What is it about?
It was found that Ren−/− rats generated in a model of salt-sensitive hypertension, exhibit severe kidney underdevelopment, polyuria, and lower body weight and blood pressure compared to their wild-type littermates. Renin deficiency led to decreased expression of the Na+/H+ exchanger involved in Na+ absorption in the proximal tubules, but did not affect the expression of Na-K-Cl cotransporter, the main transporter in the loop of Henle. In the distal parts of nephron, the expression of NCC and activity of ENaC were also decreased.
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Why is it important?
The renin-angiotensin-aldosterone system (RAAS) is the central regulator of water and salt homeostasis in the body. Components of this hormonal cascade are major targets for pharmaceutical agents aimed at controlling blood pressure, and heart and kidney functions. Regulation of sodium balance by the kidney is the key factor responsible for long-term blood pressure control. Therefore it is highly important to understand how RAAS is controlling renal transport.
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This page is a summary of: Renal sodium transport in renin-deficient Dahl salt-sensitive rats, Journal of the Renin-Angiotensin-Aldosterone System, July 2016, SAGE Publications,
DOI: 10.1177/1470320316653858.
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