scholarly journals Combined knockout of collecting duct endothelin A and B receptors causes hypertension and sodium retention

2008 ◽  
Vol 295 (6) ◽  
pp. F1635-F1640 ◽  
Author(s):  
Yuqiang Ge ◽  
Alan Bagnall ◽  
Peter K. Stricklett ◽  
David Webb ◽  
Yuri Kotelevtsev ◽  
...  
Keyword(s):  
Salt Intake ◽  
Collecting Duct ◽  
Plasma Renin ◽  
Hypotensive Effect ◽  
Sodium Retention ◽  
High Salt Intake ◽  
Eta Receptor ◽  
Etb Receptor ◽  
Endothelin A ◽  
Salt Sensitive Hypertension

The collecting duct (CD) endothelin (ET) system regulates blood pressure (BP) and Na excretion. CD-specific knockout (KO) of ET-1 causes hypertension, CD-specific KO of the ETA receptor does not alter BP, while CD-specific KO of the ETB receptor increases BP to a lesser extent than CD ET-1 KO. These findings suggest a paracrine role for CD-derived ET-1; however, they do not exclude compensation for the loss of one ET receptor by the other. To examine this, mice with CD-specific KO of both ETA and ETB receptors were generated (CD ETA/B KO). CD ETA/B KO mice excreted less urinary Na than controls during acute or chronic Na loading. Urinary aldosterone excretion and plasma renin concentration were similar during Na intake and both fell comparably during Na loading. On a normal sodium diet, CD ETA/B KO mice had increased BP, which increased further with high salt intake. The degree of BP elevation during normal Na intake was similar to CD ET-1 KO mice and higher than CD ETB KO animals. During 1 wk of Na loading, CD ETA/B KO mice had higher BPs than CD ETB KO, while BP was less than CD ET-1 KOs until the latter days of Na loading. These studies suggest that 1) CD ETA/B deficiency causes salt-sensitive hypertension, 2) CD ETA/B KO-associated Na retention is associated with failure to suppress the renin-angiotensin-aldosterone system, and 3) CD ETA and ETB receptors exerts a combined hypotensive effect that exceeds that of either receptor alone.

Collecting duct-specific knockout of the endothelin B receptor causes hypertension and sodium retention

2006 ◽  
Vol 291 (6) ◽  
pp. F1274-F1280 ◽  
Author(s):  
Yuqiang Ge ◽  
Alan Bagnall ◽  
Peter K. Stricklett ◽  
Kevin Strait ◽  
David J. Webb ◽  
...  
Keyword(s):  
Collecting Duct ◽  
Receptor Gene ◽  
Plasma Renin ◽  
High Salt ◽  
Paracrine Effects ◽  
High Sodium ◽  
Eta Receptor ◽  
Etb Receptor ◽  
Endothelin B

Collecting duct (CD)-derived endothelin-1 (ET-1) inhibits renal Na reabsorption and its deficiency increases blood pressure (BP). The role of CD endothelin B (ETB) receptors in mediating these effects is unknown. CD-specific knockout of the ETB receptor was achieved using an aquaporin-2 promoter-Cre recombinase transgene and the loxP-flanked ETB receptor gene (CD ETB KO). Systolic BP in mice with CD-specific knockout of the ETB receptor, ETA receptor (CD ETA KO) and ET-1 (CD ET-1 KO), and their respective controls were compared during normal- and high-salt diet. On a normal-sodium diet, CD ETB KO mice had elevated BP, which increased further during high salt feeding. However, the degree of hypertension in CD ETB KO mice and the further increase in BP during salt feeding were lower than that of CD ET-1 KO mice, whereas CD ETA KO mice were normotensive. CD ETB KO mice had impaired sodium excretion following acute sodium loading. Aldosterone and plasma renin activity were decreased in CD ETB KO mice on normal- and high-sodium diets, while plasma and urinary ET-1 levels did not differ from controls. In conclusion, the CD ETB receptor partially mediates the antihypertensive and natriuretic effects of ET-1. CD ETA and ETB receptors do not fully account for the antihypertensive and natriuretic effects of CD-derived ET-1, suggesting paracrine effects of this peptide.

scholarly journals Salt-sensitive hypertension in ANP knockout mice: potential role of abnormal plasma renin activity

1998 ◽  
Vol 274 (1) ◽  
pp. R255-R261 ◽  
Author(s):  
L. G. Melo ◽  
A. T. Veress ◽  
C. K. Chong ◽  
S. C. Pang ◽  
T. G. Flynn ◽  
...  
Keyword(s):  
Plasma Renin Activity ◽  
Knockout Mice ◽  
Salt Intake ◽  
Plasma Renin ◽  
Peptide Hormone ◽  
Hypotensive Effect ◽  
The State ◽  
Renin Activity ◽  
Arterial Blood ◽  
Salt Sensitive Hypertension

Atrial natriuretic peptide (ANP), a peptide hormone produced by the heart, exerts a chronic hypotensive effect. Knockout mice with a homozygous disruption of the pro-ANP gene (−/−) are incapable of producing ANP and are hypertensive relative to their wild-type (+/+) siblings. Previous studies showed that arterial blood pressure (ABP) was further increased in conscious −/− mice kept for 2 wk on 2% salt, but not in anesthetized −/− mice after 1 wk on 8% salt. To determine whether inconsistencies in observed effects of salt on ABP of −/− mice are due to duration of increased salt intake and/or the state of consciousness of the animals, we measured ABP from an exteriorized carotid catheter during and after recovery from anesthesia with ketamine-xylazine in adult +/+ and −/− mice kept on low (LS; 0.008% NaCl)- or high (HS; 8% NaCl)-salt diets for 3–4 wk. Conscious ABP ± SE (mmHg) of +/+ mice did not differ significantly on either diet (HS, 113 ± 3; LS, 110 ± 5). However, on HS diet −/− mice had significantly higher ABP (135 ± 3; P < 0.001) than both −/− (115 ± 2) and +/+ (110 ± 5) mice on LS diet. Anesthesia decreased ABP in all groups, but the genotype- and diet-related differences were preserved. Plasma renin activity (PRA, ng ANG I ⋅ ml−1 ⋅ h−1) in blood collected at termination of experiment was appropriately different on the 2 diets in +/+ mice (HS, 4.9 ± 1.9; LS, 21 ± 2.8). However, PRA failed to decrease in −/− mice on HS diet (HS, 18 ± 2.9; LS, 19 ± 3.7). Independent of genotype, concentration of endothelin-1 (ET-1, pg/mg protein) and endothelial constitutive NOS (ecNOS, density/100 μg protein) was significantly elevated in kidneys of mice fed on HS diet (ET-1 −/−, 31 ± 4.7 and +/+, 32 ± 4.1; ecNOS −/−, 160 ± 19 and +/+, 156 ± 19) compared with mice fed on LS diet (ET-1 −/−, 19 ± 1.9 and +/+, 21 ± 1.8; ecNOS −/−, 109 ± 13 and +/+, 112 ± 18). We conclude that, regardless of the state of alertness, −/− mice develop salt-sensitive hypertension after prolonged feeding on HS, in part due to their inability to reduce PRA, whereas the specific renal upregulation of ecNOS and ET-1 in response to HS intake may be an ANP-independent adaptive adjustment aimed at improving kidney function and counteracting the pressor effect of salt.

Abstract 097: Effects of Lysine-specific Demethylase 1 Deficiency on Aldosterone Production and Salt-sensitive Hypertension in Female Mice

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Yuefei Huang ◽  
Tham M Yao ◽  
Paul Loutraris ◽  
Isis K Rangel ◽  
Pei Yee Ting ◽  
...  
Keyword(s):  
Salt Intake ◽  
Ex Vivo ◽  
Plasma Renin ◽  
Zona Glomerulosa ◽  
Cardiovascular Outcomes ◽  
Female Mice ◽  
Urine Albumin ◽  
Aldosterone Production ◽  
Similar Phenotype ◽  
Salt Sensitive Hypertension

Lysine-Specific Demethylase1 (LSD1) is an epigenetic factor modulated by salt intake. Previously, we documented the male heterozygote LSD1 knockout mice (LSD1+/-) had dysregulation of aldosterone (ALDO) production on a liberal salt diet (1.6% Na+) associated with salt-sensitive hypertension. This study assessed if: 1) female LSD1+/- mice have a similar phenotype; and 2) the effect of aging on this phenotype. Methods: Female LSD1+/- and wild type mice (LSD1+/+) were randomly assigned for sacrifice at the ages of 18-week, 52-week, and 75-week and the following were assessed at each time point: blood pressure (BP); plasma renin activity (PRA) and ALDO; urine albumin; and ex vivo ALDO production from isolated adrenal zona glomerulosa cells. Results: BP and urine albumin in the LSD1+/- compared to the LSD1+/+ were not different at any age (Table). However, the LSD1+/- had greater ALDO/PRA ratios at 18 weeks compared with the LSD1+/+, but lower ALDO levels and ex vivo ALDO production at 52 and 75 weeks. Associated with this phenotype, the LSD1+/- showed significantly higher rate of all-cause mortality than the LSD1+/+. Conclusion: Lack of LSD1 caused dysregulation of ALDO production in both male and female mice. But the cardiovascular outcomes are different. The LSD1+/- females in contrast to males do not develop hypertension or albuminuria even at 75 weeks of age. However, the females do die at a faster rate than the males of a variety of causes. Thus, there is considerable sexual dimorphism in the pathogenesis of cardiovascular outcomes associated with dysregulation of adrenal ALDO production mediated by lack of LSD1.

Effect of high salt intake on sodium, potassium-dependent adenosine triphosphatase activity in the erythrocytes of normotensive men

1988 ◽  
Vol 75 (2) ◽  
pp. 167-170 ◽  
Author(s):  
Antonio P. Quintanilla ◽  
Maria I. Weffer ◽  
Haengil Koh ◽  
Mohammed Rahman ◽  
Agostino Molteni ◽  
...  
Keyword(s):  
Atpase Activity ◽  
Inorganic Phosphate ◽  
Adenosine Triphosphatase ◽  
Salt Intake ◽  
Control Period ◽  
Plasma Renin ◽  
Normal Diet ◽  
High Salt ◽  
Sodium Potassium ◽  
High Salt Intake

1. We measured ouabain-insensitive adenosine triphosphatase (ATPase), sodium, potassium-dependent adenosine triphosphatase (Na+,K+-ATPase) and intracellular Na+ and K+ in the erythrocytes of 19 healthy volunteers, before and after supplementation of their normal diet with 6.0–8.9 g of salt (102–137 mmol of NaCl) per day, for 5 days. 2. The subjects had a small but significant gain in weight. Mean plasma renin activity decreased from 1.57 to 0.73 pmol of angiotensin I h−1 ml−1 and plasma aldosterone from 0.46 to 0.24 nmol/l. 3. Total ATPase activity fell from 197.9 nmol of inorganic phosphate h−1 mg−1 during the control period to 173.5 during the high-salt period (P < 0.0125). Na+,K+-ATPase activity fell from 162.2 to 141.4 nmol of inorganic phosphate h−1 mg−1 (P < 0.05). Intracellular Na + and intracellular K+ did not change. 4. These results are consistent with the hypothesis that salt-induced volume expansion causes the release of a factor inhibitory to the Na+ pump.

Abstract 040: Upregulation Of Cyp Epoxygenase In The Connecting Tubule(cnt)/cortical Collecting Duct (ccd) Is Essential For High Potassium (k) Intake-induced Antihypertensive Effect

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Daohong Lin ◽  
Chengbiao Zhang ◽  
Lijun Wang ◽  
Wenhui Wang
Keyword(s):  
Antihypertensive Effect ◽  
Salt Intake ◽  
Collecting Duct ◽  
Smooth Muscles ◽  
High Salt ◽  
Conditional Knockout ◽  
Na Channel ◽  
Thick Ascending Limb ◽  
High K ◽  
High Salt Intake

Cyp epoxygenase is responsible for metabolizing arachidonic acid to epoxyeicosatrienoic acid (EET) in the kidney and vascular tissues. EET has been shown to cause vasodilation by stimulating Ca 2+ -activated K channels in vascular smooth muscles and to have natriuretic effect by inhibiting the epithelial Na channel (ENaC) in the kidney. In the present study we used real time PCR technique to examine the effect of high salt intake or high K intake on Cyp2c44 (a major type of Cyp epoxygenase in the mouse kidney) in the proximal tubule (PxT), thick ascending limb (TAL), distal convoluted tubule (DCT) and the CNT/CCD. An increase in dietary Na content stimulates the expression of Cyp2c4 in TAL, DCT and CNT/CCD but not in PxT while an increase in dietary K intake augments the expression of Cyp2c44 only in DCT and CNT/CCD. Neither high salt intake nor high K intake has a significant effect on the blood pressure (BP) in wt mice. However, high K intake increased BP in CNT/CCD specific conditional knockout (KO) mice. In contrast, the high Na intake did not significantly increase the BP in those KO mice. This suggests that Cyp2c44 in the CNT/CCD plays a key role in preventing hypertension induced by increasing dietary K intake. Administration of amiloride (a ENaC inhibitor) restored the normal BP in KO mice fed high K diet, suggesting that down-regulation of Cyp2c44 may enhance the Na absorption in the CNT/CCD. This notion was also supported by metabolic cage study demonstrating that renal Na excretion was compromised in KO mice. We conclude that Cyp2c44 plays a key role in stimulating renal Na excretion during increasing dietary K intake and that Cyp-epoxygenase is required for antihypertensive effect induced by high K intake.

Hemodynamics, fluid volume, and hormonal responses to chronic high-salt intake in dogs

1990 ◽  
Vol 259 (6) ◽  
pp. H1629-H1636 ◽  
Author(s):  
J. E. Krieger ◽  
J. F. Liard ◽  
A. W. Cowley
Keyword(s):  
Angiotensin Ii ◽  
Salt Intake ◽  
Peripheral Resistance ◽  
Plasma Renin ◽  
Total Body Weight ◽  
High Salt ◽  
Plasma Sodium ◽  
Plasma Protein Concentration ◽  
Hormonal Responses ◽  
High Salt Intake

The sequential hemodynamics, fluid and electrolyte balances, and the hormonal responses to a 7-day high-salt (NaCl) intake were investigated in sodium-depleted conscious dogs (n = 6). Studies were carried out in metabolic cages mounted on sensitive load cells, which enabled continuous 24 h/day monitoring of total body weight (TBW) as an index of changes in body water. Beat-by-beat hemodynamics were determined 24 h/day. Water (700 ml/day iv) intake was maintained constant. Daily fluid and electrolyte balances and hormonal analyses were performed. An increase of daily salt intake from 8 to 120 meq increased TBW 251 +/- 44 g (P less than 0.05), which was sustained thereafter. Average 24-h mean arterial pressure (MAP) and heart rate (HR) remained unchanged. Average cardiac output (CO) increased 11% (P less than 0.05) above control values by day 2, while total peripheral resistance (TPR) decreased proportionally. CO and TPR returned to control values only when low salt was resumed. Blood volume (BV) was unchanged on day 2 as indicated by direct measurement of BV (51Cr-labeled red blood cells) or by analysis of plasma protein concentration. A 92-meq (P less than 0.05) sodium retention was observed initially, and plasma sodium concentration increased slightly. Plasma renin activity, angiotensin II, and aldosterone levels decreased significantly, whereas vasopressin and atrial natriuretic peptide levels remained unchanged. In summary, chronic high-salt intake resulted in a net retention of water and sodium with no changes in MAP, HR, or BV. The rise in CO was offset by a reduction in TPR, which appeared at least in part related to angiotensin II suppression.

Assessment of atrial natriuretic peptide resistance in cirrhosis with head-out water immersion and atrial natriuretic peptide infusion

1993 ◽  
Vol 71 (2) ◽  
pp. 157-164 ◽  
Author(s):  
Louis Legault ◽  
Leonard C. Warner ◽  
Wai Ming Leung ◽  
Alexander G. Logan ◽  
Laurence M. Blendis ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Collecting Duct ◽  
Water Immersion ◽  
Plasma Renin ◽  
Sodium Balance ◽  
Plasma Sodium ◽  
Sodium Retention ◽  
Serum Aldosterone ◽  
Atrial Natriuretic

The nature of sodium retention in cirrhosis complicated by ascites has been studied for the last 30 years. Resistance to the natriuretic action of atrial natriuretic peptide (ANP) may play a potential role in this sodium retention. To further evaluate this possibility, we studied 12 patients with biopsy-proven cirrhosis and ascites on 2 consecutive days after a 7-day period off diuretics while receiving a 20 mmol/day sodium restricted diet. Following a crossover design, patients underwent head-out water immersion (HWI) for 3 h and were infused with a α-human ANP for 2 h on 2 consecutive days. Blood and urine samples were collected hourly. Five patients displayed a natriuretic response to HWI, sufficient to achieve negative sodium balance, and these patients were termed responders. Each of these five patients also displayed a natriuretic response to ANP infusion. In contrast, the other seven patients (nonresponders) consistently failed to develop a natriuretic response to either maneuver. The two groups had similar elevations in plasma ANP concentrations, but at baseline differed in terms of plasma sodium, plasma renin activity, and serum aldosterone. Despite higher serum aldosterone concentrations, nonresponders excreted less potassium than responders during the peak effect of the interventions, suggesting greater sodium delivery to the aldosterone-sensitive nephron segment in responders. We conclude that the inability to mount an adequate sodium excretory response to HWI in patients with cirrhosis may be conveyed through increased antinatriuretic factors that decrease the sodium delivery to the medullary collecting duct and inhibit the natriuretic effect of ANP at that site.Key words: atrial natriuretic peptide, cirrhosis, ascites, sodium.

scholarly journals Chronic glucose infusion causes sustained increases in tubular sodium reabsorption and renal blood flow in dogs

2009 ◽  
Vol 296 (2) ◽  
pp. R265-R271 ◽  
Author(s):  
Michael W. Brands ◽  
Tracy D. Bell ◽  
Nancy A. Rodriquez ◽  
Praveen Polavarapu ◽  
Dmitriy Panteleyev
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Salt Intake ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Glucose Infusion ◽  
Sodium Reabsorption ◽  
Tubular Sodium Reabsorption ◽  
High Salt Intake ◽  
Sustained Increase

This study tested the hypothesis that inducing hyperinsulinemia and hyperglycemia in dogs, by infusing glucose chronically intravenously, would increase tubular sodium reabsorption and cause hypertension. Glucose was infused for 6 days (14 mg·kg−1·min−1 iv) in five uninephrectomized (UNX) dogs. Mean arterial pressure (MAP) and renal blood flow (RBF) were measured 18 h/day using DSI pressure units and Transonic flow probes, respectively. Urinary sodium excretion (UNaV) decreased significantly on day 1 and remained decreased over the 6 days, coupled with a significant, sustained increase in RBF, averaging ∼20% above control on day 6. Glomerular filtration rate and plasma renin activity (PRA) also increased. However, although MAP tended to increase, this was not statistically significant. Therefore, the glucose infusion was repeated in six dogs with 70% surgical reduction in kidney mass (RKM) and high salt intake. Blood glucose and plasma insulin increased similar to the UNX dogs, and there was significant sodium retention, but MAP still did not increase. Interestingly, the increases in PRA and RBF were prevented in the RKM dogs. The decrease in UNaV, increased RBF, and slightly elevated MAP show that glucose infusion in dogs caused a sustained increase in tubular sodium reabsorption by a mechanism independent of pressure natriuresis. The accompanying increase in PRA, together with the failure of either RBF or PRA to increase in the RKM dogs, suggests the site of tubular reabsorption was before the macula densa. However, the volume retention and peripheral edema suggest that systemic vasodilation offsets any potential renal actions to increase MAP in this experimental model in dogs.

Enhanced sympathoexcitatory and pressor responses to central Na+ in Dahl salt-sensitive vs. -resistant rats

2001 ◽  
Vol 281 (5) ◽  
pp. H1881-H1889 ◽  
Author(s):  
Bing S. Huang ◽  
Hao Wang ◽  
Frans H. H. Leenen
Keyword(s):  
Wistar Rats ◽  
Salt Intake ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Intracerebroventricular Infusion ◽  
Air Jet ◽  
Adrenoceptor Agonist ◽  
Pressor Responses ◽  
High Salt Intake ◽  
Salt Sensitive Hypertension

An enhanced responsiveness to increases in cerebrospinal fluid (CSF) Na+ by high salt intake may contribute to salt-sensitive hypertension in Dahl salt-sensitive (S) rats. To test this hypothesis, sympathetic and pressor responses to acute and chronic increases in CSF Na+were evaluated. In conscious young (5–6 wk old) and adult (10–11 wk old) Dahl S and salt-resistant (R) rats as well as weight-matched Wistar rats, hemodynamic [blood pressure (BP) and heart rate (HR)] and sympathetic [renal sympathetic nerve activity (RSNA)] responses to 10-min intracerebroventricular infusions of artificial CSF (aCSF) and Na+-rich aCSF (containing 0.2–0.45 M Na+) were evaluated. Intracerebroventricular Na+-rich aCSF increased BP, RSNA, and HR in a dose-related manner. The extent of these increases was significantly larger in Dahl S versus Dahl R or Wistar rats and young versus adult Dahl S rats. In a second set of experiments, young Dahl S and R rats received a chronic intracerebroventricular infusion of aCSF or Na+-rich (0.8 M) aCSF (5 μl/h) for 14 days, with the use of osmotic minipumps. On day 14 in conscious rats, CSF was sampled and BP, HR, and RSNA were recorded at rest and in response to air stress, intracerebroventricular α2-adrenoceptor agonist guanabenz, intracerebroventricular ouabain, and intravenous phenylephrine and nitroprusside to estimate baroreflex function. The infusion of Na+-rich aCSF versus aCSF increased CSF Na+ concentration to the same extent but caused severe versus mild hypertension in Dahl S and Dahl R rats, respectively. After central Na+ loading, hypothalamus “ouabain” significantly increased in Dahl S and only tended to increase in Dahl R rats. Moreover, sympathoexcitatory and pressor responses to intracerebroventricular exogenous ouabain were attenuated by Na+-rich aCSF to a greater extent in Dahl S versus Dahl R rats. Responses to air-jet stress or intracerebroventricular guanabenz were enhanced by Na+-rich aCSF in both strains, but the extent of enhancement was significantly larger in Dahl S versus Dahl R. Na+-rich aCSF impaired arterial baroreflex control of RSNA more markedly in Dahl S versus R rats. These findings indicate that genetic control of mechanisms linking CSF Na+ with brain “ouabain” is altered in Dahl S rats toward sympathetic hyperactivity and hypertension.

scholarly journals Collecting duct-specific endothelin B receptor knockout increases ENaC activity

2012 ◽  
Vol 302 (1) ◽  
pp. C188-C194 ◽  
Author(s):  
Vladislav Bugaj ◽  
Elena Mironova ◽  
Donald E. Kohan ◽  
James D. Stockand
Keyword(s):  
Blood Pressure ◽  
Collecting Duct ◽  
Endothelin Receptors ◽  
Sodium Retention ◽  
Wild Type ◽  
Open Probability ◽  
Endothelin System ◽  
Etb Receptor ◽  
Endothelin B ◽  
Patch Clamp Electrophysiology

Collecting duct (CD)-derived endothelin-1 (ET-1) acting via endothelin B (ETB) receptors promotes Na+ excretion. Compromise of ET-1 signaling or ETB receptors in the CD cause sodium retention and increase blood pressure. Activity of the epithelial Na+ channel (ENaC) is limiting for Na+ reabsorption in the CD. To test for ETB receptor regulation of ENaC, we combined patch-clamp electrophysiology with CD-specific knockout (KO) of endothelin receptors. We also tested how ET-1 signaling via specific endothelin receptors influences ENaC activity under differing dietary Na+ regimens. ET-1 significantly decreased ENaC open probability in CD isolated from wild-type (WT) and CD ETA KO mice but not CD ETB KO and CD ETA/B KO mice. ENaC activity in WT and CD ETA but not CD ETB and CD ETA/B KO mice was inversely related to dietary Na+ intake. ENaC activity in CD ETB and CD ETA/B KO mice tended to be elevated under all dietary Na+ regimens compared with WT and CD ETA KO mice, reaching significance with high (2%) Na+ feeding. These results show that the bulk of ET-1 inhibition of ENaC activity is mediated by the ETB receptor. In addition, they could explain the Na+ retention and elevated blood pressure observed in CD ET-1 KO, CD ETB KO, and CD ETA/B KO mice consistent with ENaC regulation by ET-1 via ETB receptors contributing to the antihypertensive and natriuretic effects of the local endothelin system in the mammalian CD.

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