Antidipsogenic role of the E-prostaglandins

Prostaglandin E1 (PGE1) is antidipsogenic when administered into the lateral cerebral ventricle of the rat. In these experiments PGE1, at a dose of 1 microgram, suppressed water intake induced by centrally administered angiotensin II (AII) or carbachol, subcutaneously administered polyethylene glycol, and water deprivation. Even at this high dose, PGE1 did not reduce water 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 microgram), the PGE1 suppression of ingestion was specific to water 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. Since PGE-like substances are synthesized in the brain, these data suggest the possibility that the prostaglandin may be involved in the regulation of water balance as a component of a reciprocal system in which water intake initiated by the activation of the renin-angiotensin system is halted by the synthesis and release of PGE.