Septal hyperdipsia: Specific enhancement of drinking to angiotensin in rats

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Conducted 3 experiments with a total of 126 hyperdipsic and 123 normal female Sprague-Dawley rats. Ss made hyperdipsic by destruction of the septal nuclei drank more water than normal Ss to thirst stimuli considered to be mediated, at least in part, by angiotensin. Specifically, they drank more than normal Ss to caval ligation, hypotension induced by the b-adrenergic agonist isoproterenol, intraperitoneal injections of renin, and intravenous infusions of angiotensin. Overdrinking was enhanced by nephrectomy when renin or angiotensin were introduced exogenously, but nephrectomy reduced drinking to hypotension. Septal hyperdipsic Ss drank more water than normal Ss when polyethylene glycol was delivered intraperitoneally but not subcutaneously. They did not drink more to cellular dehydration produced by the intravenous or intragastric injection of hypertonic saline or sucrose. The contributions of the septum to angiotensin-mediated drinking and to nonhomeostatic determinants of drinking are discussed, as are the possible mechanisms controlling drinking to intravascular depletions. (38 ref) (PsycINFO Database Record (c) 2006 APA, all rights reserved)

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