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We evaluated the dipsogenic effects of angiotensin II (Ang II) in relation to the steady-state level of the endogenous renin-angiotensin system (RAS) by measuring water intake in 22 trained dogs during three 20 min intravenous (i.v.) infusions of Ile5 Ang II (10, 15 and 50 ng/kg/min). Measurements obtained in normally hydrated (NHyd) dogs were compared with those obtained in dogs pretreated as follows: 24 hr water deprivation (WD); WD combined with chronic blockade of the RAS (300 mg/day X 3 days of SQ 14225) (WD + SQ); and 48 hr after bilateral nephrectomy (BNX). Both WD and WD + SQ were given water before Ang II infusion. Plasma renin activity (PRA) and serum and CSF electrolytes (cisterna magna catheter) were measured. All treatments caused a significant (p less than 0.05) increase in CSF sodium (Na+) that was not paralleled by hypernatremia in BNX dogs (142 +/- 1 vs 144 +/- 1 mEq/L in NHyd). WD and WD + SQ caused a 2- and 12-fold increase in PRA, respectively; PRA was not detectable in BNX. Suppression of blood Ang II by WD + SQ produced a reduced latency and significant enhancement of the thirst behavior elicited by Ang II at all doses; however, i.v. Ang II did not elicit drinking in the WD state. Furthermore, in BNX, the same phenomenon as in WD + SQ was observed. These data are compatible with the concept that endogenous levels of Ang II play a key role in regulating drinking behavior. However, these findings do not negate the possibility that Ang II acts synergistically with CSF Na+, but not plasma Na+, to modulate drinking behavior.
Suzuki et al. (1987) studied this question.