Renal sodium transport in renin-deficient Dahl salt-sensitive rats. (July 2016)

• Record Type: Journal Article
• Authors: Pavlov, Tengis S; Levchenko, Vladislav; Ilatovskaya, Daria V; Moreno, Carol; Staruschenko, Alexander
• Is Part Of: Journal of the renin-angiotensin-aldosterone system. Volume 17:Number 3(2016:Sep.)
• Publication Date: 2016-07
• Subjects: Renin-angiotensin-aldosterone system -- sodium-hydrogen antiporter -- sodium chloride cotransporter -- Na-K-Cl cotransporter -- epithelial sodium channel -- aldosterone-sensitive distal nephron; Renin-angiotensin system -- Periodicals; 616.132
• DOI: 10.1177/1470320316653858
• Languages: English
• ISSNs: 1470-3203

Abstract

Objective: The Dahl salt-sensitive rat is a well-established model of salt-sensitive hypertension. The goal of this study was to assess the expression and activity of renal sodium channels and transporters in the renin-deficient salt-sensitive rat. Methods: Renin knockout (Ren −/− ) rats created on the salt-sensitive rat background were used to investigate the role of renin in the regulation of ion transport in salt-sensitive hypertension. Western blotting and patch-clamp analyses were utilized to assess the expression level and activity of Na + transporters. Results: It has been described previously that Ren −/− rats exhibit severe kidney underdevelopment, polyuria, and lower body weight and blood pressure compared to their wild-type littermates. Here we found that renin deficiency led to decreased expression of sodium-hydrogen antiporter (NHE3), the Na + /H + exchanger involved in Na + absorption in the proximal tubules, but did not affect the expression of Na-K-Cl cotransporter (NKCC2), the main transporter in the loop of Henle. In the distal nephron, the expression of sodium chloride cotransporter (NCC) was lower in Ren −/− rats. Single-channel patch clamp analysis detected decreased ENaC activity in Ren −/− rats which was mediated via changes in the channel open probability. Conclusion: These data illustrate that renin deficiency leads to significant dysregulation of ion transporters.