneously active during SNA and can already generate several intrinsic activity patterns including repetitive-spiking and sodium-dependent plateau potential that rely on the presence of persistent sodium currents (INap). Sodium 241-247 NFKB inhibitor zeta Homo sapiens 258-262 30012693-13 2018 We uncover a new role for persistent sodium currents (INaP) in driving plateau potential in V1R and in SNA patterning in the embryonic SC. Sodium 37-43 NFKB inhibitor zeta Homo sapiens 54-58 30135311-7 2018 These data demonstrate a direct role for insulin receptor-stimulated sodium and glucose transport and a functional interaction of insulin signaling with mineralocorticoids in vivo. Sodium 69-75 insulin receptor Mus musculus 41-57 30106376-4 2018 Smart patch clamp (SPC) indicated greater sodium current density (INa) at perinexi, relative to non-junctional sites. Sodium 42-48 alpha-internexin Cavia porcellus 66-69 30089272-5 2018 Mechanistically, PKD2L1 deficiency increased p300-mediated acetylation of histone 3 lysine 27 on the promoter of sodium/calcium exchange 1 (NCX1) by repressing AMP-activated protein kinase (AMPK) activity, resulting in NCX1 overexpression and mitochondrial Ca2+ overload. Sodium 113-119 E1A binding protein p300 Homo sapiens 45-49 29978166-5 2018 Observed negative capacitance behaviour in impedance spectra of mc-Si solar cells after PID-s has been attributed to structural deformation caused by potential induced migration of sodium ions (Na+) into mc-Si. Sodium 181-187 metastasis associated 1 family member 2 Homo sapiens 88-91 30116758-6 2018 However, a positive correlation was detected between sodium intake and levels of CD4+CD25+Foxp3+ Treg cells in SLE and a negative association between CD4+CD69+Foxp3- Treg cells and sodium intake in RA. Sodium 53-59 forkhead box P3 Homo sapiens 90-95 31949699-9 2018 Cells treated with NaHS for 24 h showed significant upregulation of p-JAK2, and p-STAT3 expression, as well as increased cell viability when compared to the control cells. Sodium 19-23 Janus kinase 2 Homo sapiens 70-74 29924756-13 2018 HbA1c positively correlated with pre-dialysis sodium gradient (r=0.66 p<0.05). Sodium 46-52 hemoglobin subunit alpha 1 Homo sapiens 0-4 29787809-5 2018 Knockout of PGC-1alpha in EET-treated mice resulted in a reversal of these beneficial effects including a decrease in sodium excretion, elevation of blood pressure and an increase in the pro-inflammatory adipokine nephroblastoma overexpressed gene (NOV). Sodium 118-124 peroxisome proliferative activated receptor, gamma, coactivator 1 alpha Mus musculus 12-22 29925695-8 2018 Consistent with altered pain signaling in NF1, dysregulation of calcium and sodium channels was observed in dorsal root ganglia expressing mutant NF1. Sodium 76-82 neurofibromin 1 Sus scrofa 146-149 29875317-3 2018 We previously reported that the 1.1 subtype of the voltage-gated sodium (NaV; NaV1.1) channel family regulates the excitability of sensory nerve fibers that transmit a mechanical pain message to the spinal cord. Sodium 65-71 sodium voltage-gated channel alpha subunit 1 Homo sapiens 78-84 29524392-0 2018 Sodium functions as a negative allosteric modulator of the oxytocin receptor. Sodium 0-6 oxytocin receptor Homo sapiens 59-76 29524392-3 2018 Using displacement assays with a high-affinity fluorescent antagonist (OTAN-A647), we now show that sodium functions as a negative allosteric modulator of the oxytocin receptor. Sodium 100-106 oxytocin receptor Homo sapiens 159-176 29524392-10 2018 Thus, the oxytocin receptor is allosterically controlled by sodium similar to other GPCRs, but it behaves differently concerning the involvement of the conserved Asp 85. Sodium 60-66 oxytocin receptor Homo sapiens 10-27 29806494-2 2018 The sodium current mediated by Nav1.5 consists of peak and late components (INa-P and INa-L). Sodium 4-10 NFKB inhibitor zeta Homo sapiens 76-81 29516664-0 2018 A Simple One-Pot Strategy for Synthesizing Ultrafine SnS2 Nanoparticle/Graphene Composites as Anodes for Lithium/Sodium-Ion Batteries. Sodium 113-119 sodium voltage-gated channel alpha subunit 11 Homo sapiens 53-57 29516664-4 2018 Through this method, ultrafine SnS2 nanoparticles anchored on graphene nanosheets are prepared and exhibit excellent electrochemical performance for both lithium and sodium storage. Sodium 166-172 sodium voltage-gated channel alpha subunit 11 Homo sapiens 31-35 29408101-6 2018 With the advantages of unique architecture and excellent sodium storage performances, the NF/RGO/SnS2 composite shows promising application potential in the sodium ion batteries. Sodium 57-63 sodium voltage-gated channel alpha subunit 11 Homo sapiens 97-101 29408101-6 2018 With the advantages of unique architecture and excellent sodium storage performances, the NF/RGO/SnS2 composite shows promising application potential in the sodium ion batteries. Sodium 157-163 sodium voltage-gated channel alpha subunit 11 Homo sapiens 97-101 29310825-8 2018 Disruption of Kir4.1 significantly increased basal urinary sodium excretion but it abolished the natriuretic effect of hydrochlorothiazide. Sodium 59-65 potassium inwardly-rectifying channel, subfamily J, member 10 Mus musculus 14-20 29973322-16 2018 The mRNA levels of 5-HIAA and MAO-A increased in the gastric tissues, and IDO1, 5-HT1A and 5-HT3A mRNAs decreased in the sodium chromate group. Sodium 121-127 5-hydroxytryptamine (serotonin) receptor 3A Mus musculus 91-97 29556787-6 2018 Thirdly, the cooperative action of Ang II acting on AT1R and AVP stimulating both V1aR and V2 receptors in the kidney is necessary for the appropriate regulation of renal blood flow and the efficient resorption of sodium and water. Sodium 214-220 angiotensin II receptor type 1 Homo sapiens 52-56 29556787-6 2018 Thirdly, the cooperative action of Ang II acting on AT1R and AVP stimulating both V1aR and V2 receptors in the kidney is necessary for the appropriate regulation of renal blood flow and the efficient resorption of sodium and water. Sodium 214-220 arginine vasopressin receptor 1A Homo sapiens 82-86 29319903-0 2018 SnS2 /Sb2 S3 Heterostructures Anchored on Reduced Graphene Oxide Nanosheets with Superior Rate Capability for Sodium-Ion Batteries. Sodium 110-116 sodium voltage-gated channel alpha subunit 11 Homo sapiens 0-4 29182730-7 2018 RESULTS: In the process of acute sodium loading, after adjusting for age and 24-hour urinary sodium concentration, SNPs in CYP11B2, PRKG1, SLC8A1 genes were significantly associated with systolic BP (SBP) rising in the additive and recessive model; SNPs in CYP4A11, PRKG1, SLC8A1, and ADRB2 genes were significantly associated with diastolic BP (DBP) rising. Sodium 33-39 cytochrome P450 family 4 subfamily A member 11 Homo sapiens 257-264 29593552-0 2018 KV4.3 Expression Modulates NaV1.5 Sodium Current. Sodium 34-40 potassium voltage-gated channel subfamily D member 3 Homo sapiens 0-5 29021227-11 2018 Together, these results demonstrate that the appropriate regulation of ENaC by CK2 is necessary for the normal physiological role played by this key renal ion channel in the fine-tuning of sodium excretion. Sodium 189-195 casein kinase 2, alpha prime polypeptide Mus musculus 79-82 29092848-5 2018 Endothelin type B receptors (ETB-R) can induce vasodilation of the renal vasculature and also regulate tubular sodium handling. Sodium 111-117 endothelin receptor type B Rattus norvegicus 0-27 29092848-5 2018 Endothelin type B receptors (ETB-R) can induce vasodilation of the renal vasculature and also regulate tubular sodium handling. Sodium 111-117 endothelin receptor type B Rattus norvegicus 29-34 29509976-0 2018 Sodium Threshold in Model Reduced and Low Fat Oil-in-Water Emulsion Systems. Sodium 0-6 FAT atypical cadherin 1 Homo sapiens 42-45 29509976-2 2018 Several reduced and lower fat foods have higher amounts of sodium than their regular fat counterparts, which contradict sodium and fat reduction goals for hypertensive individuals. Sodium 59-65 FAT atypical cadherin 1 Homo sapiens 26-29 29509976-3 2018 The objective of this research was to determine the threshold of sodium in a model reduced and low fat oil-in-water emulsion system analogous to salad dressings, so as to identify a reduction level of sodium that may not compromise consumer acceptability. Sodium 65-71 FAT atypical cadherin 1 Homo sapiens 99-102 29509976-8 2018 Results indicate saltiness perception is increased when fat content is decreased, and threshold for sodium in the reduced fat emulsion system is higher than the low fat emulsion system with lower fat content. Sodium 100-106 FAT atypical cadherin 1 Homo sapiens 122-125 29509976-8 2018 Results indicate saltiness perception is increased when fat content is decreased, and threshold for sodium in the reduced fat emulsion system is higher than the low fat emulsion system with lower fat content. Sodium 100-106 FAT atypical cadherin 1 Homo sapiens 122-125 29509976-8 2018 Results indicate saltiness perception is increased when fat content is decreased, and threshold for sodium in the reduced fat emulsion system is higher than the low fat emulsion system with lower fat content. Sodium 100-106 FAT atypical cadherin 1 Homo sapiens 122-125 29509976-10 2018 PRACTICAL APPLICATION: Study results demonstrated sodium difference thresholds for the reduced and low fat emulsions were at levels lower than the mean sodium content found in comparable processed food emulsion systems. Sodium 50-56 FAT atypical cadherin 1 Homo sapiens 103-106 29509976-10 2018 PRACTICAL APPLICATION: Study results demonstrated sodium difference thresholds for the reduced and low fat emulsions were at levels lower than the mean sodium content found in comparable processed food emulsion systems. Sodium 152-158 FAT atypical cadherin 1 Homo sapiens 103-106 29509976-12 2018 Having insight for where consumers are able to detect a difference in sodium levels within reduced and low fat food systems can contribute to a successful reduction of sodium in reduced and lower fat food systems and benefit individuals requiring reductions of sodium and fat in processed food systems. Sodium 70-76 FAT atypical cadherin 1 Homo sapiens 196-199 29509976-12 2018 Having insight for where consumers are able to detect a difference in sodium levels within reduced and low fat food systems can contribute to a successful reduction of sodium in reduced and lower fat food systems and benefit individuals requiring reductions of sodium and fat in processed food systems. Sodium 70-76 FAT atypical cadherin 1 Homo sapiens 196-199 29509976-12 2018 Having insight for where consumers are able to detect a difference in sodium levels within reduced and low fat food systems can contribute to a successful reduction of sodium in reduced and lower fat food systems and benefit individuals requiring reductions of sodium and fat in processed food systems. Sodium 168-174 FAT atypical cadherin 1 Homo sapiens 107-110 29509976-12 2018 Having insight for where consumers are able to detect a difference in sodium levels within reduced and low fat food systems can contribute to a successful reduction of sodium in reduced and lower fat food systems and benefit individuals requiring reductions of sodium and fat in processed food systems. Sodium 168-174 FAT atypical cadherin 1 Homo sapiens 196-199 29509976-12 2018 Having insight for where consumers are able to detect a difference in sodium levels within reduced and low fat food systems can contribute to a successful reduction of sodium in reduced and lower fat food systems and benefit individuals requiring reductions of sodium and fat in processed food systems. Sodium 168-174 FAT atypical cadherin 1 Homo sapiens 196-199 29360682-13 2018 CONCLUSION: Considering that the renin-angiotensin pathway plays a central role in blood pressure and plasma sodium concentration, and our observation that ACE and PTPRD expression increased over the spectrum of childhood development, this finding could potentially impact the dosing of an entire class of drugs known as ACE-inhibitors in pediatric patients. Sodium 109-115 protein tyrosine phosphatase receptor type D Homo sapiens 164-169 29289466-2 2018 Activation of angiotensin II type 2 receptor (AT2R) decreases sodium reabsorption in renal proximal tubule (RPT) cells, whereas insulin produces the opposite effect. Sodium 62-68 angiotensin II receptor, type 2 Rattus norvegicus 14-44 29289466-2 2018 Activation of angiotensin II type 2 receptor (AT2R) decreases sodium reabsorption in renal proximal tubule (RPT) cells, whereas insulin produces the opposite effect. Sodium 62-68 angiotensin II receptor, type 2 Rattus norvegicus 46-50 29289466-3 2018 We presume that AT2R has an inhibitory effect on insulin receptor expression in RPT cells, which may affect renal sodium transport and therefore be of physiological or pathological significance. Sodium 114-120 angiotensin II receptor, type 2 Rattus norvegicus 16-20 29289466-3 2018 We presume that AT2R has an inhibitory effect on insulin receptor expression in RPT cells, which may affect renal sodium transport and therefore be of physiological or pathological significance. Sodium 114-120 insulin receptor Rattus norvegicus 49-65 29305116-3 2018 Plasmin activates the epithelial sodium channel in the collecting ducts potentially causing impaired sodium excretion, suppression of the renin-angiotensin-aldosterone system, and hypertension in PE. Sodium 33-39 plasminogen Homo sapiens 0-7 28752895-3 2018 As previously reported, resurgent and persistent sodium currents (INaR and INaP , respectively) may carry small currents at subthreshold voltages that contribute to generation of spike firing. Sodium 49-55 NFKB inhibitor zeta Homo sapiens 75-79 28281179-9 2018 Nut intake frequency was higher in cluster 2 (P < .001), which was characterized by a higher intake frequency of fruits and vegetables, but high mean daily intake of added sugar (12.26 +- 7.67 tsp) and sodium (2800 +- 881 mg). Sodium 202-208 NUT midline carcinoma family member 1 Homo sapiens 0-3 29373601-16 2018 A time effect was observed for the cell membrane sodium-dependent glucose transporter SLC5A1, for the major carbohydrate facilitated transporter SLC2A2, and water transport function AQP3, where SLC5A1 and AQP3 had a negative quadratic effect over time. Sodium 49-55 solute carrier family 5 member 1 Bos taurus 86-92 29373601-16 2018 A time effect was observed for the cell membrane sodium-dependent glucose transporter SLC5A1, for the major carbohydrate facilitated transporter SLC2A2, and water transport function AQP3, where SLC5A1 and AQP3 had a negative quadratic effect over time. Sodium 49-55 solute carrier family 5 member 1 Bos taurus 194-200 29373601-16 2018 A time effect was observed for the cell membrane sodium-dependent glucose transporter SLC5A1, for the major carbohydrate facilitated transporter SLC2A2, and water transport function AQP3, where SLC5A1 and AQP3 had a negative quadratic effect over time. Sodium 49-55 aquaporin 3 Bos taurus 205-209 29281247-0 2018 Promising Dual-Doped Graphene Aerogel/SnS2 Nanocrystal Building High Performance Sodium Ion Batteries. Sodium 81-87 sodium voltage-gated channel alpha subunit 11 Homo sapiens 38-42 30393695-0 2018 Improved Electrochemical Performance Based on Nanostructured SnS2@CoS2-rGO Composite Anode for Sodium-Ion Batteries. Sodium 95-101 sodium voltage-gated channel alpha subunit 11 Homo sapiens 61-65 30393695-2 2018 The presence of rGO and the combined merits of SnS2 and CoS2 endow the SnS2@CoS2-rGO composite with high conductivity pathways and channels for electrons and with excellent properties as an anode material for sodium-ion batteries (SIBs). Sodium 209-215 sodium voltage-gated channel alpha subunit 11 Homo sapiens 47-51 30393695-2 2018 The presence of rGO and the combined merits of SnS2 and CoS2 endow the SnS2@CoS2-rGO composite with high conductivity pathways and channels for electrons and with excellent properties as an anode material for sodium-ion batteries (SIBs). Sodium 209-215 sodium voltage-gated channel alpha subunit 11 Homo sapiens 71-75 30393695-4 2018 The defined structure and good sodium-storage performance of the SnS2@CoS2-rGO composite demonstrate its promising application in high-performance SIBs. Sodium 31-37 sodium voltage-gated channel alpha subunit 11 Homo sapiens 65-69 28744670-1 2017 Mineralocorticoid receptor (MR) mediates the sodium-retaining action of aldosterone in the distal nephron. Sodium 45-51 nuclear receptor subfamily 3 group C member 2 Homo sapiens 0-26 28744670-1 2017 Mineralocorticoid receptor (MR) mediates the sodium-retaining action of aldosterone in the distal nephron. Sodium 45-51 nuclear receptor subfamily 3 group C member 2 Homo sapiens 28-30 28744670-7 2017 Our data shed new light on the crucial role of HuR as a stabilizing factor for the MR transcript and provide evidence for a short autoregulatory loop in which expression of a nuclear receptor transcriptionally regulating water and sodium balance is controlled by osmotic tone. Sodium 231-237 nuclear receptor subfamily 3 group C member 2 Homo sapiens 83-85 28940861-7 2017 Thus, Ang-(1-7)-induced increases in sodium and water excretion are dependent upon functional Mas and AT1 receptors. Sodium 37-43 angiotensin II receptor, type 1a Rattus norvegicus 102-105 28940861-9 2017 The renin-angiotensin system was enhanced in anaesthetized rats by prior manipulation of dietary sodium intake. Sodium 97-103 renin Rattus norvegicus 4-9 29106511-4 2017 The sodium acetate tolerance was dependent on the extrusion of intracellular sodium ions by the plasma membrane-localized sodium pumps Ena1, Ena2, and Ena5 (Ena1/2/5) and two known upstream regulators: the Rim101 pH signaling pathway and the Hog1 mitogen-activated protein kinase. Sodium 4-10 putative Na(+)-exporting P-type ATPase ENA5 Saccharomyces cerevisiae S288C 151-155 29106511-4 2017 The sodium acetate tolerance was dependent on the extrusion of intracellular sodium ions by the plasma membrane-localized sodium pumps Ena1, Ena2, and Ena5 (Ena1/2/5) and two known upstream regulators: the Rim101 pH signaling pathway and the Hog1 mitogen-activated protein kinase. Sodium 4-10 putative Na(+)-exporting P-type ATPase ENA5 Saccharomyces cerevisiae S288C 157-165 28934190-0 2017 People with the major alleles of ATP2B1 rs17249754 increases the risk of hypertension in high ratio of sodium and potassium, and low calcium intakes. Sodium 103-109 ATPase plasma membrane Ca2+ transporting 1 Homo sapiens 33-39 29076723-0 2017 Rapidly Synthesized, Few-Layered Pseudocapacitive SnS2 Anode for High-Power Sodium Ion Batteries. Sodium 76-82 sodium voltage-gated channel alpha subunit 11 Homo sapiens 50-54 29076723-5 2017 SnS2 possesses a large number of active surface sites and exhibits high-capacity, rapid sodium ion storage kinetics induced by quick, nondestructive pseudocapacitance. Sodium 88-94 sodium voltage-gated channel alpha subunit 11 Homo sapiens 0-4 29076723-7 2017 Additionally, a rationally designed sodium ion full cell coupled with SnS2//Na3V2(PO4)3 exhibited exceptional performance with high initial Coulombic efficiency (99%), high capacity, high stability, and a retention of ~53% of the initial capacity even after the current density was increased by a factor of 140. Sodium 36-42 sodium voltage-gated channel alpha subunit 11 Homo sapiens 70-74 29116128-0 2017 Salt stress-induced FERROCHELATASE 1 improves resistance to salt stress by limiting sodium accumulation in Arabidopsis thaliana. Sodium 84-90 ferrochelatase 1 Arabidopsis thaliana 20-36 28614116-5 2017 In addition, PTH alters sodium transport that indirectly leads to enhanced TRPV5 activity. Sodium 24-30 transient receptor potential cation channel subfamily V member 5 Homo sapiens 75-80 28617689-3 2017 RECENT FINDINGS: Recent studies have identified the paracellular channel, claudin-2, that is responsible for paracellular reabsorption of sodium in the proximal renal tubule. Sodium 138-144 claudin 2 Mus musculus 74-83 28617689-4 2017 Knockout of claudin-2 in mice impairs proximal sodium and fluid reabsorption but is compensated by upregulation of sodium reabsorption in the loop of Henle. Sodium 47-53 claudin 2 Mus musculus 12-21 28617689-4 2017 Knockout of claudin-2 in mice impairs proximal sodium and fluid reabsorption but is compensated by upregulation of sodium reabsorption in the loop of Henle. Sodium 115-121 claudin 2 Mus musculus 12-21 28793216-9 2017 We conclude that, independent of its transport activity and indirect regulatory mechanisms involving inositol-derived increases in PIP2, SMIT1, and likely other related sodium-dependent solute transporters, regulates KCNQ channel ion selectivity, gating, and pharmacology by direct physical interaction with the pore module. Sodium 169-175 solute carrier family 5 member 3 Homo sapiens 137-142 28684740-0 2017 HuR-Dependent Editing of a New Mineralocorticoid Receptor Splice Variant Reveals an Osmoregulatory Loop for Sodium Homeostasis. Sodium 108-114 nuclear receptor subfamily 3 group C member 2 Homo sapiens 31-57 28007400-3 2017 METHODS: We used patch-clamp electrophysiology to record sodium currents encoded by either Nav1.1 or Nav1.6 channels stably expressed in HEK293 cells. Sodium 57-63 sodium voltage-gated channel alpha subunit 1 Homo sapiens 91-97 28007400-3 2017 METHODS: We used patch-clamp electrophysiology to record sodium currents encoded by either Nav1.1 or Nav1.6 channels stably expressed in HEK293 cells. Sodium 57-63 neuron navigator 1 Homo sapiens 91-95 28452575-4 2017 Paracellular reabsorption of sodium occurs in the proximal tubule and is mediated by claudin-2. Sodium 29-35 claudin 2 Mus musculus 85-94 28196676-4 2017 Similarly, brequinar sodium is another DHODH inhibitor that showed anti-tumour effect in MC38 colon carcinoma cells when used in combination with fluorouracil. Sodium 21-27 dihydroorotate dehydrogenase Mus musculus 39-44 27995414-2 2017 Since the upregulation of Fe2+ and H+ cotransporter, divalent metal transporter (DMT)-1, has been shown to correlate with thalassemia-induced intestinal calcium absorption impairment, the inhibition of the apical Na+/H+ exchanger (NHE)-3 that is essential for cytoplasmic pH regulation and transepithelial sodium absorption was hypothesized to negatively affect hepcidin action. Sodium 306-312 solute carrier family 11 (proton-coupled divalent metal ion transporters), member 2 Mus musculus 53-87 28137877-0 2017 CaMKII modulates sodium current in neurons from epileptic Scn2a mutant mice. Sodium 17-23 sodium channel, voltage-gated, type II, alpha Mus musculus 58-63 28137877-2 2017 In the Scn2aQ54 mouse model of epilepsy, a focal epilepsy phenotype is caused by transgenic expression of an engineered NaV1.2 mutation displaying enhanced persistent sodium current. Sodium 167-173 sodium channel, voltage-gated, type II, alpha Mus musculus 120-126 28038937-8 2017 In a neuronal cell line expressing TRPM8 channels, voltage-gated sodium currents are blocked in the presence of the cell-impermeable, charged lidocaine derivative QX-314 and WS-12. Sodium 65-71 transient receptor potential cation channel subfamily M member 8 Homo sapiens 35-40 27920129-1 2017 The renal outer medullary potassium (ROMK) channel mediates potassium recycling and facilitates sodium reabsorption through the Na+/K+/2Cl- cotransporter in the loop of Henle and potassium secretion at the cortical collecting duct. Sodium 96-102 potassium inwardly rectifying channel subfamily J member 1 Homo sapiens 37-41 27999940-0 2017 FHF2 isoforms differentially regulate Nav1.6-mediated resurgent sodium currents in dorsal root ganglion neurons. Sodium 64-70 neuron navigator 1 Homo sapiens 38-42 28017718-0 2017 Maturation and processing of the amyloid precursor protein is regulated by the potassium/sodium hyperpolarization-activated cyclic nucleotide-gated ion channel 2 (HCN2). Sodium 89-95 hyperpolarization activated cyclic nucleotide gated potassium and sodium channel 2 Rattus norvegicus 163-167 28017718-4 2017 Interestingly, one of the purified proteins was potassium/sodium hyperpolarization-activated cyclic nucleotide-gated ion channel 2 (HCN2), which has been shown to be involved in epilepsy. Sodium 58-64 hyperpolarization activated cyclic nucleotide gated potassium and sodium channel 2 Rattus norvegicus 132-136 27867157-8 2016 Further analyses revealed that the OPG concentration positively correlated with 24-h urinary sodium excretion (r=0.497, P<0.01). Sodium 93-99 TNF receptor superfamily member 11b Homo sapiens 35-38 27725978-4 2016 To this end, we explored using first-principles calculations the strategy of doping of STO at the Sr site with sodium and potassium. Sodium 111-117 nuclear receptor binding SET domain protein 1 Homo sapiens 87-90 27214087-2 2016 The study was designed to test the hypothesis that the epithelial sodium channel is activated proteolytically by urine plasmin in diabetic nephropathy and mediates renal sodium retention. Sodium 66-72 plasminogen Homo sapiens 119-126 27463191-0 2016 Loss of Renal Tubular PGC-1alpha Exacerbates Diet-Induced Renal Steatosis and Age-Related Urinary Sodium Excretion in Mice. Sodium 98-104 peroxisome proliferative activated receptor, gamma, coactivator 1 alpha Mus musculus 22-32 27463191-5 2016 Moreover, we demonstrate that mice with an inducible nephron-specific inactivation of PGC-1alpha in the kidney display elevated urinary sodium excretion, exacerbated renal steatosis during metabolic stress but normal blood pressure regulation. Sodium 136-142 peroxisome proliferative activated receptor, gamma, coactivator 1 alpha Mus musculus 86-96 27443990-0 2016 Renal sodium transport in renin-deficient Dahl salt-sensitive rats. Sodium 6-12 renin Rattus norvegicus 26-31 26615605-2 2016 Mineralocorticoid receptor antagonists (MRAs) in natriuretic doses may improve spot urine sodium excretion and outcomes. Sodium 90-96 nuclear receptor subfamily 3 group C member 2 Homo sapiens 0-26 27107134-2 2016 Activation of dopamine receptor inhibits sodium reabsorption, whereas activation of insulin receptor increases sodium reabsorption in RPTs, and hyperinsulinemic animals and patients have defective renal dopaminergic system. Sodium 111-117 insulin receptor Homo sapiens 84-100 27043552-5 2016 The 24 h urinary sodium excretion of the DS and SS.13BN rats increased after the 6-week high salt diet intervention, while sodium excretion was increased in DS rats with daidzein (agonist of ERRalpha) treatment. Sodium 123-129 estrogen related receptor, alpha Rattus norvegicus 191-199 27043552-6 2016 ERRalpha expression was decreased, while beta- and gamma-ENaC mRNA expressions were increased upon high sodium diet treatment in the DS rats. Sodium 104-110 estrogen related receptor, alpha Rattus norvegicus 0-8 26464215-4 2016 Compared with others, MOG-A showed higher peptide purity (99.2 %) and content (92.2 %) and presented a sheet shape with additional sodium and chloride chemical elements. Sodium 131-137 myelin oligodendrocyte glycoprotein Homo sapiens 22-25 27032980-1 2016 The serotonin transporter (SERT) is an integral membrane protein that exploits preexisting sodium-, chloride-, and potassium ion gradients to catalyze the thermodynamically unfavorable movement of synaptic serotonin into the presynaptic neuron. Sodium 91-97 Serotonin transporter Drosophila melanogaster 4-25 27032980-1 2016 The serotonin transporter (SERT) is an integral membrane protein that exploits preexisting sodium-, chloride-, and potassium ion gradients to catalyze the thermodynamically unfavorable movement of synaptic serotonin into the presynaptic neuron. Sodium 91-97 Serotonin transporter Drosophila melanogaster 27-31 26702152-8 2016 These findings suggest that aging attenuates the responsiveness of the adrenocortical AT1R to a sodium load through impaired regulation of AT1bR mRNA, and that this dysregulation contributes to the defects in water and electrolyte homeostasis observed in aging. Sodium 96-102 angiotensin II receptor, type 1a Rattus norvegicus 86-90 26937967-8 2016 In comparison with the classical model, the action potential shapes for power-law behaving potassium conductance (n gate) showed a longer peak and shallow hyperpolarization; for power-law activation of the sodium conductance (m gate), the action potentials had a sharp rise time; and for power-law inactivation of the sodium conductance (h gate) the spikes had wider peak that for low values of eta replicated pituitary- and cardiac-type action potentials. Sodium 206-212 endothelin receptor type A Homo sapiens 395-398 26882503-0 2016 An external sodium ion binding site controls allosteric gating in TRPV1 channels. Sodium 12-18 transient receptor potential cation channel subfamily V member 1 Homo sapiens 66-71 26882503-2 2016 Here, we show that external sodium ions stabilize the TRPV1 channel in a closed state, such that removing the external ion leads to channel activation. Sodium 28-34 transient receptor potential cation channel subfamily V member 1 Homo sapiens 54-59 26882503-3 2016 In studying the underlying mechanism, we find that the temperature sensors in TRPV1 activate in two steps to favor opening, and that the binding of sodium to an extracellular site exerts allosteric control over temperature-sensor activation and opening of the pore. Sodium 148-154 transient receptor potential cation channel subfamily V member 1 Homo sapiens 78-83 26712462-4 2016 Here we report that IL-1 receptor (IL-1R1) deficiency or blockade limits blood pressure elevation in this model by mitigating sodium reabsorption via the NKCC2 co-transporter in the nephron. Sodium 126-132 interleukin 1 complex Mus musculus 20-24 26747232-10 2016 Furthermore, the toxin also slightly slowed down sodium inactivation on Nav1.3 and Nav1.6 channels. Sodium 49-55 neuron navigator 1 Homo sapiens 72-76 26537257-4 2015 With increased extracellular sodium, Nax up-regulates prostasin, which results in activation of the sodium channel ENaC, resulting in increased sodium flux and increased downstream mRNA synthesis of inflammatory mediators. Sodium 29-35 serine protease 8 Homo sapiens 54-63 26537257-4 2015 With increased extracellular sodium, Nax up-regulates prostasin, which results in activation of the sodium channel ENaC, resulting in increased sodium flux and increased downstream mRNA synthesis of inflammatory mediators. Sodium 100-106 serine protease 8 Homo sapiens 54-63 26358148-1 2015 The lateral parabrachial nucleus (LPBN) and the central nucleus of the amygdala (CeA) are important central areas for the control of sodium appetite. Sodium 133-139 carcinoembryonic antigen gene family 4 Rattus norvegicus 81-84 26495835-2 2015 In this issue of the JCI, a study by Zhang and associates shows that consumption of a high-sodium diet induces expression of cyclooxygenase-2 (COX-2) in macrophages, resulting in enhanced levels of prostaglandin E2 (PGE2), autocrine activation of the macrophage E-prostanoid 4 (EP4) receptor, and subsequent triggering of parallel pathways in the kidney and in skin that help dispose of excess sodium. Sodium 394-400 prostaglandin-endoperoxide synthase 2 Mus musculus 143-148 26344240-0 2015 AT1 receptor blockade in the central nucleus of the amygdala attenuates the effects of muscimol on sodium and water intake. Sodium 99-105 angiotensin II receptor, type 1a Rattus norvegicus 0-3 26344240-1 2015 The blockade of the central nucleus of the amygdala (CeA) with the GABAA receptor agonist muscimol significantly reduces hypertonic NaCl and water intake by sodium-depleted rats. Sodium 157-163 carcinoembryonic antigen gene family 4 Rattus norvegicus 53-56 26203193-1 2015 Aldosterone regulates sodium homeostasis by activating the mineralocorticoid receptor (MR), a member of the nuclear receptor superfamily. Sodium 22-28 nuclear receptor subfamily 3 group C member 2 Homo sapiens 59-85 26203193-1 2015 Aldosterone regulates sodium homeostasis by activating the mineralocorticoid receptor (MR), a member of the nuclear receptor superfamily. Sodium 22-28 nuclear receptor subfamily 3 group C member 2 Homo sapiens 87-89 26147879-5 2015 Intracerebroventricular infusion of an RXFP3 antagonist reduced in a dose-dependent manner the volume of 0.3 m NaCl consumed by sodium-depleted C57Bl/6J (wild-type) mice. Sodium 128-134 relaxin family peptide receptor 3 Mus musculus 39-44 26147879-7 2015 Our findings identify endogenous relaxin-3-RXFP3 signalling as a modulator of sodium appetite. Sodium 78-84 relaxin family peptide receptor 3 Mus musculus 43-48 26147879-12 2015 infusion of the selective RXFP3 antagonist, R3(B1-22)R, reduced in a dose-dependent manner the volume of 0.3 m NaCl solution consumed when offered to sodium-depleted C57Bl/6J wild-type mice, relative to vehicle-treated control animals. Sodium 150-156 relaxin family peptide receptor 3 Mus musculus 26-31 26190808-3 2015 We further discovered that SMA MNs exhibit enhanced sodium channel activities with increased current amplitude and facilitated recovery, which was corrected by restoration of SMN1 in SMA MNs. Sodium 52-58 survival of motor neuron 1, telomeric Homo sapiens 175-179 25841323-8 2015 In summary, the results show that 5HT-mechanisms in the LPBN modulate sodium intake during the delay of SA when the renin angiotensin aldosterone system (RAAS) is increased. Sodium 70-76 renin Rattus norvegicus 116-121 25669316-7 2015 Systolic and diastolic BP (SBP and DBP, respectively) significantly increased from the lower to the higher tertile of sodium from snacks and with increasing frequency of salty snacks consumption. Sodium 118-124 selenium binding protein 1 Homo sapiens 27-30 25669316-9 2015 In the 400 individuals, the average total sodium intake was 3.1 g/day and was significantly higher in individuals belonging to the highest quartile of SBP and DBP. Sodium 42-48 selenium binding protein 1 Homo sapiens 151-154 25992725-0 2015 Identification of the first sodium binding site of the phosphate cotransporter NaPi-IIa (SLC34A1). Sodium 28-34 solute carrier family 34 member 1 Homo sapiens 79-87 25992725-0 2015 Identification of the first sodium binding site of the phosphate cotransporter NaPi-IIa (SLC34A1). Sodium 28-34 solute carrier family 34 member 1 Homo sapiens 89-96 25961826-1 2015 Nax is a sodium-concentration ([Na+])-sensitive Na channel with a gating threshold of ~150 mM for extracellular [Na+] ([Na+]o) in vitro. Sodium 9-15 sodium channel, voltage-gated, type VII, alpha Mus musculus 0-3 25767117-0 2015 Amyloid precursor protein enhances Nav1.6 sodium channel cell surface expression. Sodium 42-48 sodium channel, voltage-gated, type VIII, alpha Mus musculus 35-41 25767117-3 2015 Because mouse models of gain of function and loss of function of APP and Nav1.6 share some similar phenotypes, we hypothesized that APP might be a candidate molecule for sodium channel modulation. Sodium 170-176 sodium channel, voltage-gated, type VIII, alpha Mus musculus 73-79 25767117-5 2015 Knocking down APP decreased Nav1.6 sodium channel currents and cell surface expression. Sodium 35-41 sodium channel, voltage-gated, type VIII, alpha Mus musculus 28-34 25767117-8 2015 JNK inhibition attenuated increases in cell surface expression of Nav1.6 sodium channels induced by overexpression of APP. Sodium 73-79 sodium channel, voltage-gated, type VIII, alpha Mus musculus 66-72 25767117-10 2015 Nav1.6 sodium channel surface expression was increased by T668E and decreased by T668A, mutations of APP695 mimicking and preventing Thr-668 phosphorylation, respectively. Sodium 7-13 sodium channel, voltage-gated, type VIII, alpha Mus musculus 0-6 25767117-12 2015 Therefore, we show that APP enhances Nav1.6 sodium channel cell surface expression through a Go-coupled JNK pathway. Sodium 44-50 sodium channel, voltage-gated, type VIII, alpha Mus musculus 37-43 25014399-1 2015 PURPOSE: The main goal of this study is to investigate the existence of sodium-dependent vitamin C transport system (SVCT2) and to define time-dependent uptake mechanism and intracellular regulation of ascorbic acid (AA) in human corneal epithelial (HCEC) and human retinal pigment epithelial (D407) cells. Sodium 72-78 solute carrier family 23 member 2 Homo sapiens 117-122 25812049-0 2015 A phase-transfer assisted solvo-thermal strategy for low-temperature synthesis of Na3(VO1-xPO4)2F1+2x cathodes for sodium-ion batteries. Sodium 115-121 exportin 4 Homo sapiens 90-94 25858030-2 2015 The sympathetic control of renal sodium tubular reabsorption is dependent on activation of the intrarenal renin-angiotensin system and activation of the angiotensin II type 1 (AT1 ) receptor by angiotensin II. Sodium 33-39 angiotensin II receptor type 1 Homo sapiens 153-190 25858030-11 2015 Pharmacological blockade of the AT1 receptor with losartan prior to RNS abolished both the functional and the molecular responses, suggesting that intrarenal Ang II acting via the AT1 receptor is a major factor for NHE3-mediated sodium and water reabsorption induced by RNS. Sodium 229-235 angiotensin II receptor type 1 Homo sapiens 32-35 25858030-11 2015 Pharmacological blockade of the AT1 receptor with losartan prior to RNS abolished both the functional and the molecular responses, suggesting that intrarenal Ang II acting via the AT1 receptor is a major factor for NHE3-mediated sodium and water reabsorption induced by RNS. Sodium 229-235 angiotensin II receptor type 1 Homo sapiens 180-183 25781322-0 2015 Deletion of PDK1 causes cardiac sodium current reduction in mice. Sodium 32-38 3-phosphoinositide dependent protein kinase 1 Mus musculus 12-16 25781322-4 2015 Thus, the aim of this study was to investigate the potential mechanisms between PDK1 signaling pathway and cardiac sodium current. Sodium 115-121 3-phosphoinositide dependent protein kinase 1 Mus musculus 80-84 25781322-7 2015 Furthermore, the peak sodium current is decreased by 33% in cells lacking PDK1. Sodium 22-28 3-phosphoinositide dependent protein kinase 1 Mus musculus 74-78 25781322-9 2015 The role of the PDK1-Foxo1 pathway in regulating Nav1.5 levels and sodium current density was verified using selective PDK1, Akt and Foxo1 inhibitors and isolated neonatal rat cardiomyocytes. Sodium 67-73 pyruvate dehydrogenase kinase 1 Rattus norvegicus 16-20 25781322-9 2015 The role of the PDK1-Foxo1 pathway in regulating Nav1.5 levels and sodium current density was verified using selective PDK1, Akt and Foxo1 inhibitors and isolated neonatal rat cardiomyocytes. Sodium 67-73 forkhead box O1 Rattus norvegicus 21-26 25368031-11 2015 We suggest that an aberrant interaction between D4 and AT1 receptors may play a role in the abnormal regulation of sodium excretion in hypertension. Sodium 115-121 angiotensin II receptor, type 1a Rattus norvegicus 55-58 25415435-0 2015 mTORC2 regulates renal tubule sodium uptake by promoting ENaC activity. Sodium 30-36 CREB regulated transcription coactivator 2 Mus musculus 0-6 25088759-10 2014 Dynamitin overexpression in HEK-293 (human embryonic kidney 293) cells expressing Nav1.5 resulted in a decrease in sodium current density in the membrane with no modification of the channel-gating properties. Sodium 115-121 dynactin subunit 2 Homo sapiens 0-9 25102111-1 2014 The main goal of this study is to investigate the expression of sodium dependent vitamin C transport system (SVCT2). Sodium 64-70 solute carrier family 23 member 2 Homo sapiens 109-114 25010575-0 2014 Enhanced sodium-ion battery performance by structural phase transition from two-dimensional hexagonal-SnS2 to orthorhombic-SnS. Sodium 9-15 sodium voltage-gated channel alpha subunit 11 Homo sapiens 102-106 25010575-2 2014 It was found that the hexagonal-SnS2 phase can be transformed into the orthorhombic-SnS phase after an annealing step in an argon atmosphere, and the thus transformed SnS shows enhanced sodium-ion storage performance over that of the SnS2, which is attributed to its structural advantages. Sodium 186-192 sodium voltage-gated channel alpha subunit 11 Homo sapiens 32-36 24729583-0 2014 SnS2 nanoplatelet@graphene nanocomposites as high-capacity anode materials for sodium-ion batteries. Sodium 79-85 sodium voltage-gated channel alpha subunit 11 Homo sapiens 0-4 24729583-4 2014 When applied as the anode material for Na-ion batteries, the SnS2/graphene nanosheets achieved a high reversible specific sodium-ion storage capacity of 725 mA h g(-1), stable cyclability, and an enhanced high-rate capability. Sodium 122-128 sodium voltage-gated channel alpha subunit 11 Homo sapiens 61-65 24729583-5 2014 The improved electrochemical performance for reversible sodium-ion storage could be ascribed to the synergistic effects of the SnS2 nanoplatelet/graphene nanosheets as an integrated hybrid nanoarchitecture, in which the graphene nanosheets provide electronic conductivity and cushion for the active SnS2 nanoplatelets during Na-ion insertion and extraction processes. Sodium 56-62 sodium voltage-gated channel alpha subunit 11 Homo sapiens 127-131 24729583-5 2014 The improved electrochemical performance for reversible sodium-ion storage could be ascribed to the synergistic effects of the SnS2 nanoplatelet/graphene nanosheets as an integrated hybrid nanoarchitecture, in which the graphene nanosheets provide electronic conductivity and cushion for the active SnS2 nanoplatelets during Na-ion insertion and extraction processes. Sodium 56-62 sodium voltage-gated channel alpha subunit 11 Homo sapiens 299-303 24590923-1 2014 The aim of this study was to assess whether endogenous Ang II and oxidative stress produced by acute hypertonic sodium overload may regulate the expression of aquaporin-1 (AQP-1) and aquaporin-2 (AQP-2) in the kidney. Sodium 112-118 aquaporin 1 Rattus norvegicus 159-170 24590923-1 2014 The aim of this study was to assess whether endogenous Ang II and oxidative stress produced by acute hypertonic sodium overload may regulate the expression of aquaporin-1 (AQP-1) and aquaporin-2 (AQP-2) in the kidney. Sodium 112-118 aquaporin 1 Rattus norvegicus 172-177 24252256-6 2014 FGF14 regulates brain sodium channels, especially in the cerebellum. Sodium 22-28 fibroblast growth factor 14 Homo sapiens 0-5 24596098-5 2014 This unique splicing of turret residues offers T-type channels a capacity to serve as a pacemaking sodium current in the primitive heart and brain in lieu of Nav1-type sodium channels and to substitute for voltage-gated sodium channels lacking in many invertebrates. Sodium 99-105 neuron navigator 1 Homo sapiens 158-162 24610784-6 2014 The goal of this study was to test if Per1 regulates sodium transport in the DCT through modulation of NCC and the WNK kinases, WNK1 and WNK4. Sodium 53-59 WNK lysine deficient protein kinase 1 Mus musculus 128-132 24610784-6 2014 The goal of this study was to test if Per1 regulates sodium transport in the DCT through modulation of NCC and the WNK kinases, WNK1 and WNK4. Sodium 53-59 WNK lysine deficient protein kinase 4 Mus musculus 137-141 24795654-2 2014 BGT1 is a member of the solute carrier family 6 (the neurotransmitter, sodium symporter transporter family) and mediates cellular uptake of betaine and GABA in a sodium- and chloride-dependent process. Sodium 71-77 solute carrier family 6 member 12 Homo sapiens 0-4 24523339-8 2014 Thus, we have identified a novel peptide encoded within the rAT1aR E2 that selectively inhibits Erk1/2 activation, resulting in physiological consequences for sodium ingestion and arterial pressure that may have implications for treating sodium-sensitive diseases like hypertension and chronic kidney disease. Sodium 159-165 mitogen activated protein kinase 3 Rattus norvegicus 96-102 24523339-8 2014 Thus, we have identified a novel peptide encoded within the rAT1aR E2 that selectively inhibits Erk1/2 activation, resulting in physiological consequences for sodium ingestion and arterial pressure that may have implications for treating sodium-sensitive diseases like hypertension and chronic kidney disease. Sodium 238-244 mitogen activated protein kinase 3 Rattus norvegicus 96-102 24515291-7 2014 T-type channels possess an ion selectivity that can resemble not only the calcium ion exclusive Cav1 and Cav2 channels but also the sodium ion selectivity of Nav1 sodium channels too. Sodium 132-138 Caveolin;Caveolin-1 Caenorhabditis elegans 96-100 24365600-4 2014 In this study, we knocked-down the sodium-dependent vitamin C transporter, SVCT2, the only known transporter of vitamin C in BMSCs, and performed cell adhesion, migration, in-vitro scratch wound healing and F-actin re-arrangement studies. Sodium 35-41 solute carrier family 23 member 2 Homo sapiens 75-80 24439681-4 2014 Central to this novel avenue of sodium channel drug discovery is that fact that Na(V)1.1 comprises the majority of the sodium current in specific inhibitory interneurons. Sodium 32-38 sodium voltage-gated channel alpha subunit 1 Homo sapiens 80-88 23979127-10 2014 There was a significant inverse correlation between plasma BNP levels of EOP patients and sodium (p<0.05) and total protein concentrations (p<0.05). Sodium 90-96 natriuretic peptide B Homo sapiens 59-62 24366341-9 2014 The plasma membrane translocation of MLKL or MLKL(ND) leads to sodium influx, and depletion of sodium from the cell culture medium inhibits necroptosis. Sodium 63-69 mixed lineage kinase domain like pseudokinase Homo sapiens 37-41 24366341-9 2014 The plasma membrane translocation of MLKL or MLKL(ND) leads to sodium influx, and depletion of sodium from the cell culture medium inhibits necroptosis. Sodium 63-69 mixed lineage kinase domain like pseudokinase Homo sapiens 45-49 24366341-11 2014 Thus, the MLKL oligomerization leads to translocation of MLKL to lipid rafts of plasma membrane, and the plasma membrane MLKL complex acts either by itself or via other proteins to increase the sodium influx, which increases osmotic pressure, eventually leading to membrane rupture. Sodium 194-200 mixed lineage kinase domain like pseudokinase Homo sapiens 10-14 24026042-7 2014 Ang II (100 nmol l(-1)) significantly increased ERK 1/2 phosphorylation and cell proliferation in the both medium containing standard sodium and high sodium. Sodium 150-156 mitogen activated protein kinase 3 Rattus norvegicus 48-55 24026042-8 2014 High-sodium level augmented Ang II-induced ERK 1/2 phosphorylation and cell proliferation compared with standard sodium. Sodium 5-11 mitogen activated protein kinase 3 Rattus norvegicus 43-50 24026042-9 2014 Pre-treatment with candesartan (1 mumol l(-1), Ang II type 1 receptor blocker) or PD98095 (10 mumol l(-1), ERK kinase iinhibitor) abolished the proliferative effect induced by high sodium/Ang II. Sodium 181-187 mitogen activated protein kinase 3 Rattus norvegicus 107-110 24026042-14 2014 These data suggest that high-sodium level directly augments Ang II-induced VSMC proliferation through NHE-1- and ERK 1/2-dependent pathways and may offer new insights into the mechanisms of vascular remodeling by high-sodium/Ang II. Sodium 29-35 mitogen activated protein kinase 3 Rattus norvegicus 113-120 25866303-7 2014 These results suggest that [6]-gingerol induced the electrogenic absorption of sodium in the rat colon via TRPV1. Sodium 79-85 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 107-112 25376899-10 2014 While a better understanding of the molecular mechanisms is needed and will provide new therapeutic options, current pharmacological interventions that target both salt retention and sodium appetite include mineralocorticoid receptor antagonists and potentially inhibitors of angiotensin II and ENaC. Sodium 183-189 nuclear receptor subfamily 3 group C member 2 Homo sapiens 207-233 24310820-0 2014 The sodium chloride cotransporter SLC12A3: new roles in sodium, potassium, and blood pressure regulation. Sodium 4-10 solute carrier family 12 member 3 Homo sapiens 34-41 24118094-9 2013 SNAP-5114, a specific GAT-2/3 antagonist, induced an elevation of intracellular sodium concentration ([Na(+) ]i ) under resting conditions and in the presence of d-aspartate, indicating that GAT-2/3 operates in reverse mode. Sodium 80-86 solute carrier family 6 (neurotransmitter transporter, betaine/GABA), member 12 Mus musculus 191-196 23760292-10 2013 Thus, impaired tissue kallikrein stimulation by a low-sodium/high-potassium diet in R53H subjects with partial tissue kallikrein deficiency highlights an inappropriate renal adaptation to potassium load, consistent with experimental data in mice. Sodium 54-60 kallikrein 1 Homo sapiens 15-32 24233809-8 2013 Magnesium deficiency by interfering with ATPase functions causes increased intracellular calcium and sodium and decreases intracellular potassium concentration. Sodium 101-107 dynein axonemal heavy chain 8 Homo sapiens 41-47 24207066-8 2013 Serum Gal3 levels above median (13.8 ng/ml) was a significant predictor of primary endpoint risk after adjustment for age, estimated glomerular filtration rate, anemia, diabetes, serum sodium, brain natriuretic peptide levels, NYHA class and urea, respectively (hazard ratio 1.43, 95% CI 1.07-1.91 P=0.015). Sodium 185-191 galectin 3 Homo sapiens 6-10 24132903-6 2013 We use this approach to determine if prior data implicating the sodium/hydrogen exchanger 9 gene (SLC9A9) in ADHD implicate sodium/hydrogen exchange (NHE) inhibitors as potential treatments. Sodium 64-70 solute carrier family 9 member C1 Homo sapiens 150-153 23833257-3 2013 Compared with wild-type mice, Slc26a6-null mice exhibited increased renal and intestinal sodium-dependent succinate uptake, as well as urinary hyperoxaluria and hypocitraturia, but no change in urinary pH, indicating enhanced transport activity of NaDC-1. Sodium 89-95 solute carrier family 26, member 6 Mus musculus 30-37 24040049-1 2013 Aldosterone binds to the mineralocorticoid receptor (MR) and exerts pleiotropic effects beyond enhancing renal sodium reabsorption. Sodium 111-117 nuclear receptor subfamily 3 group C member 2 Homo sapiens 53-55 23958258-10 2013 CONCLUSION: The minor alleles of 3 SNPs at the NPPA-NPPB locus are associated with a lower risk of PAD, especially in the subjects of high sodium intake. Sodium 139-145 natriuretic peptide B Homo sapiens 52-56 23940334-8 2013 The recovery was sodium-dependent and sensitive to Na(+)/H(+)-exchanger (NHE) inhibitors. Sodium 17-23 solute carrier family 9 member C1 Homo sapiens 51-71 23940334-8 2013 The recovery was sodium-dependent and sensitive to Na(+)/H(+)-exchanger (NHE) inhibitors. Sodium 17-23 solute carrier family 9 member C1 Homo sapiens 73-76 23977363-8 2013 Owing to the enhanced sodium excretion, NDP-alpha-MSH-treated mice were protected from DOCA-salt-induced hypernatremia. Sodium 22-28 Norrie disease (pseudoglioma) (human) Mus musculus 40-43 23977363-8 2013 Owing to the enhanced sodium excretion, NDP-alpha-MSH-treated mice were protected from DOCA-salt-induced hypernatremia. Sodium 22-28 pro-opiomelanocortin-alpha Mus musculus 44-53 23977363-10 2013 In conclusion, treatment with NDP-alpha-MSH increases urinary sodium excretion and protects against DOCA-salt-induced hypertension. Sodium 62-68 Norrie disease (pseudoglioma) (human) Mus musculus 30-33 23977363-10 2013 In conclusion, treatment with NDP-alpha-MSH increases urinary sodium excretion and protects against DOCA-salt-induced hypertension. Sodium 62-68 pro-opiomelanocortin-alpha Mus musculus 34-43 23615500-6 2013 Activating CaSR by either raising the luminal calcium ion concentration or by the calcimimetic caused a concomitant increase in sodium-dependent proton extrusion and fluid reabsorption, whereas in proximal tubules isolated from CaSR knockout mice varying calcium ion concentration had no effect. Sodium 128-134 calcium-sensing receptor Mus musculus 11-15 23503750-1 2013 BACKGROUND: Urinary plasmin activates the epithelial Na(+) channel (ENaC) in vitro and may possibly be a mechanism of sodium retention in nephrotic syndrome (NS). Sodium 118-124 plasminogen Homo sapiens 20-27 23503750-10 2013 CONCLUSIONS: These findings support the hypothesis that aberrantly filtered plasminogen-plasmin may contribute to ENaC activation and mediate primary renal sodium retention during active childhood NS. Sodium 156-162 plasminogen Homo sapiens 76-83 23582189-2 2013 Here, we demonstrate transcriptional and protein expression of OATP members in human melanoma cell lines with sodium-independent organic anion uptake activity. Sodium 110-116 solute carrier organic anion transporter family member 1A2 Homo sapiens 63-67 23656866-6 2013 SO2, together with the Ca (2+)-activated sensor of sodium ions, SOS3, activates SOS1. Sodium 51-57 Calcium-binding EF-hand family protein Arabidopsis thaliana 64-68 23840884-9 2013 In response to both AngII infusion and AT1R blockade via losartan, renal hemodynamic responses and tubular sodium excretion were significantly attenuated in uni-x animals compared to sham. Sodium 107-113 type-1 angiotensin II receptor Ovis aries 39-43 23677982-1 2013 Sodium-hydrogen exchangers (NHE) of the Slc9 gene family are the major regulators of intracellular pH against acidosis in mammalian cells. Sodium 0-6 solute carrier family 9 member C1 Homo sapiens 28-31 23561701-1 2013 Na(+)/K(+)-ATPase alpha 2 (Atp1a2) is an integral plasma membrane protein belonging to the P-type ATPase family that is responsible for maintaining the sodium (Na(+)) and potassium (K(+)) gradients across cellular membranes with hydrolysis of ATP. Sodium 152-158 ATPase, Na+/K+ transporting, alpha 2 polypeptide Mus musculus 27-33 23344662-4 2013 Recent clinical and experimental data indicate that proteinuria may mediate sodium retention and hypertension via plasmin-mediated activation of the epithelial sodium channel. Sodium 76-82 plasminogen Homo sapiens 114-121 23391983-10 2013 sodium loading evoked profound natriuresis, suppression of plasma renin activity (PRA) and global sympathoinhibition. Sodium 0-6 renin Rattus norvegicus 66-71 23360087-2 2013 The thyroid transcription factors-NKx2 homeobox 1 (NKx2-1, formerly called TTF-1) and Paired box gene 8 (Pax8)-are known to associate biochemically and synergistically in the activation of thyroid functional genes including the sodium/iodide symporter (NIS), thyrotropin (TSH) receptor (TSHR), thyroglobulin (Tg), and thyroid peroxidase (TPO) genes. Sodium 228-234 paired box 8 Mus musculus 86-103 23360087-2 2013 The thyroid transcription factors-NKx2 homeobox 1 (NKx2-1, formerly called TTF-1) and Paired box gene 8 (Pax8)-are known to associate biochemically and synergistically in the activation of thyroid functional genes including the sodium/iodide symporter (NIS), thyrotropin (TSH) receptor (TSHR), thyroglobulin (Tg), and thyroid peroxidase (TPO) genes. Sodium 228-234 paired box 8 Mus musculus 105-109 23360087-2 2013 The thyroid transcription factors-NKx2 homeobox 1 (NKx2-1, formerly called TTF-1) and Paired box gene 8 (Pax8)-are known to associate biochemically and synergistically in the activation of thyroid functional genes including the sodium/iodide symporter (NIS), thyrotropin (TSH) receptor (TSHR), thyroglobulin (Tg), and thyroid peroxidase (TPO) genes. Sodium 228-234 thyroglobulin Mus musculus 294-307 23360087-2 2013 The thyroid transcription factors-NKx2 homeobox 1 (NKx2-1, formerly called TTF-1) and Paired box gene 8 (Pax8)-are known to associate biochemically and synergistically in the activation of thyroid functional genes including the sodium/iodide symporter (NIS), thyrotropin (TSH) receptor (TSHR), thyroglobulin (Tg), and thyroid peroxidase (TPO) genes. Sodium 228-234 thyroglobulin Mus musculus 309-311 23459041-6 2013 The most commonly missed items related to diet, such as the sodium content of sea salt, as well as the safety of medications, such as acetaminophen and statins. Sodium 60-66 S13 erythroblastosis (avian) oncogene homolog Homo sapiens 78-81 23324381-5 2013 These observations suggest that kallikrein can have antihypertensive function in physiological situations where sodium retention can trigger blood pressure elevation. Sodium 112-118 kallikrein 1-related peptidase b9 Mus musculus 32-42 23224894-4 2013 Sodium-calcium exchange (NCX) is the dominant calcium (Ca2+) efflux mechanism in cardiac cells. Sodium 0-6 T cell leukemia, homeobox 2 Mus musculus 25-28 23224874-2 2013 Na(+)/Ca(2+) exchangers, NCX and NCKX, play a critical role in the transport of one [Ca(2+)](i) and potassium ion across the cell membrane in exchange for four extracellular sodium ions [Na(+)](e). Sodium 174-180 solute carrier family 24 member 1 Homo sapiens 33-37 22826127-3 2012 Cells expressing hNav1.5-F1486del exhibited a loss-of-function alteration, reflected by an 80% reduction of peak current density, and several gain-of-function alterations, including reduced channel inactivation, enlarged window current, substantial augmentation of persistent late sodium current and an increase in ramp current. Sodium 281-287 sodium voltage-gated channel alpha subunit 5 Homo sapiens 17-24 22820370-9 2012 SUMMARY: Modulation of WNK4 activity by AngII underlies the effects of AngII on NCC activity and this is probably important for the stimulation of renal sodium retention, as well as for the prevention of potassium loss, during hypovolemia. Sodium 153-159 WNK lysine deficient protein kinase 4 Homo sapiens 23-27 22802227-4 2012 In the present studies we assessed whether Nedd4-2 knockout (-/-) mice have the following: (1) increased brain ENaC; (2) elevated cerebrospinal fluid (CSF) sodium on a high-salt diet; and (3) enhanced pressor responses to CSF sodium and hypertension on a high-salt diet, both mediated by brain ENaC. Sodium 156-162 neural precursor cell expressed, developmentally down-regulated gene 4-like Mus musculus 43-50 22802227-4 2012 In the present studies we assessed whether Nedd4-2 knockout (-/-) mice have the following: (1) increased brain ENaC; (2) elevated cerebrospinal fluid (CSF) sodium on a high-salt diet; and (3) enhanced pressor responses to CSF sodium and hypertension on a high-salt diet, both mediated by brain ENaC. Sodium 226-232 neural precursor cell expressed, developmentally down-regulated gene 4-like Mus musculus 43-50 22802227-10 2012 We conclude that increased ENaC expression in the brain of Nedd4-2 -/- mice mediates their hypertensive response to a high-salt diet by causing increased sodium levels in the CSF, as well as hyperresponsiveness to CSF sodium. Sodium 154-160 sodium channel, nonvoltage-gated 1 alpha Mus musculus 27-31 22802227-10 2012 We conclude that increased ENaC expression in the brain of Nedd4-2 -/- mice mediates their hypertensive response to a high-salt diet by causing increased sodium levels in the CSF, as well as hyperresponsiveness to CSF sodium. Sodium 154-160 neural precursor cell expressed, developmentally down-regulated gene 4-like Mus musculus 59-66 22802227-10 2012 We conclude that increased ENaC expression in the brain of Nedd4-2 -/- mice mediates their hypertensive response to a high-salt diet by causing increased sodium levels in the CSF, as well as hyperresponsiveness to CSF sodium. Sodium 218-224 sodium channel, nonvoltage-gated 1 alpha Mus musculus 27-31 22802227-10 2012 We conclude that increased ENaC expression in the brain of Nedd4-2 -/- mice mediates their hypertensive response to a high-salt diet by causing increased sodium levels in the CSF, as well as hyperresponsiveness to CSF sodium. Sodium 218-224 neural precursor cell expressed, developmentally down-regulated gene 4-like Mus musculus 59-66 22575762-5 2012 Cells cotransduced with Tbx5, Mef2c, Myocd expressed cardiac contractile proteins, had cardiac-like potassium and sodium currents and action potentials could be elicited. Sodium 114-120 myocardin Mus musculus 37-42 22587908-7 2012 KEY FINDINGS: A high-sodium diet downregulated AQP-1 and AQP-2 expression levels in the proximal tubule and collecting duct, respectively. Sodium 21-27 aquaporin 2 Rattus norvegicus 57-62 22647294-0 2012 Possible role of brain salt-inducible kinase 1 in responses to central sodium in Dahl rats. Sodium 71-77 salt-inducible kinase 1 Rattus norvegicus 23-46 22617007-0 2012 A sodium channel myotonia due to a novel SCN4A mutation accompanied by acquired autoimmune myasthenia gravis. Sodium 2-8 sodium voltage-gated channel alpha subunit 4 Homo sapiens 41-46 22617007-1 2012 Mutations of the voltage gated sodium channel gene (SCN4A) are responsible for non-dystrophic myotonia including hyperkalemic periodic paralysis, paramyotonia congenita, and sodium channel myotonia, as well as congenital myasthenic syndrome. Sodium 31-37 sodium voltage-gated channel alpha subunit 4 Homo sapiens 52-57 22617007-1 2012 Mutations of the voltage gated sodium channel gene (SCN4A) are responsible for non-dystrophic myotonia including hyperkalemic periodic paralysis, paramyotonia congenita, and sodium channel myotonia, as well as congenital myasthenic syndrome. Sodium 174-180 sodium voltage-gated channel alpha subunit 4 Homo sapiens 52-57 22087608-7 2012 AM5 infusion also induced significant increases in urine volume (HD 2-fold increment, P<0.05) and urine sodium (2.7-fold increment, P<0.01), potassium (1.7-fold increment, P<0.05) and creatinine (1.4-fold increment, P<0.05) excretion and creatinine clearance (60% increment, P<0.05). Sodium 107-113 adrenomedullin 5 (putative) Homo sapiens 0-3 22746038-7 2012 An aquaporin-4 inhibitor recovered sodium ion concentration in blood to normal. Sodium 35-41 aquaporin 4 Rattus norvegicus 3-14 22129970-4 2012 Expression of a dominant negative (DN) form of Rab11a or Rab11b significantly reduced the basal and cAMP-stimulated ENaC-dependent sodium (Na(+)) transport. Sodium 131-137 sodium channel, nonvoltage-gated 1 alpha Mus musculus 116-120 22271663-12 2012 Upregulated expression of sodium channel subunits Nav1.7 and Nav1.8 in both small dorsal root ganglion neurons and peripheral C-fibres as well as enhanced transient and persistent sodium current and increased excitability in small dorsal root ganglion neurons from diabetic rats might underlie the reduced conduction failure in the diabetic high-firing-frequency polymodal nociceptive C-fibres. Sodium 26-32 sodium voltage-gated channel alpha subunit 9 Rattus norvegicus 50-56 22025386-7 2012 Pharmacological inhibition of mGluR1/5 slightly dampened the spread of sodium, whereas inhibition of glutamate uptake or purinergic receptors had no effect. Sodium 71-77 glutamate receptor, metabotropic 1 Mus musculus 30-36 21204798-6 2011 Currently, four genes are identified to be involved in myotonia: the muscle voltage-gated sodium and chloride channel genes SCN4A and CLCN1, the myotonic dystrophy protein kinase (DMPK) gene, and the CCHC-type zinc finger, nucleic acid binding protein gene CNBP. Sodium 90-96 sodium voltage-gated channel alpha subunit 4 Homo sapiens 124-129 21666503-0 2011 Nucleotide sequence of the Na+/H+ exchanger-8 in patients with congenital sodium diarrhea. Sodium 74-80 solute carrier family 9 member A8 Homo sapiens 27-45 21666503-1 2011 Sodium absorption by the intestine is mediated by brush border Na/H exchangers, which include the NHE3 and NHE8 isoforms. Sodium 0-6 solute carrier family 9 member A8 Homo sapiens 107-111 21666503-5 2011 Because some patients with congenital sodium diarrhea improve with age and knowing the developmental switch from NHE8 to NHE3, NHE8 may be a candidate gene for this disorder. Sodium 38-44 solute carrier family 9 member A8 Homo sapiens 127-131 24319568-1 2011 The SNTA1-encoded alpha1-syntrophin (SNTA1) missense mutation, p.A257G, causes long QT syndrome (LQTS) by pathogenic accentuation of Nav1.5"s sodium current (INa). Sodium 142-148 sodium voltage-gated channel alpha subunit 5 Homo sapiens 133-139 22028644-9 2011 Analysis of all sodium flux pathways suggests that the sodium-potassium pump (NaK) plays the largest role in exacerbated sodium overload during reperfusion, and that reduced NaK flux is largely the result of impaired pH recovery. Sodium 16-22 TANK binding kinase 1 Homo sapiens 78-81 22028644-9 2011 Analysis of all sodium flux pathways suggests that the sodium-potassium pump (NaK) plays the largest role in exacerbated sodium overload during reperfusion, and that reduced NaK flux is largely the result of impaired pH recovery. Sodium 55-61 TANK binding kinase 1 Homo sapiens 78-81 21907141-6 2011 In mice, extracellular fluid volume depletion shifts SPAK isoform abundance to favor NaCl retention along both segments, indicating that a SPAK isoform switch modulates sodium avidity along the distal nephron. Sodium 169-175 serine/threonine kinase 39 Mus musculus 139-143 21488862-5 2011 proposes provisional safety margins for QRS prolongation in man based on retrospective clinical data and a single in vitro approach to assess potency of block of cardiac sodium current (hNav1.5), the ionic current responsible for ventricular conduction (observed as QRS prolongation). Sodium 170-176 sodium voltage-gated channel alpha subunit 5 Homo sapiens 186-193 21610494-10 2011 SUMMARY: SPAK and OSR1 kinases regulate SCL12A transporters with important physiological effects for sodium homeostasis by the kidney, aortic contractility and neuronal excitability. Sodium 101-107 serine/threonine kinase 39 Mus musculus 9-13 21720262-9 2011 Compared with metoprolol alone (which tended to reduce urine output and creatinine excretion/clearance), Ucn2 + metoprolol increased urine volume, sodium and creatinine excretion and clearance. Sodium 147-153 urocortin-2 Ovis aries 105-109 21699903-1 2011 Renalase is a recently discovered flavoprotein that regulates blood pressure, regulates sodium and phosphate excretion, and displays cardioprotectant action through a mechanism that is barely understood to date. Sodium 88-94 renalase, FAD dependent amine oxidase Homo sapiens 0-8 21631568-11 2011 Urinary sodium excretion was greater (P < 0.01) during the HS diet (253 +- 10 vs 281 +- 27 mmol/24 h for PL vs CX2, respectively) compared with the LS diet (14 +- 3 vs 17 +- 7 mmol/24 h for PL vs CX2, respectively; P(drug) = 0.26). Sodium 8-14 interleukin 17C Homo sapiens 114-117 21631568-11 2011 Urinary sodium excretion was greater (P < 0.01) during the HS diet (253 +- 10 vs 281 +- 27 mmol/24 h for PL vs CX2, respectively) compared with the LS diet (14 +- 3 vs 17 +- 7 mmol/24 h for PL vs CX2, respectively; P(drug) = 0.26). Sodium 8-14 interleukin 17C Homo sapiens 199-202 21536685-5 2011 Knockdown of cortactin in mpkCCD(c14) principal cells results in an increase in ENaC activity and sodium reabsorption. Sodium 98-104 cortactin Mus musculus 13-22 21653227-0 2011 TWIK-1 two-pore domain potassium channels change ion selectivity and conduct inward leak sodium currents in hypokalemia. Sodium 89-95 potassium two pore domain channel subfamily K member 1 Homo sapiens 0-6 21385947-2 2011 Prompted by a case of autopsy-negative SUD in a 23-year-old African American man who collapsed while playing football, we hypothesized that S1103Y interacted with other SCN5A variants to pathologically modify sodium current (I(Na)). Sodium 209-215 sodium voltage-gated channel alpha subunit 5 Homo sapiens 169-174 21499270-4 2011 In this study, we found that beta(2)-adrenergic receptor (beta(2)AR) stimulation led to decreased transcription of the gene encoding WNK4, a regulator of sodium reabsorption. Sodium 154-160 adrenoceptor beta 2 Rattus norvegicus 29-56 21499270-4 2011 In this study, we found that beta(2)-adrenergic receptor (beta(2)AR) stimulation led to decreased transcription of the gene encoding WNK4, a regulator of sodium reabsorption. Sodium 154-160 adrenoceptor beta 2 Rattus norvegicus 58-67 21372286-0 2011 FKBP12 is a critical regulator of the heart rhythm and the cardiac voltage-gated sodium current in mice. Sodium 81-87 FK506 binding protein 1a Mus musculus 0-6 20167245-3 2011 Highly metastatic breast cancer cells express Na(V)1.5, the main isoform expressed in cardiac cells, where the current generated by the flux of sodium ions is responsible for the excitability. Sodium 144-150 immunoglobulin lambda variable 2-18 Homo sapiens 46-54 21893992-3 2011 A large number of in vitro studies have supported this notion of an autocrine function for ET-1, demonstrating that the peptide, largely through activation of the ET(B) receptor, inhibits both sodium (Na) and water reabsorption in the CD. Sodium 193-199 endothelin 1 Mus musculus 91-95 20852447-7 2011 Salt-sensitive CYP2C9*3 carriers exhibited the lowest PRA values and significantly lower 24 h sodium excretion rates during high-salt intake (P = 0.005 vs. CYP2C9*1/*1). Sodium 94-100 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 15-21 32272545-0 2011 Functional Analysis of Human Sodium-Phosphate Transporter 4 (NPT4/SLC17A3) Polymorphisms. Sodium 29-35 solute carrier family 17 member 3 Homo sapiens 61-65 32272545-0 2011 Functional Analysis of Human Sodium-Phosphate Transporter 4 (NPT4/SLC17A3) Polymorphisms. Sodium 29-35 solute carrier family 17 member 3 Homo sapiens 66-73 20805697-8 2011 RESULTS: beta(2)M levels predict increased PP (p = 0.02) adjusting for age, HD modalities, HD duration, HOMA-IR and percent sodium removal. Sodium 124-130 beta-2-microglobulin Homo sapiens 9-17 20805697-11 2011 CONCLUSIONS: beta(2)M levels were positively associated with PP, which was influenced mainly by dialysis modality fluid and sodium balance and less by arterial stiffness. Sodium 124-130 beta-2-microglobulin Homo sapiens 13-21 21887217-0 2011 Sodium coupled bicarbonate influx regulates intracellular and apical pH in cultured rat caput epididymal epithelium. Sodium 0-6 glucose-6-phosphate isomerase Rattus norvegicus 69-71 20817076-3 2010 In a follow-up study, we reported that elevated BACE1 activity regulates total and surface expression of voltage-gated sodium channels (Na(v)1 channels) and thereby modulates sodium currents in neuronal cells and mouse brains. Sodium 119-125 beta-site APP cleaving enzyme 1 Mus musculus 48-53 20817076-3 2010 In a follow-up study, we reported that elevated BACE1 activity regulates total and surface expression of voltage-gated sodium channels (Na(v)1 channels) and thereby modulates sodium currents in neuronal cells and mouse brains. Sodium 175-181 beta-site APP cleaving enzyme 1 Mus musculus 48-53 20347966-0 2010 Intracellular sodium sensing: SIK1 network, hormone action and high blood pressure. Sodium 14-20 salt inducible kinase 1 Homo sapiens 30-34 20347966-5 2010 One of these pathways relies on an intracellular sodium-sensor network with the salt-inducible kinase 1 (SIK1) at its core. Sodium 49-55 salt inducible kinase 1 Homo sapiens 80-103 20347966-5 2010 One of these pathways relies on an intracellular sodium-sensor network with the salt-inducible kinase 1 (SIK1) at its core. Sodium 49-55 salt inducible kinase 1 Homo sapiens 105-109 20347966-7 2010 The SIK1 network also mediates sodium-independent signals that modulate the activity of the Na(+),K(+)-ATPase, like dopamine and angiotensin, which are relevant per se in the development of high blood pressure. Sodium 31-37 salt inducible kinase 1 Homo sapiens 4-8 21167004-0 2010 SCN5A rare variants in familial dilated cardiomyopathy decrease peak sodium current depending on the common polymorphism H558R and common splice variant Q1077del. Sodium 69-75 sodium voltage-gated channel alpha subunit 5 Homo sapiens 0-5 20621122-4 2010 Consequently, studies were undertaken to characterize the effects of MB on voltage-gated sodium currents (I(Na)) in hippocampal CA1 neurons. Sodium 89-95 carbonic anhydrase 1 Rattus norvegicus 128-131 21105923-6 2010 Expression of the gene encoding Arabidopsis high-affinity K(+) transporter 1;1 (AtHKT1;1), a gene responsible for removing sodium ions from the root xylem, was repressed by cytokinin treatment, but showed significantly elevated expression in the cytokinin response double mutant arr1-3 arr12-1. Sodium 123-129 high-affinity K+ transporter 1 Arabidopsis thaliana 80-88 21105923-7 2010 Our data suggest that cytokinin, acting through the transcription factors ARR1 and ARR12, regulates sodium accumulation in the shoots by controlling the expression of AtHKT1;1 in the roots. Sodium 100-106 high-affinity K+ transporter 1 Arabidopsis thaliana 167-175 20817733-1 2010 PiT1/SLC20A1 is a sodium-dependent P(i) transporter expressed by most mammalian cells. Sodium 18-24 solute carrier family 20 member 1 Homo sapiens 0-4 20817733-1 2010 PiT1/SLC20A1 is a sodium-dependent P(i) transporter expressed by most mammalian cells. Sodium 18-24 solute carrier family 20 member 1 Homo sapiens 5-12 20949524-2 2010 Gilfillan et al.2008] reported mutations in SLC9A6, the gene encoding the sodium/hydrogen exchanger NHE6, in the family first reported and in three others. Sodium 74-80 solute carrier family 9 member A6 Homo sapiens 44-50 20949524-2 2010 Gilfillan et al.2008] reported mutations in SLC9A6, the gene encoding the sodium/hydrogen exchanger NHE6, in the family first reported and in three others. Sodium 74-80 solute carrier family 9 member A6 Homo sapiens 100-104 21104767-2 2010 NCKX3 (gene SLC24A3), a potassium-dependent sodium-/calcium exchanger, plays a critical role in the transport of one intracellular calcium and potassium ion across the cell membrane in exchange for four extracellular sodium ions. Sodium 44-50 solute carrier family 24 member 3 Rattus norvegicus 0-5 21104767-2 2010 NCKX3 (gene SLC24A3), a potassium-dependent sodium-/calcium exchanger, plays a critical role in the transport of one intracellular calcium and potassium ion across the cell membrane in exchange for four extracellular sodium ions. Sodium 44-50 solute carrier family 24 member 3 Rattus norvegicus 12-19 20696009-0 2010 The SOS1 transporter of Physcomitrella patens mediates sodium efflux in planta. Sodium 55-61 ribosomal 60S subunit protein L35A Saccharomyces cerevisiae S288C 4-8 20403459-10 2010 However, in the context of H558R-SCN5A, persistent late sodium current emerges, indicating that A572D/H558R could be a proarrhythmic factor akin to S1103Y. Sodium 56-62 sodium voltage-gated channel alpha subunit 5 Homo sapiens 33-38 20483727-6 2010 RANK represents the longest TNFR with four full cysteine-rich domains (CRDs) in which the CRD4 is stabilized by a sodium ion and a rigid linkage with CRD3. Sodium 114-120 TNF receptor superfamily member 1A Homo sapiens 28-32 20529371-0 2010 Effect of thyroid statuses on sodium/iodide symporter (NIS) gene expression in the extrathyroidal tissues in mice. Sodium 30-36 solute carrier family 5 (sodium iodide symporter), member 5 Mus musculus 55-58 20042427-9 2010 Co-expression of Nav1.5 with Navbeta3-V54G (with or without co-expression of the Navbeta1 subunit) in both HEK-293 cells and COS cells revealed a significant decrease in peak sodium current and a positive shift of inactivation compared with WT. Sodium 175-181 sodium voltage-gated channel alpha subunit 5 Homo sapiens 17-23 20065149-4 2010 After 2 weeks of DOCA plus 1% NaCl as drinking fluid, hypertension and sodium retention were more severe in mPGES-1 knockout (KO) mice than in wild-type (WT) controls. Sodium 71-77 prostaglandin E synthase Mus musculus 108-115 20091493-11 2010 Urinary sodium excretion was low when protein levels of E-cadherin and claudin-4 were high. Sodium 8-14 cadherin 1 Rattus norvegicus 56-66 20091493-14 2010 The dynamic change in protein levels of E-cadherin and claudin-4 seems to coincide with that in the level of sodium excretion. Sodium 109-115 cadherin 1 Rattus norvegicus 40-50 19688719-6 2010 Also, in acutely isolated rat hippocampal CA1 pyramidal neurons, quercetin (0.3, 3 and 30 microm) decreased the amplitude of voltage-dependent sodium currents in a dose- and voltage-dependent manner. Sodium 143-149 carbonic anhydrase 1 Rattus norvegicus 42-45 19858225-4 2009 We found that short bursts of Schaffer collateral stimulation evoke sodium transients in the millimolar range in both CA1 pyramidal neurons and in SR101-positive astrocytes of the stratum radiatum. Sodium 68-74 carbonic anhydrase 1 Mus musculus 118-121 19943938-18 2009 CNGC19 and CNGC20 could assist the plant to cope with toxic effects caused by salt stress, probably by contributing to a re-allocation of sodium within the plant. Sodium 138-144 cyclic nucleotide-binding transporter 1 Arabidopsis thaliana 11-17 19919977-4 2009 Compared with time-matched controls, separate Ucn2 and furosemide administration significantly increased urine output (furosemide>Ucn2), urine sodium (furosemide>Ucn2), potassium (furosemide>Ucn2), and creatinine excretion (Ucn2>furosemide) and creatinine clearance (Ucn2>furosemide). Sodium 146-152 urocortin-2 Ovis aries 46-50 19567370-6 2009 In vivo, CNKSR3 was highly expressed in the renal cortical collecting duct (CCD), the prime target segment of aldosterone-regulated sodium retention in the kidney. Sodium 132-138 CNKSR family member 3 Homo sapiens 9-15 19567370-7 2009 CCD cell lines stably overexpressing or silencing CNKSR3 were electrophysiologically analyzed and show that CNKSR3 expression correlated with and is required for ENaC-mediated transepithelial sodium transport. Sodium 192-198 CNKSR family member 3 Homo sapiens 50-56 19567370-7 2009 CCD cell lines stably overexpressing or silencing CNKSR3 were electrophysiologically analyzed and show that CNKSR3 expression correlated with and is required for ENaC-mediated transepithelial sodium transport. Sodium 192-198 CNKSR family member 3 Homo sapiens 108-114 19567370-9 2009 We conclude that CNKSR3, a homologue of scaffold proteins involved in MAPK pathway regulation, is a direct target of MR and is required for the maintenance of transepithelial sodium transport in the kidney. Sodium 175-181 CNKSR family member 3 Homo sapiens 17-23 19717569-2 2009 For numerous gammaretroviruses, such as the gibbon ape leukemia virus, woolly monkey virus, feline leukemia virus subgroup B, feline leukemia virus subgroup T, and 10A1 murine leukemia virus, this receptor is the human type III sodium-dependent inorganic phosphate transporter, SLC20A1, formerly known as PiT1. Sodium 228-234 solute carrier family 20 member 1 Homo sapiens 278-285 19717569-2 2009 For numerous gammaretroviruses, such as the gibbon ape leukemia virus, woolly monkey virus, feline leukemia virus subgroup B, feline leukemia virus subgroup T, and 10A1 murine leukemia virus, this receptor is the human type III sodium-dependent inorganic phosphate transporter, SLC20A1, formerly known as PiT1. Sodium 228-234 solute carrier family 20 member 1 Homo sapiens 305-309 19666841-1 2009 The SCN5A-encoded cardiac sodium channel underlies excitability in the heart, and dysfunction of sodium current (I(Na)) can cause fatal ventricular arrhythmia in maladies such as long QT syndrome, Brugada syndrome (BrS), and sudden infant death syndrome (SIDS). Sodium 26-32 sodium voltage-gated channel alpha subunit 5 Homo sapiens 4-9 19648062-9 2009 CONCLUSION: Our study supports the concept that febrile illness predisposes individuals who carry a loss of function SCN5A mutation, such as V1340I, to fever-induced ventricular arrhythmias in BrS by significantly reducing the sodium currents in the hyperthermic state. Sodium 227-233 sodium voltage-gated channel alpha subunit 5 Homo sapiens 117-122 19571313-8 2009 RNAi-based interference of SOS1 caused cell death in the root elongation zone, accompanied by fragmentation of vacuoles, inhibition of endocytosis, and apoplastic sodium influx into the stele and hence the shoot. Sodium 163-169 sodium proton exchanger, putative (NHX7) (SOS1) Arabidopsis thaliana 27-31 19713338-9 2009 Renal medullary ischemia after hypothermic circulatory arrest was ameliorated by atrial natriuretic peptide which increased medullary blood flow and reduced sodium reabsorption in the medulla. Sodium 157-163 natriuretic peptides A Sus scrofa 81-107 19341767-5 2009 EGF induced concentration-dependent increases in proton efflux in renal podocytes as assessed using a Cytosensor microphysiometer, were diminished in the presence of 5-(N-methyl-N-isobutyl) amiloride or in a sodium-free solution. Sodium 208-214 epidermal growth factor Homo sapiens 0-3 20641261-6 2004 Although different AA transport systems are involved in the uptake of AAs, the AAs are transported primarily by the l AA transport systems (designated as LAT1 and LAT2), which are not sodium-dependent and can transport both the l- and d-isomers (7, 13), including those containing a branched chain or an aromatic moiety (14). Sodium 184-190 linker for activation of T cells family, member 2 Mus musculus 163-167 20031595-7 2009 Coexpression of SCN5A/WT+SCN1B/WT+SCN3B/L10P resulted in an 82.6% decrease in peak sodium current density, accelerated inactivation, slowed reactivation, and a -9.6-mV shift of half-inactivation voltage compared with SCN5A/WT+SCN1B/WT+SCN3B/WT. Sodium 83-89 sodium voltage-gated channel alpha subunit 5 Homo sapiens 16-21 19501014-0 2009 Potassium nutrition, sodium toxicity, and calcium signaling: connections through the CBL-CIPK network. Sodium 21-27 Cbl proto-oncogene Homo sapiens 85-88 19162162-0 2009 The alpha-like scorpion toxin BmK I enhances membrane excitability via persistent sodium current by preventing slow inactivation and deactivation of rNav1.2a expressed in Xenopus Oocytes. Sodium 82-88 mitogen-activated protein kinase 7 L homeolog Xenopus laevis 30-35 19162162-4 2009 The results showed that BmK I prevented the development of slow inactivation of rNav1.2a from the open-state and enhanced the persistent sodium current (I(NaP)) at suprathreshold potentials in concentration-dependence, whereas it hardly affected the fast inactivation. Sodium 137-143 mitogen-activated protein kinase 7 L homeolog Xenopus laevis 24-29 19035761-1 2009 Sodium amalgam reduction of the aryl-substituted bis(imino)pyridine iron dibromide complex, ((Et)PDI)FeBr2 ((Et)PDI = 2,6-(2,6-Et2-C6H3N=CMe)2C5H3N), under a dinitrogen atmosphere in pentane furnished the bis(chelate)iron compound, ((Et)PDI)2Fe. Sodium 0-6 peptidyl arginine deiminase 1 Homo sapiens 97-100 19035761-1 2009 Sodium amalgam reduction of the aryl-substituted bis(imino)pyridine iron dibromide complex, ((Et)PDI)FeBr2 ((Et)PDI = 2,6-(2,6-Et2-C6H3N=CMe)2C5H3N), under a dinitrogen atmosphere in pentane furnished the bis(chelate)iron compound, ((Et)PDI)2Fe. Sodium 0-6 peptidyl arginine deiminase 1 Homo sapiens 112-115 19035761-1 2009 Sodium amalgam reduction of the aryl-substituted bis(imino)pyridine iron dibromide complex, ((Et)PDI)FeBr2 ((Et)PDI = 2,6-(2,6-Et2-C6H3N=CMe)2C5H3N), under a dinitrogen atmosphere in pentane furnished the bis(chelate)iron compound, ((Et)PDI)2Fe. Sodium 0-6 peptidyl arginine deiminase 1 Homo sapiens 112-115 19211916-1 2009 The human sodium-dependent multivitamin transporter (hSMVT) mediates sodium-dependent uptake of biotin in renal and intestinal epithelia. Sodium 10-16 solute carrier family 5 member 6 Homo sapiens 53-58 19176528-2 2009 MDA-MB-231 breast cancer cells express functional sodium channel complexes, consisting of Na(V)1.5 and associated auxiliary beta-subunits, that are responsible for a sustained inward sodium current at the membrane potential. Sodium 50-56 immunoglobulin lambda variable 2-18 Homo sapiens 90-98 19251209-0 2009 Type of SCN5A mutation determines clinical severity and degree of conduction slowing in loss-of-function sodium channelopathies. Sodium 105-111 sodium voltage-gated channel alpha subunit 5 Homo sapiens 8-13 19129479-1 2009 The newly described yeast endosomal sorting complexes required for transport (ESCRT) protein increased sodium tolerance-1 (Ist1p) binds the late-acting ESCRT proteins Did2p/charged MVB protein (CHMP) 1 and Vps4p and exhibits synthetic vacuolar protein sorting defects when combined with mutations in the Vta1p/LIP5-Vps60p/CHMP5 complex. Sodium 103-109 AAA family ATPase VPS4 Saccharomyces cerevisiae S288C 206-211 19146874-2 2009 The results indicated that: (1) in the present of final concentration of 10(-4)g/ml nano-ZnO, the current-voltage curve of sodium current (I(Na)) was decreased, and the peak amplitudes of I(Na) were increased considerably from -50 to +20mV (p<0.05). Sodium 123-129 internexin neuronal intermediate filament protein, alpha Rattus norvegicus 139-144 19028991-0 2009 Nociceptin/orphanin FQ peptide receptor agonist Ac-RYYRWKKKKKKK-NH2 (ZP120) induces antinatriuresis in rats by stimulation of amiloride-sensitive sodium reabsorption. Sodium 146-152 prepronociceptin Rattus norvegicus 0-10 19885019-12 2009 These findings suggest that the increased renal ANP synthesis in association with decreased metabolism via NEP and NPR-C may play a compensatory role against the development of sodium retention in nephrotic syndrome. Sodium 177-183 natriuretic peptide receptor 3 Rattus norvegicus 115-120 19885019-14 2009 The subsequent recovery of NPR-A expression may play a role in promoting sodium excretion in later stage (at day 14). Sodium 73-79 natriuretic peptide receptor 1 Rattus norvegicus 27-32 19054333-6 2009 RESULTS: Uroguanylin did not increase urinary excretion of sodium and water in normal rats, but significantly increased urinary sodium excretion during the sodium retention phase in nephrotic rats (untreated vs uroguanylin-treated nephrotic rats in mmol/mmol creatinine; 2.92 +/- 0.65 vs 8.93 +/- 2.53 on day 6, P < 0.05; 3.55 +/- 0.47 vs 10.37 +/- 1.73 on day 7, P < 0.01; 14.88 +/- 2.32 vs 24.47 +/- 2.86 on day 8, P < 0.05). Sodium 128-134 guanylate cyclase activator 2B Rattus norvegicus 9-20 19054333-6 2009 RESULTS: Uroguanylin did not increase urinary excretion of sodium and water in normal rats, but significantly increased urinary sodium excretion during the sodium retention phase in nephrotic rats (untreated vs uroguanylin-treated nephrotic rats in mmol/mmol creatinine; 2.92 +/- 0.65 vs 8.93 +/- 2.53 on day 6, P < 0.05; 3.55 +/- 0.47 vs 10.37 +/- 1.73 on day 7, P < 0.01; 14.88 +/- 2.32 vs 24.47 +/- 2.86 on day 8, P < 0.05). Sodium 128-134 guanylate cyclase activator 2B Rattus norvegicus 9-20 19054333-8 2009 CONCLUSION: Uroguanylin increased urinary sodium excretion in rats with PAN-induced nephrosis, and might be useful for treating sodium retention in patients with nephrotic syndrome. Sodium 42-48 guanylate cyclase activator 2B Rattus norvegicus 12-23 19054333-8 2009 CONCLUSION: Uroguanylin increased urinary sodium excretion in rats with PAN-induced nephrosis, and might be useful for treating sodium retention in patients with nephrotic syndrome. Sodium 128-134 guanylate cyclase activator 2B Rattus norvegicus 12-23 19097948-2 2009 Veratridine prevents inactivation of Na(+) channel via binding the receptor site 2, causes influx of sodium ion and depolarization and induces apoptosis of neuronal cells. Sodium 101-107 sodium voltage-gated channel alpha subunit 8 Rattus norvegicus 37-50 19071883-9 2009 In addition to the clinical pharmacokinetic analysis, the ability of mipomersen sodium to inhibit the major CYP isoform enzymes (namely CYP1A2, CYP2C9, CYP2C19, CYP2D6 and CYP3A4) was evaluated in cryo-preserved human hepatocytes in vitro. Sodium 80-86 cytochrome P450 family 1 subfamily A member 2 Homo sapiens 136-142 19071883-9 2009 In addition to the clinical pharmacokinetic analysis, the ability of mipomersen sodium to inhibit the major CYP isoform enzymes (namely CYP1A2, CYP2C9, CYP2C19, CYP2D6 and CYP3A4) was evaluated in cryo-preserved human hepatocytes in vitro. Sodium 80-86 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 144-150 19093733-9 2009 TRPV4 and intracellular Ca(2+), PKC and Ca/CaMKII participate in the hypotonic modifications of sodium currents. Sodium 96-102 transient receptor potential cation channel, subfamily V, member 4 Rattus norvegicus 0-5 19053274-4 2008 Our biophysical experiments indicate that the c-MYC quadruplex under physiological conditions is stable and dominates the quadruplex-WC duplex equilibrium in both sodium and potassium buffers. Sodium 163-169 MYC proto-oncogene, bHLH transcription factor Homo sapiens 46-51 18799550-7 2008 Administration of VEGF-121 from day 0 to 14, day 0 to 35, or day 3 to 35 after I/R suppressed the effects of sodium diet on CKD development, while delayed administration of VEGF-121 from day 21 to 35 had no effect. Sodium 109-115 vascular endothelial growth factor A Rattus norvegicus 18-22 18799550-10 2008 These data suggest that early, but not delayed, treatment with VEGF-121 can preserve vascular structure after ischemia and influence chronic renal function in response to elevated sodium intake. Sodium 180-186 vascular endothelial growth factor A Rattus norvegicus 63-67 18816377-0 2008 The chemokine CXCL1/growth related oncogene increases sodium currents and neuronal excitability in small diameter sensory neurons. Sodium 54-60 C-X-C motif chemokine ligand 1 Rattus norvegicus 14-19 18591664-7 2008 A390V-SNTA1 expressed with SCN5A, nNOS, and PMCA4b in heterologous cells increased peak and late sodium current compared with WT-SNTA1, and the increase was partially inhibited by NOS blockers. Sodium 97-103 sodium voltage-gated channel alpha subunit 5 Homo sapiens 27-32 18591664-9 2008 We conclude that the A390V mutation disrupted binding with PMCA4b, released inhibition of nNOS, caused S-nitrosylation of SCN5A, and was associated with increased late sodium current, which is the characteristic biophysical dysfunction for sodium-channel-mediated LQTS (LQT3). Sodium 168-174 sodium voltage-gated channel alpha subunit 5 Homo sapiens 122-127 18591664-10 2008 These results establish an SNTA1-based nNOS complex attached to SCN5A as a key regulator of sodium current and suggest that SNTA1 be considered a rare LQTS-susceptibility gene. Sodium 92-98 sodium voltage-gated channel alpha subunit 5 Homo sapiens 64-69 18388193-6 2008 Our findings provide the first evidence that GH, in concert with IGF-I, stimulates ENaC-mediated sodium transport in the late distal nephron, accounting for the pathogenesis of sodium retention in acromegaly. Sodium 97-103 insulin-like growth factor 1 Rattus norvegicus 65-70 18388193-6 2008 Our findings provide the first evidence that GH, in concert with IGF-I, stimulates ENaC-mediated sodium transport in the late distal nephron, accounting for the pathogenesis of sodium retention in acromegaly. Sodium 177-183 insulin-like growth factor 1 Rattus norvegicus 65-70 18391099-13 2008 These data demonstrate that collecting duct-derived endothelin-1 is important in the following: (1) chronic N(G)-nitro-l-arginine methyl ester-induced hypertension; (2) full expression of pressure-dependent changes in sodium excretion; and (3) control of inner medullary NOS1 and NOS3 activity. Sodium 218-224 endothelin 1 Mus musculus 52-64 18464934-2 2008 Loss-of-function mutations in SCN5A, which encodes the predominant cardiac sodium channel alpha subunit NaV1.5, can cause Brugada syndrome and cardiac conduction disease. Sodium 75-81 sodium voltage-gated channel alpha subunit 5 Homo sapiens 30-35 18464934-2 2008 Loss-of-function mutations in SCN5A, which encodes the predominant cardiac sodium channel alpha subunit NaV1.5, can cause Brugada syndrome and cardiac conduction disease. Sodium 75-81 sodium voltage-gated channel alpha subunit 5 Homo sapiens 104-110 18464934-8 2008 Sodium current was lower when NaV1.5 was coexpressed with mutant beta1 or beta1B subunits than when it was coexpressed with WT subunits. Sodium 0-6 sodium voltage-gated channel alpha subunit 5 Homo sapiens 30-36 18291093-7 2008 These results reveal a new mechanism by which BK can modulate renal sodium excretion: coupling between B2 receptor and activation of membrane-associated iPLA2. Sodium 68-74 bradykinin receptor B2 Homo sapiens 103-114 18052934-8 2008 Ucn2, both separately and in conjunction with captopril, increased urine output, sodium and creatinine excretion and creatinine clearance. Sodium 81-87 urocortin-2 Ovis aries 0-4 18633183-13 2008 In conclusion, the interaction of Ang II with acute-sodium overload exacerbated intrarenal TGF-beta1, alpha-SMA and NF-kappaB expression, independently from changes in blood pressure levels, in normal rats. Sodium 52-58 actin gamma 2, smooth muscle Rattus norvegicus 102-111 18184654-5 2008 Co-expression of MOG1 with Nav1.5 in HEK293 cells increased sodium current densities. Sodium 60-66 sodium voltage-gated channel alpha subunit 5 Homo sapiens 27-33 18184654-7 2008 Western blot analysis revealed that MOG1 increased cell surface expression of Nav1.5, which may be the underlying mechanism by which MOG1 increased sodium current densities. Sodium 148-154 sodium voltage-gated channel alpha subunit 5 Homo sapiens 78-84 18178722-1 2008 Changes in dietary sodium intake are associated with changes in vascular volume and reactivity that may be mediated, in part, by alterations in endothelial nitric oxide synthase (eNOS) activity. Sodium 19-25 nitric oxide synthase 3, endothelial cell Mus musculus 144-177 18178722-1 2008 Changes in dietary sodium intake are associated with changes in vascular volume and reactivity that may be mediated, in part, by alterations in endothelial nitric oxide synthase (eNOS) activity. Sodium 19-25 nitric oxide synthase 3, endothelial cell Mus musculus 179-183 18178722-3 2008 To test the hypothesis that endothelial Cav-1 participates in the dietary sodium-mediated effects on vascular function, we assessed vascular responses and nitric oxide (NO)-mediated mechanisms of vascular relaxation in Cav-1 knockout mice (Cav-1-/-) and wild-type control mice (WT; Cav-1+/+) placed on a high-salt (HS; 4% NaCl) or low-salt (LS; 0.08% NaCl) diet for 16 days. Sodium 74-80 caveolin 1, caveolae protein Mus musculus 40-45 18203179-0 2008 Severe neonatal non-dystrophic myotonia secondary to a novel mutation of the voltage-gated sodium channel (SCN4A) gene. Sodium 91-97 sodium voltage-gated channel alpha subunit 4 Homo sapiens 107-112 18203179-6 2008 Mutations within the voltage-gated sodium channel alpha-subunit gene (SCN4A) have been described in association with several phenotypes including paramyotonia congenita, hyperkalemic or hypokalemic periodic paralysis, and potassium-aggravated myotonias. Sodium 35-41 sodium voltage-gated channel alpha subunit 4 Homo sapiens 70-75 18161988-3 2008 The citrate Km and sodium KNa values are much larger in human than rabbit NaDC1. Sodium 19-25 solute carrier family 13 member 2 Oryctolagus cuniculus 74-79 17977906-12 2008 NHE8 activity, measured as the sodium-dependent rate of intracellular pH recovery from an acid load, was less with thyroid treatment than control. Sodium 31-37 solute carrier family 9 member A8 Rattus norvegicus 0-4 18209489-2 2008 Sodium selenite treatment exerted a profound preventive effect on apoptotic cell death, including p-P38, p-SAPK/JNK, caspases, and PARP activity, and ameliorated astrogliosis and hypomyelination, which occurs in regions of active cell death in the spinal cords of SCI rats. Sodium 0-6 mitogen-activated protein kinase 8 Rattus norvegicus 112-115 20021424-0 2008 Pharmacologic intervention in axonal excitability: in vivo assessment of nodal persistent sodium currents in human neuropathies. Sodium 90-96 nodal growth differentiation factor Homo sapiens 73-78 20021424-8 2008 Administration of sodium channel blockers such as mexiletine, results in marked alleviation of muscle cramping in parallel with a decrease in nodal persistent sodium currents. Sodium 18-24 nodal growth differentiation factor Homo sapiens 142-147 20021424-8 2008 Administration of sodium channel blockers such as mexiletine, results in marked alleviation of muscle cramping in parallel with a decrease in nodal persistent sodium currents. Sodium 159-165 nodal growth differentiation factor Homo sapiens 142-147 20021424-10 2008 Aldose reductase inhibitiors improve nodal sodium currents, as well as nerve conduction, and this can be objectively assessed by threshold tracking. Sodium 43-49 nodal growth differentiation factor Homo sapiens 37-42 17935523-1 2007 AIM: Sodium current (I(Na)) of the mammalian heart is resistant to tetrodotoxin (TTX) due to low TTX affinity of the cardiac sodium channel (Na(v)) isoform Na(v)1.5. Sodium 5-11 immunoglobulin lambda variable 2-18 Homo sapiens 156-164 17959796-6 2007 Coexpression of Fyn with Na(V)1.2 channels decreases sodium currents by increasing the rate of inactivation and causing a negative shift in the voltage dependence of inactivation. Sodium 53-59 FYN proto-oncogene, Src family tyrosine kinase Homo sapiens 16-19 17959797-3 2007 Here we have identified the amino acid residues on Na(V)1.2 channels that coordinate binding of Fyn kinase and mediate inhibition of sodium currents by enhancing fast inactivation. Sodium 133-139 FYN proto-oncogene, Src family tyrosine kinase Homo sapiens 96-99 17959797-4 2007 Fyn kinase binds to a Src homology 3 (SH3)-binding motif in the second half of the intracellular loop connecting domains I and II (L(I-II)) of Na(V)1.2, and mutation of that SH3-binding motif prevents Fyn binding and Fyn enhancement of fast inactivation of sodium currents. Sodium 257-263 FYN proto-oncogene, Src family tyrosine kinase Homo sapiens 0-3 17939993-0 2007 SIK1 is part of a cell sodium-sensing network that regulates active sodium transport through a calcium-dependent process. Sodium 23-29 salt inducible kinase 1 Homo sapiens 0-4 17939993-0 2007 SIK1 is part of a cell sodium-sensing network that regulates active sodium transport through a calcium-dependent process. Sodium 68-74 salt inducible kinase 1 Homo sapiens 0-4 17939993-2 2007 Here we report the existence of a salt-inducible kinase-1 (SIK1) that associates constitutively with the NK regulatory complex and is responsible for increases in its catalytic activity following small elevations in intracellular sodium concentrations. Sodium 230-236 salt inducible kinase 1 Homo sapiens 34-57 17939993-2 2007 Here we report the existence of a salt-inducible kinase-1 (SIK1) that associates constitutively with the NK regulatory complex and is responsible for increases in its catalytic activity following small elevations in intracellular sodium concentrations. Sodium 230-236 salt inducible kinase 1 Homo sapiens 59-63 17939993-3 2007 Increases in intracellular sodium are paralleled by elevations in intracellular calcium through the reversible Na(+)/Ca(2+) exchanger, leading to the activation of SIK1 (Thr-322 phosphorylation) by a calcium calmodulin-dependent kinase. Sodium 27-33 salt inducible kinase 1 Homo sapiens 164-168 17939993-6 2007 These observations illustrate the existence of a distinct intracellular signaling network, with SIK1 at its core, which is triggered by a monovalent cation (Na(+)) and links sodium permeability to its active transport. Sodium 174-180 salt inducible kinase 1 Homo sapiens 96-100 17638382-6 2007 Coexpression of each splice form in Xenopus oocytes with either the human muscle sodium channel gene, hNav1.4, or a Sternopygus ortholog, smNav1.4b, sped the rate of inactivation of the sodium current and shifted the steady-state inactivation toward less negative membrane potentials. Sodium 81-87 sodium voltage-gated channel alpha subunit 4 Homo sapiens 102-109 17512504-7 2007 CONCLUSIONS: Our findings indicate that a decrease in Scn5a expression and significant reduction in sodium current can result in DCM, and support the hypothesis that some mutations in the human SCN5A gene can lead to DCM. Sodium 100-106 sodium voltage-gated channel alpha subunit 5 Homo sapiens 194-199 17712719-1 2007 BACKGROUND: Impaired 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) has been suggested in patients with hypertension or renal disease, where it may contribute to sodium retention and hypertension. Sodium 172-178 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 21-76 17430990-2 2007 Decreased activity of the amiloride-sensitive epithelial Na(+) channel (ENaC) in the apical membrane of alveolar epithelial cells impairs sodium-driven alveolar fluid clearance (AFC) and predisposes to pulmonary oedema. Sodium 138-144 sodium channel, nonvoltage-gated 1 alpha Mus musculus 46-70 17430990-2 2007 Decreased activity of the amiloride-sensitive epithelial Na(+) channel (ENaC) in the apical membrane of alveolar epithelial cells impairs sodium-driven alveolar fluid clearance (AFC) and predisposes to pulmonary oedema. Sodium 138-144 sodium channel, nonvoltage-gated 1 alpha Mus musculus 72-76 17430990-11 2007 These data show that constitutive ENaC activation improved sodium-driven AFC in the mouse lung, and attenuated the severity of hydrostatic pulmonary oedema. Sodium 59-65 sodium channel, nonvoltage-gated 1 alpha Mus musculus 34-38 17630587-8 2007 Although the relevance of endogenous leptin needs further clarification for the control of renal sodium excretion and vascular tone, it appears to be a potential pressure and volume-regulating factor in normal situations. Sodium 97-103 leptin Homo sapiens 37-43 17591909-0 2007 Expression of the sodium-coupled monocarboxylate transporters SMCT1 (SLC5A8) and SMCT2 (SLC5A12) in retina. Sodium 18-24 solute carrier family 5 (sodium/glucose cotransporter), member 12 Mus musculus 81-86 17591909-0 2007 Expression of the sodium-coupled monocarboxylate transporters SMCT1 (SLC5A8) and SMCT2 (SLC5A12) in retina. Sodium 18-24 solute carrier family 5 (sodium/glucose cotransporter), member 12 Mus musculus 88-95 17255103-2 2007 We have identified and characterized two different sodium-coupled monocarboxylate cotransporters (SMCT) from zebrafish (Danio rerio), electrogenic (zSMCTe) and electroneutral (zSMCTn). Sodium 51-57 solute carrier family 5 member 12 Danio rerio 176-182 17068143-5 2007 The CSF-1-induced rise in pH(i) is not blocked by 4,4"-diisothiocyanatostilbene-2,2"-disulfonic acid, an inhibitor of HCO(3)(-) transporters but is abolished by removing extracellular sodium. Sodium 184-190 colony stimulating factor 1 Homo sapiens 4-9 17241128-0 2007 Critical role of sodium in cytosolic [Ca2+] elevations in cultured hippocampal CA1 neurons during anoxic depolarization. Sodium 17-23 carbonic anhydrase 1 Rattus norvegicus 79-82 17382577-1 2007 BACKGROUND: Epidermal growth factor (EGF) has been shown to play a role in the nephromegaly and enhanced sodium reabsorption observed in diabetic nephropathy. Sodium 105-111 epidermal growth factor Homo sapiens 12-35 17382577-1 2007 BACKGROUND: Epidermal growth factor (EGF) has been shown to play a role in the nephromegaly and enhanced sodium reabsorption observed in diabetic nephropathy. Sodium 105-111 epidermal growth factor Homo sapiens 37-40 16868309-5 2006 On a normal-sodium diet, CD ETB KO mice had elevated BP, which increased further during high salt feeding. Sodium 12-18 endothelin receptor type B Mus musculus 28-31 16868309-7 2006 CD ETB KO mice had impaired sodium excretion following acute sodium loading. Sodium 28-34 endothelin receptor type B Mus musculus 3-6 16868309-7 2006 CD ETB KO mice had impaired sodium excretion following acute sodium loading. Sodium 61-67 endothelin receptor type B Mus musculus 3-6 17108170-0 2006 Physiologic regulation of a tetrodotoxin-sensitive sodium influx that mediates a slow afterdepolarization potential in gonadotropin-releasing hormone neurons: possible implications for the central regulation of fertility. Sodium 51-57 gonadotropin releasing hormone 1 Mus musculus 119-149 17200691-6 2006 Both gammaENaC and neutralizing syntaxin1A antibodies blocked native expression as amiloride-sensitive sodium currents were inhibited while munc18-1 antibody reversed this effect. Sodium 103-109 syntaxin 1A Homo sapiens 32-42 16959493-7 2006 Sodium-dependent glutamate uptake, which is mostly mediated by the glutamate transporter GLAST expressed by Muller glial cells, was reduced dose-dependently by rotenone with no changes in GLAST expression. Sodium 0-6 solute carrier family 1 member 3 Rattus norvegicus 89-94 16418303-7 2006 Intrarenal octreotide administration (IROA) prevented sodium retention in CBL rats without changes in renal plasma flow, glomerular filtration rate, or circulating levels of aldosterone and vasopressin. Sodium 54-60 Cbl proto-oncogene Rattus norvegicus 74-77 16908340-6 2006 Though the metal ion transport by Smf1p, the yeast homolog of DCT1, is also a protonmotive force, a slippage of sodium ions was observed. Sodium 112-118 solute carrier family 11 member 2 Homo sapiens 62-66 16773405-5 2006 During the first days after birth, higher urinary AQP2 was observed in boys than in girls (P=0.01) and positively correlated with urinary sodium/potassium (Na/K) ratio (r=0.33, P=0.01). Sodium 138-144 aquaporin 2 Homo sapiens 50-54 16571785-0 2006 Dietary sodium intake regulates the ubiquitin-protein ligase nedd4-2 in the renal collecting system. Sodium 8-14 neural precursor cell expressed, developmentally down-regulated gene 4-like Mus musculus 61-68 16459033-10 2006 A human sodium-dependant multivitamin transporter, hSMVT, was identified by RT-PCR in Y-79. Sodium 8-14 solute carrier family 5 member 6 Homo sapiens 51-56 16284089-11 2006 The observations reveal a pivotal role of SGK1 in insulin-mediated sodium retention and the salt-sensitizing hypertensive effect of high fructose intake. Sodium 67-73 serum/glucocorticoid regulated kinase 1 Mus musculus 42-46 16778331-2 2006 In AME, defective HSD11B2 enzyme activity results in overstimulation of the mineralocorticoid receptor (MR) by cortisol, causing sodium retention, hypokalemia, and salt-dependent hypertension. Sodium 129-135 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 18-25 17319461-4 2006 Leptin has been shown to influence nitric oxide production and natriuresis, and along with chronic sympathetic activation, especially to the kidney, it may lead to sodium retention, systemic vasoconstriction, and blood pressure elevation. Sodium 164-170 leptin Homo sapiens 0-6 16251242-1 2005 Hypertension and sodium retention are features of a diminished 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2). Sodium 17-23 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 63-118 16093448-3 2005 Patients who have congenital NDI and bear mutations in the AVPR2 or AQP2 genes have a "pure" NDI phenotype with loss of water but normal conservation of sodium, potassium, chloride, and calcium. Sodium 153-159 aquaporin 2 Homo sapiens 68-72 16105045-6 2005 Incubation of finely minced mouse renal cortical tissue in tissue culture media for 3 hours resulted in a reduction in brush border membrane vesicles (BBMV) sodium-dependent phosphate transport (NaPi-2A) protein abundance in the presence but not in the absence of heparin. Sodium 157-163 solute carrier family 34 (sodium phosphate), member 1 Mus musculus 195-202 15913580-4 2005 Here, we review the causal link between SIDS and mutations involving the SCN5A-encoded cardiac sodium channel, provide new findings following extensive postmortem genetic testing of long QT syndrome (LQTS)-associated potassium channel genes in a population-based cohort of SIDS, and summarize the current understanding regarding the spectrum and prevalence of cardiac channelopathies in the pathogenesis of SIDS. Sodium 95-101 sodium voltage-gated channel alpha subunit 5 Homo sapiens 73-78 16083715-9 2005 CONCLUSIONS: Chronic inflammation uncovers a potentiating effect of EGFR activation on epithelial electrogenic sodium absorption that would be expected to ameliorate diarrheal symptoms associated with colitis. Sodium 111-117 epidermal growth factor receptor Mus musculus 68-72 15805112-11 2005 TAp73 also activated the bradykinin B2 receptor (B2R) promoter, a developmentally regulated gene involved in regulation of sodium excretion. Sodium 123-129 bradykinin receptor B2 Homo sapiens 49-52 15681398-1 2005 The amiloride-sensitive epithelial sodium channel (ENaC) constitutes a rate-limiting step for sodium (Na+) and water absorption across lung alveolar epithelium. Sodium 35-41 sodium channel, nonvoltage-gated 1 alpha Mus musculus 51-55 15955065-0 2005 Evolutionary and experimental analyses of inorganic phosphate transporter PiT family reveals two related signature sequences harboring highly conserved aspartic acids critical for sodium-dependent phosphate transport function of human PiT2. Sodium 180-186 solute carrier family 20 member 2 Homo sapiens 235-239 15955065-1 2005 The mammalian members of the inorganic phosphate (P(i)) transporter (PiT) family, the type III sodium-dependent phosphate (NaP(i)) transporters PiT1 and PiT2, have been assigned housekeeping P(i) transport functions and are suggested to be involved in chondroblastic and osteoblastic mineralization and ectopic calcification. Sodium 95-101 solute carrier family 20 member 2 Homo sapiens 153-157 15894890-0 2005 Correlation between left ventricular mass and urinary sodium excretion in specific genotypes of CYP11B2. Sodium 54-60 cytochrome P450 family 11 subfamily B member 2 Homo sapiens 96-103 15894890-9 2005 CONCLUSIONS: The -344CC or intron 2 conversion (-/-) genotype in CYP11B2 may be a risk factor for developing sodium-sensitive cardiac hypertrophy. Sodium 109-115 cytochrome P450 family 11 subfamily B member 2 Homo sapiens 65-72 15831816-3 2005 Sodium currents were acquired by whole cell recording on HEK-293 cells transiently expressing Na(V)1.5. Sodium 0-6 immunoglobulin lambda variable 2-18 Homo sapiens 94-102 15772302-0 2005 SGK1: a rapid aldosterone-induced regulator of renal sodium reabsorption. Sodium 53-59 serum/glucocorticoid regulated kinase 1 Mus musculus 0-4 15528393-8 2005 Sodium depletion with furosemide and low-sodium diet produced a strong sodium appetite and induced Fos-ir in SFO and MnPO. Sodium 0-6 FBJ osteosarcoma oncogene Mus musculus 99-102 15528393-8 2005 Sodium depletion with furosemide and low-sodium diet produced a strong sodium appetite and induced Fos-ir in SFO and MnPO. Sodium 41-47 FBJ osteosarcoma oncogene Mus musculus 99-102 15467005-6 2005 The sodium-retaining effect of ANG II is greatly influenced by O2- generation, particularly in the condition of NO deficiency. Sodium 4-10 ANG Canis lupus familiaris 31-34 15638689-3 2005 A sub-monolayer of atomic sodium was deposited on a LiF(001) surface at 40 K. The adsorbed sodium exists at the surface as single atoms and clusters. Sodium 26-32 LIF interleukin 6 family cytokine Homo sapiens 52-55 15638689-3 2005 A sub-monolayer of atomic sodium was deposited on a LiF(001) surface at 40 K. The adsorbed sodium exists at the surface as single atoms and clusters. Sodium 91-97 LIF interleukin 6 family cytokine Homo sapiens 52-55 15596759-2 2004 OBJECTIVE: To describe new mutations in the muscle sodium channel gene SCN4A that cause periodic paralysis. Sodium 51-57 sodium voltage-gated channel alpha subunit 4 Homo sapiens 71-76 15191892-1 2004 We hypothesized that caloric restriction (CR)-induced hypotension would correlate with increased sodium excretion through an atrial natriuretic peptide (ANP)-dependent mechanism. Sodium 97-103 natriuretic peptide type A Mus musculus 125-151 15240817-4 2004 These mice are viable and fertile, and in contrast to mice lacking SGK1 or Akt2, respectively, display normal sodium handling and glucose tolerance. Sodium 110-116 thymoma viral proto-oncogene 2 Mus musculus 75-79 15100098-7 2004 To further establish that the stimulation of sodium transport induced by insulin is related to PIP(3) levels, we transfected A6 cells with human PTEN cDNA and observed a 30% decrease in the natriferic effect of insulin. Sodium 45-51 phosphatase and tensin homolog Homo sapiens 145-149 15100098-8 2004 Similarly, the increase in sodium transport observed by addition of permeant PIP(3) was also reduced by 30% in PTEN-overexpressing cells. Sodium 27-33 phosphatase and tensin homolog Homo sapiens 111-115 15238568-8 2004 In subjects with sodium excretion >190 mmol/d, these associations with the CYP11B2 and AT1R polymorphisms were nonsignificant or in the opposite direction, respectively. Sodium 17-23 cytochrome P450 family 11 subfamily B member 2 Homo sapiens 78-85 15238568-0 2004 Genetic variation in CYP11B2 and AT1R influences heart rate variability conditional on sodium excretion. Sodium 87-93 cytochrome P450 family 11 subfamily B member 2 Homo sapiens 21-28 15238568-7 2004 In subjects with sodium excretion <190 mmol/d (median), supine heart rate, LF, and LF:HF increased and HF decreased with the number of CYP11B2 -344T alleles, and the orthostatic changes in LF, HF, and LF:HF were blunted in carriers of the AT1R 1166C allele. Sodium 17-23 cytochrome P450 family 11 subfamily B member 2 Homo sapiens 138-145 15253723-7 2004 In contrast, EPO treatment at the time of ischemia of rats with ARF significantly prevented the ischemia-induced down-regulation of renal AQPs and sodium transporters and in parallel improved the urinary concentrating capability and renal sodium reabsorption. Sodium 147-153 erythropoietin Rattus norvegicus 13-16 15282825-2 2004 However, the multicomponent transverse relaxation of 23Na (spin 3/2) complicates the determination of tissue sodium concentration from 23Na images with nonzero echo-time. Sodium 109-115 spindlin family member 3 Homo sapiens 59-67 15140887-8 2004 Dimerization of PGRP-Ialpha, which occurs through three-dimensional domain swapping, is mediated by specific binding of sodium ions to a flexible hinge loop, stabilizing the conformation found in the dimer. Sodium 120-126 peptidoglycan recognition protein 3 Homo sapiens 16-27 15140887-9 2004 We further demonstrate sodium-dependent dimerization of PGRP-Ialpha in solution, suggesting a possible mechanism for modulating PGRP activity through the formation of multivalent adducts. Sodium 23-29 peptidoglycan recognition protein 3 Homo sapiens 56-67 15140887-9 2004 We further demonstrate sodium-dependent dimerization of PGRP-Ialpha in solution, suggesting a possible mechanism for modulating PGRP activity through the formation of multivalent adducts. Sodium 23-29 peptidoglycan recognition protein 1 Homo sapiens 56-60 15497505-8 2004 Expression of Hsp9alpha and Hsp90beta was upregulated in the renal cortex during sodium restriction. Sodium 81-87 heat shock protein 90 alpha family class B member 1 Rattus norvegicus 28-37 15497505-12 2004 Hsp90alpha and Hsp90beta upregulation induced by a low-sodium diet together with redistribution in thick ascending limb cells suggests that Hsp90 plays a role in the modulation of sodium reabsorption under these circumstances. Sodium 55-61 heat shock protein 90 alpha family class B member 1 Rattus norvegicus 15-24 15497505-12 2004 Hsp90alpha and Hsp90beta upregulation induced by a low-sodium diet together with redistribution in thick ascending limb cells suggests that Hsp90 plays a role in the modulation of sodium reabsorption under these circumstances. Sodium 180-186 heat shock protein 90 alpha family class B member 1 Rattus norvegicus 15-24 12959947-1 2004 Human prostasin is a membrane-anchored serine peptidase hypothesized to regulate lung epithelial sodium transport. Sodium 97-103 protease, serine 8 (prostasin) Mus musculus 6-15 14670806-0 2004 Changes in dietary sodium consumption modulate GLUT4 gene expression and early steps of insulin signaling. Sodium 19-25 solute carrier family 2 member 4 Rattus norvegicus 47-52 14670806-2 2004 In the present study we investigated the influence of dietary sodium on 1) GLUT4 gene expression, by No the n and Western blotting analysis; 2) in vivo GLUT4 protein translocation, by measuring the GLUT4 protein in plasma membrane and microsome, before and after insulin injection; and 3) insulin signaling, by analyzing basal and insulin-stimulated tyrosine phosphorylation of insulin receptor (IR)-beta, insulin receptor substrate (IRS)-1, and IRS-2. Sodium 62-68 solute carrier family 2 member 4 Rattus norvegicus 75-80 15074615-14 2004 Most chloride and sodium components were shown to originate from sea-salt particles. Sodium 18-24 S13 erythroblastosis (avian) oncogene homolog Homo sapiens 65-68 15016907-1 2004 The mammalian, highly amiloride-sensitive epithelial sodium channel (ENaC) is member of the degenerin/ENaC superfamily of ion channels known to be implicated in sodium homeostasis, mechanosensation, and mechanoperception. Sodium 53-59 sodium channel, nonvoltage-gated 1 alpha Mus musculus 69-73 15016907-1 2004 The mammalian, highly amiloride-sensitive epithelial sodium channel (ENaC) is member of the degenerin/ENaC superfamily of ion channels known to be implicated in sodium homeostasis, mechanosensation, and mechanoperception. Sodium 53-59 sodium channel, nonvoltage-gated 1 alpha Mus musculus 102-106 15261163-0 2004 Altered cyclic expression of epithelial Na+ channel subunits and cystic fibrosis transmembrane conductance regulator in mouse endometrium by a low sodium diet. Sodium 147-153 sodium channel, nonvoltage-gated 1 alpha Mus musculus 29-51 15261163-7 2004 Isc measurements showed that treatment of cultured endometrial epithelial cells with aldosterone, the major hormone expected to be elevated during the low sodium diet, resulted in prominent increase in ENaC channel activity. Sodium 155-161 sodium channel, nonvoltage-gated 1 alpha Mus musculus 202-206 15261163-8 2004 The altered cyclic expression of uterine ENaC and CFTR by a low sodium diet suggests that these ion channels may be affected by elevated circulating aldosterone, which may disrupt reproductive events in the uterus. Sodium 64-70 sodium channel, nonvoltage-gated 1 alpha Mus musculus 41-45 15183505-7 2004 Microinjection of NPY inhibited NMDA-induced phase advances during the late subjective night, even when sodium-dependent action potentials were inhibited by tetrodotoxin. Sodium 104-110 neuropeptide Y Homo sapiens 18-21 14656289-2 2003 Here we identify two novel variants of the sodium-driven chloride bicarbonate exchanger (NCBE) from brain. Sodium 43-49 solute carrier family 4 member 10 Rattus norvegicus 89-93 14534366-5 2003 [3H][Dmt1]DALDA binds with very high affinity to human mu opioid receptor (hMOR) (Kd = 0.199 nM), and Kd and Bmax were reduced by sodium but not Gpp(NH)p [guanosine 5"-(beta,gamma-imido)triphosphate]. Sodium 130-136 doublesex and mab-3 related transcription factor 1 Homo sapiens 5-9 12783779-3 2003 In the present study, a continuous infusion of synthetic human UII (hUII) into the renal artery (RA) in anesthetized rats was found to increase renal blood flow (RBF) and urinary water and sodium excretion (UV and UNaV) in a dose-dependent manner. Sodium 189-195 urotensin 2 Homo sapiens 63-66 12783779-3 2003 In the present study, a continuous infusion of synthetic human UII (hUII) into the renal artery (RA) in anesthetized rats was found to increase renal blood flow (RBF) and urinary water and sodium excretion (UV and UNaV) in a dose-dependent manner. Sodium 189-195 urotensin 2 Homo sapiens 68-72 12783779-7 2003 Nitric oxide (NO) synthase inhibitor NG-nitro-l-arginine methyl ester (l-NAME) completely abolished hUII-induced increases in RBF and water/sodium excretion. Sodium 140-146 urotensin 2 Homo sapiens 100-104 14618246-10 2003 Serum sodium concentrations increased with HYPER-HES and HYPER-DEX to maximal values of 150+/-3 mmol/l and 149+/-4 mmol/l, respectively (baseline 141+/-3 mmol/l, 141+/-1 mmol/l) CONCLUSIONS: Compared to isotonic saline solution, preoperative volume replacement with hyperoncotic colloids improves haemodynamic conditions during the pre-bypass period in patients with normal left ventricular function undergoing coronary artery bypass grafting. Sodium 6-12 ribosome binding protein 1 Homo sapiens 49-52 12906334-8 2003 Western blot analysis indicated that neither sodium supplementation nor deprivation altered hepatic microsomal CYP3A2 levels; however, hepatic CYP2C11 levels significantly increased in rats receiving the largest sodium supplement. Sodium 212-218 cytochrome P450, subfamily 2, polypeptide 11 Rattus norvegicus 143-150 12906334-10 2003 Activity of CYP2C11 was significantly reduced in both rat groups receiving additional sodium supplements. Sodium 86-92 cytochrome P450, subfamily 2, polypeptide 11 Rattus norvegicus 12-19 22063117-9 2003 NAC increases, however, the sodium content of the product. Sodium 28-34 synuclein alpha Homo sapiens 0-3 12878321-1 2003 Microsomal epoxide hydrolase (mEH) is a bifunctional protein that plays a central role in carcinogen metabolism and is also able to mediate the sodium-dependent uptake of bile acids into hepatocytes. Sodium 144-150 epoxide hydrolase 1 Homo sapiens 0-28 12586353-0 2003 NHERF-1 uniquely transduces the cAMP signals that inhibit sodium-hydrogen exchange in mouse renal apical membranes. Sodium 58-64 solute carrier family 9 (sodium/hydrogen exchanger), member 3 regulator 1 Mus musculus 0-7 12506330-0 2002 [Inhibition of sodium currents in acutely isolated hippocampal CA1 neurons of rats by magnesium sulfate]. Sodium 15-21 carbonic anhydrase 1 Rattus norvegicus 63-66 12411468-1 2002 The role of cyclooxygenase-2 (COX-2) in the prolonged regulation of renal function was evaluated during changes in sodium intake and reduction of NO synthesis. Sodium 115-121 prostaglandin-endoperoxide synthase 2 Canis lupus familiaris 30-35 12411468-5 2002 During low sodium intake, COX-2 inhibition elicited a decrease (P<0.05) of both glomerular filtration rate (34%) and renal blood flow (31%). Sodium 11-17 prostaglandin-endoperoxide synthase 2 Canis lupus familiaris 26-31 12411468-6 2002 Sodium excretion only decreased (P<0.05) during the first day of COX-2 inhibition in dogs with normal or high sodium load. Sodium 0-6 prostaglandin-endoperoxide synthase 2 Canis lupus familiaris 68-73 12411468-7 2002 The increase in plasma potassium levels elicited by COX-2 inhibition was greater in dogs with low sodium intake and was enhanced when NO production was inhibited. Sodium 98-104 prostaglandin-endoperoxide synthase 2 Canis lupus familiaris 52-57 12411468-9 2002 The results of this study suggest that COX-2-derived metabolites (1) play a more important role in the long-term regulation of renal hemodynamic when sodium intake is low, (2) protect the renal vasculature from the vasoconstriction secondary to a reduction in NO, (3) are only acutely involved in regulating urinary sodium excretion, and (4) play a more important role in regulating plasma potassium concentration when NO synthesis is reduced. Sodium 150-156 prostaglandin-endoperoxide synthase 2 Canis lupus familiaris 39-44 12411468-9 2002 The results of this study suggest that COX-2-derived metabolites (1) play a more important role in the long-term regulation of renal hemodynamic when sodium intake is low, (2) protect the renal vasculature from the vasoconstriction secondary to a reduction in NO, (3) are only acutely involved in regulating urinary sodium excretion, and (4) play a more important role in regulating plasma potassium concentration when NO synthesis is reduced. Sodium 316-322 prostaglandin-endoperoxide synthase 2 Canis lupus familiaris 39-44 12356854-0 2002 Extracellular sodium interacts with the HERG channel at an outer pore site. Sodium 14-20 potassium voltage-gated channel subfamily H member 2 Homo sapiens 40-44 12230479-22 2002 The metabolism of absorbed icodextrin and the resultant rise in plasma levels of small glucose polymers (DP2 to DP4) do not result in hyperglycemia or hyperinsulinemia, but may result in a small decrease in serum sodium and chloride. Sodium 213-219 transcription factor Dp-2 Homo sapiens 105-108 12091564-0 2002 NRSF causes cAMP-sensitive suppression of sodium current in cultured hippocampal neurons. Sodium 42-48 RE1-silencing transcription factor Rattus norvegicus 0-4 12075477-0 2002 [Effect of SO2 derivatives on sodium currents in acutely isolated rat hippocampal CA1 neurons]. Sodium 30-36 carbonic anhydrase 1 Rattus norvegicus 82-85 12034882-4 2002 The predicted SOS1 protein sequence and comparisons of sodium ion accumulation in wild-type and sos1 plants suggest that SOS1 is involved directly in the transport of sodium ions across the plasma membrane. Sodium 55-61 sodium proton exchanger, putative (NHX7) (SOS1) Arabidopsis thaliana 96-100 12034882-4 2002 The predicted SOS1 protein sequence and comparisons of sodium ion accumulation in wild-type and sos1 plants suggest that SOS1 is involved directly in the transport of sodium ions across the plasma membrane. Sodium 55-61 sodium proton exchanger, putative (NHX7) (SOS1) Arabidopsis thaliana 121-125 12034882-4 2002 The predicted SOS1 protein sequence and comparisons of sodium ion accumulation in wild-type and sos1 plants suggest that SOS1 is involved directly in the transport of sodium ions across the plasma membrane. Sodium 167-173 sodium proton exchanger, putative (NHX7) (SOS1) Arabidopsis thaliana 14-18 12034882-4 2002 The predicted SOS1 protein sequence and comparisons of sodium ion accumulation in wild-type and sos1 plants suggest that SOS1 is involved directly in the transport of sodium ions across the plasma membrane. Sodium 167-173 sodium proton exchanger, putative (NHX7) (SOS1) Arabidopsis thaliana 96-100 12034882-4 2002 The predicted SOS1 protein sequence and comparisons of sodium ion accumulation in wild-type and sos1 plants suggest that SOS1 is involved directly in the transport of sodium ions across the plasma membrane. Sodium 167-173 sodium proton exchanger, putative (NHX7) (SOS1) Arabidopsis thaliana 121-125 12090248-7 2002 whi2 and psr1 psr2 mutants had similar phenotypes, including reduced STRE-mediated gene expression, higher sensitivity to sodium ions and heat shock, and hyper-phosphorylation of Msn2. Sodium 122-128 phosphatase Saccharomyces cerevisiae S288C 9-13 11988490-5 2002 (3) Alterations of I(Ks), I(Kr), and I(Na) (fast sodium current) in long-QT syndrome (LQT1, LQT2, and LQT3, respectively) are reflected in characteristic QT-interval and T-wave changes; LQT1 prolongs QT without widening the T wave. Sodium 49-55 sodium voltage-gated channel alpha subunit 5 Homo sapiens 102-106 11988490-5 2002 (3) Alterations of I(Ks), I(Kr), and I(Na) (fast sodium current) in long-QT syndrome (LQT1, LQT2, and LQT3, respectively) are reflected in characteristic QT-interval and T-wave changes; LQT1 prolongs QT without widening the T wave. Sodium 49-55 potassium voltage-gated channel subfamily Q member 1 Homo sapiens 86-90 11933197-1 2002 Pure non-syndromic, non-dystrophic myotonia in humans is caused by mutations in the genes coding for the skeletal muscle sodium channel (SCN5A) or the skeletal muscle chloride channel (CLCN1) with similar phenotypes. Sodium 121-127 sodium voltage-gated channel alpha subunit 5 Homo sapiens 137-142 11744737-2 2002 In the inner medullary collecting duct of the terminal nephron, the type A natriuretic peptide receptor (NPR-A) plays a major role in determining urinary sodium content. Sodium 154-160 natriuretic peptide receptor 1 Rattus norvegicus 105-110 11922146-5 2001 However, beta3 is unique in causing increased persistent sodium currents. Sodium 57-63 eukaryotic translation elongation factor 1 beta 2 pseudogene 2 Homo sapiens 9-14 11487618-10 2001 The rapid repriming of Nav1.3 suggests that it contributes to the acceleration of repriming of TTX-sensitive (TTX-S) sodium currents that are seen after peripheral axotomy of DRG neurons. Sodium 117-123 sodium voltage-gated channel alpha subunit 3 Homo sapiens 23-29 11390018-0 2001 Blockade of pancreatic polypeptide-sensitive neuropeptide Y (NPY) receptors by agonist peptides is prevented by modulators of sodium transport. Sodium 126-132 neuropeptide Y Homo sapiens 61-64 11390018-2 2001 Ligand binding to rodent pancreatic polypeptide-responding neuropeptide Y (NPY) receptors (here termed PP/NPY receptors), or to cloned Y4 or Y5 receptors, is selectively inhibited by amiloride, peptide or alkylating modulators of sodium transport. Sodium 230-236 neuropeptide Y Homo sapiens 59-73 11380523-9 2001 Omission of sodium from the perfusate resulted in a smooth decline in pHi. Sodium 12-18 glucose-6-phosphate isomerase Rattus norvegicus 70-73 11318960-6 2001 CONCLUSIONS: This study demonstrates that renal glomerular and adrenal AT1 receptors in the dog are coordinately down-regulated by dietary sodium restriction compared with sodium loading, which is distinctly different from the reciprocal regulation observed for rat AT1 receptors in these tissues. Sodium 139-145 angiotensin II receptor type 1 Canis lupus familiaris 71-74 11318960-6 2001 CONCLUSIONS: This study demonstrates that renal glomerular and adrenal AT1 receptors in the dog are coordinately down-regulated by dietary sodium restriction compared with sodium loading, which is distinctly different from the reciprocal regulation observed for rat AT1 receptors in these tissues. Sodium 172-178 angiotensin II receptor type 1 Canis lupus familiaris 71-74 11430469-1 2001 The effects of bidisomide, an antiarrhythmic agent, on sodium current (I(Na)) in isolated rat ventricular myocytes were investigated using a whole cell voltage clamp method. Sodium 55-61 internexin neuronal intermediate filament protein, alpha Rattus norvegicus 71-76 11306713-5 2001 When expressed in Xenopus laevis oocytes, hOAT3 mediated the transport of estrone sulfate (K(m) = 3.1 microM), p-aminohippurate (K(m) = 87.2 microM), methotrexate (K(m) = 10.9 microM), and cimetidine (K(m) = 57.4 microM) in a sodium-independent manner. Sodium 226-232 solute carrier family 22 member 8 Homo sapiens 42-47 11437250-5 2001 VCX1-expressing Arabidopsis plants displayed increased sensitivity to sodium and other ions. Sodium 70-76 Vcx1p Saccharomyces cerevisiae S288C 0-4 11254668-6 2001 Disruption of the dADAR gene results in totally unedited sodium (Para), calcium (Dmca1A), and chloride (DrosGluCl-alpha) channels, a very prolonged recovery from anoxic stupor, a vulnerability to heat shock and increased O2 demands, and neuronal degeneration in aged flies. Sodium 57-63 Adenosine deaminase acting on RNA Drosophila melanogaster 18-23 11160618-3 2001 In the current study, the wild-type D4 dopamine receptor showed an 8-fold decrease in zinc affinity in the presence of 120 mM NaCl, but the binding of zinc to the neutral TMS2 D4-D77N mutant was completely sodium-insensitive. Sodium 206-212 dopamine receptor D4 Homo sapiens 36-56 11130776-2 2000 This association causes the following changes: insulin and leptin resistance with a suppressed biologic activity of natriuretic peptide, which contributes to sodium retention with concomitant expanded cardiopulmonary volume and increased cardiac output. Sodium 158-164 leptin Homo sapiens 59-65 11053350-3 2000 The reduction in submandibular blood flow, which occurred in response to the infusion of ET-1, was associated with a decreased flow of saliva and a diminished output of both sodium and protein. Sodium 174-180 endothelin 1 Felis catus 89-93 10966927-10 2000 Transport by mNaDC-1 is electrogenic, and substrates produced inward currents in the presence of sodium. Sodium 97-103 solute carrier family 13 (sodium-dependent dicarboxylate transporter), member 2 Mus musculus 13-20 10966927-11 2000 The sodium affinity was relatively high in mNaDC-1, with half-saturation constants for sodium of 10 mM (radiotracer experiments) and 28 mM at -50 mV (2-electrode voltage clamp experiments). Sodium 4-10 solute carrier family 13 (sodium-dependent dicarboxylate transporter), member 2 Mus musculus 43-50 10966927-11 2000 The sodium affinity was relatively high in mNaDC-1, with half-saturation constants for sodium of 10 mM (radiotracer experiments) and 28 mM at -50 mV (2-electrode voltage clamp experiments). Sodium 87-93 solute carrier family 13 (sodium-dependent dicarboxylate transporter), member 2 Mus musculus 43-50 10919843-1 2000 Previous electrophysiological experiments on renal cortical collecting ducts indicated that dietary sodium intake and variations in aldosterone plasma levels regulate the abundance of functional epithelial Na channels (ENaC) in the apical plasma membrane. Sodium 100-106 sodium channel, nonvoltage-gated 1 alpha Mus musculus 219-223 11009046-17 2000 Furthermore, ibuprofen decreased lithium excretion suggesting that COX-1 is involved in the re-absorption of sodium and/or water in the proximal tubuli. Sodium 109-115 mitochondrially encoded cytochrome c oxidase I Homo sapiens 67-72 10948090-0 2000 Renal changes induced by a cyclooxygenase-2 inhibitor during normal and low sodium intake. Sodium 76-82 prostaglandin-endoperoxide synthase 2 Canis lupus familiaris 27-43 10948090-1 2000 Cyclooxygenase-2 (COX-2) has been identified in renal tissues under normal conditions, with its expression enhanced during sodium restriction. Sodium 123-129 prostaglandin-endoperoxide synthase 2 Canis lupus familiaris 0-16 10948090-1 2000 Cyclooxygenase-2 (COX-2) has been identified in renal tissues under normal conditions, with its expression enhanced during sodium restriction. Sodium 123-129 prostaglandin-endoperoxide synthase 2 Canis lupus familiaris 18-23 10948090-11 2000 These results suggest that COX-2-derived metabolites (1) are involved in the regulation of sodium excretion in dogs with normal sodium intake, (2) play an important role in the regulation of renal hemodynamic and excretory function in dogs with low sodium intake, and (3) are not involved in the maintenance of the high renin levels during a long-term decrease in sodium intake. Sodium 91-97 prostaglandin-endoperoxide synthase 2 Canis lupus familiaris 27-32 10948090-11 2000 These results suggest that COX-2-derived metabolites (1) are involved in the regulation of sodium excretion in dogs with normal sodium intake, (2) play an important role in the regulation of renal hemodynamic and excretory function in dogs with low sodium intake, and (3) are not involved in the maintenance of the high renin levels during a long-term decrease in sodium intake. Sodium 128-134 prostaglandin-endoperoxide synthase 2 Canis lupus familiaris 27-32 10948090-11 2000 These results suggest that COX-2-derived metabolites (1) are involved in the regulation of sodium excretion in dogs with normal sodium intake, (2) play an important role in the regulation of renal hemodynamic and excretory function in dogs with low sodium intake, and (3) are not involved in the maintenance of the high renin levels during a long-term decrease in sodium intake. Sodium 128-134 prostaglandin-endoperoxide synthase 2 Canis lupus familiaris 27-32 10948090-11 2000 These results suggest that COX-2-derived metabolites (1) are involved in the regulation of sodium excretion in dogs with normal sodium intake, (2) play an important role in the regulation of renal hemodynamic and excretory function in dogs with low sodium intake, and (3) are not involved in the maintenance of the high renin levels during a long-term decrease in sodium intake. Sodium 128-134 prostaglandin-endoperoxide synthase 2 Canis lupus familiaris 27-32 10942166-5 2000 COX inhibition reduced the hypertension and renal vasoconstriction, but enhanced the sodium retention, induced by the lower dose angiotensin II infusion (n = 6). Sodium 85-91 prostaglandin-endoperoxide synthase 1 Canis lupus familiaris 0-3 11015600-6 2000 These findings imply that genetic deficiencies in ANP or natriuretic receptor activity may be underlying causative factors in the etiology of salt-sensitive variants of hypertensive disease and other sodium-retaining disorders, such as congestive heart failure and cirrhosis. Sodium 200-206 natriuretic peptide type A Mus musculus 50-53 10777497-0 2000 Psr1p/Psr2p, two plasma membrane phosphatases with an essential DXDX(T/V) motif required for sodium stress response in yeast. Sodium 93-99 phosphatase Saccharomyces cerevisiae S288C 0-5 10777497-2 2000 In this study, we report the identification of two previously uncharacterized genes, PSR1 and PSR2, that perform an essential function under conditions of sodium ion stress in the yeast Saccharomyces cerevisiae. Sodium 155-161 phosphatase Saccharomyces cerevisiae S288C 85-89 10777497-5 2000 Growth of the psr1psr2 mutant is severely inhibited under conditions of sodium but not potassium ion or sorbitol stress. Sodium 72-78 phosphatase Saccharomyces cerevisiae S288C 14-22 10851391-2 2000 This phenotype is associated with a novel mutation in the voltage-dependent skeletal muscle sodium channel alpha subunit (SCN4A). Sodium 92-98 sodium voltage-gated channel alpha subunit 4 Homo sapiens 122-127 10851391-3 2000 This Pro1158Ser mutation is localized between the fourth and fifth transmembrane segments of domain III in SCN4A and may give rise to a new function; that is, thermosensitive permeability changes of the sodium channel. Sodium 203-209 sodium voltage-gated channel alpha subunit 4 Homo sapiens 107-112 10912759-1 2000 The alpha-adducin gene contributes significantly to hypertension in MHS rats (rats of the Milan hypertensive strain) and in some white and Japanese populations, causing a low renin, sodium, and diuretic-sensitive hypertension. Sodium 182-188 adducin 1 Rattus norvegicus 4-17 10770960-3 2000 This result indicated that serine proteases may be implicated in the regulation of ENaC-mediated sodium transport. Sodium 97-103 sodium channel, nonvoltage-gated 1 alpha Mus musculus 83-87 10792624-1 2000 BACKGROUND: Enhanced expression of the kidney-specific sodium transporter, rBSC1, in the thick ascending limb of Henle (TAL) and of the renal water channel, aquaporin-2 (AQP2), in collecting duct has been identified in rats with congestive heart failure (CHF) as a cause for enhanced sodium and water retention in this condition. Sodium 55-61 aquaporin 2 Rattus norvegicus 157-168 10792624-1 2000 BACKGROUND: Enhanced expression of the kidney-specific sodium transporter, rBSC1, in the thick ascending limb of Henle (TAL) and of the renal water channel, aquaporin-2 (AQP2), in collecting duct has been identified in rats with congestive heart failure (CHF) as a cause for enhanced sodium and water retention in this condition. Sodium 55-61 aquaporin 2 Rattus norvegicus 170-174 10750033-1 2000 Corticosteroid control of distal nephron sodium handling, particularly through the amiloride-sensitive sodium channel (ENaC), has a key role in blood pressure regulation. Sodium 41-47 sodium channel, nonvoltage-gated 1 alpha Mus musculus 119-123 10675242-7 2000 Compared to control monolayers, lipopolysaccharide, prostaglandin E2, IL-1alpha, and TNF-alpha decreased mucosal-to-serosal and net sodium and chloride fluxes and increased serosal-to-mucosal movement of sodium and unmeasured ions. Sodium 132-138 interleukin 1 alpha Homo sapiens 70-79 10675242-7 2000 Compared to control monolayers, lipopolysaccharide, prostaglandin E2, IL-1alpha, and TNF-alpha decreased mucosal-to-serosal and net sodium and chloride fluxes and increased serosal-to-mucosal movement of sodium and unmeasured ions. Sodium 204-210 interleukin 1 alpha Homo sapiens 70-79 10726708-1 2000 The 11 beta-hydroxysteroid dehydrogenase type 2 (11 PHSD2) enzyme inactivates 11 betahydroxy steroids in sodium-transporting epithelia such as the kidney, thus protecting the non-selective mineralocorticoid receptor (MR) from occupation by cortisol in humans. Sodium 105-111 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 4-47 10684301-4 2000 Overexpression of epsilon-epitope-tagged Pit-2 transporters in NIH 3T3 cells resulted in a marked increase in sodium-dependent P(i) uptake. Sodium 110-116 solute carrier family 20, member 2 Mus musculus 41-46 10617665-2 2000 The retinal rod Na/Ca-K exchanger (NCKX) is a unique calcium extrusion protein utilizing both inward sodium gradient and outward potassium gradient. Sodium 101-107 solute carrier family 24 member 1 Homo sapiens 35-39 10567848-0 2000 Effect of epidermal growth factor on sodium-dependent L-alanine transport in LLC-PK1 cells. Sodium 37-43 epidermal growth factor Sus scrofa 10-33 10567848-3 2000 However, prolonged (16 h) incubation with 2 and 20 ng/ml of EGF resulted in significant increases in sodium-dependent L-alanine uptake as compared with controls. Sodium 101-107 epidermal growth factor Sus scrofa 60-63 10567848-4 2000 Treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA; 20 ng/ ml) caused a marked increase in sodium-dependent L-alanine uptake after both 2 and 16 h of incubation, and the treatment with TPA (20 ng/ml) EGF (20 ng/ml) for 16 h resulted in significant acceleration of the TPA-stimulated increase in L-alanine uptake by LLC-PK1 cells. Sodium 97-103 epidermal growth factor Sus scrofa 206-209 10765110-10 2000 Water, sodium and urea excretion rates were increased in all groups infused with Ang-(1-7); after the combination of Ang-(1-7) + EXP 3174, all increases were higher than after every substance alone; however, statistical significance (p<0.05) was reached in sodium excretion values only. Sodium 7-13 ANG Canis lupus familiaris 81-84 10707899-9 1999 Moreover, this pHi recovery was completely blocked in the absence of sodium or on addition of DIDS, confirming that the Na+-HCO3 cotransporter (NBC) is present. Sodium 69-75 glucose-6-phosphate isomerase Rattus norvegicus 15-18 10599760-4 1999 METHODS: Single-stranded conformational polymorphism (SSCP) analysis and PCR direct sequencing were used to screen the skeletal muscle alpha1-sodium channel gene (SCN4A) for a mutation in our family. Sodium 142-148 sodium voltage-gated channel alpha subunit 4 Homo sapiens 163-168 10556521-0 1999 Cloning and functional characterization of the human sodium-dependent vitamin C transporters hSVCT1 and hSVCT2. Sodium 53-59 solute carrier family 23 member 1 Homo sapiens 93-99 10555096-1 1999 BACKGROUND: Earlier studies have indicated that the atrial natriuretic factor prohormone fragment 31-67 (Pro ANF31-67) has important effects for the promotion of sodium excretion and vasodilation in several animal species. Sodium 162-168 natriuretic peptide A Canis lupus familiaris 52-77 10521407-2 1999 Here we report that the vesicle traffic regulatory (SNARE (soluble N-ethylmaleimide-sensitive factor attachment protein receptor)) protein, syntaxin 1A (S1A), inhibits ENaC mediated sodium entry. Sodium 182-188 syntaxin 1A Homo sapiens 140-151 10521407-2 1999 Here we report that the vesicle traffic regulatory (SNARE (soluble N-ethylmaleimide-sensitive factor attachment protein receptor)) protein, syntaxin 1A (S1A), inhibits ENaC mediated sodium entry. Sodium 182-188 syntaxin 1A Homo sapiens 153-156 10521407-7 1999 Immunoprecipitation of syntaxin 1A from the sodium-transporting epithelial cell line, A6, co-precipitates ENaC. Sodium 44-50 syntaxin 1A Homo sapiens 23-34 10521407-8 1999 These findings indicate that syntaxin 1A and other members of the SNARE machinery are involved in the control of plasma membrane ENaC content, and they suggest that SNARE proteins participate in the regulation of sodium absorption in relation to agonist mediated vesicle insertion-retrieval processes. Sodium 213-219 syntaxin 1A Homo sapiens 29-40 10515937-4 1999 Deletion of CKB1 increased the salt sensitivity of a strain lacking Ena1 ATPase, the major determinant for sodium efflux, suggesting that the function of the kinase is not mediated by Ena1. Sodium 107-113 casein kinase 2 regulatory subunit CKB1 Saccharomyces cerevisiae S288C 12-16 11245090-0 1999 Bepridil inhibition of sodium current in rat hippocampal CA1 neurons. Sodium 23-29 carbonic anhydrase 1 Rattus norvegicus 57-60 11245090-7 1999 CONCLUSION: Bepridil blocked voltage-dependent sodium current of hippocampal CA1 neurons and might have therapeutic actions for ischemia-induced brain damage. Sodium 47-53 carbonic anhydrase 1 Rattus norvegicus 77-80 10478474-1 1999 Collision-induced dissociation (CID) spectra of sodium ion complexes ([M+Na]+ ions), produced by FAB-MS of methyl ester derivatives of ganglioside, indicate the length of the fatty acyl chain of the ceramide moieties without chemical degradation. Sodium 48-54 FA complementation group B Homo sapiens 97-100 10444029-0 1999 Glomerular ultrafiltration of IGF-I may contribute to increased renal sodium retention in diabetic nephropathy. Sodium 70-76 insulin-like growth factor 1 Rattus norvegicus 30-35 10444029-3 1999 By this route, ultrafiltered IGF-I may increase tubular epithelial cell sodium absorption in overt diabetic nephropathy. Sodium 72-78 insulin-like growth factor 1 Rattus norvegicus 29-34 10391915-3 1999 The amino acid transport activity induced by the co-expression of 4F2hc and LAT-2 was sodium-independent and showed broad specificity for small and large zwitterionic amino acids, as well as bulky analogs (e.g. BCH (2-aminobicyclo-(2,2,1)-heptane-2-carboxylic acid)). Sodium 86-92 solute carrier family 3 member 2 Homo sapiens 66-71 10681655-9 1999 Indeed, recent findings indicate that besides regulating appetite leptin may play a role in sympathico-activation, insulin metabolism, renal sodium handling and hematopoiesis. Sodium 141-147 leptin Homo sapiens 66-72 10358072-3 1999 LST-1 transports taurocholate (Km = 13.6 microM) in a sodium-independent manner. Sodium 54-60 leukocyte specific transcript 1 Homo sapiens 0-5 10435855-2 1999 Moreover, recent studies in rodents have shown that leptin in high doses decreases urine osmolality and increases water intake, together with renal sodium and water excretion. Sodium 148-154 leptin Homo sapiens 52-58 10411326-6 1999 Mutations in 11beta-HSD2 result in sodium retention and severe hypertension, account for the syndrome of apparent mineralocorticoid excess and may be responsible for other forms of hypertension. Sodium 35-41 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 13-24 10334808-10 1999 In congenital 11beta-HSD deficiency and after administration of 11beta-HSD inhibitors, suppression of 11beta-HSD2 activity in the kidney has been believed to cause renal mineralocorticoid excess, resulting in sodium retention and hypertension. Sodium 209-215 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 102-113 10207057-6 1999 In addition, hal4 hal5 and trk1 trk2 mutants exhibit similar phenotypes: (i) they are deficient in potassium uptake; (ii) their growth is sensitive to a variety of toxic cations, including lithium, sodium, calcium, tetramethylammonium, hygromycin B, and low pH; and (iii) they exhibit increased uptake of methylammonium, an indicator of membrane potential. Sodium 198-204 Trk2p Saccharomyces cerevisiae S288C 32-36 10218481-1 1999 An unusual form of painful congenital myotonia is associated with a novel SCN4A mutation causing a valine to methionine substitution in the domain 1/S6 segment of the skeletal muscle sodium channel. Sodium 183-189 sodium voltage-gated channel alpha subunit 4 Homo sapiens 74-79 10205232-1 1999 Heart-transplant recipients (Htx) generally present with body fluid and sodium handling abnormalities and hypertension. Sodium 72-78 Zic family member 3 Homo sapiens 29-32 10205232-7 1999 Enhanced urinary sodium (1650+/-370% versus 450+/-150%, P=0.01), cGMP, and water excretions were observed in Htx and urinary cGMP positively correlated with natriuresis in 6 of the Htx subjects. Sodium 17-23 Zic family member 3 Homo sapiens 109-112 10419018-3 1999 Loss of 11beta-HSD2 expression may be important in sodium balance and blood pressure control in some patients with renal disease. Sodium 51-57 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 8-19 10074485-1 1999 Deficiency of 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) in humans leads to the syndrome of apparent mineralocorticoid excess (SAME), in which cortisol illicitly occupies mineralocorticoid receptors, causing sodium retention, hypokalemia, and hypertension. Sodium 222-228 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 14-69 10334590-4 1999 Mucosal application of C. perfringens enterotoxin resulted in prompt increases in short-circuit current coupled with a reduction in transepithelial resistance consistent with movement of sodium and other cations smaller than diethanolamine from mucosa to serosa. Sodium 187-193 cpe Clostridium perfringens 38-49 9920939-3 1999 Sodium reabsorption was decreased within 2 h by 3-deazaadenosine, a competitive inhibitor of SAHHase, with a half inhibitory concentration between 40 and 50 microM. Sodium 0-6 adenosylhomocysteinase Homo sapiens 93-100 9950958-9 1999 These data indicate that under normal sodium intake, increases in MBF and CBF caused by ACE inhibition are primarily due to reduced intrarenal ANG II levels. Sodium 38-44 angiotensin I converting enzyme Canis lupus familiaris 88-91 10233691-0 1999 Granulocyte-macrophage colony-stimulating factor and interleukin-3 cause basophil histamine release by a common pathway: downregulation by sodium. Sodium 139-145 colony stimulating factor 2 Homo sapiens 0-48 10233691-0 1999 Granulocyte-macrophage colony-stimulating factor and interleukin-3 cause basophil histamine release by a common pathway: downregulation by sodium. Sodium 139-145 interleukin 3 Homo sapiens 53-66 9856972-1 1998 -Dopamine, via D1-like receptors, stimulates the activity of both protein kinase A (PKA) and protein kinase C (PKC), which results in inhibition of renal sodium transport. Sodium 154-160 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 66-82 9856972-1 1998 -Dopamine, via D1-like receptors, stimulates the activity of both protein kinase A (PKA) and protein kinase C (PKC), which results in inhibition of renal sodium transport. Sodium 154-160 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 84-87 9851798-11 1998 The data indicate that 11betaHSD2 in fetal life principally modulates ligand access to the GR in most fetal tissues, notably glomeruli and tubules in the developing kidney, testis, and periderm, and this may be have ramifications for fetal sodium homeostasis and differentiation. Sodium 240-246 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 23-33 10048495-11 1998 Taken together our studies suggest that the abundance of NPr-C in adipose tissue may play a significant role in explaining at least part of the sodium retention characteristic of obesity associated hypertension. Sodium 144-150 natriuretic peptide receptor 3 Homo sapiens 57-62 9731751-0 1998 Activation of the sodium/hydrogen exchanger via the fibronectin-integrin pathway results in hematopoietic stimulation. Sodium 18-24 fibronectin 1 Mus musculus 52-63 9729514-10 1998 Proximal and distal fractional reabsorption of sodium decreased in the ADM-infused kidney. Sodium 47-53 adrenomedullin Canis lupus familiaris 71-74 9750952-5 1998 Amylin stimulates sodium/water reabsorption from the basolateral side of the proximal tubules and plays a role in sodium homeostasis. Sodium 18-24 islet amyloid polypeptide Rattus norvegicus 0-6 9750952-5 1998 Amylin stimulates sodium/water reabsorption from the basolateral side of the proximal tubules and plays a role in sodium homeostasis. Sodium 114-120 islet amyloid polypeptide Rattus norvegicus 0-6 9725828-3 1998 Cells with null alleles in both STD1 and its homologue, MTH1, manifest numerous phenotypes observed in calcineurin mutants, including sodium, lithium, manganese, and hydroxyl ion sensitivity, as well as alpha factor toxicity. Sodium 134-140 Mth1p Saccharomyces cerevisiae S288C 56-60 9727364-0 1998 Function and expression of a novel rat salt-tolerant protein: evidence of a role in cellular sodium metabolism. Sodium 93-99 thyroid hormone receptor interactor 10 Rattus norvegicus 39-60 9727364-8 1998 These results suggest that STP may play an important role in salt sensitivity through cellular sodium metabolism by mediating signal transduction and a hormone-dependent transcription mechanism. Sodium 95-101 thyroid hormone receptor interactor 10 Rattus norvegicus 27-30 9739038-0 1998 Epidermal growth factor and human growth hormone induce two sodium-dependent arginine transport systems after massive enterectomy. Sodium 60-66 epidermal growth factor Homo sapiens 0-23 9692746-0 1998 Sodium currents in isolated rat CA1 neurons after kindling epileptogenesis. Sodium 0-6 carbonic anhydrase 1 Rattus norvegicus 32-35 9692746-3 1998 We compared sodium currents in acutely isolated CA1 neurons from kindled rats with those in matched controls, one day and five weeks after cessation of kindling stimulations. Sodium 12-18 carbonic anhydrase 1 Rattus norvegicus 48-51 9692746-4 1998 The sodium current in CA1 neurons was tetrodotoxin sensitive and inactivated completely with two time-constants. Sodium 4-10 carbonic anhydrase 1 Rattus norvegicus 22-25 9888610-1 1998 The stimulation of the zona glomerulosa phenotype by a low sodium diet is characterised by increased expression of aldosterone synthase accompanied by increases in (pro)renin, bFGF, c-fos and c-jun gene transcription. Sodium 59-65 cytochrome P450, family 11, subfamily b, polypeptide 1 Rattus norvegicus 115-135 9693717-4 1998 The Pho84 protein catalyzes a proton-coupled phosphate transport at acidic pH, while the Pho89 protein catalyzes a sodium-dependent phosphate uptake at alkaline pH. Sodium 115-121 Pho89p Saccharomyces cerevisiae S288C 89-94 9654228-1 1998 INTRODUCTION: Inherited long QT syndrome (LQTS) recently has been associated with mutations in genes coding for potassium (KVLQT1, KCNE1, and HERG) or sodium (SCN5A) ion channels involved in regulating either sodium inward or potassium outward currents of heart cells, resulting in prolongation of the repolarization period. Sodium 151-157 sodium voltage-gated channel alpha subunit 5 Homo sapiens 159-164 9654228-1 1998 INTRODUCTION: Inherited long QT syndrome (LQTS) recently has been associated with mutations in genes coding for potassium (KVLQT1, KCNE1, and HERG) or sodium (SCN5A) ion channels involved in regulating either sodium inward or potassium outward currents of heart cells, resulting in prolongation of the repolarization period. Sodium 209-215 potassium voltage-gated channel subfamily Q member 1 Homo sapiens 123-129 9654228-1 1998 INTRODUCTION: Inherited long QT syndrome (LQTS) recently has been associated with mutations in genes coding for potassium (KVLQT1, KCNE1, and HERG) or sodium (SCN5A) ion channels involved in regulating either sodium inward or potassium outward currents of heart cells, resulting in prolongation of the repolarization period. Sodium 209-215 potassium voltage-gated channel subfamily H member 2 Homo sapiens 142-146 9654228-1 1998 INTRODUCTION: Inherited long QT syndrome (LQTS) recently has been associated with mutations in genes coding for potassium (KVLQT1, KCNE1, and HERG) or sodium (SCN5A) ion channels involved in regulating either sodium inward or potassium outward currents of heart cells, resulting in prolongation of the repolarization period. Sodium 209-215 sodium voltage-gated channel alpha subunit 5 Homo sapiens 159-164 9570196-3 1998 Genes responsible for LQT1, LQT2, and LQT3 have been identified as cardiac potassium channel genes (KVLQT1, HERG) and the cardiac sodium channel gene (SCN5A). Sodium 130-136 potassium voltage-gated channel subfamily Q member 1 Homo sapiens 22-26 9570196-3 1998 Genes responsible for LQT1, LQT2, and LQT3 have been identified as cardiac potassium channel genes (KVLQT1, HERG) and the cardiac sodium channel gene (SCN5A). Sodium 130-136 potassium voltage-gated channel subfamily H member 2 Homo sapiens 28-32 9570196-3 1998 Genes responsible for LQT1, LQT2, and LQT3 have been identified as cardiac potassium channel genes (KVLQT1, HERG) and the cardiac sodium channel gene (SCN5A). Sodium 130-136 sodium voltage-gated channel alpha subunit 5 Homo sapiens 38-42 9570196-3 1998 Genes responsible for LQT1, LQT2, and LQT3 have been identified as cardiac potassium channel genes (KVLQT1, HERG) and the cardiac sodium channel gene (SCN5A). Sodium 130-136 sodium voltage-gated channel alpha subunit 5 Homo sapiens 151-156 9597116-10 1998 In conclusion, COMT inhibition using entacapone results in a mainly DA1 receptor mediated natriuresis involving inhibition of tubular transport processes, supporting a role for dopamine metabolism in sodium homeostasis. Sodium 200-206 catechol-O-methyltransferase Rattus norvegicus 15-19 9561804-7 1998 Further studies showed that cyclohexyladenosine and insulin, additional agonists of sodium transport in A6 cells, also stimulated phosphorylation of MARCKS. Sodium 84-90 insulin S homeolog Xenopus laevis 52-59 9495259-1 1998 Endothelin-1 (ET-1) is a cardiovascular peptide that binds to two distinct receptors, ET(A) and ET(B), resulting in systemic and regional vasoconstriction, alteration in sodium excretion, mitogenesis, and release of other vasoactive peptides such as atrial natriuretic peptide (ANP). Sodium 170-176 endothelin receptor type A Canis lupus familiaris 86-91 9495259-11 1998 Despite the lower mean arterial pressure and circulating ANP in the ET(A) receptor antagonist group, the absolute decrease in sodium excretion from baseline was less compared with the untreated CHF control group. Sodium 126-132 endothelin receptor type A Canis lupus familiaris 68-73 9493562-18 1998 For example, leptin increases renal sodium and water excretion, apparently through a direct tubular action. Sodium 36-42 leptin Homo sapiens 13-19 9493562-21 1998 In conclusion, leptin may act as a mediator linking body adiposity with changes in insulin action, sympathetic neural outflow and renal sodium excretion. Sodium 136-142 leptin Homo sapiens 15-21 9670610-4 1998 The dose-limiting toxicities of RTA ITs include manifestation of VLS presenting as decreased urinary sodium excretion, hypoalbuminemia, fatigue, hypotonia, myalgia, pulmonary edema, or rhabdomyolysis. Sodium 101-107 MAS related GPR family member F Homo sapiens 32-35 9359910-0 1997 Changes in subsarcolemmal sodium concentration measured by Na-Ca exchanger activity during Na-pump inhibition and beta-adrenergic stimulation in guinea-pig ventricular myocytes. Sodium 26-32 nascent polypeptide-associated complex subunit alpha Cavia porcellus 59-64 9359910-1 1997 Measurement of Na-Ca exchange activity was used to examine subsarcolemmal sodium levels ([Na+]s) in single, voltage-clamped guinea-pig cardiac myocytes while Na-K pump activity was modulated pharmacologically. Sodium 74-80 nascent polypeptide-associated complex subunit alpha Cavia porcellus 15-20 9439811-1 1997 The norepinephrine transporter (NET) terminates noradrenergic neurotransmission at synapse by high-affinity sodium-dependent reuptake into presynaptic terminals, and thus serves as a marker of differentiation of noradrenergic neurons. Sodium 108-114 solute carrier family 6 member 2 Rattus norvegicus 4-30 9392583-1 1997 Mutations in the skeletal muscle voltage-gated sodium channel alpha-subunit gene (SCN4A) have been associated with a spectrum of inherited nondystrophic myotonias and periodic paralyses. Sodium 47-53 sodium voltage-gated channel alpha subunit 4 Homo sapiens 82-87 9322991-11 1997 Leptin in high doses increases renal sodium and water excretion, apparently through a direct tubular action. Sodium 37-43 leptin Homo sapiens 0-6 9284273-9 1997 The expression of alpha mENaC transcripts increases transiently in the lungs at birth (2.5-fold), as for alpha1 Na+-K+-ATPase mRNAs (1.5-fold), suggesting that the expression of several components of the sodium transport system is modulated in the lungs at that time. Sodium 204-210 sodium channel, nonvoltage-gated 1 alpha Mus musculus 24-29 9236220-5 1997 Phosphorylation at the second PKA site (serine-573) was necessary and sufficient to diminish sodium current amplitude. Sodium 93-99 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 30-33 9236220-7 1997 Introduction of a negative charge at site 2 by substitution of serine-573 with an aspartate constitutively reduced the basal level of sodium current, indicating that the attenuation of sodium current by phosphorylation of site 2 by PKA results from the introduction of a negative charge at this site. Sodium 134-140 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 232-235 9236220-7 1997 Introduction of a negative charge at site 2 by substitution of serine-573 with an aspartate constitutively reduced the basal level of sodium current, indicating that the attenuation of sodium current by phosphorylation of site 2 by PKA results from the introduction of a negative charge at this site. Sodium 185-191 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 232-235 9276478-2 1997 We examined the effect of a recombinant mouse DMPK on the functional properties of human skeletal muscle (hSkM1) and cardiac (hH1) voltage-gated sodium channels in the Xenopus oocyte expression system. Sodium 145-151 H1.5 linker histone, cluster member Homo sapiens 126-129 9276478-3 1997 Co-expression of DMPK with hSkM1 in oocytes resulted in significantly lower peak sodium current amplitude as compared to cells expressing hSkM1 alone in agreement with a previous report. Sodium 81-87 DM1 protein kinase Rattus norvegicus 17-21 9276478-3 1997 Co-expression of DMPK with hSkM1 in oocytes resulted in significantly lower peak sodium current amplitude as compared to cells expressing hSkM1 alone in agreement with a previous report. Sodium 81-87 sodium voltage-gated channel alpha subunit 4 Homo sapiens 27-32 9258207-4 1997 Atrial natriuretic factor alone increased sodium excretion from a baseline of 25 +/- 7 microEq/min to 158 +/- 24 microEq/min (P < 0.05), whereas creatinine clearance was elevated by 9 mL/min (P < 0.05). Sodium 42-48 natriuretic peptide A Canis lupus familiaris 0-25 9142203-6 1997 The unusual well being with very high sodium concentrations may have resulted from osmoreceptor dysfunction, presumably caused by hypothalamic involvement as well as by the high CSF protein. Sodium 38-44 colony stimulating factor 2 Homo sapiens 178-181 9312939-5 1997 Elevation of extracellular concentration of sodium ions (from 140 mM till 200-220 mM), but did not tonicity reduced cellular swelling, water accumulation in tissue, prevented loss of myoglobin and ATP, phosphocreatine level. Sodium 44-50 myoglobin Homo sapiens 183-192 9186871-3 1997 Since plasminogen activator inhibitor type 1 (PAI-1) is a major inhibitor of matrix degradation and elevated plasma PAI-1 levels are reported to be associated with increased low-density lipoprotein (LDL) cholesterol, PAI-1 was examined in the kidneys of rats fed a sodium-deficient diet, with or without cholesterol. Sodium 265-271 serpin family E member 2 Rattus norvegicus 46-51 9186871-3 1997 Since plasminogen activator inhibitor type 1 (PAI-1) is a major inhibitor of matrix degradation and elevated plasma PAI-1 levels are reported to be associated with increased low-density lipoprotein (LDL) cholesterol, PAI-1 was examined in the kidneys of rats fed a sodium-deficient diet, with or without cholesterol. Sodium 265-271 serpin family E member 2 Rattus norvegicus 116-121 9186871-3 1997 Since plasminogen activator inhibitor type 1 (PAI-1) is a major inhibitor of matrix degradation and elevated plasma PAI-1 levels are reported to be associated with increased low-density lipoprotein (LDL) cholesterol, PAI-1 was examined in the kidneys of rats fed a sodium-deficient diet, with or without cholesterol. Sodium 265-271 serpin family E member 2 Rattus norvegicus 116-121 9039044-0 1997 Amylin stimulates proximal tubular sodium transport and cell proliferation in the rat kidney. Sodium 35-41 islet amyloid polypeptide Rattus norvegicus 0-6 9039044-7 1997 We conclude that amylin acts on renal proximal tubules to promote sodium and water reabsorption and cell proliferation. Sodium 66-72 islet amyloid polypeptide Rattus norvegicus 17-23 8995537-3 1997 Here we report that nociceptin is physiologically active in vivo and produces marked changes in the renal excretion of water and sodium. Sodium 129-135 prepronociceptin Rattus norvegicus 20-30 8995537-4 1997 In conscious Sprague-Dawley rats, intravenous infusion of nociceptin produced a profound increase in urine flow rate and decrease in urinary sodium excretion. Sodium 141-147 prepronociceptin Rattus norvegicus 58-68 8942728-7 1996 IGF-I in vivo reversed most of these changes; IGF-I in vitro enhanced sodium-dependent glucose absorption but had no other effects. Sodium 70-76 insulin-like growth factor 1 Rattus norvegicus 46-51 8917568-3 1996 One form of LQTS (LQT3) has been linked to the human cardiac voltage-gated sodium channel gene (SCN5A). Sodium 75-81 sodium voltage-gated channel alpha subunit 5 Homo sapiens 96-101 8945974-1 1996 The purpose of this study was to determine whether high plasma levels of atrial natriuretic peptide (ANP) in compensated heart failure are important in the maintenance of sodium balance. Sodium 171-177 natriuretic peptide A Canis lupus familiaris 73-99 8945974-1 1996 The purpose of this study was to determine whether high plasma levels of atrial natriuretic peptide (ANP) in compensated heart failure are important in the maintenance of sodium balance. Sodium 171-177 natriuretic peptide A Canis lupus familiaris 101-104 8945974-8 1996 These results indicate that ANP plays a critical role in promoting sodium excretion in the early stages of cardiac dysfunction. Sodium 67-73 natriuretic peptide A Canis lupus familiaris 28-31 8831588-5 1996 RESULTS: Jejunal and ileal tissue responded to serosal addition of IL-10 with a transient decrease in short-circuit current reflecting an IL-10-induced increase in net sodium and chloride absorption because of an increase in mucosal to serosal ion movement. Sodium 168-174 interleukin 10 Rattus norvegicus 67-72 8831588-5 1996 RESULTS: Jejunal and ileal tissue responded to serosal addition of IL-10 with a transient decrease in short-circuit current reflecting an IL-10-induced increase in net sodium and chloride absorption because of an increase in mucosal to serosal ion movement. Sodium 168-174 interleukin 10 Rattus norvegicus 138-143 8831588-10 1996 CONCLUSIONS: This study shows that IL-10 enhances intestinal electroneutral sodium and chloride absorption, inhibits stimulated chloride secretion, and under some secretory conditions stimulates bicarbonate secretion. Sodium 76-82 interleukin 10 Rattus norvegicus 35-40 8770164-2 1996 It has been suggested that medullary ET-1 may affect water and sodium absorption along the collecting ducts in an autocrine fashion. Sodium 63-69 endothelin 1 Mus musculus 37-41 8760245-14 1996 beta 2-Adrenoceptor activation results in increases in Na-K-ATPase and Na transport as a consequence of increased apical sodium entry. Sodium 121-127 adrenoceptor beta 2 Rattus norvegicus 0-19 8613987-4 1996 The enthalpic contribution to the free energy of sodium binding is equal to -27 kcal/mol and -21 kcal/mol in the TM-free and TM-bound thrombin forms, respectively. Sodium 49-55 thrombomodulin Homo sapiens 125-127 8613987-5 1996 Finally, the entropy change for sodium binding was also affected by TM, being equal to -83 cal/(mol deg) and -58 cal/(mol deg) in TM-free and TM-bound thrombin species, respectively. Sodium 32-38 thrombomodulin Homo sapiens 68-70 8613987-5 1996 Finally, the entropy change for sodium binding was also affected by TM, being equal to -83 cal/(mol deg) and -58 cal/(mol deg) in TM-free and TM-bound thrombin species, respectively. Sodium 32-38 thrombomodulin Homo sapiens 130-132 8613987-5 1996 Finally, the entropy change for sodium binding was also affected by TM, being equal to -83 cal/(mol deg) and -58 cal/(mol deg) in TM-free and TM-bound thrombin species, respectively. Sodium 32-38 thrombomodulin Homo sapiens 130-132 8613987-10 1996 Therefore, the effect of sodium binding to thrombin on the hydrolysis of human Protein C was extensively investigated. Sodium 25-31 protein C, inactivator of coagulation factors Va and VIIIa Homo sapiens 79-88 8613987-12 1996 Application of thermodynamic principles demonstrated that the Na+-thrombomodulin linkage contributes, under physiological conditions of sodium activity and temperature, to reduce significantly the transition-state stabilization free energy for Protein C hydrolysis. Sodium 136-142 thrombomodulin Homo sapiens 66-80 8613987-12 1996 Application of thermodynamic principles demonstrated that the Na+-thrombomodulin linkage contributes, under physiological conditions of sodium activity and temperature, to reduce significantly the transition-state stabilization free energy for Protein C hydrolysis. Sodium 136-142 protein C, inactivator of coagulation factors Va and VIIIa Homo sapiens 244-253 8867036-0 1996 Veratridine-enhanced persistent sodium current induces bursting in CA1 pyramidal neurons. Sodium 32-38 carbonic anhydrase 1 Rattus norvegicus 67-70 8867036-8 1996 The present results demonstrate that veratridine enhances the slowly inactivating sodium current, leading to the development of negative slope resistance and induction of bursting in rat hippocampal CA1 pyramidal neurons. Sodium 82-88 carbonic anhydrase 1 Rattus norvegicus 199-202 8603590-1 1996 Atrial (ANP), brain (BNP), and C-type natriuretic peptide (CNP) belong to a family of hormones important in blood pressure and sodium homeostasis. Sodium 127-133 natriuretic peptide type B Mus musculus 21-24 8589728-3 1996 In vivo, ENaC constitutes the limiting step for sodium absorption in epithelial cells that line the distal renal tubule, distal colon and the duct of several exocrine glands. Sodium 48-54 sodium channel, nonvoltage-gated 1 alpha Mus musculus 9-13 8671811-10 1996 Sodium-dependent glucose transport was preserved in monolayers exposed to HDL. Sodium 0-6 HDL Sus scrofa 74-77 8833340-0 1996 Paramyotonia congenita mutations reveal different roles for segments S3 and S4 of domain D4 in hSkM1 sodium channel gating. Sodium 101-107 sodium voltage-gated channel alpha subunit 4 Homo sapiens 95-100 8611352-2 1996 In cell culture, lowering sodium in the medium reduces growth factor-stimulated Na+/H+ exchange activity, intracellular pH (pHi), and DNA synthesis. Sodium 26-32 glucose-6-phosphate isomerase Rattus norvegicus 124-127 8596711-6 1996 The kinetics of sodium activation of succinate transport by NaDC-1 were sigmoidal, with an apparent Hill coefficient of 2.9, indicating that three sodium ions are involved in the transport of each succinate. Sodium 16-22 solute carrier family 13 member 2 Oryctolagus cuniculus 60-66 8596711-6 1996 The kinetics of sodium activation of succinate transport by NaDC-1 were sigmoidal, with an apparent Hill coefficient of 2.9, indicating that three sodium ions are involved in the transport of each succinate. Sodium 147-153 solute carrier family 13 member 2 Oryctolagus cuniculus 60-66 9005073-3 1996 The judicious employment in a complex of therapeutic measures of aerosols of hydrocarbonate of sodium and heparin promotes neutralization of cationic proteins and large major protein of eosinophiles in the bronchial lumen whereby there occurs normalization of Ig A levels in the sputum along with lowering of its fibrinolytic activity. Sodium 95-101 immunoglobulin heavy variable 4-38-2-like Homo sapiens 260-264 8584433-1 1996 Conflicting results have been reported in literature about the influence of beta-adrenergic stimulation on the fast cardiac sodium current (INa+). Sodium 124-130 internexin neuronal intermediate filament protein, alpha Rattus norvegicus 140-143 8668674-6 1996 The incorporation into the hepatocytes was found essentially depending on the FABPPM transport system whenever BLA was bound to albumin or to galactosylated albumin in the incubation medium: indeed, the transport was inhibited by phloretin (inhibitor of sodium dependent transport), increased when the free part of BLA was higher, and BLA was recovered in the cytosolic fraction of the hepatocytes. Sodium 254-260 glutamic-oxaloacetic transaminase 2 Homo sapiens 78-84 7479969-6 1995 For the GAT1 (gamma-aminobutyric acid,Na,Cl) cotransporter, expressed in Xenopus oocyte membrane, we find that chloride binding from the cytoplasmic side, and probably sodium binding from the extracellular side, results in a decrease of membrane capacitance monitored with 1- to 50-kHz perturbation frequencies. Sodium 168-174 solute carrier family 6 (neurotransmitter transporter), member 1 S homeolog Xenopus laevis 8-12 8563702-8 1995 These results suggest that the augmentation of renal dopaminergic activity which may in part cause sodium escape appears at the early stage of DOCA-salt treatment, but this augmentation is subsequently blunted; volume and sodium retention may be associated with the blood pressure elevation at the late stage of DOCA-salt treatment, and that the augmentation of renal kallikrein-kinin system may be a compensatory response to sodium and volume retention in DOCA-salt treated rats. Sodium 99-105 kallikrein related-peptidase 5 like Rattus norvegicus 368-378 8580427-2 1995 This phenotype is clearly different from classical paramyotonia congenita Eulenburg, which has been shown to be a sodium channelopathy resulting from mutations in the gene for the alpha-subunit of the human skeletal muscle sodium channel gene (SCN4A). Sodium 114-120 sodium voltage-gated channel alpha subunit 4 Homo sapiens 244-249 8580427-2 1995 This phenotype is clearly different from classical paramyotonia congenita Eulenburg, which has been shown to be a sodium channelopathy resulting from mutations in the gene for the alpha-subunit of the human skeletal muscle sodium channel gene (SCN4A). Sodium 223-229 sodium voltage-gated channel alpha subunit 4 Homo sapiens 244-249 8541846-2 1995 We used single-strand conformation polymorphism (SSCP) and DNA sequence analyses to identify mutations in the cardiac sodium channel gene, SCN5A, in affected members of four LQT families. Sodium 118-124 sodium voltage-gated channel alpha subunit 5 Homo sapiens 139-144 7581380-3 1995 In contrast, dominant myotonias sensitive to potassium are caused by point mutations in SCN4A on chromosome 17q, the gene for the alpha subunit of the adult skeletal muscle sodium channel. Sodium 173-179 sodium voltage-gated channel alpha subunit 4 Homo sapiens 88-93 7611264-7 1995 After rIL-2 withdrawal, these alterations persisted and were associated with a reduction in urinary output, sodium urinary excretion, and plasma protein. Sodium 108-114 interleukin 2 Rattus norvegicus 6-11 7611264-10 1995 Similarly, the decline in urinary output and sodium excretion during rIL-2 was promptly counteracted by dopamine; in addition, after withdrawal of rIL-2 and dopamine, plasma protein levels were normalized. Sodium 45-51 interleukin 2 Rattus norvegicus 69-74 7744735-2 1995 The mechanism of sodium movement across apical membrane of colonic crypt cells of rat distal colon was examined in studies of both 22Na uptake by apical membrane vesicles (AMV) and the rate of intracellular pH (pHi) recovery from an acid load by the addition of lumen sodium. Sodium 17-23 glucose-6-phosphate isomerase Rattus norvegicus 211-214 7744735-5 1995 pHi recovery from an acid load was both lumen sodium- and chloride-dependent, and the rate of pHi recovery by lumen sodium in the presence of chloride was 65-fold greater than that in the absence of chloride (dpH/dt is 655.4 and 10.2 in the presence and absence of chloride, respectively). Sodium 46-52 glucose-6-phosphate isomerase Rattus norvegicus 0-3 7744735-5 1995 pHi recovery from an acid load was both lumen sodium- and chloride-dependent, and the rate of pHi recovery by lumen sodium in the presence of chloride was 65-fold greater than that in the absence of chloride (dpH/dt is 655.4 and 10.2 in the presence and absence of chloride, respectively). Sodium 116-122 glucose-6-phosphate isomerase Rattus norvegicus 0-3 7744735-5 1995 pHi recovery from an acid load was both lumen sodium- and chloride-dependent, and the rate of pHi recovery by lumen sodium in the presence of chloride was 65-fold greater than that in the absence of chloride (dpH/dt is 655.4 and 10.2 in the presence and absence of chloride, respectively). Sodium 116-122 glucose-6-phosphate isomerase Rattus norvegicus 94-97 7889574-3 1995 Here we report genetic linkage between LQT3 and polymorphisms within SCN5A, the cardiac sodium channel gene. Sodium 88-94 sodium voltage-gated channel alpha subunit 5 Homo sapiens 39-43 7889574-3 1995 Here we report genetic linkage between LQT3 and polymorphisms within SCN5A, the cardiac sodium channel gene. Sodium 88-94 sodium voltage-gated channel alpha subunit 5 Homo sapiens 69-74 7736494-3 1995 During reperfusion the activity of the Na+/H+ exchanger recovers, allowing extrusion of protons at the expense of increases in intracellular sodium. Sodium 141-147 solute carrier family 9 member A1 Canis lupus familiaris 39-55 7736494-5 1995 These data are in keeping with the pathophysiological model that the Na+/H+ exchanger is an important part of a cascade leading from intracellular acidosis to intracellular sodium loading followed by calcium overload. Sodium 173-179 solute carrier family 9 member A1 Canis lupus familiaris 69-85 7588410-1 1995 Excessive aldosterone secretion in some hypertensive patients may result from abnormal aldosterone synthase (AS) gene regulation in response to changes in dietary sodium intake. Sodium 163-169 cytochrome P450 family 11 subfamily B member 2 Homo sapiens 87-107 7588410-1 1995 Excessive aldosterone secretion in some hypertensive patients may result from abnormal aldosterone synthase (AS) gene regulation in response to changes in dietary sodium intake. Sodium 163-169 cytochrome P450 family 11 subfamily B member 2 Homo sapiens 109-111 8846725-3 1995 Inward sodium current (INa) in isolated rat ventricular and guinea pig and human atrial cells was also inhibited by prazosin (1 to 10 microM) dose-dependently. Sodium 7-13 internexin neuronal intermediate filament protein, alpha Rattus norvegicus 23-26 7982958-0 1994 Conformation-dependent phosphorylation of Na,K-ATPase by protein kinase A and protein kinase C. Phosphorylation of sodium and potassium ion-activated adenosine triphosphatase (Na,K-ATPase) by protein kinase A (PKA) and protein kinase C (PKC) was investigated in vitro, where substrate conformation, kinase activity, and consequent effects on Na,K-ATPase activity could be controlled. Sodium 115-121 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 57-73 7982958-0 1994 Conformation-dependent phosphorylation of Na,K-ATPase by protein kinase A and protein kinase C. Phosphorylation of sodium and potassium ion-activated adenosine triphosphatase (Na,K-ATPase) by protein kinase A (PKA) and protein kinase C (PKC) was investigated in vitro, where substrate conformation, kinase activity, and consequent effects on Na,K-ATPase activity could be controlled. Sodium 115-121 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 192-208 7982958-0 1994 Conformation-dependent phosphorylation of Na,K-ATPase by protein kinase A and protein kinase C. Phosphorylation of sodium and potassium ion-activated adenosine triphosphatase (Na,K-ATPase) by protein kinase A (PKA) and protein kinase C (PKC) was investigated in vitro, where substrate conformation, kinase activity, and consequent effects on Na,K-ATPase activity could be controlled. Sodium 115-121 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 210-213 7810724-3 1994 Oral administration of the selective AVP V2 receptor antagonist OPC-31260 induced marked water diuresis, which resulted in significant increases in serum sodium concentration, plasma renin activity, and plasma concentration of AVP, although it did not produce hemodynamic improvement. Sodium 154-160 arginine vasopressin Canis lupus familiaris 37-40 7832493-0 1994 Bombesin, gastrin-releasing peptide, and neuromedin B attenuate the salt appetite of sodium-depleted rats. Sodium 85-91 neuromedin B Rattus norvegicus 41-53 9420635-6 1994 In separate groups of dogs, low-dose intrarenal cGMP PDI potentiated the actions of exogenous ANF on glomerular filtration and distal nephron sodium reabsorption, leading to enhanced natriuresis in the presence or absence of severe CHF. Sodium 142-148 natriuretic peptide A Canis lupus familiaris 94-97 9420635-7 1994 These studies support a link between ANF and the renal actions of cGMP PDI, and indicate that cGMP phosphodiesterases may contribute to sodium retention in advanced CHF by limiting the renal actions of increased endogenous ANF. Sodium 136-142 natriuretic peptide A Canis lupus familiaris 223-226 7821363-4 1994 Infusion of adrenomedullin at the rates of 4 and 20 ng.kg-1.min-1 increased urine flow and the urinary excretion of sodium and potassium dose dependently. Sodium 116-122 adrenomedullin Canis lupus familiaris 12-26 8046459-1 1994 The dopamine transporter (DAT) and norepinephrine transporter (NET) terminate catecholaminergic neurotransmission at synapses by high-affinity sodium-dependent reuptake into presynaptic terminals, and are the initial sites of action for drugs of abuse and antidepressants. Sodium 143-149 solute carrier family 6 member 2 Rattus norvegicus 35-61 8046459-1 1994 The dopamine transporter (DAT) and norepinephrine transporter (NET) terminate catecholaminergic neurotransmission at synapses by high-affinity sodium-dependent reuptake into presynaptic terminals, and are the initial sites of action for drugs of abuse and antidepressants. Sodium 143-149 solute carrier family 6 member 2 Rattus norvegicus 63-66 8024004-6 1994 Plasma renin activity (PRA) was elevated (47.9 +/- 9.7 vs. 8.8 +/- 3.3 ng angiotensin I.ml-1.h-1) after sodium depletion (P < 0.05). Sodium 104-110 renin Macaca fascicularis 7-12 8062506-10 1994 Also des-(1-3)-insulin-like growth factor-1 significantly increased creatinine clearance and reduced fractional excretion of filtered sodium. Sodium 134-140 insulin-like growth factor 1 Rattus norvegicus 15-43 8084540-0 1994 Fast sodium action potentials are generated in the distal apical dendrites of rat hippocampal CA1 pyramidal cells. Sodium 5-11 carbonic anhydrase 1 Rattus norvegicus 94-97 8046774-1 1994 Met5-enkephalin inhibits sodium and water excretion and antagonizes the central actions of angiotensin II in subfornical organ of rat brain. Sodium 25-31 proenkephalin Rattus norvegicus 5-15 8037884-2 1994 In contrast to nontransgenic CD-1 mice, immobility in the swim test was longer and sodium intake higher in the male TGF alpha mice than in the female TGF alpha mice. Sodium 83-89 transforming growth factor alpha Mus musculus 116-125 8019852-0 1994 Removal of extracellular sodium prevents anoxia-induced injury in freshly dissociated rat CA1 hippocampal neurons. Sodium 25-31 carbonic anhydrase 1 Rattus norvegicus 90-93 8011980-1 1994 The capillary leak syndrome with decreased GFR and renal water and sodium retention after recombinant interleukin-2 (IL-2) administration may arise from endothelial activation via an increase in prostaglandin synthesis. Sodium 67-73 interleukin 2 Rattus norvegicus 102-115 8011980-1 1994 The capillary leak syndrome with decreased GFR and renal water and sodium retention after recombinant interleukin-2 (IL-2) administration may arise from endothelial activation via an increase in prostaglandin synthesis. Sodium 67-73 interleukin 2 Rattus norvegicus 117-121 8011980-3 1994 The chronic administration of IL-2 (100,000 U/kg, thrice daily, ip) resulted in a significant increase in body weight, a decrease in GFR and in the urinary excretion of sodium and potassium, and an increase in the urinary excretion of thromboxane (TXB2). Sodium 169-175 interleukin 2 Rattus norvegicus 30-34 7905839-4 1994 The expressed mu OR1 recognized tested opiate drugs and opioid peptides in a sodium- and GTP-sensitive fashion with affinities virtually identical to those displayed by the rat mu opiate receptor. Sodium 77-83 opioid receptor, mu 1 Rattus norvegicus 14-20 7976661-3 1994 Mepyramine and ranitidine given 2 h before the induction of EBP prevented the accumulation of water, sodium and albumin in samples taken from the parietal cortex. Sodium 101-107 EBP, cholestenol delta-isomerase Rattus norvegicus 60-63 8044656-0 1994 Mutations in the muscle sodium channel gene (SCN4A) in 13 French families with hyperkalemic periodic paralysis and paramyotonia congenita: phenotype to genotype correlations and demonstration of the predominance of two mutations. Sodium 24-30 sodium voltage-gated channel alpha subunit 4 Homo sapiens 45-50 8404675-7 1993 Thus, it appears that sodium restriction specifically increases late pathway aldosterone synthase mRNA levels, resulting in an increase in enzyme levels, followed by an increase in late pathway activity and an increase in aldosterone output. Sodium 22-28 cytochrome P450, family 11, subfamily b, polypeptide 1 Rattus norvegicus 77-97 8301099-6 1993 In both sodium-depleted and sodium-replete monkeys the AT1 antagonist and ACE inhibitors caused similar increases in PRA and active renin. Sodium 8-14 angiotensin-converting enzyme Macaca fascicularis 74-77 8301099-6 1993 In both sodium-depleted and sodium-replete monkeys the AT1 antagonist and ACE inhibitors caused similar increases in PRA and active renin. Sodium 28-34 angiotensin-converting enzyme Macaca fascicularis 74-77 8238378-0 1993 Oxytocin affects apical sodium conductance in rabbit cortical collecting duct. Sodium 24-30 oxytocin Oryctolagus cuniculus 0-8 8270912-1 1993 M-1 cells, derived from a microdissected cortical collecting duct of a transgenic mouse, grown to confluence on a permeable support, develop a lumen-negative amiloride-sensitive transepithelial potential, reabsorb sodium, and secrete potassium. Sodium 214-220 cholinergic receptor, muscarinic 1, CNS Mus musculus 0-3 8276134-0 1993 A tetrapeptide within a receptor-binding region of human follicle-stimulating hormone beta-subunit, hFSH-beta-(34-37), regulates sodium-calcium exchange in Sertoli cells. Sodium 129-135 follicle stimulating hormone subunit beta Homo sapiens 100-109 8365363-7 1993 Atrial natriuretic peptide, which is known to affect sodium transport in various cell types, did not alter the [Na+]i response elicited by Ang II. Sodium 53-59 natriuretic peptide A Bos taurus 0-26 8393484-9 1993 Replacement of external sodium (80%) with Tris or choline caused (1) an outward current with a decrease in input conductance and (2) an approximately 50% decrease in the met-ENK-induced outward current with a shift in its reversal potential toward EK. Sodium 24-30 proenkephalin Rattus norvegicus 174-177 8393484-11 1993 The met-ENK-induced outward current was almost totally abolished by combined sodium substitution and extracellular Ba2+ in an additive manner. Sodium 77-83 proenkephalin Rattus norvegicus 8-11 8342649-0 1993 Sodium hyperosmolarity of intestinal lymph causes arteriolar vasodilation in part mediated by EDRF. Sodium 0-6 alpha hemoglobin stabilizing protein Homo sapiens 94-98 8342649-5 1993 After EDRF blockade, the responses to sodium hypertonicity decreased by about one-half; blockade reduced mannitol-induced dilation by 22%. Sodium 38-44 alpha hemoglobin stabilizing protein Homo sapiens 6-10 8342649-6 1993 These results indicate that sodium hypertonicity, as occurs during absorption, can play a major role in absorptive hyperemia, and about one-half of the dilation is related to a sodium-coupled release of EDRF. Sodium 177-183 alpha hemoglobin stabilizing protein Homo sapiens 203-207 8342659-1 1993 Atrial natriuretic factor (ANF) is a circulating 28-amino acid peptide that functions in the regulation of sodium homeostasis and vascular tone. Sodium 107-113 natriuretic peptide A Canis lupus familiaris 0-25 8342659-1 1993 Atrial natriuretic factor (ANF) is a circulating 28-amino acid peptide that functions in the regulation of sodium homeostasis and vascular tone. Sodium 107-113 natriuretic peptide A Canis lupus familiaris 27-30 8097382-7 1993 In the pre-DOCA experiments, ANF infusions at 15, 30, and 100 ng.kg-1.min-1 produced dose-related increases in urinary sodium excretion and significant elevations in creatinine clearance. Sodium 119-125 natriuretic peptide A Canis lupus familiaris 29-32 8097382-8 1993 In the presence of DOCA, urinary sodium excretion was markedly attenuated during identical ANF infusions. Sodium 33-39 natriuretic peptide A Canis lupus familiaris 91-94 8511189-1 1993 Rats exposed to low levels of dietary sodium throughout development exhibit reduced chorda tympani nerve taste responses to sodium stimuli during adulthood, apparently due to altered activity of some hormone(s) or growth factor(s) during early development. Sodium 38-44 myotrophin Rattus norvegicus 214-227 8467324-0 1993 Atrial natriuretic factor and changes in the aldosterone response to angiotensin II in sodium depleted dogs. Sodium 87-93 natriuretic peptide A Canis lupus familiaris 0-25 8467324-6 1993 These data suggest subtle shifts in endogenous levels of plasma ANF, accompanying changes in sodium status, are a major contributor to the associated alterations in angiotensin II/aldosterone relationships. Sodium 93-99 natriuretic peptide A Canis lupus familiaris 64-67 8507814-5 1993 EPO administration resulted in a dose-dependent decrease in sodium excretion to a maximum of 50% at the 1,000 mU/mL dose. Sodium 60-66 erythropoietin Rattus norvegicus 0-3 8507814-7 1993 The administration of EPO resulted in an immediate decrease in average sodium excretion (30%) with no change in GFR or other renal function parameters. Sodium 71-77 erythropoietin Rattus norvegicus 22-25 8507814-11 1993 It was concluded that EPO acts within the kidney to cause the production of angiotensin II, which mediates the increased reabsorption of sodium. Sodium 137-143 erythropoietin Rattus norvegicus 22-25 8423477-8 1993 At the same time, voltage-clamp recordings revealed significant ontogenetic modifications in several key properties of the sodium currents (INa). Sodium 123-129 internexin neuronal intermediate filament protein alpha Felis catus 140-143 22217827-2 1992 Low sodium and high potassium intake promoted time-dependent increases in the zona glomerulosa cytochrome P450scc (P450scc) and cytochrome P450c11 (P450c11) protein and mRNA levels, but no changes were found in the zona fasciculata-reticularis. Sodium 4-10 cytochrome P450, family 11, subfamily b, polypeptide 1 Rattus norvegicus 139-146 22217827-2 1992 Low sodium and high potassium intake promoted time-dependent increases in the zona glomerulosa cytochrome P450scc (P450scc) and cytochrome P450c11 (P450c11) protein and mRNA levels, but no changes were found in the zona fasciculata-reticularis. Sodium 4-10 cytochrome P450, family 11, subfamily b, polypeptide 1 Rattus norvegicus 148-155 1482638-6 1992 Insulin-like growth factor-1 (IGF-1), which is depressed in calorie-deficient growth failure, was depressed in all the rats on the low-sodium intakes relative to ad libitum-fed controls, but did not vary in relation to dietary sodium or weight gain within those groups. Sodium 135-141 insulin-like growth factor 1 Rattus norvegicus 0-28 1482638-6 1992 Insulin-like growth factor-1 (IGF-1), which is depressed in calorie-deficient growth failure, was depressed in all the rats on the low-sodium intakes relative to ad libitum-fed controls, but did not vary in relation to dietary sodium or weight gain within those groups. Sodium 135-141 insulin-like growth factor 1 Rattus norvegicus 30-35 1328299-0 1992 Renal tubular responsiveness to atrial natriuretic peptide in sodium-retaining chronic caval dogs. Sodium 62-68 natriuretic peptide A Canis lupus familiaris 32-58 1338909-1 1992 Mutations in the skeletal muscle sodium channel gene (SCN4A) have been described in paramyotonia congenita (PMC) and hyperkalaemic periodic paralysis (HPP). Sodium 33-39 sodium voltage-gated channel alpha subunit 4 Homo sapiens 54-59 1338909-2 1992 We have found two mutations in SCN4A which affect regions of the sodium channel not previously associated with a disease phenotype. Sodium 65-71 sodium voltage-gated channel alpha subunit 4 Homo sapiens 31-36 1329522-3 1992 Stimulation of the beta 2-adrenergic receptor or treatment with dibutyryl cAMP resulted in increased sodium current amplitudes without affecting the voltage dependence of channel activation or inactivation. Sodium 101-107 adrenoceptor beta 2 Rattus norvegicus 19-45 1639774-17 1992 Dibasic amino acids are taken up by both 4F2 and D2 cRNA-injected oocytes in a sodium-independent manner. Sodium 79-85 solute carrier family 3 (amino acid transporter heavy chain), member 2 L homeolog Xenopus laevis 41-44 1639774-18 1992 In contrast, 4F2-induced but not D2-induced neutral amino acid uptake has a significant component of sodium dependence. Sodium 101-107 solute carrier family 3 (amino acid transporter heavy chain), member 2 L homeolog Xenopus laevis 13-16 1639774-19 1992 Likewise, neutral amino acids in excess inhibit the 4F2-induced uptake of radiolabeled arginine but not leucine in a sodium-dependent manner. Sodium 117-123 solute carrier family 3 (amino acid transporter heavy chain), member 2 L homeolog Xenopus laevis 52-55 1683643-2 1991 In this study multipoint linkage analysis of two Duffy-linked families given a combined LOD score of 8.65 to establish that the Duffy-linked CMT1B gene exists in the 18 centimorgan region between the antithrombin III gene and the Duffy/sodium-potassium ATPase loci. Sodium 236-242 serpin family C member 1 Homo sapiens 200-216 34512393-1 2021 The activity of the Epithelial Na+ Channel (ENaC) in renal principal cells (PC) fine-tunes sodium excretion and consequently, affects blood pressure. Sodium 91-97 sodium channel, nonvoltage-gated 1 alpha Mus musculus 20-42 34512393-1 2021 The activity of the Epithelial Na+ Channel (ENaC) in renal principal cells (PC) fine-tunes sodium excretion and consequently, affects blood pressure. Sodium 91-97 sodium channel, nonvoltage-gated 1 alpha Mus musculus 44-48 34433864-3 2021 We aim to knockout (KO) NaV1.5, the cardiac sodium channel, in a healthy human iPSC line, characterize the model and then, use it to express variants of NaV1.5. Sodium 44-50 sodium voltage-gated channel alpha subunit 5 Homo sapiens 24-30 34429341-0 2021 Anti-contactin-1 Antibodies Affect Surface Expression and Sodium Currents in Dorsal Root Ganglia. Sodium 58-64 contactin 1 Homo sapiens 5-16 34429341-4 2021 RESULTS: We found a reduction in contactin-1 expression levels on dorsal root ganglion neurons, cerebellar granule neurons, and contactin-1-transfected human embryonic kidney 293 cells and decreased dorsal root ganglion sodium currents after long-term exposure to anti-contactin-1 autoantibodies. Sodium 220-226 contactin 1 Homo sapiens 269-280 34429341-6 2021 DISCUSSION: Our results demonstrate a direct effect of anti-contactin-1 autoantibodies on the surface expression of contactin-1 and sodium currents in dorsal root ganglion neurons. Sodium 132-138 contactin 1 Homo sapiens 60-71 34425903-1 2021 BACKGROUND: Genetic variants in the voltage-gated sodium channels SCN1A, SCN2A, SCN3A, and SCN8A are leading causes of epilepsy, developmental delay, and autism spectrum disorder. Sodium 50-56 sodium voltage-gated channel alpha subunit 3 Homo sapiens 80-85 34373326-0 2021 Functional cross-talk between phosphorylation and disease-causing mutations in the cardiac sodium channel Nav1.5. Sodium 91-97 sodium voltage-gated channel alpha subunit 5 Homo sapiens 106-112 34373326-1 2021 The voltage-gated sodium channel Nav1.5 initiates the cardiac action potential. Sodium 18-24 sodium voltage-gated channel alpha subunit 5 Homo sapiens 33-39 34422849-1 2021 Objective: Voltage-gated sodium channel Nav1.5 encoded by the SCN5A gene plays crucial roles in cardiac electrophysiology. Sodium 25-31 sodium voltage-gated channel alpha subunit 5 Homo sapiens 40-46 34421659-0 2021 Editorial: Inherited Arrhythmias of the Cardiac Sodium Channel Nav1.5. Sodium 48-54 sodium voltage-gated channel alpha subunit 5 Homo sapiens 63-69 34115435-0 2021 Flower-like Spherical alpha-Ni(OH)2 Derived NiP2 as Superior Anode Material of Sodium Ion Batteries. Sodium 79-85 BCL2 interacting protein 2 Homo sapiens 44-48 34115435-4 2021 When used as a sodium-ion batteries anode material, NiP 2 @rGO composite shows excellent cycling performance (117 mA h g -1 at 10 A g -1 after 8000 cycles). Sodium 15-21 BCL2 interacting protein 2 Homo sapiens 52-57 34337820-7 2021 Western blotting, real-time polymerase chain reaction, immunostaining, intrathecal injection, and chromatin immunoprecipitation (ChIP) assay were performed to determine whether the sodium channel protein Nav1.7 plays a role in CFA-induced pain and whether GR regulates Nav1.7 expression during analgesia following EA stimulation. Sodium 181-187 sodium voltage-gated channel alpha subunit 9 Rattus norvegicus 204-210 34325884-7 2021 Inhibition of SGLT2 may also lead to a reduction in the activity of sodium-hydrogen exchangers in the kidney (leading to diuresis) and in the heart (attenuating the development of cardiac hypertrophy and systolic dysfunction). Sodium 68-74 solute carrier family 5 member 2 Homo sapiens 14-19 34327875-2 2021 For example, long QT syndrome-3 (LQTS3) is caused by mutations in the Nav 1.5 sodium channel that debilitate channel inactivation and cause arrhythmias. Sodium 78-84 sodium voltage-gated channel alpha subunit 5 Homo sapiens 70-77 34331631-5 2021 out of five GNAI2 single nucleotide polymorphisms (SNPs) tested, rs4547694 significantly moderated the relationship of dietary sodium intake on BP in KAIs. Sodium 127-133 G protein subunit alpha i2 Homo sapiens 12-17 34272444-1 2021 Activity of the Epithelial Na+ Channel (ENaC) in the distal nephron fine-tunes renal sodium excretion. Sodium 85-91 sodium channel, nonvoltage-gated 1 alpha Mus musculus 16-38 34272444-1 2021 Activity of the Epithelial Na+ Channel (ENaC) in the distal nephron fine-tunes renal sodium excretion. Sodium 85-91 sodium channel, nonvoltage-gated 1 alpha Mus musculus 40-44 34272444-12 2021 In the principal cell-specific Ank-3 KO mouse, ENaC activity and sodium excretion were significantly decreased and increased, respectively. Sodium 65-71 ankyrin 3, epithelial Mus musculus 31-36 34234096-1 2021 BACKGROUND Brugada syndrome is a rare ion channelopathy that can lead to sudden cardiac death and lethal arrhythmias in patients without a structural cardiac defect, the most common of which being the gain-of-function mutation of the SCN5a sodium ion channel involving phase 0 of the cardiac action potential. Sodium 240-246 sodium voltage-gated channel alpha subunit 5 Homo sapiens 234-239 34209614-1 2021 The SCN4B gene, coding for the NaVbeta4 subunit of voltage-gated sodium channels, was recently found to be expressed in normal epithelial cells and down-regulated in several cancers. Sodium 65-71 sodium voltage-gated channel beta subunit 4 Homo sapiens 4-9 34209614-1 2021 The SCN4B gene, coding for the NaVbeta4 subunit of voltage-gated sodium channels, was recently found to be expressed in normal epithelial cells and down-regulated in several cancers. Sodium 65-71 sodium voltage-gated channel beta subunit 4 Homo sapiens 31-39 34234493-0 2021 An Overview of Similarities and Differences in Metabolic Actions and Effects of Central Nervous System Between Glucagon-Like Peptide-1 Receptor Agonists (GLP-1RAs) and Sodium Glucose Co-Transporter-2 Inhibitors (SGLT-2is). Sodium 168-174 solute carrier family 5 member 2 Homo sapiens 212-218 34126732-0 2021 (Research update on post-translational modification of cardiac sodium channel Nav1.5). Sodium 63-69 sodium voltage-gated channel alpha subunit 5 Homo sapiens 78-84 34206182-2 2021 We aimed to determine the impact of three macrolides, azithromycin, clarithromycin and erythromycin, on cardiac electrophysiology, cardiac enzyme activities, histopathological changes, and sodium voltage-gated alpha subunit 5 (Nav1.5) channel expression. Sodium 189-195 sodium voltage-gated channel alpha subunit 5 Homo sapiens 227-233 34317510-2 2021 We describe a patient who presented after a cardiac arrest with Bi-MVP and variants in Lamin A/C (LMNA) and the sodium channel alpha-subunit 5a (SCN5A). Sodium 112-118 sodium voltage-gated channel alpha subunit 5 Homo sapiens 145-150 35605014-4 2022 Solute carrier family 20 member 1 (SLC20A1) is a sodium/inorganic phosphate symporter that has been proposed to be a viable prognostic marker for the luminal A and luminal B types of ER+ breast cancer. Sodium 49-55 solute carrier family 20 member 1 Homo sapiens 0-33 35438990-3 2022 Reduction of this precursor using excess sodium amalgam afforded (Ph2PPrPDI)Fe, which possesses an Fe(II) center that is supported by a dianionic PDI ligand. Sodium 41-47 peptidyl arginine deiminase 1 Homo sapiens 146-149 35353937-7 2022 In the presence of Abeta oligomers, knockdown of Nav1.6 reduces intracellular calcium overload by suppressing reverse sodium-calcium exchange channel, consequently increasing inactive NFAT1 (the nuclear factor of activated T cells) levels and thus reducing BACE1 transcription. Sodium 118-124 amyloid beta (A4) precursor protein Mus musculus 19-24 35483793-0 2022 Impact of SGLT2 Inhibitors on Serum Sodium in Heart Failure With Reduced Ejection Fraction. Sodium 36-42 solute carrier family 5 member 2 Homo sapiens 10-15 35528832-2 2022 In rat cardiomyocytes, IGF-I has been shown to regulate sarcolemmal potassium channel activity and late sodium current thus impacting cardiac repolarization and the heart rate-corrected QT (QTc). Sodium 104-110 insulin-like growth factor 1 Rattus norvegicus 23-28 35563683-1 2022 The Mineralocorticoid Receptor (MR) mediates the sodium-retaining action of aldosterone in the distal nephron, but mechanisms regulating MR expression are still poorly understood. Sodium 49-55 nuclear receptor subfamily 3, group C, member 2 Mus musculus 4-30 35563683-1 2022 The Mineralocorticoid Receptor (MR) mediates the sodium-retaining action of aldosterone in the distal nephron, but mechanisms regulating MR expression are still poorly understood. Sodium 49-55 nuclear receptor subfamily 3, group C, member 2 Mus musculus 32-34 35447164-7 2022 For instance, central infusion of IL-1beta or TNF-alpha can directly affect sodium and water consumption in animal models. Sodium 76-82 interleukin 1 alpha Homo sapiens 34-42 35453812-0 2022 Kinetic Alterations in Resurgent Sodium Currents of Mutant Nav1.4 Channel in Two Patients Affected by Paramyotonia Congenita. Sodium 33-39 sodium voltage-gated channel alpha subunit 4 Homo sapiens 59-65 35428804-1 2022 Renal type II sodium-dependent inorganic phosphate (Pi) transporters NaPi2a and NaPi2c cooperate with other organs to strictly regulate the plasma Pi concentration. Sodium 14-20 solute carrier family 34 (sodium phosphate), member 1 Mus musculus 69-75 35428804-1 2022 Renal type II sodium-dependent inorganic phosphate (Pi) transporters NaPi2a and NaPi2c cooperate with other organs to strictly regulate the plasma Pi concentration. Sodium 14-20 solute carrier family 34 (sodium phosphate), member 3 Mus musculus 80-86 35320795-3 2022 Brugada Syndrome is related to mutations in the genes that encode SCN5A, a subunit of sodium ion channel (NaV). Sodium 86-92 sodium voltage-gated channel alpha subunit 5 Homo sapiens 66-71 35320795-4 2022 This computational study investigates the mechanism of loss of function gene mutation (SCN5A L812Q) in sodium ion channel that leads to spiral wave and further develops into VF in an epicardial tissue with homozygous condition. Sodium 103-109 sodium voltage-gated channel alpha subunit 5 Homo sapiens 87-92 35454100-9 2022 Through compartmentalization of sodium and potassium ions, a significant effect of Na+ upon AQP2 water permeability was highlighted as well. Sodium 32-38 aquaporin 2 Homo sapiens 92-96 35332400-1 2022 Nav1.3, encoded by the SCN3A gene, is a voltage-gated sodium channel on the cell membrane. Sodium 54-60 sodium voltage-gated channel alpha subunit 3 Homo sapiens 0-6 35332400-1 2022 Nav1.3, encoded by the SCN3A gene, is a voltage-gated sodium channel on the cell membrane. Sodium 54-60 sodium voltage-gated channel alpha subunit 3 Homo sapiens 23-28 35391843-16 2022 This suggests that still other factors than sustained glycosuria or proximal sodium excretion may contribute to the resetting to lower blood pressure levels with SGLT2 inhibition. Sodium 77-83 solute carrier family 5 member 2 Homo sapiens 162-167 35303888-4 2022 SGLT2is acutely and directly (1) inhibit cardiac sodium transporters and alter ion homeostasis, (2) reduce inflammation and oxidative stress, (3) influence metabolism, and (4) improve cardiac function. Sodium 49-55 solute carrier family 5 member 2 Homo sapiens 0-5 35303888-5 2022 We postulate that cardiac benefit modulated by SGLT2i"s can be commonly attributed to their inhibition of sodium-loaders in the plasma membrane (NHE-1, Nav1.5, SGLT) affecting intracellular sodium-homeostasis (the sodium-interactome), thereby providing a unifying view on the various effects reported in separate studies. Sodium 106-112 solute carrier family 5 member 2 Homo sapiens 47-52 35303888-5 2022 We postulate that cardiac benefit modulated by SGLT2i"s can be commonly attributed to their inhibition of sodium-loaders in the plasma membrane (NHE-1, Nav1.5, SGLT) affecting intracellular sodium-homeostasis (the sodium-interactome), thereby providing a unifying view on the various effects reported in separate studies. Sodium 106-112 sodium voltage-gated channel alpha subunit 5 Homo sapiens 152-158 35303888-5 2022 We postulate that cardiac benefit modulated by SGLT2i"s can be commonly attributed to their inhibition of sodium-loaders in the plasma membrane (NHE-1, Nav1.5, SGLT) affecting intracellular sodium-homeostasis (the sodium-interactome), thereby providing a unifying view on the various effects reported in separate studies. Sodium 190-196 solute carrier family 5 member 2 Homo sapiens 47-52 35303888-5 2022 We postulate that cardiac benefit modulated by SGLT2i"s can be commonly attributed to their inhibition of sodium-loaders in the plasma membrane (NHE-1, Nav1.5, SGLT) affecting intracellular sodium-homeostasis (the sodium-interactome), thereby providing a unifying view on the various effects reported in separate studies. Sodium 190-196 sodium voltage-gated channel alpha subunit 5 Homo sapiens 152-158 35303888-5 2022 We postulate that cardiac benefit modulated by SGLT2i"s can be commonly attributed to their inhibition of sodium-loaders in the plasma membrane (NHE-1, Nav1.5, SGLT) affecting intracellular sodium-homeostasis (the sodium-interactome), thereby providing a unifying view on the various effects reported in separate studies. Sodium 214-220 solute carrier family 5 member 2 Homo sapiens 47-52 35303888-6 2022 The SGLT2is effects are most apparent when cells or hearts are subjected to pathological conditions (reactive oxygen species, inflammation, acidosis, hypoxia, high saturated fatty acids, hypertension, hyperglycemia, and heart failure sympathetic stimulation) that are known to prime these plasmalemmal sodium-loaders. Sodium 302-308 solute carrier family 5 member 2 Homo sapiens 4-9 35303888-7 2022 In conclusion, the cardiac sodium-interactome provides a unifying testable working hypothesis and a possible, at least partly, explanation to the clinical benefits of SGLT2is observed in the diseased patient. Sodium 27-33 solute carrier family 5 member 2 Homo sapiens 167-172 35434529-1 2022 Sodium-dependent glucose cotransporter 2 inhibitors (SGLT2) are recently approved drugs for the treatment of diabetes that regulate blood glucose levels by inhibiting reabsorption of glucose and sodium in the proximal tubules of the kidney. Sodium 0-6 solute carrier family 5 member 2 Homo sapiens 53-58 35434529-1 2022 Sodium-dependent glucose cotransporter 2 inhibitors (SGLT2) are recently approved drugs for the treatment of diabetes that regulate blood glucose levels by inhibiting reabsorption of glucose and sodium in the proximal tubules of the kidney. Sodium 195-201 solute carrier family 5 member 2 Homo sapiens 53-58 35104250-2 2022 We previously discovered that GRP170 regulates the degradation and assembly of the epithelial sodium channel (ENaC), which reabsorbs sodium in the distal nephron and thereby regulates salt-water homeostasis and blood pressure. Sodium 94-100 sodium channel, nonvoltage-gated 1 alpha Mus musculus 110-114 35104250-2 2022 We previously discovered that GRP170 regulates the degradation and assembly of the epithelial sodium channel (ENaC), which reabsorbs sodium in the distal nephron and thereby regulates salt-water homeostasis and blood pressure. Sodium 133-139 sodium channel, nonvoltage-gated 1 alpha Mus musculus 110-114 35268096-6 2022 In addition, the ratio of sodium to potassium (Na/K ratio) was positively associated with the risk of CVD (HR comparing extreme quintiles = 1.26, 95% CI: 1.14-1.39, p trend < 0.0001). Sodium 26-32 TANK binding kinase 1 Homo sapiens 47-51 35570989-1 2022 Introduction: Proximal tubule sodium uptake is diminished following sodium glucose cotransporter 2 (SGLT2) inhibition. Sodium 30-36 solute carrier family 5 member 2 Homo sapiens 68-98 35570989-1 2022 Introduction: Proximal tubule sodium uptake is diminished following sodium glucose cotransporter 2 (SGLT2) inhibition. Sodium 30-36 solute carrier family 5 member 2 Homo sapiens 100-105 35570989-2 2022 We previously showed that during SGLT2 inhibition, the kidneys adapt by increasing sodium uptake at distal tubular segments, thereby maintaining body sodium balance. Sodium 83-89 solute carrier family 5 member 2 Homo sapiens 33-38 35570989-2 2022 We previously showed that during SGLT2 inhibition, the kidneys adapt by increasing sodium uptake at distal tubular segments, thereby maintaining body sodium balance. Sodium 150-156 solute carrier family 5 member 2 Homo sapiens 33-38 35165201-0 2022 NPRL2 Inhibition of mTORC1 Controls Sodium Channel Expression and Brain Amino Acid Homeostasis. Sodium 36-42 NPR2 like, GATOR1 complex subunit Homo sapiens 0-5 35165201-6 2022 The increased action potential strength is consistent with elevated expression of epilepsy-linked, voltage-gated sodium channels in the NPRL2-deficient brain. Sodium 113-119 NPR2 like, GATOR1 complex subunit Homo sapiens 136-141 35165201-7 2022 Targeted deletion of NPRL2 in primary neurons increases the expression of sodium channel Scn1A, whereas treatment with the pharmacological mTORC1 inhibitor called rapamycin prevents Scn1A upregulation. Sodium 74-80 NPR2 like, GATOR1 complex subunit Homo sapiens 21-26 35165201-8 2022 These studies demonstrate a novel role of NPRL2 and mTORC1 signaling in the regulation of sodium channels, which can contribute to seizures and early lethality.Significance StatementNPRL2 is a requisite subunit of the epilepsy-linked GATOR1 complex that functions as a negative regulator of mTORC1 kinase when intracellular amino acids are limited. Sodium 90-96 NPR2 like, GATOR1 complex subunit Homo sapiens 42-47 35165201-11 2022 In addition, loss of NPRL2 increases the strength of electrically stimulated action potentials and the expression of epilepsy-linked sodium channels. Sodium 133-139 NPR2 like, GATOR1 complex subunit Homo sapiens 21-26 35257103-0 2022 Missense Variant E1295K of Sodium Channel SCN5A Associated With Recurrent Ventricular Fibrillation and Myocardial Inflammation. Sodium 27-33 sodium voltage-gated channel alpha subunit 5 Homo sapiens 42-47 34994586-1 2022 Background: Multiple reports associate the cardiac sodium channel gene (SCN5A) variants S1103Y and R1193Q with type 3 congenital long QT syndrome (LQTS) and drug-induced LQTS. Sodium 51-57 sodium voltage-gated channel alpha subunit 5 Homo sapiens 72-77 35582188-3 2022 Methods: We systematically searched PubMed, EMBASE, CENTRAL, and ClinicalTrials.gov up to January 2021 to identify eligible randomized controlled trials (RCTs) of SGLT2is that reported mean changes in serum electrolytes, including magnesium, sodium, potassium, phosphate, and calcium. Sodium 242-248 solute carrier family 5 member 2 Homo sapiens 163-168 35039597-9 2022 An increased number of SGLT2+ tubular epithelia may be an adaptive response against hyperglycemia, and linked to the hyper-reabsorption of sodium and glucose observed in type 2 diabetes patients. Sodium 139-145 solute carrier family 5 member 2 Homo sapiens 23-28 35053120-1 2022 Hypertension is associated with an increased renal expression and activity of the epithelial sodium channel (ENaC) and iron deficiency. Sodium 93-99 sodium channel, nonvoltage-gated 1 alpha Mus musculus 109-113 35069250-2 2021 Studies in FHHt mice engineered to constitutively activate SPAK specifically in the DCT (CA-SPAK mice) revealed maladaptive remodeling of the aldosterone sensitive distal nephron (ASDN), characterized by decrease in the potassium excretory channel, renal outer medullary potassium (ROMK), and epithelial sodium channel (ENaC), that contributes to the hyperkalemia. Sodium 304-310 serine/threonine kinase 39 Mus musculus 59-63 35058797-0 2021 Selective Deletion of the Mechanistic Target of Rapamycin From the Renal Collecting Duct Principal Cell in Mice Down-Regulates the Epithelial Sodium Channel. Sodium 142-148 mechanistic target of rapamycin kinase Mus musculus 26-57 35058797-2 2021 In the collecting duct (CD) of the kidney, the epithelial sodium channel (ENaC) essential in the determination of final urine Na+ losses, has been demonstrated to be upregulated by mTOR, using cell culture and mTOR inhibition in ex vivo preparations. Sodium 58-64 mechanistic target of rapamycin kinase Mus musculus 181-185 35058797-2 2021 In the collecting duct (CD) of the kidney, the epithelial sodium channel (ENaC) essential in the determination of final urine Na+ losses, has been demonstrated to be upregulated by mTOR, using cell culture and mTOR inhibition in ex vivo preparations. Sodium 58-64 mechanistic target of rapamycin kinase Mus musculus 210-214 35058797-3 2021 We tested whether CD-principal cell (PC) targeted deletion of mTOR using Cre-lox recombination would affect whole-body sodium homeostasis, blood pressure, and ENaC regulation in mice. Sodium 119-125 mechanistic target of rapamycin kinase Mus musculus 62-66 35058797-14 2021 These data support a role for mTOR in the collecting duct in the maintenance of body sodium homeostasis. Sodium 85-91 mechanistic target of rapamycin kinase Mus musculus 30-34 35418262-0 2022 Extracellular signal-regulated kinase phosphorylation enhancement and NaV1.7 sodium channel upregulation in rat dorsal root ganglia neurons contribute to resiniferatoxin-induced neuropathic pain: The efficacy and mechanism of pulsed radiofrequency therapy. Sodium 77-83 sodium voltage-gated channel alpha subunit 9 Rattus norvegicus 70-76 35040153-8 2022 The traits associated with this Meta-QTL were root and shoot sodium and potassium concentration and leaf chlorophyll content. Sodium 61-67 homoserine O-succinyltransferase Glycine max 32-36 35284224-2 2021 A new variant c.6023C>T p.Pro2008Leu of the SCN5A protein, responsible for the sodium inward current (INa) through the cardiomyocytes, was found. Sodium 79-85 sodium voltage-gated channel alpha subunit 5 Homo sapiens 44-49 35465284-3 2022 The sodium-potassium-chloride co-transporter isoform 1 (NKCC1), localized at the basolateral surface of the lung epithelium, drives water transport via back transport of Na+ and Cl- to the alveolar air space. Sodium 4-10 solute carrier family 12 member 2 Homo sapiens 56-61 2557347-0 1989 The human 5-HT1A receptor expressed in HeLa cells stimulates sodium-dependent phosphate uptake via protein kinase C. Regulation of phosphate uptake was studied in HeLa cell lines after transfection with DNA encoding the human 5-HT1A receptor. Sodium 61-67 5-hydroxytryptamine receptor 1A Homo sapiens 10-25 2561148-1 1989 The non-laminar (rather turbulent) flow induced by cell washings was able to reversibly increase the sodium ion (Na+) content in cultured A10 aortic smooth muscle cells. Sodium 101-107 immunoglobulin kappa variable 6D-21 (non-functional) Homo sapiens 138-141 2531552-9 1989 We conclude that there is reversible attenuation of the ANF natriuretic effect in 50% of chronic caval dogs, which disappears when they lose avidity for sodium retention. Sodium 153-159 natriuretic peptide A Canis lupus familiaris 56-59 2531554-3 1989 Sodium excretion was significantly higher during ANP infusion at RPP of 122 +/- 3 mmHg, averaging 55.8 +/- 13.7 during control and 113.3 +/- 23.3 mueq/min during ANP infusion. Sodium 0-6 natriuretic peptide A Canis lupus familiaris 49-52 2531554-3 1989 Sodium excretion was significantly higher during ANP infusion at RPP of 122 +/- 3 mmHg, averaging 55.8 +/- 13.7 during control and 113.3 +/- 23.3 mueq/min during ANP infusion. Sodium 0-6 natriuretic peptide A Canis lupus familiaris 162-165 2557451-5 1989 N-bromoacetamide (NBA) and N-bromosuccinimide (NBS), reagents which remove inactivation gating in physiological preparations, transiently stimulate the sodium permeability of inside-out facing channels to high levels. Sodium 152-158 nibrin Homo sapiens 47-50 2776021-1 1989 The effects of chlordiazepoxide, chlorpromazine, diazepam, diphenylhydantoin, flunitrazepam and haloperidol on the voltage-dependent sodium current (INa) were studied on the hippocampal pyramidal neurons, isolated acutely from rats, using a concentration clamp technique. Sodium 133-139 internexin neuronal intermediate filament protein, alpha Rattus norvegicus 149-152 2539922-2 1989 Diprafenone (20 mumol/l) and lidocaine (300 mumol/l) induced a voltage- and time-dependent block of reconstructed macroscopic sodium current (INa). Sodium 126-132 internexin neuronal intermediate filament protein, alpha Rattus norvegicus 142-145 2705532-6 1989 Urine flow and sodium excretion were changed significantly only at doses of NPY that significantly reduced renal blood flow and filtration rate. Sodium 15-21 neuropeptide Y Homo sapiens 76-79 2539816-10 1989 These results suggest (1) that sodium ions may have a selective and positive regulatory role in hormonal activation of adenylate cyclase in mouse exocrine tissue, and (2) that sodium ions enhance hormonal activation of enzyme by interacting at a site on the adenylate cyclase complex which is independent of the hormone receptor (Rs) and the stimulatory guanine nucleotide binding protein (Ns). Sodium 31-37 nuclear receptor subfamily 4, group A, member 1 Mus musculus 312-328 2539816-10 1989 These results suggest (1) that sodium ions may have a selective and positive regulatory role in hormonal activation of adenylate cyclase in mouse exocrine tissue, and (2) that sodium ions enhance hormonal activation of enzyme by interacting at a site on the adenylate cyclase complex which is independent of the hormone receptor (Rs) and the stimulatory guanine nucleotide binding protein (Ns). Sodium 176-182 nuclear receptor subfamily 4, group A, member 1 Mus musculus 312-328 2525634-6 1989 The infusion of ANP increased the urine volume, absolute sodium excretion, and osmolar clearance in the control and CRF groups. Sodium 57-63 natriuretic peptide A Canis lupus familiaris 16-19 2521228-0 1989 Alterations in serum sodium in relation to atrial natriuretic factor and other neuroendocrine variables in experimental pacing-induced heart failure. Sodium 21-27 natriuretic peptide A Canis lupus familiaris 43-68 2847552-4 1988 Saralasin infused intra-arterially to the kidney significantly blocked the increase in RBF seen after angiotensin-converting enzyme (ACE) inhibition in sodium-replete dogs, and reduced the increase in RBF in sodium-restricted dogs, but the latter effect was not statistically significant. Sodium 152-158 angiotensin I converting enzyme Canis lupus familiaris 133-136 2847552-7 1988 The results suggest that blockade of the influence of the renin-angiotensin system and possibly another vasodilator mechanism, such as kinin potentiation, account for the increase in RBF after ACE inhibition in the low-sodium state. Sodium 219-225 angiotensin I converting enzyme Canis lupus familiaris 193-196 2970801-10 1988 Intrarenal ANP prevents the ANG II-induced decrement in urinary sodium excretion and urine flow rate. Sodium 64-70 natriuretic peptide A Canis lupus familiaris 11-14 2970801-11 1988 ANP may play an important role in escape from the sodium-retaining action of intrarenal ANG II. Sodium 50-56 natriuretic peptide A Canis lupus familiaris 0-3 2970433-3 1988 In contrast, ANF-(99-122), 10 micrograms/kg, significantly increased renal blood flow (26 +/- 4.5%), reduced renal vascular resistance (24 +/- 2.9%) and arterial pressure (5.5 +/- 1.9%), and markedly increased urine flow rate (198 +/- 34%) and sodium (206 +/- 32%) and potassium (75 +/- 27%) excretion (p less than 0.05), being almost twice as effective in the first 10 minutes as was ANF-(99-119) infusion. Sodium 244-250 natriuretic peptide A Canis lupus familiaris 13-16 2970433-4 1988 During a brief infusion, ANF-(99-122) (10 micrograms/kg/min for 4 minutes) increased renal blood flow (24 +/- 2.7%), heart rate (18 +/- 5.7%), urine flow rate (199 +/- 25%), and sodium (290 +/- 81%) and potassium (104 +/- 17%) excretion. Sodium 178-184 natriuretic peptide A Canis lupus familiaris 25-28 2976824-21 1988 These results suggest that a Na+-H+ exchange and an influx of bicarbonate coupled to sodium influx are of importance for pHi control in these vessels. Sodium 85-91 glucose-6-phosphate isomerase Rattus norvegicus 121-124 2964794-1 1988 The present study in anesthetized dogs (n = 8) was designed to test the hypothesis that intrarenal angiotensin II (ANG II) attenuates the increase in sodium excretion in response to atrial natriuretic factor (ANF). Sodium 150-156 natriuretic peptide A Canis lupus familiaris 182-207 2964794-3 1988 During ANF infusion, absolute increases in urinary sodium excretion (delta + 160.8 +/- 44.7 vs. delta + 369.4 +/- 56.9 mu eq/min, P less than 0.005) and fractional sodium excretion (delta + 2.55 +/- 0.62 vs. delta + 4.26 +/- 0.82%, P less than 0.03) were markedly attenuated in the ANG II K compared with CK. Sodium 51-57 natriuretic peptide A Canis lupus familiaris 7-10 2964794-3 1988 During ANF infusion, absolute increases in urinary sodium excretion (delta + 160.8 +/- 44.7 vs. delta + 369.4 +/- 56.9 mu eq/min, P less than 0.005) and fractional sodium excretion (delta + 2.55 +/- 0.62 vs. delta + 4.26 +/- 0.82%, P less than 0.03) were markedly attenuated in the ANG II K compared with CK. Sodium 164-170 natriuretic peptide A Canis lupus familiaris 7-10 2454285-0 1988 The sodium current underlying action potentials in guinea pig hippocampal CA1 neurons. Sodium 4-10 carbonic anhydrase 1 Cavia porcellus 74-77 2965177-2 1988 In four female calves fitted with a Foley catheter, an intravenous administration of ANF (Ile-ANF 26; 1.6 micrograms/kg body wt during 30 min) induced an increase (P less than 0.01) in urine flow rate (from 1.8 +/- 0.2 to 12.8 +/- 1.1 ml/min), sodium excretion (from 0.15 +/- 0.02 to 0.81 +/- 0.06 mmol/min) and free water clearance (from 0.13 +/- 0.9 to 5.16 +/- 0.5 ml/min). Sodium 244-250 natriuretic peptide A Bos taurus 85-88 2965177-2 1988 In four female calves fitted with a Foley catheter, an intravenous administration of ANF (Ile-ANF 26; 1.6 micrograms/kg body wt during 30 min) induced an increase (P less than 0.01) in urine flow rate (from 1.8 +/- 0.2 to 12.8 +/- 1.1 ml/min), sodium excretion (from 0.15 +/- 0.02 to 0.81 +/- 0.06 mmol/min) and free water clearance (from 0.13 +/- 0.9 to 5.16 +/- 0.5 ml/min). Sodium 244-250 natriuretic peptide A Bos taurus 90-100 3280170-5 1988 The chronic elevation of ANG II in the CSF plus an increase in NaCl intake produces a low renin, sodium dependent, expanded volume hypertension. Sodium 97-103 ANG Canis lupus familiaris 25-28 2825538-5 1987 The rate of rise in pHi was a function of extracellular sodium concentration with a Km for Na+ of 30 +/- 12 mM (n = 6). Sodium 56-62 glucose-6-phosphate isomerase Rattus norvegicus 20-23 2958169-6 1987 We suggest that chronic decreases in the secretion of atrial natriuretic factor might contribute to the inability of the dog with constriction of the thoracic inferior vena cava to excrete sodium normally. Sodium 189-195 natriuretic peptide A Canis lupus familiaris 54-79 2957698-6 1987 Infusion of ANF(8-33) decreased blood pressure by 14% (P less than 0.01) and increased sodium excretion by a factor of 10 (P less than 0.01). Sodium 87-93 natriuretic peptide A Canis lupus familiaris 12-15 2956890-2 1987 During administration of 25 and 125 pmol X kg-1 X min-1 of ANF 101-126, fractional sodium excretion (FENa) rose from 1.4 +/- 0.3 to 6.6 +/- 1.1 and 5.6 +/- 1.3% when renal perfusion pressure (RPP) was at its basal level (112 +/- 5 mmHg). Sodium 83-89 natriuretic peptide A Canis lupus familiaris 59-62 2955951-3 1987 At the lowest infusion rate, circulating ANF increased 31 +/- 3 pg/ml, resulting in a significant increase in absolute sodium excretion, fractional excretion of sodium, and fractional excretion of lithium, and a significant decrease in urine osmolality. Sodium 119-125 natriuretic peptide A Canis lupus familiaris 41-44 2955951-3 1987 At the lowest infusion rate, circulating ANF increased 31 +/- 3 pg/ml, resulting in a significant increase in absolute sodium excretion, fractional excretion of sodium, and fractional excretion of lithium, and a significant decrease in urine osmolality. Sodium 161-167 natriuretic peptide A Canis lupus familiaris 41-44 2957298-3 1987 These data suggest that atrial natriuretic factor may affect sodium secretion through the modulation of aldosterone secretion. Sodium 61-67 natriuretic peptide A Bos taurus 24-49 3028491-9 1987 Under both experimental conditions, the pHi recovery after an intracellular acidification, introduced by exposure to 20% CO2 and by removal of NH4+, was found to be inhibited by 53% and 63%, respectively, in the absence of sodium and 60% and 72%, respectively, by 1 mM amiloride. Sodium 223-229 vasoactive intestinal peptide Sus scrofa 40-43 2943930-2 1986 Intrarenal infusion of synthetic atrial natriuretic peptide (0.3 micrograms/kg/min) significantly increased glomerular filtration rate from 29.3 +/- 3.0 to 43.2 +/- 4.4 ml/min, urinary sodium excretion from 20.1 +/- 10.3 to 223.3 +/- 52.3 microEq/min, fractional sodium excretion from 0.47 +/- 0.19 to 3.75 +/- 0.59%. Sodium 185-191 natriuretic peptide A Canis lupus familiaris 33-59 2943930-2 1986 Intrarenal infusion of synthetic atrial natriuretic peptide (0.3 micrograms/kg/min) significantly increased glomerular filtration rate from 29.3 +/- 3.0 to 43.2 +/- 4.4 ml/min, urinary sodium excretion from 20.1 +/- 10.3 to 223.3 +/- 52.3 microEq/min, fractional sodium excretion from 0.47 +/- 0.19 to 3.75 +/- 0.59%. Sodium 263-269 natriuretic peptide A Canis lupus familiaris 33-59 2940094-7 1986 These findings, however, do not necessarily exclude the possibility that ANP also inhibits renal sodium reabsorption by a direct action. Sodium 97-103 natriuretic peptide A Canis lupus familiaris 73-76 3961009-5 1986 These results indicate that, in the pig, drinking in response to Ang II requires the presence of sodium ions. Sodium 97-103 angiogenin Sus scrofa 65-68 6722263-6 1984 The model consists of: Ix, which underlies the repolarization phase of the action potential, IK2, a time-dependent potassium ion pacemaker current, Ibg, a background or time-independent current, and INa, an inward sodium ion current that underlies the upstroke of the action potential. Sodium 214-220 internexin neuronal intermediate filament protein alpha Gallus gallus 199-202 6323226-9 1984 These data indicate that the long-term hypotensive and natriuretic actions of inhibitors of ACE are mediated by inhibition of AngII formation and that the renin-angiotensin system plays an essential role in regulating aldosterone secretion, renal function, and AP during sodium deficiency. Sodium 271-277 angiotensin I converting enzyme Canis lupus familiaris 92-95 6308231-1 1983 The time course of the rise in sodium conductance during positive voltage-clamp pulses was measured in squid giant axons perfused with CsF and immersed in low-sodium solutions. Sodium 31-37 colony stimulating factor 2 Homo sapiens 135-138 238725-0 1975 Natriuresis following fourth ventricle perfusion with high-sodium artificial CSF. Sodium 59-65 granulocyte-macrophage colony-stimulating factor Felis catus 77-80 163797-0 1975 Analysis of unidirectional fluxes of sodium during diarrhea induced by Clostridium perfringens enterotoxin in the rat terminal ileum. Sodium 37-43 cpe Clostridium perfringens 95-106 163797-1 1975 Net intestinal transport of sodium in vivo, in control and enterotoxin (Clostridium perfringens)-treated rats, was resolved into two unidirectional fluxes, influx from and efflux into the lumen of the terminal ileum. Sodium 28-34 cpe Clostridium perfringens 59-70 4448413-5 1974 With a saline bicarbonate solution (Na 145 or 140 m-equiv/1, K 5, or 10 m-equiv/1) in the dialysis tube, considerable absorption of fluid and sodium was demonstrable with little change in sodium concentration. Sodium 142-148 keratin 5 Homo sapiens 61-64 4140229-6 1974 Removal of sodium or potassium from Krebs solution markedly inhibited the transport of DBH. Sodium 11-17 dopamine beta-hydroxylase Homo sapiens 87-90 11344563-2 1974 Preferential expansion of the plasma volume by infusion of salt-poor hyperoncotic albumin solution decreases sodium reabsorption by the proximal tubule. Sodium 109-115 albumin Canis lupus familiaris 82-89 11344563-4 1974 Infusion of salt-poor hyperoncotic albumin significantly decreased plasma ionized calcium, increased immunoreactive PTH (iPTH) in plasma, decreased sodium reabsorption by the proximal tubule, and increased phosphate clearance. Sodium 148-154 albumin Canis lupus familiaris 35-42 11344563-8 1974 These findings (a) indicate that PTH plays a significant role in the decrease in sodium reabsorption by the renal proximal tubule after salt-poor hyperoncotic albumin infusion, and (b) dissociate preferential expansion of the plasma volume from decreases in sodium reabsorption by the proximal tubule. Sodium 81-87 albumin Canis lupus familiaris 159-166 5793683-0 1969 Sodium transfer from plasma to CSF in severe depressive illness. Sodium 0-6 colony stimulating factor 2 Homo sapiens 31-34 6058244-0 1967 The distribution and variations of cholinesterase activity in the nephron and in other tissues concerned with sodium transport. Sodium 110-116 butyrylcholinesterase Homo sapiens 35-49 33713776-0 2021 Aldosterone alleviates lipopolysaccharide-induced acute lung injury by regulating epithelial sodium channel through PI3K/Akt/SGK1 signaling pathway. Sodium 93-99 serum/glucocorticoid regulated kinase 1 Mus musculus 125-129 33713776-2 2021 Epithelial sodium channel (ENaC) plays a key role in regulating the transport of Na+ and clearing alveolar edema fluid effectively. Sodium 11-17 sodium channel, nonvoltage-gated 1 alpha Mus musculus 27-31 33989615-1 2021 Type 1 salt-inducible kinases (SIK1) has been shown to act as a mediator during the cellular adaptation to variations in intracellular sodium in a variety of cell types. Sodium 135-141 salt inducible kinase 1 Mus musculus 31-35 34019817-1 2021 Mutations in SCN5A, encoding the cardiac sodium channel, are linked with familial atrial fibrillation (AF) but the underlying pathophysiologic mechanisms and implications for therapy remain unclear. Sodium 41-47 sodium voltage-gated channel alpha subunit 5 Homo sapiens 13-18 33974881-0 2021 New generation ENaC inhibitors detach cystic fibrosis airway mucus bundles via Sodium/Hydrogen Exchanger inhibition. Sodium 79-85 sodium channel, nonvoltage-gated 1 alpha Mus musculus 15-19 33974881-3 2021 Several drug targets are under evaluation to alleviate airway mucus obstruction in CF and one of these targets is the epithelial sodium channel ENaC. Sodium 129-135 sodium channel, nonvoltage-gated 1 alpha Mus musculus 144-148 33650216-0 2021 Zymogen-locked mutant prostasin (Prss8) leads to incomplete proteolytic activation of the epithelial sodium channel (ENaC) and severely compromises triamterene tolerance in mice. Sodium 101-107 protease, serine 8 (prostasin) Mus musculus 22-31 33650216-0 2021 Zymogen-locked mutant prostasin (Prss8) leads to incomplete proteolytic activation of the epithelial sodium channel (ENaC) and severely compromises triamterene tolerance in mice. Sodium 101-107 protease, serine 8 (prostasin) Mus musculus 33-38 33650216-0 2021 Zymogen-locked mutant prostasin (Prss8) leads to incomplete proteolytic activation of the epithelial sodium channel (ENaC) and severely compromises triamterene tolerance in mice. Sodium 101-107 sodium channel, nonvoltage-gated 1 alpha Mus musculus 117-121 33650216-1 2021 AIM: The serine protease prostasin (Prss8) is expressed in the distal tubule and stimulates proteolytic activation of the epithelial sodium channel (ENaC) in co-expression experiments in vitro. Sodium 133-139 protease, serine 8 (prostasin) Mus musculus 25-34 33650216-1 2021 AIM: The serine protease prostasin (Prss8) is expressed in the distal tubule and stimulates proteolytic activation of the epithelial sodium channel (ENaC) in co-expression experiments in vitro. Sodium 133-139 protease, serine 8 (prostasin) Mus musculus 36-41 33650216-1 2021 AIM: The serine protease prostasin (Prss8) is expressed in the distal tubule and stimulates proteolytic activation of the epithelial sodium channel (ENaC) in co-expression experiments in vitro. Sodium 133-139 sodium channel, nonvoltage-gated 1 alpha Mus musculus 149-153 33650216-8 2021 Sodium conservation under low sodium diet was preserved in Prss8-S238A and Prss8-R44Q mice but with higher plasma aldosterone concentrations in Prss8-R44Q mice. Sodium 0-6 protease, serine 8 (prostasin) Mus musculus 59-64 33650216-8 2021 Sodium conservation under low sodium diet was preserved in Prss8-S238A and Prss8-R44Q mice but with higher plasma aldosterone concentrations in Prss8-R44Q mice. Sodium 0-6 protease, serine 8 (prostasin) Mus musculus 75-80 33650216-8 2021 Sodium conservation under low sodium diet was preserved in Prss8-S238A and Prss8-R44Q mice but with higher plasma aldosterone concentrations in Prss8-R44Q mice. Sodium 0-6 protease, serine 8 (prostasin) Mus musculus 75-80 33953928-1 2021 The sodium potassium ion channel (NaK) is a nonselective ion channel that conducts both sodium and potassium across the cellular membrane. Sodium 4-10 TANK binding kinase 1 Homo sapiens 34-37 33953928-1 2021 The sodium potassium ion channel (NaK) is a nonselective ion channel that conducts both sodium and potassium across the cellular membrane. Sodium 88-94 TANK binding kinase 1 Homo sapiens 34-37 33547739-0 2021 Expansion of the ophthalmic phenotype of SPINT2-related syndromic congenital sodium diarrhea. Sodium 77-83 serine peptidase inhibitor, Kunitz type 2 Homo sapiens 41-47 33745603-13 2021 There was a positive relationship between participant dipstick estimated chloride concentration and laboratory sodium (Kendall"s tau = 0.45; P < 0.001; Spearman"s rs = 0.58 P < 0.001; 47 pairs). Sodium 111-117 microtubule associated protein tau Homo sapiens 129-132 33853169-7 2021 Recent developments shift the focus towards classes of drugs ameliorating prognosis in CKD: sodium-glucose linked transporter 2 (SGLT2) inhibitors have proven beneficial in heart and renal failure - by sodium and fluid excretion, among others; additionally, a novel mineralocorticoid receptor antagonist (MRA), finerenone, was recently shown to improve prognosis in CKD. Sodium 92-98 solute carrier family 5 member 2 Homo sapiens 129-134 33670307-1 2021 Non-dystrophic myotonias have been linked to loss-of-function mutations in the ClC-1 chloride channel or gain-of-function mutations in the Nav1.4 sodium channel. Sodium 146-152 sodium voltage-gated channel alpha subunit 4 Homo sapiens 139-145 33342222-1 2021 Rationale: The cardiac sodium channel NaV1.5 has a fundamental role in excitability and conduction. Sodium 23-29 sodium voltage-gated channel alpha subunit 5 Homo sapiens 38-44 33342222-10 2021 Preferential localization of NCLX to this domain allows for functional coupling where the extrusion of Ca2+ from the mitochondria is powered, at least in part, by the entry of sodium through NaV1.5 channels. Sodium 176-182 sodium voltage-gated channel alpha subunit 5 Homo sapiens 191-197 33318125-1 2021 OBJECTIVE: Sodium-glucose cotransporter 2 (SGLT2) inhibitors reduce the risk for heart failure hospitalization potentially by inducing sodium excretion, osmotic diuresis, and plasma volume contraction. Sodium 135-141 solute carrier family 5 member 2 Homo sapiens 11-41 33318125-1 2021 OBJECTIVE: Sodium-glucose cotransporter 2 (SGLT2) inhibitors reduce the risk for heart failure hospitalization potentially by inducing sodium excretion, osmotic diuresis, and plasma volume contraction. Sodium 135-141 solute carrier family 5 member 2 Homo sapiens 43-48 33318125-2 2021 Few studies have investigated this hypothesis, but none have assessed cumulative sodium excretion with SGLT2 inhibition during standardized sodium intake in patients with type 2 diabetes. Sodium 81-87 solute carrier family 5 member 2 Homo sapiens 103-108 32490567-4 2021 SGLT2-I prevent sodium and glucose reabsorption in proximal convoluted tubule (PCT) of kidneys which is similar to loop diuretics. Sodium 16-22 solute carrier family 5 member 2 Homo sapiens 0-5 32956652-1 2021 NHA2 is a sodium/proton exchanger associated with arterial hypertension in humans, but the role of NHA2 in kidney function and blood pressure homeostasis is currently unknown. Sodium 10-16 solute carrier family 9 member B2 Homo sapiens 0-4 32956652-4 2021 Phosphorylation of the thiazide-sensitive sodium/chloride cotransporter NCC and its upstream activating kinase Ste20/SPS1-related proline/alanine rich kinase (SPAK), as well as the abundance of with no lysine kinase 4 (WNK4), were significantly reduced in the kidneys of NHA2 knock-out mice. Sodium 42-48 serine/threonine kinase 39 Mus musculus 159-163 33190196-8 2021 In conclusion, our findings pointed for significant interactions between genetic polymorphisms (rs699-AGT and rs1799722-BDKRB2) and the consumption of micronutrients (sodium, magnesium, and calcium) on the BP variation. Sodium 167-173 bradykinin receptor B2 Homo sapiens 120-126 32868747-8 2021 Furthermore, Foxo1 interacted with voltage gated sodium Nav1.7 channels and increased the Nav1.7 current density by accelerating activation rather than by changing the expression of Nav1.7 in dorsal root ganglia neurons. Sodium 49-55 sodium voltage-gated channel alpha subunit 9 Rattus norvegicus 56-62 33137501-2 2021 Two polymorphisms, H558R and A572D, of the voltage-gated sodium channel alpha-subunit SCN5A gene were studied in chagasic patients in order to determine their contribution to the susceptibility to the development and/or to the progression of the cardiovascular disease. Sodium 57-63 sodium voltage-gated channel alpha subunit 5 Homo sapiens 86-91 33290383-1 2021 SLC13A5/NaCT is a sodium-coupled citrate transporter expressed in the plasma membrane of the liver, testis, and brain. Sodium 18-24 solute carrier family 13 member 5 Homo sapiens 0-7 33290383-1 2021 SLC13A5/NaCT is a sodium-coupled citrate transporter expressed in the plasma membrane of the liver, testis, and brain. Sodium 18-24 solute carrier family 13 member 5 Homo sapiens 8-12 33534341-10 2021 CONCLUSION: The deletion of CD-S1PR1 reduced sodium excretion, promoted sodium retention, and accelerated DOCA-salt-induced salt-sensitive hypertension, suggesting that the CD-S1PR1 signaling is an important antihypertensive pathway by promoting sodium excretion and that impairment of renal medullary S1PR1 may represent a novel mechanism for salt-sensitive hypertension. Sodium 45-51 sphingosine-1-phosphate receptor 1 Mus musculus 31-36 33534341-10 2021 CONCLUSION: The deletion of CD-S1PR1 reduced sodium excretion, promoted sodium retention, and accelerated DOCA-salt-induced salt-sensitive hypertension, suggesting that the CD-S1PR1 signaling is an important antihypertensive pathway by promoting sodium excretion and that impairment of renal medullary S1PR1 may represent a novel mechanism for salt-sensitive hypertension. Sodium 72-78 sphingosine-1-phosphate receptor 1 Mus musculus 31-36 33534341-10 2021 CONCLUSION: The deletion of CD-S1PR1 reduced sodium excretion, promoted sodium retention, and accelerated DOCA-salt-induced salt-sensitive hypertension, suggesting that the CD-S1PR1 signaling is an important antihypertensive pathway by promoting sodium excretion and that impairment of renal medullary S1PR1 may represent a novel mechanism for salt-sensitive hypertension. Sodium 72-78 sphingosine-1-phosphate receptor 1 Mus musculus 31-36 33510259-4 2021 In DM1-1300, we identified a switch in the cardiac sodium channel SCN5A from the adult to the neonatal isoform. Sodium 51-57 sodium voltage-gated channel alpha subunit 5 Homo sapiens 66-71 33510259-5 2021 The down-regulation of adult SCN5A isoforms is consistent with a shift in the sodium current activation to depolarized potentials observed in DM1-1300. Sodium 78-84 sodium voltage-gated channel alpha subunit 5 Homo sapiens 29-34 33478555-9 2021 Our study shows that the endocytic complex composed of Numb, Nedd4-2 and Eps15, is necessary for non-SUMOylated CRMP2-mediated internalization of sodium channels in vivo. Sodium 146-152 NUMB endocytic adaptor protein Mus musculus 55-59 33478555-9 2021 Our study shows that the endocytic complex composed of Numb, Nedd4-2 and Eps15, is necessary for non-SUMOylated CRMP2-mediated internalization of sodium channels in vivo. Sodium 146-152 neural precursor cell expressed, developmentally down-regulated gene 4-like Mus musculus 61-68 32833340-2 2021 This study aimed to uncover the roles of miR-3175 in regulating cell growth and migration, as well as the expression of its predicted target gene cardiac sodium channel beta4-subunit gene (SCN4B). Sodium 154-160 sodium voltage-gated channel beta subunit 4 Homo sapiens 189-194 33478705-0 2021 Long-Term Efficacy and Safety of Sodium Channel Antagonists in Patients With p.R222Q SCN5A-Related Arrhythmic Dilated Cardiomyopathy. Sodium 33-39 sodium voltage-gated channel alpha subunit 5 Homo sapiens 85-90 32410367-8 2021 CONCLUSIONS: The presence of sodium is important for the absorption of intravesical fluid through aquaporin-2 in the urinary bladders of rats. Sodium 29-35 aquaporin 2 Rattus norvegicus 98-109 33252993-3 2021 Previously, we have shown PVN specific GPCR-coupled Galphai2 subunit proteins are essential to counter the development of salt-sensitive hypertension by mediating the sympathoinhibitory and natriuretic responses to increased dietary sodium intake to maintain sodium homeostasis and normotension. Sodium 233-239 G protein subunit alpha i2 Rattus norvegicus 52-60 33252993-3 2021 Previously, we have shown PVN specific GPCR-coupled Galphai2 subunit proteins are essential to counter the development of salt-sensitive hypertension by mediating the sympathoinhibitory and natriuretic responses to increased dietary sodium intake to maintain sodium homeostasis and normotension. Sodium 259-265 G protein subunit alpha i2 Rattus norvegicus 52-60 33410279-1 2021 BACKGROUND: In the aldosterone-sensitive distal nephron (ASDN), epithelial sodium channel (ENaC)-mediated Na+ absorption drives K+ excretion. Sodium 75-81 sodium channel, nonvoltage-gated 1 alpha Mus musculus 91-95 31882264-3 2021 The availability of the sodium glucose transport protein-2 (SGLT2) inhibitors and glucagon-like peptide -1 receptor antagonists (GLP1-RA) for managing diabetes have shifted our focus in diabetes care beyond glucose lowering to addressing cardiovascular risk reduction. Sodium 24-30 solute carrier family 5 member 2 Homo sapiens 60-65 33135259-2 2021 Several of the sodium-glucose linked transporter 2 inhibitors (SGLT2is) and glucagon-like peptide 1 receptor agonists (GLP1-RAs) dramatically improve outcomes of individuals with type 2 diabetes with and without chronic kidney disease, which is, as heart failure and atherosclerotic cardiovascular disease differentially affected by both drug classes (presumably). Sodium 15-21 solute carrier family 5 member 2 Homo sapiens 63-68 33313626-4 2020 By employing CoP/FeP@PCNFs as the anode for sodium-ion batteries, a large reversible specific capacity (459 mA h g-1 at 0.05 A g-1), excellent rate performance (46.4% capacity retention rate at 10 A g-1 relative to 0.05 A g-1) and long-term cycling stability (208 mA h g-1 at 5 A g-1 over 1000 cycles and 73.5% capacity retention) can be obtained. Sodium 44-50 caspase recruitment domain family member 16 Homo sapiens 13-16 33519442-2 2020 The heterozygous SCN5A V411M mutation of the human sodium channel leads to a LQTS type 3 with severe proarrhythmic effects due to an increase in the late component of the sodium current (INaL). Sodium 51-57 sodium voltage-gated channel alpha subunit 5 Homo sapiens 17-22 33519442-2 2020 The heterozygous SCN5A V411M mutation of the human sodium channel leads to a LQTS type 3 with severe proarrhythmic effects due to an increase in the late component of the sodium current (INaL). Sodium 171-177 sodium voltage-gated channel alpha subunit 5 Homo sapiens 17-22 33322108-2 2020 A high sodium diet is associated with increased expression of beta-myosin heavy chain, decreased expression of alpha/beta-myosin heavy chain, increased myocyte enhancer factor 2/nuclear factor of activated T cell transcriptional activity, and increased salt-inducible kinase 1 expression, which leads to alteration in myocardial mechanical performance. Sodium 7-13 salt inducible kinase 1 Homo sapiens 253-276 33284715-2 2021 All function as cation channels; AMPAR and KAR are more permeable to sodium and NMDAR to calcium ions. Sodium 69-75 KAR Homo sapiens 43-46 32962518-3 2020 The underlying ionic mechanisms by which reduced sodium channel availability in Fhf2 knockout mice predisposes to abnormal excitability at the tissue level are not well defined. Sodium 49-55 fibroblast growth factor 13 Mus musculus 80-84 32962518-4 2020 Objective: Using animal models and theoretical multicellular linear strands, we examined how FHF2 orchestrates the interdependency of sodium, calcium, and gap junctional conductances to safeguard cardiac conduction. Sodium 134-140 fibroblast growth factor 13 Mus musculus 93-97 32962518-7 2020 To explore the ionic mechanisms of block in Fhf2KO hearts, multicellular linear strand models incorporating FHF2-deficient sodium channel inactivation properties were constructed and faithfully recapitulated conduction abnormalities seen in mutant hearts. Sodium 123-129 fibroblast growth factor 13 Mus musculus 108-112 32962518-11 2020 Conclusions: FHF2-dependent effects on sodium channel inactivation ensure adequate sodium current reserve to safeguard against numerous threats to reliable cardiac impulse propagation. Sodium 39-45 fibroblast growth factor 13 Mus musculus 13-17 32962518-11 2020 Conclusions: FHF2-dependent effects on sodium channel inactivation ensure adequate sodium current reserve to safeguard against numerous threats to reliable cardiac impulse propagation. Sodium 83-89 fibroblast growth factor 13 Mus musculus 13-17 33108349-2 2020 The cardiac voltage gated sodium channel alpha-subunit (SCN5A), encoding the Nav1.5 current, plays a key role in the cardiac electrical conduction and arrhythmic risk. Sodium 26-32 sodium voltage-gated channel alpha subunit 5 Homo sapiens 56-61 33108349-2 2020 The cardiac voltage gated sodium channel alpha-subunit (SCN5A), encoding the Nav1.5 current, plays a key role in the cardiac electrical conduction and arrhythmic risk. Sodium 26-32 sodium voltage-gated channel alpha subunit 5 Homo sapiens 77-83 32815768-0 2020 Calmodulin binds to the N-terminal domain of the cardiac sodium channel Nav1.5. Sodium 57-63 sodium voltage-gated channel alpha subunit 5 Homo sapiens 72-78 32815768-1 2020 The cardiac voltage-gated sodium channel Nav1.5 conducts the rapid inward sodium current crucial for cardiomyocyte excitability. Sodium 26-32 sodium voltage-gated channel alpha subunit 5 Homo sapiens 41-47 32815768-1 2020 The cardiac voltage-gated sodium channel Nav1.5 conducts the rapid inward sodium current crucial for cardiomyocyte excitability. Sodium 74-80 sodium voltage-gated channel alpha subunit 5 Homo sapiens 41-47 33190567-6 2020 The administration of SGLT2 inhibitors to patients with diabetes mellitus enhances sodium and glucose excretion, leading to a reduction of the glycosuria threshold and tubular maximal transport of glucose. Sodium 83-89 solute carrier family 5 member 2 Homo sapiens 22-27 32853180-0 2020 Selective pharmacological inhibition of the sodium-dependent phosphate co-transporter NPT2a promotes phosphate excretion. Sodium 44-50 solute carrier family 34 (sodium phosphate), member 1 Mus musculus 86-91 32780153-1 2020 This study analyzed the effects of combination therapy with sodium-glucose transporter-2 inhibitors (SGLT2is) and metformin on fracture risk. Sodium 60-66 solute carrier family 5 member 2 Homo sapiens 101-106 32612066-1 2020 Sodium-glucose cotransporter-2 inhibitors (SGLT2Is) are reported to prevent cardiovascular events by a mechanism possibly including diuresis and sodium excretion. Sodium 145-151 solute carrier family 5 member 2 Homo sapiens 0-30 33213388-1 2020 BACKGROUND: Alterations in the SCN5A gene encoding the cardiac sodium channel Nav1.5 have been linked to a number of arrhythmia syndromes and diseases including long-QT syndrome (LQTS), Brugada syndrome (BrS) and dilative cardiomyopathy (DCM), which may predispose to fatal arrhythmias and sudden death. Sodium 63-69 sodium voltage-gated channel alpha subunit 5 Homo sapiens 31-36 33213388-1 2020 BACKGROUND: Alterations in the SCN5A gene encoding the cardiac sodium channel Nav1.5 have been linked to a number of arrhythmia syndromes and diseases including long-QT syndrome (LQTS), Brugada syndrome (BrS) and dilative cardiomyopathy (DCM), which may predispose to fatal arrhythmias and sudden death. Sodium 63-69 sodium voltage-gated channel alpha subunit 5 Homo sapiens 78-84 33208364-2 2020 Airway dehydration and impaired mucociliary clearance in CF is proposed to result in tonic epithelial sodium channel (ENaC) activity, which drives amiloride-sensitive electrogenic sodium absorption. Sodium 102-108 sodium channel, nonvoltage-gated 1 alpha Mus musculus 118-122 33208364-2 2020 Airway dehydration and impaired mucociliary clearance in CF is proposed to result in tonic epithelial sodium channel (ENaC) activity, which drives amiloride-sensitive electrogenic sodium absorption. Sodium 180-186 sodium channel, nonvoltage-gated 1 alpha Mus musculus 118-122 33208364-3 2020 Decreasing sodium absorption by inhibiting ENaC can reverse airway surface liquid dehydration. Sodium 11-17 sodium channel, nonvoltage-gated 1 alpha Mus musculus 43-47 32791143-0 2020 Reduction of extracellular sodium evokes nociceptive behaviors in the chicken via activation of TRPV1. Sodium 27-33 transient receptor potential cation channel subfamily V member 1 Gallus gallus 96-101 32791143-3 2020 Extracellular sodium ions ([Na+]o) regulate TRPV1 activity in mammals, but their regulatory role on chicken TRPV1 (cTRPV1) is unknown. Sodium 14-20 transient receptor potential cation channel subfamily V member 1 Gallus gallus 44-49 32387251-2 2020 Mutations in CAV3 have caused an LQT3-like accentuation in late sodium current, INa (Nav1.5). Sodium 64-70 sodium voltage-gated channel alpha subunit 5 Homo sapiens 85-91 33294215-2 2020 Previous large-scale cardiovascular outcomes trials of sodium.glucose co-transporter 2 (SGLT2) inhibitors in patients with type 2 diabetes (T2D) have suggested that these agents may help to prevent primary and secondary hospitalisation due to heart failure and cardiovascular death in these patients. Sodium 55-61 solute carrier family 5 member 2 Homo sapiens 88-93 33186352-1 2020 The central pattern generator (CPG) for locomotion is a set of pacemaker neurons endowed with inherent bursting driven by the persistent sodium current (INaP). Sodium 137-143 nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, zeta Mus musculus 153-157 33176139-4 2020 We show that leptin activates the sodium leak channel (NALCN), thereby depolarizing a subset of glutamatergic (VGluT2) LepRb NTS neurons expressing galanin. Sodium 34-40 leptin Mus musculus 13-19 33176139-4 2020 We show that leptin activates the sodium leak channel (NALCN), thereby depolarizing a subset of glutamatergic (VGluT2) LepRb NTS neurons expressing galanin. Sodium 34-40 solute carrier family 17 (sodium-dependent inorganic phosphate cotransporter), member 6 Mus musculus 111-117 33343341-2 2020 Gastrin, a gastrointestinal hormone, is involved in the regulation of kidney function of sodium excretion. Sodium 89-95 gastrin Homo sapiens 0-7 32910945-4 2020 We found that CBD inhibits with comparable micromolar potencies the peak and late components of the NaV1.5 sodium current, the CaV1.2 mediated L-type calcium current, as well as all the repolarizing potassium currents examined except Kir2.1. Sodium 107-113 sodium voltage-gated channel alpha subunit 5 Homo sapiens 100-106 32931730-4 2020 Using iterative cycles of medicinal chemistry synthesis and testing, we identified drug analogs with increased potency and selectivity for inhibiting late sodium current across a panel of 7 LQT3 sodium channel variants and suppressing arrhythmic activity across multiple genetic and pharmacological hiPSC-CM models of LQT3 with diverse backgrounds. Sodium 155-161 sodium voltage-gated channel alpha subunit 5 Homo sapiens 190-194 32931730-4 2020 Using iterative cycles of medicinal chemistry synthesis and testing, we identified drug analogs with increased potency and selectivity for inhibiting late sodium current across a panel of 7 LQT3 sodium channel variants and suppressing arrhythmic activity across multiple genetic and pharmacological hiPSC-CM models of LQT3 with diverse backgrounds. Sodium 155-161 sodium voltage-gated channel alpha subunit 5 Homo sapiens 318-322 32931730-4 2020 Using iterative cycles of medicinal chemistry synthesis and testing, we identified drug analogs with increased potency and selectivity for inhibiting late sodium current across a panel of 7 LQT3 sodium channel variants and suppressing arrhythmic activity across multiple genetic and pharmacological hiPSC-CM models of LQT3 with diverse backgrounds. Sodium 195-201 sodium voltage-gated channel alpha subunit 5 Homo sapiens 190-194 33167351-3 2020 Characterized by increased blood pressure due to excessive sodium retention and plasma volume, it is caused by a mutation in the HSD11B2 gene encoding the oxydoreductase enzyme 11beta-hydroxysteroide dehydrogenase type 2. Sodium 59-65 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 129-136 32882214-0 2020 Norquetiapine blocks the human cardiac sodium channel Nav1.5 in a state-dependent manner. Sodium 39-45 sodium voltage-gated channel alpha subunit 5 Homo sapiens 54-60 32882214-3 2020 In the present study, we used the whole-cell patch-clamp technique to investigate the effect that quetiapine and its major metabolite norquetiapine can exert on human cardiac sodium channels (hNav1.5). Sodium 175-181 sodium voltage-gated channel alpha subunit 5 Homo sapiens 192-199 33066406-1 2020 The human L-type amino acid transporters LAT1 and LAT2 mediate the transport of amino acids and amino acid derivatives across plasma membranes in a sodium-independent, obligatory antiport mode. Sodium 148-154 solute carrier family 7 member 5 Homo sapiens 41-45 33163493-8 2020 Overexpression of CG4928 resulted in induced apoptosis and cytotoxicity, which could be restored when cells were kept in high-sodium media. Sodium 126-132 uncharacterized protein Drosophila melanogaster 18-24 32840624-9 2020 Gene-based tests identified 1 significant gene for sodium excretion, CDC42 small effector 1 (CDC42SE1), which is associated with blood pressure regulation. Sodium 51-57 CDC42 small effector 1 Homo sapiens 69-91 32840624-9 2020 Gene-based tests identified 1 significant gene for sodium excretion, CDC42 small effector 1 (CDC42SE1), which is associated with blood pressure regulation. Sodium 51-57 CDC42 small effector 1 Homo sapiens 93-101 32822653-8 2020 The SGLT2 inhibitor group showed higher sodium concentrations compared with the placebo group and the DPP4 inhibitor group (145.89 vs 143.89 and 144.79 mmol/l, respectively; P = 0.00 and P = 0.04) at 24 weeks. Sodium 40-46 solute carrier family 5 member 2 Homo sapiens 4-9 32304618-4 2020 Expression of Nav1.7 mRNA, the prevailing, pro-invasive voltage-gated sodium channel alpha-subunit (VGSCalpha), was upregulated by hypoxia. Sodium 70-76 sodium voltage-gated channel alpha subunit 9 Rattus norvegicus 14-20 32454217-1 2020 BACKGROUND: Gain-of-function variants in the SCN5A-encoded Nav1.5 sodium channel cause type 3 long QT syndrome (LQT3) and multifocal ectopic Purkinje-related premature contractions (MEPPC). Sodium 66-72 sodium voltage-gated channel alpha subunit 5 Homo sapiens 45-50 32454217-1 2020 BACKGROUND: Gain-of-function variants in the SCN5A-encoded Nav1.5 sodium channel cause type 3 long QT syndrome (LQT3) and multifocal ectopic Purkinje-related premature contractions (MEPPC). Sodium 66-72 sodium voltage-gated channel alpha subunit 5 Homo sapiens 59-65 32454217-1 2020 BACKGROUND: Gain-of-function variants in the SCN5A-encoded Nav1.5 sodium channel cause type 3 long QT syndrome (LQT3) and multifocal ectopic Purkinje-related premature contractions (MEPPC). Sodium 66-72 sodium voltage-gated channel alpha subunit 5 Homo sapiens 112-116 32696547-2 2020 In a recent study, a strong relationship between semi-quantitative abnormalities in sodium MRI and the mutational status of the isocitrate dehydrogenase enzyme (IDH) with untreated cerebral gliomas was observed. Sodium 84-90 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 161-164 32696547-8 2020 Thus, quantitative analysis of relaxation rates, intra- and extracellular sodium concentrations, intracellular molar and volume fractions based on enhanced SISTINA confirmed a relationship between abnormalities in sodium parameters and the IDH mutational status in cerebral gliomas, hence catering for the potential to provide further insights into the status of the disease. Sodium 214-220 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 240-243 32940654-0 2020 GRK4-Mediated Adiponectin Receptor-1 Phosphorylative Desensitization as a Novel Mechanism of Reduced Renal Sodium Excretion in Hypertension. Sodium 107-113 G protein-coupled receptor kinase 4 Rattus norvegicus 0-4 32940654-6 2020 We found that sodium excretion was reduced in adiponectin knockout (Adipo-/-) mice; intrarenal arterial infusion of adiponectin induced natriuresis and diuresis in Wistar-Kyoto (WKY) rats. Sodium 14-20 adiponectin, C1Q and collagen domain containing Mus musculus 46-57 32940654-6 2020 We found that sodium excretion was reduced in adiponectin knockout (Adipo-/-) mice; intrarenal arterial infusion of adiponectin induced natriuresis and diuresis in Wistar-Kyoto (WKY) rats. Sodium 14-20 adiponectin, C1Q and collagen domain containing Mus musculus 68-73 32940654-6 2020 We found that sodium excretion was reduced in adiponectin knockout (Adipo-/-) mice; intrarenal arterial infusion of adiponectin induced natriuresis and diuresis in Wistar-Kyoto (WKY) rats. Sodium 14-20 adiponectin, C1Q and collagen domain containing Mus musculus 116-127 32940654-9 2020 Finally, we identified G protein-coupled receptor kinase 4 (GRK4) as a mediator of adiponectin receptor hyper-phosphorylation; mice transgenic for a hyperphosphorilating variant of GRK4 replicated the abnormal adiponectin function observed in SHRs, whereas down-regulation of GRK4 by renal-ultrasound-directed siRNA restored the adiponectin-mediated sodium excretion and reduced the blood pressure in SHRs. Sodium 350-356 adiponectin, C1Q and collagen domain containing Mus musculus 83-94 32940654-10 2020 We conclude that the stimulatory effect of adiponectin on sodium excretion is impaired in hypertension, which is ascribed to the increased renal GRK4 expression and activity. Sodium 58-64 adiponectin, C1Q and collagen domain containing Mus musculus 43-54 32940654-11 2020 Targeting GRK4 restores impaired adiponectin-mediated sodium excretion in hypertension, thus representing a novel strategy against hypertension. Sodium 54-60 adiponectin, C1Q and collagen domain containing Mus musculus 33-44 32701600-1 2020 PURPOSE OF REVIEW: Sodium-glucose cotransporter 2 (SGLT2) inhibitors are antihyperglycemic drugs that act by inhibiting renal sodium-glucose cotransport. Sodium 126-132 solute carrier family 5 member 2 Homo sapiens 19-49 32701600-1 2020 PURPOSE OF REVIEW: Sodium-glucose cotransporter 2 (SGLT2) inhibitors are antihyperglycemic drugs that act by inhibiting renal sodium-glucose cotransport. Sodium 126-132 solute carrier family 5 member 2 Homo sapiens 51-56 32707593-0 2020 Effects of Child-Pugh B Cirrhosis on Pharmacokinetics of Tofogliflozin, a New Sodium-Glucose Co-Transporter (SGLT2) Inhibitor. Sodium 78-84 solute carrier family 5 member 2 Homo sapiens 109-114 32652691-3 2020 A well characterized aldosterone-induced gene is the serum and glucocorticoid-induced kinase (SGK1), which acts downstream to increase sodium transport in distal kidney nephron epithelial cells. Sodium 135-141 serum/glucocorticoid regulated kinase 1 Mus musculus 94-98 32687659-1 2020 The endothelin receptor type B (ETBR) regulates water and electrolyte balance and blood pressure, in part, by inhibiting renal sodium transport. Sodium 127-133 endothelin receptor type B Mus musculus 4-30 32687659-1 2020 The endothelin receptor type B (ETBR) regulates water and electrolyte balance and blood pressure, in part, by inhibiting renal sodium transport. Sodium 127-133 endothelin receptor type B Mus musculus 32-36 32515017-1 2020 OBJECTIVE: Pathogenic variants in SCN3A, encoding the voltage-gated sodium channel subunit Nav1.3, cause severe childhood-onset epilepsy and malformation of cortical development. Sodium 68-74 sodium voltage-gated channel alpha subunit 3 Homo sapiens 34-39 31828722-4 2020 NaF exposure markedly increased testicular oxidative load, inflammatory (NF-kB/COX-2), and apoptotic (caspase-3) protein expression. Sodium 0-3 caspase-3 Mesocricetus auratus 102-111 32691498-8 2020 One is through the upregulation of early growth response-1 (EGR1) via increased phosphorylation of extracellular signal-regulated protein kinases 1 and 2; and the other is through a reduced serum glucocorticoid-induced kinase-1 (SGK1)-mediated downregulation of epithelial sodium channel-alpha and the induction of oxidative stress. Sodium 273-279 early growth response 1 Homo sapiens 35-58 32691498-8 2020 One is through the upregulation of early growth response-1 (EGR1) via increased phosphorylation of extracellular signal-regulated protein kinases 1 and 2; and the other is through a reduced serum glucocorticoid-induced kinase-1 (SGK1)-mediated downregulation of epithelial sodium channel-alpha and the induction of oxidative stress. Sodium 273-279 early growth response 1 Homo sapiens 60-64 32588437-2 2020 TCAP is shown to modulate alpha-subunit of the human cardiac sodium channel (hNav 1.5) by direct interactions. Sodium 61-67 sodium voltage-gated channel alpha subunit 5 Homo sapiens 77-85 32850980-0 2020 Compound Heterozygous SCN5A Mutations in Severe Sodium Channelopathy With Brugada Syndrome: A Case Report. Sodium 48-54 sodium voltage-gated channel alpha subunit 5 Homo sapiens 22-27 32850980-2 2020 About 20% of BrS cases are explained by mutations in the SCN5A gene, encoding the main cardiac sodium Nav1.5 channel. Sodium 95-101 sodium voltage-gated channel alpha subunit 5 Homo sapiens 57-62 32850980-2 2020 About 20% of BrS cases are explained by mutations in the SCN5A gene, encoding the main cardiac sodium Nav1.5 channel. Sodium 95-101 sodium voltage-gated channel alpha subunit 5 Homo sapiens 102-108 32850980-3 2020 Here we present a severe case of cardiac sodium channelopathy with BrS caused by SCN5A compound heterozygous mutations. Sodium 41-47 sodium voltage-gated channel alpha subunit 5 Homo sapiens 81-86 32850980-14 2020 Conclusion: This is the first report providing support for the pathogenicity of the p.Phe1571Leu SCN5A variant which, together with the c.4813+3_4813+6dupGGGT founder mutation, explains the severity of the phenotype of cardiac sodium channelopathy with BrS in the presented case. Sodium 227-233 sodium voltage-gated channel alpha subunit 5 Homo sapiens 97-102 32774738-2 2020 Our study aim to investigate the underlying mechanism by which IP3R1 signaling mediates the process of homocysteine (Hcy)-induced Ca2+ accumulation via interaction with sodium current (Nav1.5) in atrium. Sodium 169-175 inositol 1,4,5-trisphosphate receptor 1 Mus musculus 63-68 32818118-3 2020 Up to 35% of healthy individuals below 25 years of age, trained athletes, and those with a rare form of the familial syndrome with potassium/sodium hyperpolarization-activated cyclic nucleotide-gated channel 4 (HCN4) mutation may have asymptomatic sinus bradycardia without any heart diseases. Sodium 141-147 hyperpolarization activated cyclic nucleotide gated potassium channel 4 Homo sapiens 148-209 32818118-3 2020 Up to 35% of healthy individuals below 25 years of age, trained athletes, and those with a rare form of the familial syndrome with potassium/sodium hyperpolarization-activated cyclic nucleotide-gated channel 4 (HCN4) mutation may have asymptomatic sinus bradycardia without any heart diseases. Sodium 141-147 hyperpolarization activated cyclic nucleotide gated potassium channel 4 Homo sapiens 211-215 32409841-6 2020 Although there have been trials with various drugs as adjunctive therapy to insulin in T1DM currently in the UK, there is only one sodium glucose transport protein 2 (SGLT2) inhibitor with a marketing authorization for use in this indication. Sodium 131-137 solute carrier family 5 member 2 Homo sapiens 167-172 32645929-4 2020 Pulmonary sodium-potassium-chloride co-transporter 1 (NKCC1) regulates the net influx of ions and water into alveolar cells. Sodium 10-16 solute carrier family 12 member 2 Homo sapiens 54-59 32615940-1 2020 BACKGROUND: Loss-of-function mutations of human cardiac sodium channel gene SCN5A induce a wide range of arrhythmic disorders. Sodium 56-62 sodium voltage-gated channel alpha subunit 5 Homo sapiens 76-81 32077098-3 2020 We hypothesized that high glucose, could adversely affect Nav1.5, the major cardiac sodium channel isoform of the heart, at least partially via oxidative stress. Sodium 84-90 sodium voltage-gated channel alpha subunit 5 Homo sapiens 58-64 32775991-0 2020 Do SGLT-2 Inhibitors Act Only Through a Functional Tubuloglomerular Feedback Induced by the Increased Outflow of Sodium? Sodium 113-119 solute carrier family 5 member 2 Homo sapiens 3-9 32277752-8 2020 The gills of otx2bhu3625/hu3625 fish have weak sodium influx, consistent with the role of prolactin in osmoregulation. Sodium 47-53 orthodenticle homeobox 2b Danio rerio 13-17 32591971-11 2020 MR analysis revealed that the odds ratio for hypertension per 1 mg/day increment of dietary sodium intake was 2.24 in participants with the PRKG1 rs12414562 AA genotype. Sodium 92-98 protein kinase cGMP-dependent 1 Homo sapiens 140-145 32572427-4 2020 Serum 5-HT levels were detected with ELISA, and potassium/sodium hyperpolarization activated cyclic nucleotide-gated channel 2 (HCN2) and tryptophan hydroxylase 1 (TPH1) expression levels in colon epithelium of offspring were detected by Western blot and RT-qPCR. Sodium 58-64 hyperpolarization-activated, cyclic nucleotide-gated K+ 2 Mus musculus 128-132 32545865-4 2020 During the ischemic state, excessive sodium ions enter neurons and inappropriately activate the sodium-calcium exchanger (NCX). Sodium 37-43 T cell leukemia, homeobox 2 Mus musculus 122-125 32545865-4 2020 During the ischemic state, excessive sodium ions enter neurons and inappropriately activate the sodium-calcium exchanger (NCX). Sodium 96-102 T cell leukemia, homeobox 2 Mus musculus 122-125 32550094-2 2020 Due to sodium channel mutations in the cardiac membrane, most commonly SCN5A and SCN10A, the heart can be triggered into a fatal arrhythmia. Sodium 7-13 sodium voltage-gated channel alpha subunit 5 Homo sapiens 71-76 32229307-6 2020 Together, sodium taste is mediated by cells expressing ENaC and CALHM1/3, where oral Na+ entry elicits suprathreshold depolarization for action potentials driving voltage-dependent neurotransmission via the channel synapse. Sodium 10-16 calcium homeostasis modulator 3 Homo sapiens 64-72 32496703-1 2020 The gene SCN5A encodes the cardiac sodium channel which, through the conduction of Na+ current into the cell, generates the fast upstroke of the action potential of cardiomyocytes. Sodium 35-41 sodium voltage-gated channel alpha subunit 5 Homo sapiens 9-14 32338037-0 2020 Differences in renal BMAL1 contribution to sodium homeostasis and blood pressure control in male and female mice. Sodium 43-49 aryl hydrocarbon receptor nuclear translocator-like Mus musculus 21-26 32338037-7 2020 In addition, male KS-BMAL1 KO had less sodium retention compared to CNTL in response to a potassium-restricted diet (15% less following 5 days of treatment). Sodium 39-45 aryl hydrocarbon receptor nuclear translocator-like Mus musculus 21-26 32338037-10 2020 We propose that BMAL1 in the distal nephron and collecting duct contributes to blood pressure regulation and sodium handling in a sex-specific manner. Sodium 109-115 aryl hydrocarbon receptor nuclear translocator-like Mus musculus 16-21 31802037-0 2020 Dietary sodium modulates nephropathy in Nedd4-2-deficient mice. Sodium 8-14 neural precursor cell expressed, developmentally down-regulated gene 4-like Mus musculus 40-47 31797525-11 2020 The expression of Ki67 and c-Myc protein was increased in tissues treated with 50 muM NaF and the expression of Fibronectin and Vimentin in the 50 muM NaF treated tissues was stimulated. Sodium 151-154 fibronectin 1 Rattus norvegicus 112-123 32112796-8 2020 Intestinal tissues and derived enteroids from MYO5B(P663L) piglets had reduced apical levels and diffuse sub-apical levels of NHE3 and SGLT1, which regulate transport of sodium, glucose, and water, compared with tissues from control piglets. Sodium 170-176 solute carrier family 5 member 1 Sus scrofa 135-140 32279611-1 2020 Background: To verify the hypothesis that the nature of trigeminal neuralgia (TN) is an ectopic impulse induced by sodium channel modulated by cytokines, we conducted an animal study using the infraorbital nerve chronic constriction injury (CCI) model in rats.Method: The expression of Nav1.3 or IL-6 in the infraorbital nerve (ION) and trigeminal ganglion (TG) were detected by western blot and immunocytochemistry after administration of antisense oligodeoxynucleotide sequence (AS), IL-6 or Anti-IL-6.Results: With intrathecal administration of AS or mismatch oligodeoxynucleotide sequence (MM) in the CCI rats, the Nav1.3-IR in ION and TG accounted for 2.2 +- 0.51% and 8.5 +- 3.1% in AS+CCI group vs. 6.9 +- 1.3% and 38.7 +- 4.8% in MM+CCI group (p < 0.05), respectively. Sodium 115-121 sodium voltage-gated channel alpha subunit 3 Rattus norvegicus 286-292 32279611-1 2020 Background: To verify the hypothesis that the nature of trigeminal neuralgia (TN) is an ectopic impulse induced by sodium channel modulated by cytokines, we conducted an animal study using the infraorbital nerve chronic constriction injury (CCI) model in rats.Method: The expression of Nav1.3 or IL-6 in the infraorbital nerve (ION) and trigeminal ganglion (TG) were detected by western blot and immunocytochemistry after administration of antisense oligodeoxynucleotide sequence (AS), IL-6 or Anti-IL-6.Results: With intrathecal administration of AS or mismatch oligodeoxynucleotide sequence (MM) in the CCI rats, the Nav1.3-IR in ION and TG accounted for 2.2 +- 0.51% and 8.5 +- 3.1% in AS+CCI group vs. 6.9 +- 1.3% and 38.7 +- 4.8% in MM+CCI group (p < 0.05), respectively. Sodium 115-121 sodium voltage-gated channel alpha subunit 3 Rattus norvegicus 619-625 31977939-1 2020 Sodium channel Nav1.7, encoded by the SCN9A gene, is a well validated target that plays a key role in controlling pain sensation. Sodium 0-6 sodium voltage-gated channel alpha subunit 9 Rattus norvegicus 15-21 31977939-1 2020 Sodium channel Nav1.7, encoded by the SCN9A gene, is a well validated target that plays a key role in controlling pain sensation. Sodium 0-6 sodium voltage-gated channel alpha subunit 9 Rattus norvegicus 38-43 32485919-0 2020 Regulators of Epithelial Sodium Channels in Aldosterone-Sensitive Distal Nephrons (ASDN): Critical Roles of Nedd4L/Nedd4-2 and Salt-Sensitive Hypertension. Sodium 25-31 neural precursor cell expressed, developmentally down-regulated gene 4-like Mus musculus 108-114 32315024-5 2020 Western blot analysis and patch-clamping recordings showed that overexpression of UBE1 or UBA6 increased ubiquitination of Nav1.5 and significantly reduced Nav1.5 expression and sodium current density, and knockdown of UBE1 or UBA6 expression significantly increased Nav1.5 expression and sodium current density in HEK293/Nav1.5 cells. Sodium 289-295 ubiquitin like modifier activating enzyme 1 Homo sapiens 82-86 32315024-5 2020 Western blot analysis and patch-clamping recordings showed that overexpression of UBE1 or UBA6 increased ubiquitination of Nav1.5 and significantly reduced Nav1.5 expression and sodium current density, and knockdown of UBE1 or UBA6 expression significantly increased Nav1.5 expression and sodium current density in HEK293/Nav1.5 cells. Sodium 289-295 sodium voltage-gated channel alpha subunit 5 Homo sapiens 123-129 32315024-8 2020 Mutations of K590 and K591 to K590A and K591A abolished the effects of overexpression or knockdown of UBE1 or UBA6 on Nav1.5 expression and sodium current density. Sodium 140-146 ubiquitin like modifier activating enzyme 1 Homo sapiens 102-106 32509969-2 2020 A subset of infants with the neuromuscular disorder sodium channel myotonia, due to mutations in the SCN4A gene, experience apnoeic events due to laryngospasm (myotonia) of the upper airway muscles that may present as a BRUE. Sodium 52-58 sodium voltage-gated channel alpha subunit 4 Homo sapiens 101-106 32431610-2 2020 This electrical impulse is governed by the intricate activity of cardiac ion channels, among them the cardiac voltage-gated potassium (Kv) channels KCNQ1 and hERG as well as the voltage-gated sodium (Nav) channel encoded by SCN5A. Sodium 192-198 sodium voltage-gated channel alpha subunit 5 Homo sapiens 224-229 31925815-5 2020 The peak sodium current density (INa -Peak) was reduced from -84.02 +- 5.68 pA/pF to -65.78 +- 3.96 pA/pF with 1 mumol/L, -54.45 +- 5.18 pA/pF with 3 mumol/L, and -44.20 +- 4.35 pA/pF with 10 mumol/L, respectively. Sodium 9-15 internexin neuronal intermediate filament protein, alpha Rattus norvegicus 33-36 31904424-2 2020 In the heart, the protein CASK (Calcium/CAlmodulin-dependent Serine protein Kinase) negatively regulates the main cardiac sodium channel, NaV1.5, which carries the sodium current (INa) by preventing its anterograde trafficking. Sodium 122-128 sodium voltage-gated channel alpha subunit 5 Homo sapiens 138-144 32245797-4 2020 METHODS: To investigate whether transcellular sodium transport controls tight-junction composition and paracellular permeability via modulating expression of the transmembrane protein claudin-8, we used cultured mouse cortical collecting duct cells to see how overexpression or silencing of epithelial sodium channel (ENaC) subunits and claudin-8 affect paracellular permeability. Sodium 46-52 claudin 8 Mus musculus 184-193 32245797-7 2020 Increased claudin-8 abundance was associated with a reduction in paracellular permeability to sodium, whereas decreased claudin-8 abundance was associated with the opposite effect. Sodium 94-100 claudin 8 Mus musculus 10-19 31420581-8 2020 QR showed that the consumption of sodium was positively associated with SBP (P10) and DBP (P10) in males, and positively associated with DBP (P80-P90) alone in females. Sodium 34-40 coiled-coil domain containing 8 Homo sapiens 146-149 32323320-10 2020 Peak sodium current densities in SCN5A -R800H were larger than those in wild type but the difference was not statistically significantly. Sodium 5-11 sodium voltage-gated channel alpha subunit 5 Homo sapiens 33-38 32372285-4 2020 In the present study, we screened for novel [Na+] sensors involved in water intake control and identified SLC9A4 (also called sodium (Na+)/hydrogen (H+) exchanger 4 (NHE4)). Sodium 126-132 solute carrier family 9 (sodium/hydrogen exchanger), member 4 Mus musculus 106-112 32372285-4 2020 In the present study, we screened for novel [Na+] sensors involved in water intake control and identified SLC9A4 (also called sodium (Na+)/hydrogen (H+) exchanger 4 (NHE4)). Sodium 126-132 solute carrier family 9 (sodium/hydrogen exchanger), member 4 Mus musculus 166-170 32372285-6 2020 Sodium-imaging experiments using cultured cells transfected with slc9a4 revealed that SLC9A4 was activated by increases in extracellular [Na+] ([Na+]o), but not osmolality. Sodium 0-6 solute carrier family 9 (sodium/hydrogen exchanger), member 4 Mus musculus 65-71 32372285-6 2020 Sodium-imaging experiments using cultured cells transfected with slc9a4 revealed that SLC9A4 was activated by increases in extracellular [Na+] ([Na+]o), but not osmolality. Sodium 0-6 solute carrier family 9 (sodium/hydrogen exchanger), member 4 Mus musculus 86-92 32415460-3 2020 We studied gf and gK1 in single HEK293 cells expressing cardiac sodium current channel Nav1.5 (SCN5A). Sodium 64-70 sodium voltage-gated channel alpha subunit 5 Homo sapiens 87-93 32415460-3 2020 We studied gf and gK1 in single HEK293 cells expressing cardiac sodium current channel Nav1.5 (SCN5A). Sodium 64-70 sodium voltage-gated channel alpha subunit 5 Homo sapiens 95-100 32411069-0 2020 Sodium Channel Myotonia Due to Novel Mutations in Domain I of Nav1.4. Sodium 0-6 sodium voltage-gated channel alpha subunit 4 Homo sapiens 62-68 32411069-1 2020 Sodium channel myotonia is a form of muscle channelopathy due to mutations that affect the Nav1.4 channel. Sodium 0-6 sodium voltage-gated channel alpha subunit 4 Homo sapiens 91-97 32411069-8 2020 We characterized two novel mutations of the SCN4A gene expanding the knowledge about genetics of mild forms of myotonia, and we present, to our knowledge, the first homozygous patient with sodium channel myotonia. Sodium 189-195 sodium voltage-gated channel alpha subunit 4 Homo sapiens 44-49 32403855-1 2020 Compact high-power yellow laser is a critical part for sodium beacon adaptive optical systems. Sodium 55-61 ubiquitin like 5 Homo sapiens 62-68 32734255-3 2020 Clinical trials examining inhibitors of the type 2 sodium glucose cotransporter (SGLT2) show small but significant increases in serum magnesium levels in diabetic patients. Sodium 51-57 solute carrier family 5 member 2 Homo sapiens 81-86 31954305-8 2020 SNP/NaHS under stress increased activation of superoxide dismutase (SOD), peroxidase (POX), APX, glutathione reductase (GR), monodehydroascorbate reductase (MDHAR), dehydroascorbate reductase (DHAR), ascorbate (tAsA) and glutathione (GSH). Sodium 4-8 peroxidase-like Triticum aestivum 74-84 31954305-8 2020 SNP/NaHS under stress increased activation of superoxide dismutase (SOD), peroxidase (POX), APX, glutathione reductase (GR), monodehydroascorbate reductase (MDHAR), dehydroascorbate reductase (DHAR), ascorbate (tAsA) and glutathione (GSH). Sodium 4-8 peroxidase-like Triticum aestivum 86-89 32009028-1 2020 Epithelial sodium channel (ENaC) is an amiloride-sensitive sodium ion channel that is expressed in epithelial tissues. Sodium 11-17 sodium channel, nonvoltage-gated 1 alpha Mus musculus 27-31 32009028-1 2020 Epithelial sodium channel (ENaC) is an amiloride-sensitive sodium ion channel that is expressed in epithelial tissues. Sodium 59-65 sodium channel, nonvoltage-gated 1 alpha Mus musculus 27-31 32009028-2 2020 ENaC overexpression and/or hyperactivation in airway epithelial cells cause sodium over-absorption and dysregulated ciliary movement for mucus clearance; however, the agents that suppress constitutive airway ENaC activation are yet to be clinically available. Sodium 76-82 sodium channel, nonvoltage-gated 1 alpha Mus musculus 0-4 32112267-6 2020 In addition, we have shown that ATRAP functions as an endogenous modulator so as to prevent hypertension in response to pathological stimuli, by regulating renal sodium handling. Sodium 162-168 angiotensin II, type I receptor-associated protein Mus musculus 32-37 32037492-5 2020 The further optimization tests indicate that the highest chlorine removal efficiency of 39.06% was observed when the ultrasonic time was 15 min, the sodium dosage and the ethanol dosage were 0.5 g mL-1 and 1.1 mL mL-1, respectively. Sodium 149-155 L1 cell adhesion molecule Mus musculus 197-217 32037659-0 2020 Autophagy stimulation and intracellular sodium reduction as mediators of the cardioprotective effect of sodium-glucose cotransporter 2 inhibitors. Sodium 40-46 solute carrier family 5 member 2 Homo sapiens 104-134 32037659-6 2020 By contrast, experimental studies suggest that SGLT2 inhibitors may reduce intracellular sodium, thereby preventing oxidative stress and cardiomyocyte death. Sodium 89-95 solute carrier family 5 member 2 Homo sapiens 47-52 32114848-2 2020 SGLT2 inhibitors inhibit the coupled reabsorption of sodium and glucose from the proximal tubules, thereby increasing renal glucose and sodium excretion, but they have more widespread renal effects, including inhibition of the sodium:proton exchanger. Sodium 53-59 solute carrier family 5 member 2 Homo sapiens 0-5 32114848-2 2020 SGLT2 inhibitors inhibit the coupled reabsorption of sodium and glucose from the proximal tubules, thereby increasing renal glucose and sodium excretion, but they have more widespread renal effects, including inhibition of the sodium:proton exchanger. Sodium 136-142 solute carrier family 5 member 2 Homo sapiens 0-5 32148128-1 2020 We have previously reported that in salt-resistant rat phenotypes brain, Galphai2 (guanine nucleotide-binding protein alpha inhibiting activity polypeptide 2) proteins are required to maintain blood pressure and sodium balance. Sodium 212-218 G protein subunit alpha i2 Rattus norvegicus 73-81 32148128-4 2020 Furthermore, in response to chronically elevated dietary sodium intake, PVN-specific Galphai2 proteins are essential to counter renal nerve-dependent salt-sensitive hypertension (mean arterial pressure [mm Hg] 8% NaCl; SCR oligodeoxynucleotide 128+-2 versus Galphai2 oligodeoxynucleotide 147+-3; P<0.05). Sodium 57-63 G protein subunit alpha i2 Rattus norvegicus 85-93 32148128-4 2020 Furthermore, in response to chronically elevated dietary sodium intake, PVN-specific Galphai2 proteins are essential to counter renal nerve-dependent salt-sensitive hypertension (mean arterial pressure [mm Hg] 8% NaCl; SCR oligodeoxynucleotide 128+-2 versus Galphai2 oligodeoxynucleotide 147+-3; P<0.05). Sodium 57-63 G protein subunit alpha i2 Rattus norvegicus 258-266 31771816-6 2020 NaHS also upregulated prolyl hydroxylase (PHD)2, and suppressed hypoxia-inducible factor (HIF)-1alpha expression in vivo and in vitro, suggesting H2S inhibits CS-induced activation of PHD2/HIF-1alpha axis. Sodium 0-4 egl-9 family hypoxia-inducible factor 1 Mus musculus 42-47 31771816-6 2020 NaHS also upregulated prolyl hydroxylase (PHD)2, and suppressed hypoxia-inducible factor (HIF)-1alpha expression in vivo and in vitro, suggesting H2S inhibits CS-induced activation of PHD2/HIF-1alpha axis. Sodium 0-4 hypoxia inducible factor 1, alpha subunit Mus musculus 64-101 31771816-6 2020 NaHS also upregulated prolyl hydroxylase (PHD)2, and suppressed hypoxia-inducible factor (HIF)-1alpha expression in vivo and in vitro, suggesting H2S inhibits CS-induced activation of PHD2/HIF-1alpha axis. Sodium 0-4 egl-9 family hypoxia-inducible factor 1 Mus musculus 184-188 31771816-6 2020 NaHS also upregulated prolyl hydroxylase (PHD)2, and suppressed hypoxia-inducible factor (HIF)-1alpha expression in vivo and in vitro, suggesting H2S inhibits CS-induced activation of PHD2/HIF-1alpha axis. Sodium 0-4 hypoxia inducible factor 1, alpha subunit Mus musculus 189-199 31771816-8 2020 These results suggest that NaHS may prevent emphysema via the suppression of PHD2/HIF-1alpha/MAPK signaling pathway, and subsequently inhibition of inflammation, epithelial cell injury and apoptosis, and may be a novel strategy for the treatment of COPD. Sodium 27-31 egl-9 family hypoxia-inducible factor 1 Mus musculus 77-81 31771816-8 2020 These results suggest that NaHS may prevent emphysema via the suppression of PHD2/HIF-1alpha/MAPK signaling pathway, and subsequently inhibition of inflammation, epithelial cell injury and apoptosis, and may be a novel strategy for the treatment of COPD. Sodium 27-31 hypoxia inducible factor 1, alpha subunit Mus musculus 82-92 32027092-10 2020 These data suggest that a relationship exists between NaX and NaV 1.5 and that NaX may play a role in excitation-contraction coupling. Sodium 54-57 sodium voltage-gated channel alpha subunit 5 Homo sapiens 62-69 32059758-6 2020 We show a polymorph-dependent differential synaptic redistribution of alpha3-Na+/K+-ATPase, GluA2 subunit containing alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors, and GluN2B-subunit containing N-methyl-D-aspartate receptors, but not GluA1 subunit containing alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid and metabotropic glutamate receptor 5 receptors. Sodium 70-79 glutamate receptor, ionotropic, NMDA2B (epsilon 2) Mus musculus 189-195 31770723-6 2020 Finally, by using Ce-doped Co CNTs as the precursor, the target catalyst (Ce0.05-doped CoP CNTs) was obtained through a chemical vapour deposition (CVD) process in the presence of NaH2PO2. Sodium 180-187 caspase recruitment domain family member 16 Homo sapiens 87-90 32054691-5 2020 RESULTS: Ablation of the intercalated cell mineralocorticoid receptor in CCDs from aldosterone-treated mice reduced chloride absorption and epithelial sodium channel activity, despite principal cell mineralocorticoid receptor expression in the knockout mice. Sodium 151-157 nuclear receptor subfamily 3, group C, member 2 Mus musculus 43-69 32054691-8 2020 CONCLUSIONS: With high circulating aldosterone, intercalated cell mineralocorticoid receptor ablation reduces chloride absorption in the CCD and indirectly reduces principal cell epithelial sodium channel abundance and function. Sodium 190-196 nuclear receptor subfamily 3, group C, member 2 Mus musculus 66-92 31897553-4 2020 In order to construct the aptasensor, an amino-modified aptamer was immobilized on CdS-Cu2O NAs/TM to serve as a recognition unit for PSA. Sodium 83-95 kallikrein related peptidase 3 Homo sapiens 134-137 31738900-0 2020 Substituted cysteine scanning in D1-S6 of the sodium channel hNav1.4 alters kinetics and structural interactions of slow inactivation. Sodium 46-52 sodium voltage-gated channel alpha subunit 4 Homo sapiens 61-68 31928070-3 2020 Methods - We have developed and validated a method to perform a DMS of variants in SCN5A, which encodes the major voltage-gated sodium channel in the heart. Sodium 128-134 sodium voltage-gated channel alpha subunit 5 Homo sapiens 83-88 32031527-6 2020 Here, we report a patient with a severe phenotype of Mowat-Wilson syndrome, associated with a novel heterozygous de novo frame-shift variant in the ZEB2 gene, as well as an additional novel heterozygous missense variant in the SCN1A gene, the mutation of which is known to affect NaV1.1-mediated sodium current in GABAergic interneurons. Sodium 296-302 zinc finger E-box binding homeobox 2 Homo sapiens 148-152 30345606-8 2020 Our results indicate that a sodium channel consisting, at minimum, of ppk25, ppk29 and ppk23, can sense 7,11-HD, most likely as a receptor. Sodium 28-34 pickpocket 25 Drosophila melanogaster 70-75 30345606-8 2020 Our results indicate that a sodium channel consisting, at minimum, of ppk25, ppk29 and ppk23, can sense 7,11-HD, most likely as a receptor. Sodium 28-34 pickpocket 29 Drosophila melanogaster 77-82 32037601-0 2020 The geography of grassland plant chemistry and productivity accounts for ant sodium and sugar usage. Sodium 77-83 solute carrier family 25 member 6 Homo sapiens 29-32 31596966-8 2020 Ocn-/- VSMCs showed reduced mRNA expression of the osteogenic marker Runx2 (0.51 fold, p < 0.01) and the sodium-dependent phosphate transporter, PiT1 (0.70 fold, p < 0.001), with an increase in the calcification inhibitor Mgp (1.42 fold, p < 0.05) compared to WT. Sodium 108-114 bone gamma-carboxyglutamate protein 2 Mus musculus 0-3 31794424-0 2020 Stomach gastrin is regulated by sodium via PPAR-alpha and dopamine D1 receptor. Sodium 32-38 gastrin Homo sapiens 8-15 31794424-0 2020 Stomach gastrin is regulated by sodium via PPAR-alpha and dopamine D1 receptor. Sodium 32-38 peroxisome proliferator activated receptor alpha Homo sapiens 43-53 31794424-1 2020 Gastrin, secreted by stomach G cells in response to ingested sodium, stimulates the renal cholecystokinin B receptor (CCKBR) to increase renal sodium excretion. Sodium 61-67 gastrin Homo sapiens 0-7 31794424-1 2020 Gastrin, secreted by stomach G cells in response to ingested sodium, stimulates the renal cholecystokinin B receptor (CCKBR) to increase renal sodium excretion. Sodium 143-149 gastrin Homo sapiens 0-7 31794424-2 2020 It is not known how dietary sodium, independent of food, can increase gastrin secretion in human G cells. Sodium 28-34 gastrin Homo sapiens 70-77 31794424-5 2020 the sodium sensor in G cells plays a critical role in the sodium-mediated increase in gastrin expression/secretion, and (2.) Sodium 4-10 gastrin Homo sapiens 86-93 31794424-5 2020 the sodium sensor in G cells plays a critical role in the sodium-mediated increase in gastrin expression/secretion, and (2.) Sodium 58-64 gastrin Homo sapiens 86-93 31794424-8 2020 When extra- or intracellular sodium was increased in human antrum, human G cells, and adenocarcinoma cells, gastrin mRNA and protein expression/secretion were increased. Sodium 29-35 gastrin Homo sapiens 108-115 31794424-12 2020 G cells in the stomach may be the sodium sensor that stimulates gastrin secretion, which enables the kidney to eliminate acutely an oral sodium load. Sodium 34-40 gastrin Homo sapiens 64-71 31794424-12 2020 G cells in the stomach may be the sodium sensor that stimulates gastrin secretion, which enables the kidney to eliminate acutely an oral sodium load. Sodium 137-143 gastrin Homo sapiens 64-71 31851560-3 2020 We have hypothesized that sustained sodium influx due to the expression of SFN-associated sodium channel variants may trigger an energetic deficit in neurons which contributes to degeneration and loss of nerve fibers in SFN. Sodium 36-42 RNA exonuclease 2 Homo sapiens 75-78 31851560-3 2020 We have hypothesized that sustained sodium influx due to the expression of SFN-associated sodium channel variants may trigger an energetic deficit in neurons which contributes to degeneration and loss of nerve fibers in SFN. Sodium 36-42 RNA exonuclease 2 Homo sapiens 220-223 31851560-3 2020 We have hypothesized that sustained sodium influx due to the expression of SFN-associated sodium channel variants may trigger an energetic deficit in neurons which contributes to degeneration and loss of nerve fibers in SFN. Sodium 90-96 RNA exonuclease 2 Homo sapiens 75-78 31851560-3 2020 We have hypothesized that sustained sodium influx due to the expression of SFN-associated sodium channel variants may trigger an energetic deficit in neurons which contributes to degeneration and loss of nerve fibers in SFN. Sodium 90-96 RNA exonuclease 2 Homo sapiens 220-223 30989437-11 2020 CONCLUSIONS: Sodium MRI appears to be more strongly related to the IDH mutational status than are [18F]FET-PET parameters. Sodium 13-19 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 67-70 31950584-8 2020 We mapped the localization of the epithelial sodium channel (ENaC), aquaporin-9 (AQP9), and cystic fibrosis transmembrane conductance regulator (CFTR) in the rat and mouse vas deferens. Sodium 45-51 CF transmembrane conductance regulator Rattus norvegicus 145-149 32026654-0 2020 Role of sodium-dependent Pi transporter/Npt2c on Pi homeostasis in klotho knockout mice different properties between juvenile and adult stages. Sodium 8-14 solute carrier family 34 (sodium phosphate), member 3 Mus musculus 40-45 31776304-10 2020 In addition, glucose-free medium and knockdown of SGLT2 by siRNA suppressed the glucose-induced whole-cell current of MCF-7 cells, suggesting that ipragliflozin inhibits sodium and glucose cotransport through SGLT2. Sodium 170-176 solute carrier family 5 member 2 Homo sapiens 50-55 31721323-0 2020 Fe doped CoP flower-like microstructure on carbon membrane as integrated electrode with enhanced sodium ion storage. Sodium 97-103 caspase recruitment domain family member 16 Homo sapiens 9-12 31721323-6 2020 The hierarchical Fe doped CoP directly grown on the carbon membrane could increase the active sites for sodium species intercalation and further promote the internal electron conduction in the Fe doped CoP/CM electrode. Sodium 104-110 caspase recruitment domain family member 16 Homo sapiens 26-29 31721323-6 2020 The hierarchical Fe doped CoP directly grown on the carbon membrane could increase the active sites for sodium species intercalation and further promote the internal electron conduction in the Fe doped CoP/CM electrode. Sodium 104-110 caspase recruitment domain family member 16 Homo sapiens 202-205 31721323-7 2020 Thereby, the Fe doped CoP/CM as anode electrode for sodium ion batteries exhibits high specific capacity of 515 mAh g-1 at 100 mA g-1 after 100 cycles. Sodium 52-58 caspase recruitment domain family member 16 Homo sapiens 22-25 31979418-8 2020 Exposure of the thyroid to NaI modulates 15 cellular pathways, most of which are also affected by ICM treatment (including the elF4 and P706SK cell signaling pathway and INSR identified as an upstream activator in both treatments). Sodium 27-30 E74 like ETS transcription factor 4 Homo sapiens 127-131 31993492-2 2020 Originally believed to be predominantly associated with mutations in SCN5A encoding for the cardiac sodium channel, mutations of 18 genes other than SCN5A have been implicated in the pathogenesis of BrS to date. Sodium 100-106 sodium voltage-gated channel alpha subunit 5 Homo sapiens 69-74 31866066-1 2020 Voltage-gated sodium channel Nav1.5 generates cardiac action potentials and initiates the heartbeat. Sodium 14-20 sodium voltage-gated channel alpha subunit 5 Homo sapiens 29-35 31866066-3 2020 NaV1.5 is distinguished from other sodium channels by a unique glycosyl moiety and loss of disulfide-bonding capability at the NaVbeta subunit-interaction sites. Sodium 35-41 sodium voltage-gated channel alpha subunit 5 Homo sapiens 0-6 31970162-5 2019 SGLT2 inhibitors also promote sodium metabolism-mediated cardioprotective effects. Sodium 30-36 solute carrier family 5 member 2 Homo sapiens 0-5 31920633-1 2019 The cardiac Nav1.5 mediated sodium current (INa) generates the upstroke of the action potential in atrial and ventricular myocytes. Sodium 28-34 sodium voltage-gated channel alpha subunit 5 Homo sapiens 12-18 31559679-3 2019 The subsequent reduction of MTC1 and palladium acetate with NaBH4 afforded cage-supported highly dispersed ultrafine palladium nanoparticles with a narrow particle size distribution of 1.9 +- 0.4 nm, denoted as Pd@MTC1-1/5. Sodium 60-65 ret proto-oncogene Homo sapiens 214-218 31559679-4 2019 Such ultrafine palladium nanoparticles in Pd@MTC1-1/5, in cooperation with photocatalytically active MTC1, enable efficient cascade reactions including visible light-induced aerobic hydroxylation of 4-nitrophenylboronic acid to 4-nitrophenol and the following hydrogenation reduction with NaBH4. Sodium 289-294 ret proto-oncogene Homo sapiens 45-49 31559679-4 2019 Such ultrafine palladium nanoparticles in Pd@MTC1-1/5, in cooperation with photocatalytically active MTC1, enable efficient cascade reactions including visible light-induced aerobic hydroxylation of 4-nitrophenylboronic acid to 4-nitrophenol and the following hydrogenation reduction with NaBH4. Sodium 289-294 ret proto-oncogene Homo sapiens 101-105 31631436-7 2019 Researchers in our laboratory have reported that hypothalamic paraventricular nucleus (PVN) Galphai2 proteins mediate the sympathoinhibitory and normotensive responses to high sodium intake in salt-resistant rats. Sodium 176-182 G protein subunit alpha i2 Rattus norvegicus 92-100 31549401-8 2019 Here, we analyzed the relation between different patterns of activity-induced [Na+ ]i signalling and ATP in mouse hippocampal CA1 pyramidal neurons by Na+ -imaging with SBFI (sodium-binding benzofurane isophthalate) and employing the genetically-encoded nanosensor ATeam1.03YEMK ("ATeam"). Sodium 175-181 carbonic anhydrase 1 Mus musculus 126-129 31728700-0 2019 beta1 and beta3 subunits amplify mechanosensitivity of the cardiac voltage-gated sodium channel Nav1.5. Sodium 81-87 sodium voltage-gated channel alpha subunit 5 Homo sapiens 96-102 31728700-2 2019 The voltage-gated sodium channel Nav1.5 is the main contributor to the rising phase of the action potential in the heart. Sodium 18-24 sodium voltage-gated channel alpha subunit 5 Homo sapiens 33-39 31398537-2 2019 Inflammatory mediators can act on multiple receptors expressed in airway C-fibers, nonetheless, the action potential initiation in C-fibers depends on a limited number of voltage-gated sodium channel (NaV1) subtypes. Sodium 185-191 neuron navigator 1 Cavia porcellus 201-205 31795454-7 2019 We found phosphorylated Akt, a downstream target of the PI3 kinase pathway, phosphor- mitogen-activated protein kinase kinase 1/2 (ERK), and intracellular reactive oxygen species (ROS) were predominantly induced by NaIO3. Sodium 215-220 mitogen-activated protein kinase kinase 1 Homo sapiens 86-129 31852640-12 2019 Compared with those in BCNI group, the rats in BCNI+NaHS group had significantly decreased expressions of caspase-3 and Bax proteins (P < 0.05) with significantly enhanced Bcl-2 protein expression and an increased Bcl-2/Bax ratio (P < 0.05). Sodium 52-56 BCL2 associated X, apoptosis regulator Rattus norvegicus 120-123 31852640-12 2019 Compared with those in BCNI group, the rats in BCNI+NaHS group had significantly decreased expressions of caspase-3 and Bax proteins (P < 0.05) with significantly enhanced Bcl-2 protein expression and an increased Bcl-2/Bax ratio (P < 0.05). Sodium 52-56 BCL2 associated X, apoptosis regulator Rattus norvegicus 223-226 31621295-4 2019 These mass peaks were identified to be protonated and sodium adducts of LPC 16:0 by using tandem mass spectra (MS2 and MS3) of purely synthesized LPC 16:0 and extracted LPC 16:0 from a healthy control and a sepsis patient. Sodium 54-60 MS2 Homo sapiens 111-114 31705320-1 2019 xCT is a sodium-independent amino acid antiporter that imports L-cystine and exports L-glutamate in a 1:1 ratio. Sodium 9-15 solute carrier family 7 member 11 Homo sapiens 0-3 31570523-9 2019 Co-localization of epithelial sodium channel (ENaC) with the plasma membrane was reduced in cysts in PKD1-knockout mice, consistent with an inability of the cysts to absorb fluid. Sodium 30-36 sodium channel, nonvoltage-gated 1 alpha Mus musculus 46-50 31570523-9 2019 Co-localization of epithelial sodium channel (ENaC) with the plasma membrane was reduced in cysts in PKD1-knockout mice, consistent with an inability of the cysts to absorb fluid. Sodium 30-36 polycystin 1, transient receptor potential channel interacting Mus musculus 101-105 31482509-2 2019 In this study, we aimed to characterise the 1-year switching, adherence, and persistence patterns among people with diabetes aged 18 years and older prescribed sodium-glucose co-transporter 2 inhibitors (SGLT2is) in Australia. Sodium 160-166 solute carrier family 5 member 2 Homo sapiens 204-209 31518570-0 2019 Carbonic anhydrase II/sodium-proton exchanger 1 metabolon complex in cardiomyopathy of ob-/- type 2 diabetic mice. Sodium 22-28 leptin Mus musculus 87-89 31257412-0 2019 Sex and body mass index modify the association between leptin and sodium excretion: a cross-sectional study in an African population. Sodium 66-72 leptin Homo sapiens 55-61 31257412-2 2019 The aim of the study was to assess the relationship of leptin with urinary sodium excretion and proximal sodium reabsorption in humans. Sodium 75-81 leptin Homo sapiens 55-61 31257412-9 2019 Leptin was associated positively with daytime (coefficient (c): 0.16, standard deviation (sd): 0.03, p<0.001), nighttime urinary sodium excretion (c: 017, sd: 0.04), p<0.019), daytime lithium clearance (c: 0.40, sd: 0.08, p<0.001) and nighttime lithium clearance (c: 0.39, sd: 0.10, p<0.001) after adjusting for sex. Sodium 132-138 leptin Homo sapiens 0-6 31257412-11 2019 When BMI was categorized in normal vs overweight participant, leptin was associated with daytime and nighttime sodium excretion rates (c: 0.14, sd: 0.05, p=0.011 and c: 0.22, sd: 0.07, p=0.002 respectively) only in overweight participants. Sodium 111-117 leptin Homo sapiens 62-68 31257412-12 2019 CONCLUSION: Leptin is associated positively with daytime and nighttime sodium excretion and lithium clearance suggesting a natriuretic rather than a sodium retaining effect of leptin. Sodium 71-77 leptin Homo sapiens 12-18 31257412-14 2019 These results highlight the importance of sex and obesity in our understanding of the relationships between leptin, blood pressure and renal sodium handling. Sodium 141-147 leptin Homo sapiens 108-114 31614475-2 2019 SCN5A mutations associated with long QT syndrome type 3 (LQT3) lead to enhanced late sodium current and consequent action potential (AP) prolongation. Sodium 85-91 sodium voltage-gated channel alpha subunit 5 Homo sapiens 57-61 31614475-5 2019 We found that in HEK293 cells, the SCN5A-p.Y1977N mutation abolished the interaction between Nav1.5 and Nedd4-2, suppressed PY-motif-dependent ubiquitylation of Nav1.5, and consequently abrogated Nedd4-2 induced sodium current (INa) decrease. Sodium 212-218 sodium voltage-gated channel alpha subunit 5 Homo sapiens 35-40 31614475-5 2019 We found that in HEK293 cells, the SCN5A-p.Y1977N mutation abolished the interaction between Nav1.5 and Nedd4-2, suppressed PY-motif-dependent ubiquitylation of Nav1.5, and consequently abrogated Nedd4-2 induced sodium current (INa) decrease. Sodium 212-218 sodium voltage-gated channel alpha subunit 5 Homo sapiens 93-99 31680960-10 2019 Our findings indicated that the phosphorylated activation of Akt played a role in the proliferation of HaCat cells upon long-term, low-dose NaAsO2 exposure through the phosphorylative regulation of its downstream cell cycle regulating factors of GSK-3beta/cyclin D1, p21 and p27, which could induce the promotion of cell cycle progression from G1 to S/G2M phase. Sodium 140-146 interferon alpha inducible protein 27 Homo sapiens 275-278 31559991-2 2019 The results demonstrate that the as-synthesized CoP/CNs as electrocatalysts exhibit high electrocatalytic activity toward the N2 reduction reaction (NRR), affording a large NH3 yield rate of 48.9 mug h-1 mgcat.-1 with a faradaic efficiency (FE) of 8.7% at -0.4 V (vs. RHE) in 0.1 M Na2SO4 electrolyte. Sodium 282-288 caspase recruitment domain family member 16 Homo sapiens 48-51 31538763-7 2019 Therefore, the SnSe/FLG composite is a promising anode for high-performance lithium/sodium-ion batteries. Sodium 84-90 filaggrin Homo sapiens 20-23 31523904-2 2019 Independently of their actions on blood glucose, sodium-glucose co-transporter 2 (SGLT2) inhibitors exert a broad range of biological effects (including actions to inhibit cardiac inflammation and fibrosis, antagonize sodium retention and improve glomerular function) that can ameliorate the pathophysiological derangements in HFpEF. Sodium 49-55 solute carrier family 5 member 2 Homo sapiens 82-87 31302244-5 2019 These age-dependent cortical excitability dysfunctions correlate with a similar time-dependent trend of the persistent sodium current (INaP) amplitude alterations, suggesting that INaP may play a crucial role in the G93A cortical excitability aberrations. Sodium 119-125 nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, zeta Mus musculus 135-139 31302244-5 2019 These age-dependent cortical excitability dysfunctions correlate with a similar time-dependent trend of the persistent sodium current (INaP) amplitude alterations, suggesting that INaP may play a crucial role in the G93A cortical excitability aberrations. Sodium 119-125 nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, zeta Mus musculus 180-184 31611837-2 2019 Molecular mechanisms responsible for DM cardiac defects are still unclear; however, missplicing of the cardiac isoform of troponin T (TNNT2) and of the cardiac sodium channel (SCN5A) genes might contribute to the reduced myocardial function and conduction abnormalities seen in DM patients. Sodium 160-166 sodium voltage-gated channel alpha subunit 5 Homo sapiens 176-181 31627867-3 2019 Mutations in SCN5A gene coding for the alpha-subunit of the NaV1.5 cardiac sodium channel are identified in 15-30% of BrS cases. Sodium 75-81 sodium voltage-gated channel alpha subunit 5 Homo sapiens 13-18 31627867-3 2019 Mutations in SCN5A gene coding for the alpha-subunit of the NaV1.5 cardiac sodium channel are identified in 15-30% of BrS cases. Sodium 75-81 sodium voltage-gated channel alpha subunit 5 Homo sapiens 60-66 31257483-1 2019 Voltage-gated sodium channel beta2 (Navbeta2), as an unconventional substrate of beta-site amyloid precursor protein cleaving enzyme 1, is involved in regulating the neuronal surface expression of sodium channels. Sodium 14-20 beta-site APP cleaving enzyme 1 Mus musculus 81-134 31257483-1 2019 Voltage-gated sodium channel beta2 (Navbeta2), as an unconventional substrate of beta-site amyloid precursor protein cleaving enzyme 1, is involved in regulating the neuronal surface expression of sodium channels. Sodium 197-203 beta-site APP cleaving enzyme 1 Mus musculus 81-134 31365577-4 2019 Sodium storage capacity was decreased in Ext1+/-Ext2+/- mice as reflected by a 77% reduction in endothelial surface layer thickness and a lower skin sodium-to-glycosaminoglycan ratio. Sodium 0-6 exostosin glycosyltransferase 2 Mus musculus 48-52 31365577-4 2019 Sodium storage capacity was decreased in Ext1+/-Ext2+/- mice as reflected by a 77% reduction in endothelial surface layer thickness and a lower skin sodium-to-glycosaminoglycan ratio. Sodium 149-155 exostosin glycosyltransferase 2 Mus musculus 48-52 31384471-1 2019 Selective analogs of the natural glycoside phloridzin are marketed drugs that reduce hyperglycemia in diabetes by inhibiting the active sodium glucose cotransporter SGLT2 in the kidneys. Sodium 136-142 solute carrier family 5 member 2 Homo sapiens 165-170 31362426-2 2019 In particular, the human adenosine A2A receptor (A2A AR) is the first GPCR in which a monovalent sodium ion was crystallized in a distal site from the canonical orthosteric one, corroborating, from a structural point of view, its role as a negative allosteric modulator. Sodium 97-103 adenosine A2a receptor Homo sapiens 25-47 31534500-0 2019 Focused ultrasound activates voltage-gated calcium channels through depolarizing TRPC1 sodium currents in kidney and skeletal muscle. Sodium 87-93 transient receptor potential cation channel, subfamily C, member 1 Mus musculus 81-86 31312012-0 2019 Bisphenol A Regulates Sodium Ramp Currents in Mouse Dorsal Root Ganglion Neurons and Increases Nociception. Sodium 22-28 peptidase domain containing associated with muscle regeneration 1 Mus musculus 29-33 31054938-0 2019 MiR-30b-5p attenuates oxaliplatin-induced peripheral neuropathic pain through the voltage-gated sodium channel Nav1.6 in rats. Sodium 96-102 microRNA 30b Rattus norvegicus 0-7 31054938-0 2019 MiR-30b-5p attenuates oxaliplatin-induced peripheral neuropathic pain through the voltage-gated sodium channel Nav1.6 in rats. Sodium 96-102 neuron navigator 1 Rattus norvegicus 111-115 30980865-6 2019 As a nonselective monovalent cation channel, TRPM4 upregulation and activation enhance sodium entry, which leads to depolarization of the membrane potential. Sodium 87-93 transient receptor potential cation channel subfamily M member 4 Homo sapiens 45-50 31283756-6 2019 For drugs eliciting block of the inward sodium or calcium currents (mexiletine, lidocaine), the TrX effect profiles were consistent with accelerated electrical activity in the initial repolarization phase. Sodium 40-46 thioredoxin Homo sapiens 96-99 30588669-2 2019 This study aims at providing more evidence on this regard by addressing the effects of feeding cycle on the voltage-gated sodium (Na+ ) currents of acutely isolated Wistar rat hippocampal CA1 neurones. Sodium 122-128 carbonic anhydrase 1 Rattus norvegicus 188-191 30997701-8 2019 The presence of abundant sodium adducts of beta-casein further complicated the spectra. Sodium 25-31 casein beta Homo sapiens 43-54 30905471-0 2019 The TNF-derived TIP peptide activates the epithelial sodium channel and ameliorates experimental nephrotoxic serum nephritis. Sodium 53-59 TOR signaling pathway regulator Homo sapiens 16-19 30905471-9 2019 We show that TIP peptide activates the epithelial sodium channel(ENaC), which is expressed by GEC, upon binding to the channel"s alpha subunit. Sodium 50-56 TOR signaling pathway regulator Homo sapiens 13-16 30914445-9 2019 This work identifies a critical and important new role for MAP1B in the regulation of neuronal excitability and adds to our understanding of AIS maintenance and plasticity, in addition to identifying new target residues for pathogenic mutations of SCN8A SIGNIFICANCE STATEMENT Nav1.6 is a major voltage-gated sodium channel in human brain, where it regulates neuronal activity due to its localization at the axon initial segment (AIS). Sodium 309-315 microtubule associated protein 1B Homo sapiens 59-64 30914445-13 2019 This work confirms a new biological role of MAP1B in the regulation of sodium channel localization and will contribute to future analysis of patient mutations in the cytoplasmic N terminus of Nav1.6. Sodium 71-77 microtubule associated protein 1B Homo sapiens 44-49 31118417-3 2019 Cardiomyocytes differentiated from these iPSCs, and which thus carry K219T-LMNA, have altered action potential, reduced peak sodium current and diminished conduction velocity. Sodium 125-131 lamin A/C Homo sapiens 75-79 31118417-7 2019 Thus, K219T-LMNA cooperates with PRC2 in downregulating SCN5A, leading to decreased sodium current density and slower conduction velocity. Sodium 84-90 lamin A/C Homo sapiens 12-16 31118417-7 2019 Thus, K219T-LMNA cooperates with PRC2 in downregulating SCN5A, leading to decreased sodium current density and slower conduction velocity. Sodium 84-90 sodium voltage-gated channel alpha subunit 5 Homo sapiens 56-61 30649746-1 2019 Plecanatide, a uroguanylin analog, activates the guanylate cyclase C receptors in the epithelial lining of the gastrointestinal tract in a pH-dependent fashion initiating (1) the conversion of intracellular guanosine triphosphate to cyclic guanosine monophosphate, which increases the activity of the cystic fibrosis transmembrane conductance regulator to increase chloride and bicarbonate secretion into the intestinal lumen and (2) a decrease in activity of the sodium-hydrogen ion exchanger. Sodium 464-470 natriuretic peptide receptor 3 Homo sapiens 49-68 29522854-6 2019 In addition, we found upregulation of neuronal inhibitory ligands and their cognate microglial receptors, while downregulation of Esr1 and Scn1a, encoding estrogen receptor alpha and voltage-gated sodium-channel Na(v)1.1, respectively, was observed. Sodium 197-203 estrogen receptor 1 Rattus norvegicus 130-134 30635397-6 2019 ASCT2 deficiency was compensated by increased levels of sodium neutral amino acid transporter 1 (SNAT1 or SLC38A1) and SNAT2 (SLC38A2) in ASCT2ko 143B cells, mediated by a GCN2 EIF2alpha kinase (GCN2)-dependent pathway, but this compensation was not observed in ASCT2ko HCC1806 cells. Sodium 56-62 solute carrier family 38 member 1 Homo sapiens 97-102 30566002-0 2019 G protein-coupled receptor 37L1 regulates renal sodium transport and blood pressure. Sodium 48-54 G protein-coupled receptor 37 like 1 Homo sapiens 0-31 30566002-8 2019 Inhibition of Na+/H+ exchanger isoform 3 (NHE3) activity abrogated the GPR37L1-mediated increase in intracellular sodium. Sodium 114-120 G protein-coupled receptor 37 like 1 Homo sapiens 71-78 30566002-11 2019 Our findings show that in the kidney, GPR37L1 participates in renal proximal tubule luminal sodium transport and regulation of blood pressure by increasing the renal expression and function of NHE3 by decreasing cAMP production. Sodium 92-98 G protein-coupled receptor 37 like 1 Homo sapiens 38-45 30445423-0 2019 SPINT2 (HAI-2) missense variants identified in congenital sodium diarrhea/tufting enteropathy affect the ability of HAI-2 to inhibit prostasin but not matriptase. Sodium 58-64 serine peptidase inhibitor, Kunitz type 2 Homo sapiens 0-6 30445423-0 2019 SPINT2 (HAI-2) missense variants identified in congenital sodium diarrhea/tufting enteropathy affect the ability of HAI-2 to inhibit prostasin but not matriptase. Sodium 58-64 serine peptidase inhibitor, Kunitz type 2 Homo sapiens 8-13 30445423-0 2019 SPINT2 (HAI-2) missense variants identified in congenital sodium diarrhea/tufting enteropathy affect the ability of HAI-2 to inhibit prostasin but not matriptase. Sodium 58-64 serine peptidase inhibitor, Kunitz type 2 Homo sapiens 116-121 30488537-7 2019 Electrophysiological studies show that mutation p.Arg399Cys decreases the peak cardiac sodium current by decreasing the cell surface expression level of cardiac sodium channel Nav 1.5, but does not affect IKr potassium current. Sodium 87-93 sodium voltage-gated channel alpha subunit 5 Homo sapiens 176-183 30636551-4 2019 Although cardiac (echocardiography) and resistance artery (perfusion myography) functions were normal, metabolic cage studies revealed that c-myb h/h mice had increased 24-hour urine output and sodium excretion versus WT. Sodium 194-200 myeloblastosis oncogene Mus musculus 140-145 30606887-1 2019 The SALT-OVERLY-SENSITIVE (SOS) pathway in Arabidopsis (Arabidopsis thaliana) functions to prevent the toxic accumulation of sodium in the cytosol when plants are grown in salt-affected soils. Sodium 125-131 sodium proton exchanger, putative (NHX7) (SOS1) Arabidopsis thaliana 27-30 30637460-3 2019 We investigated several Markov models for the human cardiac sodium channel NaV1.5 to derive a minimal mathematical model that describes the reported experimental data obtained using major voltage clamp protocols. Sodium 60-66 sodium voltage-gated channel alpha subunit 5 Homo sapiens 75-81 30569925-4 2019 Due to this multiscale coordinated design, the CoP@DC@GR nanocomposite demonstrates high charge capacity, remarkable cycle stability, and distinguished rate performance; therefore, it possesses fascinating potential in anodes for lithium and sodium storage. Sodium 242-248 caspase recruitment domain family member 16 Homo sapiens 47-50 30285481-2 2019 Humans obtain vitamin C from dietary sources via intestinal absorption, a process that involves the sodium-dependent vitamin C transporters-1 and -2 (SVCT1 and SVCT2). Sodium 100-106 solute carrier family 23 member 1 Homo sapiens 150-155 30394905-3 2019 Although there are 17 types of LQTS, most patients have types 1 or 2 which are due to mutations in KCNQ1 and KCNH2 (encoding for the cardiac potassium channels), and type 3 which is due to a mutation in SCN5A (encoding for the sodium channel). Sodium 227-233 sodium voltage-gated channel alpha subunit 5 Homo sapiens 203-208 29136153-0 2018 Reverse NCX Attenuates Cellular Sodium Loading in Metabolically Compromised Cortex. Sodium 32-38 T cell leukemia, homeobox 2 Mus musculus 8-11 29136153-7 2018 In both cell types, inhibition of sodium/calcium exchange (NCX) increased sodium transients. Sodium 34-40 T cell leukemia, homeobox 2 Mus musculus 59-62 29136153-7 2018 In both cell types, inhibition of sodium/calcium exchange (NCX) increased sodium transients. Sodium 74-80 T cell leukemia, homeobox 2 Mus musculus 59-62 30524708-5 2018 In the kidney, increased sodium delivery to the macula densa mediated by SGLT-2 inhibition has the potential to reduce intraglomerular pressure, which may explain why SGLT-2 inhibitors reduce albuminuria and appear to slow kidney function decline in people with diabetes. Sodium 25-31 solute carrier family 5 member 2 Homo sapiens 73-79 30524708-5 2018 In the kidney, increased sodium delivery to the macula densa mediated by SGLT-2 inhibition has the potential to reduce intraglomerular pressure, which may explain why SGLT-2 inhibitors reduce albuminuria and appear to slow kidney function decline in people with diabetes. Sodium 25-31 solute carrier family 5 member 2 Homo sapiens 167-173 30019930-5 2018 Multiple mechanisms were required to explain the observed response: 1) direct inhibition of sodium and glucose reabsorption through SGLT2, 2) SGLT2-driven inhibition of Na+/H+ exchanger 3 sodium reabsorption, and 3) osmotic diuresis coupled with peripheral sodium storage. Sodium 92-98 solute carrier family 5 member 2 Homo sapiens 132-137 30019930-5 2018 Multiple mechanisms were required to explain the observed response: 1) direct inhibition of sodium and glucose reabsorption through SGLT2, 2) SGLT2-driven inhibition of Na+/H+ exchanger 3 sodium reabsorption, and 3) osmotic diuresis coupled with peripheral sodium storage. Sodium 92-98 solute carrier family 5 member 2 Homo sapiens 142-147 30019930-5 2018 Multiple mechanisms were required to explain the observed response: 1) direct inhibition of sodium and glucose reabsorption through SGLT2, 2) SGLT2-driven inhibition of Na+/H+ exchanger 3 sodium reabsorption, and 3) osmotic diuresis coupled with peripheral sodium storage. Sodium 188-194 solute carrier family 5 member 2 Homo sapiens 142-147 30019930-5 2018 Multiple mechanisms were required to explain the observed response: 1) direct inhibition of sodium and glucose reabsorption through SGLT2, 2) SGLT2-driven inhibition of Na+/H+ exchanger 3 sodium reabsorption, and 3) osmotic diuresis coupled with peripheral sodium storage. Sodium 188-194 solute carrier family 5 member 2 Homo sapiens 142-147 29797427-8 2018 Aquaporin-2 siRNA treatment suppressed aquaporin-2 expression and the change of intravesical fluid volume from 0 to 3 h (1.00 +- 0.00 and 0.99 +- 0.02 mL), which was related to the suppression of sodium concentration change in comparison with control siRNA treatment (149.6 +- 2.4 vs 143.6 +- 3.67 mEq/mL, P < 0.05). Sodium 196-202 aquaporin 2 Rattus norvegicus 0-11 29797427-10 2018 Aquaporin-2 plays an important role in the transport of water, accompanied by sodium concentration change. Sodium 78-84 aquaporin 2 Rattus norvegicus 0-11 30216136-3 2018 Umod-/- mice have significantly lower blood pressure than Umod+/+ mice, are resistant to salt-induced changes in blood pressure, and show a leftward shift in pressure-natriuresis curves reflecting changes of sodium reabsorption. Sodium 208-214 uromodulin Mus musculus 0-4 30216136-12 2018 This direction of effect in Umod+/+ tubules suggest the difference is due to the presence of Umod facilitating greater sodium entry into the tubule cell reflecting a specific response to salt stress. Sodium 119-125 uromodulin Mus musculus 28-32 30216136-12 2018 This direction of effect in Umod+/+ tubules suggest the difference is due to the presence of Umod facilitating greater sodium entry into the tubule cell reflecting a specific response to salt stress. Sodium 119-125 uromodulin Mus musculus 93-97 30289240-0 2018 Hierarchical Nanosheet-Based MS2 (M = Re, Mo, W) Nanotubes Prepared by Templating Sacrificial Te Nanowires with Superior Lithium and Sodium Storage Capacity. Sodium 133-139 MS2 Homo sapiens 29-32 30377822-7 2018 Inversely, deficiency of IL-17a in mice blunts the hypertensive response and attenuates renal sodium retention via a serum- and glucocorticoid-regulated kinase 1 (SGK1)-dependent pathway. Sodium 94-100 serum/glucocorticoid regulated kinase 1 Mus musculus 163-167 30286162-10 2018 In conclusion, our findings indicate that the deletion [DeltaM500] in hSGLT3 inhibits membrane targeting and thus largely disrupts glucose-induced sodium conductance, which may, in interaction with other ADHD risk-related gene variants, influence the risk for ADHD in deletion carriers. Sodium 147-153 solute carrier family 5 member 4 Homo sapiens 70-76 30132034-5 2018 However, unlike the glucose-lowering effects of SGLT2 inhibitors, the spill-over of sodium and glucose beyond the proximal nephron following SGLT2 inhibition triggers dynamic and reversible realignment of energy metabolism, renal filtration and plasma volume without relying on losses into the urine. Sodium 84-90 solute carrier family 5 member 2 Homo sapiens 141-146 29465422-0 2018 Elevated Postmortem Vitreous Sodium and Chloride Level in a Salt Water Drowning Death During Self-Contained Underwater Breathing Apparatus Diving With Diving Mask in Place: Case Report. Sodium 29-35 ankyrin repeat and KH domain containing 1 Homo sapiens 158-162 30012693-7 2018 In addition, we discovered that V1R are spontaneously active during SNA and can already generate several intrinsic activity patterns including repetitive-spiking and sodium-dependent plateau potential that rely on the presence of persistent sodium currents (INap). Sodium 166-172 vomeronasal 1 receptor 51 Mus musculus 32-35 30012693-7 2018 In addition, we discovered that V1R are spontaneously active during SNA and can already generate several intrinsic activity patterns including repetitive-spiking and sodium-dependent plateau potential that rely on the presence of persistent sodium currents (INap). Sodium 241-247 vomeronasal 1 receptor 51 Mus musculus 32-35 30012693-13 2018 We uncover a new role for persistent sodium currents (INaP) in driving plateau potential in V1R and in SNA patterning in the embryonic SC. Sodium 37-43 vomeronasal 1 receptor 51 Mus musculus 92-95 30143662-1 2018 Mutations in SCN5A can alter the cardiac sodium current INa and increase the risk of potentially lethal conditions such as Brugada and long-QT syndromes. Sodium 41-47 sodium voltage-gated channel alpha subunit 5 Homo sapiens 13-18 31549035-0 2018 Rechargeable Na-CO2 Batteries Starting from Cathode of Na2CO3 and Carbon Nanotubes. Sodium 55-61 complement C2 Homo sapiens 16-19 31549035-4 2018 Here we report the Na-CO2 batteries, starting from the cathode of cheap Na2CO3 and multiwalled carbon nanotubes (CNTs). Sodium 72-78 complement C2 Homo sapiens 22-25 31549035-8 2018 This work reveals that safe rechargeable Na-CO2 batteries could be constructed by cheap Na2CO3 and multiwalled carbon nanotubes. Sodium 88-94 complement C2 Homo sapiens 44-47 30118514-11 2018 We conclude that obesity induced sodium retention and elevated SBP are mediated by the PRR-SGK-1- alpha-ENaC pathway independent of Ang II. Sodium 33-39 serum/glucocorticoid regulated kinase 1 Mus musculus 91-96 30118514-11 2018 We conclude that obesity induced sodium retention and elevated SBP are mediated by the PRR-SGK-1- alpha-ENaC pathway independent of Ang II. Sodium 33-39 sodium channel, nonvoltage-gated 1 alpha Mus musculus 98-108 30116045-2 2018 Here, we developed a positron emission tomography (PET) technique based on the sodium-iodide symporter (NIS) gene fused with the carboxyl-terminal of ornithine decarboxylase (cODC) that noninvasively images cancer cells with inhibited proteasome activity. Sodium 79-85 solute carrier family 5 (sodium iodide symporter), member 5 Mus musculus 104-107 30062333-6 2018 Furthermore, the self-diffusivity of water molecules and sodium dramatically increases with the elevation of temperature, because the decrease in connectivity of the aluminosilicate network reduces the chemical and geometric restriction on the water and ions in NASH gel under higher temperatures. Sodium 57-63 SAM domain, SH3 domain and nuclear localization signals 1 Homo sapiens 262-266 30089272-5 2018 Mechanistically, PKD2L1 deficiency increased p300-mediated acetylation of histone 3 lysine 27 on the promoter of sodium/calcium exchange 1 (NCX1) by repressing AMP-activated protein kinase (AMPK) activity, resulting in NCX1 overexpression and mitochondrial Ca2+ overload. Sodium 113-119 polycystin 2 like 1, transient receptor potential cation channel Homo sapiens 17-23 29966028-4 2018 In contrast, up to 36.4% of the counter sodium ions, originally caged in the vacancies on the NASH surface, gradually dissociate from the silicate-aluminate skeleton and migrate into the bulk solution, which is consistent with the experimentally observed leaching process of alkali ions in the geopolymer material. Sodium 40-46 SAM domain, SH3 domain and nuclear localization signals 1 Homo sapiens 94-98 30079156-7 2018 Results: Sodium As induced hepatic injury as indicated by significant increase in AST, ALT, ALP, and LDH in serum and pathologic evidences. Sodium 9-15 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 82-85 30079156-7 2018 Results: Sodium As induced hepatic injury as indicated by significant increase in AST, ALT, ALP, and LDH in serum and pathologic evidences. Sodium 9-15 glutamic pyruvic transaminase, soluble Mus musculus 87-90 29946067-1 2018 Dominantly inherited channelopathies of the skeletal muscle voltage-gated sodium channel NaV1.4 include hypokalaemic and hyperkalaemic periodic paralysis (hypoPP and hyperPP) and myotonia. Sodium 74-80 sodium voltage-gated channel alpha subunit 4 Homo sapiens 89-95 29359851-5 2018 Interestingly, leptin-mediated neurohormonal activation appears to enhance the expression of SGLT2 in the renal tubules, and SGLT2 inhibitors exert natriuretic actions at multiple renal tubular sites in a manner that can oppose the sodium retention produced by leptin. Sodium 232-238 solute carrier family 5 member 2 Homo sapiens 93-98 29806494-2 2018 The sodium current mediated by Nav1.5 consists of peak and late components (INa-P and INa-L). Sodium 4-10 sodium voltage-gated channel alpha subunit 5 Homo sapiens 31-37 29806494-3 2018 Mutant Nav1.5 causes alterations in the peak and late sodium current and is associated with an increasingly wide range of congenital arrhythmias. Sodium 54-60 sodium voltage-gated channel alpha subunit 5 Homo sapiens 7-13 29530619-9 2018 Furthermore, patch-clamp measurements in HEK-293 T cells showed that Nav1.5 current densities decreased by 30% after high-glucose treatment, and the sodium currents increased via O-GlcNAc inhibition. Sodium 149-155 O-linked N-acetylglucosamine (GlcNAc) transferase Homo sapiens 179-187 29782000-5 2018 After the onset of proteinuria, mice exhibit increased urinary serine protease activity that leads to the activation of the epithelial sodium channel (ENaC) and sodium retention. Sodium 135-141 sodium channel, nonvoltage-gated 1 alpha Mus musculus 151-155 29493068-2 2018 These pathophysiological abnormalities may be related to the increased actions of specific adipocyte-derived signalling molecules (aldosterone, neprilysin and leptin) that work in concert with increased renal sympathetic nerve traffic and activated beta2 -adrenergic receptors to promote sodium retention, microvascular rarefaction, cardiac fibrosis and systemic inflammation. Sodium 288-294 leptin Homo sapiens 159-165 29493068-6 2018 Furthermore, as adipose tissue accumulates and becomes dysfunctional, its secretion of leptin promotes renal sodium retention, microvascular changes and fibrotic processes in the heart, and systemic inflammation; these effects may be mediated or potentiated by the activation of beta2 -adrenergic receptors. Sodium 109-115 leptin Homo sapiens 87-93 29798782-1 2018 SCN5A gene encodes the pore-forming ion-conducting alpha-subunit of the cardiac sodium channel (Nav1.5), which is responsible for the initiation and propagation of action potentials and thereby determines cardiac excitability and conduction of electrical stimuli through the heart. Sodium 80-86 sodium voltage-gated channel alpha subunit 5 Homo sapiens 0-5 29798782-1 2018 SCN5A gene encodes the pore-forming ion-conducting alpha-subunit of the cardiac sodium channel (Nav1.5), which is responsible for the initiation and propagation of action potentials and thereby determines cardiac excitability and conduction of electrical stimuli through the heart. Sodium 80-86 sodium voltage-gated channel alpha subunit 5 Homo sapiens 96-102 29798782-3 2018 Gain-of-function mutations in SCN5A lead to more sodium influx into cardiomyocytes through aberrant channel gating and cause long QT syndrome, a primary electrical disease of the heart. Sodium 49-55 sodium voltage-gated channel alpha subunit 5 Homo sapiens 30-35 29989584-0 2018 [Effect of Sodium Selenite on Gene Expression of SELF, SELW, and TGR Selenoproteins in Adenocarcinoma Cells of the Human Prostate]. Sodium 11-17 thioredoxin reductase 3 Homo sapiens 65-68 29973322-16 2018 The mRNA levels of 5-HIAA and MAO-A increased in the gastric tissues, and IDO1, 5-HT1A and 5-HT3A mRNAs decreased in the sodium chromate group. Sodium 121-127 indoleamine 2,3-dioxygenase 1 Mus musculus 74-78 30250892-2 2018 We recently identified a conceptually novel mechanism for how dysregulated pH in hypoxic cells causes chemoresistance which is based on the aberrant cellular distribution of the endosomal pH regulator, the sodium/hydrogen exchanger 6 (NHE6). Sodium 206-212 solute carrier family 9 member A6 Homo sapiens 235-239 29182730-7 2018 RESULTS: In the process of acute sodium loading, after adjusting for age and 24-hour urinary sodium concentration, SNPs in CYP11B2, PRKG1, SLC8A1 genes were significantly associated with systolic BP (SBP) rising in the additive and recessive model; SNPs in CYP4A11, PRKG1, SLC8A1, and ADRB2 genes were significantly associated with diastolic BP (DBP) rising. Sodium 33-39 cytochrome P450 family 11 subfamily B member 2 Homo sapiens 123-130 29182730-7 2018 RESULTS: In the process of acute sodium loading, after adjusting for age and 24-hour urinary sodium concentration, SNPs in CYP11B2, PRKG1, SLC8A1 genes were significantly associated with systolic BP (SBP) rising in the additive and recessive model; SNPs in CYP4A11, PRKG1, SLC8A1, and ADRB2 genes were significantly associated with diastolic BP (DBP) rising. Sodium 33-39 protein kinase cGMP-dependent 1 Homo sapiens 132-137 29182730-7 2018 RESULTS: In the process of acute sodium loading, after adjusting for age and 24-hour urinary sodium concentration, SNPs in CYP11B2, PRKG1, SLC8A1 genes were significantly associated with systolic BP (SBP) rising in the additive and recessive model; SNPs in CYP4A11, PRKG1, SLC8A1, and ADRB2 genes were significantly associated with diastolic BP (DBP) rising. Sodium 33-39 protein kinase cGMP-dependent 1 Homo sapiens 266-271 29182730-7 2018 RESULTS: In the process of acute sodium loading, after adjusting for age and 24-hour urinary sodium concentration, SNPs in CYP11B2, PRKG1, SLC8A1 genes were significantly associated with systolic BP (SBP) rising in the additive and recessive model; SNPs in CYP4A11, PRKG1, SLC8A1, and ADRB2 genes were significantly associated with diastolic BP (DBP) rising. Sodium 93-99 cytochrome P450 family 11 subfamily B member 2 Homo sapiens 123-130 29593552-0 2018 KV4.3 Expression Modulates NaV1.5 Sodium Current. Sodium 34-40 sodium voltage-gated channel alpha subunit 5 Homo sapiens 27-33 29251736-10 2018 Amiloride (ENaC) and hydrochlorothiazide (pendrin inhibitor) equally attenuated the effect of PGE2 on sodium transport. Sodium 102-108 sodium channel, nonvoltage-gated 1 alpha Mus musculus 11-15 29251736-10 2018 Amiloride (ENaC) and hydrochlorothiazide (pendrin inhibitor) equally attenuated the effect of PGE2 on sodium transport. Sodium 102-108 solute carrier family 26, member 4 Mus musculus 42-49 29483621-2 2018 The charge reversal mutant enhances the late sodium current (INa) passed by the cardiac voltage-gated sodium channel (NaV1.5), delaying cardiac repolarization. Sodium 45-51 sodium voltage-gated channel alpha subunit 5 Homo sapiens 118-124 29473904-1 2018 The SCN5A gene encodes the pore-forming alpha-subunit of the ion channel that carries the cardiac fast sodium current (INa). Sodium 103-109 sodium voltage-gated channel alpha subunit 5 Homo sapiens 4-9 29459730-1 2018 NaK and other non-selective channels are able to conduct both sodium (Na+) and potassium (K+) with equally high efficiency. Sodium 62-68 TANK binding kinase 1 Homo sapiens 0-3 28861610-1 2018 The epithelial sodium channel (ENaC) marks the tightly regulated, rate-limiting step of sodium re-absorption in the aldosterone-sensitive distal nephron (ASDN). Sodium 15-21 sodium channel, nonvoltage-gated 1 alpha Mus musculus 31-35 29255002-5 2018 Whole-cell patch-clamp recordings in rat DRG neurons revealed that paclitaxel induced an enhancement of ProTx II (a selective Nav1.7 channel blocker)-sensitive sodium currents. Sodium 160-166 sodium voltage-gated channel alpha subunit 9 Rattus norvegicus 126-132 29386206-3 2018 A sodium-coupled bicarbonate exchanger (NCBE) encoded by solute carrier family 4 member 10 gene is expressed on the choroid plexus basolateral membrane and may play a role in cerebrospinal fluid production and the development of PHH. Sodium 2-8 solute carrier family 4 member 10 Rattus norvegicus 40-44 28939973-1 2018 The NaV1.4 sodium channel is highly expressed in skeletal muscle, where it carries almost all of the inward Na+ current that generates the action potential, but is not present at significant levels in other tissues. Sodium 11-17 sodium voltage-gated channel alpha subunit 4 Homo sapiens 4-10 28939973-2 2018 Consequently, mutations of SCN4A encoding NaV1.4 produce pure skeletal muscle phenotypes that now include six allelic disorders: sodium channel myotonia, paramyotonia congenita, hyperkalemic periodic paralysis, hypokalemic periodic paralysis, congenital myasthenia, and congenital myopathy with hypotonia. Sodium 129-135 sodium voltage-gated channel alpha subunit 4 Homo sapiens 27-32 28939973-2 2018 Consequently, mutations of SCN4A encoding NaV1.4 produce pure skeletal muscle phenotypes that now include six allelic disorders: sodium channel myotonia, paramyotonia congenita, hyperkalemic periodic paralysis, hypokalemic periodic paralysis, congenital myasthenia, and congenital myopathy with hypotonia. Sodium 129-135 sodium voltage-gated channel alpha subunit 4 Homo sapiens 42-48 30580866-6 2018 Several beneficial factors beyond glucose control, such as weight loss, lowering blood pressure, sodium depletion, renal hemodynamic effects, effects on myocardial energetics, and/or neurohormonal effects, have been seen with SGLT2 inhibition. Sodium 97-103 solute carrier family 5 member 2 Homo sapiens 226-231 28744670-7 2017 Our data shed new light on the crucial role of HuR as a stabilizing factor for the MR transcript and provide evidence for a short autoregulatory loop in which expression of a nuclear receptor transcriptionally regulating water and sodium balance is controlled by osmotic tone. Sodium 231-237 ELAV like RNA binding protein 1 Homo sapiens 47-50 29106511-3 2017 The T255A mutation selectively increased the resistance of cells against sodium acetate, suggesting that S. cerevisiae cells possess an Rsp5-mediated mechanism to cope with the composite stress of sodium and acetate. Sodium 73-79 NEDD4 family E3 ubiquitin-protein ligase Saccharomyces cerevisiae S288C 136-140 28809766-7 2017 Rats with truncation of neurofibromin, showed increases in voltage-gated calcium (specifically N-type or CaV2.2) and voltage-gated sodium (particularly tetrodotoxin-sensitive) currents in dorsal root ganglion neurons. Sodium 131-137 neurofibromin 1 Rattus norvegicus 24-37 29132091-9 2017 SGLT2 inhibitors may cause bone loss or increase fracture risk due to altered calcium, phosphate and sodium concentration. Sodium 101-107 solute carrier family 5 member 2 Homo sapiens 0-5 28637969-7 2017 CONCLUSIONS: This study successfully demonstrated diminished sodium currents resulting from lower NaV1.5 protein levels, which is dependent on proteasomal degradation, using a hiPSC-based model forSCN5A-D1275N-related sodium channelopathy. Sodium 61-67 sodium voltage-gated channel alpha subunit 5 Homo sapiens 98-104 28779003-0 2017 Novel idiopathic DCM-related SCN5A variants localised in DI-S4 predispose electrical disorders by reducing peak sodium current density. Sodium 112-118 sodium voltage-gated channel alpha subunit 5 Homo sapiens 29-34 28779003-12 2017 CONCLUSION: Our results suggest that the iDCM-related SCN5A variants in the DI-S4 could predispose electrical disorders by reducing peak sodium current density. Sodium 137-143 sodium voltage-gated channel alpha subunit 5 Homo sapiens 54-59 29084222-8 2017 Furthermore, evidence indicated that Tsu-1 AtHKT1 is highly expressed in stems and is more effective compared to Col-0 AtHKT1 at limiting sodium flow to the flowers. Sodium 138-144 high-affinity K+ transporter 1 Arabidopsis thaliana 43-49 29084222-8 2017 Furthermore, evidence indicated that Tsu-1 AtHKT1 is highly expressed in stems and is more effective compared to Col-0 AtHKT1 at limiting sodium flow to the flowers. Sodium 138-144 high-affinity K+ transporter 1 Arabidopsis thaliana 113-125 28793271-0 2017 Loss of Navbeta4-Mediated Regulation of Sodium Currents in Adult Purkinje Neurons Disrupts Firing and Impairs Motor Coordination and Balance. Sodium 40-46 sodium voltage-gated channel beta subunit 4 Homo sapiens 8-16 26311058-8 2017 All interventions also reduced focal glomerulosclerosis and interstitial expression of alpha-SMA during the low-sodium diet, while similar trends were observed during the high-sodium diet. Sodium 112-118 actin gamma 2, smooth muscle Rattus norvegicus 87-96 28248529-6 2017 The main cardiovascular and autonomic responses to a change in plasma sodium concentration are: i) changes in arterial blood pressure and heart rate; ii) changes in sympathetic activity to the renal system in order to ensure adequate renal sodium excretion/absorption, and iii) the secretion of compounds involved in sodium ion homeostasis (ANP, Ang-II, and ADH, for example). Sodium 70-76 alcohol dehydrogenase 1A (class I), alpha polypeptide Homo sapiens 346-361 28684740-0 2017 HuR-Dependent Editing of a New Mineralocorticoid Receptor Splice Variant Reveals an Osmoregulatory Loop for Sodium Homeostasis. Sodium 108-114 ELAV like RNA binding protein 1 Homo sapiens 0-3 28120456-7 2017 Because vitamin D-induced hypercalcaemia increases the renal expression of endothelin (ET)-1, we hypothesized that ET-1 mediates the effects of hypercalcaemia on renal sodium and water handling. Sodium 168-174 endothelin 1 Mus musculus 75-92 28420122-3 2017 Gastrin, which is produced by the G-cells of the stomach and duodenum, can increase renal sodium excretion and regulate blood pressure by acting on the cholecystokinin B receptor. Sodium 90-96 gastrin Homo sapiens 0-7 28420122-9 2017 Further analyses revealed that serum gastrin was positively correlated with 24 h urinary sodium excretion (r = 0.476, p < 0.001). Sodium 89-95 gastrin Homo sapiens 37-44 28162808-6 2017 FGF13 increased Nav1.7 sodium currents and maintained the membrane localization of Nav1.7 during noxious heat stimulation, enabling the sustained firing of action potentials. Sodium 23-29 fibroblast growth factor 13 Mus musculus 0-5 28137877-0 2017 CaMKII modulates sodium current in neurons from epileptic Scn2a mutant mice. Sodium 17-23 calcium/calmodulin-dependent protein kinase II alpha Mus musculus 0-6 28137877-12 2017 We conclude that CaMKII-mediated modulation of neuronal sodium current impacts neuronal excitability in Scn2aQ54 mice and may represent a therapeutic target for the treatment of epilepsy. Sodium 56-62 calcium/calmodulin-dependent protein kinase II alpha Mus musculus 17-23 27743286-9 2017 These results suggest that the inhibition of Nav1.6 sodium currents may be the underlying mechanism of GAS"s anticonvulsant properties. Sodium 52-58 neuron navigator 1 Rattus norvegicus 45-49 28125689-1 2017 Mutations of hepatocyte growth factor activator inhibitor (HAI)-2 in humans cause sodium loss in the gastrointestinal (GI) tract in patients with syndromic congenital sodium diarrhea (SCSD). Sodium 82-88 serine peptidase inhibitor, Kunitz type 2 Homo sapiens 13-65 27903222-9 2017 Prior to high-salt diet, a reduction in the fractional sodium and chloride excretion was observed in rats given the AAV9-ELA vector. Sodium 55-61 apelin receptor early endogenous ligand Homo sapiens 121-124 27748201-1 2017 Sodium-glucose co-transporter 2 (SGLT2) inhibitors are a new class of antidiabetic drugs that inhibit glucose and sodium reabsorption at proximal tubules. Sodium 114-120 solute carrier family 5 member 2 Homo sapiens 0-31 27748201-1 2017 Sodium-glucose co-transporter 2 (SGLT2) inhibitors are a new class of antidiabetic drugs that inhibit glucose and sodium reabsorption at proximal tubules. Sodium 114-120 solute carrier family 5 member 2 Homo sapiens 33-38 27690427-1 2016 Late sodium current (late INa) is enhanced during ischemia by reactive oxygen species (ROS) modifying the Nav 1.5 channel, resulting in incomplete inactivation. Sodium 5-11 sodium voltage-gated channel alpha subunit 5 Homo sapiens 106-113 27792639-1 2016 BACKGROUND: G protein-coupled receptor kinase type 4 (GRK4) plays a vital role in the long-term control of blood pressure (BP) and sodium excretion by regulating renal G protein-coupled receptor phosphorylation, including dopamine type 1 receptor (D1R). Sodium 131-137 G protein-coupled receptor kinase 4 Rattus norvegicus 12-52 27792639-1 2016 BACKGROUND: G protein-coupled receptor kinase type 4 (GRK4) plays a vital role in the long-term control of blood pressure (BP) and sodium excretion by regulating renal G protein-coupled receptor phosphorylation, including dopamine type 1 receptor (D1R). Sodium 131-137 G protein-coupled receptor kinase 4 Rattus norvegicus 54-58 27792639-7 2016 The present study revealed that UTMD-mediated renal GRK4 siRNA delivery efficiently reduced GRK4 expression and lowered BP in spontaneously hypertensive rats, accompanied by increased sodium excretion. Sodium 184-190 G protein-coupled receptor kinase 4 Rattus norvegicus 52-56 27364017-2 2016 The main cardiac sodium channel, NaV1.5, carries the sodium current (INa) that provides a rapid depolarizing current during the upstroke of the action potential. Sodium 17-23 sodium voltage-gated channel alpha subunit 5 Homo sapiens 33-39 27440829-9 2016 SGLT2 inhibitors reduce sodium reabsorption in the proximal tubule, causing, through tubuloglomerular feedback, afferent arteriole vasoconstriction and reduction in hyperfiltration. Sodium 24-30 solute carrier family 5 member 2 Homo sapiens 0-5 26701978-8 2016 In conclusion, lack of ENaC-mediated sodium transport along the nephron cannot be compensated for by other sodium channels and/or transporters, only by a high-sodium and reduced-potassium diet. Sodium 37-43 sodium channel, nonvoltage-gated 1 alpha Mus musculus 23-27 26635128-9 2016 Immunohistochemistry using an antibody against type III sodium-dependent phosphate transporter 2 (PiT-2), the SLC20A2 product, demonstrated that astrocytic processes were labeled in several regions in control brains, whereas in the patient, reactivity in astrocytes was apparently weak. Sodium 56-62 solute carrier family 20 member 2 Homo sapiens 98-103 26635128-9 2016 Immunohistochemistry using an antibody against type III sodium-dependent phosphate transporter 2 (PiT-2), the SLC20A2 product, demonstrated that astrocytic processes were labeled in several regions in control brains, whereas in the patient, reactivity in astrocytes was apparently weak. Sodium 56-62 solute carrier family 20 member 2 Homo sapiens 110-117 27525866-3 2016 Compared with the normal controls (C57BL/6J mice) bearing the wild-type KCNQ1 gene, J343 mice bearing KCNQ1 A340E demonstrated a much higher 24-h intake of electrolytes (potassium, sodium, and chloride). Sodium 181-187 potassium voltage-gated channel, subfamily Q, member 1 Mus musculus 102-107 27436489-7 2016 Hypoxia-mediated direct activation of TRPV4 may be the reason of anti-dipsogenic effects because the serum sodium, pH, and intracranial temperature are unaltered. Sodium 107-113 transient receptor potential cation channel, subfamily V, member 4 Rattus norvegicus 38-43 25842276-1 2016 AIMS: The expression of sodium channel Nav1.8 in cardiac nervous systems has been identified, and variants of SCN10A that encodes Nav1.8 contribute to the development of Brugada syndrome (BrS) by modifying the function of Nav1.5 or directly reducing the sodium current. Sodium 24-30 sodium voltage-gated channel alpha subunit 5 Homo sapiens 222-228 25829471-11 2016 The reduced sodium current in mutant LMNA may account for the advent of malignant ventricular arrhythmias. Sodium 12-18 lamin A/C Homo sapiens 37-41 26854262-3 2016 This review describes the role of gastrin in the cross-talk between the stomach and the kidney following the ingestion of sodium. Sodium 122-128 gastrin Homo sapiens 34-41 26854262-6 2016 It is proposed that gastrin produced by G-cells via its receptor, cholecystokinin B receptor, interacts with renal D1 -like dopamine receptors to increase renal sodium excretion. Sodium 161-167 gastrin Homo sapiens 20-27 26854262-9 2016 The natriuresis following the ingestion of a certain amount of sodium may be due to an enterokine, gastrin, secreted by G-cells in the stomach and duodenum and released into the circulation. Sodium 63-69 gastrin Homo sapiens 99-106 26854262-12 2016 Gastrin, via its receptor, the cholecystokinin type B receptor (CCKBR), is natriuretic in mammals, including humans, by inhibition of renal sodium transport. Sodium 140-146 gastrin Homo sapiens 0-7 26854262-14 2016 Selective silencing of Gast in the stomach and duodenum impairs the ability to excrete an oral sodium load and also increases blood pressure. Sodium 95-101 gastrin Homo sapiens 23-27 26854262-15 2016 Thus, the gastrorenal axis, mediated by gastrin, can complement pronatriuretic hormones, such as dopamine, to increase sodium excretion after an oral sodium load. Sodium 119-125 gastrin Homo sapiens 40-47 26854262-15 2016 Thus, the gastrorenal axis, mediated by gastrin, can complement pronatriuretic hormones, such as dopamine, to increase sodium excretion after an oral sodium load. Sodium 150-156 gastrin Homo sapiens 40-47 26412230-1 2016 AIM: We determined the role of brain Galphai2 proteins in mediating the neural and humoral responses of conscious male Sprague-Dawley rats to acute peripheral sodium challenge. Sodium 159-165 G protein subunit alpha i2 Rattus norvegicus 37-45 26747232-8 2016 Interestingly, the toxin also inhibited sodium current on all the mammalian channels tested, with the higher current inhibition on Nav1.3 (38.43 +- 8.04%, IC50 = 1.5 muM). Sodium 40-46 sodium voltage-gated channel alpha subunit 3 Homo sapiens 131-137 26747232-9 2016 Analysis of activation curves on Nav1.3 and Nav1.5 showed that the toxin shifts channel activation to more depolarized potentials, which can explain the sodium current inhibition. Sodium 153-159 sodium voltage-gated channel alpha subunit 3 Homo sapiens 33-39 26747232-9 2016 Analysis of activation curves on Nav1.3 and Nav1.5 showed that the toxin shifts channel activation to more depolarized potentials, which can explain the sodium current inhibition. Sodium 153-159 sodium voltage-gated channel alpha subunit 5 Homo sapiens 44-50 26747232-10 2016 Furthermore, the toxin also slightly slowed down sodium inactivation on Nav1.3 and Nav1.6 channels. Sodium 49-55 sodium voltage-gated channel alpha subunit 3 Homo sapiens 72-78 26787348-5 2016 We show that the N-cadherin-NaV1.5 association is not random, that NaV1.5 molecules in these clusters are major contributors to cardiac sodium current, and that loss of NaV1.5 expression reduces intercellular adhesion strength. Sodium 136-142 sodium voltage-gated channel alpha subunit 5 Homo sapiens 67-73 26787348-5 2016 We show that the N-cadherin-NaV1.5 association is not random, that NaV1.5 molecules in these clusters are major contributors to cardiac sodium current, and that loss of NaV1.5 expression reduces intercellular adhesion strength. Sodium 136-142 sodium voltage-gated channel alpha subunit 5 Homo sapiens 67-73 26708501-1 2016 We expressed rat Nav1.6 sodium channels with or without the rat beta1 subunit in human embryonic kidney (HEK293) cells and evaluated the effects of the pyrethroid insecticides tefluthrin and deltamethrin on whole-cell sodium currents. Sodium 24-30 neuron navigator 1 Rattus norvegicus 17-21 26494691-6 2016 RESULTS: We demonstrated that the initial sodium signal of a treatment-naive brain tumor is a significant predictor of isocitrate dehydrogenase (IDH) mutation status (P < .001). Sodium 42-48 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 119-143 26494691-6 2016 RESULTS: We demonstrated that the initial sodium signal of a treatment-naive brain tumor is a significant predictor of isocitrate dehydrogenase (IDH) mutation status (P < .001). Sodium 42-48 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 145-148 26494691-8 2016 Compared with the molecular signature of IDH mutation status, information criteria of model comparison revealed that the sodium signal is even superior to IDH in progression prediction. Sodium 121-127 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 41-44 27247938-7 2016 Insulin signaling via IRS2 continues to stimulate sodium reabsorption in the proximal tubule and causes sodium retention, edema, and hypertension. Sodium 50-56 insulin receptor substrate 2 Homo sapiens 22-26 27247938-7 2016 Insulin signaling via IRS2 continues to stimulate sodium reabsorption in the proximal tubule and causes sodium retention, edema, and hypertension. Sodium 104-110 insulin receptor substrate 2 Homo sapiens 22-26 27855391-11 2016 Expression of antisense of miR-219-5p significantly attenuated the levels of liver fibrosis, portal hypertension and sodium retention caused by CCl4. Sodium 117-123 C-C motif chemokine ligand 4 Homo sapiens 144-148 26343338-8 2015 Differences in selected sites in the nd4 and atp6 could be caused by superfamily-level differences in sodium transport or ATP synthesis functions, respectively. Sodium 102-108 ATP6 Sinonovacula constricta 45-49 26666158-1 2015 SGLT2 is a glucose transporter which plays an important role for reabsorption of urinary glucose depending on the sodium concentration gradient. Sodium 114-120 solute carrier family 5 member 2 Homo sapiens 0-5 26451045-1 2015 The renal epithelial sodium channel (ENaC) provides regulated sodium transport in the distal nephron. Sodium 21-27 sodium channel, nonvoltage-gated 1 alpha Mus musculus 37-41 26324167-8 2015 Replacement of extracellular sodium by other monovalent cations revealed that human NaCT was markedly less dependent on extracellular sodium than mouse NaCT. Sodium 29-35 solute carrier family 13 member 5 Homo sapiens 84-88 26324167-8 2015 Replacement of extracellular sodium by other monovalent cations revealed that human NaCT was markedly less dependent on extracellular sodium than mouse NaCT. Sodium 134-140 solute carrier family 13 member 5 Homo sapiens 84-88 26479925-6 2015 Activation of TLR5 with its ligand flagellin results in neuronal entry of the membrane-impermeable lidocaine derivative QX-314, leading to TLR5-dependent blockade of sodium currents, predominantly in A-fiber neurons of mouse DRGs. Sodium 166-172 toll-like receptor 5 Mus musculus 14-18 26479925-6 2015 Activation of TLR5 with its ligand flagellin results in neuronal entry of the membrane-impermeable lidocaine derivative QX-314, leading to TLR5-dependent blockade of sodium currents, predominantly in A-fiber neurons of mouse DRGs. Sodium 166-172 toll-like receptor 5 Mus musculus 139-143 26209011-6 2015 With Western blot assays and electrophysiological studies, we demonstrated that miR-192-5p significantly reduced expression of SCN5A and Nav1.5 as well as peak sodium current density INa generated by Nav1.5. Sodium 160-166 sodium voltage-gated channel alpha subunit 5 Homo sapiens 200-206 25735906-0 2015 New phenotype and neonatal onset of sodium channel myotonia in a child with a novel mutation of SCN4A gene. Sodium 36-42 sodium voltage-gated channel alpha subunit 4 Homo sapiens 96-101 25735906-2 2015 Mutations of the skeletal muscle sodium channel gene SCN4A are associated with several neuromuscular disorders including sodium channel myotonias. Sodium 33-39 sodium voltage-gated channel alpha subunit 4 Homo sapiens 53-58 25735906-2 2015 Mutations of the skeletal muscle sodium channel gene SCN4A are associated with several neuromuscular disorders including sodium channel myotonias. Sodium 121-127 sodium voltage-gated channel alpha subunit 4 Homo sapiens 53-58 26159698-4 2015 Although NHE8, the newest addition of intestinal NHE family, is involved in sodium absorption in the intestinal tract, whether butyrate modulates NHE8 expression in the intestinal epithelial cells is not known. Sodium 76-82 solute carrier family 9 member A8 Homo sapiens 9-13 26159698-11 2015 Thus butyrate is involved in intestinal regulation of NHE8 resulting enhanced sodium absorption. Sodium 78-84 solute carrier family 9 member A8 Homo sapiens 54-58 26125643-5 2015 By targeting WNK4, FGF23 has been shown to increase the membrane abundance of the epithelial calcium channel TRPV5 and of the sodium-chloride cotransporter NCC, resulting in augmented renal calcium and sodium reabsorption. Sodium 126-132 WNK lysine deficient protein kinase 4 Homo sapiens 13-17 26195795-1 2015 In sinoatrial node (SAN) cells, electrogenic sodium-calcium exchange (NCX) is the dominant calcium (Ca) efflux mechanism. Sodium 45-51 T cell leukemia, homeobox 2 Mus musculus 70-73 25534867-7 2015 In multivariate analyses adjusting for covariates, there were stepwise decreases in the baPWV (P = 0.003) and CIMT (P = 0.001) values as the estimated 24-hour urinary sodium excretion increased, whereas no significant differences in left ventricular (LV) structural and functional parameters were observed across the tertiles of estimated 24-hour urinary sodium excretion. Sodium 167-173 CIMT Homo sapiens 110-114 25534867-8 2015 Multiple linear regression analyses revealed that the estimated 24-hour urinary sodium excretion was independently and inversely associated with baPWV (P < 0.001) and CIMT (P = 0.001), but not with LV parameters. Sodium 80-86 CIMT Homo sapiens 170-174 25534867-9 2015 CONCLUSIONS: In the nonhypertensive population, urinary sodium excretion was inversely related to baPWV and CIMT. Sodium 56-62 CIMT Homo sapiens 108-112 26083731-3 2015 We found that Tf2 selectively activates human (h)Nav1.3, a neuronal voltage-gated sodium (Nav) subtype implicated in epilepsy and nociception. Sodium 82-88 sodium voltage-gated channel alpha subunit 3 Homo sapiens 49-55 25903070-3 2015 In addition, cell type- and segment-specific expression of 11beta-HSD2 and sodium transporters such as Na-Cl cotransporter (NCC), epithelial sodium channel (ENaC), and pendrin/Na(+)-driven Cl(-)/HCO3 (-) exchanger (NDCBE) builds a distinctive model of sodium transport in the aldosterone-sensitive distal nephron. Sodium 75-81 solute carrier family 4 member 8 Homo sapiens 215-220 25992604-2 2015 Microsomal epoxide hydrolase (mEH) is a bifunctional protein that plays a central role in the metabolism of numerous xenobiotics as well as mediating the sodium-dependent transport of bile acids into hepatocytes. Sodium 154-160 epoxide hydrolase 1 Homo sapiens 0-28 25740157-4 2015 We were surprised to find that simultaneous loss of Tmod1 and CP49, which disrupts cytoskeletal networks in lens fiber cells, results in increased gap junction coupling resistance, hydrostatic pressure, and sodium concentration. Sodium 207-213 tropomodulin 1 Mus musculus 52-57 25767117-0 2015 Amyloid precursor protein enhances Nav1.6 sodium channel cell surface expression. Sodium 42-48 amyloid beta (A4) precursor protein Mus musculus 0-25 25701724-3 2015 At 0.3muM and greater, A-803467 blocked cardiac sodium currents in a dose-dependent manner in both ventricular myocytes and in SCN5A-expressing HEK293 cell lines. Sodium 48-54 sodium voltage-gated channel alpha subunit 5 Homo sapiens 127-132 25608453-1 2015 Urotensin II (U-II) was thought to be one of the mediators of primary renal sodium retention due to effects on renal sodium excretion. Sodium 76-82 urotensin 2 Homo sapiens 0-12 25608453-1 2015 Urotensin II (U-II) was thought to be one of the mediators of primary renal sodium retention due to effects on renal sodium excretion. Sodium 76-82 urotensin 2 Homo sapiens 14-18 25608453-1 2015 Urotensin II (U-II) was thought to be one of the mediators of primary renal sodium retention due to effects on renal sodium excretion. Sodium 117-123 urotensin 2 Homo sapiens 0-12 25608453-1 2015 Urotensin II (U-II) was thought to be one of the mediators of primary renal sodium retention due to effects on renal sodium excretion. Sodium 117-123 urotensin 2 Homo sapiens 14-18 25860756-2 2015 Compression of metallic sodium (Na) to 200 GPa leads to the stability of a wide-band-gap insulator with the double hexagonal hP4 structure. Sodium 24-30 solute carrier family 10 member 4 Homo sapiens 125-128 25792129-8 2015 CONCLUSIONS: These results demonstrated that distal tubule-dominant enhancement of ATRAP inhibits pathological renal sodium reabsorption and blood pressure elevation in response to HS loading. Sodium 117-123 angiotensin II, type I receptor-associated protein Mus musculus 83-88 25792129-9 2015 The findings suggest that ATRAP-mediated modulation of sodium handling in renal distal tubules could be a target of interest in salt-sensitive blood pressure regulation. Sodium 55-61 angiotensin II, type I receptor-associated protein Mus musculus 26-31 25477470-8 2015 The rates of sodium absorption in cTAL and mTAL of SPAK-KO mice were 34.5 and 12.5% of WT tubules, respectively. Sodium 13-19 serine/threonine kinase 39 Mus musculus 51-55 25477470-10 2015 We next examined the role of SPAK in the regulation of sodium reabsorption by vasopressin in TAL. Sodium 55-61 serine/threonine kinase 39 Mus musculus 29-33 25477470-13 2015 In conclusion, the combined net effect of SPAK isoforms on sodium reabsorption in TAL is stimulatory. Sodium 59-65 serine/threonine kinase 39 Mus musculus 42-46 25798240-4 2015 Studies suggest that the epithelial sodium channel (ENaC) is important for regulating sodium transport across epithelia. Sodium 36-42 sodium channel, nonvoltage-gated 1 alpha Mus musculus 52-56 25371970-9 2015 Other experiments demonstrate that the activation of COX-2 in response to increased sodium flux is mediated through the PIK3/Akt pathway. Sodium 84-90 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma Homo sapiens 120-124 26261452-6 2015 RESULTS: There was no association between the amounts of sodium intake and serum Cr concentration (r = 0.138, P = 0.174), however, an association was revealed between sodium intake and value of CrCl (r = 0.303, P = 0.003). Sodium 167-173 CRCL Homo sapiens 194-198 26261452-7 2015 Multivariable linear regression model showed that sodium intake could effectively predict renal function assessed by CrCl (Beta = 0.070, P = 0.016). Sodium 50-56 CRCL Homo sapiens 117-121 25012180-9 2015 Notably, membrane staining of beta1 was reduced throughout collecting ducts of AE1-null mouse kidney, where increased fractional excretion of sodium has been reported. Sodium 142-148 hemoglobin, beta adult major chain Mus musculus 30-35 25312437-0 2015 Galphai2-protein-mediated signal transduction: central nervous system molecular mechanism countering the development of sodium-dependent hypertension. Sodium 120-126 G protein subunit alpha i2 Rattus norvegicus 0-8 25312437-3 2015 We hypothesized that impairment of brain Galphai2-protein-gated signal transduction pathways would result in increased sympathetically mediated renal sodium retention, thus promoting the development of salt-sensitive hypertension. Sodium 150-156 G protein subunit alpha i2 Rattus norvegicus 41-49 25312437-6 2015 In Dahl salt-resistant rats, Galphai2 downregulation evoked rapid renal nerve-dependent hypertension, sodium retention, and sympathoexcitation. Sodium 102-108 G protein subunit alpha i2 Rattus norvegicus 29-37 25312437-8 2015 Congenic-8 DSS rats exhibited sodium-evoked paraventricular nucleus-specific Galphai2-protein upregulation and attenuated hypertension, sodium retention, and global sympathoexcitation compared with DSS rats. Sodium 30-36 G protein subunit alpha i2 Rattus norvegicus 77-85 25312437-9 2015 These data demonstrate that paraventricular nucleus Galphai2-protein-gated pathways represent a conserved central molecular pathway mediating sympathoinhibitory renal nerve-dependent responses evoked to maintain sodium homeostasis and a salt-resistant phenotype. Sodium 212-218 G protein subunit alpha i2 Rattus norvegicus 52-60 25821630-5 2015 Strong correlation was observed between the sodium and calcium ion levels with acetylcholinesterase activity in the brain and serum. Sodium 44-50 acetylcholinesterase Rattus norvegicus 79-99 25556802-11 2015 This in vitro preparation also revealed that riluzole, a blocker of the persistent sodium current (INap), abolished the modulatory effect on sighs, while flufenamic acid, an antagonist for the calcium-activated non-selective cation conductance (ICAN ) abolished the effect of PGE2 on fictive eupnoea at higher concentrations. Sodium 83-89 nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, zeta Mus musculus 99-103 25681084-5 2015 This case of Leigh syndrome caused by the m.13513G>A mutation in the ND5 gene illustrates that hyponatraemia due to renal sodium loss and inappropriate ADH secretion and hypertension can be features of this entity in addition to the previously reported cardiomyopathy and WPW-like conduction pattern and that they present additional challenges in diagnosis and management. Sodium 125-131 mitochondrially encoded NADH dehydrogenase 5 Homo sapiens 72-75 25395996-1 2014 Sodium current in the heart flows principally through the pore protein NaV1.5, which is part of a complex of interacting proteins that serve both to target and localize the complex in the membrane, and to modulate function by such post-translational modifications as phosphorylation and nitrosylation. Sodium 0-6 sodium voltage-gated channel alpha subunit 5 Homo sapiens 71-77 25395996-2 2014 Multiple mutations in seven different NaV1.5 interacting proteins have been associated with dysfunctional sodium current and inherited cardiac diseases, including long QT syndrome, Brugada syndrome, atrial fibrillation, and cardiomyopathy, as well as sudden infant death syndrome (SIDS). Sodium 106-112 sodium voltage-gated channel alpha subunit 5 Homo sapiens 38-44 25484998-3 2014 The voltage-dependent cardiac sodium channel, encoded by SCN5A, conducts the main cardiac inward sodium current (INa) and is responsible for the upstroke of the atrial action potential. Sodium 30-36 sodium voltage-gated channel alpha subunit 5 Homo sapiens 57-62 25267718-2 2014 Both reentrant hairpin loops, HP1 and -2, have been shown to take part in binding the substrate and the more deeply buried sodium ion, and might therefore be a part of the intra- or extracellular gate of the transporter. Sodium 123-129 chromobox 5 Homo sapiens 30-40 25209412-9 2014 Sodium reabsorption was 98% less in LPK than Lewis rats, but renal oxygen consumption did not significantly differ between the two groups. Sodium 0-6 pyruvate kinase L/R Rattus norvegicus 36-39 25088759-10 2014 Dynamitin overexpression in HEK-293 (human embryonic kidney 293) cells expressing Nav1.5 resulted in a decrease in sodium current density in the membrane with no modification of the channel-gating properties. Sodium 115-121 sodium voltage-gated channel alpha subunit 5 Homo sapiens 82-88 25088311-2 2014 They are caused by mutations in either the CLCN1 gene in myotonia congenita or in the SCN4A gene in paramyotonia congenita and sodium channel myotonias. Sodium 127-133 sodium voltage-gated channel alpha subunit 4 Homo sapiens 86-91 25164814-0 2014 Role of Rho GDP dissociation inhibitor alpha in control of epithelial sodium channel (ENaC)-mediated sodium reabsorption. Sodium 70-76 Rho GDP dissociation inhibitor alpha Rattus norvegicus 8-44 25164814-6 2014 Knockdown of RhoGDIalpha in cultured cortical collecting duct principal cells increased ENaC subunits expression and ENaC-mediated sodium reabsorption. Sodium 131-137 Rho GDP dissociation inhibitor alpha Rattus norvegicus 13-24 23223089-0 2014 Mineralocorticoid receptor blockade inhibits accelerated atherosclerosis induced by a low sodium diet in apolipoprotein E-deficient mice. Sodium 90-96 nuclear receptor subfamily 3, group C, member 2 Mus musculus 0-26 24694992-0 2014 Deletion of the angiotensin II type 1 receptor-associated protein enhances renal sodium reabsorption and exacerbates angiotensin II-mediated hypertension. Sodium 81-87 angiotensin II, type I receptor-associated protein Mus musculus 16-46 24694992-2 2014 However, the functional significance of ATRAP in renal sodium handling and blood pressure regulation under pathological stimuli is not fully resolved. Sodium 55-61 angiotensin II, type I receptor-associated protein Mus musculus 40-45 24694992-4 2014 However, in ATRAP-knockout mice, angiotensin II-induced hypertension was exacerbated and the extent of positive sodium balance was increased by angiotensin II. Sodium 112-118 angiotensin II, type I receptor-associated protein Mus musculus 12-17 25133511-2 2014 The isozyme 11beta-HSD2 is selectively expressed in mineralocorticoid target tissues and its activity is reduced in various disease states with abnormal sodium retention and hypertension, including the apparent mineralocorticoid excess. Sodium 153-159 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 12-23 24556999-6 2014 We also discuss recent work describing the identification of a novel "NCC-like" transport system mediated by pendrin and the sodium-driven chloride/bicarbonate exchanger (NDCBE) in the beta-intercalated cells of the collecting system. Sodium 125-131 solute carrier family 4 member 8 Homo sapiens 171-176 24590923-1 2014 The aim of this study was to assess whether endogenous Ang II and oxidative stress produced by acute hypertonic sodium overload may regulate the expression of aquaporin-1 (AQP-1) and aquaporin-2 (AQP-2) in the kidney. Sodium 112-118 aquaporin 2 Rattus norvegicus 183-194 24590923-1 2014 The aim of this study was to assess whether endogenous Ang II and oxidative stress produced by acute hypertonic sodium overload may regulate the expression of aquaporin-1 (AQP-1) and aquaporin-2 (AQP-2) in the kidney. Sodium 112-118 aquaporin 2 Rattus norvegicus 196-201 24590923-12 2014 This study is a novel demonstration that renal endogenous Ang II-oxidative stress, induced in vivo in hypernatremic rats by an acute sodium overload, regulates AQP-2 expression. Sodium 133-139 aquaporin 2 Rattus norvegicus 160-165 25223087-0 2014 Ethanol increases astrocyte aquaporin-4 expression under hyper-sodium condition. Sodium 63-69 aquaporin 4 Rattus norvegicus 28-39 25223087-4 2014 From these findings, we hypothesized that ethanol may have different effects on AQP4 expression in hypo- or hyper-sodium condition. Sodium 114-120 aquaporin 4 Rattus norvegicus 80-84 25223087-7 2014 And to check whether hypo/hyper-sodium condition could change AQP4 expression after ethanol exposure or not, astrocytes were incubated in iso-sodium with ethanol, followed by changed to hypo/hyper-sodium with the same concentration of ethanol. Sodium 32-38 aquaporin 4 Rattus norvegicus 62-66 25223087-7 2014 And to check whether hypo/hyper-sodium condition could change AQP4 expression after ethanol exposure or not, astrocytes were incubated in iso-sodium with ethanol, followed by changed to hypo/hyper-sodium with the same concentration of ethanol. Sodium 31-38 aquaporin 4 Rattus norvegicus 62-66 25223087-8 2014 Astrocyte AQP4 expression was increased in hypo-sodium exposure. Sodium 48-54 aquaporin 4 Rattus norvegicus 10-14 24725019-2 2014 The etiology of CPM remains unclear, although the rapid correction of the serum sodium and CNI concentrations may be associated with the development of CPM. Sodium 80-86 carboxypeptidase M Homo sapiens 152-155 24617758-7 2014 When compared to wild-type controls, nhd1 T-DNA insertion mutants showed decreased biomasses and lower chlorophyll levels after sodium feeding. Sodium 128-134 sodium:hydrogen antiporter 1 Arabidopsis thaliana 37-41 24733925-2 2014 Here we identify plasma sodium concentration as a factor that modulates blood coagulability by affecting the production of von Willebrand factor (vWF), a key initiator of the clotting cascade. Sodium 24-30 Von Willebrand factor Mus musculus 123-144 24733925-2 2014 Here we identify plasma sodium concentration as a factor that modulates blood coagulability by affecting the production of von Willebrand factor (vWF), a key initiator of the clotting cascade. Sodium 24-30 Von Willebrand factor Mus musculus 146-149 24733925-10 2014 Multivariate regression analysis of clinical data from the Atherosclerosis Risk in Communities Study demonstrated that serum sodium significantly contributes to prediction of plasma vWF and risk of stroke. Sodium 125-131 Von Willebrand factor Mus musculus 182-185 24733925-11 2014 The results indicate that elevation of extracellular sodium within the physiological range raises vWF sufficiently to increase coagulability and risk of thrombosis. Sodium 53-59 Von Willebrand factor Mus musculus 98-101 24616101-6 2014 Functional studies revealed that, although both variants are activated by intracellular sodium ([Na(+)]i), NCX3-AC has a higher [Na(+)]i sensitivity, as Ca(2+) influx is observed in the presence of extracellular Na(+). Sodium 88-94 solute carrier family 8 (sodium/calcium exchanger), member 3 Mus musculus 107-111 24420571-4 2014 In the case of NaCl, an early influx of sodium through non-selective cation channels participates in the development of PCD through mitochondrial dysfunction and NADPH-oxidase-dependent O2 (-) generation. Sodium 40-46 respiratory burst oxidase homolog protein A-like Nicotiana tabacum 162-175 24488738-9 2014 Multiple linear regressions revealed that dietary sodium intake was independently associated with body weight (beta = 0.23), BMI (beta = 0.23), waist circumference (beta = 0.23), percent body fat (beta = 0.17), fat mass (beta = 0.23), subcutaneous abdominal adipose tissue (beta = 0.25), leptin (beta = 0.20), and tumor necrosis factor-alpha (beta = 0.61; all Ps < .05). Sodium 50-56 leptin Homo sapiens 288-294 24259464-0 2014 Effect of sex chromosome complement on sodium appetite and Fos-immunoreactivity induced by sodium depletion. Sodium 91-97 FBJ osteosarcoma oncogene Mus musculus 59-62 24259464-7 2014 Moreover, our results demonstrate a SCC effect on induced brain FOS-ir, showing increased brain activity in XX-SCC mice at the paraventricular nucleus, nucleus of the solitary tract, and lateral parabrachial nucleus, as well as an XX-SCC augmented effect on sodium depletion-induced brain activity at two circumventricular organs, the subfornical organ and area postrema, nuclei closely involved in fluid and blood pressure homeostasis. Sodium 258-264 FBJ osteosarcoma oncogene Mus musculus 64-67 24322815-10 2014 RESULTS: From SY 2010-2011 to SY 2011-2012, the mean unweighted sodium levels for elementary (K-5) breakfast and for secondary (6-12) breakfast and lunch decreased. Sodium 64-70 keratin 5 Homo sapiens 94-97 24418377-0 2014 Long-term dietary sodium restriction increases adiponectin expression and ameliorates the proinflammatory adipokine profile in obesity. Sodium 18-24 adiponectin, C1Q and collagen domain containing Mus musculus 47-58 24418377-3 2014 We tested if long-term dietary sodium restriction modifies the expression of adiponectin and ameliorates the pro-inflammatory profile of obese, diabetic mice. Sodium 31-37 adiponectin, C1Q and collagen domain containing Mus musculus 77-88 24245744-1 2013 As part of a strategy to identify good fluorescent probes based on two-photon excited fluorescence (TPEF), the sensor for sodium cation has been designed bearing a rhodol chromophore linked with an aza-crown ether. Sodium 122-128 transmembrane protein with EGF like and two follistatin like domains 2 Homo sapiens 100-104 24060890-1 2013 The inability of mineralocorticoid receptor (MR) blockade to reduce hypertension associated with high angiotensin (Ang) II suggests direct actions of Ang II to regulate tubular sodium reabsorption via the epithelial Na(+) channel (ENaC) in the aldosterone-sensitive distal nephron. Sodium 177-183 sodium channel, nonvoltage-gated 1 alpha Mus musculus 205-229 24060892-0 2013 cGMP-dependent protein kinase 1 polymorphisms underlie renal sodium handling impairment. Sodium 61-67 protein kinase cGMP-dependent 1 Homo sapiens 0-31 24270425-5 2013 PTEN KO lenses exhibited a progressive age-related increase in intracellular hydrostatic pressure, along with, increased intracellular sodium concentrations, and reduced Na+/K+-ATPase activity. Sodium 135-141 phosphatase and tensin homolog Homo sapiens 0-4 23707769-7 2013 Moreover, at higher concentrations, the drug also reduced human Nav1.5 sodium and Cav1.2 calcium currents. Sodium 71-77 sodium voltage-gated channel alpha subunit 5 Homo sapiens 64-70 24244710-3 2013 The LRRK2 knockout rat, starting at 2-months of age, displayed abnormal kidney staining patterns and/or morphologic changes that were associated with higher serum phosphorous, creatinine, cholesterol, and sorbitol dehydrogenase, and lower serum sodium and chloride compared to the LRRK2 wild-type rat. Sodium 245-251 leucine-rich repeat kinase 2 Rattus norvegicus 4-9 24244710-4 2013 Urinalysis indicated pronounced changes in LRRK2 knockout rats in urine specific gravity, total volume, urine potassium, creatinine, sodium, and chloride that started as early as 1- to 2-months of age. Sodium 133-139 leucine-rich repeat kinase 2 Rattus norvegicus 43-48 24132903-6 2013 We use this approach to determine if prior data implicating the sodium/hydrogen exchanger 9 gene (SLC9A9) in ADHD implicate sodium/hydrogen exchange (NHE) inhibitors as potential treatments. Sodium 64-70 solute carrier family 9 member A9 Homo sapiens 98-104 23714182-1 2013 Microsomal epoxide hydrolase (mEH) is a bifunctional protein that plays a central role in the metabolism of numerous xenobiotics as well as mediating the sodium-dependent transport of bile acids into hepatocytes where they are involved in cholesterol excretion and metabolism, lipid digestion and regulating numerous signaling pathways. Sodium 154-160 epoxide hydrolase 1 Homo sapiens 0-28 23612729-1 2013 AIMS: Long QT syndrome (LQTS) type 3 is characterized by prolonged ventricular repolarization due to persistent sodium inward current secondary to a mutation in SCN5a, the gene encoding for the alpha-subunit of the sodium channel. Sodium 112-118 sodium voltage-gated channel alpha subunit 5 Homo sapiens 161-166 24098284-0 2013 Sodium overload due to a persistent current that attenuates the arrhythmogenic potential of a novel LQT3 mutation. Sodium 0-6 sodium voltage-gated channel alpha subunit 5 Homo sapiens 100-104 24048831-0 2013 Persistent sodium current drives conditional pacemaking in CA1 pyramidal neurons under muscarinic stimulation. Sodium 11-17 carbonic anhydrase 1 Mus musculus 59-62 23883673-3 2013 Both relaxin and its receptor, RXFP1, are expressed in the kidney, and relaxin has been shown to play a role in renal vasodilation, in sodium excretion, and as an antifibrotic agent. Sodium 135-141 relaxin family peptide receptor 1 Homo sapiens 31-36 23698114-0 2013 Endothelin-1 inhibits sodium reabsorption by ET(A) and ET(B) receptors in the mouse cortical collecting duct. Sodium 22-28 endothelin 1 Mus musculus 0-12 23446772-8 2013 Thus, HSD11B2 CA-repeat genotype is not associated with hypertension itself, but with renal sodium excretion, probably through salt intake/appetite. Sodium 92-98 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 6-13 23895837-3 2013 Patch-clamp recording was applied to analyze the changes in whole-cell sodium current after desmoplakin silencing. Sodium 71-77 desmoplakin Homo sapiens 92-103 23656866-6 2013 SO2, together with the Ca (2+)-activated sensor of sodium ions, SOS3, activates SOS1. Sodium 51-57 sodium proton exchanger, putative (NHX7) (SOS1) Arabidopsis thaliana 80-84 23688374-1 2013 OBJECTIVE: To investigate how the sodium/calcium exchanger subtype 3 (NCX3) and its reverse mode contribute to the function of interstitial cells of Cajal (ICCs) from the rat bladder. Sodium 34-40 solute carrier family 8 member A3 Rattus norvegicus 70-74 23364531-0 2013 The tight junction protein claudin-b regulates epithelial permeability and sodium handling in larval zebrafish, Danio rerio. Sodium 75-81 claudin b Danio rerio 27-36 23288201-0 2013 Leukotrienes, but not angiotensin II, are involved in the renal effects elicited by the prolonged cyclooxygenase-2 inhibition when sodium intake is low. Sodium 131-137 prostaglandin-endoperoxide synthase 2 Canis lupus familiaris 98-114 23288201-1 2013 It is known that cyclooxygenase-2 (COX-2) inhibition elicits significant renal hemodynamics alterations when sodium intake is low. Sodium 109-115 prostaglandin-endoperoxide synthase 2 Canis lupus familiaris 17-33 23288201-1 2013 It is known that cyclooxygenase-2 (COX-2) inhibition elicits significant renal hemodynamics alterations when sodium intake is low. Sodium 109-115 prostaglandin-endoperoxide synthase 2 Canis lupus familiaris 35-40 23288201-3 2013 Our objective was to evaluate the role of angiotensin II and 5-lipooxygenase-derived metabolites in the renal effects induced by prolonged COX-2 inhibition when sodium intake is low. Sodium 161-167 prostaglandin-endoperoxide synthase 2 Canis lupus familiaris 139-144 23288201-8 2013 Our data suggest that leukotrienes but not angiotensin II are involved in the renal effects induced by COX-2 inhibition when sodium intake is low. Sodium 125-131 prostaglandin-endoperoxide synthase 2 Canis lupus familiaris 103-108 23391983-0 2013 Brain Galphai2-subunit protein-gated pathways are required to mediate the centrally evoked sympathoinhibitory mechanisms activated to maintain sodium homeostasis. Sodium 143-149 G protein subunit alpha i2 Rattus norvegicus 6-14 23862391-7 2013 Sodium independent effect of dipeptides assimilation decreasing with pH caused by, apparently, functioning of proton-dependent transporter PepT1 for oligopeptides in the apical membrane of enterocytes. Sodium 0-6 solute carrier family 15 member 1 Rattus norvegicus 139-144 23360087-2 2013 The thyroid transcription factors-NKx2 homeobox 1 (NKx2-1, formerly called TTF-1) and Paired box gene 8 (Pax8)-are known to associate biochemically and synergistically in the activation of thyroid functional genes including the sodium/iodide symporter (NIS), thyrotropin (TSH) receptor (TSHR), thyroglobulin (Tg), and thyroid peroxidase (TPO) genes. Sodium 228-234 NK2 homeobox 1 Mus musculus 51-57 23360087-2 2013 The thyroid transcription factors-NKx2 homeobox 1 (NKx2-1, formerly called TTF-1) and Paired box gene 8 (Pax8)-are known to associate biochemically and synergistically in the activation of thyroid functional genes including the sodium/iodide symporter (NIS), thyrotropin (TSH) receptor (TSHR), thyroglobulin (Tg), and thyroid peroxidase (TPO) genes. Sodium 228-234 transcription termination factor, RNA polymerase I Mus musculus 75-80 23360087-2 2013 The thyroid transcription factors-NKx2 homeobox 1 (NKx2-1, formerly called TTF-1) and Paired box gene 8 (Pax8)-are known to associate biochemically and synergistically in the activation of thyroid functional genes including the sodium/iodide symporter (NIS), thyrotropin (TSH) receptor (TSHR), thyroglobulin (Tg), and thyroid peroxidase (TPO) genes. Sodium 228-234 thyroid peroxidase Mus musculus 318-336 23360087-2 2013 The thyroid transcription factors-NKx2 homeobox 1 (NKx2-1, formerly called TTF-1) and Paired box gene 8 (Pax8)-are known to associate biochemically and synergistically in the activation of thyroid functional genes including the sodium/iodide symporter (NIS), thyrotropin (TSH) receptor (TSHR), thyroglobulin (Tg), and thyroid peroxidase (TPO) genes. Sodium 228-234 thyroid peroxidase Mus musculus 338-341 22954532-0 2013 Attenuated effect of tungsten carbide nanoparticles on voltage-gated sodium current of hippocampal CA1 pyramidal neurons. Sodium 69-75 carbonic anhydrase 1 Homo sapiens 99-102 23450472-1 2013 OBJECTIVE: To screening mutations of exons 15, 18 and 26 of sodium channel Nav1.7 (SCN9A) gene, and to assess its association with pain related to Parkinsonism. Sodium 60-66 sodium voltage-gated channel alpha subunit 9 Homo sapiens 83-88 23224874-2 2013 Na(+)/Ca(2+) exchangers, NCX and NCKX, play a critical role in the transport of one [Ca(2+)](i) and potassium ion across the cell membrane in exchange for four extracellular sodium ions [Na(+)](e). Sodium 174-180 T cell leukemia homeobox 2 Homo sapiens 25-28 23382806-8 2013 These sodium current increases were unaffected by acyclovir pre-treatment but were abolished by exposure to Tetrodotoxin (TTX) which blocks the TTX-sensitive fast Nav 1.6 and Nav 1.7 channels but not the TTX-resistant slow Nav 1.8 channel. Sodium 6-12 sodium voltage-gated channel alpha subunit 9 Homo sapiens 175-182 23382806-8 2013 These sodium current increases were unaffected by acyclovir pre-treatment but were abolished by exposure to Tetrodotoxin (TTX) which blocks the TTX-sensitive fast Nav 1.6 and Nav 1.7 channels but not the TTX-resistant slow Nav 1.8 channel. Sodium 6-12 sodium voltage-gated channel alpha subunit 10 Homo sapiens 223-230 23577024-8 2013 In addition, thiazolidinediones may augment sodium reabsorption in the proximal tubule by stimulating the expression and activity of apical Na(+)/H(+) exchanger-3 and basolateral Na(+)-HCO3 (-) cotransporter as well as of Na(+),K(+)-ATPase. Sodium 44-50 solute carrier family 9 member A3 Homo sapiens 140-207 23116249-6 2012 We discovered that (1) glucose binding involves CH-pi stacking with Y290, (2) pi T-stacking interactions between Y290 and W291 and H-bonding between Y290 and N78 (TM1) are essential to form the sodium and sugar binding sites, (3) the Na(+):sugar stoichiometry is determined by these residues, and (4) W289 may be important in stabilizing the structure through H-bonding to TM3. Sodium 194-200 tropomyosin 3 Homo sapiens 373-376 22473870-6 2012 The non-synonymous rs6746030 single nucleotide polymorphism (SNP) of the SCN9A gene, which alters the coding sequence of the sodium channel Nav1.7 (arginine to tryptophan), was nominally associated with PD-related pain susceptibility (p = 0.037), as well as with central and musculoskeletal pain subtypes independently. Sodium 125-131 sodium voltage-gated channel alpha subunit 9 Homo sapiens 73-78 22592667-3 2012 On the basis of a genome-wide association study, single-nucleotide polymorphisms in the uromodulin (UMOD) promoter region had been considered to influence both renal sodium reabsorption and BP. Sodium 166-172 uromodulin Homo sapiens 88-98 22592667-3 2012 On the basis of a genome-wide association study, single-nucleotide polymorphisms in the uromodulin (UMOD) promoter region had been considered to influence both renal sodium reabsorption and BP. Sodium 166-172 uromodulin Homo sapiens 100-104 22592667-10 2012 Urinary UMOD excretion was correlated with urinary sodium excretion (R=0.239, P=0.656*10(-13)). Sodium 51-57 uromodulin Homo sapiens 8-12 21630263-8 2012 Functional activity of Na(V) 1.6 channels in the plasma membrane of CaC cells was confirmed by whole-cell patch-clamp experiments using Cn2, a Na(V) 1.6-specific toxin, which blocked ~30% of the total sodium current. Sodium 201-207 sodium voltage-gated channel alpha subunit 8 Homo sapiens 23-32 21630263-8 2012 Functional activity of Na(V) 1.6 channels in the plasma membrane of CaC cells was confirmed by whole-cell patch-clamp experiments using Cn2, a Na(V) 1.6-specific toxin, which blocked ~30% of the total sodium current. Sodium 201-207 carnosine dipeptidase 2 Homo sapiens 136-139 22315453-9 2012 These studies demonstrate that the T158A mutation of the KCNJ5 gene produces a marked stimulation in aldosterone biosynthesis that is dependent on membrane depolarization and sodium and calcium influx into the HAC15 adrenal cortical carcinoma cells. Sodium 175-181 potassium inwardly rectifying channel subfamily J member 5 Homo sapiens 57-62 22331379-4 2012 Mutations in the potassium channel KCNJ5 have been identified in APAs that result in sodium influx and membrane depolarization and are postulated to result in calcium influx in adrenal glomerulosa cells. Sodium 85-91 potassium inwardly rectifying channel subfamily J member 5 Homo sapiens 35-40 22129970-4 2012 Expression of a dominant negative (DN) form of Rab11a or Rab11b significantly reduced the basal and cAMP-stimulated ENaC-dependent sodium (Na(+)) transport. Sodium 131-137 RAB11A, member RAS oncogene family Mus musculus 47-53 21966935-1 2012 Sodium retention has been proposed as the cause of hypertension in the LP rat (offspring exposed to a maternal low-protein diet in utero) model of developmental programming because of increased renal NKCC2 (Na+/K+/2Cl- co-transporter 2) expression. Sodium 0-6 solute carrier family 12 member 1 Rattus norvegicus 200-205 21966935-1 2012 Sodium retention has been proposed as the cause of hypertension in the LP rat (offspring exposed to a maternal low-protein diet in utero) model of developmental programming because of increased renal NKCC2 (Na+/K+/2Cl- co-transporter 2) expression. Sodium 0-6 solute carrier family 12 member 1 Rattus norvegicus 207-235 22293193-8 2012 To clarify the effects of AII, a second group of mice was infused with AII via an osmotic pump, which led to higher systolic blood pressure, and decreases in urinary sodium excretion and the expression of AMPK, in a manner similar to those observed in the HFD mice. Sodium 166-172 arginase type II Mus musculus 71-74 22293193-9 2012 However, treatment with an AMPK activator, metformin, improved the changes induced by the AII, suggesting that AII induced sodium retention works by acting on AMPK activity. Sodium 123-129 arginase type II Mus musculus 90-93 22293193-9 2012 However, treatment with an AMPK activator, metformin, improved the changes induced by the AII, suggesting that AII induced sodium retention works by acting on AMPK activity. Sodium 123-129 arginase type II Mus musculus 111-114 22293193-12 2012 These findings indicate that AII suppresses AMPK activity in the kidney, leading to sodium retention and enhanced salt-sensitivity, and that AMPK activation may represent a new therapeutic target for obesity-related salt-sensitive hypertension. Sodium 84-90 arginase type II Mus musculus 29-32 21863227-2 2012 Expression of the renal thick ascending limb (TAL) sodium transporter NKCC2 is up-regulated, which has been predicted to result in greater sodium reabsorption. Sodium 51-57 solute carrier family 12 member 1 Rattus norvegicus 70-75 21863227-4 2012 The aim of this study was to determine whether the increased abundance of sodium:potassium:chloride (Na(+):K(+):2Cl(-)) co-transporter (NKCC2) leads to enhanced sodium uptake by the TAL. Sodium 74-80 solute carrier family 12 member 1 Rattus norvegicus 136-141 21863227-4 2012 The aim of this study was to determine whether the increased abundance of sodium:potassium:chloride (Na(+):K(+):2Cl(-)) co-transporter (NKCC2) leads to enhanced sodium uptake by the TAL. Sodium 161-167 solute carrier family 12 member 1 Rattus norvegicus 136-141 22937490-10 2012 Correction of these defects in PHD2/HIF-1alpha-associated molecular adaptation in the renal medulla improves sodium excretion, reduces sodium retention and attenuates saltsensitive hypertension in Dahl/ss rats. Sodium 109-115 egl-9 family hypoxia-inducible factor 1 Rattus norvegicus 31-35 22937490-10 2012 Correction of these defects in PHD2/HIF-1alpha-associated molecular adaptation in the renal medulla improves sodium excretion, reduces sodium retention and attenuates saltsensitive hypertension in Dahl/ss rats. Sodium 109-115 hypoxia inducible factor 1 subunit alpha Rattus norvegicus 36-46 22937490-10 2012 Correction of these defects in PHD2/HIF-1alpha-associated molecular adaptation in the renal medulla improves sodium excretion, reduces sodium retention and attenuates saltsensitive hypertension in Dahl/ss rats. Sodium 135-141 egl-9 family hypoxia-inducible factor 1 Rattus norvegicus 31-35 22937490-10 2012 Correction of these defects in PHD2/HIF-1alpha-associated molecular adaptation in the renal medulla improves sodium excretion, reduces sodium retention and attenuates saltsensitive hypertension in Dahl/ss rats. Sodium 135-141 hypoxia inducible factor 1 subunit alpha Rattus norvegicus 36-46 21998139-0 2012 Functional analysis of the human concentrative nucleoside transporter-1 variant hCNT1S546P provides insight into the sodium-binding pocket. Sodium 117-123 solute carrier family 28 member 1 Homo sapiens 33-71 21998139-0 2012 Functional analysis of the human concentrative nucleoside transporter-1 variant hCNT1S546P provides insight into the sodium-binding pocket. Sodium 117-123 solute carrier family 28 member 1 Homo sapiens 80-85 23177983-3 2012 GLUT2 (glucose transporter), as representative of the latter, facilitates the sodium-independent exit of sugars from cells. Sodium 78-84 solute carrier family 2 member 2 Homo sapiens 0-5 23177985-2 2012 Although termed solute carriers (SLCs), only three out of seven (i.e. SLC10A1, SLC10A2, and SLC10A6) show sodium-dependent uptake of organic substrates across the cell membrane. Sodium 106-112 solute carrier family 10 member 2 Homo sapiens 79-86 23177985-2 2012 Although termed solute carriers (SLCs), only three out of seven (i.e. SLC10A1, SLC10A2, and SLC10A6) show sodium-dependent uptake of organic substrates across the cell membrane. Sodium 106-112 solute carrier family 10 member 6 Homo sapiens 92-99 22948718-6 2012 RESULTS: Treatment with the sEH inhibitor elicited similar BP decreases that were associated with increases in daily sodium excretion in 2K1C eNOS+/+ as well as 2K1C eNOS-/- mice. Sodium 117-123 epoxide hydrolase 2, cytoplasmic Mus musculus 28-31 21204798-6 2011 Currently, four genes are identified to be involved in myotonia: the muscle voltage-gated sodium and chloride channel genes SCN4A and CLCN1, the myotonic dystrophy protein kinase (DMPK) gene, and the CCHC-type zinc finger, nucleic acid binding protein gene CNBP. Sodium 90-96 chloride voltage-gated channel 1 Homo sapiens 134-139 21940906-6 2011 All compounds tested were transported by Oatp1b4 and uptake intrinsic clearance (CL(int, uptake)) in dog hepatocytes in sodium-free buffer was correlated significantly with CL(int, uptake) in Oatp1b4-expressing cells. Sodium 120-126 solute carrier organic anion transporter family member 1B3 Canis lupus familiaris 192-199 21666503-1 2011 Sodium absorption by the intestine is mediated by brush border Na/H exchangers, which include the NHE3 and NHE8 isoforms. Sodium 0-6 solute carrier family 9 member A3 Homo sapiens 98-102 21666503-5 2011 Because some patients with congenital sodium diarrhea improve with age and knowing the developmental switch from NHE8 to NHE3, NHE8 may be a candidate gene for this disorder. Sodium 38-44 solute carrier family 9 member A3 Homo sapiens 121-125 21813872-8 2011 These data suggest that activation of the JAK/STAT pathway is critical for the development of ANG II-induced hypertension by mediating its effects on renal sodium excretory capability, but the physiological control of blood pressure by ANG II with a low-salt diet does not require JAK2 activation. Sodium 156-162 angiogenin Rattus norvegicus 94-97 22028644-3 2011 The resulting sodium overload drives increased reverse-mode sodium-calcium exchanger (NCX) activity, creating a secondary calcium overload that has pathologic consequences. Sodium 14-20 T cell leukemia homeobox 2 Homo sapiens 86-89 21556912-3 2011 Comparisons of control, overexpressing (OX), and knockout (KO) lines indicated that higher than wild type levels of EARLI1 improved germinability, root elongation, and reduction of sodium accumulation in leaves under salt stress, as well as germinability under low-temperature stress. Sodium 181-187 Bifunctional inhibitor/lipid-transfer protein/seed storage 2S albumin superfamily protein Arabidopsis thaliana 116-122 21613418-8 2011 A high sodium intake increased basolateral Na(+)/H(+) exchange activity by 89% in association with an increase in NHE1 expression. Sodium 7-13 solute carrier family 9 member A1 Rattus norvegicus 114-118 21613418-10 2011 These results suggest that high sodium intake increases HCO(3)(-) absorptive capacity in the MTAL through 1) an adaptive increase in basolateral NHE1 activity that results secondarily in an increase in apical NHE3 activity; and 2) an adaptive increase in NHE3 activity, independent of NHE1 activity. Sodium 32-38 solute carrier family 9 member A1 Rattus norvegicus 145-149 21613418-10 2011 These results suggest that high sodium intake increases HCO(3)(-) absorptive capacity in the MTAL through 1) an adaptive increase in basolateral NHE1 activity that results secondarily in an increase in apical NHE3 activity; and 2) an adaptive increase in NHE3 activity, independent of NHE1 activity. Sodium 32-38 solute carrier family 9 member A1 Rattus norvegicus 285-289 21815750-5 2011 Uroguanylin may act as a hormone in a novel endocrine axis linking the digestive system and kidney as well as a paracrine system intrarenally to increase sodium excretion in the postprandial period. Sodium 154-160 guanylate cyclase activator 2B Homo sapiens 0-11 21427176-7 2011 However, levels of anti-CA II, VI and XIII antibodies correlated significantly with urinary pH, and inversely with serum sodium concentrations. Sodium 121-127 carbonic anhydrase 2 Homo sapiens 24-29 21539900-3 2011 Both H-EVE (0.30M NaCl, 2mL/100g of body weight, in 1 minute) and 24 hours of WD significantly increased plasma sodium concentrations, producing, respectively, either an increase or a decrease in extracellular volume. Sodium 112-118 complement factor D Rattus norvegicus 7-10 21218498-0 2011 Nano-CuO inhibited voltage-gated sodium current of hippocampal CA1 neurons via reactive oxygen species but independent from G-proteins pathway. Sodium 33-39 carbonic anhydrase 1 Homo sapiens 63-66 21218498-1 2011 The aim of this study was to investigate the effects of nano-CuO on voltage-gated sodium current (I(Na) ) in hippocampal CA1 neurons. Sodium 82-88 carbonic anhydrase 1 Homo sapiens 121-124 21199648-3 2011 Recent work in rodents has also identified important effects of MSH"s, particularly gamma-MSH, on sodium metabolism and blood pressure regulation. Sodium 98-104 msh homeobox 1 Mus musculus 64-67 21199648-6 2011 Mice lacking the gamma-MSH receptor (the melanocortin 3 receptor, Mc3r) also become hypertensive on a high sodium diet but remain so when administered gamma-MSH, and infusions of physiologic levels of the peptide stimulate urinary sodium excretion in normal rats and mice, but not in mice with deletion of Mc3r. Sodium 107-113 msh homeobox 1 Mus musculus 23-26 21199648-6 2011 Mice lacking the gamma-MSH receptor (the melanocortin 3 receptor, Mc3r) also become hypertensive on a high sodium diet but remain so when administered gamma-MSH, and infusions of physiologic levels of the peptide stimulate urinary sodium excretion in normal rats and mice, but not in mice with deletion of Mc3r. Sodium 107-113 melanocortin 3 receptor Mus musculus 41-64 21199648-6 2011 Mice lacking the gamma-MSH receptor (the melanocortin 3 receptor, Mc3r) also become hypertensive on a high sodium diet but remain so when administered gamma-MSH, and infusions of physiologic levels of the peptide stimulate urinary sodium excretion in normal rats and mice, but not in mice with deletion of Mc3r. Sodium 107-113 melanocortin 3 receptor Mus musculus 66-70 21199648-6 2011 Mice lacking the gamma-MSH receptor (the melanocortin 3 receptor, Mc3r) also become hypertensive on a high sodium diet but remain so when administered gamma-MSH, and infusions of physiologic levels of the peptide stimulate urinary sodium excretion in normal rats and mice, but not in mice with deletion of Mc3r. Sodium 231-237 msh homeobox 1 Mus musculus 23-26 21199648-6 2011 Mice lacking the gamma-MSH receptor (the melanocortin 3 receptor, Mc3r) also become hypertensive on a high sodium diet but remain so when administered gamma-MSH, and infusions of physiologic levels of the peptide stimulate urinary sodium excretion in normal rats and mice, but not in mice with deletion of Mc3r. Sodium 231-237 melanocortin 3 receptor Mus musculus 41-64 21199648-6 2011 Mice lacking the gamma-MSH receptor (the melanocortin 3 receptor, Mc3r) also become hypertensive on a high sodium diet but remain so when administered gamma-MSH, and infusions of physiologic levels of the peptide stimulate urinary sodium excretion in normal rats and mice, but not in mice with deletion of Mc3r. Sodium 231-237 melanocortin 3 receptor Mus musculus 66-70 21384128-7 2011 This suggested that external sodium increased the probability of NaPi-IIb occupying a conformation that favours interaction between sites in the re-entrant domains. Sodium 29-35 solute carrier family 34 member 2 L homeolog Xenopus laevis 65-73 21430243-0 2011 Sodium intake is associated with carotid artery structure alterations and plasma matrix metalloproteinase-9 upregulation in hypertensive adults. Sodium 0-6 matrix metallopeptidase 9 Homo sapiens 81-107 21430243-11 2011 The present findings also suggest that increased MMP-9 activity might play a role in sodium-induced vascular remodeling. Sodium 85-91 matrix metallopeptidase 9 Homo sapiens 49-54 21499270-4 2011 In this study, we found that beta(2)-adrenergic receptor (beta(2)AR) stimulation led to decreased transcription of the gene encoding WNK4, a regulator of sodium reabsorption. Sodium 154-160 WNK lysine deficient protein kinase 4 Rattus norvegicus 133-137 21335042-1 2011 Gamma-Melanocyte Stimulating Hormone (Gamma-MSH) regulates sodium (Na(+)) balance and blood pressure through activation of the melanocortin receptor 3 (MC3-R). Sodium 59-65 melanocortin 3 receptor Mus musculus 127-150 21335042-1 2011 Gamma-Melanocyte Stimulating Hormone (Gamma-MSH) regulates sodium (Na(+)) balance and blood pressure through activation of the melanocortin receptor 3 (MC3-R). Sodium 59-65 melanocortin 3 receptor Mus musculus 152-157 21178974-8 2011 The mCCD(c11) cell line is a first example of a mammalian tight epithelium allowing quantitative study of the coupling between sodium and water transport. Sodium 127-133 RNA polymerase III subunit K Homo sapiens 9-12 21155863-4 2011 Sodium transport in the proximal tubule is increased in diabetes mellitus as a result of enhanced activity of the sodium-hydrogen exchanger-3 (NHE3), the key transporter for transcellular reabsorption of sodium. Sodium 0-6 solute carrier family 9 member A3 Homo sapiens 114-141 21155863-4 2011 Sodium transport in the proximal tubule is increased in diabetes mellitus as a result of enhanced activity of the sodium-hydrogen exchanger-3 (NHE3), the key transporter for transcellular reabsorption of sodium. Sodium 0-6 solute carrier family 9 member A3 Homo sapiens 143-147 21155863-4 2011 Sodium transport in the proximal tubule is increased in diabetes mellitus as a result of enhanced activity of the sodium-hydrogen exchanger-3 (NHE3), the key transporter for transcellular reabsorption of sodium. Sodium 114-120 solute carrier family 9 member A3 Homo sapiens 143-147 21155863-7 2011 Enhanced sodium and water reabsorption, occurring as a consequence of endogenous or pharmacological stimulation of the peroxisome proliferator-activated receptor gamma is Sgk1 mediated. Sodium 9-15 serum/glucocorticoid regulated kinase 1 Homo sapiens 171-175 20923597-9 2011 Intakes of PUFA (6-12 years), vitamins B1 (2-5 and 13-18 years), B2 (13-18 years), A (2-5 and 13-18 years) and E (13-18 years) were higher in those groups consuming >= 3 0 servings of WG/d; intakes of added sugars (2-5 years), vitamin C (2-5 and 6-12 years), potassium and sodium (6-12 years) were lower. Sodium 276-282 pumilio RNA binding family member 3 Homo sapiens 11-15 21097500-3 2011 hPAT4 in Xenopus oocytes mediated sodium-independent, electroneutral uptake of [(3)H]proline, with the highest rate of uptake when the uptake medium pH was 7.4 and an affinity of 3.13 muM. Sodium 34-40 solute carrier family 36 member 4 Homo sapiens 0-5 21629870-3 2011 Sodium-proton exchanger type 3 (NHE3) is a main regulator of sodium reabsorption in the luminal side of proximal tubule. Sodium 61-67 solute carrier family 9 member A3 Homo sapiens 32-36 21750640-1 2011 Pseudohypoaldosteronism type 1 (PHA-1, MIM #264350) is caused by defective transepithelial sodium transport. Sodium 91-97 sodium channel epithelial 1 subunit gamma Homo sapiens 0-37 21076398-2 2011 Cardiac glycosides increase the intracellular sodium concentration, which appears to inhibit the ATPase activity of the RNA sensor RIG-I, an essential and early component in the IFNbeta activation pathway. Sodium 46-52 DExD/H-box helicase 58 Homo sapiens 131-136 20947508-1 2010 Serum- and glucocorticoid-induced kinase 1 (SGK1) is a multifunctional protein kinase that markedly influences various cellular processes such as proliferation, apoptosis, glucose metabolism, and sodium (Na(+)) transport via the epithelial Na(+) channel, ENaC. Sodium 196-202 serum/glucocorticoid regulated kinase 1 Homo sapiens 0-42 20947508-1 2010 Serum- and glucocorticoid-induced kinase 1 (SGK1) is a multifunctional protein kinase that markedly influences various cellular processes such as proliferation, apoptosis, glucose metabolism, and sodium (Na(+)) transport via the epithelial Na(+) channel, ENaC. Sodium 196-202 serum/glucocorticoid regulated kinase 1 Homo sapiens 44-48 21105923-6 2010 Expression of the gene encoding Arabidopsis high-affinity K(+) transporter 1;1 (AtHKT1;1), a gene responsible for removing sodium ions from the root xylem, was repressed by cytokinin treatment, but showed significantly elevated expression in the cytokinin response double mutant arr1-3 arr12-1. Sodium 123-129 response regulator 1 Arabidopsis thaliana 279-283 21105923-7 2010 Our data suggest that cytokinin, acting through the transcription factors ARR1 and ARR12, regulates sodium accumulation in the shoots by controlling the expression of AtHKT1;1 in the roots. Sodium 100-106 response regulator 1 Arabidopsis thaliana 74-78 20571087-5 2010 In particular, we identify a highly influential cluster of 13 genes--including three transcription factors (Arntl, Bhlhe41 and Npas2)-that is implicated as being protective against hypertension in response to increased dietary sodium. Sodium 227-233 aryl hydrocarbon receptor nuclear translocator-like Rattus norvegicus 108-113 20571087-5 2010 In particular, we identify a highly influential cluster of 13 genes--including three transcription factors (Arntl, Bhlhe41 and Npas2)-that is implicated as being protective against hypertension in response to increased dietary sodium. Sodium 227-233 neuronal PAS domain protein 2 Rattus norvegicus 127-132 20525693-4 2010 SGK1 increases membrane expression of the epithelial sodium channel (ENaC) and sodium reabsorption via phosphorylation and sequestering of the E3 ubiquitin ligase neural precursor cell expressed, developmentally down-regulated 4-2 (Nedd4-2), which otherwise promotes ENaC endocytosis. Sodium 53-59 serum/glucocorticoid regulated kinase 1 Homo sapiens 0-4 20525693-4 2010 SGK1 increases membrane expression of the epithelial sodium channel (ENaC) and sodium reabsorption via phosphorylation and sequestering of the E3 ubiquitin ligase neural precursor cell expressed, developmentally down-regulated 4-2 (Nedd4-2), which otherwise promotes ENaC endocytosis. Sodium 53-59 NEDD4 like E3 ubiquitin protein ligase Homo sapiens 163-230 20472302-0 2010 Effects of brain-derived neurotrophic factor on sodium-induced apoptosis in human olfactory neuroepithelial progenitor cells. Sodium 48-54 brain derived neurotrophic factor Homo sapiens 11-44 20472302-3 2010 Since both elevated intracellular sodium and apoptosis are believed to contribute to cellular dysfunction in bipolar disorder, it is important to determine the effect of exogenous BDNF on apoptosis induced by the high levels of intracellular sodium seen in ill bipolar patients. Sodium 242-248 brain derived neurotrophic factor Homo sapiens 180-184 20472302-9 2010 Co-treatment of BDNF and monensin increased intracellular sodium concentration and reduced apoptosis by 66%. Sodium 58-64 brain derived neurotrophic factor Homo sapiens 16-20 20430871-7 2010 Inhibition of the sodium/hydrogen exchanger 3 (NHE3) had an additive effect to AICAR, suggesting that the AMPK effect is not via NHE3. Sodium 18-24 solute carrier family 9 member A3 Homo sapiens 47-51 20427726-5 2010 The protein expression of the NAD(P)H oxidase subunits NOX2 and p47(phox) and overall NAD(P)H oxidase activity were approximately doubled in the cortex of the rats on the high-sodium diet compared with those on the normal sodium intake while both SOD activity and expression were unchanged. Sodium 176-182 cytochrome b-245 beta chain Rattus norvegicus 55-59 20427726-5 2010 The protein expression of the NAD(P)H oxidase subunits NOX2 and p47(phox) and overall NAD(P)H oxidase activity were approximately doubled in the cortex of the rats on the high-sodium diet compared with those on the normal sodium intake while both SOD activity and expression were unchanged. Sodium 222-228 cytochrome b-245 beta chain Rattus norvegicus 55-59 20211600-0 2010 Sodium-coupled electrogenic transport of pyroglutamate (5-oxoproline) via SLC5A8, a monocarboxylate transporter. Sodium 0-6 solute carrier family 5 member 8 Homo sapiens 74-80 20404220-1 2010 D(5) dopamine receptor (D(5)R)-deficient (D(5)(-/-)) mice have hypertension that is aggravated by an increase in sodium intake. Sodium 113-119 dopamine receptor D5 Mus musculus 0-22 20308610-11 2010 Overexpression of PHD2 transgene in the renal medulla impaired renal sodium excretion after salt loading. Sodium 69-75 egl-9 family hypoxia-inducible factor 1 Rattus norvegicus 18-22 20079461-7 2010 Oatp1b4 mediates sodium-independent transport of typical organic anions including bromosulfophthalein (BSP), [D-penicillamine(2,5)]enkephalin (DPDPE), estradiol-17beta-glucuronide (E17betaG), estrone-3-sulfate and taurocholate. Sodium 17-23 solute carrier organic anion transporter family member 1B3 Canis lupus familiaris 0-7 20008467-0 2010 Sodium accumulation promotes diastolic dysfunction in end-stage heart failure following Serca2 knockout. Sodium 0-6 ATPase, Ca++ transporting, cardiac muscle, slow twitch 2 Mus musculus 88-94 19943938-18 2009 CNGC19 and CNGC20 could assist the plant to cope with toxic effects caused by salt stress, probably by contributing to a re-allocation of sodium within the plant. Sodium 138-144 cyclic nucleotide gated channel 19 Arabidopsis thaliana 0-6 19713312-7 2009 In the kidney, klotho(-/-) mice exhibited increased expression of TRPV5 and decreased expression of the sodium/calcium exchanger (NCX1) and calbindin-D(28K), implying a failure to absorb Ca(2+) through the distal convoluted tubule/connecting tubule (DCT/CNT) via TRPV5. Sodium 104-110 klotho Mus musculus 15-21 19723921-0 2009 A possible relationship between brain-derived adrenomedullin and oxytocin in the regulation of sodium balance. Sodium 95-101 oxytocin/neurophysin I prepropeptide Homo sapiens 65-73 19723921-4 2009 When plasma tonicity was elevated with sodium, ribozyme-induced compromise of central AM production significantly blunted the release of OT into plasma. Sodium 39-45 oxytocin/neurophysin I prepropeptide Homo sapiens 137-139 19723921-6 2009 Thus, brain-derived AM controls OT release in response to altered plasma sodium levels. Sodium 73-79 oxytocin/neurophysin I prepropeptide Homo sapiens 32-34 19683029-0 2009 Action potential changes associated with the inhibitory effects on voltage-gated sodium current of hippocampal CA1 neurons by silver nanoparticles. Sodium 81-87 carbonic anhydrase 1 Homo sapiens 111-114 19664597-6 2009 Additionally, in experiments using a model of salt-sensitive hypertension in Dahl rats, we provided evidence suggesting that transcriptional regulation and activation of NPC2 protein depends on sodium intake. Sodium 194-200 NPC intracellular cholesterol transporter 2 Rattus norvegicus 170-174 19664597-7 2009 NPC2 might regulate sodium reabsorption in the terminal nephron by interacting with ENaC-Nedd4L system. Sodium 20-26 NEDD4 like E3 ubiquitin protein ligase Homo sapiens 89-95 20641261-6 2004 Although different AA transport systems are involved in the uptake of AAs, the AAs are transported primarily by the l AA transport systems (designated as LAT1 and LAT2), which are not sodium-dependent and can transport both the l- and d-isomers (7, 13), including those containing a branched chain or an aromatic moiety (14). Sodium 184-190 solute carrier family 7 (cationic amino acid transporter, y+ system), member 5 Mus musculus 154-158 19299496-8 2009 In cftr knockout mice, a normalizing effect was observed on sodium but not on chloride conductance. Sodium 60-66 cystic fibrosis transmembrane conductance regulator Mus musculus 3-7 19335336-2 2009 The heterodimeric complexes of CD98hc and the light chains LAT1 (L-type amino acid transporter 1) or LAT2 specifically promote sodium-independent System L exchange of neutral amino acids, including leucine. Sodium 127-133 CD98 heavy chain Drosophila melanogaster 31-37 19403809-7 2009 We show that changes in firing patterns are caused by neurotrophin-dependent regulation of at least four voltage-gated currents: the sodium current and the M-type, delayed rectifier, and calcium-dependent potassium currents. Sodium 133-139 brain derived neurotrophic factor Homo sapiens 54-66 19171180-9 2009 The difference between the results obtained with the generic inhibitor for Trk receptors and the specific inhibitors for TrkA and p75(NTR) receptors in CM-treated cells, suggested that alternative pathways could be used to regulate neurite elongation, axon specification and sodium currents in PC12 cells. Sodium 275-281 neurotrophic receptor tyrosine kinase 1 Rattus norvegicus 121-125 19185581-11 2009 As a consequence, transcription of the ENaC beta- and gamma-subunits was up-regulated, increasing ENaC-dependent sodium absorption. Sodium 113-119 sodium channel epithelial 1 subunit beta Homo sapiens 39-48 19129479-1 2009 The newly described yeast endosomal sorting complexes required for transport (ESCRT) protein increased sodium tolerance-1 (Ist1p) binds the late-acting ESCRT proteins Did2p/charged MVB protein (CHMP) 1 and Vps4p and exhibits synthetic vacuolar protein sorting defects when combined with mutations in the Vta1p/LIP5-Vps60p/CHMP5 complex. Sodium 103-109 Ist1p Saccharomyces cerevisiae S288C 123-128 19885019-12 2009 These findings suggest that the increased renal ANP synthesis in association with decreased metabolism via NEP and NPR-C may play a compensatory role against the development of sodium retention in nephrotic syndrome. Sodium 177-183 natriuretic peptide A Rattus norvegicus 48-51 19885019-12 2009 These findings suggest that the increased renal ANP synthesis in association with decreased metabolism via NEP and NPR-C may play a compensatory role against the development of sodium retention in nephrotic syndrome. Sodium 177-183 membrane metallo-endopeptidase Rattus norvegicus 107-110 19054333-1 2009 AIM: Uroguanylin, isolated from human and opossum urine, is a candidate intestinal natriuretic hormone that controls the sodium and water balance between the intestine and the kidneys. Sodium 121-127 guanylate cyclase activator 2B Homo sapiens 5-16 19071883-9 2009 In addition to the clinical pharmacokinetic analysis, the ability of mipomersen sodium to inhibit the major CYP isoform enzymes (namely CYP1A2, CYP2C9, CYP2C19, CYP2D6 and CYP3A4) was evaluated in cryo-preserved human hepatocytes in vitro. Sodium 80-86 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 152-159 18417280-3 2008 The selectivity sequence for NH4+ entering the sodium form of the three materials was Na-clinoptilolite>Na-Y>Na-P, as indicated by values of DeltaG degrees . Sodium 47-53 catenin beta like 1 Homo sapiens 115-119 18716027-2 2008 Mouse CYP2J5 is abundant in the kidney where its products, the cis-epoxyeicosatrienoic acids (EETs), modulate sodium transport and vascular tone. Sodium 110-116 cytochrome P450, family 2, subfamily j, polypeptide 5 Mus musculus 6-12 18805957-2 2008 In the absence of the cystic fibrosis transmembrane regulator (CFTR), chloride secretion is diminished and sodium reabsorption exaggerated. Sodium 107-113 cystic fibrosis transmembrane conductance regulator Mus musculus 22-61 18805957-2 2008 In the absence of the cystic fibrosis transmembrane regulator (CFTR), chloride secretion is diminished and sodium reabsorption exaggerated. Sodium 107-113 cystic fibrosis transmembrane conductance regulator Mus musculus 63-67 19037590-6 2008 High-fat, high-sodium diet increased systolic blood pressure in LDLR(-/-) mice but not in C57Bl/6 mice, whereas it induced cardiac hypertrophy in both mouse strains. Sodium 15-21 low density lipoprotein receptor Mus musculus 64-68 19037590-7 2008 Dietary combination of fat and sodium induced endothelial dysfunction in LDLR(-/-) mice. Sodium 31-37 low density lipoprotein receptor Mus musculus 73-77 19037590-9 2008 High sodium intake induced superoxide formation in LDLR(-/-) mice on high-fat diet. Sodium 5-11 low density lipoprotein receptor Mus musculus 51-55 18661192-0 2008 Sodium-coupled transport of the short chain fatty acid butyrate by SLC5A8 and its relevance to colon cancer. Sodium 0-6 solute carrier family 5 member 8 Homo sapiens 67-73 18620340-7 2008 This finding also suggests that human Phox2b mutations, which cause the central congenital hypoventilation syndrome (CCHS, also known as Ondine"s curse), may also produce deficits in central aldosterone signaling and appetitive or autonomic responses to sodium deficiency. Sodium 254-260 paired like homeobox 2B Homo sapiens 38-44 18667581-6 2008 Similarly, the transcriptional activation of ENA1 is impaired in the nsf1Delta mutant in response to high concentrations of NaCl, implying that NSF1 is also needed for the yeast response to sodium stress. Sodium 190-196 Na(+)/Li(+)-exporting P-type ATPase ENA1 Saccharomyces cerevisiae S288C 45-49 18668436-2 2008 hCNT1 and hCNT2 translocate pyrimidine- and purine-nucleosides, respectively, by a sodium-dependent mechanism, whereas hCNT3 shows broad substrate selectivity and the unique ability of translocating nucleosides both in a sodium- and a proton-coupled manner. Sodium 83-89 solute carrier family 28 member 1 Homo sapiens 0-5 18668436-2 2008 hCNT1 and hCNT2 translocate pyrimidine- and purine-nucleosides, respectively, by a sodium-dependent mechanism, whereas hCNT3 shows broad substrate selectivity and the unique ability of translocating nucleosides both in a sodium- and a proton-coupled manner. Sodium 83-89 solute carrier family 28 member 2 Homo sapiens 10-15 18668436-2 2008 hCNT1 and hCNT2 translocate pyrimidine- and purine-nucleosides, respectively, by a sodium-dependent mechanism, whereas hCNT3 shows broad substrate selectivity and the unique ability of translocating nucleosides both in a sodium- and a proton-coupled manner. Sodium 221-227 solute carrier family 28 member 1 Homo sapiens 0-5 18668436-2 2008 hCNT1 and hCNT2 translocate pyrimidine- and purine-nucleosides, respectively, by a sodium-dependent mechanism, whereas hCNT3 shows broad substrate selectivity and the unique ability of translocating nucleosides both in a sodium- and a proton-coupled manner. Sodium 221-227 solute carrier family 28 member 2 Homo sapiens 10-15 18464934-8 2008 Sodium current was lower when NaV1.5 was coexpressed with mutant beta1 or beta1B subunits than when it was coexpressed with WT subunits. Sodium 0-6 alpha-1-B glycoprotein Homo sapiens 74-80 18520136-5 2008 Thus, sodium-dependent glucose transport has been studied on sodium-dependent glucose transporters such as SGLT1 and SGLT2 using cell lines of porcelain renal cell, LLC-PK(1), and murine renal cell, NRK-52E. Sodium 6-12 solute carrier family 5 (sodium/glucose cotransporter), member 1 Mus musculus 107-112 18520136-5 2008 Thus, sodium-dependent glucose transport has been studied on sodium-dependent glucose transporters such as SGLT1 and SGLT2 using cell lines of porcelain renal cell, LLC-PK(1), and murine renal cell, NRK-52E. Sodium 6-12 solute carrier family 5 (sodium/glucose cotransporter), member 2 Mus musculus 117-122 18356541-2 2008 Given the important roles of these genes in the control of arterial pressure, the present study was to test the hypothesis that HIF-1alpha-mediated gene activation serves as an antihypertensive pathway by regulating renal medullary function and sodium excretion. Sodium 245-251 hypoxia inducible factor 1 subunit alpha Rattus norvegicus 128-138 18319257-7 2008 These results were interpreted as a reduction of Na(+) affinity caused by the Asn(82) mutations, suggesting that these mutations interfere with the interaction of SNAT2 with the sodium ion. Sodium 178-184 solute carrier family 38 member 2 Homo sapiens 163-168 18296494-4 2008 After 6 weeks on a high-sodium diet (4% NaCl), the activity of ACE2 was reduced in the renal cortex by 31%, which was mirrored by similar decreases in ACE2 protein (30%) and mRNA expression (36%) in the ovariectomized RW rat (RW-OVX); E2 replacement prevented these effects. Sodium 24-30 angiotensin I converting enzyme 2 Rattus norvegicus 63-67 18256274-10 2008 Because these transcriptional effects of ANG II in isolated nuclei were induced by ANG II in the absence of cell surface receptor-mediated signaling and completely blocked by losartan, we concluded that ANG II may directly stimulate nuclear AT(1a) receptors to induce transcriptional responses that are associated with tubular epithelial sodium transport, cellular growth and hypertrophy, and proinflammatory cytokines. Sodium 338-344 angiogenin Rattus norvegicus 41-44 18470417-2 2008 METHODS: Using SPDP((N-Succinimidyl-3-(2-pyridyldithio)) propionate) as cross-linker, anti-VEGFR2/KDR monoclone antibody was combined to the liposome surface to prepare immunolipo-sodium morrhuate by extruding method, and then its effect on human hemangioma endothelial cells in vitro was observed by laser scanning confocal microscope, inverted microscope, Gimsa staining, transmission electron microscope, MTT and flow cytometry. Sodium 180-186 kinase insert domain receptor Homo sapiens 91-97 18470417-2 2008 METHODS: Using SPDP((N-Succinimidyl-3-(2-pyridyldithio)) propionate) as cross-linker, anti-VEGFR2/KDR monoclone antibody was combined to the liposome surface to prepare immunolipo-sodium morrhuate by extruding method, and then its effect on human hemangioma endothelial cells in vitro was observed by laser scanning confocal microscope, inverted microscope, Gimsa staining, transmission electron microscope, MTT and flow cytometry. Sodium 180-186 kinase insert domain receptor Homo sapiens 98-101 18270170-1 2008 Calmodulin (CaM) regulates steady-state inactivation of sodium currents (Na(V)1.4) in skeletal muscle. Sodium 56-62 immunoglobulin lambda variable 2-14 Homo sapiens 73-81 18166528-0 2008 SLC24A5 encodes a trans-Golgi network protein with potassium-dependent sodium-calcium exchange activity that regulates human epidermal melanogenesis. Sodium 71-77 solute carrier family 24 member 5 Homo sapiens 0-7 18221922-0 2008 Detection and quantification of ppb level potassium in biological samples in the presence of high sodium by ion chromatographic method. Sodium 98-104 histatin 1 Homo sapiens 32-35 18252953-1 2008 Using a highly sensitive quantitative RT-PCR method for the measurement of CYP11B1 (11beta-hydroxylase) and CYP11B2 (aldosterone synthase) mRNAs, we previously demonstrated that CYP11B2 expression in the central nervous system (CNS) is subject to regulation by dietary sodium. Sodium 269-275 cytochrome P450, family 11, subfamily b, polypeptide 2 Rattus norvegicus 178-185 17767805-1 2008 OBJECTIVES: This study was carried out to investigate the effects of WIN55,212-2, a potential cannabinoid receptor agonist, on voltage-gated sodium currents I(Na) in cultured trigeminal ganglion neurons of rats, and to investigate whether the anti-nociceptive effects of cannabinoid receptor subtype 1 (CB1) were produced through its modulation on I(Na). Sodium 141-147 cannabinoid receptor 1 Rattus norvegicus 271-301 17767805-1 2008 OBJECTIVES: This study was carried out to investigate the effects of WIN55,212-2, a potential cannabinoid receptor agonist, on voltage-gated sodium currents I(Na) in cultured trigeminal ganglion neurons of rats, and to investigate whether the anti-nociceptive effects of cannabinoid receptor subtype 1 (CB1) were produced through its modulation on I(Na). Sodium 141-147 cannabinoid receptor 1 Rattus norvegicus 303-306 18441515-2 2008 When expressed in Xenopus oocytes, UST1r mediated uptake of ochratoxin A (OTA; K(m) = 1.0 microM) and sulfate conjugates of steroids, such as estrone-3-sulfate (ES; K(m) = 3.1 microM) and dehydroepiandrosterone sulfate (DHEAS; K(m) = 2.1 microM) in a sodium-independent manner. Sodium 251-257 solute carrier family 22, member 25 Rattus norvegicus 35-40 17931606-16 2007 Assessment of amino acid uptake into cortical synaptosomes of v7-3 knockouts identified 15% and 40% reductions in sodium-dependent proline and leucine transport, respectively, compared to wild type controls. Sodium 114-120 solute carrier family 6 (neurotransmitter transporter), member 15 Mus musculus 62-66 17973873-2 2007 The renal bumetanide-sensitive Na-K-2Cl cotransporter (BSC-1) is expressed only in the thick ascending limb and selectively traffics from intracellular vesicles (IVs) to apical plasma membranes (PMs), where BSC-1 regulates sodium reabsorption. Sodium 223-229 solute carrier family 12 member 1 Rattus norvegicus 55-60 17986147-0 2007 GM1 in the nuclear envelope regulates nuclear calcium through association with a nuclear sodium-calcium exchanger. Sodium 89-95 coenzyme Q10A Mus musculus 0-3 17704762-4 2007 The crystal structure of LeuT reveals an occluded binding pocket containing leucine and two sodium ions, and is highly relevant for the neurotransmitter transporters. Sodium 92-98 Leucine transport, high Homo sapiens 25-29 17663450-3 2007 After 8-day dietary sodium deprivation, immunoreactivity for c-Fos (a neuronal activity marker) increased markedly within the aldosterone-sensitive neurons of the NTS, which express the enzyme 11-beta-hydroxysteroid dehydrogenase type 2 (HSD2). Sodium 20-26 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 61-66 17663450-3 2007 After 8-day dietary sodium deprivation, immunoreactivity for c-Fos (a neuronal activity marker) increased markedly within the aldosterone-sensitive neurons of the NTS, which express the enzyme 11-beta-hydroxysteroid dehydrogenase type 2 (HSD2). Sodium 20-26 hydroxysteroid 11-beta dehydrogenase 2 Rattus norvegicus 193-236 17663450-3 2007 After 8-day dietary sodium deprivation, immunoreactivity for c-Fos (a neuronal activity marker) increased markedly within the aldosterone-sensitive neurons of the NTS, which express the enzyme 11-beta-hydroxysteroid dehydrogenase type 2 (HSD2). Sodium 20-26 hydroxysteroid 11-beta dehydrogenase 2 Rattus norvegicus 238-242 17644362-4 2007 The BP of those mice increased when they were put on a high-salt diet, suggesting that the EP2 receptor is involved in sodium handling by the kidney. Sodium 119-125 prostaglandin E receptor 2 (subtype EP2) Mus musculus 91-103 17255103-2 2007 We have identified and characterized two different sodium-coupled monocarboxylate cotransporters (SMCT) from zebrafish (Danio rerio), electrogenic (zSMCTe) and electroneutral (zSMCTn). Sodium 51-57 solute carrier family 5 member 8 Homo sapiens 98-102 17068161-4 2007 Unlike thirst-associated sensory neurons in the hypothalamus, the 11-beta-hydroxysteroid dehydrogenase type 2 (HSD2) neurons in the rat nucleus tractus solitarius (NTS) are activated in close association with sodium appetite (16). Sodium 209-215 hydroxysteroid 11-beta dehydrogenase 2 Rattus norvegicus 66-109 17068161-4 2007 Unlike thirst-associated sensory neurons in the hypothalamus, the 11-beta-hydroxysteroid dehydrogenase type 2 (HSD2) neurons in the rat nucleus tractus solitarius (NTS) are activated in close association with sodium appetite (16). Sodium 209-215 hydroxysteroid 11-beta dehydrogenase 2 Rattus norvegicus 111-115 17068161-8 2007 The HSD2 neurons were, however, activated by prolonged hypovolemia, which also stimulated sodium appetite. Sodium 90-96 hydroxysteroid 11-beta dehydrogenase 2 Rattus norvegicus 4-8 17068161-9 2007 Twelve hours after PEG was injected in rats that had been sodium deprived for 4 days, the HSD2 neurons showed a consistent increase in c-Fos immunoreactivity. Sodium 58-64 hydroxysteroid 11-beta dehydrogenase 2 Rattus norvegicus 90-94 17068161-10 2007 In summary, the HSD2 neurons are activated specifically in association with sodium appetite and appear not to function in thirst. Sodium 76-82 hydroxysteroid 11-beta dehydrogenase 2 Rattus norvegicus 16-20 17214984-7 2007 Furthermore, Fos-Li IR in the MnPO was increased following AngII infusion in rats consuming a high sodium diet, but not in animals drinking Tap. Sodium 99-105 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 13-16 17230192-4 2007 At least two sodium ions bind in close proximity to the substrate and these sodium-binding sites, together with the sodium-binding sites in another sodium-coupled transporter, LeuT, define an unwound alpha-helix as the central element of the ion-binding motif, a motif well suited to the binding of sodium and to participation in conformational changes that accompany ion binding and unbinding during the transport cycle. Sodium 13-19 Leucine transport, high Homo sapiens 176-180 17230192-4 2007 At least two sodium ions bind in close proximity to the substrate and these sodium-binding sites, together with the sodium-binding sites in another sodium-coupled transporter, LeuT, define an unwound alpha-helix as the central element of the ion-binding motif, a motif well suited to the binding of sodium and to participation in conformational changes that accompany ion binding and unbinding during the transport cycle. Sodium 76-82 Leucine transport, high Homo sapiens 176-180 17230192-4 2007 At least two sodium ions bind in close proximity to the substrate and these sodium-binding sites, together with the sodium-binding sites in another sodium-coupled transporter, LeuT, define an unwound alpha-helix as the central element of the ion-binding motif, a motif well suited to the binding of sodium and to participation in conformational changes that accompany ion binding and unbinding during the transport cycle. Sodium 76-82 Leucine transport, high Homo sapiens 176-180 17230192-4 2007 At least two sodium ions bind in close proximity to the substrate and these sodium-binding sites, together with the sodium-binding sites in another sodium-coupled transporter, LeuT, define an unwound alpha-helix as the central element of the ion-binding motif, a motif well suited to the binding of sodium and to participation in conformational changes that accompany ion binding and unbinding during the transport cycle. Sodium 76-82 Leucine transport, high Homo sapiens 176-180 16917017-1 2007 Downregulation of the renal glucocorticoid-metabolizing enzyme 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD-2) during liver cirrhosis may allow activation of the mineralocorticoid receptor (MR) by glucocorticoids and contribute to sodium retention. Sodium 241-247 hydroxysteroid 11-beta dehydrogenase 2 Rattus norvegicus 107-119 17164836-9 2007 IGF-1 could play an important physiological role in regulating basal sodium transport via the PI3-K/Sgk1 pathway in ASDN. Sodium 69-75 serum/glucocorticoid regulated kinase 1 Homo sapiens 100-104 17082729-1 2006 OBJECTIVE: The Na-K-2Cl cotransporter (NKCC2 isoform) of the thick ascending limb of Henle"s loop (TAL) plays an important role in renal sodium handling, and the vascular isoform (NKCC1) participates in the response to vasoconstrictors. Sodium 137-143 solute carrier family 12 member 1 Rattus norvegicus 39-44 16870839-3 2006 Here we show that the persistent sodium (Na(P)) current in mouse neocortical slices is associated with cellular bursting and our data suggest that these cells are capable of driving networks into a bursting state. Sodium 33-39 catenin, beta like 1 Mus musculus 41-46 17081065-8 2006 Proteins validated by confirming their intracellular localization include PEDF (pigment-epithelium derived factor) and SLC24A5 (sodium/potassium/calcium exchanger 5, NCKX5). Sodium 128-134 solute carrier family 24 member 5 Homo sapiens 119-126 16828976-5 2006 We found that some of the aldosterone-sensitive neurons received close appositions from processes originating in the area postrema, suggesting that input to the HSD2 neurons could be involved in the inhibition of sodium appetite by this site. Sodium 213-219 hydroxysteroid 11-beta dehydrogenase 2 Rattus norvegicus 161-165 16828976-9 2006 A local microcircuit involving the area postrema, HSD2 neurons, and neurotensinergic neurons may play a major role in the regulation of sodium appetite. Sodium 136-142 hydroxysteroid 11-beta dehydrogenase 2 Rattus norvegicus 50-54 16804091-0 2006 Combined behavioral and c-Fos studies elucidate the vital role of sodium for odor detection. Sodium 66-72 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 24-29 16804091-5 2006 In the presence of sodium in the mucus covering the OE, all odorants induce odorant-specific c-Fos expression in the olfactory bulb. Sodium 19-25 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 93-98 16477455-2 2006 Activation of the CNP/NPR-B pathway in pulmonary epithelium has been linked to the inhibition of amiloride-sensitive sodium absorption and to the stimulation of the cystic fibrosis transmembrane conductance regulator (CFTR). Sodium 117-123 C-type natriuretic peptide Ovis aries 18-21 16705681-10 2006 The efferent projections of the HSD2 neurons may provide new insights into the brain circuitry responsible for sodium appetite. Sodium 111-117 hydroxysteroid 11-beta dehydrogenase 2 Rattus norvegicus 32-36 16843877-2 2006 The aim of the present study was to clarify whether fecal stream is required for the enhancement of SGLT-1-mediated sodium transport. Sodium 116-122 solute carrier family 5 member 1 Rattus norvegicus 100-106 16843877-6 2006 Villous height and crypt depth were measured to test for correlations between mucosal structure and SGLT-1-mediated sodium transport or mRNA expression levels. Sodium 116-122 solute carrier family 5 member 1 Rattus norvegicus 100-106 16843877-9 2006 Comparative studies of proximal and distal mucosae demonstrated that in addition to hormonal changes, fecal stream is required for full induction of the sodium transport system (which includes SGLT-1-mediated transport) in the remnant ileum following total proctocolectomy. Sodium 153-159 solute carrier family 5 member 1 Rattus norvegicus 193-199 16805843-6 2006 These results suggest that down-regulation of beta4 may lead to abnormalities of sodium channel and neurite degeneration in the striatum of HD transgenic mice and patients with HD. Sodium 81-87 ATPase, H+ transporting, lysosomal V0 subunit A4 Mus musculus 46-51 16691295-5 2006 These studies (a) establish a physiological role for the arachidonate monooxygenases in renal sodium reabsorption and blood pressure regulation, (b) demonstrate that a dysfunctional Cyp4a10 gene causes alterations in the gating activity of the kidney epithelial sodium channel, and (c) identify a conceptually novel approach for studies of the molecular basis of human hypertension. Sodium 94-100 cytochrome P450, family 4, subfamily a, polypeptide 10 Mus musculus 182-189 16571019-1 2006 The distribution of sodium, choline, sulfate, and chloride ions around two proteins, horseradish peroxidase (HRP) and bovine pancreatic trypsin inhibitor (BPTI), is investigated by means of molecular dynamics simulations with the aim to elucidate ion adsorption at the protein surface. Sodium 20-26 spleen trypsin inhibitor I Bos taurus 155-159 16189294-13 2006 These results suggest that increased apical targeting of ENaC subunits combined with diminished abundance of 11betaHSD2 may contribute to sodium retention associated with HgCl(2)-induced nephrotic syndrome. Sodium 138-144 hydroxysteroid 11-beta dehydrogenase 2 Rattus norvegicus 109-119 16189294-14 2006 The decreased abundance of NHE3, NKCC2, NCC, and Na-K-ATPase may play a compensatory role in promoting sodium excretion. Sodium 103-109 solute carrier family 12 member 1 Rattus norvegicus 33-38 16195498-1 2006 Gamma-melanocyte stimulating hormone (gamma-MSH) is a circulating natriuretic peptide hormone derived from proopiomelanocortin (POMC); its concentration in plasma and pituitary POMC mRNA abundance, increase in rats ingesting a high-sodium diet (HSD, 8% NaCl) compared with a low-sodium diet (LSD, 0.07% NaCl). Sodium 232-238 proopiomelanocortin Rattus norvegicus 128-132 16195498-1 2006 Gamma-melanocyte stimulating hormone (gamma-MSH) is a circulating natriuretic peptide hormone derived from proopiomelanocortin (POMC); its concentration in plasma and pituitary POMC mRNA abundance, increase in rats ingesting a high-sodium diet (HSD, 8% NaCl) compared with a low-sodium diet (LSD, 0.07% NaCl). Sodium 279-285 proopiomelanocortin Rattus norvegicus 128-132 24459482-7 2006 Immunolabeling intensity of 11betaHSD2 in the connecting tubule and cortical collecting duct was significantly reduced in sodium retaining phase of liver cirrhosis, and this was confirmed by immunoblotting. Sodium 122-128 hydroxysteroid 11-beta dehydrogenase 2 Rattus norvegicus 28-38 16541252-6 2006 SOAT specifically transports steroid sulfates such as oestrone-3-sulfate and dehydroepiandrosterone sulfate in a sodium-dependent manner, and is considered to play an important role for the cellular delivery of these prohormones in testes, placenta, adrenal gland and probably other peripheral tissues. Sodium 113-119 solute carrier family 10 member 6 Homo sapiens 0-4 16192299-9 2006 However, further isolation of background currents by recording in solutions that contained only sodium or only potassium revealed that both leptin and CCK were capable of increasing a sodium-dependent conductance or inhibiting a potassium-dependent conductance. Sodium 96-102 cholecystokinin Rattus norvegicus 151-154 16192299-9 2006 However, further isolation of background currents by recording in solutions that contained only sodium or only potassium revealed that both leptin and CCK were capable of increasing a sodium-dependent conductance or inhibiting a potassium-dependent conductance. Sodium 184-190 cholecystokinin Rattus norvegicus 151-154 16417554-4 2006 Mutations in the voltage-gated sodium channel alpha2 subunit (SCN2A) gene on chromosome 2 were recently identified in families affected by neonatal and infantile seizures (benign familial neonatal-infantile seizures, BFNIS) with typical onset before 4 months of life. Sodium 31-37 sodium voltage-gated channel alpha subunit 2 Homo sapiens 62-67 16633989-8 2006 Quantitative polymerase chain reaction (PCR) and Western blot analysis reveal that in diabetic rats compared with controls, mRNA and protein abundance was higher for type 3 sodium/hydrogen exchanger (NHE3) in proximal tubule and ascending limbs of Henle"s loop, and higher for bumetanide-sensitive sodium-potassium-2 chloride cotransporter (NKCC2) in ascending limbs of Henle"s loop. Sodium 173-179 solute carrier family 12 member 1 Rattus norvegicus 341-346 16785747-2 2006 The cloning and identification of sodium transporting genes and proteins like NHE3, NKCC2, ROMK, CLCNKB, NCC, and EnaC has considerably improved our understanding of renal salt handling. Sodium 34-40 solute carrier family 9 member A3 Homo sapiens 78-82 16079298-4 2005 When expressed in Xenopus laevis oocytes, rOat5 mediated the transport of sulfate conjugates of steroids such as estrone-3-sulfate (E(1)S; K(m) = 18.9 +/- 3.9 microM) and dehydroepiandrosterone sulfate (K(m) = 2.3 +/- 0.2 microM) in a sodium-independent manner, in addition to OTA. Sodium 235-241 solute carrier family 22, member 24 Rattus norvegicus 42-47 16045453-1 2005 Many of the sodium-dependent neurotransmitter transporters are rapidly (within minutes) regulated by protein kinase C (PKC), with changes in activity being correlated with changes in transporter trafficking to or from the plasma membrane. Sodium 12-18 protein kinase C, alpha Rattus norvegicus 119-122 16103375-1 2005 Proximal tubular reabsorption of filtered sodium by the sodium/hydrogen exchanger isoform 3 (NHE3), located on the apical membrane, is fundamental to the maintenance of systemic volume and pH homeostasis. Sodium 42-48 solute carrier family 9 member A3 Homo sapiens 93-97 16103375-7 2005 Regulation of the interaction of NHE3 with the actin cytoskeleton can therefore provide a new mode of regulation of sodium and hydrogen transport. Sodium 116-122 solute carrier family 9 member A3 Homo sapiens 33-37 15958509-2 2005 We describe a novel mutation in a family with erythromelalgia in SCN9A, the gene that encodes the Na(v)1.7 sodium channel. Sodium 107-113 sodium voltage-gated channel alpha subunit 9 Homo sapiens 65-70 16043776-7 2005 Taken together, our data suggest that changes in resting potential toward more positive potentials favor states of Nav1.4 with depolarized voltage dependence of gating and thus shift voltage dependence of the sodium current. Sodium 209-215 sodium voltage-gated channel alpha subunit 4 Rattus norvegicus 115-121 16076377-6 2005 The present study suggests that FGF23(R179Q) reduces intestinal sodium-dependent Pi transport activity and type IIb NaPi protein levels by a mechanism that is dependent on VDR. Sodium 64-70 fibroblast growth factor 23 Mus musculus 32-37 16076377-6 2005 The present study suggests that FGF23(R179Q) reduces intestinal sodium-dependent Pi transport activity and type IIb NaPi protein levels by a mechanism that is dependent on VDR. Sodium 64-70 vitamin D (1,25-dihydroxyvitamin D3) receptor Mus musculus 172-175 15955217-9 2005 Somatostatin did not alter portal hemodynamics whereas it significantly reduced MAP, heart rate (HR) and CO (86.9 vs 98.6 mmHg, 65 vs 73 bpm and 8.4 vs 9.1 L/min, respectively) and, in patients with ascites, sodium excretion (0.13 vs 0.23%). Sodium 208-214 somatostatin Homo sapiens 0-12 16109662-10 2005 In contrast, epithelial cells in the crypt also showed immunoreactivity for 11beta-HSD2 in the proximal colon of dietary sodium-depleted and aldosterone-infused rats. Sodium 121-127 hydroxysteroid 11-beta dehydrogenase 2 Rattus norvegicus 76-87 15955112-0 2005 SCN9A mutations define primary erythermalgia as a neuropathic disorder of voltage gated sodium channels. Sodium 88-94 sodium voltage-gated channel alpha subunit 9 Homo sapiens 0-5 15955112-3 2005 Recently, Yang et al identified two missense mutations of the sodium channel alpha subunit SCN9A in patients with erythermalgia. Sodium 62-68 sodium voltage-gated channel alpha subunit 9 Homo sapiens 91-96 15651982-0 2005 Sodium-coupled and electrogenic transport of B-complex vitamin nicotinic acid by slc5a8, a member of the Na/glucose co-transporter gene family. Sodium 0-6 solute carrier family 5 member 8 Homo sapiens 81-87 15721482-1 2005 Adrenomedullin reduces systemic blood pressure and increases urinary sodium excretion partly through the release of nitric oxide. Sodium 69-75 adrenomedullin Rattus norvegicus 0-14 15721482-4 2005 The high sodium diet resulted in an increase in blood pressure and a reduction of urinary sodium excretion in association with increased renal adrenomedullin concentrations and decreased expression of renal neuronal NOS (nNOS) and renal medullary endothelial NOS (eNOS) in DS rats compared with DR rats. Sodium 9-15 adrenomedullin Rattus norvegicus 143-157 15721482-4 2005 The high sodium diet resulted in an increase in blood pressure and a reduction of urinary sodium excretion in association with increased renal adrenomedullin concentrations and decreased expression of renal neuronal NOS (nNOS) and renal medullary endothelial NOS (eNOS) in DS rats compared with DR rats. Sodium 9-15 nitric oxide synthase 1 Rattus norvegicus 207-219 15721482-4 2005 The high sodium diet resulted in an increase in blood pressure and a reduction of urinary sodium excretion in association with increased renal adrenomedullin concentrations and decreased expression of renal neuronal NOS (nNOS) and renal medullary endothelial NOS (eNOS) in DS rats compared with DR rats. Sodium 9-15 nitric oxide synthase 1 Rattus norvegicus 221-225 15721482-5 2005 Chronic adrenomedullin infusion partly inhibited the increase of blood pressure and proteinuria in association with a restoration of renal nNOS and medullary eNOS expression in DS rats under the high sodium diet. Sodium 200-206 adrenomedullin Rattus norvegicus 8-22 15888650-5 2005 Instead, tonic neurons were found to express a persistent sodium current, I(Na,P), that amplified and prolonged depolarization in response to brief stimulation. Sodium 58-64 catenin, beta like 1 Rattus norvegicus 76-80 15804582-5 2005 Functional expression of one of the DMIH variants with a long N-terminus in HEK293 cells produced unitary currents that were preferentially selective for potassium over sodium ions and were activated by hyperpolarizing voltage steps. Sodium 169-175 I[[h]] channel Drosophila melanogaster 36-40 15836629-0 2005 Transport characteristics of N-acetyl-L-aspartate in rat astrocytes: involvement of sodium-coupled high-affinity carboxylate transporter NaC3/NaDC3-mediated transport system. Sodium 84-90 solute carrier family 13 member 3 Rattus norvegicus 137-141 15836629-0 2005 Transport characteristics of N-acetyl-L-aspartate in rat astrocytes: involvement of sodium-coupled high-affinity carboxylate transporter NaC3/NaDC3-mediated transport system. Sodium 84-90 solute carrier family 13 member 3 Rattus norvegicus 142-147 15831236-2 2005 T138067-sodium is a unique new chemotherapy agent that inhibits microtubule formation by binding irreversibly and specifically to beta(1), beta(2)and beta(4) isotypes of 3-tubulin, causing cell arrest at G(2)/M and inducing apoptosis. Sodium 8-14 UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2 Homo sapiens 130-137 15690192-2 2005 Urine steroid profiling substantiated the diagnosis and DNA analysis of the epithelial sodium channel (ENaC) revealed a novel heterozygous beta ENaC mutation in the patient and in her hypertensive father. Sodium 87-93 sodium channel epithelial 1 subunit beta Homo sapiens 139-148 15660328-4 2005 Specifically, we review the evidence that the mutation of uricase that occurred in the Miocene that resulted in a higher serum uric acid in humans compared with most other mammals may have occurred as a means to increase blood pressure in early hominoids in response to a low-sodium and low-purine diet. Sodium 276-282 urate oxidase (pseudogene) Homo sapiens 58-65 15614284-0 2005 Induction of 11beta-hydroxysteroid dehydrogenase type 2 and hyperaldosteronism are essential for enhanced sodium absorption after total colectomy in rats. Sodium 106-112 hydroxysteroid 11-beta dehydrogenase 2 Rattus norvegicus 13-55 15452200-1 2004 The serum and glucocorticoid induced kinase 1 (SGK1) participates in the regulation of sodium reabsorption in the distal segment of the renal tubule, where it may modify the function of the epithelial sodium channel (ENaC). Sodium 87-93 serum/glucocorticoid regulated kinase 1 Homo sapiens 47-51 15333707-1 2004 We evaluated the hypothesis that sodium-dependent vitamin C (ascorbate) transporters SVCT1 and SVCT2 (encoded by genes Slc23a1 and Slc23a2) regulate ascorbate concentrations in tissues of adult mice. Sodium 33-39 solute carrier family 23 (nucleobase transporters), member 1 Mus musculus 85-90 15333707-1 2004 We evaluated the hypothesis that sodium-dependent vitamin C (ascorbate) transporters SVCT1 and SVCT2 (encoded by genes Slc23a1 and Slc23a2) regulate ascorbate concentrations in tissues of adult mice. Sodium 33-39 solute carrier family 23 (nucleobase transporters), member 1 Mus musculus 119-126 15217911-1 2004 Sodium/calcium (Na+/Ca2+) exchange (NCX) overexpression is common to human heart failure and heart failure in many animal models, but its specific contribution to the cellular Ca2+ ([Ca2+]i) handling deficit is unclear. Sodium 0-6 T cell leukemia homeobox 2 Homo sapiens 36-39 15513697-10 2004 It is speculated that the adaptive allostatic renal response to a high sodium diet (an increase in GFR) may result in loss of the ability to appropriately vary renal filtration if that diet is chronically maintained. Sodium 71-77 Rap guanine nucleotide exchange factor 5 Homo sapiens 99-102 15010500-10 2004 By contrast, KB-R7943 [(2-[2-[4-nitrobenzyloxy]phenyl]ethyl)-isothioureamethanesulfonate] preferentially blocks sodium-dependent calcium influx by NCX (reverse mode) and was nontoxic to glioma cells. Sodium 112-118 T cell leukemia homeobox 2 Homo sapiens 147-150 15219883-6 2004 ATB(0) was capable of d-serine transport, and the transport process is obligatorily dependent on sodium (Na+) with a Na(+):substrate stoichiometry of 1:1 and saturable with a Michaelis-Menten constant of 310 +/- 30 microM. Sodium 97-103 solute carrier family 1 member 5 Homo sapiens 0-6 15202772-1 2004 The dopamine transporter (DAT) regulates the extent and duration of dopamine receptor activation through sodium-dependant reuptake of dopamine into presynaptic neurons, resulting in termination of dopaminergic neurotransmission. Sodium 105-111 solute carrier family 6 member 3 Homo sapiens 4-24 15202772-1 2004 The dopamine transporter (DAT) regulates the extent and duration of dopamine receptor activation through sodium-dependant reuptake of dopamine into presynaptic neurons, resulting in termination of dopaminergic neurotransmission. Sodium 105-111 solute carrier family 6 member 3 Homo sapiens 26-29 15170065-4 2004 Sodium transport in the thick ascending limb of Henle (TAL) is the initial process of this system. Sodium 0-6 transaldolase 1 Homo sapiens 55-58 15170065-6 2004 Two additional findings, namely, a lack of the ability to increase BSC1 expression leads to urinary concentrating defect and an enhanced BSC1 expression underlies the edema-forming condition, confirm the close association between sodium handling in TAL and body fluid accumulation. Sodium 230-236 transaldolase 1 Homo sapiens 249-252 15170065-8 2004 Because those genes directly or indirectly regulate sodium transport by the Na-Cl co-transporter or the epithelial sodium channel in the distal convoluted tubule to the collecting duct (distal tubular segments after TAL), sodium handling in this part of the renal tubule may be, at least in part, involved in blood pressure regulation. Sodium 52-58 transaldolase 1 Homo sapiens 216-219 15170065-8 2004 Because those genes directly or indirectly regulate sodium transport by the Na-Cl co-transporter or the epithelial sodium channel in the distal convoluted tubule to the collecting duct (distal tubular segments after TAL), sodium handling in this part of the renal tubule may be, at least in part, involved in blood pressure regulation. Sodium 115-121 transaldolase 1 Homo sapiens 216-219 15148385-3 2004 Using triple-labeled fluorescent immunocytochemistry, we also show that Nav1.6, which is known to produce a persistent sodium current, and the Na+/Ca2+ exchanger, which can be driven by persistent sodium current to import damaging levels of calcium into axons, are colocalized with beta-amyloid precursor protein, a marker of axonal injury, in acute MS lesions. Sodium 119-125 sodium voltage-gated channel alpha subunit 8 Homo sapiens 72-78 15148385-3 2004 Using triple-labeled fluorescent immunocytochemistry, we also show that Nav1.6, which is known to produce a persistent sodium current, and the Na+/Ca2+ exchanger, which can be driven by persistent sodium current to import damaging levels of calcium into axons, are colocalized with beta-amyloid precursor protein, a marker of axonal injury, in acute MS lesions. Sodium 197-203 sodium voltage-gated channel alpha subunit 8 Homo sapiens 72-78 15048685-5 2004 By comparison, dietary sodium restriction instituted during pre- and postnatal development results in small taste buds at adulthood as a result of fewer cytokeratin-19-positive cells. Sodium 23-29 keratin 19 Rattus norvegicus 153-167 14747378-4 2004 Administration of 10(9) total viral particles of Adeno-beta(2)-AR induced an approximately threefold increase in beta(2)-AR density in the renal tissue, which 2 wk after delivery, enhanced GFR and sodium reabsorption compared with control rats. Sodium 197-203 adrenoceptor beta 2 Homo sapiens 49-65 14747378-4 2004 Administration of 10(9) total viral particles of Adeno-beta(2)-AR induced an approximately threefold increase in beta(2)-AR density in the renal tissue, which 2 wk after delivery, enhanced GFR and sodium reabsorption compared with control rats. Sodium 197-203 adrenoceptor beta 2 Homo sapiens 55-65 12851823-4 2004 NTCP and ASBT are cotransporters that mediate sodium-dependent, electrogenic uptake of mainly bile salts into hepatocytes (NTCP), biliary epithelial cells, ileal enterocytes and renal proximal tubular cells (ASBT). Sodium 46-52 solute carrier family 10 member 2 Homo sapiens 9-13 12851823-4 2004 NTCP and ASBT are cotransporters that mediate sodium-dependent, electrogenic uptake of mainly bile salts into hepatocytes (NTCP), biliary epithelial cells, ileal enterocytes and renal proximal tubular cells (ASBT). Sodium 46-52 solute carrier family 10 member 2 Homo sapiens 208-212 15832501-1 2004 OCTN1 (SLC22A4) transports cationic compounds such as tetraethylammonium in a pH-sensitive and sodium-independent manner in cultured cells, and is expressed in wide variety of tissues, including kidney, muscle, placenta, heart, and others. Sodium 95-101 solute carrier family 22 member 4 Homo sapiens 0-5 15832501-1 2004 OCTN1 (SLC22A4) transports cationic compounds such as tetraethylammonium in a pH-sensitive and sodium-independent manner in cultured cells, and is expressed in wide variety of tissues, including kidney, muscle, placenta, heart, and others. Sodium 95-101 solute carrier family 22 member 4 Homo sapiens 7-14 15261163-8 2004 The altered cyclic expression of uterine ENaC and CFTR by a low sodium diet suggests that these ion channels may be affected by elevated circulating aldosterone, which may disrupt reproductive events in the uterus. Sodium 64-70 cystic fibrosis transmembrane conductance regulator Mus musculus 50-54 14962074-12 2004 These results suggest ways in which oxytocin may play a cooperative role together with AVP in the regulation of sodium balance. Sodium 112-118 oxytocin Mus musculus 36-44 14654758-9 2003 In wild-type mice, the sodium-induced increase in blood pressure was completely normalized by treatment with the COMT inhibitor, nitecapone. Sodium 23-29 catechol-O-methyltransferase Mus musculus 113-117 14654758-11 2003 In COMT (-/-) and wild-type mice, a high-sodium diet increased urinary L-DOPA excretion by 405 and 660% (reflected as 102 and 212% increases in dopamine excretion), respectively. Sodium 41-47 catechol-O-methyltransferase Mus musculus 3-7 14654758-15 2003 The findings of the present study also underline the importance of COMT in the regulation of blood pressure, sodium excretion and renal dopaminergic tone. Sodium 109-115 catechol-O-methyltransferase Mus musculus 67-71 14578313-5 2003 Sodium measurements are modeled mathematically to illustrate the GUM approach to uncertainty. Sodium 0-6 OTU deubiquitinase with linear linkage specificity Homo sapiens 65-68 12865309-3 2003 Sodium restriction increased adrenal CYP11B2 expression 57-fold from 1.0 x 10(5) +/- 0.6 x 10(5) to 57 x 10(5) +/- 22 x 10(5) copies/ microg RNA (mean +/- SEM; P < 0.05);in the hippocampus, 14-fold from 5.4 x 10(2) +/- 0.8 x 10(2) to 74 x 10(2) +/- 31 x 10(2) copies/ microg RNA (P < 0.05); and in the cerebellum, 5-fold from 1.9 x 10(3) +/- 0.7 x 10(3) to 9.9 x 10(3) +/- 3.0 x 10(3) copies/ microg RNA (P < 0.01). Sodium 0-6 cytochrome P450, family 11, subfamily b, polypeptide 2 Rattus norvegicus 37-44 12865309-5 2003 High-sodium diet reduced adrenal CYP11B2 expression to 0.19 x 10(5) +/- 0.1 x 10(5) copies/ microg RNA (P < 0.05) but did not affect central nervous system (CNS) expression significantly. Sodium 5-11 cytochrome P450, family 11, subfamily b, polypeptide 2 Rattus norvegicus 33-40 12865309-8 2003 To summarize, we have identified a local CYP11B2 response to sodium depletion in the hippocampus and cerebellum. Sodium 61-67 cytochrome P450, family 11, subfamily b, polypeptide 2 Rattus norvegicus 41-48 12890054-4 2003 In this study, we compared the effects of AM and SR on the sodium current I(Na) in human atrial myocytes. Sodium 59-65 internexin neuronal intermediate filament protein alpha Homo sapiens 74-79 12777949-13 2003 rGLP-1 markedly increased urine flow and sodium excretion for the first 3 days following elevation in sodium intake. Sodium 41-47 glucagon Rattus norvegicus 0-6 12777949-13 2003 rGLP-1 markedly increased urine flow and sodium excretion for the first 3 days following elevation in sodium intake. Sodium 102-108 glucagon Rattus norvegicus 0-6 12441306-5 2003 Together, these data indicate that increased renal sympathetic nerve activity known to be present in CBL rats plays a significant role in the formation of sodium retention by stimulating sodium reabsorption in the TAL via increased renal abundance of NKCC2. Sodium 155-161 solute carrier family 12 member 1 Rattus norvegicus 251-256 12441306-5 2003 Together, these data indicate that increased renal sympathetic nerve activity known to be present in CBL rats plays a significant role in the formation of sodium retention by stimulating sodium reabsorption in the TAL via increased renal abundance of NKCC2. Sodium 187-193 solute carrier family 12 member 1 Rattus norvegicus 251-256 12586353-0 2003 NHERF-1 uniquely transduces the cAMP signals that inhibit sodium-hydrogen exchange in mouse renal apical membranes. Sodium 58-64 cathelicidin antimicrobial peptide Mus musculus 32-36 12481039-4 2002 The loss of beta2 resulted in negative shifts in the voltage dependence of inactivation as well as significant decreases in sodium current density in acutely dissociated hippocampal neurons. Sodium 124-130 hemoglobin, beta adult minor chain Mus musculus 12-17 12503866-4 2002 Because ENaC is a rate-limiting step for sodium absorption by epithelial cells, not only of the renal tubule but also of the lung epithelium, patients with PHA-1 with pulmonary symptoms have sometimes been reported. Sodium 41-47 sodium channel epithelial 1 subunit gamma Homo sapiens 156-161 12491807-2 2002 The molecular cloning of these transporters revealed that NET, DAT, and SERT are members of a sodium-dependent neurotransmitter transporter gene family, while VMATs arise from proton-dependent transporter gene family. Sodium 94-100 solute carrier family 6 member 3 Homo sapiens 63-66 12359983-7 2002 The nNOS gene expression significantly increased in rats fed with the low sodium diet compared with the standard diet group, and it significantly decreased in rats with the high sodium diet. Sodium 74-80 nitric oxide synthase 1 Rattus norvegicus 4-8 12359983-7 2002 The nNOS gene expression significantly increased in rats fed with the low sodium diet compared with the standard diet group, and it significantly decreased in rats with the high sodium diet. Sodium 178-184 nitric oxide synthase 1 Rattus norvegicus 4-8 12359983-11 2002 The parallel changes in renin and nNOS mRNA during different sodium intakes suggest that nNOS can be part of the complex, and still largely unclarified, macula densa mechanism of renin regulation. Sodium 61-67 nitric oxide synthase 1 Rattus norvegicus 34-38 12359983-11 2002 The parallel changes in renin and nNOS mRNA during different sodium intakes suggest that nNOS can be part of the complex, and still largely unclarified, macula densa mechanism of renin regulation. Sodium 61-67 nitric oxide synthase 1 Rattus norvegicus 89-93 12231642-0 2002 c-Fos expression in ouabain-treated vascular smooth muscle cells from rat aorta: evidence for an intracellular-sodium-mediated, calcium-independent mechanism. Sodium 111-117 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 0-5 12154112-6 2002 The protein expression of eNOS in the renal medulla of FFR was significantly lower than that in control rats during a high sodium load. Sodium 123-129 nitric oxide synthase 3 Rattus norvegicus 26-30 12154112-9 2002 These results suggest that the decrease in renal medullary NO production by eNOS during a high sodium load may play a role in fructose-fed, salt-sensitive hypertension. Sodium 95-101 nitric oxide synthase 3 Rattus norvegicus 76-80 12028137-0 2002 Intracellular sodium modulates the state of protein kinase C phosphorylation of rat proximal tubule Na+,K+-ATPase. Sodium 14-20 protein kinase C, gamma Rattus norvegicus 44-60 12028137-12 2002 The results imply that phosphorylation of renal Na+,K+-ATPase activity is modulated by the level of intracellular sodium and that this effect involves PKC and calcium signalling pathways. Sodium 114-120 protein kinase C, gamma Rattus norvegicus 151-154 12090248-7 2002 whi2 and psr1 psr2 mutants had similar phenotypes, including reduced STRE-mediated gene expression, higher sensitivity to sodium ions and heat shock, and hyper-phosphorylation of Msn2. Sodium 122-128 Whi2p Saccharomyces cerevisiae S288C 0-4 11988490-5 2002 (3) Alterations of I(Ks), I(Kr), and I(Na) (fast sodium current) in long-QT syndrome (LQT1, LQT2, and LQT3, respectively) are reflected in characteristic QT-interval and T-wave changes; LQT1 prolongs QT without widening the T wave. Sodium 49-55 internexin neuronal intermediate filament protein alpha Homo sapiens 37-42 11906212-3 2002 Here we report that the majority of neurons in both wild-type and tipE mutant (tipE-) embryo cultures fire sodium-dependent action potentials in response to depolarizing current injection. Sodium 107-113 temperature-induced paralytic E Drosophila melanogaster 79-83 11906212-6 2002 Analysis of underlying currents reveals a slower rate of repolarization-dependent recovery of voltage-gated sodium currents during repeated activation in tipE- neurons. Sodium 108-114 temperature-induced paralytic E Drosophila melanogaster 154-158 11906212-8 2002 These data demonstrate that tipE regulates sodium-dependent repetitive firing and recovery of sodium currents during repeated activation. Sodium 43-49 temperature-induced paralytic E Drosophila melanogaster 28-32 11906212-8 2002 These data demonstrate that tipE regulates sodium-dependent repetitive firing and recovery of sodium currents during repeated activation. Sodium 94-100 temperature-induced paralytic E Drosophila melanogaster 28-32 11906212-9 2002 Furthermore, the duration of the interstimulus interval necessary to fire a second full-sized action potential is significantly longer in single- versus multiple-spiking transgenic neurons, suggesting that a slow rate of recovery of sodium currents contributes to the decrease in repetitive firing in tipE- neurons. Sodium 233-239 temperature-induced paralytic E Drosophila melanogaster 301-305 11744737-10 2002 Collectively, the data indicate that extracellular osmolality stimulates receptor activity and receptor gene expression through a specific p38 beta-dependent mechanism, raising the possibility that changes in medullary tonicity could play an important role in the regulation of renal sodium handling in the terminal nephron. Sodium 284-290 mitogen-activated protein kinase 11 Rattus norvegicus 139-147 11742843-6 2002 The number of Fos-ir neurons within different nuclei of the raphe system was increased in spontaneous and induced sodium ingestion of CD-A and PD-A groups compared with the CD-NA and PD-NA groups. Sodium 114-120 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 14-17 12424421-5 2002 Ang-(1-7) increased absolute and fractional sodium excretion by +36 +/- 6 and +37 +/- 8%, respectively (p < 0.05). Sodium 44-50 angiogenin Rattus norvegicus 0-3 12424421-6 2002 Infusion of Ang-(1-7) did not prevent the decreases in GFR and RPF but completely blunted the decreases in absolute (-2 +/- 2%) and fractional sodium excretion (-4 +/- 4%) induced by ANG II (n = 11). Sodium 143-149 angiogenin Rattus norvegicus 12-15 12424421-7 2002 Blockade of the Ang-(1-7) receptor by [7-D-Ala]-Ang-(1-7) (5 microg/min, n = 11) significantly decreased GFR, RPF, absolute and fractional sodium excretion by -28 +/- 7, -20 +/- 5, -32 +/- 7 and -24 +/- 4%, respectively (p < 0.05), suggesting that the action of endogenous ANG II is unopposed by compensatory effect of endogenous Ang-(1-7). Sodium 139-145 angiogenin Rattus norvegicus 16-19 12424421-7 2002 Blockade of the Ang-(1-7) receptor by [7-D-Ala]-Ang-(1-7) (5 microg/min, n = 11) significantly decreased GFR, RPF, absolute and fractional sodium excretion by -28 +/- 7, -20 +/- 5, -32 +/- 7 and -24 +/- 4%, respectively (p < 0.05), suggesting that the action of endogenous ANG II is unopposed by compensatory effect of endogenous Ang-(1-7). Sodium 139-145 angiogenin Rattus norvegicus 48-51 12424421-7 2002 Blockade of the Ang-(1-7) receptor by [7-D-Ala]-Ang-(1-7) (5 microg/min, n = 11) significantly decreased GFR, RPF, absolute and fractional sodium excretion by -28 +/- 7, -20 +/- 5, -32 +/- 7 and -24 +/- 4%, respectively (p < 0.05), suggesting that the action of endogenous ANG II is unopposed by compensatory effect of endogenous Ang-(1-7). Sodium 139-145 angiogenin Rattus norvegicus 48-51 12424421-14 2002 Results obtained during blockade of Ang-(1-7) and of AT(2) receptors imply that AT(2) receptors play a role in tubular sodium reabsorption in the presence of high ANG II concentration. Sodium 119-125 angiogenin Rattus norvegicus 36-39 11738033-7 2001 This autonomous activity is periodic and depends on hyperpolarization-activated cationic (H) and persistent sodium (Na(p)) currents. Sodium 108-114 catenin, beta like 1 Mus musculus 116-121 11707620-9 2001 In particular, SGK1 plays an important role in activating certain potassium, sodium, and chloride channels, suggesting an involvement in the regulation of processes such as cell survival, neuronal excitability, and renal sodium excretion. Sodium 77-83 serum/glucocorticoid regulated kinase 1 Homo sapiens 15-19 11682659-2 2001 Inhibition of 11beta-HSD2 by liquorice-derived glycyrrhizic acid (GA) therefore results in sodium retention and hypertension. Sodium 91-97 hydroxysteroid 11-beta dehydrogenase 2 Rattus norvegicus 14-25 11922146-0 2001 Differential modulation of sodium channel gating and persistent sodium currents by the beta1, beta2, and beta3 subunits. Sodium 27-33 UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2 Homo sapiens 87-92 11553519-5 2001 These results negate the hypothesis that NHE2 plays an important renal function in sodium-fluid volume homeostasis; however, they demonstrate that NHE3 is critical for systemic electrolyte, acid-base, and fluid volume homeostasis during dietary Na+ restriction and that its absence leads to renal salt wasting. Sodium 83-89 solute carrier family 9 (sodium/hydrogen exchanger), member 2 Mus musculus 41-45 12501973-0 2001 Dietary sodium modulates mRNA abundance of enzymes involved in pituitary processing of proopiomelanocortin. Sodium 8-14 proopiomelanocortin Rattus norvegicus 87-106 11509490-15 2001 The pretreatment by the AT(1) receptor antagonist candesartan (750 ng IR) in SAL-infused rats (n=7) effectively prevented the decrease in RPF (-3+/-3%) elicited by nNOS inhibition and resulted in an increase in GFR (+25+/-12, P<0.05) and a concomitant greater increase in sodium excretion (84+/-12%, P<0.05) compared with control values. Sodium 275-281 nitric oxide synthase 1 Rattus norvegicus 164-168 11473634-13 2001 Solute clearances (+175% for sodium and +26% for potassium) were significantly increased in the H-ANP group, mainly as a result of the increased fluid removal in this group. Sodium 29-35 natriuretic peptide A Rattus norvegicus 98-101 11352505-0 2001 Sodium block and depolarization diminish P2Z-dependent Ca2+ entry in human B lymphocytes. Sodium 0-6 carbonic anhydrase 2 Homo sapiens 55-58 11424542-9 2001 Correlations between CFC scores and 24-hour recall values were 0.36 for total fat, 0.36 for saturated fat, and 0.34 for sodium; CFC scores were consistent with hypothesized gender differences in nutrient intake. Sodium 120-126 tubulin folding cofactor C Homo sapiens 21-24 11424542-10 2001 APPLICATIONS/CONCLUSIONS: The CFC is a reliable and valid tool for measuring fat, saturated fat, and sodium intake in middle school students. Sodium 101-107 tubulin folding cofactor C Homo sapiens 30-33 11375128-9 2001 Messenger RNA encoding PAR-1 was increased by dietary sodium depletion, consistent with previous reports of an increased response to trypsin after sodium depletion. Sodium 54-60 coagulation factor II (thrombin) receptor Rattus norvegicus 23-28 11375128-9 2001 Messenger RNA encoding PAR-1 was increased by dietary sodium depletion, consistent with previous reports of an increased response to trypsin after sodium depletion. Sodium 147-153 coagulation factor II (thrombin) receptor Rattus norvegicus 23-28 11427334-1 2001 To determine pharmacological specificity of intracerebroventricular (IVT) administration of adrenomedullin (AM) on water and sodium excretion, studies were performed in rats pretreated with AM (22-52), a putative AM-receptor antagonist or CGRP(8-37), a ligand that preferentially antagonizes the CGRP(1)-receptor subtype. Sodium 125-131 adrenomedullin Rattus norvegicus 92-106 11427334-3 2001 Intracerebroventricular administration of rat adrenomedullin to conscious hydrated rats resulted in a significant increase in urinary volume and sodium excretion during the 6-h period of urine collection and was most effective at 3 and 6 h. Although less effective than AM, central administration of CGRP induced diuresis and natriuresis. Sodium 145-151 adrenomedullin Rattus norvegicus 46-60 11318960-4 2001 In contrast, dietary sodium loading induced a marked increase in cAT1 receptor expression in both the glomeruli and adrenal compared with receptor expression in salt-restricted animals [H/L ratio: glomeruli (1.5), renal medulla (1.1), adrenal (1.6)] that inversely correlated with the activity of the plasma renin angiotensin system. Sodium 21-27 renin Canis lupus familiaris 308-313 11305927-1 2001 On the basis of intracellular acidifications in the presence of 30 microM cariporide, we selected a fibroblast cell line termed CR5, expressing a mutated Na(+)/H(+) exchanger NHE-1 with a low affinity for cariporide (87 +/- 11.6 microM) and extracellular sodium (248 +/- 63.7 mM). Sodium 255-261 teratocarcinoma-derived growth factor 1 pseudogene 5 Homo sapiens 128-131 11305927-3 2001 Using intracellular acidifications in the presence of 3 mM external sodium on the CR5 fibroblasts, we isolated two revertants which exhibited a complete recovery for sodium affinity but were still resistant to cariporide. Sodium 68-74 teratocarcinoma-derived growth factor 1 pseudogene 5 Homo sapiens 82-85 11305927-3 2001 Using intracellular acidifications in the presence of 3 mM external sodium on the CR5 fibroblasts, we isolated two revertants which exhibited a complete recovery for sodium affinity but were still resistant to cariporide. Sodium 166-172 teratocarcinoma-derived growth factor 1 pseudogene 5 Homo sapiens 82-85 11230727-3 2001 Expression of the apical sodium-dependent bile acid transporter (ASBT) and of the organic anion transporting polypeptide (OATP-A) was detected and associated with sodium-dependent and sodium-independent [(3)H]taurocholate uptake in BEC. Sodium 25-31 solute carrier family 10 member 2 Homo sapiens 65-69 11230727-3 2001 Expression of the apical sodium-dependent bile acid transporter (ASBT) and of the organic anion transporting polypeptide (OATP-A) was detected and associated with sodium-dependent and sodium-independent [(3)H]taurocholate uptake in BEC. Sodium 163-169 solute carrier family 10 member 2 Homo sapiens 18-63 11230727-3 2001 Expression of the apical sodium-dependent bile acid transporter (ASBT) and of the organic anion transporting polypeptide (OATP-A) was detected and associated with sodium-dependent and sodium-independent [(3)H]taurocholate uptake in BEC. Sodium 163-169 solute carrier family 10 member 2 Homo sapiens 65-69 11798865-7 2001 RESULTS: The c-fos AS ODN blocked the c-fos gene expression and reduced the content of both water and sodium in brain tissue and Ca(2+) in symptosome, thus alleviating the morphological damage in neuron. Sodium 102-108 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 13-18 11160618-3 2001 In the current study, the wild-type D4 dopamine receptor showed an 8-fold decrease in zinc affinity in the presence of 120 mM NaCl, but the binding of zinc to the neutral TMS2 D4-D77N mutant was completely sodium-insensitive. Sodium 206-212 serine incorporator 1 Homo sapiens 171-175 11340305-0 2001 Regulation of tubular cell MCP-1 production by intracellular ions: a role for sodium and calcium. Sodium 78-84 chemokine (C-C motif) ligand 2 Mus musculus 27-32 11076886-9 2000 Urinary CNP was found to be inversely related to urinary sodium excretion in cirrhotic patients (r=-0.56; p<0.01). Sodium 57-63 natriuretic peptide C Homo sapiens 8-11 11076886-11 2000 In cirrhotic patients with hepatorenal syndrome or refractory ascites (n=5), urinary CNP decreased from 132 (59) to 38 (7) ng/g creatinine (p<0.05) one week after either ornipressin infusion or insertion of a transjugular intrahepatic portosystemic shunt together with an increase in urinary sodium excretion from 27 (17) to 90 (34) mmol/24 hours. Sodium 295-301 natriuretic peptide C Homo sapiens 85-88 11076886-13 2000 Furthermore, an inverse relation between urinary CNP and urinary sodium excretion suggests a role for this peptide in renal sodium handling in patients with cirrhosis. Sodium 65-71 natriuretic peptide C Homo sapiens 49-52 11076886-13 2000 Furthermore, an inverse relation between urinary CNP and urinary sodium excretion suggests a role for this peptide in renal sodium handling in patients with cirrhosis. Sodium 124-130 natriuretic peptide C Homo sapiens 49-52 11179908-2 2000 Recent findings suggest that sgk is an important gene in the early action of corticosteroids on epithelial sodium reabsorption. Sodium 107-113 serum/glucocorticoid regulated kinase 1 Homo sapiens 29-32 10926932-2 2000 GAT-1 maintains low synaptic concentrations of neurotransmitter by coupling GABA uptake to the fluxes of sodium and chloride. Sodium 105-111 solute carrier family 6 member 12 Rattus norvegicus 0-5 10998041-5 2000 As the name implies, GIRK channels are modulated by G-proteins; they are also modulated by phosphatidylinositol 4,5-bisphosphate, intracellular sodium, ethanol and mechanical stretch. Sodium 144-150 potassium inwardly rectifying channel subfamily J member 3 S homeolog Xenopus laevis 21-25 11003661-6 2000 Ptk2 has the strongest effect on Pma1, and ptk2 mutants exhibit a pleiotropic phenotype of tolerance to toxic cations, including sodium, lithium, manganese, tetramethylammonium, hygromycin B, and norspermidine. Sodium 129-135 protein kinase PTK2 Saccharomyces cerevisiae S288C 43-47 10998198-6 2000 GH (0.1 nM) significantly increased the sodium/sulfate co-transport in MDCK/NaSi-1 cells up to 35%. Sodium 40-46 somatotropin Canis lupus familiaris 0-2 11001935-0 2000 Skeletal muscle sodium channel gating in mice deficient in myotonic dystrophy protein kinase. Sodium 16-22 dystrophia myotonica-protein kinase Mus musculus 59-92 11058023-5 2000 Variable activities of G6PD and PK, probably related to different reticulocyte number, were detected together with normal osmotic fragility and intracellular sodium and potassium concentrations. Sodium 158-164 glucose-6-phosphate dehydrogenase Canis lupus familiaris 23-27 10950861-4 2000 The purpose of this study was to directly measure the transport of nucleoside analogs by the sodium-coupled pyrimidine-selective transporter rCNT1 using electrophysiology methods. Sodium 93-99 solute carrier family 28 member 1 Rattus norvegicus 141-146 10950861-6 2000 Uridine-induced currents in voltage-clamped oocytes expressing rCNT1 were sodium-, voltage-, and concentration-dependent (K(0.5) = 21 microM), and were blocked by adenosine. Sodium 74-80 solute carrier family 28 member 1 Rattus norvegicus 63-68 10972664-0 2000 CCKB/gastrin receptors mediate changes in sodium and potassium absorption in the isolated perfused rat kidney. Sodium 42-48 gastrin Rattus norvegicus 5-12 10972664-10 2000 Compared with controls, gastrin (10-6 mol/L) caused a decrease in the fractional sodium reabsorption (basal 80%, 10 minutes after application of gastrin 71%, after 20 minutes 62%, P < 0.05). Sodium 81-87 gastrin Rattus norvegicus 24-31 10828498-1 2000 Atrial natriuretic factor (ANF) and C-type natriuretic peptide (CNP) receptors have been described in encephalic areas and nuclei related to the regulation of cardiovascular as well as sodium and water homeostasis. Sodium 185-191 natriuretic peptide A Rattus norvegicus 0-25 10828498-1 2000 Atrial natriuretic factor (ANF) and C-type natriuretic peptide (CNP) receptors have been described in encephalic areas and nuclei related to the regulation of cardiovascular as well as sodium and water homeostasis. Sodium 185-191 natriuretic peptide A Rattus norvegicus 27-30 10828498-1 2000 Atrial natriuretic factor (ANF) and C-type natriuretic peptide (CNP) receptors have been described in encephalic areas and nuclei related to the regulation of cardiovascular as well as sodium and water homeostasis. Sodium 185-191 natriuretic peptide C Rattus norvegicus 36-62 10828498-1 2000 Atrial natriuretic factor (ANF) and C-type natriuretic peptide (CNP) receptors have been described in encephalic areas and nuclei related to the regulation of cardiovascular as well as sodium and water homeostasis. Sodium 185-191 natriuretic peptide C Rattus norvegicus 64-67 10771308-2 2000 The diuretic effect of adrenomedullin occurred during the 6-h period of urine collection and was most effective during the 3 and 6 h. Most remarkably, AM given IVT induced a dose-related increase in urinary sodium excretion at all periods of urine collection. Sodium 207-213 adrenomedullin Rattus norvegicus 23-37 10771308-2 2000 The diuretic effect of adrenomedullin occurred during the 6-h period of urine collection and was most effective during the 3 and 6 h. Most remarkably, AM given IVT induced a dose-related increase in urinary sodium excretion at all periods of urine collection. Sodium 207-213 adrenomedullin Rattus norvegicus 151-153 10788509-1 2000 The neuronal glycine transporter GLYT2 takes up glycine from the extracellular space by an electrogenic process where this neurotransmitter is co-transported with sodium and chloride ions. Sodium 163-169 glycoprotein alpha-galactosyltransferase 1 (inactive) Homo sapiens 33-38 10788509-2 2000 We report in this paper that tyrosine at position 289 of GLYT2a is crucial for ion coupling, glycine affinity and sodium selectivity, stressing the essential role played by this residue of transmembrane domain III in the mechanism of transport. Sodium 114-120 glycoprotein alpha-galactosyltransferase 1 (inactive) Homo sapiens 57-62 10775148-1 2000 This study examines the amplitude of sodium-calcium exchange current (I(NaCa)) in epicardial, midmyocardial, and endocardial canine ventricular myocytes. Sodium 37-43 nascent polypeptide-associated complex subunit alpha Canis lupus familiaris 72-76 10775148-3 2000 I(NaCa) was triggered by release of calcium from the sarcoplasmic reticulum or by rapid removal of external sodium. Sodium 108-114 nascent polypeptide-associated complex subunit alpha Canis lupus familiaris 2-6 10775148-7 2000 When triggered by sodium removal, peak I(NaCa) was 0.74 +/- 0.04, 0.57 +/- 0.04, and 0.50 +/- 0.03 pA/pF, respectively, in midmyocardial, epicardial, and endocardial myocytes. Sodium 18-24 nascent polypeptide-associated complex subunit alpha Canis lupus familiaris 41-45 10775148-8 2000 Epicardial I(NaCa) was smaller than midmyocardial I(NaCa) when activated by removal of external sodium but was comparable to epicardial and midmyocardial I(NaCa) when activated by the normal calcium transient, implying possible transmural differences in excitation-contraction coupling. Sodium 96-102 nascent polypeptide-associated complex subunit alpha Canis lupus familiaris 13-17 10803602-9 2000 Aldosterone production, activity of aldosterone synthase, and expression of mRNA for CYP11B2 and AT1 receptor were increased in hearts of rats with high sodium intake. Sodium 153-159 cytochrome P450, family 11, subfamily b, polypeptide 2 Rattus norvegicus 85-92 10792624-1 2000 BACKGROUND: Enhanced expression of the kidney-specific sodium transporter, rBSC1, in the thick ascending limb of Henle (TAL) and of the renal water channel, aquaporin-2 (AQP2), in collecting duct has been identified in rats with congestive heart failure (CHF) as a cause for enhanced sodium and water retention in this condition. Sodium 55-61 solute carrier family 12 member 1 Rattus norvegicus 75-80 10792624-12 2000 CONCLUSIONS: rBSC1 is up-regulated even in rats with small to moderate myocardial infarctions, which may enhance the sodium transport in the TAL in this pathophysiologic condition. Sodium 117-123 solute carrier family 12 member 1 Rattus norvegicus 13-18 10744628-2 2000 The dopamine transporter (DAT) mediates complex actions in recognizing cocaine and in recognizing and translocating dopamine, sodium, and chloride. Sodium 126-132 solute carrier family 6 member 3 Homo sapiens 4-24 10744628-2 2000 The dopamine transporter (DAT) mediates complex actions in recognizing cocaine and in recognizing and translocating dopamine, sodium, and chloride. Sodium 126-132 solute carrier family 6 member 3 Homo sapiens 26-29 10775569-5 2000 In the present studies we have examined expression of CypB in rat proximal tubules, which contributes to the increased renal sodium reabsorption in this model of hypertension. Sodium 125-131 peptidylprolyl isomerase B Rattus norvegicus 54-58 10772659-5 2000 NHE2(-/-) and wild-type mice had comparable rates of sodium-dependent proton secretion. Sodium 53-59 solute carrier family 9 (sodium/hydrogen exchanger), member 2 Mus musculus 0-4 10772659-8 2000 Luminal sodium-dependent proton secretion was the same in NHE3(-/-)/NHE2(-/-) as in NHE3(-/-) mice. Sodium 8-14 solute carrier family 9 (sodium/hydrogen exchanger), member 2 Mus musculus 68-72 10681320-3 2000 Faropenem (an oral penem antibiotic) was transported via Npt1 with a Michaelis-Menten constant of 0.77 +/- 0.34 mM in a sodium-independent but chloride ion-sensitive manner. Sodium 120-126 solute carrier family 17 (sodium phosphate), member 1 Mus musculus 57-61 10744346-2 2000 The present study set out to explore the importance of angiotensin (Ang)II in the brain in allowing the somatosensory system to cause a reflex renal nerve-mediated reduction in renal sodium and water excretion. Sodium 183-189 angiogenin Rattus norvegicus 68-71 10729750-8 2000 Sodium restriction significantly reduced the number of PCNA-stained cells in glomeruli and tubules at days 14 and 60, but not at day 7, whereas it decreased AP-1 activation at all times of the study. Sodium 0-6 proliferating cell nuclear antigen Rattus norvegicus 55-59 10677232-0 2000 Sodium binding site of factor Xa: role of sodium in the prothrombinase complex. Sodium 42-48 coagulation factor X Homo sapiens 56-70 10974416-8 2000 We conclude that, in the renal cortex, NO produced by nNOS plays an important role in the regulation of whole-kidney GFR and excretion in normal, sodium-replete rats. Sodium 146-152 nitric oxide synthase 1 Rattus norvegicus 54-58 10717838-8 2000 It was concluded that the optimum dietary sodium concentration for maximum milk yield was greater than the published requirements, and that substantial increases in sodium intake above current requirements also reduced milk SCC. Sodium 165-171 SCC Bos taurus 224-227 10656801-0 2000 X-ray structure of yeast Hal2p, a major target of lithium and sodium toxicity, and identification of framework interactions determining cation sensitivity. Sodium 62-68 3'(2'),5'-bisphosphate nucleotidase Saccharomyces cerevisiae S288C 25-30 10656801-1 2000 The product of the yeast HAL2 gene (Hal2p) is an in vivo target of sodium and lithium toxicity and its overexpression improves salt tolerance in yeast and plants. Sodium 67-73 3'(2'),5'-bisphosphate nucleotidase Saccharomyces cerevisiae S288C 25-29 10656801-1 2000 The product of the yeast HAL2 gene (Hal2p) is an in vivo target of sodium and lithium toxicity and its overexpression improves salt tolerance in yeast and plants. Sodium 67-73 3'(2'),5'-bisphosphate nucleotidase Saccharomyces cerevisiae S288C 36-41 10691781-4 2000 In the kidney, ANG II at the AT2 receptor stimulates a vasodilator cascade of bradykinin (BK), NO and cyclic GMP which is tonically activated only during conditions of increased ANG II, such as sodium depletion. Sodium 194-200 5'-nucleotidase, cytosolic II Homo sapiens 109-112 10678288-2 2000 The kidney is an important site of action of Ang II AT1 receptor blockers because intrarenal Ang II not only vasoconstricts the renal vasculature but also reduces sodium excretion and suppresses the pressure natriuresis relationship. Sodium 163-169 angiogenin Rattus norvegicus 45-48 10644882-8 2000 CONCLUSION: These results suggest that adaptations to a high-potassium or a low-sodium diet and to metabolic acidosis involve decreases in renal 11betaHSD2 activity, enhancing the access of glucocorticoids to renal corticosteroid receptors. Sodium 80-86 hydroxysteroid 11-beta dehydrogenase 2 Rattus norvegicus 145-155 10858623-6 2000 Treatment of adrenalectomized rats with the sodium-retaining mineralocorticoid hormone, deoxycorticosterone, at the end of the fourth day, decreased Fos expression in the subfornical organ and the organum vasculosum of the lamina terminalis when NaCl solution was available but not when the NaCl solution was unavailable. Sodium 44-50 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 149-152 10858623-9 2000 Relative to sodium-deplete intact rats, however, sodium-deplete adrenalectomized rats had a greater number of neurons expressing Fos in the organum vasculosum. Sodium 49-55 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 129-132 10858623-10 2000 Treatment of sodium-deplete rats, adrenalectomized or intact, with the angiotensin II-type 1 receptor antagonist, ZD7155, decreased sodium intake and Fos expression in the subfornical organ but not in the organum vasculosum of the lamina terminalis or median preoptic nucleus. Sodium 13-19 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 150-153 10608847-8 1999 Together, the experiments indicate that sgk stimulates electrogenic sodium transport by increasing the number of ENaCs at the cell surface and suggest that sgk may mediate the early increase in aldosterone-induced sodium current. Sodium 68-74 serum/glucocorticoid regulated kinase 1 L homeolog Xenopus laevis 40-43 10555096-6 1999 This 66% fall in renin secretion was associated with significant (P < 0.05) increases in creatinine clearance (40%), renal blood flow (8%), urine flow (50%), and sodium excretion (17%). Sodium 165-171 renin Canis lupus familiaris 17-22 10555096-7 1999 CONCLUSIONS: It is suggested that this inhibition of renin secretion was mediated, at least in part, in response to a ProANF31-67-induced increment in the sodium load delivered to the macula densa. Sodium 155-161 renin Canis lupus familiaris 53-58 10515937-4 1999 Deletion of CKB1 increased the salt sensitivity of a strain lacking Ena1 ATPase, the major determinant for sodium efflux, suggesting that the function of the kinase is not mediated by Ena1. Sodium 107-113 Na(+)/Li(+)-exporting P-type ATPase ENA1 Saccharomyces cerevisiae S288C 68-72 10517637-5 1999 Here we show that polycystin-L is a calcium-modulated nonselective cation channel that is permeable to sodium, potassium and calcium ions. Sodium 103-109 polycystic kidney disease 2-like 1 Mus musculus 18-30 10360866-5 1999 METHODS: Inward sodium currents were recorded from human embryonic kidney (HEK293) cells stably expressing hH1a channels. Sodium 16-22 H1.1 linker histone, cluster member Homo sapiens 107-111 10360866-13 1999 CONCLUSIONS: In a heterologous expression system, halothane and isoflurane interact with the hH1a channels and suppress the sodium current. Sodium 124-130 H1.1 linker histone, cluster member Homo sapiens 93-97 10359563-8 1999 Blood pressure increased in these animals when they were placed on a high-salt diet, suggesting that the EP2 receptor may be involved in sodium handling by the kidney. Sodium 137-143 prostaglandin E receptor 2 (subtype EP2) Mus musculus 105-117 10234035-8 1999 We conclude that VIP excites mPRF neurons by activation of a sodium current. Sodium 61-67 Spi-C transcription factor (Spi-1/PU.1 related) Mus musculus 29-33 10207057-6 1999 In addition, hal4 hal5 and trk1 trk2 mutants exhibit similar phenotypes: (i) they are deficient in potassium uptake; (ii) their growth is sensitive to a variety of toxic cations, including lithium, sodium, calcium, tetramethylammonium, hygromycin B, and low pH; and (iii) they exhibit increased uptake of methylammonium, an indicator of membrane potential. Sodium 198-204 serine/threonine protein kinase SAT4 Saccharomyces cerevisiae S288C 13-17 10207057-6 1999 In addition, hal4 hal5 and trk1 trk2 mutants exhibit similar phenotypes: (i) they are deficient in potassium uptake; (ii) their growth is sensitive to a variety of toxic cations, including lithium, sodium, calcium, tetramethylammonium, hygromycin B, and low pH; and (iii) they exhibit increased uptake of methylammonium, an indicator of membrane potential. Sodium 198-204 protein kinase HAL5 Saccharomyces cerevisiae S288C 18-22 10196218-1 1999 Parathyroid hormone (PTH) is a potent inhibitor of mammalian renal proximal tubule sodium absorption via suppression of the apical membrane Na/H exchanger (NHE-3). Sodium 83-89 solute carrier family 9 member A3 Homo sapiens 140-161 9914451-0 1999 Antisense oligonucleotide treatment reveals a physiologically relevant role for adrenomedullin gene products in sodium intake. Sodium 112-118 adrenomedullin Homo sapiens 80-94 9914451-1 1999 Adrenomedullin (AM), a potent hypotensive peptide, is produced in numerous tissues including adrenal gland, kidney, brain and pituitary gland, where it acts to modify sodium homeostasis. Sodium 167-173 adrenomedullin Homo sapiens 0-14 9914451-4 1999 These results support a physiologic role for adrenomedullin gene products in the central regulation of sodium homeostasis. Sodium 103-109 adrenomedullin Homo sapiens 45-59 9933751-2 1999 No information, however, is available on the plasma and urine levels of uroguanylin in nephrotic syndrome (NS), the state associated with sodium and water retention. Sodium 138-144 guanylate cyclase activator 2B Homo sapiens 72-83 10068868-2 1999 Infusion of CNP induced increases in its own levels (from 1.17 +/- 0.11 up to 21.13 +/- 1.41 pmol l-1) without modifying the plasma levels of cGMP, ADM, renin and ANP, the urinary excretion rate of ADM and cGMP, renal haemodynamics and sodium excretion. Sodium 236-242 natriuretic peptide C Homo sapiens 12-15 9830050-1 1998 Nearly identical proteins (denoted NAA-Tr, rBAT, D2, NBAT), cloned from mammalian kidneys, induce a largely sodium-independent high-affinity transport system for cystine, basic amino acids, and some neutral amino acids in Xenopus oocytes (system b0,+-like). Sodium 108-114 bile acid CoA:amino acid N-acyltransferase Rattus norvegicus 43-47 9856972-1 1998 -Dopamine, via D1-like receptors, stimulates the activity of both protein kinase A (PKA) and protein kinase C (PKC), which results in inhibition of renal sodium transport. Sodium 154-160 protein kinase C, alpha Rattus norvegicus 111-114 9856972-9 1998 We conclude that there is differential regulation of PKC isoform expression by D1-like agonists that inhibits membranous PKC-delta and PKC-zeta in WKY but stimulates them in SHR; this effect in SHR is similar to the stimulatory effect of norepinephrine and angiotensin II and may be a mechanism for their differential effects on sodium transport. Sodium 329-335 protein kinase C, alpha Rattus norvegicus 53-56 9886875-8 1998 RESULTS: In the infused kidney ET-1 (2 ng/kg/min) reduced renal blood flow (RBFprobe; 52+/-8%), cortical perfusion (37+/-7%), glomerular filtration rate (GFR; 49+/-8%), urine flow (47+/-14%) and sodium excretion (49+/-13%), but not medullary perfusion (5+/-6%). Sodium 195-201 endothelin-1 Oryctolagus cuniculus 31-35 9809188-14 1998 In the rat, the CYP11B2 transcript or protein is elevated by K+ loading or sodium depletion, but not the CYP11B1 transcript or protein. Sodium 75-81 cytochrome P450, family 11, subfamily b, polypeptide 2 Rattus norvegicus 16-23 9776344-0 1998 Endothelin-1 stimulates sodium-dependent calcium efflux from bovine adrenal chromaffin cells in culture. Sodium 24-30 endothelin 1 Bos taurus 0-12 9761330-9 1998 Results are discussed in the light of a reduced sodium current modulation by carbamazepine in CA1 neurons of patients with hippocampal sclerosis and of similar observations in the kindling model of epileptogenesis. Sodium 48-54 carbonic anhydrase 1 Homo sapiens 94-97 9727369-3 1998 In normal sodium intake groups, ANP mRNA expression in the remnant kidney was significantly increased by 5.0 +/- 0.8-fold (n = 7, mean +/- SEM) at 4 d when compared with sham-operated controls (n = 6, all sham-operated groups) (*P < 0.001 by Scheffe"s test) and by 28.3 +/- 5.1-fold at 14 d. This latter response was markedly diminished to 7.6 +/- 2.1-fold (n = 7, versus sham) in rats maintained on a low sodium diet. Sodium 10-16 natriuretic peptide A Rattus norvegicus 32-35 9727369-3 1998 In normal sodium intake groups, ANP mRNA expression in the remnant kidney was significantly increased by 5.0 +/- 0.8-fold (n = 7, mean +/- SEM) at 4 d when compared with sham-operated controls (n = 6, all sham-operated groups) (*P < 0.001 by Scheffe"s test) and by 28.3 +/- 5.1-fold at 14 d. This latter response was markedly diminished to 7.6 +/- 2.1-fold (n = 7, versus sham) in rats maintained on a low sodium diet. Sodium 409-415 natriuretic peptide A Rattus norvegicus 32-35 9727369-5 1998 Because natriuretic peptides have previously been shown by us to play a major role in the adaptive responses of remnant nephrons to renal mass ablation, these data suggest that ANP of renal origin may contribute to the overall mechanism for enhancing sodium excretion in the face of declining nephron number. Sodium 251-257 natriuretic peptide A Rattus norvegicus 177-180 9733114-3 1998 A control treatment was normal tap water and the other three treatments comprised the addition to the tap water of 1,000 mg/L sodium as NaCl, 5,000 mg/L NH4Cl, or 5,000 mg/L KHCO3, supplied from age 2 to 47 d. At Day 28, equally sized subsets of these groups were moved to individual cages, where they received a severe exposure to ambient cold. Sodium 126-132 nuclear RNA export factor 1 Homo sapiens 102-105 9609738-0 1998 Regulation of amiloride-sensitive sodium absorption in murine airway epithelium by C-type natriuretic peptide. Sodium 34-40 natriuretic peptide type C Mus musculus 83-109 9609738-2 1998 In this paper, we show that CNP is also capable of reducing amiloride-sensitive sodium absorption in murine airway epithelium through a cGMP-dependent mechanism that is separate from the CFTR regulatory signaling pathway. Sodium 80-86 natriuretic peptide type C Mus musculus 28-31 9654228-1 1998 INTRODUCTION: Inherited long QT syndrome (LQTS) recently has been associated with mutations in genes coding for potassium (KVLQT1, KCNE1, and HERG) or sodium (SCN5A) ion channels involved in regulating either sodium inward or potassium outward currents of heart cells, resulting in prolongation of the repolarization period. Sodium 209-215 potassium voltage-gated channel subfamily E regulatory subunit 1 Homo sapiens 131-136 9495259-1 1998 Endothelin-1 (ET-1) is a cardiovascular peptide that binds to two distinct receptors, ET(A) and ET(B), resulting in systemic and regional vasoconstriction, alteration in sodium excretion, mitogenesis, and release of other vasoactive peptides such as atrial natriuretic peptide (ANP). Sodium 170-176 endothelin receptor type B Canis lupus familiaris 96-101 9495264-4 1998 During CNP infusion, plasma CNP increased from 1.17+/-0.23 to 41.52+/-4.61 pmol/L (ie, 4- to 10-fold higher levels than those observed in disease states) without affecting plasma and urinary cGMP, cardiac volumes, dynamics of left and right heart filling, cardiac output, arterial pressure, renal hemodynamics, intrarenal sodium handling, sodium excretion, or plasma levels of renin and aldosterone. Sodium 322-328 natriuretic peptide C Homo sapiens 7-10 9495264-4 1998 During CNP infusion, plasma CNP increased from 1.17+/-0.23 to 41.52+/-4.61 pmol/L (ie, 4- to 10-fold higher levels than those observed in disease states) without affecting plasma and urinary cGMP, cardiac volumes, dynamics of left and right heart filling, cardiac output, arterial pressure, renal hemodynamics, intrarenal sodium handling, sodium excretion, or plasma levels of renin and aldosterone. Sodium 339-345 natriuretic peptide C Homo sapiens 7-10 9533611-0 1998 Role of nitric oxide in responses to renin-angiotensin system inhibition in sodium-depleted guinea pig and rat. Sodium 76-82 renin Cavia porcellus 37-42 9503639-6 1998 Acute infusion of prolactin at the lower dose increased the fractional excretion of sodium and chloride significantly, whereas the higher dose of prolactin had no effect. Sodium 84-90 prolactin Gallus gallus 18-27 9442067-6 1998 The key differences between the structures of active horseradish peroxidase C and inactive BP 1 include the orientation of the catalytic distal histidine, disruption of a hydrogen bond between this histidine and a conserved asparagine, and apparent substitution of calcium at the distal cation binding site with sodium at pH 7.5. Sodium 312-318 prx7 Hordeum vulgare 65-75 9830516-11 1998 These results demonstrate that bradykinin counteracts ANP-stimulated sodium and water excretion, by acting directly on the kidney. Sodium 69-75 natriuretic peptide A Rattus norvegicus 54-57 9421486-13 1998 The results thus indicate that normalization of aortic cGMP and eNOS protein expression in vascular tissue is associated with increased sodium and water excretion in cirrhotic rats with ascites. Sodium 136-142 nitric oxide synthase 3 Rattus norvegicus 64-68 10806828-3 1998 The results showed that Huangdan capsule could postpone the increase in the levels of cGMP and ANP, suggesting that by regulating the water and sodium metabolism, Huangdan capsule could ameliorate the glomerular filtration rate, and that Huangdan capsule could lower the levels of cGMP and ANP in plasma via body regulation. Sodium 144-150 natriuretic peptide A Rattus norvegicus 95-98 9647500-6 1998 Proximal tubular sodium transport was the same with AcVE and ANP+AcVE suggesting that synergism is a property of more distal nephron segments. Sodium 17-23 natriuretic peptide A Rattus norvegicus 61-64 9488240-9 1997 CONCLUSIONS: Activation both of A1 and of A2 receptor causes a reduction in urinary water and sodium excretion. Sodium 94-100 UDP glucuronosyltransferase family 1 member A6 Rattus norvegicus 32-53 9370443-1 1997 The Na+-glucose cotransporter (SGLT1) expressed in Xenopus laevis oocytes was shown to generate a phlorizin-sensitive sodium leak in the absence of sugars. Sodium 118-124 solute carrier family 5 (sodium/glucose cotransporter), member 1, gene 2 L homeolog Xenopus laevis 31-36 9370443-2 1997 Using the current model for SGLT1, where the sodium leak was presumed to occur after two sodium ions are bound to the free carrier before glucose binding, a characteristic concentration constant (Kc) was introduced to describe the relative importance of the sodium leak versus Na+-glucose cotransport currents. Sodium 45-51 solute carrier family 5 (sodium/glucose cotransporter), member 1, gene 2 L homeolog Xenopus laevis 28-33 9413245-7 1997 The third hypothesis is that small changes in the time and voltage dependence of the inactivation and reactivation of the sodium ion current (INa) result in less net inward ion current for a given waveform of depolarization, and the cell therefore becomes inexcitable (eg, to every second stimulus). Sodium 122-128 LOW QUALITY PROTEIN: alpha-internexin Oryctolagus cuniculus 142-145 9362312-4 1997 CNP caused dose-dependent increases in natriuresis (U(Na)) and in the fractional excretion of sodium (FE(Na)) with no effect on diuresis (UV), renal plasma flow, and glomerular filtration rate (GFR). Sodium 94-100 natriuretic peptide C Homo sapiens 0-3 9601879-7 1997 The assembled findings support the idea that reduced tubular sodium reabsorption in the transplanted kidney (with a stabilized value of GFR) cannot be explained only as a manifestation of adaptation of tubular function as a result of the reduced number of functioning nephrons. Sodium 61-67 Rap guanine nucleotide exchange factor 5 Homo sapiens 136-139 9321816-8 1997 High-sodium diet increased vasoconstrictor responses to ANG II (P < 0.01) and nerve stimulation (P < 0.02), but not to NE or AVP, and in combination with ANG II treatment further potentiated vasoconstrictor responses to ANG II (synergism). Sodium 5-11 angiogenin Rattus norvegicus 56-59 9310074-1 1997 Atrial natriuretic peptide (ANP) is a hormone important in the cardiovascular system via its regulatory roles in sodium and water excretion, and in vasodilatation. Sodium 113-119 natriuretic peptide A Rattus norvegicus 0-26 9310074-1 1997 Atrial natriuretic peptide (ANP) is a hormone important in the cardiovascular system via its regulatory roles in sodium and water excretion, and in vasodilatation. Sodium 113-119 natriuretic peptide A Rattus norvegicus 28-31 9276478-1 1997 Altered modulation of skeletal muscle voltage-gated sodium channels by myotonic dystrophy kinase (DMPK) has been proposed as a possible mechanism underlying myotonia in this disease. Sodium 52-58 DM1 protein kinase Homo sapiens 98-102 9276478-2 1997 We examined the effect of a recombinant mouse DMPK on the functional properties of human skeletal muscle (hSkM1) and cardiac (hH1) voltage-gated sodium channels in the Xenopus oocyte expression system. Sodium 145-151 dystrophia myotonica-protein kinase Mus musculus 46-50 9236205-3 1997 Coexpression of tipE with para results in elevated levels of sodium currents and accelerated current decay. Sodium 61-67 temperature-induced paralytic E Drosophila melanogaster 16-20 9207273-7 1997 IL-10 did not prevent the IFN-gamma-induced abolishment of tight junctional charge selectivity but did attenuate the total increase in sodium and chloride permeability. Sodium 135-141 interleukin 10 Homo sapiens 0-5 9174082-13 1997 Therefore, five different treatments that induced increased sodium appetite evoked distinct patterns of c-fos expression in the anteroventral region of the third ventricle of the rat forebrain. Sodium 60-66 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 104-109 9174082-14 1997 Since the common feature was induction of c-fos in the organum vasculosum of the laminal terminalis, these results suggest a key role for this structure in the development of increased sodium appetite. Sodium 185-191 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 42-47 9176324-9 1997 These data suggest that nNOS-derived NO plays an important role in the macula densa during feedback stimulation of renin induced by dietary sodium restriction. Sodium 140-146 nitric oxide synthase 1 Rattus norvegicus 24-28 9095077-12 1997 Model-independent sib pair linkage analysis suggested that diastolic blood pressure response to sodium loading/volume depletion is linked at the beta 2-adrenergic receptor locus (P < .006). Sodium 96-102 adrenoceptor beta 2 Homo sapiens 145-171 9469794-12 1997 Subsequent infusion of ANF further reduced blood pressure but increased sodium and water excretion markedly. Sodium 72-78 natriuretic peptide A Rattus norvegicus 23-26 9094750-1 1997 Somatostatin modulates important physiologic functions of the kidney, including mesangial cell contraction, glomerular prostaglandin synthesis, and phosphate, water and sodium excretion. Sodium 169-175 somatostatin Homo sapiens 0-12 8995422-3 1997 This model (based on hydropathy analysis) was originally proposed for GAT-1 and adopted for all other members of the sodium- and chloride-dependent neurotransmitter transporter superfamily. Sodium 117-123 solute carrier family 6 member 12 Rattus norvegicus 70-75 9323436-0 1997 Effect of intravenous captopril on c-fos expression induced by sodium depletion in neurons of the lamina terminalis. Sodium 63-69 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 35-40 8978356-10 1997 CONCLUSIONS: NHE3 seems to be the Na+/H+ exchange isoform involved in the modulation of basal ileal water and sodium absorption. Sodium 110-116 solute carrier family 9 member A3 Homo sapiens 13-17 8978356-11 1997 Both Na+/H+ exchange mediated through NHE3 and Na(+)-glucose cotransport contribute to basal ileal water and sodium absorption. Sodium 109-115 solute carrier family 9 member A3 Homo sapiens 38-42 8943313-7 1996 There is a strong correlation between the degree of inhibition of PKC activity and the stimulation of sodium transport by RAP. Sodium 102-108 protein kinase C, alpha Rattus norvegicus 66-69 8943313-13 1996 The inhibition of PKC activity by RAP stimulates sodium transport in A6. Sodium 49-55 protein kinase C, alpha Rattus norvegicus 18-21 8986453-14 1996 Finally, infusion of CNP alone and in combination with (S)-thiorphan influenced the excretion of sodium and cyclic GMP only slightly. Sodium 97-103 natriuretic peptide C Rattus norvegicus 21-24 8898007-1 1996 To investigate the role of renal synthesis of atrial natriuretic peptide (ANP) as a contributor to the water-sodium homeostasis, we studied the effects of electrolyte-water imbalance on renal ANP mRNA levels, plasma ANP concentrations, and urinary ANP excretion rates by using reverse transcription-polymerase chain reaction (PCR) and radioimmunoassay. Sodium 109-115 natriuretic peptide A Rattus norvegicus 46-72 8898007-1 1996 To investigate the role of renal synthesis of atrial natriuretic peptide (ANP) as a contributor to the water-sodium homeostasis, we studied the effects of electrolyte-water imbalance on renal ANP mRNA levels, plasma ANP concentrations, and urinary ANP excretion rates by using reverse transcription-polymerase chain reaction (PCR) and radioimmunoassay. Sodium 109-115 natriuretic peptide A Rattus norvegicus 74-77 8898007-4 1996 The urinary ANP excretion rate in DOCA-salt rats was significantly increased at 2 days after treatment and was well correlated to the urinary sodium excretion rate (r = 0.76, P < 0.01). Sodium 142-148 natriuretic peptide A Rattus norvegicus 12-15 8831588-2 1996 This study examined the effects of human recombinant IL-10 on ileal sodium and chloride transport in Sprague-Dawley rats. Sodium 68-74 interleukin 10 Homo sapiens 53-58 8884981-3 1996 Results showed that in the submaxillary gland, ANF increased sodium and decreased potassium excretion when salivation was stimulated by methacholine (MC) or substance P (SP). Sodium 61-67 natriuretic peptide A Rattus norvegicus 47-50 8884981-4 1996 However, when salivation was induced by methoxamine (MX), ANF only increased sodium excretion. Sodium 77-83 natriuretic peptide A Rattus norvegicus 58-61 8884981-5 1996 On the other hand, in the parotid gland, ANF increased both sodium and potassium excretion when salivation was induced either by MC or SP but did not modify electrolyte output in MX induced salivary secretion. Sodium 60-66 natriuretic peptide A Rattus norvegicus 41-44 8707389-0 1996 Dietary sodium intake modulates pituitary proopiomelanocortin mRNA abundance. Sodium 8-14 proopiomelanocortin Rattus norvegicus 42-61 8707389-6 1996 Whole pituitary proopiomelanocortin mRNA abundance, measured with a probe to exon 3 of the rat proopiomelanocortin gene, was significantly increased after 1 week of the high sodium diet compared with the low sodium diet and increased further at 2 and 3 weeks. Sodium 174-180 proopiomelanocortin Rattus norvegicus 16-35 8707389-6 1996 Whole pituitary proopiomelanocortin mRNA abundance, measured with a probe to exon 3 of the rat proopiomelanocortin gene, was significantly increased after 1 week of the high sodium diet compared with the low sodium diet and increased further at 2 and 3 weeks. Sodium 174-180 proopiomelanocortin Rattus norvegicus 95-114 8707389-6 1996 Whole pituitary proopiomelanocortin mRNA abundance, measured with a probe to exon 3 of the rat proopiomelanocortin gene, was significantly increased after 1 week of the high sodium diet compared with the low sodium diet and increased further at 2 and 3 weeks. Sodium 208-214 proopiomelanocortin Rattus norvegicus 16-35 8707389-8 1996 These results demonstrate that high dietary sodium intake increases neurointermediate lobe proopiomelanocortin mRNA abundance compared with a very low sodium diet and also suggest that proopiomelanocortin is preferentially processed into gamma-melanocyte-stimulating hormone rather than corticotropin. Sodium 44-50 proopiomelanocortin Rattus norvegicus 91-110 8707389-8 1996 These results demonstrate that high dietary sodium intake increases neurointermediate lobe proopiomelanocortin mRNA abundance compared with a very low sodium diet and also suggest that proopiomelanocortin is preferentially processed into gamma-melanocyte-stimulating hormone rather than corticotropin. Sodium 44-50 proopiomelanocortin Rattus norvegicus 185-204 8827780-0 1996 Regulation of the renal response to atrial natriuretic peptide by sodium intake in preweaned rats. Sodium 66-72 natriuretic peptide A Rattus norvegicus 36-62 8760860-5 1996 Taken in conjunction with data that calcium channel blockade, inhibition of sodium entry or Na(+)-Ca2+ exchange in the cardiomyocyte opposes the positive chronotropic action of EGF on the cardiomyocyte, this study has identified an agent, indapamide, that accentuates the cardiomyocyte response to EGF. Sodium 76-82 epidermal growth factor Gallus gallus 177-180 8760860-5 1996 Taken in conjunction with data that calcium channel blockade, inhibition of sodium entry or Na(+)-Ca2+ exchange in the cardiomyocyte opposes the positive chronotropic action of EGF on the cardiomyocyte, this study has identified an agent, indapamide, that accentuates the cardiomyocyte response to EGF. Sodium 76-82 epidermal growth factor Gallus gallus 298-301 8864301-0 1996 Expression of Fos in rat brain in relation to sodium appetite: furosemide and cerebroventricular renin. Sodium 46-52 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 14-17 8864301-1 1996 Two experiments were performed to investigate the relationship between the expression of sodium appetite and the appearance of Fos-like immunoreactivity (Fos-IR) in the brain of rats. Sodium 89-95 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 127-130 8864301-1 1996 Two experiments were performed to investigate the relationship between the expression of sodium appetite and the appearance of Fos-like immunoreactivity (Fos-IR) in the brain of rats. Sodium 89-95 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 154-157 8713072-4 1996 Recombinant cNT1rat was sodium-dependent and selective for pyrimidine nucleosides, with approximately Km values of 21 microM, 12.5 microM and 15 microM for uridine, thymidine and adenosine, respectively. Sodium 24-30 solute carrier family 28 member 1 Rattus norvegicus 12-16 8864723-1 1996 Two renal proximal tubular apical sodium-dependent transport systems for phosphate (Na/Pi cotransporter) have been identified. Sodium 34-40 solute carrier family 17 member 1 Homo sapiens 84-103 8765995-2 1996 A sodium-dependent transport system for sulphate (NaSi-1) has recently been identified from a rat kidney cortex cDNA library. Sodium 2-8 solute carrier family 13 member 1 Rattus norvegicus 50-56 8765998-7 1996 Results of the RNase protection assay proved that the renal levels of b-NOS mRNA were significantly increased by about 50% after a low-sodium diet and hypoperfusion of the kidney. Sodium 135-141 nitric oxide synthase 1 Rattus norvegicus 70-75 8650246-0 1996 The heart communicates with the kidney exclusively through the guanylyl cyclase-A receptor: acute handling of sodium and water in response to volume expansion. Sodium 110-116 natriuretic peptide receptor 1 Mus musculus 63-81 8631857-1 1996 Several studies have shown that the cRNA of human, rabbit, or rat rBAT induces in Xenopus oocytes sodium-independent, high affinity uptake of L-cystine via a system b0,(+)-like amino acid exchanger. Sodium 98-104 bile acid CoA:amino acid N-acyltransferase Rattus norvegicus 66-70 8717064-2 1996 The effects of dietary sodium intake on active renin binding in the juxtaglomerular apparatus (JGA) of superficial and juxtamedullary cortex of the dog kidney were examined by quantitative in vitro autoradiography using a radiolabelled renin inhibitor [125I]-H77, which has high affinity for dog renin. Sodium 23-29 renin Canis lupus familiaris 47-52 8717064-4 1996 Changes in sodium intake resulted in marked alterations of active renin binding in the radiolabelled JGA. Sodium 11-17 renin Canis lupus familiaris 66-71 8717064-7 1996 Active renin binding in the labelled JGA was significantly higher in superficial JGA than in their juxtamedullary counterparts, irrespective of sodium intake. Sodium 144-150 renin Canis lupus familiaris 7-12 8717064-10 1996 The proportions of active renin as a percentage of total renin were 60, 75 and 95% in the labelled JGA of sodium-loaded, control, and sodium-depleted kidneys, respectively. Sodium 106-112 renin Canis lupus familiaris 26-31 8612770-0 1996 Multiple transduction pathways regulate the sodium-extrusion gene PMR2/ENA1 during salt stress in yeast. Sodium 44-50 Na(+)/Li(+)-exporting P-type ATPase ENA1 Saccharomyces cerevisiae S288C 66-70 8612770-0 1996 Multiple transduction pathways regulate the sodium-extrusion gene PMR2/ENA1 during salt stress in yeast. Sodium 44-50 Na(+)/Li(+)-exporting P-type ATPase ENA1 Saccharomyces cerevisiae S288C 71-75 8612770-1 1996 The yeast PMR2/ENA1 gene encodes an ATPase involved in sodium extrusion and induced by NaCl. Sodium 55-61 Na(+)/Li(+)-exporting P-type ATPase ENA1 Saccharomyces cerevisiae S288C 10-14 8612770-1 1996 The yeast PMR2/ENA1 gene encodes an ATPase involved in sodium extrusion and induced by NaCl. Sodium 55-61 Na(+)/Li(+)-exporting P-type ATPase ENA1 Saccharomyces cerevisiae S288C 15-19 8964947-0 1996 Changes of blood pressure, sodium excretion and sodium balance due to variations of the renin-angiotensin-aldosterone system. Sodium 27-33 renin Canis lupus familiaris 88-93 8964947-0 1996 Changes of blood pressure, sodium excretion and sodium balance due to variations of the renin-angiotensin-aldosterone system. Sodium 48-54 renin Canis lupus familiaris 88-93 8780244-10 1996 We conclude that chronic salt loading suppresses the postnatal rise in renal kallikrein gene expression and enzymatic activity, indicating that sodium intake is an important factor in the maturation of renal kallikrein synthesis. Sodium 144-150 kallikrein 1 Rattus norvegicus 71-87 8780244-10 1996 We conclude that chronic salt loading suppresses the postnatal rise in renal kallikrein gene expression and enzymatic activity, indicating that sodium intake is an important factor in the maturation of renal kallikrein synthesis. Sodium 144-150 kallikrein 1 Rattus norvegicus 202-218 8603590-1 1996 Atrial (ANP), brain (BNP), and C-type natriuretic peptide (CNP) belong to a family of hormones important in blood pressure and sodium homeostasis. Sodium 127-133 natriuretic peptide type C Mus musculus 31-57 8603590-1 1996 Atrial (ANP), brain (BNP), and C-type natriuretic peptide (CNP) belong to a family of hormones important in blood pressure and sodium homeostasis. Sodium 127-133 natriuretic peptide type C Mus musculus 59-62 8564984-6 1996 Together, these results suggest that sodium influx, which is a hallmark of palytoxin action, may play a key role in the activation of JNK by palytoxin. Sodium 37-43 mitogen-activated protein kinase 8 Mus musculus 134-137 8599025-11 1996 These results indicate that a constant infusion of adrenomedullin, at a dose that results in a minimal hypotensive effect increases renal plasma flow and urinary sodium excretion in the rat. Sodium 162-168 adrenomedullin Rattus norvegicus 51-65 8998365-3 1996 Results showed a significant and early decrease in urinary sodium excretion during mCP when compared to SubC and FR. Sodium 59-65 CD46 antigen, complement regulatory protein Mus musculus 83-86 8900956-4 1996 The major sodium-extrusion system of S. cerevisiae is a P-ATPase encoded by the ENA1 gene. Sodium 10-16 Na(+)/Li(+)-exporting P-type ATPase ENA1 Saccharomyces cerevisiae S288C 80-84 8883035-2 1996 Reduction in creatinine clearance and elevation in fractional excretion of sodium in mice receiving cisplatin was ameliorated by ulinastatin administration. Sodium 75-81 alpha 1 microglobulin/bikunin precursor Mus musculus 129-140 8899813-0 1996 Mammalian bombesin-like peptides suppress sham drinking of salt by sodium-deficient rats. Sodium 67-73 gastrin releasing peptide Homo sapiens 10-18 8899813-1 1996 Bombesin (BN) and its mammalian relatives, gastrin-releasing peptide (GRP) and neuromedin B (NMB), have been implicated in the control of food intake, and more recently systemic injections of BN have been shown to suppress need-free and sodium deficiency-induced salt (NaCl) intake. Sodium 237-243 gastrin releasing peptide Homo sapiens 0-8 8899813-1 1996 Bombesin (BN) and its mammalian relatives, gastrin-releasing peptide (GRP) and neuromedin B (NMB), have been implicated in the control of food intake, and more recently systemic injections of BN have been shown to suppress need-free and sodium deficiency-induced salt (NaCl) intake. Sodium 237-243 gastrin releasing peptide Homo sapiens 10-12 8899813-1 1996 Bombesin (BN) and its mammalian relatives, gastrin-releasing peptide (GRP) and neuromedin B (NMB), have been implicated in the control of food intake, and more recently systemic injections of BN have been shown to suppress need-free and sodium deficiency-induced salt (NaCl) intake. Sodium 237-243 gastrin releasing peptide Homo sapiens 43-68 8899813-1 1996 Bombesin (BN) and its mammalian relatives, gastrin-releasing peptide (GRP) and neuromedin B (NMB), have been implicated in the control of food intake, and more recently systemic injections of BN have been shown to suppress need-free and sodium deficiency-induced salt (NaCl) intake. Sodium 237-243 gastrin releasing peptide Homo sapiens 192-194 8786662-0 1995 Alterations with age of the T3-stimulated release of atrial natriuretic peptide and its effect on water and sodium metabolism in rats. Sodium 108-114 natriuretic peptide A Rattus norvegicus 53-79 7474653-1 1995 The renal kallikrein-kinin system has been implicated in the regulation of blood pressure and sodium/water excretion. Sodium 94-100 kallikrein related peptidase 4 Homo sapiens 10-20 8869083-0 1995 Inhibition of cGMP-phosphodiesterase restores the glomerular effects of atrial natriuretic factor in low sodium diet rats. Sodium 105-111 natriuretic peptide A Rattus norvegicus 72-97 8869083-1 1995 It was shown that atrial natriuretic factor (ANF)-induced increase in glomerular filtration rate (GFR) is blunted in low sodium diet. Sodium 121-127 natriuretic peptide A Rattus norvegicus 18-43 8869083-1 1995 It was shown that atrial natriuretic factor (ANF)-induced increase in glomerular filtration rate (GFR) is blunted in low sodium diet. Sodium 121-127 natriuretic peptide A Rattus norvegicus 45-48 8564890-1 1995 This study was designed to determine if tonic beta-adrenergic control of plasma renin activity (PRA) during dietary sodium restriction is due to stimulation of renal beta-adrenoceptors, extrarenal beta-adrenoceptors, or both. Sodium 116-122 renin Canis lupus familiaris 80-85 7555980-7 1995 The concomitant increases in sodium and urine excretion may be mediated by the marked increase in plasma ANP levels. Sodium 29-35 natriuretic peptide A Rattus norvegicus 105-108 7552360-6 1995 With sodium-free external solution, neurotensin also caused inward currents by reducing the inwardly rectifying potassium conductance. Sodium 5-11 neurotensin Rattus norvegicus 36-47 7611424-7 1995 Using modified Ussing chambers, we also investigated CNP"s potential modulation of sodium and chloride transport rates. Sodium 83-89 natriuretic peptide C Homo sapiens 53-56 7637582-1 1995 Synaptic reaccumulation of the neurotransmitter dopamine is mediated by the dopamine transporter (DAT), a member of the family of twelve transmembrane domain, sodium- and chloride-dependent neurotransmitter transporters. Sodium 159-165 solute carrier family 6 member 3 Homo sapiens 76-96 7637582-1 1995 Synaptic reaccumulation of the neurotransmitter dopamine is mediated by the dopamine transporter (DAT), a member of the family of twelve transmembrane domain, sodium- and chloride-dependent neurotransmitter transporters. Sodium 159-165 solute carrier family 6 member 3 Homo sapiens 98-101 7643524-5 1995 At 12.10(-11) mol.kg-1.min-1, URO and ANF increased urine flow 5.4 +/- 1.7 and 3.0 +/- 0.8-fold, increased urinary sodium excretion 20.7 +/- 8.8 and 10.3 +/- 4.0-fold, and decreased blood pressure by 13 +/- 2% and 12 +/- 1%, respectively (mean +/- SEM). Sodium 115-121 natriuretic peptide A Rattus norvegicus 38-41 7648263-0 1995 Sodium depletion induces Fos immunoreactivity in circumventricular organs of the lamina terminalis. Sodium 0-6 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 25-28 7648263-1 1995 Acute sodium depletion by peritoneal dialysis (PD) induces c-fos expression in the subfornical organ (SFO) and organum vasculosum laminae terminalis (OVLT), in conscious rats. Sodium 6-12 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 59-64 7648263-6 1995 These results demonstrate that an acute body sodium deficit induces c-fos activity in SFO and OVLT neurons, indicating the special role of these structures in sodium balance regulation. Sodium 45-51 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 68-73 7648263-6 1995 These results demonstrate that an acute body sodium deficit induces c-fos activity in SFO and OVLT neurons, indicating the special role of these structures in sodium balance regulation. Sodium 159-165 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 68-73 7648263-7 1995 They also show that the sodium-depletion-induced production of Fos in neurons of the lamina terminalis can be modulated by central or systemic reposition of sodium. Sodium 24-30 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 63-66 7648263-7 1995 They also show that the sodium-depletion-induced production of Fos in neurons of the lamina terminalis can be modulated by central or systemic reposition of sodium. Sodium 157-163 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 63-66 7740582-9 1995 RESULTS: Atrial natriuretic peptide given after a 4-hour delay significantly reduced brain water and sodium 24 hours after the injury (P < .05). Sodium 101-107 natriuretic peptide A Rattus norvegicus 9-35 7602527-2 1995 Whole-cell sodium currents (INa) were measured in mouse neuroblastoma cells (N1E-115) at different [Ca2+]i values using appropriate Ca-EGTA buffers in the pipettes. Sodium 11-17 internexin neuronal intermediate filament protein, alpha Mus musculus 28-31 7789042-8 1995 Increasing plasma atrial natriuretic peptide concentration by 60% via atrial natriuretic peptide infusion increased urinary excretion of sodium and protein in both control rats and rats with diabetic mellitus. Sodium 137-143 natriuretic peptide A Rattus norvegicus 18-44 7789042-8 1995 Increasing plasma atrial natriuretic peptide concentration by 60% via atrial natriuretic peptide infusion increased urinary excretion of sodium and protein in both control rats and rats with diabetic mellitus. Sodium 137-143 natriuretic peptide A Rattus norvegicus 70-96 7789042-10 1995 Administration of the atrial natriuretic peptide receptor antagonist HS-142-1 to diabetic rats resulted in diminished urinary excretion of both sodium (-61 +/- 14%, P < 0.02) and protein (-51 +/- 17%, P < 0.05). Sodium 144-150 natriuretic peptide A Rattus norvegicus 22-48 7900794-0 1995 Mechanism of hyperosmolality stimulation of ANP secretion: its dependency on calcium and sodium. Sodium 89-95 natriuretic peptide A Rattus norvegicus 44-47 7900794-7 1995 To determine whether calcium influx was via Na(+)-Ca2+ exchange, we determined the sodium dependency of osm-stimulated ANP secretion. Sodium 83-89 natriuretic peptide A Rattus norvegicus 119-122 7900794-9 1995 We conclude that osm-stimulated ANP secretion is calcium and sodium dependent. Sodium 61-67 natriuretic peptide A Rattus norvegicus 32-35 7784140-2 1995 Because atrial natriuretic peptide (ANP) contributes to sodium homeostasis, this study was designed to evaluate the maturational effects of increased dietary sodium intake on cardiac ANP production. Sodium 56-62 natriuretic peptide A Rattus norvegicus 8-34 7784140-2 1995 Because atrial natriuretic peptide (ANP) contributes to sodium homeostasis, this study was designed to evaluate the maturational effects of increased dietary sodium intake on cardiac ANP production. Sodium 56-62 natriuretic peptide A Rattus norvegicus 36-39 7784140-2 1995 Because atrial natriuretic peptide (ANP) contributes to sodium homeostasis, this study was designed to evaluate the maturational effects of increased dietary sodium intake on cardiac ANP production. Sodium 158-164 natriuretic peptide A Rattus norvegicus 183-186 7784140-9 1995 We conclude that chronic increase in sodium intake in the preweaning period results in increased storage of atrial pro-ANP. Sodium 37-43 natriuretic peptide A Rattus norvegicus 119-122 7724045-2 1995 With sodium-free external solution, neurotensin evoked inward currents by reducing the inwardly rectifying K+ conductance. Sodium 5-11 neurotensin Rattus norvegicus 36-47 7770642-0 1995 Age-related ANP release in response to acute vs. chronic sodium loading. Sodium 57-63 natriuretic peptide A Rattus norvegicus 12-15 7770642-6 1995 On chronic sodium load, in the young group, ANP rose significantly on days 3 and 7, subsequently declining to baseline. Sodium 11-17 natriuretic peptide A Rattus norvegicus 44-47 7770642-13 1995 (3) The role of ANP in maintaining homeostatic renal sodium excretion during short-term sodium oral loading is different in the two age groups. Sodium 53-59 natriuretic peptide A Rattus norvegicus 16-19 7770642-13 1995 (3) The role of ANP in maintaining homeostatic renal sodium excretion during short-term sodium oral loading is different in the two age groups. Sodium 88-94 natriuretic peptide A Rattus norvegicus 16-19 7777718-7 1995 It is possible that the sodium retention of these states might be the result of direct stimuli of the tubular sodium transport mechanisms in the different segments of the nephron, mediated by the co and counter transports, ATPase activity or by the second messengers cyclic AMP and cyclic GMP. Sodium 24-30 5'-nucleotidase, cytosolic II Homo sapiens 289-292 7777718-7 1995 It is possible that the sodium retention of these states might be the result of direct stimuli of the tubular sodium transport mechanisms in the different segments of the nephron, mediated by the co and counter transports, ATPase activity or by the second messengers cyclic AMP and cyclic GMP. Sodium 110-116 5'-nucleotidase, cytosolic II Homo sapiens 289-292 7792794-1 1995 It has been suggested that endogenous substances (known as ouabain-like factors, OLF), secreted from the central nervous system in response to salt and water retention, inhibit the cell membrane Na+/K+ pump in the renal tubules and reduce sodium reabsorption. Sodium 239-245 transmembrane O-mannosyltransferase targeting cadherins 1 Homo sapiens 81-84 7533632-0 1994 Tachykinin NK3 receptor agonist blocks sodium deficiency-induced shift in taste reactivity. Sodium 39-45 tachykinin receptor 3 Rattus norvegicus 11-23 7533632-2 1994 injections of tachykinin NK3 receptor agonists suppress NaCl intake by sodium deficient rats. Sodium 71-77 tachykinin receptor 3 Rattus norvegicus 25-37 7858560-6 1994 From these results, we conclude that inhibition of NEP may exaggerate the contribution of renal kinins to the renal water-sodium metabolism and overcome the contribution of ANP on that metabolism at least in normotensive rats. Sodium 122-128 membrane metallo-endopeptidase Rattus norvegicus 51-54 7896285-1 1994 Screening for cDNAs encoding proteins similar to the sodium-coupled glutamate transporter GLAST1 led to the isolation of a cDNA clone coding for a protein that turned out to be identical to the recently described neutral amino acid transporter ASCT1. Sodium 53-59 solute carrier family 1 member 4 Homo sapiens 244-249 7529926-10 1994 They also demonstrate that tachykinins endowed with high affinity for the NK3 receptor are the most potent in inhibiting sodium intake. Sodium 121-127 tachykinin receptor 3 Rattus norvegicus 74-86 7832493-0 1994 Bombesin, gastrin-releasing peptide, and neuromedin B attenuate the salt appetite of sodium-depleted rats. Sodium 85-91 gastrin releasing peptide Rattus norvegicus 10-35 7882177-6 1994 Infusion of ANF at a dose shown to reliably increase sodium excretion did not affect autoregulation or its resetting. Sodium 53-59 natriuretic peptide A Rattus norvegicus 12-15 8093022-1 1994 We have developed a new method to measure [Na+]i and Ca2+ transients of a beating cardiac myocyte using a Na(+)-sensitive fluorescent probe, sodium-binding benzofuran isophthalate (SBFI) and a Ca(2+)-sensitive fluorescent probe, fluo-3. Sodium 141-147 LOW QUALITY PROTEIN: carbonic anhydrase 2 Cavia porcellus 53-56 7882162-1 1994 The elastin-laminin receptor was shown to be present on several benign and malignant cell types and to mediate several important cell reactions such as chemotactic movements of fibroblasts and monocytes, release of lytic enzymes and oxygen free radicals from leucocytes, increased adhesion of mesenchymal cells to elastin fibers as well as modifications of ion fluxes-increase of calcium and sodium influxes and decrease of ouabain-dependent potassium influx. Sodium 392-398 elastin Rattus norvegicus 4-11 7983079-0 1994 Atrial natriuretic factor modifies noradrenaline release in a sodium-free medium. Sodium 62-68 natriuretic peptide A Rattus norvegicus 0-25 7983079-5 1994 ANF (1, 10 and 100 nM) decreased NA release evoked by the omission of sodium in a concentration-dependent way. Sodium 70-76 natriuretic peptide A Rattus norvegicus 0-3 8048533-5 1994 Feeding glucose to the rats caused a rise in sodium-dependent glucose transporter isoform (SGLT1) protein levels compared with the control diet. Sodium 45-51 solute carrier family 5 member 1 Rattus norvegicus 91-96 8175964-11 1994 Changes in sodium balance alter the actions of the two receptors (DA1 and DA2) in a coordinated fashion in the regulation of RBF. Sodium 11-17 immunoglobulin heavy diversity 4-11 (non-functional) Homo sapiens 66-69 7910657-7 1994 The delay in the restoration of the sodium gradient may in turn prolong the neuronal exposure to toxic [Ca2+]i values, due to the decrease in the efficiency of the Na+/Ca2+ exchanger to extrude calcium. Sodium 36-42 nascent polypeptide associated complex subunit alpha 2 Homo sapiens 164-171 8168694-5 1994 Here we summarize both old and new evidence that several major substances believed to be involved in the regulation of sodium metabolism and blood pressure, i.e., the antidiuretic agents angiotensin II and norepinephrine, and the diuretic agents dopamine and atrial natriuretic peptide (ANP), may achieve their effects through a common pathway that involves reversible activation/deactivation of renal tubular Na+,K(+)-ATPase. Sodium 119-125 natriuretic peptide A Rattus norvegicus 259-285 8139144-3 1994 On the other hand, the newly described atrial natriuretic peptide (ANP) hormonal system in both humans and animals appears to play an important role in sodium and water excretion. Sodium 152-158 natriuretic peptide A Rattus norvegicus 39-65 7645406-6 1994 The data indicated that even at low sodium diet ANP stimulates the diuresis and sodium excretion without changing the glomerular filtration rate (GFR). Sodium 36-42 natriuretic peptide A Rattus norvegicus 48-51 7645406-6 1994 The data indicated that even at low sodium diet ANP stimulates the diuresis and sodium excretion without changing the glomerular filtration rate (GFR). Sodium 80-86 natriuretic peptide A Rattus norvegicus 48-51 7645406-7 1994 The kidney denervation combined with ANP infusion increased twice the diuresis and four times sodium excretion vs. the control animals. Sodium 94-100 natriuretic peptide A Rattus norvegicus 37-40 7645406-9 1994 We assume that the low sodium diet attenuates the effect of ANP in respect to the excretory function. Sodium 23-29 natriuretic peptide A Rattus norvegicus 60-63 7832594-15 1994 Sodium ions specifically protected the ATPase from the modification of glutamate-65 in subunit c by dicyclohexylcarbodiimide in a pH-dependent manner indicating that the Na+ binding site is at this highly conserved acidic amino acid residue of subunit c within the middle of the membrane. Sodium 0-6 ATPase Escherichia coli 39-45 8012686-2 1994 Ang(1-7) had three major effects producing, (1) a substantial natriuresis and diuresis, (2) an increase in urinary sodium concentration associated with a fall in potassium concentration and (3) an increase in glomerular filtration rate without affecting renal vascular resistance. Sodium 115-121 angiogenin Rattus norvegicus 0-7 8014889-8 1994 Neurotensin also caused an inward current even in potassium-free internal and external solutions; this current was accompanied by a conductance increase, reversed close to 0 mV and was inhibited by reduction of the extracellular sodium concentration (from 150 to 20 mM). Sodium 229-235 neurotensin Rattus norvegicus 0-11 8301562-7 1994 ANF infusion (50 micrograms/kg/hr) increased fractional sodium excretion 46-fold in compensated rats, but only 18-fold in decompensated rats. Sodium 56-62 natriuretic peptide A Rattus norvegicus 0-3 7937350-0 1994 Modulation of the rat adrenal medulla norepinephrine secretion in a sodium-free medium by atrial natriuretic factor. Sodium 68-74 natriuretic peptide A Rattus norvegicus 90-115 7809956-7 1994 It is possible that the smallest sodium ID50 for 1-isoproterenol-stimulated adenylate cyclase is conditioned by sodium interaction with carboxylate residue of aspartate-79 from the cytoplasmic compartment of beta 2-adrenergic receptor (Horstman et al., 1990). Sodium 33-39 adrenoceptor beta 2 Homo sapiens 208-234 7809956-7 1994 It is possible that the smallest sodium ID50 for 1-isoproterenol-stimulated adenylate cyclase is conditioned by sodium interaction with carboxylate residue of aspartate-79 from the cytoplasmic compartment of beta 2-adrenergic receptor (Horstman et al., 1990). Sodium 112-118 adrenoceptor beta 2 Homo sapiens 208-234 7997816-7 1993 Sodium levels were higher in all samples from mothers of TSGA infants and in samples from mothers of PTAGA infants on the 7th, 15th and 30th days than in milk from the TAGA group. Sodium 0-6 lysine demethylase 3A Homo sapiens 57-61 8238418-1 1993 Although fast sodium current (INa) plays a major role in the generation and conduction of the cardiac impulse, the electrophysiological characteristics of INa in isolated human ventricular myocytes have not yet been fully described. Sodium 14-20 internexin neuronal intermediate filament protein alpha Homo sapiens 30-33 7505369-5 1993 Baseline mean arterial pressure (MAP) was similar among all treatment groups, but baseline plasma renin activity (PRA) was increased in the sodium-depleted dogs as compared with the sodium-replete dogs. Sodium 140-146 renin Canis lupus familiaris 98-103 7506705-0 1993 ANF decreases active sodium transport and increases alveolar epithelial permeability in rats. Sodium 21-27 natriuretic peptide A Rattus norvegicus 0-3 7904302-15 1993 With 200 microM Cd2+ present to block calcium currents, a train of brief depolarizing pulses could still elicit repetitive sodium action potentials, but these became attenuated at stimulating frequencies as low as 1 Hz. Sodium 123-129 Cd2 molecule Rattus norvegicus 16-19 8251341-1 1993 Although discovered little more than a decade ago, atrial natriuretic peptide (ANP) has been shown to play a significant role in the maintenance of sodium homeostasis. Sodium 148-154 natriuretic peptide A Rattus norvegicus 51-77 8393472-3 1993 Chronic decreases in extracellular fluid pH cause an increase in Na/H antiporter activity that is dependent on protein synthesis and associated with an increase in NHE-1 (isoform of the sodium-hydrogen antiporter) mRNA abundance. Sodium 186-192 sodium/hydrogen exchanger 1 Oryctolagus cuniculus 164-169 8505108-5 1993 Infusions of either 10 or 50 micrograms/kg per minute of synthetic atrial natriuretic factor (ANF)8-33 into sham-operated control animals produced significant increases in urine flow and fractional excretion of sodium (FENa). Sodium 211-217 natriuretic peptide A Rattus norvegicus 67-92 8505108-5 1993 Infusions of either 10 or 50 micrograms/kg per minute of synthetic atrial natriuretic factor (ANF)8-33 into sham-operated control animals produced significant increases in urine flow and fractional excretion of sodium (FENa). Sodium 211-217 natriuretic peptide A Rattus norvegicus 94-97 8315940-1 1993 The role of endogenous atrial natriuretic peptide (ANP) in the immediate response of sodium excretion to unilateral nephrectomy (UNX) was investigated in anesthetized euvolemic rats through measurement of UNX-induced change in plasma ANP concentration and the response of the remaining kidney to UNX following administration of monoclonal anti-ANP antibodies. Sodium 85-91 natriuretic peptide A Rattus norvegicus 23-49 8315940-1 1993 The role of endogenous atrial natriuretic peptide (ANP) in the immediate response of sodium excretion to unilateral nephrectomy (UNX) was investigated in anesthetized euvolemic rats through measurement of UNX-induced change in plasma ANP concentration and the response of the remaining kidney to UNX following administration of monoclonal anti-ANP antibodies. Sodium 85-91 natriuretic peptide A Rattus norvegicus 51-54 8315940-6 1993 Administration of monoclonal anti-ANP antibodies totally prevented the UNX-associated natriuresis by blunting both proximal and distal tubular reabsorption of sodium, and suppressed the rise in urinary cGMP excretion following UNX. Sodium 159-165 natriuretic peptide A Rattus norvegicus 34-37 8324893-1 1993 We investigated the effect of platelet-activating factor (PAF) on basal and insulin-stimulated sodium-dependent neutral amino acid transport by system A in rat soleus muscle. Sodium 95-101 PCNA clamp associated factor Rattus norvegicus 30-56 8324893-1 1993 We investigated the effect of platelet-activating factor (PAF) on basal and insulin-stimulated sodium-dependent neutral amino acid transport by system A in rat soleus muscle. Sodium 95-101 PCNA clamp associated factor Rattus norvegicus 58-61 7687049-10 1993 The action of neurotensin appears to be mediated, at least partially, by a TTX-insensitive but voltage-dependent inward current carried by sodium. Sodium 139-145 neurotensin Rattus norvegicus 14-25 8390506-14 1993 The present results indicate that the downregulation of glomerular ANF-R1 and the reduced cGMP response may lead to altered sodium and water handling by the kidney of 1-K,1C hypertensive rats. Sodium 124-130 natriuretic peptide A Rattus norvegicus 67-70 8390513-4 1993 More sodium, potassium and aldosterone were excreted during the daytime, but the natriuretic substance kallikrein was excreted at a fixed rate throughout the 24 h. During waking hours there was poor correlation between blood pressure and urinary sodium and potassium excretion. Sodium 246-252 kallikrein related peptidase 4 Homo sapiens 103-113 9909272-0 1993 Spin-resolved elastic scattering of electrons from sodium. Sodium 51-57 spindlin 1 Homo sapiens 0-4 8466710-5 1993 Urinary sodium and potassium excretion differences were significantly related to kallikrein differences, with urinary potassium having the strongest relationship (r = 0.46, P = .0001). Sodium 8-14 kallikrein related peptidase 4 Homo sapiens 81-91 8466710-9 1993 Therefore, urinary potassium and pH probably represent the more acute effects of recent dietary sodium and potassium intake on urinary kallikrein levels. Sodium 96-102 kallikrein related peptidase 4 Homo sapiens 135-145 8467316-5 1993 Urine flow and sodium excretion in response to ANF were significantly less in the intact kidney but not the denervated kidneys of the DOCA-salt rats compared to control rats. Sodium 15-21 natriuretic peptide A Rattus norvegicus 47-50 8490948-13 1993 Activation of neurohormonal vasoconstrictor systems and gradually decreased plasma ANF concentrations may contribute to sodium and water retention at different stages of this experimental model of heart failure. Sodium 120-126 natriuretic peptide A Rattus norvegicus 83-86 7678819-1 1993 We have previously shown that the long-term alterations in the intake of sodium and potassium which stimulated aldosterone production in the rat adrenal significantly increased cytochrome P450scc (P450scc) and P45011 beta (P45011 beta) mRNA"s and also the mRNA of their electron donor adrenodoxin. Sodium 73-79 cytochrome P450, family 11, subfamily a, polypeptide 1 Rattus norvegicus 177-195 7678819-1 1993 We have previously shown that the long-term alterations in the intake of sodium and potassium which stimulated aldosterone production in the rat adrenal significantly increased cytochrome P450scc (P450scc) and P45011 beta (P45011 beta) mRNA"s and also the mRNA of their electron donor adrenodoxin. Sodium 73-79 cytochrome P450, family 11, subfamily a, polypeptide 1 Rattus norvegicus 188-195 8381826-1 1993 We demonstrated recently that isoproterenol enhanced the cardiac voltage-dependent sodium currents (INa) in rabbit ventricular myocytes through dual G-protein regulatory pathways. Sodium 83-89 LOW QUALITY PROTEIN: alpha-internexin Oryctolagus cuniculus 100-103 8275799-0 1993 Effect of hypothyroidism on the in vitro release of atrial natriuretic peptide in response to sodium challenge in rats. Sodium 94-100 natriuretic peptide A Rattus norvegicus 52-78 8275799-12 1993 The in vitro release of ANP in response to 165 mM sodium ion was significantly lower in PTU than in saline-injected animals. Sodium 50-56 natriuretic peptide A Rattus norvegicus 24-27 15091830-1 1993 A microbiological study conducted as a complement to kinetic studies of biological denitrification as a process for treating high-sodium-nitrite wastewaters generated from ship-boiler-tube cleaning is described. Sodium 130-136 inositol polyphosphate-5-phosphatase D Homo sapiens 172-176 1471688-9 1992 In contrast, atrial natriuretic factor infusion to dehydrated fetuses significantly increased urine flow (0.17 +/- 0.03 to 0.32 +/- 0.07 ml/kg/min), osmolar clearance (0.14 +/- 0.02 to 0.28 +/- 0.06 ml/kg/min), and fractional sodium excretion (8.5% +/- 2.1% to 14.8% +/- 4.0%). Sodium 226-232 natriuretic peptides A Ovis aries 13-38 1360435-3 1992 In patients with ascites, somatostatin also reduced urinary sodium excretion. Sodium 60-66 somatostatin Homo sapiens 26-38 1360435-6 1992 These findings indicate that somatostatin administration induces renal vasoconstriction and impairs glomerular filtration rate, free water clearance, and sodium excretion in cirrhosis by a mechanism unrelated to systemic hemodynamics and endogenous neurohumoral vasoactive systems. Sodium 154-160 somatostatin Homo sapiens 29-41 1293241-4 1992 SMS 201-995 reduced the daily ileostomy output from 997 +/- 52 g to 736 +/- 28 g, P < 0.05, along with a decrease in daily sodium and chloride excretion (sodium: 92.60 +/- 8.51 to 75.22 +/- 8.64 mEq, chloride: 143.46 +/- 8.54 to 113.60 +/- 15.84 mEq; both P < 0.05). Sodium 126-132 spermine synthase Homo sapiens 0-3 1293241-4 1992 SMS 201-995 reduced the daily ileostomy output from 997 +/- 52 g to 736 +/- 28 g, P < 0.05, along with a decrease in daily sodium and chloride excretion (sodium: 92.60 +/- 8.51 to 75.22 +/- 8.64 mEq, chloride: 143.46 +/- 8.54 to 113.60 +/- 15.84 mEq; both P < 0.05). Sodium 157-163 spermine synthase Homo sapiens 0-3 22217827-2 1992 Low sodium and high potassium intake promoted time-dependent increases in the zona glomerulosa cytochrome P450scc (P450scc) and cytochrome P450c11 (P450c11) protein and mRNA levels, but no changes were found in the zona fasciculata-reticularis. Sodium 4-10 cytochrome P450, family 11, subfamily a, polypeptide 1 Rattus norvegicus 95-113 22217827-2 1992 Low sodium and high potassium intake promoted time-dependent increases in the zona glomerulosa cytochrome P450scc (P450scc) and cytochrome P450c11 (P450c11) protein and mRNA levels, but no changes were found in the zona fasciculata-reticularis. Sodium 4-10 cytochrome P450, family 11, subfamily a, polypeptide 1 Rattus norvegicus 106-113 22217827-7 1992 Captopril, an inhibitor of angiotensin-I converting enzyme, abolished the enhancing effects of the low sodium regimen on P450scc and P450c18 mRNA levels. Sodium 103-109 cytochrome P450, family 11, subfamily a, polypeptide 1 Rattus norvegicus 121-128 22217827-12 1992 In conclusion, this work demonstrates that variations in the intake of sodium and potassium act on the expression of the CYP11B2 gene, but not on that of the CYP11B1 gene. Sodium 71-77 cytochrome P450, family 11, subfamily b, polypeptide 2 Rattus norvegicus 121-128 1493157-0 1992 Adenosine deaminase restores the ability of atrial natriuretic peptide to induce glomerular hyperfiltration in low-sodium rats. Sodium 115-121 adenosine deaminase Rattus norvegicus 0-19 1493157-0 1992 Adenosine deaminase restores the ability of atrial natriuretic peptide to induce glomerular hyperfiltration in low-sodium rats. Sodium 115-121 natriuretic peptide A Rattus norvegicus 44-70 1493157-1 1992 Administration of a large dose of atrial natriuretic peptide is associated with an increase in glomerular filtration rate, diuresis and natriuresis in normal-sodium rats. Sodium 158-164 natriuretic peptide A Rattus norvegicus 34-60 1493157-2 1992 However, glomerular hyperfiltration induced by atrial natriuretic peptide is markedly decreased in low-sodium rats. Sodium 103-109 natriuretic peptide A Rattus norvegicus 47-73 1493157-4 1992 The results indicate that attenuated glomerular responses to atrial natriuretic peptide are restored by the administration of adenosine deaminase in low-sodium rats. Sodium 153-159 natriuretic peptide A Rattus norvegicus 61-87 1493157-4 1992 The results indicate that attenuated glomerular responses to atrial natriuretic peptide are restored by the administration of adenosine deaminase in low-sodium rats. Sodium 153-159 adenosine deaminase Rattus norvegicus 126-145 1379228-12 1992 6) The mRNA-induced component of L-arginine uptake which is resistant to rBAT hybrid depletion is inhibited by L-homoserine, only in the presence of sodium; thus, it is related to a system y(+)-like activity. Sodium 149-155 bile acid CoA:amino acid N-acyltransferase Rattus norvegicus 73-77 1324615-0 1992 Atrial natriuretic peptide inhibits amiloride-sensitive sodium uptake in rat brain. Sodium 56-62 natriuretic peptide A Rattus norvegicus 0-26 1425858-1 1992 Since several studies suggest that increased insulin levels may induce antinatriuresis, the present work was undertaken to determine whether a physiological increase in insulin levels in blood perfusing the kidney may exert direct effect on kidney function, and more specifically on sodium reabsorption. Sodium 283-289 insulin Canis lupus familiaris 169-176 1425858-7 1992 Even if one may assume that the baseline low insulin concentrations promote tubular sodium reabsorption, the results of the present study suggest that a moderate hyperinsulinaemia is without any additional effect on renal sodium handling. Sodium 84-90 insulin Canis lupus familiaris 45-52 1309656-1 1992 The effect of Bistramide A, a toxin isolated from Bistratum lissoclinum Sluiter (Urochordata), on the peak sodium current (INa) of frog skeletal muscle fibres was studied with the double sucrose gap voltage clamp technique. Sodium 107-113 internexin neuronal intermediate filament protein alpha Homo sapiens 123-126 1310235-2 1992 Systemic infusion of CNP (group 1; 10 and 50 ng.kg-1.min-1 iv) resulted in marked cardiovascular hemodynamic effects characterized by a decrease in mean arterial pressure, cardiac output, and atrial pressures in association with a decrease in sodium excretion. Sodium 243-249 natriuretic peptide C Canis lupus familiaris 21-24 1310235-6 1992 With both systemic infusion or bolus administration of CNP, significant increases in plasma aldosterone were observed in association with increases in distal nephron sodium reabsorption. Sodium 166-172 natriuretic peptide C Canis lupus familiaris 55-58 1343602-5 1992 This increase in Ir-ANP concentration which correlated with atrial (r = -0.93) or hypothalamic (r = -0.87) Ir-ANP content decrease, was associated with significantly enhanced levels of plasma Ir-AVP, plasma sodium, osmolarity and hematocrit. Sodium 207-213 natriuretic peptide A Rattus norvegicus 20-23 1346164-5 1992 Atrial natriuretic peptide in sham-operated rats decreased mean arterial pressure from 118 +/- 5 to 95 +/- 5 mm Hg (P less than .001), increased urine volume from 0.06 +/- 0.02 to 0.16 +/- 0.05 ml/min/kg (P less than .05), urinary sodium excretion, 14.2 +/- 3.1 to 41.4 +/- 8.9 mu eq/min/kg (P less than .02), filtration fraction from 0.30 +/- 0.03 to 0.40 +/- 0.4 (P less than .05), and the percent fractional excretion of sodium from 0.84 +/- 0.19 to 2.85 +/- 0.61 (P less than .02). Sodium 231-237 natriuretic peptide A Rattus norvegicus 0-26 1346164-5 1992 Atrial natriuretic peptide in sham-operated rats decreased mean arterial pressure from 118 +/- 5 to 95 +/- 5 mm Hg (P less than .001), increased urine volume from 0.06 +/- 0.02 to 0.16 +/- 0.05 ml/min/kg (P less than .05), urinary sodium excretion, 14.2 +/- 3.1 to 41.4 +/- 8.9 mu eq/min/kg (P less than .02), filtration fraction from 0.30 +/- 0.03 to 0.40 +/- 0.4 (P less than .05), and the percent fractional excretion of sodium from 0.84 +/- 0.19 to 2.85 +/- 0.61 (P less than .02). Sodium 424-430 natriuretic peptide A Rattus norvegicus 0-26 1320716-8 1992 Further studies will be necessary to determine whether alterations in glomerular ANP receptors contribute to renal sodium retention in the nephrotic syndrome. Sodium 115-121 natriuretic peptide A Rattus norvegicus 81-84 1386913-0 1992 Effect of dietary sodium on atrial natriuretic factor released in rats with chronic renal failure. Sodium 18-24 natriuretic peptide A Rattus norvegicus 28-53 1386913-1 1992 Studies were done in partially nephrectomized rats to examine the effect of dietary sodium intake on atrial natriuretic factor (ANF) released by the atria. Sodium 84-90 natriuretic peptide A Rattus norvegicus 101-126 1386913-1 1992 Studies were done in partially nephrectomized rats to examine the effect of dietary sodium intake on atrial natriuretic factor (ANF) released by the atria. Sodium 84-90 natriuretic peptide A Rattus norvegicus 128-131 1386913-10 1992 Atrial ANF contents were higher in partially nephrectomized rats after receiving a sodium-supplemented diet. Sodium 83-89 natriuretic peptide A Rattus norvegicus 7-10 1386913-11 1992 A reduction in atrial ANF contents occurred when fed a sodium-deficient diet. Sodium 55-61 natriuretic peptide A Rattus norvegicus 22-25 1386913-17 1992 A significant correlation existed between plasma ANF and sodium excretion in chronic renal failure rats (r = 0.78; p less than 0.01). Sodium 57-63 natriuretic peptide A Rattus norvegicus 49-52 1386913-19 1992 These results suggest that in chronic renal failure rats, ANF played a role in sodium adaptation. Sodium 79-85 natriuretic peptide A Rattus norvegicus 58-61 10044819-0 1991 Spin-resolved elastic scattering of electrons from sodium below the inelastic threshold. Sodium 51-57 spindlin 1 Homo sapiens 0-4 1659520-0 1991 Epidermal growth factor elevates intracellular pH in chicken granulosa cells by activating protein kinase C. Previous studies from our laboratory have demonstrated that epidermal growth factor (EGF), induces intracellular alkalinization in chicken granulosa cells by activating a sodium-dependent and amiloride-sensitive Na+/H+ antiporter. Sodium 280-286 epidermal growth factor Gallus gallus 0-23 1659520-0 1991 Epidermal growth factor elevates intracellular pH in chicken granulosa cells by activating protein kinase C. Previous studies from our laboratory have demonstrated that epidermal growth factor (EGF), induces intracellular alkalinization in chicken granulosa cells by activating a sodium-dependent and amiloride-sensitive Na+/H+ antiporter. Sodium 280-286 epidermal growth factor Gallus gallus 169-192 1659520-0 1991 Epidermal growth factor elevates intracellular pH in chicken granulosa cells by activating protein kinase C. Previous studies from our laboratory have demonstrated that epidermal growth factor (EGF), induces intracellular alkalinization in chicken granulosa cells by activating a sodium-dependent and amiloride-sensitive Na+/H+ antiporter. Sodium 280-286 epidermal growth factor Gallus gallus 194-197 1659520-7 1991 Like EGF-induced cytosolic alkalinization, the increases in pHi in response to TPA or OAG were dependent on the presence of sodium concentration and were inhibited by amiloride, an inhibitor of the Na+/H+ antiporter. Sodium 124-130 epidermal growth factor Gallus gallus 5-8 1752072-0 1991 Urine kallikrein excretion in relation to renal sodium handling in minimal change nephrotic syndrome. Sodium 48-54 kallikrein related peptidase 4 Homo sapiens 6-16 1683643-2 1991 In this study multipoint linkage analysis of two Duffy-linked families given a combined LOD score of 8.65 to establish that the Duffy-linked CMT1B gene exists in the 18 centimorgan region between the antithrombin III gene and the Duffy/sodium-potassium ATPase loci. Sodium 236-242 myelin protein zero Homo sapiens 141-146 1833989-9 1991 The renal nerves and ANF appear to play a larger role in the acute control of sodium and water excretion in MW rats compared to rats of the Okamoto-Aoki strain. Sodium 78-84 natriuretic peptide A Rattus norvegicus 21-24 1838024-3 1991 Patch-clamp studies conducted on rat inner medullary collecting duct cells in primary culture revealed that ANP, via its second messenger cGMP, inhibits electrogenic sodium reabsorption by reducing the open probability of a cation channel located in the apical membrane. Sodium 166-172 natriuretic peptide A Rattus norvegicus 108-111 34425903-1 2021 BACKGROUND: Genetic variants in the voltage-gated sodium channels SCN1A, SCN2A, SCN3A, and SCN8A are leading causes of epilepsy, developmental delay, and autism spectrum disorder. Sodium 50-56 sodium voltage-gated channel alpha subunit 2 Homo sapiens 73-78 34425903-1 2021 BACKGROUND: Genetic variants in the voltage-gated sodium channels SCN1A, SCN2A, SCN3A, and SCN8A are leading causes of epilepsy, developmental delay, and autism spectrum disorder. Sodium 50-56 sodium voltage-gated channel alpha subunit 8 Homo sapiens 91-96 34353840-1 2021 Erythromelalgia is a rare hereditary channelopathy affecting the Nav1.7 sodium channel. Sodium 72-78 sodium voltage-gated channel alpha subunit 9 Homo sapiens 65-71 34406040-1 2021 Dravet syndrome (DS) is a monogenic epileptic encephalopathy caused by loss-of-function mutations in the voltage-gated sodium channel (VGSC) gene SCN1A. Sodium 119-125 sodium channel, voltage-gated, type I-like, alpha Danio rerio 146-151 34196428-0 2021 The PDZ protein SCRIB regulates sodium/iodide symporter (NIS) expression at the basolateral plasma membrane. Sodium 32-38 scribble planar cell polarity protein Homo sapiens 16-21 34232678-7 2021 We describe our findings that sodium, entering antigen-presenting cells via an epithelial sodium channel, triggers a PKC (protein kinase C)- and SGK1 (serum/glucocorticoid kinase 1)-stimulated activation of nicotinamide adenine dinucleotide phosphate oxidase, which, in turn, enhances lipid oxidation with generation of highly reactive isolevuglandins. Sodium 30-36 serum/glucocorticoid regulated kinase 1 Homo sapiens 145-149 34232678-7 2021 We describe our findings that sodium, entering antigen-presenting cells via an epithelial sodium channel, triggers a PKC (protein kinase C)- and SGK1 (serum/glucocorticoid kinase 1)-stimulated activation of nicotinamide adenine dinucleotide phosphate oxidase, which, in turn, enhances lipid oxidation with generation of highly reactive isolevuglandins. Sodium 30-36 serum/glucocorticoid regulated kinase 1 Homo sapiens 151-180 34232678-7 2021 We describe our findings that sodium, entering antigen-presenting cells via an epithelial sodium channel, triggers a PKC (protein kinase C)- and SGK1 (serum/glucocorticoid kinase 1)-stimulated activation of nicotinamide adenine dinucleotide phosphate oxidase, which, in turn, enhances lipid oxidation with generation of highly reactive isolevuglandins. Sodium 90-96 serum/glucocorticoid regulated kinase 1 Homo sapiens 145-149 34232678-7 2021 We describe our findings that sodium, entering antigen-presenting cells via an epithelial sodium channel, triggers a PKC (protein kinase C)- and SGK1 (serum/glucocorticoid kinase 1)-stimulated activation of nicotinamide adenine dinucleotide phosphate oxidase, which, in turn, enhances lipid oxidation with generation of highly reactive isolevuglandins. Sodium 90-96 serum/glucocorticoid regulated kinase 1 Homo sapiens 151-180 34334139-5 2021 These actions of sodium, potassium and magnesium and other minerals, trace elements and vitamins are likely to be secondary to their action on pro-inflammatory cytokines IL-6, TNF-alpha and IL-17 and metabolism of essential fatty acids that may account for their involvement in the pathobiology of insulin resistance, T2DM, HTN and autoimmune diseases. Sodium 17-23 interleukin 17A Homo sapiens 190-195 34202119-0 2021 Distinctive Properties and Powerful Neuromodulation of Nav1.6 Sodium Channels Regulates Neuronal Excitability. Sodium 62-68 sodium voltage-gated channel alpha subunit 8 Homo sapiens 55-61 34222704-0 2021 E44Q mutation in NaV1.7 in a patient with infantile paroxysmal knee pain: electrophysiological analysis of voltage-dependent sodium current. Sodium 125-131 sodium voltage-gated channel alpha subunit 9 Homo sapiens 17-23 34222704-1 2021 Gain-of-function mutations in voltage-gated sodium channels (NaV1.7, NaV1.8, and NaV1.9) are known causes of inherited pain disorders. Sodium 44-50 sodium voltage-gated channel alpha subunit 9 Homo sapiens 61-67 34222704-1 2021 Gain-of-function mutations in voltage-gated sodium channels (NaV1.7, NaV1.8, and NaV1.9) are known causes of inherited pain disorders. Sodium 44-50 sodium voltage-gated channel alpha subunit 10 Homo sapiens 69-75 34105351-6 2021 Excellent performance of the 3D-CoO-NrGO anode and SHC is owing to the synergistic effect of the CoO conversion reaction and pseudocapacitive sodium-ion storage induced by numerous Na2O/Co/NrGO nanointerfaces. Sodium 142-148 SHC adaptor protein 1 Homo sapiens 51-54 34134742-4 2021 Mutations in the genes encoding for the subunits of the epithelial sodium channels (ENaC) are responsible for generalized PHA1. Sodium 67-73 sodium channel epithelial 1 subunit gamma Homo sapiens 122-126 34423271-0 2021 Pharmacological Inhibition of the Voltage-Gated Sodium Channel NaV1.7 Alleviates Chronic Visceral Pain in a Rodent Model of Irritable Bowel Syndrome. Sodium 48-54 sodium voltage-gated channel alpha subunit 9 Homo sapiens 63-69 34423271-1 2021 The human nociceptor-specific voltage-gated sodium channel 1.7 (hNaV1.7) is critical for sensing various types of somatic pain, but it appears not to play a primary role in acute visceral pain. Sodium 44-50 sodium voltage-gated channel alpha subunit 9 Homo sapiens 64-71 34424517-4 2021 Indeed, by accumulating mutations in genes encoding proteins that are only now being exploited as targets for new pain therapies (the nerve growth factor receptor TrkA and voltage-gated sodium channel, NaV1.7), this species mastered the art of analgesia before humans evolved. Sodium 186-192 sodium voltage-gated channel alpha subunit 9 Homo sapiens 202-208 35589927-3 2022 To trace the evolution of the 3 species, and the distribution of the kdr mutation (resistance to pyrethroid) in the para-type voltage-gated sodium channel, we genotyped 41 populations (using neutral nuclear markers) and look at the prevalence of the kdr allele. Sodium 140-146 kinase insert domain receptor Homo sapiens 69-72 35526196-2 2022 To overcome treatment resistance, we aimed to evaluate the role of the mitochondrial sodium-calcium-lithium exchanger (NCLX) and its targeting in CRC. Sodium 85-91 solute carrier family 8 member B1 Homo sapiens 119-123 35563590-0 2022 Small Extracellular Vesicles Containing miR-34c Derived from Bone Marrow Mesenchymal Stem Cells Regulates Epithelial Sodium Channel via Targeting MARCKS. Sodium 117-123 myristoylated alanine rich protein kinase C substrate Mus musculus 146-152 35591852-0 2022 Genetic and Biological Effects of SLC12A3, a Sodium-Chloride Cotransporter, in Gitelman Syndrome and Diabetic Kidney Disease. Sodium 45-51 solute carrier family 12 member 3 Danio rerio 34-41 35591852-1 2022 The SLC12A3 (Solute carrier family 12 member 3) gene encodes a sodium-chloride cotransporter and mediates Na+ and Cl- reabsorption in the distal convoluted tubule of kidneys. Sodium 63-69 solute carrier family 12 member 3 Danio rerio 4-11 35591852-1 2022 The SLC12A3 (Solute carrier family 12 member 3) gene encodes a sodium-chloride cotransporter and mediates Na+ and Cl- reabsorption in the distal convoluted tubule of kidneys. Sodium 63-69 solute carrier family 12 member 3 Danio rerio 13-46 35285452-7 2022 CONCLUSION: Inhibition of SGLT2 in combination with an angiotensin II receptor blocker effectively improved BP salt sensitivity by reducing renal expression levels of sodium transporters including NHE3 and NKCC2, which eventually led to improvement of BP salt sensitivity and cardiorenal protection. Sodium 167-173 solute carrier family 12 member 1 Rattus norvegicus 206-211 35417276-1 2022 SCN2A encodes a voltage-gated sodium channel (NaV1.2) expressed throughout the central nervous system in predominantly excitatory neurons. Sodium 30-36 sodium voltage-gated channel alpha subunit 2 Homo sapiens 0-5 35417276-1 2022 SCN2A encodes a voltage-gated sodium channel (NaV1.2) expressed throughout the central nervous system in predominantly excitatory neurons. Sodium 30-36 sodium voltage-gated channel alpha subunit 2 Homo sapiens 46-52 35348308-1 2022 This study was aimed to analyze the commonalities and distinctions of voltage-gated sodium channels, Nav1.2, Nav1.6, in neurodevelopmental disorders. Sodium 84-90 sodium voltage-gated channel alpha subunit 2 Homo sapiens 101-107 35348308-1 2022 This study was aimed to analyze the commonalities and distinctions of voltage-gated sodium channels, Nav1.2, Nav1.6, in neurodevelopmental disorders. Sodium 84-90 sodium voltage-gated channel alpha subunit 8 Homo sapiens 109-115 35448095-4 2022 After LPS treatment, the peak sodium current decreased significantly in SCN10A-hiPSC-CMs, but not in healthy donor-hiPSC-CMs. Sodium 30-36 sodium voltage-gated channel alpha subunit 10 Homo sapiens 72-78 35290799-9 2022 The depolarization-induced calcium increase is dependent on the mitochondrial sodium-calcium exchanger NCLX, suggesting initial mitochondrial calcium efflux. Sodium 78-84 solute carrier family 8 member B1 Homo sapiens 103-107 35402583-8 2022 We focused on miR-432-5p as bioinformatic analysis had shown that it could be involved in sodium transport. Sodium 90-96 microRNA 432 Homo sapiens 14-21 35402583-12 2022 Epithelial sodium channel alpha subunit (alpha-ENaC) was revealed as a direct target gene of miR-432-5p and expressed on both human peritoneum and MeT-5A cells. Sodium 11-17 microRNA 432 Homo sapiens 93-100 35153788-3 2022 Patients with SCN8A mutations are often treated with multiple antiepileptic drugs, the most common being sodium channel blockers. Sodium 105-111 sodium voltage-gated channel alpha subunit 8 Homo sapiens 14-19 35140727-7 2021 Nevertheless, more sodium ions were translocated to and accumulated in the shoots of nlp7 than that of Col-0. Sodium 19-25 NIN like protein 7 Arabidopsis thaliana 85-89 35140727-9 2021 We attributed the enhanced salt tolerance of nlp7 to the balanced accumulation of nitrate anions and sodium cations. Sodium 101-107 NIN like protein 7 Arabidopsis thaliana 45-49 34986146-5 2022 Knockdown of SBF2 exacerbated paclitaxel changes to cell viability and neurite outgrowth while attenuating paclitaxel-induced sodium current inhibition. Sodium 126-132 SET binding factor 2 Homo sapiens 13-17 34995919-11 2022 Furthermore, canonical transient receptor potential channel 6 (TRPC6) was identified as the mechanism mediating local increase of sodium (Na+) useful to drive NCX1 reverse mode and, therefore, NCX1-mediated Ca2+ refilling. Sodium 130-136 transient receptor potential cation channel, subfamily C, member 6 Rattus norvegicus 23-61 34995919-11 2022 Furthermore, canonical transient receptor potential channel 6 (TRPC6) was identified as the mechanism mediating local increase of sodium (Na+) useful to drive NCX1 reverse mode and, therefore, NCX1-mediated Ca2+ refilling. Sodium 130-136 transient receptor potential cation channel, subfamily C, member 6 Rattus norvegicus 63-68 35154493-0 2022 Erratum: Focused ultrasound activates voltage-gated calcium channels through depolarizing TRPC1 sodium currents in kidney and skeletal muscle. Sodium 96-102 transient receptor potential cation channel subfamily C member 1 Homo sapiens 90-95 35592808-11 2022 Sodium elevated between period 1 and both period 2 and period 3 (P < 0.001). Sodium 0-6 period circadian regulator 2 Homo sapiens 42-50 2555304-3 1989 Atrial natriuretic factor and enalaprilat caused similar increases in sodium excretion (10-fold and sevenfold, respectively) and glomerular filtration rate (each 34%) and similar decreases in fractional proximal reabsorption of sodium (17% and 13%, respectively) and blood pressure. Sodium 70-76 natriuretic peptide A Rattus norvegicus 0-25 2555304-3 1989 Atrial natriuretic factor and enalaprilat caused similar increases in sodium excretion (10-fold and sevenfold, respectively) and glomerular filtration rate (each 34%) and similar decreases in fractional proximal reabsorption of sodium (17% and 13%, respectively) and blood pressure. Sodium 228-234 natriuretic peptide A Rattus norvegicus 0-25 2555304-8 1989 It is concluded that failure of atrial natriuretic factor to further suppress fractional proximal sodium reabsorption during converting enzyme inhibition is caused by either prior removal of the stimulatory action of angiotensin II on proximal tubular transport or extreme changes in peritubular physical factors consequent on the high filtration fraction. Sodium 98-104 natriuretic peptide A Rattus norvegicus 32-57 2533680-1 1989 Infusion of ANP has been shown to increase the urinary excretion of sodium and water. Sodium 68-74 natriuretic peptide A Rattus norvegicus 12-15 2533680-10 1989 These results indicate that the enhancement of renal sodium excretion induced by ANP is not related to a direct inhibition of sodium transport in the proximal tubule. Sodium 53-59 natriuretic peptide A Rattus norvegicus 81-84 2531900-2 1989 Atrial natriuretic peptide (ANP) dramatically increases renal sodium excretion and has been localized to brain areas previously shown to be involved in control of sodium excretion. Sodium 62-68 natriuretic peptide A Rattus norvegicus 0-26 2531900-2 1989 Atrial natriuretic peptide (ANP) dramatically increases renal sodium excretion and has been localized to brain areas previously shown to be involved in control of sodium excretion. Sodium 62-68 natriuretic peptide A Rattus norvegicus 28-31 2531900-2 1989 Atrial natriuretic peptide (ANP) dramatically increases renal sodium excretion and has been localized to brain areas previously shown to be involved in control of sodium excretion. Sodium 163-169 natriuretic peptide A Rattus norvegicus 0-26 2531900-2 1989 Atrial natriuretic peptide (ANP) dramatically increases renal sodium excretion and has been localized to brain areas previously shown to be involved in control of sodium excretion. Sodium 163-169 natriuretic peptide A Rattus norvegicus 28-31 2531900-13 1989 Conversely, the dramatic decline in plasma ANP after AV3V lesions was accompanied by very dramatic declines in content of ANP in these same structures, which suggests that the previously shown decrease in sodium excretion obtained after these lesions may be at least in part due to a decrease in release of ANP from the brain. Sodium 205-211 natriuretic peptide A Rattus norvegicus 43-46 2531900-13 1989 Conversely, the dramatic decline in plasma ANP after AV3V lesions was accompanied by very dramatic declines in content of ANP in these same structures, which suggests that the previously shown decrease in sodium excretion obtained after these lesions may be at least in part due to a decrease in release of ANP from the brain. Sodium 205-211 natriuretic peptide A Rattus norvegicus 122-125 2531900-13 1989 Conversely, the dramatic decline in plasma ANP after AV3V lesions was accompanied by very dramatic declines in content of ANP in these same structures, which suggests that the previously shown decrease in sodium excretion obtained after these lesions may be at least in part due to a decrease in release of ANP from the brain. Sodium 205-211 natriuretic peptide A Rattus norvegicus 122-125 2529999-2 1989 Numerous studies have shown that administration of atrial natriuretic factor (ANF) increases urinary sodium excretion and urine flow, decreases blood pressure, and inhibits renin and aldosterone release. Sodium 101-107 natriuretic peptide A Rattus norvegicus 51-76 2529999-2 1989 Numerous studies have shown that administration of atrial natriuretic factor (ANF) increases urinary sodium excretion and urine flow, decreases blood pressure, and inhibits renin and aldosterone release. Sodium 101-107 natriuretic peptide A Rattus norvegicus 78-81 2529999-3 1989 However, the role of endogenous ANF in the regulation of renal sodium excretion, blood pressure, plasma renin activity, and aldosterone level remains to be elucidated. Sodium 63-69 natriuretic peptide A Rattus norvegicus 32-35 2529999-6 1989 Blockade of endogenous ANF caused a 28 +/- 0.09%, 47 +/- 0.08%, and 51 +/- 0.08% fall in sodium excretion at 15, 30, and 45 minutes after Ab injection (p less than 0.05, p less than 0.01, p less than 0.01, respectively). Sodium 89-95 natriuretic peptide A Rattus norvegicus 23-26 2529999-13 1989 In contrast to the Ab group, a challenge with exogenous ANF (500 ng) increased sodium excretion by 2.17 mueq/min in the preimmune serum group. Sodium 79-85 natriuretic peptide A Rattus norvegicus 56-59 2533609-16 1989 Urinary sodium excretion was elevated during ANF infusion in both NZGH and NZN animals. Sodium 8-14 natriuretic peptide A Rattus norvegicus 45-48 2673301-8 1989 IND significantly increased the TPR response to Ang II on low sodium intake, remarkably in NSS and NT compared with SS. Sodium 62-68 translocated promoter region, nuclear basket protein Homo sapiens 32-35 2673301-9 1989 Salt sensitivity (% decrease in MBP from high to low sodium intake) highly correlated with the increase in the TPR response to Ang II by IND on low sodium intake (r = -0.90). Sodium 53-59 translocated promoter region, nuclear basket protein Homo sapiens 111-114 2673301-9 1989 Salt sensitivity (% decrease in MBP from high to low sodium intake) highly correlated with the increase in the TPR response to Ang II by IND on low sodium intake (r = -0.90). Sodium 148-154 translocated promoter region, nuclear basket protein Homo sapiens 111-114 2532253-15 1989 It is proposed that disruption of glomerulo-tubular balance occurred in these experiments from inhibition of endogenous angiotensin II-stimulated proximal sodium reabsorption by ANF. Sodium 155-161 natriuretic peptide A Rattus norvegicus 178-181 2522979-0 1989 Effect of synthetic atrial natriuretic factor on superficial and deep proximal tubule sodium reabsorption. Sodium 86-92 natriuretic peptide A Rattus norvegicus 20-45 2522979-1 1989 The effects of synthetic atrial natriuretic factor (ANF) on sodium reabsorption by deep and superficial proximal tubules were examined in the rat. Sodium 60-66 natriuretic peptide A Rattus norvegicus 52-55 2522979-2 1989 In response to ANF infusion (4 micrograms/kg/hr), the urinary fractional excretion of sodium increased from 1.21% +/- 0.53% to 3.48% +/- 0.48%, p less than 0.05 (n = 12). Sodium 86-92 natriuretic peptide A Rattus norvegicus 15-18 2522979-7 1989 In summary, ANF infusion increased urinary fractional sodium excretion; however, fractional sodium reabsorption by the proximal tubule of superficial nephrons was unchanged. Sodium 54-60 natriuretic peptide A Rattus norvegicus 12-15 2920097-4 1989 Insulin infusion did, however, cause modest sodium retention during the first few days of infusion. Sodium 44-50 insulin Canis lupus familiaris 0-7 2521777-8 1989 The attenuated renal response to ANP may contribute to the impaired sodium and water excretion in chronic heart failure, although other mechanisms are involved. Sodium 68-74 natriuretic peptide A Rattus norvegicus 33-36 2521228-6 1989 The change in serum sodium concentration correlated with plasma renin activity and aldosterone (r = -0.77, -0.88, respectively, both p less than 0.01), but not with norepinephrine or atrial natriuretic factor. Sodium 20-26 renin Canis lupus familiaris 64-69 2473343-0 1989 Effects of the intracerebroventricular atrial natriuretic factor on angiotensin II or sodium-induced blood pressure elevation and natriuresis. Sodium 86-92 natriuretic peptide A Rattus norvegicus 39-64 2974246-1 1988 Atrial natriuretic peptide (ANP) infusion increases fractional excretion of many solutes including sodium, chloride, bicarbonate, phosphate, calcium, and magnesium. Sodium 99-105 natriuretic peptide A Rattus norvegicus 0-26 2974246-1 1988 Atrial natriuretic peptide (ANP) infusion increases fractional excretion of many solutes including sodium, chloride, bicarbonate, phosphate, calcium, and magnesium. Sodium 99-105 natriuretic peptide A Rattus norvegicus 28-31 2852059-4 1988 As a result, numerous studies have appeared that indicate that brain atrial natriuretic peptide is implicated in the regulation of blood pressure, fluid and sodium balance, cerebral blood flow, brain microcirculation, blood-brain barrier function, and cerebrospinal fluid production. Sodium 157-163 natriuretic peptide A Rattus norvegicus 69-95 2854018-7 1988 ANP produced large increases in urine volume, urinary sodium and chloride excretion, and further decreased plasma potassium concentration in the ACTH-treated sheep. Sodium 54-60 natriuretic peptides A Ovis aries 0-3 2972583-11 1988 The elevated plasma hANF levels in patients with chronic liver disease and continued sodium retention may suggest a renal insensitivity to the natriuretic effects of hANF. Sodium 85-91 HESX homeobox 1 Homo sapiens 20-24 2977195-2 1988 Administration of synthetic atrial natriuretic factor (150 micrograms/kg/day) to rats made hypertensive by 7-day infusion of aldosterone (100 micrograms/kg/day) and sodium loading with 1% NaCl as drinking water returned the blood pressure to control levels, and the antihypertensive effect was not associated with any changes in urine volume and urinary sodium excretion. Sodium 354-360 natriuretic peptide A Rattus norvegicus 28-53 2847552-5 1988 A more moderate increase in plasma renin activity was established in another group of sodium-restricted dogs, and saralasin was administered intravenously instead of intra-arterially. Sodium 86-92 renin Canis lupus familiaris 35-40 2847552-7 1988 The results suggest that blockade of the influence of the renin-angiotensin system and possibly another vasodilator mechanism, such as kinin potentiation, account for the increase in RBF after ACE inhibition in the low-sodium state. Sodium 219-225 renin Canis lupus familiaris 58-63 2976327-11 1988 Previously reported in vivo clearance data suggest that ANP causes, at least in part, a natriuresis by altering sodium transport in the medullary collecting ducts. Sodium 112-118 natriuretic peptide A Rattus norvegicus 56-59 2848091-6 1988 These data confirm previous reports of increased adrenal sensitivity to alpha-MSH and angiotensin II in sodium depletion, and also suggest the existence of intraglandular mechanisms for signal amplification which may be involved in mediating the adrenal response to very small concentrations of stimulant. Sodium 104-110 proopiomelanocortin Rattus norvegicus 72-81 2848103-7 1988 However, neuronal sodium current density was 40-60% lower in cultures prepared from both tip-E and seits1 embryos. Sodium 18-24 temperature-induced paralytic E Drosophila melanogaster 89-94 2848103-9 1988 These results indicate that both the tip-E and sei loci are important in regulation of sodium current density in embryonic neurons. Sodium 87-93 temperature-induced paralytic E Drosophila melanogaster 37-42 2848103-9 1988 These results indicate that both the tip-E and sei loci are important in regulation of sodium current density in embryonic neurons. Sodium 87-93 seizure Drosophila melanogaster 47-50 3138388-9 1988 Our results with natural, analogue, and model amino acids, and especially with sodium, suggest that threonine, but not phenylalanine, may enter the brain partly by the sodium-dependent ASC system. Sodium 168-174 PYD and CARD domain containing Rattus norvegicus 185-188 3171983-3 1988 No studies have examined the effects of SA on renal function in a situation in which the maintenance of normal kidney function is dependent upon intact renal PG synthesis (i.e., sodium restriction-elevated plasma renin activity). Sodium 178-184 renin Canis lupus familiaris 213-218 3054273-5 1988 Renal and urinary kallikrein was found to be increased under sodium restricted conditions, whereas kinin has a diuretic and natriuretic effect in the collecting tubule, when added from the basolateral surface. Sodium 61-67 kallikrein related peptidase 4 Homo sapiens 18-28 2843231-3 1988 After intracellular acidification induced by the NH4Cl-prepulse technique, there was a sodium-dependent pHi recovery towards the normal steady-state pHi. Sodium 87-93 glucose-6-phosphate isomerase Oryctolagus cuniculus 104-107 2843231-3 1988 After intracellular acidification induced by the NH4Cl-prepulse technique, there was a sodium-dependent pHi recovery towards the normal steady-state pHi. Sodium 87-93 glucose-6-phosphate isomerase Oryctolagus cuniculus 149-152 2843231-4 1988 The initial pHi recovery rate was a saturable function of extracellular sodium concentration with an apparent Km for external sodium of about 25 mM and a Vmax of about 0.28 pH units/min. Sodium 72-78 glucose-6-phosphate isomerase Oryctolagus cuniculus 12-15 2843231-4 1988 The initial pHi recovery rate was a saturable function of extracellular sodium concentration with an apparent Km for external sodium of about 25 mM and a Vmax of about 0.28 pH units/min. Sodium 126-132 glucose-6-phosphate isomerase Oryctolagus cuniculus 12-15 2842085-13 1988 We conclude that through modulation of its glomerular and vascular receptors, ANF may contribute to the differential sodium handling of saralasin-sensitive and -resistant 2K1C hypertensive rats and to the reduced vascular responsiveness to ANF observed in the saralasin-resistant hypertensive rats. Sodium 117-123 natriuretic peptide A Rattus norvegicus 78-81 2971104-7 1988 The natriuretic response to ANF was slightly, but significantly, decreased in portal hypertensive rats as compared to controls (fractional excretion of sodium, 1.8 +/- 0.4 vs. 2.9 +/- 0.3; P less than .05). Sodium 152-158 natriuretic peptide A Rattus norvegicus 28-31 2970225-9 1988 Plasma ANP and ANP mRNA decreased in the low- compared with the high-sodium state, whereas atrial ANP content was unaltered in both low- and high-sodium states. Sodium 69-75 natriuretic peptide A Rattus norvegicus 15-18 2970225-9 1988 Plasma ANP and ANP mRNA decreased in the low- compared with the high-sodium state, whereas atrial ANP content was unaltered in both low- and high-sodium states. Sodium 69-75 natriuretic peptide A Rattus norvegicus 15-18 2970225-10 1988 These results demonstrate that sodium intake affects the expression of the renin and angiotensinogen genes and slightly alters the expression of ANP gene. Sodium 31-37 natriuretic peptide A Rattus norvegicus 145-148 2970556-3 1988 Serum sodium concentrations and osmolalities were lowest on admission, and were persistently elevated following HSL resuscitation. Sodium 6-12 lipase E, hormone sensitive type Homo sapiens 112-115 2968143-1 1988 Intracerebroventricular (ICV) administration of rat atrial natriuretic peptide (99-126) (rANP) to conscious male hydrated rats resulted in a dose-related increase in urinary volume and sodium excretion over a 6-h period of urine collection. Sodium 185-191 natriuretic peptide A Rattus norvegicus 52-78 2964203-14 1988 This altered responsiveness to ANF may contribute to the sodium and water retention characteristic of this disorder. Sodium 57-63 natriuretic peptide A Rattus norvegicus 31-34 2975142-7 1988 On the other hand, central administration of synthetic rat ANF (2 micrograms) prevented the water accumulation elicited in rat brain by systemic hypoosmolar fluid load, and led to a significant sodium loss from the nervous tissue by altering the capillary sodium permeability. Sodium 194-200 natriuretic peptide A Rattus norvegicus 59-62 2975142-7 1988 On the other hand, central administration of synthetic rat ANF (2 micrograms) prevented the water accumulation elicited in rat brain by systemic hypoosmolar fluid load, and led to a significant sodium loss from the nervous tissue by altering the capillary sodium permeability. Sodium 256-262 natriuretic peptide A Rattus norvegicus 59-62 3280170-5 1988 The chronic elevation of ANG II in the CSF plus an increase in NaCl intake produces a low renin, sodium dependent, expanded volume hypertension. Sodium 97-103 renin Canis lupus familiaris 90-95 2892605-0 1988 Influence of sodium concentration in cerebrospinal fluid on plasma atrial natriuretic peptide in conscious rats. Sodium 13-19 natriuretic peptide A Rattus norvegicus 67-93 2892605-2 1988 To test the influence of a sodium (Na+) stimulus within the central nervous system on the release of atrial natriuretic peptide (ANP), we examined the effects of intracerebroventricular infusion of high Na+ artificial cerebrospinal fluid (CSF) on blood pressure, urinary Na+ excretion and plasma ANP levels in conscious Wistar rats. Sodium 27-33 natriuretic peptide A Rattus norvegicus 101-127 2892605-2 1988 To test the influence of a sodium (Na+) stimulus within the central nervous system on the release of atrial natriuretic peptide (ANP), we examined the effects of intracerebroventricular infusion of high Na+ artificial cerebrospinal fluid (CSF) on blood pressure, urinary Na+ excretion and plasma ANP levels in conscious Wistar rats. Sodium 27-33 natriuretic peptide A Rattus norvegicus 129-132 2901317-2 1988 The aim of the present experiments was to examine the question whether the rat atrial natriuretic factor (rANF 1-28) could alter the fractional excretion of sodium (FENa) and other solutes in the frog (Rana esculenta). Sodium 157-163 natriuretic peptide A Rattus norvegicus 79-104 2901317-2 1988 The aim of the present experiments was to examine the question whether the rat atrial natriuretic factor (rANF 1-28) could alter the fractional excretion of sodium (FENa) and other solutes in the frog (Rana esculenta). Sodium 157-163 natriuretic peptide A Rattus norvegicus 106-110 2977978-1 1988 Prolonged (12-day) sodium deprivation strikingly raised both basal plasma aldosterone concentration (PAC) (114%) and plasma renin activity (PRA) (200%), and lowered ANF blood level (-30%). Sodium 19-25 natriuretic peptide A Rattus norvegicus 165-168 2977978-2 1988 Acute ANF bolus administration produced a dose-dependent decrease in PAC in both normally-fed and sodium-restricted rats. Sodium 98-104 natriuretic peptide A Rattus norvegicus 6-9 2977978-8 1988 Prolonged ANF infusion significantly reduced PRA (-48%) only in sodium-restricted rats with intact RAS. Sodium 64-70 natriuretic peptide A Rattus norvegicus 10-13 2977978-9 1988 These findings suggest that (i) the long-term inhibitory effect of ANF on aldosterone secretion is due to both the block of renin release and a direct action on the zona glomerulosa; and (ii) the mechanism underlying the adrenoglomerulotrophic effect of sodium restriction involves not only the activation of RAS, but also the suppression of ANF release. Sodium 254-260 natriuretic peptide A Rattus norvegicus 67-70 2835565-3 1988 ANP administration resulted in a significant elevation of sodium excretion and glomerular filtration rate and a fall in blood pressure. Sodium 58-64 natriuretic peptide A Rattus norvegicus 0-3 2961879-1 1987 We used the kinetics of atrial natriuretic peptide (ANP) and fractional lithium excretion to test the hypothesis that ANP-induced natriuresis is related directly to the ANP perfusate concentration and is mediated by a decrease in proximal tubular sodium reabsorption. Sodium 247-253 natriuretic peptide A Rattus norvegicus 118-121 2961879-1 1987 We used the kinetics of atrial natriuretic peptide (ANP) and fractional lithium excretion to test the hypothesis that ANP-induced natriuresis is related directly to the ANP perfusate concentration and is mediated by a decrease in proximal tubular sodium reabsorption. Sodium 247-253 natriuretic peptide A Rattus norvegicus 118-121 2961879-5 1987 ANP treatment resulted in a significant peak increase in sodium (5.6-fold), lithium (2.1-fold), potassium (2.3-fold) and water (5.1-fold) excretion. Sodium 57-63 natriuretic peptide A Rattus norvegicus 0-3 3318501-9 1987 We suggest that during low sodium intake, activation of sympathetic nerve activity elicits an enhanced renin release response, whereas the renal vasculature may be protected against neurogenic vasoconstriction. Sodium 27-33 renin Canis lupus familiaris 103-108 3479549-8 1987 Abrupt and pronounced increases in urine flow and sodium excretion were observed on administration of 9 alpha, 11 beta-PGF2 at 7.5 micrograms/min. Sodium 50-56 placental growth factor Rattus norvegicus 119-122 3687594-4 1987 Sodium and potassium excretion did not vary significantly during Paf-acether infusion, but increased dramatically after discontinuation of Paf-acether infusion. Sodium 0-6 PCNA clamp associated factor Rattus norvegicus 139-142 2962708-3 1987 Partial removal of the endogenous source of atrial natriuretic factor was associated with a reduced renal response to hypervolemia, confirming that the factor is causally involved in acute sodium balance. Sodium 189-195 natriuretic peptide A Rattus norvegicus 44-69 3323013-3 1987 In each Series intravenous infusion of insulin at a rate of 0.05 U.kg-1.h-1 elicited transient increase in plasma sodium concentration and prolonged hypokalemia. Sodium 114-120 insulin Canis lupus familiaris 39-46 3323013-7 1987 Infusion of insulin in Series 1 elicited increase of sodium excretion and decrease in potassium excretion. Sodium 53-59 insulin Canis lupus familiaris 12-19 3323013-9 1987 The results indicate that depletion of electrolytes and blood aldosterone elevation modify the effects of insulin on plasma concentration and renal excretion of sodium and potassium. Sodium 161-167 insulin Canis lupus familiaris 106-113 2448367-8 1987 Our data suggest that the inhibition of kallikrein and/or other serine proteases by aprotinin can interfere with renal release of active renin and also support the hypothesis that the renal kallikrein system exerts a regulatory control on sodium excretion in salt replete hypertensives. Sodium 239-245 kallikrein related peptidase 4 Homo sapiens 40-50 2448367-8 1987 Our data suggest that the inhibition of kallikrein and/or other serine proteases by aprotinin can interfere with renal release of active renin and also support the hypothesis that the renal kallikrein system exerts a regulatory control on sodium excretion in salt replete hypertensives. Sodium 239-245 kallikrein related peptidase 4 Homo sapiens 190-200 3443953-10 1987 There was a significant negative correlation between the serum albumin concentration and the ratio of potassium to sodium ions in milk samples obtained from rats milked with varying oxytocin treatments. Sodium 115-121 albumin Rattus norvegicus 57-70 2444871-11 1987 It appears that BTX-induced phosphoinositide breakdown in guinea pig synaptoneurosomes is dependent primarily on activation of TTX-resistant, Cd2+-sensitive sodium channels that account for only a small fraction of the total sodium influx induced by BTX in synaptoneurosomes. Sodium 157-163 T-cell surface antigen CD2 Cavia porcellus 142-145 2443024-2 1987 It depresses the rapid initial depolarization of the action potential by blocking the sodium current, INa. Sodium 86-92 LOW QUALITY PROTEIN: alpha-internexin Oryctolagus cuniculus 102-105 2957927-8 1987 The augmentation of pressure natriuresis within the GFR autoregulatory range suggests an influence of ANF on the magnitude of arterial pressure-induced changes in tubular sodium reabsorption. Sodium 171-177 natriuretic peptide A Rattus norvegicus 102-105 2957323-1 1987 Although synthetic atrial natriuretic peptide is known to increase urinary volume and sodium excretion and to reduce arterial blood pressure, the physiological role of endogenous atrial natriuretic peptide is still unclear. Sodium 86-92 natriuretic peptide A Rattus norvegicus 19-45 2950776-1 1987 These experiments examined the effects of altering venous return, aortic pressure, or perfusate sodium concentration on the release of atrial natriuretic factor (ANF) from a rat heart-lung preparation. Sodium 96-102 natriuretic peptide A Rattus norvegicus 135-160 2950776-1 1987 These experiments examined the effects of altering venous return, aortic pressure, or perfusate sodium concentration on the release of atrial natriuretic factor (ANF) from a rat heart-lung preparation. Sodium 96-102 natriuretic peptide A Rattus norvegicus 162-165 2959417-2 1987 The effect of a low dose of a synthetic atrial natriuretic peptide (ANP), rat atriopeptin II (23 amino acids), on stop-flow sodium concentrations was examined in rabbits in water diuresis. Sodium 124-130 natriuretic peptide A Rattus norvegicus 40-66 2959417-2 1987 The effect of a low dose of a synthetic atrial natriuretic peptide (ANP), rat atriopeptin II (23 amino acids), on stop-flow sodium concentrations was examined in rabbits in water diuresis. Sodium 124-130 natriuretic peptide A Rattus norvegicus 68-71 3569605-1 1987 A possible involvement of oxytocin (OT) has been indicated in regulation of water and electrolyte metabolism, based on findings that the secretion of OT is increased by either water deprivation or sodium loading. Sodium 197-203 oxytocin/neurophysin I prepropeptide Homo sapiens 26-34 2953170-2 1987 Both NaCl-and DOCA-NaCl-loading increased plasma ANP levels (to 86 +/- 8.1 and 105 +/- 12 pg ml-1 respectively; 47 +/- 6.7-60 +/- 4.6 pg ml-1 in controls), which were correlated to sodium intake and excretion. Sodium 181-187 natriuretic peptide A Rattus norvegicus 49-52 2953171-1 1987 Studies were performed on anaesthetized Wistar-Kyoto rats to investigate whether the natriuretic response to stimulation of the cerebroventricular system with a hypertonic sodium solution is in part caused by increased plasma concentrations of atrial natriuretic factor (ANF). Sodium 172-178 natriuretic peptide A Rattus norvegicus 244-269 3588503-6 1987 For birds raised on tap water, unilateral sodium infusion caused a significant unilateral reduction in the glomerular filtration rate. Sodium 42-48 nuclear RNA export factor 1 Homo sapiens 20-23 2449054-9 1987 Our data suggest that the inhibition of kallikrein and/or other serine proteases by aprotinin can interfere with renal release of active renin and also support the hypothesis that the renal kallikrein system exerts a regulatory control on sodium excretion in salt replete hypertensives. Sodium 239-245 kallikrein related peptidase 4 Homo sapiens 40-50 2449054-9 1987 Our data suggest that the inhibition of kallikrein and/or other serine proteases by aprotinin can interfere with renal release of active renin and also support the hypothesis that the renal kallikrein system exerts a regulatory control on sodium excretion in salt replete hypertensives. Sodium 239-245 kallikrein related peptidase 4 Homo sapiens 190-200 3599803-8 1987 The postulated defect in sodium excretion in hypertensive patients might be related to their low kallikrein excretion. Sodium 25-31 kallikrein related peptidase 4 Homo sapiens 97-107 3481117-1 1987 The effect of vasoactive intestinal peptide (VIP), secretin, and VIP-secretin (Ala4, Val5-secretin) on the net movements of sodium, potassium, fluid, and mucus was investigated in the rat colon perfused in vivo. Sodium 124-130 secretin Rattus norvegicus 69-77 3481117-1 1987 The effect of vasoactive intestinal peptide (VIP), secretin, and VIP-secretin (Ala4, Val5-secretin) on the net movements of sodium, potassium, fluid, and mucus was investigated in the rat colon perfused in vivo. Sodium 124-130 secretin Rattus norvegicus 69-77 2944689-2 1986 ANP induced a 540% increase in sodium excretion and a 310% increase in urine flow. Sodium 31-37 natriuretic peptide A Rattus norvegicus 0-3 3524271-8 1986 These results show that high sodium intake decreased aldosterone via suppression of renin release but do not rule out a possible hypertensinogenic role for stress-induced adrenocorticotrophic hormone-sensitive corticoids. Sodium 29-35 renin Canis lupus familiaris 84-89 2427277-1 1986 The effects of a carbonic anhydrase inhibitor, acetazolamide, bound to a 72,000 dalton dextran (DBI) on bicarbonate and sodium fluxes across the isolated rabbit corneal endothelium have been examined. Sodium 120-126 acyl-CoA-binding protein Oryctolagus cuniculus 96-99 2427277-5 1986 When DBI was present on the stromal-facing surface of the endothelium, no changes were found in unidirectional or net bicarbonate fluxes; the sodium flux from stroma to endothelium was increased, however, with no change in net flux. Sodium 142-148 acyl-CoA-binding protein Oryctolagus cuniculus 5-8 3488538-11 1986 In addition, the time constant of the turning-on of sodium activation m (tau m on) was determined, assuming INa approximately m2 (with a small initial delay) or INa approximately m3 (without an initial delay). Sodium 52-58 internexin neuronal intermediate filament protein alpha Homo sapiens 161-164 2940876-0 1986 Atrial natriuretic factor inhibits sodium transport in medullary collecting duct. Sodium 35-41 natriuretic peptide A Rattus norvegicus 0-25 3636040-3 1986 Adjusted kallikrein excretion was greater in youths than in adults and correlated with potassium excretion and sodium excretion in persons with normal blood pressure. Sodium 111-117 kallikrein related peptidase 4 Homo sapiens 9-19 2936682-6 1986 Urine volume and fractional chloride excretion rose during infusions of rat or human atrial natriuretic factor in a manner that resembled the elevation in sodium excretion. Sodium 155-161 natriuretic peptide A Rattus norvegicus 85-110 2436516-3 1986 Hence, the sodium ion bonds in the minor groove of ApU and only to the phosphate backbone in GpC. Sodium 11-17 glycophorin C (Gerbich blood group) Homo sapiens 93-96 2933941-5 1985 Reduced circulating atrial natriuretic factor therefore could contribute to the previously observed impaired ability of coronary ligated rats to excrete a saline load and to the sodium retention observed in clinical heart failure. Sodium 178-184 natriuretic peptide A Rattus norvegicus 20-45 6323226-9 1984 These data indicate that the long-term hypotensive and natriuretic actions of inhibitors of ACE are mediated by inhibition of AngII formation and that the renin-angiotensin system plays an essential role in regulating aldosterone secretion, renal function, and AP during sodium deficiency. Sodium 271-277 renin Canis lupus familiaris 155-160 6435143-1 1984 Dilution of CSF sodium by infusion of hyperosmotic mannitol into the cerebral ventricles of the rat does not evoke a salt appetite, nor does the addition of sodium to the CSF of the rat suppress the preexisting salt appetites produced by the hormones of sodium conservation or by adrenalectomy. Sodium 16-22 colony stimulating factor 2 Rattus norvegicus 12-15 6435143-2 1984 CSF sodium concentration does not control sodium appetite in the rat. Sodium 4-10 colony stimulating factor 2 Rattus norvegicus 0-3 6373590-1 1984 Dissociation of blood pressure lowering and renin inhibition in sodium-deficient dogs. Sodium 64-70 renin Canis lupus familiaris 44-49 6563013-9 1984 In sodium-depleted hypertensive patients kallikrein excretion was decreased from 19.8 to 9.5 mEU /min, and in Na+-depleted normal subjects it was decreased from 15.7 to 12.6 mEU /min (p = 0.003). Sodium 3-9 kallikrein related peptidase 4 Homo sapiens 41-51 6561955-0 1984 Tissue kallikrein synthesis and its modification by testosterone or low dietary sodium. Sodium 80-86 kallikrein 1-related peptidase C12 Rattus norvegicus 0-17 6375065-4 1984 Levels of urinary kallikrein excretion in patients with primary aldosteronism due to aldosterone-producing adenoma (APA) were greater (p less than 0.05 to p less than 0.001) than those in patients with primary aldosteronism due to idiopathic adrenal hyperplasia (IHA) under any sodium diet. Sodium 278-284 kallikrein related peptidase 4 Homo sapiens 18-28 6353943-1 1983 Chronic sodium depletion is a state of reduced cardiac output in which the renin-angiotensin system is actively involved in maintenance of mean arterial blood pressure (MAP). Sodium 8-14 renin Canis lupus familiaris 75-80 6353944-3 1983 However, plasma renin activity (PRA) was 11-fold higher in sodium-deplete dogs (P less than 0.01). Sodium 59-65 renin Canis lupus familiaris 16-21 6861709-10 1983 A change in sodium-calcium exchange due to the elevation in cellular sodium is a potential mechanism by which ouabain might inhibit PTH secretion. Sodium 12-18 parathyroid hormone Bos taurus 132-135 6861709-10 1983 A change in sodium-calcium exchange due to the elevation in cellular sodium is a potential mechanism by which ouabain might inhibit PTH secretion. Sodium 69-75 parathyroid hormone Bos taurus 132-135 6351206-7 1983 Plasma renin activity was markedly elevated and further increased in the sodium-deplete group, but it was nearly unchanged in the sodium-replete group. Sodium 73-79 renin Canis lupus familiaris 7-12 6351206-8 1983 This difference in renal response to exogenous PGA1 might be due to interaction with the renin-angiotensin system, which was markedly stimulated by sodium depletion and additionally by prostaglandin infusion. Sodium 148-154 renin Canis lupus familiaris 89-94 6859924-3 1983 The concentration of sodium in the cerebrospinal fluid was such that as much as 3 mmol of sodium could have been removed with each ventricular tap. Sodium 21-27 nuclear RNA export factor 1 Homo sapiens 143-146 6859924-3 1983 The concentration of sodium in the cerebrospinal fluid was such that as much as 3 mmol of sodium could have been removed with each ventricular tap. Sodium 90-96 nuclear RNA export factor 1 Homo sapiens 143-146 6871539-5 1983 When infused into the conscious rabbit, neurotensin produces a dose-related fall in renal sodium excretion. Sodium 90-96 neurotensin/neuromedin N Oryctolagus cuniculus 40-51 6600035-8 1983 Sodium reabsorption was closely correlated to GFR in both diabetic (r = 0.99, P less than 0.0001) and healthy subjects (r = 1.00, P less than 0.0001), and both groups showed identical regression lines. Sodium 0-6 Rap guanine nucleotide exchange factor 5 Homo sapiens 46-49 6341216-3 1983 On a regular sodium intake, healthy conscious dogs apparently have a much lower plasma renin activity (PRA) than healthy human volunteers. Sodium 13-19 renin Canis lupus familiaris 87-92 6341218-2 1983 In canine neonatally-induced coarctation hypertension, we reported abnormally elevated plasma renin activity (PRA) during sodium restriction in 2-year-old dogs, but found normal PRA responses to sodium restriction +/- furosemide in coarcted dogs studied serially over the first year postaortic banding (PAB). Sodium 122-128 renin Canis lupus familiaris 94-99 6338138-9 1983 We conclude that (1) sodium depletion accentuates both the magnitude and duration of the vasoconstrictive phase of the renal blood flow response to injection of contrast medium and (2) blockade of the intrarenal renin-angiotensin system shortens the duration of this response. Sodium 21-27 renin Canis lupus familiaris 212-217 7177784-8 1982 All select lithium over sodium, but with different magnitudes of selectivity, ranging from PLi/PNa of 13 (for AS701) to PLi/PNa of 2 (for AS708). Sodium 24-30 serpin family F member 2 Homo sapiens 91-94 7159098-0 1982 The stimulation of the release of Ca2+ from mitochondria by sodium ions and its inhibition. Sodium 60-66 carbonic anhydrase 2 Homo sapiens 34-37 1149185-6 1975 Infusion of des-1-Asp-angiotensin II into sodium-depleted dogs decreased renin secretion from 1094 +/- 211 ng/min to 768 +/- 132 and 499 +/- 31 ng/min (P less than 0.025 for both values) after 10 and 30 minutes of infusion. Sodium 42-48 renin Canis lupus familiaris 73-78 1132073-5 1975 However, the rise in kallikrein shown by the SH rat on a high sodium diet is unique for this hypertensive model. Sodium 62-68 kallikrein related peptidase 4 Homo sapiens 21-31 1132073-2 1975 When dietary sodium was restricted, kallikrein excretion increased in the W/Ky but not in the SH rats. Sodium 13-19 kallikrein related peptidase 4 Homo sapiens 36-46 235594-2 1975 Two of these membrane-associated enzymes, glyceraldehyde phosphate dehydrogenase (GAPD) and phosphoglyceric kinase (PGK), have been shown to have controlling functions on intra-erythrocytic glycolysis and sodium-potassium transport. Sodium 205-211 glyceraldehyde-3-phosphate dehydrogenase Mus musculus 42-80 235594-2 1975 Two of these membrane-associated enzymes, glyceraldehyde phosphate dehydrogenase (GAPD) and phosphoglyceric kinase (PGK), have been shown to have controlling functions on intra-erythrocytic glycolysis and sodium-potassium transport. Sodium 205-211 glyceraldehyde-3-phosphate dehydrogenase Mus musculus 82-86 1120931-4 1975 The relationship between PRA and daily sodium excretion present in the low GFR group (GFR less than 80 ml. Sodium 39-45 Rap guanine nucleotide exchange factor 5 Homo sapiens 75-78 1120931-4 1975 The relationship between PRA and daily sodium excretion present in the low GFR group (GFR less than 80 ml. Sodium 39-45 Rap guanine nucleotide exchange factor 5 Homo sapiens 86-89 1183077-0 1975 Influence of plasma and extracellular fluid volumes on plasma renin activity in sodium-depleted dogs. Sodium 80-86 renin Canis lupus familiaris 62-67 4817354-2 1974 Normal human red cells which have had their intracellular sodium (Na(c)) reduced have a diminished Na-K pump rate, but only if intracellular potassium (K(c)) is high. Sodium 58-64 X-linked Kx blood group Homo sapiens 66-71 11344563-3 1974 The present micropuncture studies test the thesis that albumin infusion depresses proximal reabsorption by an effect unrelated to expansion of the plasma volume, perhaps due to an effect of parathyroid hormone (PTH) on proximal sodium reabsorption. Sodium 228-234 parathyroid hormone Canis lupus familiaris 190-209 4805251-0 1973 The effect of oxytocin and (2-tyrosine/O-methyl)-oxytocin on the sodium and potassium balance. Sodium 65-71 oxytocin/neurophysin I prepropeptide Homo sapiens 49-57 4378027-1 1972 Phentolamine-induced blockade of alpha-adrenoreceptors and subsequent beta-adrenoreceptor stimulation by intravenous injection of adrenaline or phenylephrine (Mezaton) in anaesthtized dogs was accompanied by an elevation of plasma renin activitiy in peripheral blood and a reduction of renal excretion of sodium, potassium, and water. Sodium 305-311 renin Canis lupus familiaris 231-236 5001861-0 1971 Effect of aldosterone and oxytocin on the active sodium transport across the isolated toad skin in relation to loosening of stratum corneum. Sodium 49-55 oxytocin/neurophysin I prepropeptide Homo sapiens 26-34 6020540-0 1967 Effects of mercurial diuresis and acute sodium depletion on renin release in dog. Sodium 40-46 renin Canis lupus familiaris 60-65 33832341-4 2021 Results: The SGLT2 inhibitor empagliflozin reduced late-INa in cardiomyocytes from mice with heart failure and in cardiac Nav1.5 sodium channels containing the LQT3 mutations R1623Q or KPQ. Sodium 129-135 solute carrier family 5 (sodium/glucose cotransporter), member 2 Mus musculus 13-18 33832341-4 2021 Results: The SGLT2 inhibitor empagliflozin reduced late-INa in cardiomyocytes from mice with heart failure and in cardiac Nav1.5 sodium channels containing the LQT3 mutations R1623Q or KPQ. Sodium 129-135 sodium channel, voltage-gated, type V, alpha Mus musculus 122-128 33482339-4 2021 As a neutral amino acid (AA), the transport of DL-Met is facilitated by multiple apical sodium-dependent/-independent high-/low-affinity transporters such as ASCT2, B0AT1 and rBAT/b0,+AT. Sodium 88-94 solute carrier family 1 member 5 Homo sapiens 158-163 33482339-4 2021 As a neutral amino acid (AA), the transport of DL-Met is facilitated by multiple apical sodium-dependent/-independent high-/low-affinity transporters such as ASCT2, B0AT1 and rBAT/b0,+AT. Sodium 88-94 bile acid CoA:amino acid N-acyltransferase Rattus norvegicus 175-179 33690157-7 2021 Eight children had homozygous mutations in the SCNN1A and SCNN1G genes encoding the epithelial sodium channel subunits alpha and gamma, respectively, including one novel mutation. Sodium 95-101 sodium channel epithelial 1 subunit gamma Homo sapiens 58-64 33882940-9 2021 We presume that dysfunction of the ss2AdR also leads to an insufficient stimulation of the Na+/K+-ATPase causing sodium overload which reverses the transport direction of the sodium-calcium exchanger (NCX) to import calcium instead of exporting it as is also known from the ischemia-reperfusion paradigm. Sodium 113-119 T cell leukemia homeobox 2 Homo sapiens 201-204 33406509-8 2021 Sn@C@CNF anode exhibited a stable discharge specific capacity of 610.8 mAh/g under 200 mA/g for 180 cycles in lithium ion batteries (LIBs) and 360.5 mAh/g under 100 mA/g after 100 cycles in sodium ion batteries (SIBs). Sodium 190-196 NPHS1 adhesion molecule, nephrin Homo sapiens 5-8 33916525-0 2021 DNA Methylation Patterns Correlate with the Expression of SCNN1A, SCNN1B, and SCNN1G (Epithelial Sodium Channel, ENaC) Genes. Sodium 97-103 sodium channel epithelial 1 subunit gamma Homo sapiens 78-84 33124101-1 2021 Long QT syndrome type 3 (LQT-3) is a disease related to abnormal cardiac sodium channel function (Nav 1.5), usually due to augmented late sodium current (INaL), and may lead to ventricular fibrillation. Sodium 73-79 sodium channel, voltage-gated, type V, alpha Mus musculus 98-105 33124101-1 2021 Long QT syndrome type 3 (LQT-3) is a disease related to abnormal cardiac sodium channel function (Nav 1.5), usually due to augmented late sodium current (INaL), and may lead to ventricular fibrillation. Sodium 138-144 sodium channel, voltage-gated, type V, alpha Mus musculus 98-105 33369088-2 2021 SCN2A encodes for the voltage-gated sodium channel isoform 1.2 (Nav 1.2) expressed in the neurons of the central nervous system. Sodium 36-42 sodium voltage-gated channel alpha subunit 2 Homo sapiens 0-5 33369088-2 2021 SCN2A encodes for the voltage-gated sodium channel isoform 1.2 (Nav 1.2) expressed in the neurons of the central nervous system. Sodium 36-42 sodium voltage-gated channel alpha subunit 2 Homo sapiens 64-71 33460257-10 2021 In addition, RBP4 levels presented positive (r = 0.528, P < 0.01) and negative (r = -0.506, P < 0.01) associations with 24-h urinary sodium- and potassium excretion levels. Sodium 133-139 retinol binding protein 4 Homo sapiens 13-17 33227509-6 2021 Whole-cell patch-clamp recordings on cultured sensory neurons revealed that amitriptyline was a potent inhibitor of the main voltage-gated sodium channels (Nav1.7, Nav1.8 and Nav1.9) found in nociceptors. Sodium 139-145 sodium voltage-gated channel alpha subunit 9 Homo sapiens 156-162 33915942-3 2021 Missense mutations of SCN8A, which encodes Nav1.6, one of the main voltage-gated sodium channel subunits in neurons and muscles, have been linked to early infantile SCN8A encephalopathy. Sodium 81-87 sodium voltage-gated channel alpha subunit 8 Homo sapiens 22-27 33915942-3 2021 Missense mutations of SCN8A, which encodes Nav1.6, one of the main voltage-gated sodium channel subunits in neurons and muscles, have been linked to early infantile SCN8A encephalopathy. Sodium 81-87 sodium voltage-gated channel alpha subunit 8 Homo sapiens 43-49 33915942-3 2021 Missense mutations of SCN8A, which encodes Nav1.6, one of the main voltage-gated sodium channel subunits in neurons and muscles, have been linked to early infantile SCN8A encephalopathy. Sodium 81-87 sodium voltage-gated channel alpha subunit 8 Homo sapiens 165-170 33342222-10 2021 Preferential localization of NCLX to this domain allows for functional coupling where the extrusion of Ca2+ from the mitochondria is powered, at least in part, by the entry of sodium through NaV1.5 channels. Sodium 176-182 solute carrier family 8 member B1 Homo sapiens 29-33 33144140-1 2021 BACKGROUND: High sodium intake can up-regulate the level of renal serum- and glucocorticoid-inducible kinase-1 (SGK1), which plays a pivotal role in controlling blood pressure via activation of the epithelial sodium channel (ENaC), which can lead to salt-sensitive hypertension. Sodium 17-23 serum/glucocorticoid regulated kinase 1 Homo sapiens 66-110 33144140-1 2021 BACKGROUND: High sodium intake can up-regulate the level of renal serum- and glucocorticoid-inducible kinase-1 (SGK1), which plays a pivotal role in controlling blood pressure via activation of the epithelial sodium channel (ENaC), which can lead to salt-sensitive hypertension. Sodium 17-23 serum/glucocorticoid regulated kinase 1 Homo sapiens 112-116 33144140-1 2021 BACKGROUND: High sodium intake can up-regulate the level of renal serum- and glucocorticoid-inducible kinase-1 (SGK1), which plays a pivotal role in controlling blood pressure via activation of the epithelial sodium channel (ENaC), which can lead to salt-sensitive hypertension. Sodium 209-215 serum/glucocorticoid regulated kinase 1 Homo sapiens 66-110 33144140-1 2021 BACKGROUND: High sodium intake can up-regulate the level of renal serum- and glucocorticoid-inducible kinase-1 (SGK1), which plays a pivotal role in controlling blood pressure via activation of the epithelial sodium channel (ENaC), which can lead to salt-sensitive hypertension. Sodium 209-215 serum/glucocorticoid regulated kinase 1 Homo sapiens 112-116 33144140-6 2021 RESULTS: The SGK1 gene encodes a G4 structure in the proximal upstream of promoter-2; the G4 structure is stabilized by potassium or resveratrol, but destabilized by sodium. Sodium 166-172 serum/glucocorticoid regulated kinase 1 Homo sapiens 13-17 33144140-7 2021 Super-physiological levels of sodium stimulate the transcription of all SGK1 isoforms, whereas resveratrol or potassium supplementation inhibits the transcription of iso-2 and iso-3, but not iso-1. Sodium 30-36 serum/glucocorticoid regulated kinase 1 Homo sapiens 72-76 32917465-13 2021 CONCLUSIONS: Sodium channel blockers are effective in seizure control in these patients with KCNQ2 encephalopathy. Sodium 13-19 potassium voltage-gated channel subfamily Q member 2 Homo sapiens 93-98 32956652-0 2021 The sodium/proton exchanger NHA2 regulates blood pressure through a WNK4-NCC dependent pathway in the kidney. Sodium 4-10 solute carrier family 9, subfamily B (NHA2, cation proton antiporter 2), member 2 Mus musculus 28-32 32970203-1 2021 Mutations within the SCN11A gene which encodes the voltage-gated sodium channel NaV1.9 mainly expressed in small fiber sensory neurons have been associated with neuropathic disorders; however, suitable medications have not been fully investigated. Sodium 65-71 sodium channel, voltage-gated, type XI, alpha Mus musculus 21-27 32970203-1 2021 Mutations within the SCN11A gene which encodes the voltage-gated sodium channel NaV1.9 mainly expressed in small fiber sensory neurons have been associated with neuropathic disorders; however, suitable medications have not been fully investigated. Sodium 65-71 sodium channel, voltage-gated, type XI, alpha Mus musculus 80-86 33534341-1 2021 OBJECTIVE: We have previously reported that renal medullary sphingosine-1-phosphate (S1P) regulates sodium excretion via the S1P type-1 receptor (S1PR1). Sodium 100-106 sphingosine-1-phosphate receptor 1 Homo sapiens 146-151 33842883-2 2021 Here, we focussed on correcting metabolic defects in a catastrophic paediatric epilepsy, Dravet syndrome which is caused by mutations in sodium channel NaV1.1 gene, SCN1A. Sodium 137-143 sodium channel, voltage-gated, type I-like, alpha Danio rerio 165-170 33410337-9 2021 An increased sodium conductance (up to 200%) was robustly accompanied by an increase in conduction velocity (26%), a reduction in action potential duration 90 (28%), and PWD (22%). Sodium 13-19 ATPase copper transporting beta Homo sapiens 170-173 33435938-11 2021 With RNAseq transcriptomic analysis of the expression profiling from the muscle specimens, it surprisingly discloses large downregulation of genes involved in pathways of sodium, potassium, and calcium channels, which can be rescued by L-carnitine treatment, fatty acid metabolism was differentially dysregulated in TPM3(E151G) fish and rescued by L-carnitine treatment. Sodium 171-177 tropomyosin 3 Homo sapiens 316-320 33130390-2 2021 MfVIA is a member of the muO-conotoxin family, and acts as an inhibitor of subtype 1.8 voltage-gated sodium ion channels (NaV1.8). Sodium 101-107 sodium voltage-gated channel alpha subunit 10 Homo sapiens 122-128 33361158-0 2021 Phosphorylation of a chronic pain mutation in the voltage-gated sodium channel Nav1.7 increases voltage sensitivity. Sodium 64-70 sodium voltage-gated channel alpha subunit 9 Homo sapiens 79-85 33362546-0 2020 Melatonin Attenuates Sepsis-Induced Acute Lung Injury Through Improvement of Epithelial Sodium Channel-Mediated Alveolar Fluid Clearance Via Activation of SIRT1/SGK1/Nedd4-2 Signaling Pathway. Sodium 88-94 sirtuin 1 Homo sapiens 155-160 33362546-0 2020 Melatonin Attenuates Sepsis-Induced Acute Lung Injury Through Improvement of Epithelial Sodium Channel-Mediated Alveolar Fluid Clearance Via Activation of SIRT1/SGK1/Nedd4-2 Signaling Pathway. Sodium 88-94 serum/glucocorticoid regulated kinase 1 Homo sapiens 161-165 33362546-0 2020 Melatonin Attenuates Sepsis-Induced Acute Lung Injury Through Improvement of Epithelial Sodium Channel-Mediated Alveolar Fluid Clearance Via Activation of SIRT1/SGK1/Nedd4-2 Signaling Pathway. Sodium 88-94 NEDD4 like E3 ubiquitin protein ligase Homo sapiens 166-173 33055303-1 2020 Objective: Iodide transport across thyrocytes constitutes a critical step for thyroid hormone biosynthesis, mediated mainly by the basolateral sodium-iodide-symporter (NIS (SLC5A5)) and the apical anion exchanger pendrin (PDS (SLC26A4)). Sodium 143-149 solute carrier family 26 member 4 Homo sapiens 213-220 33055303-1 2020 Objective: Iodide transport across thyrocytes constitutes a critical step for thyroid hormone biosynthesis, mediated mainly by the basolateral sodium-iodide-symporter (NIS (SLC5A5)) and the apical anion exchanger pendrin (PDS (SLC26A4)). Sodium 143-149 solute carrier family 26 member 4 Homo sapiens 227-234 33110213-4 2020 Voltage-gated sodium (NaV) channels drive neuronal excitability and three subtypes - NaV1.7, NaV1.8 and NaV1.9 - are preferentially expressed in the peripheral nervous system, suggesting that their inhibition might treat pain while avoiding central and cardiac adverse effects. Sodium 14-20 sodium voltage-gated channel alpha subunit 9 Homo sapiens 85-91 33110213-4 2020 Voltage-gated sodium (NaV) channels drive neuronal excitability and three subtypes - NaV1.7, NaV1.8 and NaV1.9 - are preferentially expressed in the peripheral nervous system, suggesting that their inhibition might treat pain while avoiding central and cardiac adverse effects. Sodium 14-20 sodium voltage-gated channel alpha subunit 10 Homo sapiens 93-99 33078551-0 2020 Salvianic Acid A Sodium Promotes the Recovery of Motor Function After Spinal Cord Injury in Rats by Reducing Microglia Inflammation through Regulating MIP2/Vdac1/Ndufa12 Signaling Axis. Sodium 17-23 voltage-dependent anion channel 1 Rattus norvegicus 156-161 32948286-3 2020 The voltage gated sodium channels contain a calmodulin (CaM)-binding IQ domain involved in channel slow inactivation, we here investigated the role of CaM regulation of Nav1.8 channel function, and showed that CaM enhanced slow inactivation of the Nav1.8 channel and hyperpolarized steady-state inactivation curve of sodium currents. Sodium 18-24 sodium voltage-gated channel alpha subunit 10 Homo sapiens 169-175 32948286-3 2020 The voltage gated sodium channels contain a calmodulin (CaM)-binding IQ domain involved in channel slow inactivation, we here investigated the role of CaM regulation of Nav1.8 channel function, and showed that CaM enhanced slow inactivation of the Nav1.8 channel and hyperpolarized steady-state inactivation curve of sodium currents. Sodium 18-24 sodium voltage-gated channel alpha subunit 10 Homo sapiens 248-254 32948286-3 2020 The voltage gated sodium channels contain a calmodulin (CaM)-binding IQ domain involved in channel slow inactivation, we here investigated the role of CaM regulation of Nav1.8 channel function, and showed that CaM enhanced slow inactivation of the Nav1.8 channel and hyperpolarized steady-state inactivation curve of sodium currents. Sodium 317-323 sodium voltage-gated channel alpha subunit 10 Homo sapiens 169-175 33203861-0 2020 Structure of the human sodium leak channel NALCN in complex with FAM155A. Sodium 23-29 NALCN channel auxiliary factor 1 Homo sapiens 65-72 33006369-11 2020 These effects were associated with renal upregulations of the oxalate transporter solute carrier family 26 (Slc26)a6 and citrate transporter sodium-dependent dicarboxylate cotransporter-1 (NaDC-1) but not Slc26a2. Sodium 141-147 solute carrier family 13 member 2 Rattus norvegicus 189-195 33023152-1 2020 Voltage-gated sodium (NaV) channel subtypes, including NaV1.7, are promising targets for the treatment of neurological diseases, such as chronic pain. Sodium 14-20 sodium voltage-gated channel alpha subunit 9 Homo sapiens 55-61 33023071-1 2020 The ENA ATPases (from exitus natru: the exit of sodium) belonging to the P-type ATPases are structurally very similar to the sarco/endoplasmic reticulum Ca2+-ATPase (SERCA); they exchange Na+ for H+ and, therefore, are also known as Na+-ATPases. Sodium 48-54 ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 3 Homo sapiens 125-164 32386467-1 2020 AIM: The voltage-gated sodium channel NaV 1.5, encoded by SCN5A, is essential for cardiac excitability and ensures proper electrical conduction. Sodium 23-29 sodium channel, voltage-gated, type V, alpha Mus musculus 58-63 32386467-4 2020 METHODS: Involvement of NaV 1.5-generated INa in murine cardiac electrical function was assessed by optical mapping in wild type embryos (Embryonic day (E)9.5 and E10.5) in the absence and presence of the sodium channel blocker tetrodotoxin (30 microM). Sodium 205-211 sodium channel, voltage-gated, type V, alpha Mus musculus 24-31 32893663-1 2020 Inhibitors of the proximal tubular sodium glucose cotransporter SGLT2 are natriuretic and they lower blood pressure. Sodium 35-41 solute carrier family 5 (sodium/glucose cotransporter), member 2 Mus musculus 64-69 32773689-4 2020 METHODS: The contribution of sodium leak channels to isoflurane-, sevoflurane-, and propofol-evoked activity of Phox2b-expressing retrotrapezoid nucleus neurons and respiratory output were evaluated in wild-type and genetically modified mice lacking sodium leak channels (both sexes). Sodium 29-35 paired-like homeobox 2b Mus musculus 112-118 32773689-8 2020 At these concentrations, isoflurane increased activity of Phox2b-expressing retrotrapezoid nucleus neurons from 1.1 +- 0.2 to 2.8 +- 0.2 Hz (P < 0.001, n = 5), which was eliminated by bath application of gadolinium or genetic silencing of sodium leak channel. Sodium 239-245 paired-like homeobox 2b Mus musculus 58-64 32663327-0 2020 Uncoupling sodium channel dimers rescues the phenotype of a pain-linked Nav1.7 mutation. Sodium 11-17 sodium voltage-gated channel alpha subunit 9 Homo sapiens 72-78 32663327-1 2020 BACKGROUND & PURPOSE: The voltage-gated sodium channel Nav1.7 is essential for adequate perception of painful stimuli. Sodium 40-46 sodium voltage-gated channel alpha subunit 9 Homo sapiens 55-61 33000761-1 2020 AIMS: We aimed to delineate the phenotypic spectrum of SCN2A-related developmental and epileptic encephalopathy (DEE) and determine the effectiveness of various treatment modalities, including sodium channel blockers and the ketogenic diet. Sodium 193-199 sodium voltage-gated channel alpha subunit 2 Homo sapiens 55-60 32778883-0 2020 Functional modulation of atrio-ventricular conduction by enhanced late sodium current and calcium-dependent mechanisms in Scn5a1798insD/+ mice. Sodium 71-77 sodium channel, voltage-gated, type V, alpha Mus musculus 122-127 32799394-2 2020 The NOX4-dependent pathway regulates many factors essential for proper sodium handling in the distal nephron. Sodium 71-77 NADPH oxidase 4 Rattus norvegicus 4-8 32799394-9 2020 These data emphasize a critical contribution of the NOX4-mediated pathway in maladaptive upregulation of ENaC-mediated sodium reabsorption in the distal nephron in the conditions of HS- and hyperglycemia-induced kidney injury. Sodium 119-125 NADPH oxidase 4 Rattus norvegicus 52-56 32699180-0 2020 Dietary sodium restriction decreases urinary NGAL in older adults with moderately elevated systolic blood pressure free from chronic kidney disease. Sodium 8-14 lipocalin 2 Homo sapiens 45-49 32897040-7 2020 Of the 57 patients, one patient without small-fibre pathology and 2 patients with small-fibre pathology had rare variants of voltage-gated sodium channels, namely SCN11A, SCN9A, and SCN1A variants. Sodium 139-145 sodium voltage-gated channel alpha subunit 9 Homo sapiens 171-176 32893499-0 2020 Anchoring SnS2 on TiC/C Backbone to Promote Sodium Ion Storage by Phosphate Ion Doping. Sodium 44-50 aryl hydrocarbon receptor nuclear translocator like Homo sapiens 18-21 32750235-1 2020 OBJECTIVE: We identified a novel de novo SCN2A variant (M1879T) associated with infantile-onset epilepsy that responded dramatically to sodium channel blocker antiepileptic drugs. Sodium 136-142 sodium voltage-gated channel alpha subunit 2 Homo sapiens 41-46 32788559-8 2020 Of those, four compounds inhibited sodium currents in Nav1.7-expressing human embryonic kidney 293 cells by 29% or greater (P < 0.05). Sodium 35-41 sodium voltage-gated channel alpha subunit 9 Homo sapiens 54-60 32701600-5 2020 Reabsorption of about 66% of sodium is accomplished in the proximal tubule and dependent on the sodium-hydrogen exchanger isoform 3 (NHE3). Sodium 29-35 solute carrier family 9 member A3 Homo sapiens 133-137 32701600-5 2020 Reabsorption of about 66% of sodium is accomplished in the proximal tubule and dependent on the sodium-hydrogen exchanger isoform 3 (NHE3). Sodium 96-102 solute carrier family 9 member A3 Homo sapiens 133-137 32653991-7 2020 This review explores the novel therapeutic concept of inhibiting the sole ileal bile acid transporter (IBAT), also known as ASBT (apical sodium-bile acid transporter, encoded by SLC10A2), as a means to reduce hepatic bile acid concentration after KPE. Sodium 137-143 solute carrier family 10 member 2 Homo sapiens 103-107 32653991-7 2020 This review explores the novel therapeutic concept of inhibiting the sole ileal bile acid transporter (IBAT), also known as ASBT (apical sodium-bile acid transporter, encoded by SLC10A2), as a means to reduce hepatic bile acid concentration after KPE. Sodium 137-143 solute carrier family 10 member 2 Homo sapiens 124-128 32653991-7 2020 This review explores the novel therapeutic concept of inhibiting the sole ileal bile acid transporter (IBAT), also known as ASBT (apical sodium-bile acid transporter, encoded by SLC10A2), as a means to reduce hepatic bile acid concentration after KPE. Sodium 137-143 solute carrier family 10 member 2 Homo sapiens 178-185 32506135-12 2020 Sodium supplementation reduced FGF23, but this was accompanied by decrease in phosphate and increase in fractional calcium excretion. Sodium 0-6 fibroblast growth factor 23 Homo sapiens 31-36 32868758-12 2020 Our results thus show that the ionic environment typical in SLT impairs IL-17 immunity, but the intracellular pathways that mediate salt-driven Th17 polarisation are intact and in vitro IL-17 responses can be reinvigorated by increasing extracellular sodium concentration. Sodium 251-257 interleukin 17A Homo sapiens 186-191 32983053-0 2020 Sodium New Houttuyfonate Inhibits Candida albicans Biofilm Formation by Inhibiting the Ras1-cAMP-Efg1 Pathway Revealed by RNA-seq. Sodium 0-6 Ras family GTPase RAS1 Saccharomyces cerevisiae S288C 87-91 32983053-0 2020 Sodium New Houttuyfonate Inhibits Candida albicans Biofilm Formation by Inhibiting the Ras1-cAMP-Efg1 Pathway Revealed by RNA-seq. Sodium 0-6 Efg1p Saccharomyces cerevisiae S288C 97-101 32824960-7 2020 Taken together, these two novel peptide toxins act as potent and sustained NaV1.7 blockers and may have potential in the pharmacological study of sodium channels. Sodium 146-152 sodium voltage-gated channel alpha subunit 9 Homo sapiens 75-81 32611770-0 2020 CaMKII enhances voltage-gated sodium channel Nav1.6 activity and neuronal excitability. Sodium 30-36 sodium voltage-gated channel alpha subunit 8 Homo sapiens 45-51 32611770-1 2020 Nav1.6 is the primary voltage-gated sodium channel isoform expressed in mature axon initial segments and nodes, making it critical for initiation and propagation of neuronal impulses. Sodium 36-42 sodium voltage-gated channel alpha subunit 8 Homo sapiens 0-6 32678707-2 2020 We previously demonstrated that varying perfusate sodium (Na+) and calcium (Ca2+) attenuates conduction slowing and arrhythmias during simulated ischemia with continuous perfusion. Sodium 50-56 LOW QUALITY PROTEIN: carbonic anhydrase 2 Cavia porcellus 76-79 31828722-3 2020 The present results indicated that sodium fluoride (NaF) exposure to adult male golden hamsters severely impairs reproductive physiology as evident from markedly reduced sperm count/viability, testosterone level, androgen receptor (AR), testicular glucose transporter (GLUT-1), gap junction (connexin-43), and survival (Bcl-2) protein expression. Sodium 52-55 androgen receptor Mesocricetus auratus 213-230 31828722-3 2020 The present results indicated that sodium fluoride (NaF) exposure to adult male golden hamsters severely impairs reproductive physiology as evident from markedly reduced sperm count/viability, testosterone level, androgen receptor (AR), testicular glucose transporter (GLUT-1), gap junction (connexin-43), and survival (Bcl-2) protein expression. Sodium 52-55 androgen receptor Mesocricetus auratus 232-234 32480218-10 2020 Parabens are blockers of hNaV1.2 channels, sharing the mechanism of action of most of sodium channel blocking antiseizure drugs. Sodium 86-92 sodium voltage-gated channel alpha subunit 2 Homo sapiens 25-32 32574916-3 2020 Here, we report the characterization of an Arabidopsis salt-tolerant mutant est1 with significantly reduced sodium content and higher Na+/H+ antiporter activity after NaCl treatment compared to the wild-type. Sodium 108-114 multidrug resistance-associated protein 1 Arabidopsis thaliana 76-80 32760780-4 2020 As part of the ingested food, salt is absorbed in the gastrointestinal tract by the sodium proton exchanger subtype 3 (NHE3 also known as Slc9a3), influencing extracellular fluid volume and blood pressure. Sodium 84-90 solute carrier family 9 member A3 Homo sapiens 119-123 32760780-4 2020 As part of the ingested food, salt is absorbed in the gastrointestinal tract by the sodium proton exchanger subtype 3 (NHE3 also known as Slc9a3), influencing extracellular fluid volume and blood pressure. Sodium 84-90 solute carrier family 9 member A3 Homo sapiens 138-144 32760780-5 2020 In this review, we discuss the beneficial effects of pharmacological inhibition of NHE3-mediated sodium absorption in the gut and focus on the effect on blood pressure and end-organ damage. Sodium 97-103 solute carrier family 9 member A3 Homo sapiens 83-87 32686994-3 2021 Sodium channels particularly Nav1.7, Nav1.8, Nav 1.9 are key stake holders in the peripheral neuropathy, activation of these sodium channels might lead to genesis and propagation. Sodium 0-6 sodium voltage-gated channel alpha subunit 9 Homo sapiens 29-35 32686994-3 2021 Sodium channels particularly Nav1.7, Nav1.8, Nav 1.9 are key stake holders in the peripheral neuropathy, activation of these sodium channels might lead to genesis and propagation. Sodium 0-6 sodium voltage-gated channel alpha subunit 10 Homo sapiens 37-43 32686994-3 2021 Sodium channels particularly Nav1.7, Nav1.8, Nav 1.9 are key stake holders in the peripheral neuropathy, activation of these sodium channels might lead to genesis and propagation. Sodium 125-131 sodium voltage-gated channel alpha subunit 9 Homo sapiens 29-35 32686994-3 2021 Sodium channels particularly Nav1.7, Nav1.8, Nav 1.9 are key stake holders in the peripheral neuropathy, activation of these sodium channels might lead to genesis and propagation. Sodium 125-131 sodium voltage-gated channel alpha subunit 10 Homo sapiens 37-43 32678535-14 2020 Fourth, the sodium-glucose cotransporter (SGLT1) was increased by acid loading in the KO kidney, but not the WT. Sodium 12-18 solute carrier family 5 (sodium/glucose cotransporter), member 1 Mus musculus 42-47 32745434-1 2020 Using parametric conversion induced by a Shapiro-type resonance, we produce and characterize a two-mode squeezed vacuum state in a sodium spin 1 Bose-Einstein condensate. Sodium 131-137 spindlin 1 Homo sapiens 138-144 32774738-2 2020 Our study aim to investigate the underlying mechanism by which IP3R1 signaling mediates the process of homocysteine (Hcy)-induced Ca2+ accumulation via interaction with sodium current (Nav1.5) in atrium. Sodium 169-175 sodium channel, voltage-gated, type V, alpha Mus musculus 185-191 32733894-1 2020 ASCT2 is a neutral amino acid transporter, which catalyzes a sodium-dependent obligatory antiport among glutamine and other neutral amino acids. Sodium 61-67 solute carrier family 1 member 5 Homo sapiens 0-5 32733894-3 2020 The experimental data highlighted that hASCT2 also catalyzes a sodium-dependent antiport of glutamate with glutamine. Sodium 63-69 solute carrier family 1 member 5 Homo sapiens 39-45 32345129-12 2020 Importantly, the expression of the sodium channel protein NaV1.5 was altered in AV nodal cells of the ZO-1cKO vs. CTL. Sodium 35-41 sodium channel, voltage-gated, type V, alpha Mus musculus 58-64 32612224-5 2020 Here we show, using atomic-scale quantitative imaging and correlative spectroscopies, that the nanoscale crystallites of hydroxylapatite (Ca5(PO4)3(OH)), which are the fundamental building blocks of enamel, comprise two nanometric layers enriched in magnesium flanking a core rich in sodium, fluoride and carbonate ions; this sandwich core is surrounded by a shell with lower concentration of substitutional defects. Sodium 284-290 carbonic anhydrase 5A Homo sapiens 138-147 32421318-2 2020 Herein, we aimed to build machine learning models for screening and design of potent and effective NaV1.7 sodium channel inhibitors. Sodium 106-112 sodium voltage-gated channel alpha subunit 9 Homo sapiens 99-105 32550094-2 2020 Due to sodium channel mutations in the cardiac membrane, most commonly SCN5A and SCN10A, the heart can be triggered into a fatal arrhythmia. Sodium 7-13 sodium voltage-gated channel alpha subunit 10 Homo sapiens 81-87 32112796-8 2020 Intestinal tissues and derived enteroids from MYO5B(P663L) piglets had reduced apical levels and diffuse sub-apical levels of NHE3 and SGLT1, which regulate transport of sodium, glucose, and water, compared with tissues from control piglets. Sodium 170-176 solute carrier family 9 member A3 Sus scrofa 126-130 32292096-1 2020 The voltage-gated sodium channel Nav1.7 is a genetically validated target for pain; pharmacological blockers are promising as a new class of nonaddictive therapeutics. Sodium 18-24 sodium voltage-gated channel alpha subunit 9 Homo sapiens 33-39 32564678-7 2020 The blood levels of sodium (Na+), iron (Fe2+), and calcium (Ca2+) were decreased in Gp3, Gp4, and Gp5 due to the chelating effects of EDTA. Sodium 20-26 glycoprotein 5 (platelet) Mus musculus 98-101 32167513-4 2020 The FeCo@C@MoS2 electrode displays high reversible capacities of 380 mA h g-1 and 147 mA h g-1 at 500 mA g-1 for sodium and potassium storage, respectively. Sodium 113-119 proline rich protein BstNI subfamily 3 Homo sapiens 74-108 32374315-4 2020 The obtained VN/CNF composite anode exhibited excellent half/full sodium and potassium storage performance. Sodium 66-72 NPHS1 adhesion molecule, nephrin Homo sapiens 16-19 32315024-5 2020 Western blot analysis and patch-clamping recordings showed that overexpression of UBE1 or UBA6 increased ubiquitination of Nav1.5 and significantly reduced Nav1.5 expression and sodium current density, and knockdown of UBE1 or UBA6 expression significantly increased Nav1.5 expression and sodium current density in HEK293/Nav1.5 cells. Sodium 178-184 ubiquitin like modifier activating enzyme 6 Homo sapiens 90-94 32315024-5 2020 Western blot analysis and patch-clamping recordings showed that overexpression of UBE1 or UBA6 increased ubiquitination of Nav1.5 and significantly reduced Nav1.5 expression and sodium current density, and knockdown of UBE1 or UBA6 expression significantly increased Nav1.5 expression and sodium current density in HEK293/Nav1.5 cells. Sodium 289-295 ubiquitin like modifier activating enzyme 6 Homo sapiens 90-94 32315024-8 2020 Mutations of K590 and K591 to K590A and K591A abolished the effects of overexpression or knockdown of UBE1 or UBA6 on Nav1.5 expression and sodium current density. Sodium 140-146 ubiquitin like modifier activating enzyme 6 Homo sapiens 110-114 32407401-1 2020 Myotonia congenita and hypokalemic periodic paralysis type 2 are both rare genetic channelopathies caused by mutations in the CLCN1 gene encoding voltage-gated chloride channel CLC-1 and the SCN4A gene encoding voltage-gated sodium channel Nav1.4. Sodium 225-231 chloride voltage-gated channel 1 Homo sapiens 126-131 31900739-0 2020 Dietary potassium restriction attenuates urinary sodium wasting in the generalized form of pseudohypoaldosteronism type 1. Sodium 49-55 sodium channel epithelial 1 subunit gamma Homo sapiens 91-121 31900739-1 2020 Owing to its rarity and severe nature, the treatment for generalized pseudohypoaldosteronism type 1 (PHA1), a genetic disorder in the epithelial sodium channel (ENaC), is exclusively experience-based. Sodium 145-151 sodium channel epithelial 1 subunit gamma Homo sapiens 69-99 31900739-1 2020 Owing to its rarity and severe nature, the treatment for generalized pseudohypoaldosteronism type 1 (PHA1), a genetic disorder in the epithelial sodium channel (ENaC), is exclusively experience-based. Sodium 145-151 sodium channel epithelial 1 subunit gamma Homo sapiens 101-105 32045596-4 2020 Using chromatin immunoprecipitation (CHIP), we verified the interaction of TCF4 and sodium voltage-gated channel alpha subunit 10A (SCN10A) enhancer in HEK293 cells and rat DRG neurons. Sodium 84-90 sodium voltage-gated channel alpha subunit 10 Homo sapiens 132-138 31635654-5 2020 In conclusion, O-2 is the main active oxidative species in the Bi2WO6/NaBiO3 nanocomposite. Sodium 70-76 immunoglobulin kappa variable 1D-39 Homo sapiens 15-18 32431783-9 2020 Furthermore, the study of human tissue demonstrates an inverse expression of sodium channel isoforms; reduction of Nav1.5 and increase of Nav1.8 in both heart failure and ventricular hypertrophy. Sodium 77-83 sodium voltage-gated channel alpha subunit 10 Homo sapiens 138-144 32295642-1 2020 BACKGROUND: Sodium channels located in the dorsal root ganglion, particularly Nav1.7 and Nav1.8, encoded by SCN9A and SCN10A, respectively, act as molecular gatekeepers for pain detection. Sodium 12-18 sodium voltage-gated channel alpha subunit 9 Homo sapiens 108-113 32295642-1 2020 BACKGROUND: Sodium channels located in the dorsal root ganglion, particularly Nav1.7 and Nav1.8, encoded by SCN9A and SCN10A, respectively, act as molecular gatekeepers for pain detection. Sodium 12-18 sodium voltage-gated channel alpha subunit 10 Homo sapiens 118-124 31954305-8 2020 SNP/NaHS under stress increased activation of superoxide dismutase (SOD), peroxidase (POX), APX, glutathione reductase (GR), monodehydroascorbate reductase (MDHAR), dehydroascorbate reductase (DHAR), ascorbate (tAsA) and glutathione (GSH). Sodium 4-8 probable glutathione S-transferase DHAR1, cytosolic Triticum aestivum 129-155 31954305-8 2020 SNP/NaHS under stress increased activation of superoxide dismutase (SOD), peroxidase (POX), APX, glutathione reductase (GR), monodehydroascorbate reductase (MDHAR), dehydroascorbate reductase (DHAR), ascorbate (tAsA) and glutathione (GSH). Sodium 4-8 probable glutathione S-transferase DHAR1, cytosolic Triticum aestivum 158-162 31758704-10 2020 Inhibition of ER stress or sEH could upregulate the expression of D1R, decrease the activity of Na+ /K+ -ATPase, increase sodium excretion, and lower BP in SKI mice. Sodium 122-128 epoxide hydrolase 2, cytoplasmic Mus musculus 27-30 31758704-12 2020 Our study highlights the importance of C674 redox status in BP control and the contribution of SERCA2 to sodium homeostasis and BP in the kidney. Sodium 105-111 ATPase, Ca++ transporting, cardiac muscle, slow twitch 2 Mus musculus 95-101 31967738-11 2020 Cox hazard analysis indicated that elevated CT-IGFBP-4 was independently associated with 1 year mortality (hazard ratio 3.26, P = 0.0008) after adjustment for age, gender, history of previous heart failure, coronary artery disease, hypertension, chronic kidney failure, history of diabetes, heart rate, haemoglobin, plasma sodium, NT-proBNP, CRP, cystatin C, and elevated cardiac troponin I or T. Patients with increased levels of either two or three of the biomarkers CT-IGFBP-4, NT-proBNP, and CRP had significantly higher mortality risk (adjusted hazard ratio 10.04, P < 0.0001) than patients with increased levels of one or none of the biomarkers. Sodium 323-329 insulin like growth factor binding protein 4 Homo sapiens 44-54 31605437-1 2020 Mutations in the voltage-gated sodium channel gene SCN8A cause a broad range of human diseases, including epilepsy, intellectual disability, and ataxia. Sodium 31-37 sodium voltage-gated channel alpha subunit 8 Homo sapiens 51-56 31771816-5 2020 NaHS significantly increased the expressions of tight junction proteins (i.e., ZO-1, Occludin and claudin-1), and reduced apoptosis and secretion of pro-inflammatory cytokines (i.e., TNF-alpha, IL-6 and IL-1beta) in CS-exposed mouse lungs and CSE-incubated A549 cells, indicating H2S inhibits CS-induced inflammation, injury and apoptosis in alveolar epithelial cells. Sodium 0-4 claudin 1 Mus musculus 98-107 31771816-7 2020 Moreover, NaHS inhibited CS-induced phosphorylation of ERK, JNK and p38 MAPK in vivo and in vitro, and treatment with their inhibitors reversed CSE-induced ZO-1 expression and inflammation in A549 cells. Sodium 10-14 mitogen-activated protein kinase 8 Mus musculus 60-63 31900034-3 2020 This study aimed to investigate the potential mechanism of diarrhea after pelvic radiotherapy in rats based on the effect of radiation on bile acid homeostasis and sodium-dependent bile acid transporter (Asbt).Methods In this experimental study, male Sprague-Dawley rats were divided into the following groups - pelvic irradiation, cholestyramine-concurrent radiation, and control groups. Sodium 164-170 solute carrier family 10 member 2 Rattus norvegicus 204-208 32025761-1 2020 Human sodium-independent glucose cotransporter 1 (hGLUT1) has been studied for its tetramerization and multimerization at the cell surface. Sodium 6-12 solute carrier family 2 member 1 Homo sapiens 50-56 32053379-2 2020 In 1.0 mol dm-3 NaBD4 aqueous solutions, about 5.6 +- 1.6 water molecules bond to BD4- via tetrahedral edges or tetrahedral corners without a very specific hydration geometry; that is, each hydrogen atom of BD4- bonds to 2.2 +- 1.0 water molecules through dihydrogen bonds with the D(B) D(W) distance of 1.95 A. Sodium 16-21 defensin beta 104A Homo sapiens 82-85 31995133-2 2020 Some forms of early-onset epileptic encephalopathy (EOEE) have been associated with variants in SCN2A, which encodes the brain voltage-gated sodium channel NaV1.2. Sodium 141-147 sodium voltage-gated channel alpha subunit 2 Homo sapiens 96-101 31995133-2 2020 Some forms of early-onset epileptic encephalopathy (EOEE) have been associated with variants in SCN2A, which encodes the brain voltage-gated sodium channel NaV1.2. Sodium 141-147 sodium voltage-gated channel alpha subunit 2 Homo sapiens 156-162 31995133-3 2020 Many voltage-gated sodium channel genes, including SCN2A, undergo developmentally regulated mRNA splicing. Sodium 19-25 sodium voltage-gated channel alpha subunit 2 Homo sapiens 51-56 31984791-2 2020 NHERF1 is involved in the regulation of the sodium hydrogen exchanger 3 (NHE3), the sodium dependent phosphate transporter 2a (Npt2a), and the sodium potassium ATPase through its ability to scaffold these transporters to the plasma membrane, allowing regulation of these protein complexes with their associated hormone receptors. Sodium 44-50 solute carrier family 9 member A3 Homo sapiens 73-77 32011655-2 2020 Gain-of-function mutations of voltage-gated sodium channel Nav1.7 underlie dorsal root ganglion neuronal hyperexcitability and pain in a subset of patients with small fibre neuropathy. Sodium 44-50 sodium voltage-gated channel alpha subunit 9 Homo sapiens 59-65 32011655-5 2020 We show that, at the clinically achievable concentration of 30 muM, lacosamide acts as a potent sodium channel inhibitor of Nav1.7 variants carried by responsive patients, via a hyperpolarizing shift of voltage-dependence of both fast and slow inactivation and enhancement of use-dependent inhibition. Sodium 96-102 sodium voltage-gated channel alpha subunit 9 Homo sapiens 124-130 31704455-1 2020 We report a novel chiral interface based on polysaccharides that was integrated via an amidation reaction between the COOH of sodium alginate and the NH2 of chitosan to form a chiral selector (SA-CS) with three dimensional N-doped graphene-CNT (NGC) as the substrate material. Sodium 126-132 sacsin molecular chaperone Homo sapiens 193-198 31908037-7 2020 Paradoxically, CTRP1-deficient mice had elevated urinary sodium and potassium excretion, partially resulting from reduced expression of genes involved in renal sodium and potassium reabsorption. Sodium 57-63 C1q and tumor necrosis factor related protein 1 Mus musculus 15-20 31908037-7 2020 Paradoxically, CTRP1-deficient mice had elevated urinary sodium and potassium excretion, partially resulting from reduced expression of genes involved in renal sodium and potassium reabsorption. Sodium 160-166 C1q and tumor necrosis factor related protein 1 Mus musculus 15-20 30345606-8 2020 Our results indicate that a sodium channel consisting, at minimum, of ppk25, ppk29 and ppk23, can sense 7,11-HD, most likely as a receptor. Sodium 28-34 pickpocket 23 Drosophila melanogaster 87-92 31851560-1 2020 Gain-of-function variants in voltage-gated sodium channel NaV1.7 that increase firing frequency and spontaneous firing of dorsal root ganglion (DRG) neurons have recently been identified in 5-10% of patients with idiopathic small fiber neuropathy (I-SFN). Sodium 43-49 sodium voltage-gated channel alpha subunit 9 Homo sapiens 58-64 31714456-12 2020 Sweat sodium losses were 0.64 +- 0.34 and 0.32 +- 0.18 g h for P1 and P2, and 0.83 +- 0.38 g during the game. Sodium 6-12 crystallin gamma F, pseudogene Homo sapiens 63-72 31820315-12 2020 Moreover, NaAsO2 triggered apoptosis in the liver by upregulating Bax and caspase-3 and downregulating Bcl-2. Sodium 10-16 BCL2-associated X protein Mus musculus 66-69 31820315-12 2020 Moreover, NaAsO2 triggered apoptosis in the liver by upregulating Bax and caspase-3 and downregulating Bcl-2. Sodium 10-16 caspase 3 Mus musculus 74-83 31931893-0 2020 Super-Resolution Imaging Using a Novel High-Fidelity Antibody Reveals Close Association of the Neuronal Sodium Channel NaV1.6 with Ryanodine Receptors in Cardiac Muscle. Sodium 104-110 sodium voltage-gated channel alpha subunit 8 Homo sapiens 119-125 31931893-1 2020 The voltage-gated sodium channel [pore-forming subunit of the neuronal voltage-gated sodium channel (NaV1.6)] has recently been found in cardiac myocytes. Sodium 18-24 sodium voltage-gated channel alpha subunit 8 Homo sapiens 101-107 31931893-1 2020 The voltage-gated sodium channel [pore-forming subunit of the neuronal voltage-gated sodium channel (NaV1.6)] has recently been found in cardiac myocytes. Sodium 85-91 sodium voltage-gated channel alpha subunit 8 Homo sapiens 101-107 31931893-5 2020 We developed and validated a novel rabbit polyclonal antibody against a C-terminal epitope on the neuronal sodium channel 1.6 (NaV1.6). Sodium 107-113 sodium voltage-gated channel alpha subunit 8 Homo sapiens 127-133 32026654-0 2020 Role of sodium-dependent Pi transporter/Npt2c on Pi homeostasis in klotho knockout mice different properties between juvenile and adult stages. Sodium 8-14 klotho Mus musculus 67-73 31871053-0 2020 Comprehensive engineering of the tarantula venom peptide huwentoxin-IV to inhibit the human voltage-gated sodium channel hNav17. Sodium 106-112 sodium voltage-gated channel alpha subunit 9 Homo sapiens 121-127 31871053-2 2020 In humans, functional loss of the voltage-gated sodium channel Nav1.7 leads to pain insensitivity without deficits in the central nervous system. Sodium 48-54 sodium voltage-gated channel alpha subunit 9 Homo sapiens 63-69 32038177-3 2020 KCNT1 and KCNT2 respectively encode the KNa1.1 (Slack) and KNa1.2 (Slick) subunits of the sodium-dependent voltage-gated potassium channel KNa. Sodium 90-96 potassium sodium-activated channel subfamily T member 2 Homo sapiens 10-15 31790574-0 2020 Enzymatic ligation of a pore blocker toxin and gating modifier toxin; creating double-knotted peptides with improved sodium channel NaV1.7 inhibition. Sodium 117-123 sodium voltage-gated channel alpha subunit 9 Homo sapiens 132-138 31790574-1 2020 Disulfide-rich animal venom peptides targeting either the voltage-sensing domain or the pore domain of voltage-gated sodium channel 1.7 (NaV1.7) have been widely studied as drug leads and pharmacological probes for the treatment of chronic pain. Sodium 117-123 sodium voltage-gated channel alpha subunit 9 Homo sapiens 137-143 31594586-2 2020 The thrombin aptamer1-functionalized magnetic sodium alginate (Malg-Apt1) hydrogel was synthesized by physical interaction between sodium alginate and Ca2+, and it was used in the biosensor for separating and enriching thrombin. Sodium 46-52 lysophospholipase 1 Homo sapiens 68-72 31594586-2 2020 The thrombin aptamer1-functionalized magnetic sodium alginate (Malg-Apt1) hydrogel was synthesized by physical interaction between sodium alginate and Ca2+, and it was used in the biosensor for separating and enriching thrombin. Sodium 131-137 lysophospholipase 1 Homo sapiens 68-72 31912282-3 2020 When placed on a glassy carbon electrode, the sensor exhibits attractive figures of merit for sensing glucose in 0.1 M NaOH solution including (a) a wide linear range (0.005-7 mM), (b) a low determination limit (0.36 muM), (c) high sensitivity (6115 muA muM-1 cm-2), (d) a relatively low working potential (0.50 V vs. Ag/AgCl), and (e) good selectivity, reproducibility, and stability. Sodium 119-123 PWWP domain containing 3A, DNA repair factor Homo sapiens 254-259 31678597-9 2020 Data are discussed aiming to interpret the importance of blockade of INa through NaV as participant of 4TERP-induced inhibition of membrane excitability. Sodium 81-84 peroxisomal trans-2-enoyl-CoA reductase Homo sapiens 104-108 31993308-3 2020 In this review, we focus on several solute carrier (SLC) transporters known to be involved in transporting clinically used radiopharmaceutical agents into cancer cells, including the sodium/iodine symporter (NIS), norepinephrine transporter (NET), glucose transporter 1 (GLUT1), and monocarboxylate transporters (MCTs). Sodium 183-189 solute carrier family 2 member 1 Homo sapiens 248-269 31993308-3 2020 In this review, we focus on several solute carrier (SLC) transporters known to be involved in transporting clinically used radiopharmaceutical agents into cancer cells, including the sodium/iodine symporter (NIS), norepinephrine transporter (NET), glucose transporter 1 (GLUT1), and monocarboxylate transporters (MCTs). Sodium 183-189 solute carrier family 2 member 1 Homo sapiens 271-276 31539779-7 2019 Our findings demonstrate that resveratrol may function as a SGK1 inhibitor, suggesting possible applications in sodium retention and cancer. Sodium 112-118 serum/glucocorticoid regulated kinase 1 Homo sapiens 60-64 31728700-4 2019 Recently, the sodium channel beta1 subunit has been described to stabilise gating against mechanical stress of Nav1.7 expressed in neurons. Sodium 14-20 sodium voltage-gated channel alpha subunit 9 Homo sapiens 111-117 32647818-6 2020 Furthermore, we show that binding of ABH involves the presence of a sodium ion close to the manganese cluster. Sodium 68-74 alkB homolog 1, histone H2A dioxygenase Homo sapiens 37-40 31718537-8 2019 In this way we attested the implication of some voltage-gated sodium (SCN1A, SCN2A, SCN4A, SCN4B, SCN5A, SCN9A) and potassium (KCNQ2, KCNH2) channels in cardiovascular diseases, epilepsies, febrile seizures, headache disorders, neuromuscular, neurodegenerative diseases or neurobehavioral manifestations. Sodium 62-68 sodium voltage-gated channel alpha subunit 2 Homo sapiens 77-82 31780884-3 2019 To date, and directly relevant to the present review, sigma1R has been found to regulate both voltage-gated ion channels (VGICs) belonging to distinct superfamilies (i.e., sodium, Na+; potassium, K+; and calcium, Ca2+ channels) and non-voltage-gated ion channels. Sodium 172-178 sigma non-opioid intracellular receptor 1 Homo sapiens 54-61 31853224-9 2019 The phosphorylation of IRE1alpha, PERK and eIF2alpha and the expression of nuclear ATF4, and GADD34 in L2 cells were all significantly reduced with NaHS. Sodium 148-152 eukaryotic translation initiation factor 2A Rattus norvegicus 43-52 31853224-9 2019 The phosphorylation of IRE1alpha, PERK and eIF2alpha and the expression of nuclear ATF4, and GADD34 in L2 cells were all significantly reduced with NaHS. Sodium 148-152 protein phosphatase 1, regulatory subunit 15A Rattus norvegicus 93-99 31672125-2 2019 Recent studies have identified an essential role of the sodium channel Nav1.6, encoded by the gene SCN8A, in epileptic encephalopathy. Sodium 56-62 sodium voltage-gated channel alpha subunit 8 Homo sapiens 71-77 31672125-2 2019 Recent studies have identified an essential role of the sodium channel Nav1.6, encoded by the gene SCN8A, in epileptic encephalopathy. Sodium 56-62 sodium voltage-gated channel alpha subunit 8 Homo sapiens 99-104 31558572-9 2019 Distinct mutations may, therefore, require tailored pharmacotherapies in order to eliminate seizures.SIGNIFICANCE STATEMENT This study expands our understanding of the pathogenic biophysical effects associated with two common epilepsy mutations in the human neuronal voltage-gated sodium channel, hNav1.2. Sodium 281-287 sodium voltage-gated channel alpha subunit 2 Homo sapiens 297-304 31623161-8 2019 We show that normal functioning of ClC-7 supports the acidification process, is associated with increased luminal concentrations of sodium, potassium, and chloride, and leads to a higher Ca2+ uptake and release. Sodium 132-138 chloride voltage-gated channel 7 Homo sapiens 35-40 31614475-1 2019 Dysfunction of the cardiac sodium channel Nav1.5 (encoded by the SCN5A gene) is associated with arrhythmias and sudden cardiac death. Sodium 27-33 sodium channel, voltage-gated, type V, alpha Mus musculus 42-48 31614475-1 2019 Dysfunction of the cardiac sodium channel Nav1.5 (encoded by the SCN5A gene) is associated with arrhythmias and sudden cardiac death. Sodium 27-33 sodium channel, voltage-gated, type V, alpha Mus musculus 65-70 31614475-2 2019 SCN5A mutations associated with long QT syndrome type 3 (LQT3) lead to enhanced late sodium current and consequent action potential (AP) prolongation. Sodium 85-91 sodium channel, voltage-gated, type V, alpha Mus musculus 0-5 31614475-5 2019 We found that in HEK293 cells, the SCN5A-p.Y1977N mutation abolished the interaction between Nav1.5 and Nedd4-2, suppressed PY-motif-dependent ubiquitylation of Nav1.5, and consequently abrogated Nedd4-2 induced sodium current (INa) decrease. Sodium 212-218 NEDD4 like E3 ubiquitin protein ligase Homo sapiens 104-111 31012583-1 2019 Voltage-gated sodium ion channel subtype 1.7 (NaV1.7) is a high interest target for the discovery of non-opioid analgesics. Sodium 14-20 sodium voltage-gated channel alpha subunit 9 Homo sapiens 46-52 31633023-4 2019 The structures reveal unique ligand-binding modes and signaling mechanisms, including lateral ligand access to the orthosteric pocket between transmembrane helices TM4 and TM5, an atypical pattern of microswitches, and a distinct four-residue-coordinated sodium site. Sodium 255-261 tropomyosin 3 Homo sapiens 172-175 31590334-2 2019 In recent years, zebrafish disease models with Scn1Lab sodium channel deficiency have been generated to seek novel anti-epileptic drug candidates, some of which are currently undergoing clinical trials. Sodium 55-61 sodium channel, voltage-gated, type I like, alpha b Danio rerio 47-54 31623375-4 2019 In the mammalian intestine, apical sodium-dependent bile acid cotransporter (ASBT; SLC10A2) is exclusively responsible for the reabsorption of bile acids in the terminal ileum. Sodium 35-41 solute carrier family 10 member 2 Homo sapiens 77-81 31623375-4 2019 In the mammalian intestine, apical sodium-dependent bile acid cotransporter (ASBT; SLC10A2) is exclusively responsible for the reabsorption of bile acids in the terminal ileum. Sodium 35-41 solute carrier family 10 member 2 Homo sapiens 83-90 31276831-0 2019 Congenital Sodium Diarrhea by mutation of the SLC9A3 gene. Sodium 11-17 solute carrier family 9 member A3 Homo sapiens 46-52 31276831-1 2019 Congenital Sodium Diarrhea (CSD) due to SLC9A3 mutation is a rare cause of neonatal diarrhea explained by dysfunction of the Na+/H+ antiporter 3 in intestine. Sodium 11-17 solute carrier family 9 member A3 Homo sapiens 40-46 31368174-5 2019 Characterizing the mouse model of podocyte inactivation of NPHS2 (Nphs2 pod ) with respect to volume handling and proteinuria revealed that sodium retention, hypertension and gross proteinuria appeared sequentially in a chronological order. Sodium 140-146 nephrosis 2, podocin Mus musculus 59-64 31551350-2 2019 Historically the evidence for ionic modulation of GPCR function dates to 1973 with studies of opioid receptors, where it was demonstrated that physiologic concentrations of sodium allosterically attenuated agonist binding. Sodium 173-179 vomeronasal 1 receptor 17 pseudogene Homo sapiens 50-54 31551350-5 2019 While ions can act selectively and nonselectively at many sites in different receptors, the discovery of the conserved sodium ion site in class A GPCR structures in 2012 revealed the unique nature of Na+ site, which has emerged as a near-universal site for allosteric modulation of class A GPCR structure and function. Sodium 119-125 vomeronasal 1 receptor 17 pseudogene Homo sapiens 146-150 31551350-5 2019 While ions can act selectively and nonselectively at many sites in different receptors, the discovery of the conserved sodium ion site in class A GPCR structures in 2012 revealed the unique nature of Na+ site, which has emerged as a near-universal site for allosteric modulation of class A GPCR structure and function. Sodium 119-125 vomeronasal 1 receptor 17 pseudogene Homo sapiens 290-294 31373846-1 2019 SLC6A14 (ATB0,+) is a sodium- and chloride-dependent neutral and dibasic amino acid transporter that regulates the distribution of amino acids across cell membranes. Sodium 22-28 solute carrier family 6 member 14 Homo sapiens 0-7 31373846-1 2019 SLC6A14 (ATB0,+) is a sodium- and chloride-dependent neutral and dibasic amino acid transporter that regulates the distribution of amino acids across cell membranes. Sodium 22-28 solute carrier family 1 member 5 Homo sapiens 9-13 31460708-7 2019 The excellent reversible capacity and cycling stability indicate MrGO-CNF a promising anode for sodium-ion batteries. Sodium 96-102 NPHS1 adhesion molecule, nephrin Homo sapiens 70-73 31333492-3 2019 Using the cell-attached patch-clamp approach on cardiomyocytes expressing Nav1.5 in which the SIV motif is deleted (DeltaSIV), sodium current (INa) recordings from the lateral membrane revealed a SIV-motif-independent INa. Sodium 127-133 sodium channel, voltage-gated, type V, alpha Mus musculus 74-80 32699619-1 2020 Background: Experimental studies have shown fibroblast growth factor 23 (FGF23)-mediated upregulation of the distal tubule sodium/chloride (Na+Cl-) co-transporter leading to increased Na reabsorption, volume expansion and hypertension. Sodium 123-129 fibroblast growth factor 23 Homo sapiens 44-71 32699619-1 2020 Background: Experimental studies have shown fibroblast growth factor 23 (FGF23)-mediated upregulation of the distal tubule sodium/chloride (Na+Cl-) co-transporter leading to increased Na reabsorption, volume expansion and hypertension. Sodium 123-129 fibroblast growth factor 23 Homo sapiens 73-78 30860870-4 2019 A competing cell-penetrating peptide mimetic derived from the NaV1.8 WW binding motif decreased sodium currents, reduced NaV1.8 protein expression, and produced hypoexcitability. Sodium 96-102 sodium voltage-gated channel alpha subunit 10 Homo sapiens 62-68 30914445-1 2019 Nav1.6 (SCN8A) is a major voltage-gated sodium channel in the mammalian CNS, and is highly concentrated at the axon initial segment (AIS). Sodium 40-46 sodium voltage-gated channel alpha subunit 8 Homo sapiens 0-6 30914445-1 2019 Nav1.6 (SCN8A) is a major voltage-gated sodium channel in the mammalian CNS, and is highly concentrated at the axon initial segment (AIS). Sodium 40-46 sodium voltage-gated channel alpha subunit 8 Homo sapiens 8-13 30914445-9 2019 This work identifies a critical and important new role for MAP1B in the regulation of neuronal excitability and adds to our understanding of AIS maintenance and plasticity, in addition to identifying new target residues for pathogenic mutations of SCN8A SIGNIFICANCE STATEMENT Nav1.6 is a major voltage-gated sodium channel in human brain, where it regulates neuronal activity due to its localization at the axon initial segment (AIS). Sodium 309-315 sodium voltage-gated channel alpha subunit 8 Homo sapiens 248-253 30914445-13 2019 This work confirms a new biological role of MAP1B in the regulation of sodium channel localization and will contribute to future analysis of patient mutations in the cytoplasmic N terminus of Nav1.6. Sodium 71-77 sodium voltage-gated channel alpha subunit 8 Homo sapiens 192-198 30301479-10 2019 The feeding treatment significantly affected creatinine, the creatinine : albumin ratio, and phosphorus and sodium levels, which were higher for ID2 heifers compared with SD and ID1. Sodium 108-114 inhibitor of DNA binding 2 Homo sapiens 145-148 30699328-1 2019 The peripherally expressed voltage-gated sodium NaV1.7 (gene SCN9A) channel boosts small stimuli to initiate firing of pain-signaling dorsal root ganglia (DRG) neurons and facilitates neurotransmitter release at the first synapse within the spinal cord. Sodium 41-47 sodium voltage-gated channel alpha subunit 9 Homo sapiens 48-54 30699328-1 2019 The peripherally expressed voltage-gated sodium NaV1.7 (gene SCN9A) channel boosts small stimuli to initiate firing of pain-signaling dorsal root ganglia (DRG) neurons and facilitates neurotransmitter release at the first synapse within the spinal cord. Sodium 41-47 sodium voltage-gated channel alpha subunit 9 Homo sapiens 61-66 30910378-8 2019 We highlight GIPR, a potential diabetes drug target, as possibly implicated in the genetic control of urinary potassium excretion, and NRBP1, a locus associated with gout, as plausibly involved in sodium and albumin excretion. Sodium 197-203 nuclear receptor binding protein 1 Homo sapiens 135-140 29518541-8 2019 In this review, we highlight the use of i) Markov State Modelling to examine sodium dynamics in the dopamine transporter, ii) Metadynamics to explore neurotransmitter binding to a ligand-gated ion channel and iii) Steered MD to investigate conformational change in ionotropic glutamate receptors. Sodium 77-83 solute carrier family 6 member 3 Homo sapiens 100-120 30785716-2 2019 Hence, heterostructured SnS2/Mn2SnS4/carbon nanoboxes (SMS/C NBs) have been developed by a facial wet-chemical method and utilized as the anode material of sodium ion batteries. Sodium 156-162 spermine synthase Homo sapiens 55-64 30949179-3 2019 On the other hand, NFAT5 is quite unique among Rel-family factors as it can be activated by hyperosmotic stress caused by elevated concentrations of extracellular sodium ions. Sodium 163-169 nuclear factor of activated T cells 5 Mus musculus 19-24 30635397-6 2019 ASCT2 deficiency was compensated by increased levels of sodium neutral amino acid transporter 1 (SNAT1 or SLC38A1) and SNAT2 (SLC38A2) in ASCT2ko 143B cells, mediated by a GCN2 EIF2alpha kinase (GCN2)-dependent pathway, but this compensation was not observed in ASCT2ko HCC1806 cells. Sodium 56-62 solute carrier family 1 member 5 Homo sapiens 0-5 30635397-6 2019 ASCT2 deficiency was compensated by increased levels of sodium neutral amino acid transporter 1 (SNAT1 or SLC38A1) and SNAT2 (SLC38A2) in ASCT2ko 143B cells, mediated by a GCN2 EIF2alpha kinase (GCN2)-dependent pathway, but this compensation was not observed in ASCT2ko HCC1806 cells. Sodium 56-62 solute carrier family 1 member 5 Homo sapiens 138-143 30635397-6 2019 ASCT2 deficiency was compensated by increased levels of sodium neutral amino acid transporter 1 (SNAT1 or SLC38A1) and SNAT2 (SLC38A2) in ASCT2ko 143B cells, mediated by a GCN2 EIF2alpha kinase (GCN2)-dependent pathway, but this compensation was not observed in ASCT2ko HCC1806 cells. Sodium 56-62 solute carrier family 1 member 5 Homo sapiens 138-143 30820499-5 2019 The NiS2NP/p-CNF nanofibers provide a huge potential for the development of massive sodium storage. Sodium 84-90 NPHS1 adhesion molecule, nephrin Homo sapiens 13-16 30539654-0 2019 Lack of urea transporters, UT-A1 and UT-A3, increases nitric oxide accumulation to dampen medullary sodium reabsorption through ENaC. Sodium 100-106 solute carrier family 14 (urea transporter), member 2 Mus musculus 27-32 30539654-0 2019 Lack of urea transporters, UT-A1 and UT-A3, increases nitric oxide accumulation to dampen medullary sodium reabsorption through ENaC. Sodium 100-106 solute carrier family 14 (urea transporter), member 2 Mus musculus 37-42 30539654-1 2019 Although the role of urea in urine concentration is known, the effect of urea handling by the urea transporters (UTs), UT-A1 and UT-A3, on sodium balance remains elusive. Sodium 139-145 solute carrier family 14 (urea transporter), member 2 Mus musculus 119-124 30539654-2 2019 Serum and urinary sodium concentration is similar between wild-type mice (WT) and UT-A3 null (UT-A3 KO) mice; however, mice lacking both UT-A1 and UT-A3 (UT-A1/A3 KO) have significantly lower serum sodium and higher urinary sodium. Sodium 198-204 solute carrier family 14 (urea transporter), member 2 Mus musculus 154-165 30539654-2 2019 Serum and urinary sodium concentration is similar between wild-type mice (WT) and UT-A3 null (UT-A3 KO) mice; however, mice lacking both UT-A1 and UT-A3 (UT-A1/A3 KO) have significantly lower serum sodium and higher urinary sodium. Sodium 198-204 solute carrier family 14 (urea transporter), member 2 Mus musculus 154-165 30566002-8 2019 Inhibition of Na+/H+ exchanger isoform 3 (NHE3) activity abrogated the GPR37L1-mediated increase in intracellular sodium. Sodium 114-120 solute carrier family 9 member A3 Homo sapiens 14-40 30566002-8 2019 Inhibition of Na+/H+ exchanger isoform 3 (NHE3) activity abrogated the GPR37L1-mediated increase in intracellular sodium. Sodium 114-120 solute carrier family 9 member A3 Homo sapiens 42-46 30566002-9 2019 Renal-selective silencing of Gpr37l1 in mice increased urine output and sodium excretion and decreased systolic and diastolic blood pressures. Sodium 72-78 G protein-coupled receptor 37-like 1 Mus musculus 29-36 30566002-11 2019 Our findings show that in the kidney, GPR37L1 participates in renal proximal tubule luminal sodium transport and regulation of blood pressure by increasing the renal expression and function of NHE3 by decreasing cAMP production. Sodium 92-98 solute carrier family 9 member A3 Homo sapiens 193-197 29936069-1 2019 BACKGROUND: In healthy lungs, epithelial sodium channel (ENaC) is regulated by short, palate, lung, and nasal clone 1 (SPLUNC1). Sodium 41-47 BPI fold containing family A, member 1 Mus musculus 119-126 30731085-1 2019 Cardiac sodium (Na+) potassium ATPase (NaK) pumps, neuronal sodium channels (INa), and sodium calcium (Ca2+) exchangers (NCX1) may co-localize to form a Na+ microdomain. Sodium 8-14 internexin neuronal intermediate filament protein alpha Canis lupus familiaris 77-80 30731085-1 2019 Cardiac sodium (Na+) potassium ATPase (NaK) pumps, neuronal sodium channels (INa), and sodium calcium (Ca2+) exchangers (NCX1) may co-localize to form a Na+ microdomain. Sodium 60-66 internexin neuronal intermediate filament protein alpha Canis lupus familiaris 77-80 30416015-1 2019 OBJECTIVES: To evaluate the clinical features of erythromelalgia in childhood associated with gain-of-function SCN9A mutations that increase activity of the Nav1.7 voltage-gated sodium channel, we conducted a systematic review of pediatric presentations of erythromelalgia related to SCN9A mutations, and compared pediatric clinical presentations of symptomatic erythromelalgia, with or without SCN9A mutations. Sodium 178-184 sodium voltage-gated channel alpha subunit 9 Homo sapiens 111-116 30416015-9 2019 SCN9A mutations resulting in greater hyperpolarizing shifts in Nav1.7 sodium channels correlated with symptom onset at younger ages (P = .016). Sodium 70-76 sodium voltage-gated channel alpha subunit 9 Homo sapiens 0-5 30416015-9 2019 SCN9A mutations resulting in greater hyperpolarizing shifts in Nav1.7 sodium channels correlated with symptom onset at younger ages (P = .016). Sodium 70-76 sodium voltage-gated channel alpha subunit 9 Homo sapiens 63-69 30604288-1 2019 Sodium-coupled monocarboxylate transporters SMCT1 (SLC5A8) and SMCT2 (SLC5A12) mediate the high- and low-affinity transport of lactate in the kidney, but their regulatory mechanism is still unknown. Sodium 0-6 solute carrier family 5 member 8 Homo sapiens 44-49 30604288-1 2019 Sodium-coupled monocarboxylate transporters SMCT1 (SLC5A8) and SMCT2 (SLC5A12) mediate the high- and low-affinity transport of lactate in the kidney, but their regulatory mechanism is still unknown. Sodium 0-6 solute carrier family 5 member 8 Homo sapiens 51-57 30839176-1 2019 Sodium transport in the thick ascending loop of Henle (TAL) is tightly regulated by numerous factors, especially angiotensin II (Ang II), a key end-product of the renin-angiotensin system (RAS). Sodium 0-6 transaldolase 1 Homo sapiens 55-58 30559144-0 2019 Kir4.1/Kir5.1 Activity Is Essential for Dietary Sodium Intake-Induced Modulation of Na-Cl Cotransporter. Sodium 48-54 potassium inwardly-rectifying channel, subfamily J, member 16 Mus musculus 7-13 30559144-4 2019 RESULTS: Low sodium intake stimulated basolateral Kir4.1/Kir5.1 activity, increased basolateral K+ conductance, and hyperpolarized the membrane. Sodium 13-19 potassium inwardly-rectifying channel, subfamily J, member 16 Mus musculus 57-63 30559144-7 2019 Thus, elevated NCC activity induced by low sodium intake was associated with upregulation of Kir4.1/Kir5.1 activity in the DCT, whereas inhibition of NCC activity by high sodium intake was associated with diminished Kir4.1/Kir5.1 activity. Sodium 43-49 potassium inwardly-rectifying channel, subfamily J, member 16 Mus musculus 100-106 30559144-11 2019 CONCLUSIONS: Stimulation of Kir4.1/Kir5.1 by low intake of dietary sodium is essential for NCC upregulation, and inhibition of Kir4.1/Kir5.1 induced by high sodium intake is a key step for downregulation of NCC. Sodium 67-73 potassium inwardly-rectifying channel, subfamily J, member 16 Mus musculus 35-41 30559144-11 2019 CONCLUSIONS: Stimulation of Kir4.1/Kir5.1 by low intake of dietary sodium is essential for NCC upregulation, and inhibition of Kir4.1/Kir5.1 induced by high sodium intake is a key step for downregulation of NCC. Sodium 157-163 potassium inwardly-rectifying channel, subfamily J, member 16 Mus musculus 35-41 30559144-11 2019 CONCLUSIONS: Stimulation of Kir4.1/Kir5.1 by low intake of dietary sodium is essential for NCC upregulation, and inhibition of Kir4.1/Kir5.1 induced by high sodium intake is a key step for downregulation of NCC. Sodium 157-163 potassium inwardly-rectifying channel, subfamily J, member 16 Mus musculus 134-140 30508412-4 2019 The present results are the first to demonstrate that PKC/p38 MAPK signaling is involved in ANGII-induced water and sodium intake and oxytocin (OT) secretion in OVX rats. Sodium 116-122 protein kinase C, alpha Rattus norvegicus 54-57 30451736-4 2019 Local and systemic factors control FGF-23 release from osteoblast/osteocytes in bone, and circulating FGF-23 activates FGFR/alpha-Klotho complexes in kidney proximal and distal renal tubules to regulate renal phosphate excretion, 1,25 (OH)2D metabolism, sodium and calcium reabsorption, and ACE2 and alpha-Klotho expression. Sodium 254-260 fibroblast growth factor 23 Homo sapiens 102-108 31018202-1 2019 OBJECTIVE: The systemic form of pseudohypoaldosteronism type 1 (PHA1) is an autosomal recessive disorder characterized by defective sodium transport in multi-organ systems. Sodium 132-138 sodium channel epithelial 1 subunit gamma Homo sapiens 64-68 31018202-2 2019 Mutations in the genes encoding the amiloride-sensitive epithelial sodium channel, ENaC, account for genetic causes of systemic PHA1. Sodium 67-73 sodium channel epithelial 1 subunit gamma Homo sapiens 128-132 30199829-5 2019 The results demonstrate that the SnO2 submicrorods-Ni foam is a highly attractive anode for sodium ion batteries, which could exhibit much better sodium storage properties than the SnO2 rod-assembly microspheres and other reported SnO2-based additive electrodes. Sodium 92-98 strawberry notch homolog 2 Homo sapiens 33-36 30199829-5 2019 The results demonstrate that the SnO2 submicrorods-Ni foam is a highly attractive anode for sodium ion batteries, which could exhibit much better sodium storage properties than the SnO2 rod-assembly microspheres and other reported SnO2-based additive electrodes. Sodium 146-152 strawberry notch homolog 2 Homo sapiens 33-36 31430745-5 2019 Klotho fractional enrichment across the kidney was inversely related to plasma sodium (r = 0.43, p = 0.045) and acid uric acid levels (r = 0.38, p = 0.084) and directly, to renal oxygen extraction (r = 0.56, p = 0.006). Sodium 79-85 klotho Homo sapiens 0-6 31067548-10 2019 A correlation between WNT4 gene expression and serum albumin and cholesterol levels was observed in patients with FSGS, while WNT4 mRNA levels correlated with plasma sodium in patients diagnosed with LN. Sodium 166-172 Wnt family member 4 Homo sapiens 126-130 30744898-7 2019 Voltage clamp analysis of Jbtx (200 nM) applied in Xenopus laevis oocytes heterologously expressed with Nav 1.1 channels showed a significant increase in the sodium currents. Sodium 158-164 sodium channel, voltage gated, type I alpha subunit S homeolog Xenopus laevis 104-111 29136153-3 2018 There is evidence that sodium influx drives PIDs, but no data exist on PID-related sodium accumulations in vivo. Sodium 23-29 preimplantation development Mus musculus 44-47 30019930-5 2018 Multiple mechanisms were required to explain the observed response: 1) direct inhibition of sodium and glucose reabsorption through SGLT2, 2) SGLT2-driven inhibition of Na+/H+ exchanger 3 sodium reabsorption, and 3) osmotic diuresis coupled with peripheral sodium storage. Sodium 188-194 solute carrier family 9 member A3 Homo sapiens 169-187 30019930-5 2018 Multiple mechanisms were required to explain the observed response: 1) direct inhibition of sodium and glucose reabsorption through SGLT2, 2) SGLT2-driven inhibition of Na+/H+ exchanger 3 sodium reabsorption, and 3) osmotic diuresis coupled with peripheral sodium storage. Sodium 188-194 solute carrier family 9 member A3 Homo sapiens 169-187 30213699-6 2018 Several lines of evidence point toward the role of high sodium intake in reversing the suppressive effects of Regulatory T cells (Tregs) and instead promoting cellular shift toward T-helper (Th)-1 and Th17 pro-inflammatory phenotypes. Sodium 56-62 negative elongation factor complex member C/D Homo sapiens 181-196 30251687-5 2018 Overexpression of dominant-negative mutant SAR1A (T39N or H79G) or SAR1B (T39N or H79G) significantly reduces the expression level of Nav1.5 on cell surface, and decreases the peak sodium current density (INa) in HEK/Nav1.5 cells and neonatal rat cardiomyocytes. Sodium 181-187 secretion associated, Ras related GTPase 1A Rattus norvegicus 43-48 29966443-3 2018 Furthermore, the possible RRF release by voltage-dependent sodium channel activation and the calcium-dependency of the RRF release were investigated. Sodium 59-65 mitochondrial ribosome recycling factor Mus musculus 26-29 30385783-7 2018 Furthermore, the seedlings presented a negative relationship between sodium (Na+) and Pi (low Na+ content and high Pi content), which is related to the genes ZmNHX1, ZmPHT1;8, and ZmPHT1;9, indicating that the exclusion of Na+ was promoted by high Pi uptake. Sodium 69-75 phosphate transporter protein 1 Zea mays 166-174 30385783-7 2018 Furthermore, the seedlings presented a negative relationship between sodium (Na+) and Pi (low Na+ content and high Pi content), which is related to the genes ZmNHX1, ZmPHT1;8, and ZmPHT1;9, indicating that the exclusion of Na+ was promoted by high Pi uptake. Sodium 69-75 phosphate transporter protein 1 Zea mays 180-188 29944390-1 2018 Oxytocin, while classically known for its role in parturition, lactation, and social behavior, also has been implicated in the control of sodium homeostasis in animal models. Sodium 138-144 oxytocin/neurophysin I prepropeptide Homo sapiens 0-8 30080995-8 2018 Markers for RBC metabolism (ATP, 2,3-DPG) were not altered but RBC sodium levels increased and potassium and calcium decreased, respectively. Sodium 67-73 RNA, 7SL, cytoplasmic 263, pseudogene Homo sapiens 63-66 29702262-7 2018 The reduction of GR content, by gene silencing, abolished the Aldo effect on NHE1, in low concentration, confirming the importance of this receptor in the rapid modulation of proximal sodium and hydrogen transports. Sodium 184-190 nuclear receptor subfamily 3, group C, member 1 Rattus norvegicus 17-19 30158152-3 2018 Tenapanor, a minimally absorbed, small-molecule inhibitor of the sodium/hydrogen exchanger isoform 3 (NHE3), acts locally in the gastrointestinal tract to inhibit sodium absorption. Sodium 65-71 solute carrier family 9 member A3 Homo sapiens 102-106 30158152-3 2018 Tenapanor, a minimally absorbed, small-molecule inhibitor of the sodium/hydrogen exchanger isoform 3 (NHE3), acts locally in the gastrointestinal tract to inhibit sodium absorption. Sodium 163-169 solute carrier family 9 member A3 Homo sapiens 102-106 30143662-1 2018 Mutations in SCN5A can alter the cardiac sodium current INa and increase the risk of potentially lethal conditions such as Brugada and long-QT syndromes. Sodium 41-47 internexin neuronal intermediate filament protein alpha Homo sapiens 56-59 30186172-0 2018 Estrone-3-Sulfate Stimulates the Proliferation of T47D Breast Cancer Cells Stably Transfected With the Sodium-Dependent Organic Anion Transporter SOAT (SLC10A6). Sodium 103-109 solute carrier family 10 member 6 Homo sapiens 146-150 30186172-0 2018 Estrone-3-Sulfate Stimulates the Proliferation of T47D Breast Cancer Cells Stably Transfected With the Sodium-Dependent Organic Anion Transporter SOAT (SLC10A6). Sodium 103-109 solute carrier family 10 member 6 Homo sapiens 152-159 30186172-3 2018 In the present study, expression of the sodium-dependent organic anion transporter SOAT was analyzed in breast cancer and its role for hormone-dependent proliferation of T47D breast cancer cells was elucidated. Sodium 40-46 solute carrier family 10 member 6 Homo sapiens 83-87 29970412-0 2018 Heat-resistant action potentials require TTX-resistant sodium channels NaV1.8 and NaV1.9. Sodium 55-61 sodium voltage-gated channel alpha subunit 10 Homo sapiens 71-77 30018331-5 2018 By targeting both the MHC class I complex (beta-2-microglobulin) and a broadly expressed sodium-potassium ATPase-subunit (CD298) with platinum-conjugated antibodies, human immune cells, stem cells as well as tumor cells could be multiplexed in the same single-cell assay. Sodium 89-95 ATPase Na+/K+ transporting subunit beta 3 Homo sapiens 122-127 29754923-1 2018 BACKGROUND: Long QT syndrome mutations in the SCN5A gene are associated with an enhanced late sodium current (INa,L) which may lead to pro-arrhythmic action potential prolongation and intracellular calcium dysregulation. Sodium 94-100 sodium channel, voltage-gated, type V, alpha Mus musculus 46-51 29754923-1 2018 BACKGROUND: Long QT syndrome mutations in the SCN5A gene are associated with an enhanced late sodium current (INa,L) which may lead to pro-arrhythmic action potential prolongation and intracellular calcium dysregulation. Sodium 94-100 internexin neuronal intermediate filament protein, alpha Mus musculus 110-113 29958388-3 2018 Sodium storage measurements demonstrate that the annealed CTS electrodes have high initial reversible capacity (447.7 mAh·g−1 at a current density of 100 mA·g−1), good capacity retention (200.6 mAh·g−1 after 50 cycles at a current density of 100 mA·g−1) and considerable rate capability because of their high crystallinity and unique morphology. Sodium 0-6 transthyretin Homo sapiens 58-61 29929539-9 2018 Furthermore, in both May 2013 and May 2016, 99-100% of CAI advertisements featured products deemed excessive in either fat (total, saturated, trans), sodium or free sugars according to the PAHO NPM. Sodium 150-156 carbonic anhydrase 1 Homo sapiens 55-58 29912865-7 2018 In CXCR4, the sodium ion is tightly bound by four protein atoms and one water molecule. Sodium 14-20 C-X-C motif chemokine receptor 4 Homo sapiens 3-8 29912865-8 2018 In CCR5, the sodium ion is mobile within the binding pocket and moves between different sites involving from one to three protein atoms and two to five water molecules. Sodium 13-19 C-C motif chemokine receptor 5 Homo sapiens 3-7 29912865-9 2018 Analysis of chemokine receptor evolution reveals that a highly constrained sodium binding site characterized most ancient receptors, and that the constraints were subsequently loosened during the divergence of this receptor family. Sodium 75-81 C-X-C motif chemokine receptor 4 Homo sapiens 12-30 29752399-11 2018 CONCLUSIONS: Our findings suggest an association between genetic variation in SCN10A, the late sodium current, and alterations in cardiac conduction. Sodium 95-101 sodium voltage-gated channel alpha subunit 10 Homo sapiens 78-84 28893621-0 2018 Rare genetic variants in the sodium-dependent organic anion transporter SOAT (SLC10A6): Effects on transport function and membrane expression. Sodium 29-35 solute carrier family 10 member 6 Homo sapiens 72-76 28893621-0 2018 Rare genetic variants in the sodium-dependent organic anion transporter SOAT (SLC10A6): Effects on transport function and membrane expression. Sodium 29-35 solute carrier family 10 member 6 Homo sapiens 78-85 28893621-3 2018 The sodium-dependent organic anion transporter SOAT, coded by the SLC10A6 gene, is specific for the transport of steroid sulfates and is highly expressed in testicular germ cells, including pachytene spermatocytes, secondary spermatocytes, and round spermatids. Sodium 4-10 solute carrier family 10 member 6 Homo sapiens 47-51 28893621-3 2018 The sodium-dependent organic anion transporter SOAT, coded by the SLC10A6 gene, is specific for the transport of steroid sulfates and is highly expressed in testicular germ cells, including pachytene spermatocytes, secondary spermatocytes, and round spermatids. Sodium 4-10 solute carrier family 10 member 6 Homo sapiens 66-73 28893621-8 2018 Other variants are located directly at (Q75R, S112F, N113K) or close to (G109S, S133F, and G263E) the supposed SOAT Na+ binding sites and thus could disable the sodium-coupled transport cycle. Sodium 161-167 solute carrier family 10 member 6 Homo sapiens 111-115 28951227-6 2018 We found significant and sodium-dependent SOAT-mediated transport of 17alpha-hydroxypregnenolone sulfate, 17beta-estradiol-17-sulfate, androsterone sulfate, epiandrosterone sulfate, testosterone sulfate, epitestosterone sulfate, and 5alpha-dihydrotestosterone sulfate. Sodium 25-31 solute carrier family 10 member 6 Homo sapiens 42-46 29756820-1 2018 The spin dynamics of a harmonically trapped Bose-Einstein condensed binary mixture of sodium atoms is experimentally investigated at finite temperature. Sodium 86-92 spindlin 1 Homo sapiens 4-8 29608553-1 2018 BACKGROUND Fibroblast growth factor 23 (FGF23), a prominent regulator of phosphate and calcium metabolism, regulates sodium excretion in distal tubules through sodium-chloride cotransporter. Sodium 117-123 fibroblast growth factor 23 Homo sapiens 11-38 29608553-1 2018 BACKGROUND Fibroblast growth factor 23 (FGF23), a prominent regulator of phosphate and calcium metabolism, regulates sodium excretion in distal tubules through sodium-chloride cotransporter. Sodium 117-123 fibroblast growth factor 23 Homo sapiens 40-45 29608553-10 2018 Furthermore, a significant inverse correlation was observed between 24-hour urinary sodium and serum concentrations of FGF23 after adjusting age, sex, BMI and hypertension status. Sodium 84-90 fibroblast growth factor 23 Homo sapiens 119-124 29469565-0 2018 Reduced Graphene Oxide-Incorporated SnSb@CNF Composites as Anodes for High-Performance Sodium-Ion Batteries. Sodium 87-93 NPHS1 adhesion molecule, nephrin Homo sapiens 41-44 29182730-7 2018 RESULTS: In the process of acute sodium loading, after adjusting for age and 24-hour urinary sodium concentration, SNPs in CYP11B2, PRKG1, SLC8A1 genes were significantly associated with systolic BP (SBP) rising in the additive and recessive model; SNPs in CYP4A11, PRKG1, SLC8A1, and ADRB2 genes were significantly associated with diastolic BP (DBP) rising. Sodium 33-39 adrenoceptor beta 2 Homo sapiens 285-290 29329358-6 2018 With Ang1-7 co-infused, SBP increased from 133 +- 5 to 161 +- 5 mm Hg (increase reduced, P < 0.002); concurrent increases in urine flow (V) and sodium excretion (UNaV) were greater. Sodium 147-153 angiogenin Rattus norvegicus 5-11 29329358-10 2018 CONCLUSIONS: The results suggest that in AngII-dependent hypertension, Ang1-7 deficit contributes to sodium and fluid retention and thereby to BP elevation; a correction by Ang1-7 infusion seems mediated by AT1 and not Mas receptors. Sodium 101-107 angiogenin Rattus norvegicus 71-77 29329358-10 2018 CONCLUSIONS: The results suggest that in AngII-dependent hypertension, Ang1-7 deficit contributes to sodium and fluid retention and thereby to BP elevation; a correction by Ang1-7 infusion seems mediated by AT1 and not Mas receptors. Sodium 101-107 angiogenin Rattus norvegicus 71-75 29146137-6 2018 RESULTS: Phosphorus, potassium, and sodium additives were present on the ingredient list in 37%, 9%, and 72% of MPF, respectively. Sodium 36-42 mesothelin Homo sapiens 112-115 29473904-1 2018 The SCN5A gene encodes the pore-forming alpha-subunit of the ion channel that carries the cardiac fast sodium current (INa). Sodium 103-109 internexin neuronal intermediate filament protein alpha Homo sapiens 119-122 29306478-1 2018 BACKGROUND: Fibroblast growth factor (FGF) 23 is a hormone that increases urinary phosphate excretion and regulates renal sodium reabsorption and plasma volume. Sodium 122-128 fibroblast growth factor 23 Homo sapiens 12-45 29467657-0 2018 Effects of Sodium and Amino Acid Substrate Availability upon the Expression and Stability of the SNAT2 (SLC38A2) Amino Acid Transporter. Sodium 11-17 solute carrier family 38 member 2 Homo sapiens 97-102 29467657-0 2018 Effects of Sodium and Amino Acid Substrate Availability upon the Expression and Stability of the SNAT2 (SLC38A2) Amino Acid Transporter. Sodium 11-17 solute carrier family 38 member 2 Homo sapiens 104-111 29357199-1 2018 Creatine kinase (CK) rapidly regenerates ATP for Na+ /K+ -ATPase driven sodium retention throughout the kidney. Sodium 72-78 cytidine/uridine monophosphate kinase 1 Homo sapiens 0-20 29357199-2 2018 Therefore, we assessed whether resting plasma CK is associated with sodium retention after a high sodium diet. Sodium 68-74 cytidine/uridine monophosphate kinase 1 Homo sapiens 46-48 29357199-2 2018 Therefore, we assessed whether resting plasma CK is associated with sodium retention after a high sodium diet. Sodium 98-104 cytidine/uridine monophosphate kinase 1 Homo sapiens 46-48 29357199-4 2018 Sodium excretion (mmol/24-h) after high sodium was 260.4 (28.3) in the high CK tertile versus 415.2 (26.3) mmol/24-h in the low CK tertile (P < .001), with a decrease in urinary sodium excretion of 98.4 mmol/24-h for each increase in log CK, adjusted for age and African ancestry. Sodium 0-6 cytidine/uridine monophosphate kinase 1 Homo sapiens 76-78 29361765-2 2018 Physiologically, THP is implicated in renal countercurrent gradient formation, sodium homeostasis, blood pressure regulation, and a defense molecule against infections in the urinary system. Sodium 79-85 uromodulin Homo sapiens 17-20 28940861-2 2017 Dietary sodium manipulation alters the magnitude of angiotensin-(1-7) [Ang-(1-7)]-induced natriuresis. Sodium 8-14 angiogenin Rattus norvegicus 71-79 28940861-7 2017 Thus, Ang-(1-7)-induced increases in sodium and water excretion are dependent upon functional Mas and AT1 receptors. Sodium 37-43 angiogenin Rattus norvegicus 6-14 28940861-14 2017 Interstitial Ang-(1-7) infusion increased urine flow twofold and fractional sodium excretion threefold (P < 0.05) in rats receiving a normal-sodium diet and to a greater extent, approximately three- and fourfold, respectively, in rats receiving the low-sodium diet (both P < 0.05). Sodium 76-82 angiogenin Rattus norvegicus 13-21 28940861-14 2017 Interstitial Ang-(1-7) infusion increased urine flow twofold and fractional sodium excretion threefold (P < 0.05) in rats receiving a normal-sodium diet and to a greater extent, approximately three- and fourfold, respectively, in rats receiving the low-sodium diet (both P < 0.05). Sodium 144-150 angiogenin Rattus norvegicus 13-21 28940861-14 2017 Interstitial Ang-(1-7) infusion increased urine flow twofold and fractional sodium excretion threefold (P < 0.05) in rats receiving a normal-sodium diet and to a greater extent, approximately three- and fourfold, respectively, in rats receiving the low-sodium diet (both P < 0.05). Sodium 144-150 angiogenin Rattus norvegicus 13-21 29106511-4 2017 The sodium acetate tolerance was dependent on the extrusion of intracellular sodium ions by the plasma membrane-localized sodium pumps Ena1, Ena2, and Ena5 (Ena1/2/5) and two known upstream regulators: the Rim101 pH signaling pathway and the Hog1 mitogen-activated protein kinase. Sodium 4-10 Na(+)/Li(+)-exporting P-type ATPase ENA1 Saccharomyces cerevisiae S288C 135-139 29106511-4 2017 The sodium acetate tolerance was dependent on the extrusion of intracellular sodium ions by the plasma membrane-localized sodium pumps Ena1, Ena2, and Ena5 (Ena1/2/5) and two known upstream regulators: the Rim101 pH signaling pathway and the Hog1 mitogen-activated protein kinase. Sodium 4-10 Na(+)-exporting P-type ATPase ENA2 Saccharomyces cerevisiae S288C 141-145 28576404-4 2017 We found that the increase in urinary output and urinary sodium excretion in response to systemic infusion of GLP-1 for 30min in SHRs was much less pronounced than in normotensive rats. Sodium 57-63 glucagon Rattus norvegicus 110-115 28900153-2 2017 The bone-derived phosphaturic and sodium-conserving hormone fibroblast growth factor-23 (FGF23) and its co-receptor Klotho have been implicated in the development of uremic LVH. Sodium 34-40 fibroblast growth factor 23 Mus musculus 60-87 28900153-2 2017 The bone-derived phosphaturic and sodium-conserving hormone fibroblast growth factor-23 (FGF23) and its co-receptor Klotho have been implicated in the development of uremic LVH. Sodium 34-40 fibroblast growth factor 23 Mus musculus 89-94 28900153-2 2017 The bone-derived phosphaturic and sodium-conserving hormone fibroblast growth factor-23 (FGF23) and its co-receptor Klotho have been implicated in the development of uremic LVH. Sodium 34-40 klotho Mus musculus 116-122 27622885-8 2017 The newly described sodium- and calcium-conserving functions of FGF23 may have major implications for the pathophysiology of diseases characterized by chronically increased circulating FGF23 concentrations such as chronic kidney disease. Sodium 20-26 fibroblast growth factor 23 Homo sapiens 64-69 27622885-8 2017 The newly described sodium- and calcium-conserving functions of FGF23 may have major implications for the pathophysiology of diseases characterized by chronically increased circulating FGF23 concentrations such as chronic kidney disease. Sodium 20-26 fibroblast growth factor 23 Homo sapiens 185-190 28369721-4 2017 Moreover, we generated a homology model of the EBI2 receptor to investigate the structural basis of the allosteric modulation by sodium. Sodium 129-135 G protein-coupled receptor 183 Homo sapiens 47-51 28369721-10 2017 CONCLUSIONS AND IMPLICATIONS: Collectively, our data point to N114 as a key residue for EBI2 signalling controlling the balance between G protein-dependent and -independent pathways and facilitating sodium binding. Sodium 199-205 G protein-coupled receptor 183 Homo sapiens 88-92 28407399-7 2017 Furthermore, they support the notion that mislocalization of transporters, such as NHE3 substantially contributes to the reported sodium loss diarrhea. Sodium 130-136 solute carrier family 9 member A3 Homo sapiens 83-87 28654017-3 2017 The importance of Vit C for CNS function has been proven by the fact that targeted deletion of the sodium-vitamin C co-transporter in mice results in widespread cerebral hemorrhage and death on post-natal day one. Sodium 99-105 vitrin Mus musculus 18-21 28432123-1 2017 The electrogenic sodium/calcium exchanger (NCX) mediates bidirectional calcium transport controlled by the transmembrane sodium gradient. Sodium 17-23 T cell leukemia homeobox 2 Homo sapiens 43-46 27987209-0 2017 The sodium transporter encoded by the HKT1;2 gene modulates sodium/potassium homeostasis in tomato shoots under salinity. Sodium 4-10 sodium transporter HKT1,2 Solanum lycopersicum 38-44 26801191-3 2017 This article first describes the distribution, function and regulation of glucose transporters at the blood-brain barrier, the major ones being the sodium-independent facilitative transporters GLUT1 and GLUT3. Sodium 148-154 solute carrier family 2 member 1 Homo sapiens 193-198 26801191-3 2017 This article first describes the distribution, function and regulation of glucose transporters at the blood-brain barrier, the major ones being the sodium-independent facilitative transporters GLUT1 and GLUT3. Sodium 148-154 solute carrier family 2 member 3 Homo sapiens 203-208 28243920-0 2017 Involvement of Glucagon-Like Peptide-1 in the Regulation of Selective Excretion of Sodium or Chloride Ions by the Kidneys. Sodium 83-89 glucagon Rattus norvegicus 15-38 28243920-5 2017 These findings suggest that GLP-1 participates in selective regulation of the balance of sodium and chloride ions. Sodium 89-95 glucagon Rattus norvegicus 28-33 27999940-0 2017 FHF2 isoforms differentially regulate Nav1.6-mediated resurgent sodium currents in dorsal root ganglion neurons. Sodium 64-70 fibroblast growth factor 13 Homo sapiens 0-4 28045581-10 2017 We hypothesize that these vacuolar chloride channel proteins might be PP2A-C5"s substrates in vivo, and the action of PP2A-C5 on these channel proteins could increase or activate their activities, thereby result in accumulation of the chloride and sodium contents in vacuoles, leading to increased salt tolerance in plants. Sodium 248-254 serine/threonine protein phosphatase 2A Arabidopsis thaliana 70-74 28045581-10 2017 We hypothesize that these vacuolar chloride channel proteins might be PP2A-C5"s substrates in vivo, and the action of PP2A-C5 on these channel proteins could increase or activate their activities, thereby result in accumulation of the chloride and sodium contents in vacuoles, leading to increased salt tolerance in plants. Sodium 248-254 serine/threonine protein phosphatase 2A Arabidopsis thaliana 118-122 28017718-0 2017 Maturation and processing of the amyloid precursor protein is regulated by the potassium/sodium hyperpolarization-activated cyclic nucleotide-gated ion channel 2 (HCN2). Sodium 89-95 amyloid beta precursor protein Rattus norvegicus 33-58 28059145-0 2017 A Markov State-based Quantitative Kinetic Model of Sodium Release from the Dopamine Transporter. Sodium 51-57 solute carrier family 6 member 3 Homo sapiens 75-95 28059145-3 2017 We have constructed Markov State Models (MSMs) from extensive molecular dynamics simulations of human DAT (hDAT) to explore the mechanism of this sodium release. Sodium 146-152 solute carrier family 6 member 3 Homo sapiens 102-105 28059145-3 2017 We have constructed Markov State Models (MSMs) from extensive molecular dynamics simulations of human DAT (hDAT) to explore the mechanism of this sodium release. Sodium 146-152 solute carrier family 6 member 3 Homo sapiens 107-111 28059145-6 2017 An intermediate state is discovered on the sodium release pathway, and the results reveal the importance of various modes of interaction of the N-terminus of hDAT in controlling the pathways of release. Sodium 43-49 solute carrier family 6 member 3 Homo sapiens 158-162 28287879-5 2017 The serum sodium level was correlated with the average 24-h ABP and NDR, after adjustment for other clinical variables, such as the increase in body weight, serum albumin level, and urinary protein excretion. Sodium 10-16 serine/threonine kinase 38 Homo sapiens 68-71 28287879-7 2017 Furthermore, change in the serum sodium level was significantly correlated with the change in NDR. Sodium 33-39 serine/threonine kinase 38 Homo sapiens 94-97 29276908-0 2017 [Correlations of IL-18 and IL-6 with sodium consumption in patients with arterial hypertension and diabetes mellitus]. Sodium 37-43 interleukin 18 Homo sapiens 17-22 29276908-1 2017 AIM: To determine correlations of AH-associated interleukins (IL-18, IL-6) with sodium consumption in AH patients with and without DM. Sodium 80-86 interleukin 18 Homo sapiens 34-67 27713141-0 2016 Fibroblast growth factor 23 dysregulates late sodium current and calcium homeostasis with enhanced arrhythmogenesis in pulmonary vein cardiomyocytes. Sodium 46-52 fibroblast growth factor 23 Homo sapiens 0-27 27475229-7 2016 In contrast, selective SDF-1 receptor blockade with AMD3100 reduced urinary sodium excretion and aggravated glomerular hypertension in the Glp1r(+/+) diabetic-prone mice. Sodium 76-82 chemokine (C-X-C motif) receptor 4 Mus musculus 23-37 30193436-4 2016 In contrast to analogs of neurohypophysial nonapeptides, glucagon-like peptide-1 mimetic (exenatide) did not exert its physiological effects after oral administration, whereas it increased urinary sodium and potassium excretion following intramuscular injection. Sodium 197-203 glucagon Rattus norvegicus 57-80 27685945-9 2016 In summary, our results demonstrate that loss of the sodium/hydrogen exchanger NHA2 exacerbates obesity- and aging-induced glucose intolerance in mice. Sodium 53-59 solute carrier family 9, subfamily B (NHA2, cation proton antiporter 2), member 2 Mus musculus 79-83 27259686-1 2016 The concentration-sensitive sodium channel (Nac) is activated by an increase in the extracellular sodium concentration. Sodium 28-34 NLR family, pyrin domain containing 1A Mus musculus 44-47 27259686-3 2016 We characterized Nac expression and examined amiloride-insensitive sodium transport mediated by Nac in mouse lung. Sodium 67-73 NLR family, pyrin domain containing 1A Mus musculus 96-99 27259686-8 2016 We conclude that Nac expressed in PMVECs and AEC II contributes to the reabsorption of sodium via an amiloride-insensitive pathway during alveolar fluid clearance. Sodium 87-93 NLR family, pyrin domain containing 1A Mus musculus 17-20 27517916-0 2016 Serum and Glucocorticoid Regulated Kinase 1 in Sodium Homeostasis. Sodium 47-53 serum/glucocorticoid regulated kinase 1 Homo sapiens 0-43 27517916-2 2016 Recently, SGK1 has been implicated as a signal hub for the regulation of sodium transport. Sodium 73-79 serum/glucocorticoid regulated kinase 1 Homo sapiens 10-14 27517916-5 2016 Here, we focus particularly on recent findings of SGK1"s involvement in Na+ transport in renal sodium reabsorption, hormone-stimulated salt appetite and fluid balance and discuss the abnormal SGK1-mediated Na+ reabsorption in hypertension, heart disease, edema with diabetes, and embryo implantation failure. Sodium 95-101 serum/glucocorticoid regulated kinase 1 Homo sapiens 50-54 26789642-7 2016 The early supernormality changes indicate that sodium currents were reduced in DM1, whereas the weakness-associated slow recovery after repetitive stimulation may provide an indication of reduced Na(+) /K(+) -ATPase activation. Sodium 47-53 DM1 protein kinase Homo sapiens 79-82 27392042-0 2016 Atrial Natriuretic Peptide Stimulates Dopamine Tubular Transport by Organic Cation Transporters: A Novel Mechanism to Enhance Renal Sodium Excretion. Sodium 132-138 natriuretic peptide A Rattus norvegicus 0-26 25842276-1 2016 AIMS: The expression of sodium channel Nav1.8 in cardiac nervous systems has been identified, and variants of SCN10A that encodes Nav1.8 contribute to the development of Brugada syndrome (BrS) by modifying the function of Nav1.5 or directly reducing the sodium current. Sodium 24-30 sodium voltage-gated channel alpha subunit 10 Homo sapiens 39-45 27711263-5 2016 Based on these results, a nonflammable sodium-ion battery is constructed by use of Sb anode, NaNi0.35Mn0.35Fe0.3O2 cathode, and TMP + 10 vol% FEC electrolyte, which works very well with considerable capacity and cyclability, demonstrating a promising prospect to build safer sodium-ion batteries for large-scale energy storage applications. Sodium 39-45 oligodendrocytic myelin paranodal and inner loop protein Homo sapiens 128-136 27165083-0 2016 Effects of Selective Agonists of V1a, V2, and V1b Receptors on Sodium Transport in Rat Kidney. Sodium 63-69 arginine vasopressin receptor 1A Rattus norvegicus 33-36 27165083-2 2016 Selective V1a receptor agonist reduced sodium reabsorption in the kidneys and expression of these receptors increased by practically 100 times. Sodium 39-45 arginine vasopressin receptor 1A Rattus norvegicus 10-13 27165083-6 2016 Our findings attest to the key role of V1a receptors in the regulation of renal excretion of sodium ions. Sodium 93-99 arginine vasopressin receptor 1A Rattus norvegicus 39-42 26854262-5 2016 Neural mechanisms and several gut hormones, including cholecystokinin and uroguanylin, have been suggested to mediate the natriuresis after an oral sodium load. Sodium 148-154 guanylate cyclase activator 2B Homo sapiens 74-85 26791475-1 2016 The present study aimed to investigate the potential physiological role of vasopressin and the incretin hormone of the gastrointestinal tract (glucagon-like peptide-1; GLP-1) in the regulation of the water-salt balance in a hyperosmolar state as a result of sodium loadings. Sodium 258-264 glucagon Rattus norvegicus 143-166 26791475-1 2016 The present study aimed to investigate the potential physiological role of vasopressin and the incretin hormone of the gastrointestinal tract (glucagon-like peptide-1; GLP-1) in the regulation of the water-salt balance in a hyperosmolar state as a result of sodium loadings. Sodium 258-264 glucagon Rattus norvegicus 168-173 26791475-7 2016 It was hypothesised that the basis for the fast elimination of excess sodium following an oral NaCl load could be the involvement of GLP-1 in osmoregulation combined with vasopressin. Sodium 70-76 glucagon Rattus norvegicus 133-138 26791475-8 2016 It was demonstrated that GLP-1 mimetic exenatide (1.5 nmol/kg) produced a significant decrease in proximal reabsorption and an increase in fractional sodium excretion (from 0.15 +- 0.04% to 9 +- 1%). Sodium 150-156 glucagon Rattus norvegicus 25-30 26791475-11 2016 These data suggest that GLP-1 combined with vasopressin could be involved in the regulation of sodium balance in the hyperosmolar state as a result of NaCl loading. Sodium 95-101 glucagon Rattus norvegicus 24-29 27010853-8 2016 Collectively, our data revealed that NHA1 and NHA2 function as a key sodium-hydrogen exchanger responsible for sperm motility after leaving the cauda epididymidis. Sodium 69-75 solute carrier family 9, subfamily B (NHA2, cation proton antiporter 2), member 2 Mus musculus 46-50 26906748-1 2016 The ion exchange mechanism of the sodium/calcium exchanger (NCX) crystallized by Liao et al. Sodium 34-40 T cell leukemia homeobox 2 Homo sapiens 60-63 26224401-5 2016 RESULTS: SNP rs5063 in the NPPA gene and SNP rs2077386 in the NPPC gene exhibited significant associations with BP response to low-sodium dietary intervention under recessive genetic model. Sodium 131-137 natriuretic peptide C Homo sapiens 62-66 28510148-4 2016 In recent years developments in genetics have shed new light on the types and physiology of various glucose transporters, of which there are two main types-sodium-glucose linked transporters (SGLTs) and facilitated diffusion glucose transporters (GLUT)-which can be divided into many more subclasses. Sodium 156-162 solute carrier family 2 member 1 Homo sapiens 100-120 28510148-4 2016 In recent years developments in genetics have shed new light on the types and physiology of various glucose transporters, of which there are two main types-sodium-glucose linked transporters (SGLTs) and facilitated diffusion glucose transporters (GLUT)-which can be divided into many more subclasses. Sodium 156-162 solute carrier family 2 member 1 Homo sapiens 247-251 26787348-5 2016 We show that the N-cadherin-NaV1.5 association is not random, that NaV1.5 molecules in these clusters are major contributors to cardiac sodium current, and that loss of NaV1.5 expression reduces intercellular adhesion strength. Sodium 136-142 cadherin 2 Homo sapiens 17-27 26751218-1 2016 Renal dopamine D1-like receptors (D1R and D5R) and the gastrin receptor (CCKBR) are involved in the maintenance of sodium homeostasis. Sodium 115-121 cholecystokinin B receptor Mus musculus 73-78 26751218-4 2016 Hence, we sought to investigate the interaction between D5R and CCKBR in the regulation of renal sodium excretion. Sodium 97-103 cholecystokinin B receptor Mus musculus 64-69 26751218-10 2016 Disruption of CCKBR in mice caused hypertension and decreased sodium excretion. Sodium 62-68 cholecystokinin B receptor Mus musculus 14-19 26751218-13 2016 Taken together, our findings indicate that CCKBR and D5R synergistically interact in the kidney, which may contribute to the maintenance of normal sodium balance following an increase in sodium intake. Sodium 147-153 cholecystokinin B receptor Mus musculus 43-48 26751218-13 2016 Taken together, our findings indicate that CCKBR and D5R synergistically interact in the kidney, which may contribute to the maintenance of normal sodium balance following an increase in sodium intake. Sodium 187-193 cholecystokinin B receptor Mus musculus 43-48 26683887-8 2016 The fractional excretions of urate and sodium showed a strong positive correlation with uromodulin, likely linked to the extracellular volume status. Sodium 39-45 uromodulin Homo sapiens 88-98 26683887-11 2016 The strongest associations were between uric acid, sodium, and uromodulin excretions and are likely linked to the extracellular volume status. Sodium 51-57 uromodulin Homo sapiens 63-73 26779035-5 2015 To illustrate this subtlety, we simulated this phenomenon using two approaches; (1) by using the standard, i.e., S1S2 protocol to quantify restitution and disabling the slow inactivation gate j of the sodium current (INa), and (2) by using the dynamic, i.e., S1S1 protocol for quantification of restitution and increasing INa at different cycle lengths (CL). Sodium 201-207 internexin neuronal intermediate filament protein alpha Homo sapiens 217-220 27666396-8 2016 However, only tempol increased the expression of eNOS elicited by sodium overload in the medial layer of the aorta and small arteries respect to HS group. Sodium 66-72 nitric oxide synthase 3 Rattus norvegicus 49-53 26440927-4 2016 Sensitivity to high Na(+) concentrations of the erv14 mutant associated to the intracellular mislocalization of Nha1p-GFP, together with a lower Na(+) efflux, indicate the involvement of this mutual association to accomplish the survival of the yeast cell upon sodium stress. Sodium 261-267 cornichon family protein Saccharomyces cerevisiae S288C 48-53 26429937-1 2015 Many spider-venom peptides are known to modulate the activity of the voltage-gated sodium (NaV) subtype 1.7 (NaV1.7) channel, which has emerged as a promising analgesic target. Sodium 83-89 sodium voltage-gated channel alpha subunit 9 Homo sapiens 109-115 26297688-4 2015 In the present work, we evaluated the effect of sodium intake on Fos-ir produced by WD-PR in brain areas operationally defined according to the literature as either facilitatory or inhibitory to sodium intake. Sodium 48-54 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 65-68 26297688-6 2015 Sodium intake decreased Fos-ir in facilitatory areas such as the lamina terminalis (particularly subfornical organ and median preoptic nucleus), central amygdala and hypothalamic parvocellular paraventricular nucleus in the forebrain. Sodium 0-6 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 24-27 26297688-7 2015 Sodium intake also decreased Fos-ir in inhibitory areas such as the area postrema, lateral parabrachial nucleus and nucleus of the solitary tract in the hindbrain. Sodium 0-6 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 29-32 26297688-8 2015 In contrast, sodium intake further increased Fos-ir that was activated by water deprivation in the dorsal raphe nucleus, another inhibitory area localized in the hindbrain. Sodium 13-19 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 45-48 26297688-10 2015 Sodium intake reduced Fos-ir in both parts of the accumbens. Sodium 0-6 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 22-25 26297688-11 2015 In summary, sodium intake following WD-PR reduced Fos-ir in most facilitatory and inhibitory areas, but increased Fos-ir in another inhibitory area. Sodium 12-18 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 50-53 26297688-11 2015 In summary, sodium intake following WD-PR reduced Fos-ir in most facilitatory and inhibitory areas, but increased Fos-ir in another inhibitory area. Sodium 12-18 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 114-117 26159698-3 2015 Butyrate has been shown to stimulate electroneutral sodium absorption through its regulation on sodium/hydrogen exchanger 3 (NHE3). Sodium 52-58 solute carrier family 9 member A3 Homo sapiens 125-129 26125643-5 2015 By targeting WNK4, FGF23 has been shown to increase the membrane abundance of the epithelial calcium channel TRPV5 and of the sodium-chloride cotransporter NCC, resulting in augmented renal calcium and sodium reabsorption. Sodium 126-132 fibroblast growth factor 23 Homo sapiens 19-24 26125643-7 2015 The calcium- and sodium-conserving functions of FGF23 may have major implications for the pathophysiology of cardiovascular diseases. Sodium 17-23 fibroblast growth factor 23 Homo sapiens 48-53 26147879-7 2015 Our findings identify endogenous relaxin-3-RXFP3 signalling as a modulator of sodium appetite. Sodium 78-84 relaxin 3 Mus musculus 33-42 26259032-15 2015 Our results indicate that PCSK6 is the long-sought corin activator and is important for sodium homeostasis and normal blood pressure. Sodium 88-94 proprotein convertase subtilisin/kexin type 6 Homo sapiens 26-31 26100633-2 2015 Activation of SLICK channels may be important during pathological states such as ischemia, in which an increase in intracellular sodium and chloride can perturb membrane potential and ion homeostasis. Sodium 129-135 potassium sodium-activated channel subfamily T member 2 Rattus norvegicus 14-19 26109717-11 2015 The study of the nodal/paranodal architecture demonstrated that sodium channels and Caspr were correctly localized in patients with CMT2E. Sodium 64-70 neurofilament light chain Homo sapiens 132-137 25078966-7 2015 A reduced total scan time of 22 min was achieved under the SAR restriction for human studies in quantifying both total and bound sodium concentrations. Sodium 129-135 sarcosine dehydrogenase Homo sapiens 59-62 26157341-6 2015 Treatment with sodium selenite reduced cell death, stabilized mitochondrial membrane potential and oxygen consumption rate, and prevented accumulation of ROS and activation of caspase-3. Sodium 15-21 caspase 3 Mus musculus 176-185 25715988-5 2015 In offspring of both sexes at 12 mo of age, there were no differences in kidney weights, urine output, or urinary sodium excretion; however, prenatal CORT exposure increased the urinary albumin/creatinine ratio and 24-h urinary albumin excretion. Sodium 114-120 cortistatin Mus musculus 150-154 25767117-8 2015 JNK inhibition attenuated increases in cell surface expression of Nav1.6 sodium channels induced by overexpression of APP. Sodium 73-79 mitogen-activated protein kinase 8 Mus musculus 0-3 25767117-12 2015 Therefore, we show that APP enhances Nav1.6 sodium channel cell surface expression through a Go-coupled JNK pathway. Sodium 44-50 mitogen-activated protein kinase 8 Mus musculus 104-107 25524356-5 2015 Declining serum sodium levels were associated with increasing age, a higher number of comorbidities, a more advanced TNM stage and worsening biochemical parameters. Sodium 16-22 teneurin transmembrane protein 1 Homo sapiens 117-120 25776075-4 2015 Given the proximity of macula densa to the juxtaglomerular area and the importance of macula densa released prostanoids in renin synthesis and release, we hypothesized that chronic sodium deprivation induces macula densa release of prostanoids, stimulating renal CD44+ cell activation and differentiation. Sodium 181-187 CD44 antigen Mus musculus 263-267 25776075-6 2015 Low sodium stimulated prostaglandin E2 production by MMDD1 and induced migration of CD44+ cells. Sodium 4-10 CD44 antigen Mus musculus 84-88 25744892-7 2015 Furthermore, TEH4 enhanced persistent current and slowed sodium current decay. Sodium 57-63 tipE homolog 4 Drosophila melanogaster 13-17 25750424-8 2015 In the yeast cornichon mutant erv14, OsHKT1;3 is mistargeted, preventing the toxic effects of sodium transport in the cell observed in wild-type cells or in the erv14 mutant that co-expressed OsHKT1;3 with either OsCNIH1 or Erv14p. Sodium 94-100 cornichon family protein Saccharomyces cerevisiae S288C 30-35 25858030-11 2015 Pharmacological blockade of the AT1 receptor with losartan prior to RNS abolished both the functional and the molecular responses, suggesting that intrarenal Ang II acting via the AT1 receptor is a major factor for NHE3-mediated sodium and water reabsorption induced by RNS. Sodium 229-235 solute carrier family 9 member A3 Homo sapiens 215-219 25859219-4 2015 Sodium-calcium exchange (NCX) is most often considered in the context of mediating membrane depolarisation after spark-like events. Sodium 0-6 T cell leukemia homeobox 2 Homo sapiens 25-28 25617595-1 2015 Oxytocin (OT), a neurohormone, has been related to natriuretic and diuretic effects and also to water intake and sodium appetite. Sodium 113-119 oxytocin/neurophysin I prepropeptide Homo sapiens 0-8 25617595-1 2015 Oxytocin (OT), a neurohormone, has been related to natriuretic and diuretic effects and also to water intake and sodium appetite. Sodium 113-119 oxytocin/neurophysin I prepropeptide Homo sapiens 10-12 25617595-3 2015 Experiment 1 showed that OT administration increases the urine volume, urinary sodium concentration, and natriuresis and reduces the water intake, water and sodium balances, and estimated plasma sodium concentration induced by hypertonic NaCl administration. Sodium 79-85 oxytocin/neurophysin I prepropeptide Homo sapiens 25-27 25617595-3 2015 Experiment 1 showed that OT administration increases the urine volume, urinary sodium concentration, and natriuresis and reduces the water intake, water and sodium balances, and estimated plasma sodium concentration induced by hypertonic NaCl administration. Sodium 157-163 oxytocin/neurophysin I prepropeptide Homo sapiens 25-27 25617595-3 2015 Experiment 1 showed that OT administration increases the urine volume, urinary sodium concentration, and natriuresis and reduces the water intake, water and sodium balances, and estimated plasma sodium concentration induced by hypertonic NaCl administration. Sodium 157-163 oxytocin/neurophysin I prepropeptide Homo sapiens 25-27 25601932-8 2015 Our results suggest that during Ang-II hypertension both IFN-gamma and IL-17A production interfere with the pressure natriuretic decrease in proximal tubule sodium transport and that IFN-gamma production is necessary to activate distal sodium reabsorption. Sodium 157-163 interleukin 17A Mus musculus 71-77 25347571-2 2015 These mutations abolish the K(+) selectivity of Kir3.4 and, consequently, cause sodium (Na(+)) leak, depolarized membrane potential, and nonsuppressible aldosterone secretion. Sodium 80-86 potassium inwardly rectifying channel subfamily J member 5 Homo sapiens 48-54 26277930-0 2015 Common Variants in Serum/Glucocorticoid Regulated Kinase 1 (SGK1) and Blood Pressure Responses to Dietary Sodium or Potassium Interventions: A family-Based Association Study. Sodium 106-112 serum/glucocorticoid regulated kinase 1 Homo sapiens 60-64 26277930-2 2015 This study aimed to assess the association of common genetic variants in the SGK1 gene with BP responses to controlled dietary sodium or potassium interventions. Sodium 127-133 serum/glucocorticoid regulated kinase 1 Homo sapiens 77-81 26277930-7 2015 However, the associations between selected SNPs in the SGK1 gene and BP responses to high-sodium or high-sodium plus potassium-supplementation intervention did not reach statistical significance. Sodium 90-96 serum/glucocorticoid regulated kinase 1 Homo sapiens 55-59 26277930-7 2015 However, the associations between selected SNPs in the SGK1 gene and BP responses to high-sodium or high-sodium plus potassium-supplementation intervention did not reach statistical significance. Sodium 105-111 serum/glucocorticoid regulated kinase 1 Homo sapiens 55-59 26277930-10 2015 CONCLUSION: Our study indicates that the genetic polymorphism in the SGK1 gene is significantly associated with BP responses to dietary sodium intervention. Sodium 136-142 serum/glucocorticoid regulated kinase 1 Homo sapiens 69-73 25618976-0 2014 Electroacupuncture of neiguan (PC 6) inhibits enhanced voltage-gated sodium currents in ischemic ventricular myocytes. Sodium 69-75 proprotein convertase subtilisin/kexin type 5 Rattus norvegicus 31-35 25053638-0 2014 SCN10A/Nav1.8 modulation of peak and late sodium currents in patients with early onset atrial fibrillation. Sodium 42-48 sodium voltage-gated channel alpha subunit 10 Homo sapiens 0-6 25053638-0 2014 SCN10A/Nav1.8 modulation of peak and late sodium currents in patients with early onset atrial fibrillation. Sodium 42-48 sodium voltage-gated channel alpha subunit 10 Homo sapiens 7-13 25088311-0 2014 Heterozygous CLCN1 mutations can modulate phenotype in sodium channel myotonia. Sodium 55-61 chloride voltage-gated channel 1 Homo sapiens 13-18 25265491-1 2014 Sodium reabsorption via Na-K-2Cl cotransporter 2 (NKCC2) in the thick ascending limbs has a major role for medullary osmotic gradient and subsequent water reabsorption in the collecting ducts. Sodium 0-6 solute carrier family 12 member 1 Rattus norvegicus 24-48 25265491-1 2014 Sodium reabsorption via Na-K-2Cl cotransporter 2 (NKCC2) in the thick ascending limbs has a major role for medullary osmotic gradient and subsequent water reabsorption in the collecting ducts. Sodium 0-6 solute carrier family 12 member 1 Rattus norvegicus 50-55 25022513-5 2014 Uptake of [(3)H]ergothioneine occurred by the organic cation transporter novel type-1 (OCTN-1), was sodium-dependent, and was reduced when expression of OCTN-1 was silenced by small interfering RNA (siRNA). Sodium 100-106 solute carrier family 22 member 4 Homo sapiens 87-93 25022513-5 2014 Uptake of [(3)H]ergothioneine occurred by the organic cation transporter novel type-1 (OCTN-1), was sodium-dependent, and was reduced when expression of OCTN-1 was silenced by small interfering RNA (siRNA). Sodium 100-106 solute carrier family 22 member 4 Homo sapiens 153-159 24797667-0 2014 FGF23 regulates renal sodium handling and blood pressure. Sodium 22-28 fibroblast growth factor 23 Mus musculus 0-5 24797667-3 2014 Renal sodium (Na(+)) reabsorption and distal tubular membrane expression of NCC are reduced in mouse models of Fgf23 and alphaKlotho deficiency. Sodium 6-12 fibroblast growth factor 23 Mus musculus 111-116 24582607-4 2014 RESULTS: The mutant channel expressed alone caused a 70% reduction in inward sodium current (INa) density compared to WT currents, which was consistent with its partial proteasomal degradation. Sodium 77-83 internexin neuronal intermediate filament protein alpha Homo sapiens 93-96 24590923-12 2014 This study is a novel demonstration that renal endogenous Ang II-oxidative stress, induced in vivo in hypernatremic rats by an acute sodium overload, regulates AQP-2 expression. Sodium 133-139 angiogenin Rattus norvegicus 58-61 25206775-5 2014 These results suggest that matrix metalloproteinase-9 upregulation is associated with increased regional angiogenesis and degradation of collagen IV, the major component of the basal lamina, in stroke-prone spontaneously hypertensive rats with high-sodium water-induced focal cerebral infarction. Sodium 249-255 matrix metallopeptidase 9 Rattus norvegicus 27-53 24878720-8 2014 RESULTS: In single-marker association analyses, SGK1 marker rs2758151 was significantly associated with diastolic BP (DBP) response to high-sodium intervention (P = 0.0010). Sodium 140-146 serum/glucocorticoid regulated kinase 1 Homo sapiens 48-52 24878720-11 2014 In addition, gene-based analyses demonstrated significant associations between SGK1 and SBP, DBP and MAP responses to high sodium intervention (P = 0.0002, 0.0076, and 0.00001, respectively). Sodium 123-129 serum/glucocorticoid regulated kinase 1 Homo sapiens 79-83 23636436-10 2014 In multivariate analysis, serum sodium correlated significantly and independently with residual renal function (RRF: r = 0.463, p = 0.0001) and negatively with the daily volume of instilled icodextrin (r = -0.476, p = 0.0001). Sodium 32-38 mitochondrial ribosome recycling factor Homo sapiens 112-115 23636436-17 2014 Serum sodium is strongly correlated with RRF, hyponatremia being associated with lower RRF. Sodium 6-12 mitochondrial ribosome recycling factor Homo sapiens 41-44 23636436-17 2014 Serum sodium is strongly correlated with RRF, hyponatremia being associated with lower RRF. Sodium 6-12 mitochondrial ribosome recycling factor Homo sapiens 87-90 24767681-0 2014 Allosteric sodium in class A GPCR signaling. Sodium 11-17 vomeronasal 1 receptor 17 pseudogene Homo sapiens 29-33 24767681-4 2014 New insights help to explain allosteric effects of sodium on GPCR agonist binding and activation, and sodium"s role as a potential co-factor in class A GPCR function. Sodium 51-57 vomeronasal 1 receptor 17 pseudogene Homo sapiens 61-65 24608976-0 2014 A novel tescalcin-sodium/hydrogen exchange axis underlying sorafenib resistance in FLT3-ITD+ AML. Sodium 18-24 tescalcin Homo sapiens 8-17 24401712-7 2014 Our observations demonstrate changes in sodium influx that provide a mechanistic link between the altered biophysical properties of a mutant Nav1.7 channel and nociceptor hyperexcitability underlying the pain phenotype in IEM. Sodium 40-46 sodium voltage-gated channel alpha subunit 9 Homo sapiens 141-147 24530955-1 2014 A new method is proposed for acquiring 3D biexponential-weighted sodium images with two instead of three RF pulses to allow for shorter repetition time at high magnetic fields (B0>=7 T) and reduced SAR. Sodium 65-71 sarcosine dehydrogenase Homo sapiens 201-204 24659330-1 2014 The Salt Overly Sensitive (SOS) pathway regulates intracellular sodium ion (Na(+)) homeostasis and salt tolerance in plants. Sodium 64-70 Protein kinase superfamily protein Arabidopsis thaliana 27-30 24291282-10 2014 Patch-clamp analysis of isolated CAR+/- myocytes showed reduced sodium current magnitude specifically at the intercalated disk. Sodium 64-70 CXADR Ig-like cell adhesion molecule Homo sapiens 33-36 23919677-3 2014 Sodium calcium exchangers (NCXs) play important roles in regulating intracellular calcium, and accumulating data suggests that reduced NCX function, following aberrant proteolytic cleavage of these exchangers, may contribute to neurodegeneration. Sodium 0-6 T cell leukemia homeobox 2 Homo sapiens 27-30 24262505-8 2014 Multivariate analysis found that age, PSTR, daily ultrafiltration, and sodium removal were significant predictors of Pcl when adjusted for sex, comorbidity, glucose exposure, and residual renal function. Sodium 71-77 PHD finger protein 1 Homo sapiens 117-120 24158986-6 2014 Elevated FGF-23 was associated more strongly with CHF than with atherosclerotic events (P=0.02), and uniformly was associated with greater risk of CHF events across subgroups stratified by eGFR, proteinuria, prior heart disease, diabetes, BP control, anemia, sodium intake, income, fat-free mass, left ventricular mass index, and ejection fraction. Sodium 259-265 fibroblast growth factor 23 Homo sapiens 9-15 24026042-14 2014 These data suggest that high-sodium level directly augments Ang II-induced VSMC proliferation through NHE-1- and ERK 1/2-dependent pathways and may offer new insights into the mechanisms of vascular remodeling by high-sodium/Ang II. Sodium 29-35 solute carrier family 9 member A1 Rattus norvegicus 102-107 24572816-1 2014 Ranolazine (RAN), a novel antianginal agent, inhibits the increased late sodium current (INa.L) under many pathological conditions. Sodium 73-79 LOW QUALITY PROTEIN: alpha-internexin Oryctolagus cuniculus 89-92 24349144-6 2013 The inserted sequence included the META motif, which has previously been implicated in increased sodium tolerance of the Hal2 homologue from a related fungal species. Sodium 97-103 3'(2'),5'-bisphosphate nucleotidase Saccharomyces cerevisiae S288C 121-125 24049115-0 2013 ENaC-expressing neurons in the sensory circumventricular organs become c-Fos activated following systemic sodium changes. Sodium 106-112 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 71-76 24049115-5 2013 These neurons become c-Fos activated, a marker for neuronal activity, after various manipulations of peripheral levels of sodium including systemic injections with hypertonic saline, dietary sodium deprivation, and sodium repletion after prolonged sodium deprivation. Sodium 122-128 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 21-26 24049115-5 2013 These neurons become c-Fos activated, a marker for neuronal activity, after various manipulations of peripheral levels of sodium including systemic injections with hypertonic saline, dietary sodium deprivation, and sodium repletion after prolonged sodium deprivation. Sodium 191-197 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 21-26 24049115-5 2013 These neurons become c-Fos activated, a marker for neuronal activity, after various manipulations of peripheral levels of sodium including systemic injections with hypertonic saline, dietary sodium deprivation, and sodium repletion after prolonged sodium deprivation. Sodium 191-197 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 21-26 24049115-5 2013 These neurons become c-Fos activated, a marker for neuronal activity, after various manipulations of peripheral levels of sodium including systemic injections with hypertonic saline, dietary sodium deprivation, and sodium repletion after prolonged sodium deprivation. Sodium 191-197 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 21-26 24049115-6 2013 The increases seen c-Fos activity in the CVOs were correlated with parallel increases in plasma sodium levels. Sodium 96-102 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 19-24 24045943-6 2013 Kinetic studies with conservative and non-conservative mutants of sodium sensitive residues further underscored the importance of Gln(75), Phe(76), Met(79), Gly(83), Leu(86), Phe(90), and Asp(91) in hASBT function. Sodium 66-72 solute carrier family 10 member 2 Homo sapiens 199-204 24045943-8 2013 Combined, our data propose that a consortium of sodium-sensitive residues along with previously reported residues (Thr(134), Leu(138), and Thr(149)) from TM3 may form the sodium binding and translocation pathway. Sodium 48-54 tropomyosin 3 Homo sapiens 154-157 24045943-8 2013 Combined, our data propose that a consortium of sodium-sensitive residues along with previously reported residues (Thr(134), Leu(138), and Thr(149)) from TM3 may form the sodium binding and translocation pathway. Sodium 171-177 tropomyosin 3 Homo sapiens 154-157 23810808-7 2013 TGF-beta2 treatment of ARPE-19 cells resulted in a time-dependent decrease in Na,K-ATPase beta1 mRNA and protein levels while Na,K-ATPase alpha1 levels, Na,K-ATPase activity, and intracellular sodium levels remained largely unchanged. Sodium 193-199 transforming growth factor beta 2 Homo sapiens 0-9 24204233-1 2013 LeuT-like fold Na-dependent secondary active transporters form a large family of integral membrane proteins that transport various substrates against their concentration gradient across lipid membranes, using the free energy stored in the downhill concentration gradient of sodium ions. Sodium 274-280 Leucine transport, high Homo sapiens 0-4 24204233-5 2013 Using a multi-dimensional path sampling (string-method) followed by all-atom free energy simulations, we established the principal thermodynamic and kinetic components governing the ion-dependent conformational dynamics of a LeuT-like fold transporter, the sodium/benzyl-hydantoin symporter Mhp1, for an entire conformational cycle. Sodium 257-263 Leucine transport, high Homo sapiens 225-229 24204233-5 2013 Using a multi-dimensional path sampling (string-method) followed by all-atom free energy simulations, we established the principal thermodynamic and kinetic components governing the ion-dependent conformational dynamics of a LeuT-like fold transporter, the sodium/benzyl-hydantoin symporter Mhp1, for an entire conformational cycle. Sodium 257-263 calcium voltage-gated channel subunit alpha1 A Homo sapiens 291-295 24073217-0 2013 Body sodium overload modulates the firing rate and fos immunoreactivity of serotonergic cells of dorsal raphe nucleus. Sodium 5-11 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 51-54 24073217-7 2013 Both Fos-OT immunoreactive and plasma OT concentration increased after s.c. hypertonic sodium infusion. Sodium 87-93 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 5-8 23794401-10 2013 Robust associations between Delta BMC and Delta [Na+]p suggest that sodium status and bone density may be inter-related during endurance exercise and should be considered in future investigations of athletic osteopenia. Sodium 68-74 catenin beta like 1 Homo sapiens 49-54 23872594-6 2013 Experiments involving heterologous expression in HEK293 cells further showed that TMEM16C modulated the single-channel activity of Slack channels and increased its sodium sensitivity. Sodium 164-170 anoctamin 3 Homo sapiens 82-89 24009611-6 2013 Finally, adenosine diphosphoribose (ADPR) a breakdown product of both NAD and cADPR activates a plasma membrane cation channel termed TRPM2 thereby facilitating calcium (and sodium) entry into T cells. Sodium 174-180 transient receptor potential cation channel subfamily M member 2 Homo sapiens 134-139 23836888-12 2013 Diminution of sodium currents, largely NaV1.7, was recapitulated in sensory neurons expressing CRMP2-K374A. Sodium 14-20 sodium voltage-gated channel alpha subunit 9 Homo sapiens 39-45 23897888-4 2013 Cells lacking IST1 (increased sodium tolerance 1), an endosomal sorting complex required for transport (ESCRT) component to which spastin binds, also had increased endosomal tubulation. Sodium 30-36 spastin Danio rerio 130-137 23903415-3 2013 NHE3 is required for sodium and fluid absorption, and its activity is coupled to passive reabsorption of a major fraction of calcium through the paracellular route. Sodium 21-27 solute carrier family 9 member A3 Homo sapiens 0-4 23874427-8 2013 Both TipE and TEH1 enhanced the amplitude of sodium current and accelerated current decay of all three sodium channels tested. Sodium 45-51 temperature-induced paralytic E Drosophila melanogaster 5-9 23874427-8 2013 Both TipE and TEH1 enhanced the amplitude of sodium current and accelerated current decay of all three sodium channels tested. Sodium 45-51 tipE homolog 1 Drosophila melanogaster 14-18 23853500-5 2013 Herein we present a 42-yr-old Korean male of DM1 with abnormally elevated serum sodium and potassium. Sodium 80-86 DM1 protein kinase Homo sapiens 45-48 23825530-6 2013 FGF23 concentration correlated with the MELD score, serum sodium concentration, and GFR. Sodium 58-64 fibroblast growth factor 23 Homo sapiens 0-5 23720317-1 2013 NHA2 is a sodium/hydrogen exchanger with unknown physiological function. Sodium 10-16 solute carrier family 9, subfamily B (NHA2, cation proton antiporter 2), member 2 Mus musculus 0-4 23739961-5 2013 In response to changing synaptic excitation, Pum regulates the translation of the voltage-gated sodium conductance, leading to a concomitant adjustment in action potential firing. Sodium 96-102 pumilio Drosophila melanogaster 45-48 23545808-2 2013 The aim of the present study was to investigate the direct effects of acid loading on the proliferation of rat glomerular mesangial cells (GMCs) in vitro and the possible role of sodium-hydrogen ion exchanger isoform 1 (NHE1). Sodium 179-185 solute carrier family 9 member A1 Rattus norvegicus 220-224 23360087-2 2013 The thyroid transcription factors-NKx2 homeobox 1 (NKx2-1, formerly called TTF-1) and Paired box gene 8 (Pax8)-are known to associate biochemically and synergistically in the activation of thyroid functional genes including the sodium/iodide symporter (NIS), thyrotropin (TSH) receptor (TSHR), thyroglobulin (Tg), and thyroid peroxidase (TPO) genes. Sodium 228-234 thyroid stimulating hormone receptor Mus musculus 287-291