Journal
JOURNAL OF THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM
Volume 17, Issue 3, Pages -Publisher
SAGE PUBLICATIONS LTD
DOI: 10.1177/1470320316653858
Keywords
Renin-angiotensin-aldosterone system; sodium-hydrogen antiporter; sodium chloride cotransporter; Na-K-Cl cotransporter; epithelial sodium channel; aldosterone-sensitive distal nephron
Categories
Funding
- National Institutes of Health [HL108880, HL122662, HL82798, HL116603, DK105160]
- American Diabetes Association [1-15-BS-172]
- American Heart Association [16EIA26720006]
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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.
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