The antidipsogenic action of peripheral prostaglandin E2

Intraperitoneal (IP) injection of 50 μg/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 μg/kg, IP PGE₂ reduces drinking to all of these stimuli as well as to hypovolemia. A 10 μg/kg dose of PGE₂ has not effect on drinking under any of the conditions tested. Intraperitoneal PGE₂, at either 50 or 100 μg/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.