Central inhibition of nitric oxide synthase preferentially augments release of oxytocin during dehydration

Intracerebroventricular (i.c.v.) administration of N^G-monomethyl-l-arginine monoacetate (NMMA; 500 μg; 402 mM) and ^G-nitro-l-arginine methyl ester (NAME; 270 μg; 200 mM), inhibitors of nitric oxide synthase, enhanced the rise in oxytocin but not vasopressin levels in plasma of conscious rats following 24 h of water deprivation. This effect of NMMA occurred by 10 min after administration, reached its peak at 15 min and decreased by 20 min. Daily administration of lower doses (50 μg and 0.5 μg 5 μl, i.c.v.) of another inhibitor of nitric oxide synthase, N^G-nitro-l-arginine, just before and after 24 h of water deprivation and in control animals treated similarly were without effect on either vasopression or oxytocin levels. Nitric oxide, therefore, attenuates preferentially the release of oxytocin during dehydration.