Nitric oxide and drinking behaviour.

Abstract

The role of brain L-arginine/nitric oxide biochemical pathway in the regulation of drinking behaviour was investigated. Drinking was induced by water deprivation or by intracerebroventricularly (i.c.v.) injected angiotensin II. L-Arginine, the amino-acid precursor of nitric oxide, i.c.v. injected, caused a dose-dependent reduction of the intake of water induced both by water deprivation and i.c.v. angiotensin II (P < 0.001). L-NAME, inhibitor of nitric oxide synthase, reverted L-arginine antidipsogenic effect. L-Arginine, given into the preoptic area (POA) caused a potent antidipsogenic effect (P < 0.001). Either methylene blue (inhibitor of guanylate cyclase activation) or acetylsalicylic acid (ASA), injected into the POA, antagonized the antidipsogenic effect of i.c.v. injected L-arginine. The results indicate that nitric oxide acts as an inhibitory mechanism into the POA and that its antidipsogenic effect requires prostaglandin synthesis.