PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 12154110-1 2002 Renal endothelin-1 participates in sodium and water handling, and its urinary excretion is increased in sodium-retentive states. Sodium 35-41 endothelin 1 Homo sapiens 6-18 15328386-9 2004 Finally, ET-1 decreased sodium excretion by 58% and VML 588 reduced this decrease dose-independently by two-thirds. Sodium 24-30 endothelin 1 Homo sapiens 9-13 12154110-6 2002 In the renal cortex, low sodium diet caused a 194% increase in prepro-endothelin-1 mRNA (P<0.05), whereas endothelin-converting enzyme-1 type B and type A receptors remained unchanged. Sodium 25-31 endothelin 1 Homo sapiens 70-82 12154110-9 2002 In conclusion, during low sodium diet, renal prepro-endothelin-1 synthesis increases mainly in the renal cortex (where no changes in receptors occur), whereas type B receptor is selectively enhanced in the renal medulla. Sodium 26-32 endothelin 1 Homo sapiens 52-64 12887970-0 2003 Sodium-calcium exchange influences the response to endothelin-1 in lens epithelium. Sodium 0-6 endothelin 1 Homo sapiens 51-63 12887970-9 2003 The half-time for decay of the ET-1 and ATP calcium peak was increased several folds by bepridil, ouabain and low-sodium conditions. Sodium 114-120 endothelin 1 Homo sapiens 31-35 12887970-11 2003 Taken together findings suggest inhibition of sodium-calcium exchange increases the magnitude of the receptor-initiated store-release phase of the ET-1 calcium signaling response as the result of impaired calcium clearance from the cytoplasm. Sodium 46-52 endothelin 1 Homo sapiens 147-151 12154110-1 2002 Renal endothelin-1 participates in sodium and water handling, and its urinary excretion is increased in sodium-retentive states. Sodium 104-110 endothelin 1 Homo sapiens 6-18 11811373-11 2001 There is some evidence for a role of ET-1 in blood pressure elevation in some experimental forms of hypertension, particularly severe, sodium-sensitive hypertension, in which it may play a role in accentuating rather than initiating blood pressure elevation. Sodium 135-141 endothelin 1 Homo sapiens 37-41 10928293-6 2000 The relationship between urinary volume and urinary ET-1 was stronger than that of urinary sodium with ET-1 excretion because sodium was excluded from the multivariable model when urinary volume was introduced. Sodium 91-97 endothelin 1 Homo sapiens 103-107 11011335-1 2000 BACKGROUND: Recent studies have shown that endothelin-1 (ET-1) antagonists increase sodium excretion and improve renal blood flow in experimental heart failure (HF). Sodium 84-90 endothelin 1 Homo sapiens 43-55 11011335-1 2000 BACKGROUND: Recent studies have shown that endothelin-1 (ET-1) antagonists increase sodium excretion and improve renal blood flow in experimental heart failure (HF). Sodium 84-90 endothelin 1 Homo sapiens 57-61 11011335-3 2000 Our aim was to investigate renal ET-1 formation and its relation to sodium excretion in patients with HF. Sodium 68-74 endothelin 1 Homo sapiens 33-37 11011335-8 2000 In the 71 subjects who were not receiving diuretic treatment, urinary ET-1 was selected as the strongest predictor of sodium excretion by multivariate stepwise analysis. Sodium 118-124 endothelin 1 Homo sapiens 70-74 11011335-9 2000 CONCLUSIONS: Urinary ET-1 excretion increases in an earlier phase of HF than plasma ET-1 and appears to be closely correlated with sodium excretion, indicating renal ET-1 is a target for ET-1 antagonists in patients with HF. Sodium 131-137 endothelin 1 Homo sapiens 21-25 11710777-5 2001 CONCLUSIONS: The association of renal ET-1 and NO activity with sodium excretion supports the hypothesis that these factors play a role in the physiologic response to acute changes in sodium intake, particularly in African Americans. Sodium 64-70 endothelin 1 Homo sapiens 38-42 11710777-5 2001 CONCLUSIONS: The association of renal ET-1 and NO activity with sodium excretion supports the hypothesis that these factors play a role in the physiologic response to acute changes in sodium intake, particularly in African Americans. Sodium 184-190 endothelin 1 Homo sapiens 38-42 11566009-2 2001 In the kidney, ET-1 not only produces vasoconstriction, but also vasodilation in the renal medulla, stimulation of sodium reabsorption in the proximal tubule, and inhibition of reabsorption in a variety of nephron segments. Sodium 115-121 endothelin 1 Homo sapiens 15-19 11274080-10 2001 Sodium content was detectably increased in lenses exposed to ET-1 for 24 hours. Sodium 0-6 endothelin 1 Homo sapiens 61-65 10928293-11 2000 Since urinary ET-1 reflects its renal synthesis, our data support the notion that renal ET-1 plays a role in the regulation of sodium balance in patients with mild hypertension. Sodium 127-133 endothelin 1 Homo sapiens 88-92 9832178-8 1998 Our results suggest that renal ET-1 may be responsible for the renal handling of sodium homeostasis, and alteration of renal ET-1 synthesis may be a contributory factor in the pathogenesis of essential hypertension and salt sensitivity. Sodium 81-87 endothelin 1 Homo sapiens 31-35 10344351-13 1999 We observed a highly significant inverse correlation between the plasma endothelin-1 concentrations and the ability to excrete a given water and sodium load, suggesting that the endothelin system plays a role in the regulation of water excretion in patients with liver cirrhosis. Sodium 145-151 endothelin 1 Homo sapiens 72-84 9791046-6 1998 During atrial natriuretic peptide infusion, urinary endothelin-1 directly correlated with plasma atrial natriuretic peptide, urinary cGMP and sodium excretion.3. Sodium 142-148 endothelin 1 Homo sapiens 52-64 10906163-7 2000 Infusion of ET-1 significantly decreased effective renal plasma flow, GFR, sodium excretion, and urine flow. Sodium 75-81 endothelin 1 Homo sapiens 12-16 10757221-4 2000 Evidence suggests that endothelin-1 within the renal medulla is activated in conditions of salt loading and inhibits reabsorption of sodium in a nitric oxide-dependent manner. Sodium 133-139 endothelin 1 Homo sapiens 23-35 9830275-4 1998 The 24-hour urinary excretion of ET-1 in patients with GN or CRF showed significant correlation with the urinary excretion of sodium (r = 0.27, p < 0.05). Sodium 126-132 endothelin 1 Homo sapiens 33-37 9724315-3 1998 Renal ET-1 formation is affected by sodium intake, because 1 wk of high sodium decreased urinary ET-1 excretion (-34%, P < 0.05), whereas a low-sodium diet increased ET-1 excretion (66%, P < 0.05) and mRNA expression for preproendothelin-1 in epithelial cells of medullary collecting ducts and endothelial cells of the peritubular capillary network. Sodium 72-78 endothelin 1 Homo sapiens 227-245 9724315-3 1998 Renal ET-1 formation is affected by sodium intake, because 1 wk of high sodium decreased urinary ET-1 excretion (-34%, P < 0.05), whereas a low-sodium diet increased ET-1 excretion (66%, P < 0.05) and mRNA expression for preproendothelin-1 in epithelial cells of medullary collecting ducts and endothelial cells of the peritubular capillary network. Sodium 72-78 endothelin 1 Homo sapiens 227-245 10684103-0 1998 [Effects of plasma endothelin-1 and aldosterone on sodium retention in children with nephrotic syndrome]. Sodium 51-57 endothelin 1 Homo sapiens 19-31 10684103-6 1998 Plasma ET-1 was positively correlated with the serum sodium ionic concentration and negatively correlated with the serum Alb(r = 0.486, P < 0.01; r = 0.490, P < 0.01, respectively). Sodium 53-59 endothelin 1 Homo sapiens 7-11 10684103-7 1998 In conclusion, the sodium retention with nephrotic syndrome might be correlated with reduction of secreted sodium in the kidney, suggesting that ET-1 plays an important role in pathogenesis. Sodium 19-25 endothelin 1 Homo sapiens 145-149 10684103-7 1998 In conclusion, the sodium retention with nephrotic syndrome might be correlated with reduction of secreted sodium in the kidney, suggesting that ET-1 plays an important role in pathogenesis. Sodium 107-113 endothelin 1 Homo sapiens 145-149 9002526-3 1997 ET-1 exerts a wide range of biologic effects in the kidney, including constriction of most renal vessels, mesangial cell contraction, inhibition of sodium and water reabsorption by the nephron, enhancement of glomerular cell proliferation, and stimulation of extracellular matrix accumulation. Sodium 148-154 endothelin 1 Homo sapiens 0-4 9231815-2 1997 We recently reported strong sodium retention and renal vasoconstriction during pathophysiological increments in plasma ET-1. Sodium 28-34 endothelin 1 Homo sapiens 119-123 9002526-10 1997 Deranged ET-1 production in the nephron may cause inappropriate sodium and water retention, thereby contributing to the development and/or maintenance of hypertension. Sodium 64-70 endothelin 1 Homo sapiens 9-13 9013446-1 1997 The authors recently reported that infusion of endothelin-1 in humans to obtain pathophysiological plasma levels causes profound renal vasoconstriction and sodium retention. Sodium 156-162 endothelin 1 Homo sapiens 47-59 9013446-9 1997 Sodium excretion rate decreased during endothelin-1 infusion, from a baseline value of 182 +/- 33 to 84 +/- 28 mumol/min at the end of the endothelin-1 infusion. Sodium 0-6 endothelin 1 Homo sapiens 39-51 9013446-9 1997 Sodium excretion rate decreased during endothelin-1 infusion, from a baseline value of 182 +/- 33 to 84 +/- 28 mumol/min at the end of the endothelin-1 infusion. Sodium 0-6 endothelin 1 Homo sapiens 139-151 8907569-8 1996 In patients with ascites, endothelin-1 was inversely correlated with both glomerular filtration rate (upright: r = -0.62; p = 0.06; supine: r = -0.71, p < 0.05) and renal sodium excretion (upright: r = -0.82; p < 0.01; supine: r = -0.88; p < 0.001). Sodium 174-180 endothelin 1 Homo sapiens 26-38 7562563-1 1995 Infusion of endothelin-1 in humans to obtain pathophysiological plasma levels causes mild hypertension, strong sodium retention and renal vasoconstriction. Sodium 111-117 endothelin 1 Homo sapiens 12-24 8547550-11 1995 Venous ET-1 levels were significantly correlated with venous oxygen content, pH, PO2, oxygen saturation, base excess, blood sodium concentration, and potassium concentration. Sodium 124-130 endothelin 1 Homo sapiens 7-11 7965436-1 1994 We investigated the role of endothelin-1 in the renal adaptation to alterations in sodium balance in premature infants. Sodium 83-89 endothelin 1 Homo sapiens 28-40 7721406-1 1995 Endothelin-1 infusion into humans to obtain pathophysiological plasma levels causes mild hypertension, strong renal vasoconstriction, and sodium retention. Sodium 138-144 endothelin 1 Homo sapiens 0-12 7565483-5 1995 Lastly, ET-1 is also an autocrine inhibitor of collecting duct sodium and water reabsorption; reduced nephron ET-1 production may result in fluid retention in essential hypertension. Sodium 63-69 endothelin 1 Homo sapiens 8-12 8538922-8 1995 Likewise the changes in renal handling of sodium and water in response to ET-1 infusion were unaffected by pretreatment with placebo or isradipine, e.g. sodium excretion (-44.6% versus -40.8%), urine flow rate (-49.8% versus -38.9%) and clearance of lithium (-32.0% versus -29.1%). Sodium 42-48 endothelin 1 Homo sapiens 74-78 8538922-9 1995 CONCLUSIONS: Intravenous infusion of ET-1 in healthy humans discretely increases diastolic blood pressure and profoundly decreases renal haemodynamics and excretion of sodium and water. Sodium 168-174 endothelin 1 Homo sapiens 37-41 7965436-6 1994 We conclude that in sodium-depleted premature infants with high urinary sodium excretion, an angiotensin II-mediated increase in renal endothelin-1 production occurs, which acts in concert with angiotensin II to restore sodium balance. Sodium 20-26 endothelin 1 Homo sapiens 135-147 7965436-6 1994 We conclude that in sodium-depleted premature infants with high urinary sodium excretion, an angiotensin II-mediated increase in renal endothelin-1 production occurs, which acts in concert with angiotensin II to restore sodium balance. Sodium 72-78 endothelin 1 Homo sapiens 135-147 7965436-6 1994 We conclude that in sodium-depleted premature infants with high urinary sodium excretion, an angiotensin II-mediated increase in renal endothelin-1 production occurs, which acts in concert with angiotensin II to restore sodium balance. Sodium 72-78 endothelin 1 Homo sapiens 135-147 7967349-1 1994 Elevated levels of the vasocontrictor peptide endothelin-1 have been demonstrated in various pathological conditions that are characterized by sodium retention and/or renal vasoconstriction, such as heart failure, hepatorenal syndrome, renal failure and during administration of cyclosporin and radiocontrast. Sodium 143-149 endothelin 1 Homo sapiens 46-58 7967349-4 1994 Infusion of low dosages of endothelin-1, that result in a twofold increase in plasma levels, decreased sodium excretion by 36%, without a significant effect on systemic and renal hemodynamics. Sodium 103-109 endothelin 1 Homo sapiens 27-39 7967349-5 1994 Infusion of 2.5 ng/kg/min of endothelin-1 further enhanced sodium retention and, in addition, increased renal vascular resistance by 37%. Sodium 59-65 endothelin 1 Homo sapiens 29-41 32343134-3 2020 ET-1, a 21-amino acid residue peptide, plays fundamental roles in basal vascular tone, sodium balance, cell proliferation, and stress-responsive regulation. Sodium 87-93 endothelin 1 Homo sapiens 0-4 7958155-7 1994 Furthermore, there was a significant positive relationship between ET-1 excretion and urine flow rate (r = 0.67, P < 0.0001), CCR (r = 0.40, P < 0.0025), Cosm (r = 0.58, P < 0.001), sodium (r = 0.56, P < 0.001) and potassium excretion (r = 0.42, P < 0.001). Sodium 191-197 endothelin 1 Homo sapiens 67-71 8160789-8 1994 It is suggested that ET-1 at plasma concentrations found in certain pathophysiological conditions in humans may influence renal perfusion and renal sodium and water excretion. Sodium 148-154 endothelin 1 Homo sapiens 21-25 33063475-9 2020 CONCLUSIONS: Elevation of ET-1 is related to clinical signs of peripheral congestion, low urine sodium excretion, and poor outcome in AHF. Sodium 96-102 endothelin 1 Homo sapiens 26-30 8301063-3 1993 In patients with cirrhosis ET-1 was directly correlated to serum creatinine (r = 0.70, P < 0.0001) and aspartate aminotransferase (r = 0.44, P < 0.03) and negatively correlated to serum sodium (r = -0.58, P < 0.003). Sodium 192-198 endothelin 1 Homo sapiens 27-31 28507171-9 2017 Big ET-1 increased the fractional excretion of sodium (from 0.5 to 1.0%). Sodium 47-53 endothelin 1 Homo sapiens 4-8 29246686-2 2018 Our preclinical studies demonstrate an important role for renal endothelin-1 (ET-1) in regulating sodium excretion. Sodium 98-104 endothelin 1 Homo sapiens 64-76 29246686-2 2018 Our preclinical studies demonstrate an important role for renal endothelin-1 (ET-1) in regulating sodium excretion. Sodium 98-104 endothelin 1 Homo sapiens 78-82 29246686-4 2018 We hypothesize that reduced renal ET-1 accounts for derangements in sodium handling under stress, a link never explored in a large human cohort. Sodium 68-74 endothelin 1 Homo sapiens 34-38 29246686-12 2018 Thus, loss of ET-1-dependent natriuresis may account for sodium retention during stress and may predispose retainers to renal diseases such as hypertension and kidney disease. Sodium 57-63 endothelin 1 Homo sapiens 14-18 28507171-12 2017 Sodium and water excretion increased in the absence of significant hemodynamic perturbation, supporting a direct action of ET-1 on the renal tubule. Sodium 0-6 endothelin 1 Homo sapiens 123-127 28507171-13 2017 Our data also suggest that sodium reabsorption is stimulated by ET-1 in the thick ascending limb and suppressed in the distal renal tubule. Sodium 27-33 endothelin 1 Homo sapiens 64-68 25530107-4 2015 Thus, we hypothesized that compared to high dialysate sodium, low dialysate sodium concentration would lower endothelin 1 levels, increase NO release, and reduce BP. Sodium 76-82 endothelin 1 Homo sapiens 109-121 28205210-0 2017 Urinary sodium and calcium excretion: via endothelin-1 do they part? Sodium 8-14 endothelin 1 Homo sapiens 42-54 25530107-9 2015 MEASUREMENTS: Mixed linear regression was used to compare the effect of dialysate sodium (low vs high) and randomization arm (low-then-high vs high-then-low) on intradialytic changes in endothelin 1, NO2(-), and BP values. Sodium 82-88 endothelin 1 Homo sapiens 186-198 22859405-1 2012 Endothelin-1 inhibits collecting duct sodium reabsorption and stimulates proximal and distal tubule acidification in experimental animals both directly and indirectly via increased mineralocorticoid activity. Sodium 38-44 endothelin 1 Homo sapiens 0-12 16133044-8 2005 The association of renal ET-1 and AVP activity with sodium excretion in premature infants treated with indomethacin and ibuprofen supports the hypothesis that these factors may play a role in the physiologic changes in sodium excretion. Sodium 52-58 endothelin 1 Homo sapiens 25-29 16982943-2 2006 The aim of the present study was to investigate the effects of ET-1 antagonism on pulmonary hypertension, renal water, and sodium balance under acute and prolonged exposure to high-altitude-associated hypoxia. Sodium 123-129 endothelin 1 Homo sapiens 63-67 16919017-2 2006 ET-1 exerts a wide variety of biological effects, including constriction of cortical and medullary vessels, mesangial cell contraction, stimulation of extracellular matrix production, and inhibition of sodium and water reabsorption along the collecting duct, effects that are primarily mediated in an autocrine/paracrine manner. Sodium 202-208 endothelin 1 Homo sapiens 0-4 17027026-0 2006 How does endothelin-1 cause a sustained increase in intracellular sodium and calcium which lead to hypertrophy? Sodium 66-72 endothelin 1 Homo sapiens 9-21 16133044-8 2005 The association of renal ET-1 and AVP activity with sodium excretion in premature infants treated with indomethacin and ibuprofen supports the hypothesis that these factors may play a role in the physiologic changes in sodium excretion. Sodium 219-225 endothelin 1 Homo sapiens 25-29