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Am J Physiol Regul Integr Comp Physiol (March 6, 2003). doi:10.1152/ajpregu.00658.2002
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Submitted on October 25, 2002
Accepted on February 18, 2003

Elevated Dietary Salt Suppresses Renin Secretion But Not Thirst Evoked by Arterial Hypotension in Rats

Sean D Stocker1, Carrie Smith1, Celeste Kimbrough1, Edward M Stricker1, and Alan F Sved1*

1 Department of Neuroscience, University of Pittsburgh, Pittsburgh, PA, USA

* To whom correspondence should be addressed. E-mail: sved{at}bns.pitt.edu.

Increased dietary salt intake was used as a non-pharmacological tool to blunt hypotension-induced increases in plasma renin activity (PRA), in order to evaluate the contribution of the renin-angiotensin system (RAS) to hypotension-induced thirst. Rats were maintained on 8% NaCl (high) or 1% NaCl (standard) diet for at least two weeks, and then arterial hypotension was produced by administration of the arteriolar vasodilator diazoxide. Despite marked reductions in PRA, rats maintained on the high salt diet drank similar amounts of water, displayed similar latencies to drink, and had similar degrees of hypotension compared to rats maintained on the standard diet. Furthermore, blockade of ANG II production by an intravenous infusion of the angiotensin-converting enzyme inhibitor captopril attenuated the hypotension-induced water intake similarly in rats fed standard and high salt diet. Additional experiments showed that increases in dietary salt did not alter thirst stimulated by the acetylcholine agonist carbachol administered into the lateral ventricle; however, increases in dietary salt did enhance thirst evoked by central ANG II. Collectively, the present findings suggest that hypotension-evoked thirst in rats fed a high salt diet is dependent upon the peripheral RAS despite marked reductions in PRA.




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