Cerebral prostaglandin biosynthesis and angiotensin-induced drinking in rats

Prostaglandin E2 (PGE2) suppressed drinking induced by angiotensin II (A II) when both were injected into the cerebral ventricles of the rat. This antidipsogenic effect of PGE2 was correlated with its known pyrexic actions. Intracerebroventricular injection of arachidonic acid (AA), the precursor of PGE2, also suppressed A II-induced drinking. This antidipsogenic effect of AA was similarly correlated with pyrexia and was dependent upon the conversion of the precursor to a prostaglandin within the brain. These observations are consistent with the hypothesis that newly synthesized cerebral PGEs, in response to elevated A II levels, contribute to the cessation of drinking by opposing the dipsogenic action of A II. However, blockade of cerebral prostaglandin biosynthesis by central injection of indomethacin did not enhance drinking elicited by A II even at doses that completely eliminated the antidipsogenic and pyrexic actions of AA. Collectively, the results suggest that exogenous PGEs or AA may inhibit A II-induced drinking by elevating body temperature or some other pharmacological action and that endogenously synthesized PGEs of cerebral origin do not play an important role in the normal termination of drinking induced by centrally administered A II.