Elevated dietary salt suppresses renin secretion but not thirst evoked by arterial
hypotension in rats.
Stocker, Sean D., Carrie A. Smith, Celeste M. Kimbrough, Edward M. Stricker, and Alan
F. Sved.
Department of Neuroscience, University of Pittsburgh, Pittsburgh, Pennsylvania
15260
APStracts 10:0080R, 2003.
Increased dietary salt intake was used as a nonpharmacological 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 2 wk, 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 with 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 on the peripheral RAS despite marked reductions in
PRA.
Received 25 October 2002; accepted in final form 18 February 2003
APS Manuscript Number R658-2.
Article publication pending Am J Physiol Regul Integr Comp Physiol
ISSN 1080-4757 Copyright 2003 The American Physiological Society.
Published in APStracts on 14 April 2003