E Prostanoid-1 receptor regulates renal medullary αENaC in rats infused with angiotensin II

Alexis A. González; Carlos Céspedes; Sandra Villanueva; Luis Michea; Carlos P. Vio

doi:10.1016/j.bbrc.2009.08.157

E Prostanoid-1 receptor regulates renal medullary αENaC in rats infused with angiotensin II

Alexis A. González^*, Carlos Céspedes, Sandra Villanueva, Luis Michea, Carlos P. Vio

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

28 Scopus citations

Abstract

E Prostanoid (EP) receptors play an important role in urinary Na⁺ excretion. In the kidney, the epithelial sodium channel (ENaC) is the rate-limiting-step for Na⁺ reabsorption. We hypothesized that activation of EP1/EP3 regulates the expression of ENaC in the face of renin-angiotensin-aldosterone-system (RAAS) activation. In primary cultures of inner medullary collecting duct (IMCD) cells, sulprostone (EP1 > EP3 agonist, 1 μM) and 17 Phenyl trinor (17 Pt, EP1 agonist, 10 μM) prevented the up-regulation of αENaC mRNA induced by aldosterone (10 nM). In Sprague-Dawley rats infused with angiotensin II (0.4 μg/kg/min), αENaC expression was up-regulated in renal cortex and medulla coincidently with high plasma aldosterone levels. Sulprostone and/or 17 Pt prevented this effect in renal medulla but not in cortex. Immunocytochemistry demonstrated that IMCD cells express EP1. Our results suggest that specific activation of EP1 receptor during RAAS activation antagonizes the action of aldosterone on αENaC expression in the renal medulla.

Original language	English
Pages (from-to)	372-377
Number of pages	6
Journal	Biochemical and Biophysical Research Communications
Volume	389
Issue number	2
DOIs	https://doi.org/10.1016/j.bbrc.2009.08.157
State	Published - 2009
Externally published	Yes

Bibliographical note

Funding Information:
This work was supported by grants FONDECYT 1080590 and Programa de Financiamiento Basal PFB 12-2007 (C.P. Vio), FONDECYT 1090223 (L. Michea) and doctoral fellowship from MECESUP and CONICYT (A.A. Gonzalez). Technical assistance of Maria Alcoholado is acknowledged.

ASJC Scopus subject areas

Biophysics
Biochemistry
Molecular Biology
Cell Biology

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10.1016/j.bbrc.2009.08.157

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title = "E Prostanoid-1 receptor regulates renal medullary αENaC in rats infused with angiotensin II",

abstract = "E Prostanoid (EP) receptors play an important role in urinary Na+ excretion. In the kidney, the epithelial sodium channel (ENaC) is the rate-limiting-step for Na+ reabsorption. We hypothesized that activation of EP1/EP3 regulates the expression of ENaC in the face of renin-angiotensin-aldosterone-system (RAAS) activation. In primary cultures of inner medullary collecting duct (IMCD) cells, sulprostone (EP1 > EP3 agonist, 1 μM) and 17 Phenyl trinor (17 Pt, EP1 agonist, 10 μM) prevented the up-regulation of αENaC mRNA induced by aldosterone (10 nM). In Sprague-Dawley rats infused with angiotensin II (0.4 μg/kg/min), αENaC expression was up-regulated in renal cortex and medulla coincidently with high plasma aldosterone levels. Sulprostone and/or 17 Pt prevented this effect in renal medulla but not in cortex. Immunocytochemistry demonstrated that IMCD cells express EP1. Our results suggest that specific activation of EP1 receptor during RAAS activation antagonizes the action of aldosterone on αENaC expression in the renal medulla.",

keywords = "Aldosterone, Angiotensin II, Epithelial sodium channel (ENaC), Prostaglandins, Prostanoid receptor, Renin-angiotensin-aldosterone-system",

author = "Gonz{\'a}lez, {Alexis A.} and Carlos C{\'e}spedes and Sandra Villanueva and Luis Michea and Vio, {Carlos P.}",

note = "Funding Information: This work was supported by grants FONDECYT 1080590 and Programa de Financiamiento Basal PFB 12-2007 (C.P. Vio), FONDECYT 1090223 (L. Michea) and doctoral fellowship from MECESUP and CONICYT (A.A. Gonzalez). Technical assistance of Maria Alcoholado is acknowledged.",

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AU - Villanueva, Sandra

AU - Michea, Luis

AU - Vio, Carlos P.

N1 - Funding Information: This work was supported by grants FONDECYT 1080590 and Programa de Financiamiento Basal PFB 12-2007 (C.P. Vio), FONDECYT 1090223 (L. Michea) and doctoral fellowship from MECESUP and CONICYT (A.A. Gonzalez). Technical assistance of Maria Alcoholado is acknowledged.

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N2 - E Prostanoid (EP) receptors play an important role in urinary Na+ excretion. In the kidney, the epithelial sodium channel (ENaC) is the rate-limiting-step for Na+ reabsorption. We hypothesized that activation of EP1/EP3 regulates the expression of ENaC in the face of renin-angiotensin-aldosterone-system (RAAS) activation. In primary cultures of inner medullary collecting duct (IMCD) cells, sulprostone (EP1 > EP3 agonist, 1 μM) and 17 Phenyl trinor (17 Pt, EP1 agonist, 10 μM) prevented the up-regulation of αENaC mRNA induced by aldosterone (10 nM). In Sprague-Dawley rats infused with angiotensin II (0.4 μg/kg/min), αENaC expression was up-regulated in renal cortex and medulla coincidently with high plasma aldosterone levels. Sulprostone and/or 17 Pt prevented this effect in renal medulla but not in cortex. Immunocytochemistry demonstrated that IMCD cells express EP1. Our results suggest that specific activation of EP1 receptor during RAAS activation antagonizes the action of aldosterone on αENaC expression in the renal medulla.

AB - E Prostanoid (EP) receptors play an important role in urinary Na+ excretion. In the kidney, the epithelial sodium channel (ENaC) is the rate-limiting-step for Na+ reabsorption. We hypothesized that activation of EP1/EP3 regulates the expression of ENaC in the face of renin-angiotensin-aldosterone-system (RAAS) activation. In primary cultures of inner medullary collecting duct (IMCD) cells, sulprostone (EP1 > EP3 agonist, 1 μM) and 17 Phenyl trinor (17 Pt, EP1 agonist, 10 μM) prevented the up-regulation of αENaC mRNA induced by aldosterone (10 nM). In Sprague-Dawley rats infused with angiotensin II (0.4 μg/kg/min), αENaC expression was up-regulated in renal cortex and medulla coincidently with high plasma aldosterone levels. Sulprostone and/or 17 Pt prevented this effect in renal medulla but not in cortex. Immunocytochemistry demonstrated that IMCD cells express EP1. Our results suggest that specific activation of EP1 receptor during RAAS activation antagonizes the action of aldosterone on αENaC expression in the renal medulla.

KW - Aldosterone

KW - Angiotensin II

KW - Epithelial sodium channel (ENaC)

KW - Prostaglandins

KW - Prostanoid receptor

KW - Renin-angiotensin-aldosterone-system

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E Prostanoid-1 receptor regulates renal medullary αENaC in rats infused with angiotensin II

Abstract

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