EFFECTS OF ANGIOTENSIN-II AT(1)-RECEPTOR OR AT(2)-RECEPTOR ANTAGONISTS ON DRINKING EVOKED BY ANGIOTENSIN-II OR WATER-DEPRIVATION IN RATS

In previous studies, we found that central administration of the AT(1) -receptor antagonist, EXP 3174, and the AT(2)-receptor antagonist, PD 123319, blocked the cardiovascular response to centrally-injected angi otensin II (AII), although another AT(2)-receptor antagonist (PD 12317 7) was ineffective. In the present study, we examined the effects of t hese three compounds on the presser and dipsogenic response to central ly-injected AII in conscious, male Long Evans rats, and the effect of EXP 3174 and PD 123319 on drinking in response to water-deprivation in Brattleboro rats. In Long Evans rats, AII-induced water intake and pr esser effects were inhibited by EXP 3174 and PD 123319 (although with different time courses). In contrast, PD 123177 had little effect on t he presser response to i.c.v. AII, but enhanced its dipsogenic action. Following 8 h water deprivation in Brattleboro rats, neither EXP 3174 nor PD 123319 inhibited drinking when water was returned. These data indicate that EXP 3174 and PD 123319 inhibit thirst evoked by centrall y injected AII, but not that caused by extracellular dehydration. In a ddition, since the putative AT(2)-receptor antagonists PD 123319 and P D 123177 have the opposite effects on i.c.v. AII-induced water intake, these results cannot be easily reconciled with a simple model of thir st in which AT(2)-receptors are involved in a final common pathway for drinking [19].