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

Research output: Contribution to journalArticlepeer-review

26 Scopus citations


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 languageEnglish
Pages (from-to)372-377
Number of pages6
JournalBiochemical and Biophysical Research Communications
Issue number2
StatePublished - 13 Nov 2009
Externally publishedYes


  • Aldosterone
  • Angiotensin II
  • Epithelial sodium channel (ENaC)
  • Prostaglandins
  • Prostanoid receptor
  • Renin-angiotensin-aldosterone-system


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