PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 12011484-9 2002 1-aminobenzotriazole, a suicidal P450 enzyme inhibitor, attenuated the effects of acrylonitrile on catalase and xanthine oxidase in SHE cells, suggesting that P450 metabolism is required for acrylonitrile to produce its effects on these enzymes. 1-aminobenzotriazole 0-20 catalase Rattus norvegicus 99-107 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 33828490-0 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 28445205-6 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 27627464-3 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 27627464-4 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 22957745-2 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 19171180-5 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 10608847-1 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 9174082-0 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 9176324-9 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 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 9134052-3 1997 D-Fructose induced a sodium-independent release of GLP-1. Sodium 21-27 glucagon Rattus norvegicus 51-56 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 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 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 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 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 8897973-8 1996 Furthermore, intracerebroventricular GLP-1 stimulated urinary excretion of water and sodium. Sodium 85-91 glucagon Rattus norvegicus 37-42 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 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 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 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 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 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 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 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 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 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 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 8869083-0 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 2974246-1 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 3488538-11 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 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 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 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 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 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 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 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 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 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 6373590-1 1984 Dissociation of blood pressure lowering and renin inhibition in sodium-deficient dogs. Sodium 64-70 renin Canis lupus familiaris 44-49 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 33921209-7 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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