The role of endogenous prostaglandin E in angiotensin-II-induced drinking in rats.

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Abstract
Oral administration of indomethacin, a nonsteroidal anti-inflammatory agent which suppresses endogenous prostaglandin E2 (PGE2) levels in plasma, results in an augmentation of total water intake and a shortening of the latency to drink in response to an i.v. infusion of angiotensin [A] II. This same treatment has no effect on water intake stimulated by the intracranial injection of the dipsogen. Plasma PGE2 may act as both a tonic inhibitor of drinking and a satiety indicator in situations in which water intake is stimulated by increases in blood levels of AII. While peripheral PGE2 levels do not appear to be involved in the control of drinking to increased brain levels of AII, the role of endogenous central PGE in this phenomenon remains unknown.