The antidipsogenic action of peripheral prostaglandin E2.

Intraperitoneal (IP) injection of 50 micrograms/kg prostaglandin E2 (PGE2) suppresses water intake elicited by cellular dehydration, intracerebroventricular injection of angiotensin II (A II) and, for a shorter duration, water deprivation. At a dose of 100 micrograms/kg, IP PGE2 reduces drinking to all of these stimuli as well as to hypovolemia. A 10 microgram/kg dose of PGE2 has no effect on drinking under any of the conditions tested. Intraperitoneal PGE2, at either 50 or 100 micrograms/kg, does not support the formation of a conditioned taste aversion suggesting that PGE may act via specific inhibition of drinking rather than by producing a generalized malaise. Although both central and peripheral administration of PGE suppresses water intake, the findings that peripheral PGE2 reduces drinking to cellular dehydration but has minimal effects on drinking due to hypovolemia are in marked contrast to the actions reported for intracranial PGE. In addition, peripheral PGE2 reduces body temperature whereas centrally applied PGE induces thermogenesis. These data may indicate differential roles and/or mechanisms by which central and peripheral PGE may control water intake.