Renal sodium transport in renin-deficient Dahl salt-sensitive rats

Tengis S. Pavlov, Vladislav Levchenko, Daria V. Ilatovskaya, Carol Moreno, Alexander Staruschenko

Research output: Contribution to journalArticlepeer-review

19 Scopus citations


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.

Original languageEnglish (US)
JournalJRAAS - Journal of the Renin-Angiotensin-Aldosterone System
Issue number3
StatePublished - 2016
Externally publishedYes


  • Aldosterone-sensitive distal nephron
  • Epithelial sodium channel
  • Na-K-Cl cotransporter
  • Renin-angiotensin-aldosterone system
  • Sodium chloride cotransporter
  • Sodium-hydrogen antiporter

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology


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