Antidipsogenic role of the E-prostaglandins.

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Abstract
Prostaglandin E1 (PGE1) is antidipsogenic when administered into the lateral cerebral ventricle of the rat. PGE1, at a dose of 1 .mu.g, suppressed H2O intake induced by centrally administered angiotensin II (AII) or carbachol, s.c. administered polyethylene glycol and H2O deprivation. Even at this high dose, PGE1 did not reduce H2O intake due to cellular dehydration. As the dose of PGE1 was reduced, its suppressant effects became more specific to AII-induced drinking, with a dose of 10 ng yielding a significant suppression only in the case of AII-induced drinking. Even at a high dose (1 .mu.g), the PGE1 suppression of ingestion was specific to H2O intake. Although PGE1-treated rats reduced food intake if they were not hydrated prior to access to food, no reduction in food intake was seen when they received water by gavage before food presentation. PGE-like substances are synthesized in the brain, suggesting that the prostaglandin may be involved in the regulation of H2O balance as a component of a reciprocal system in which H2O intake initiated by the activation of the renin-angiotensin system is halted by the synthesis and release of PGE.