Vasopressin does not mediate the inhibition of ethanol drinking by the renin-angiotensin system.

Manipulations which are known to enhance activity in the renin-angiotensin system (RAS) have been found to reduce the voluntary consumption of ethanol in rats. Since angiotensin II is a potent stimulus for the release of vasopressin (VP), it is possible that the RAS modulates ethanol (ETOH) consumption through a mechanism involving VP. The present investigation examined the effect of peripheral injections of arginine-VP (AVP) and desglycinamide-AVP (DGAVP) on ETOH consumption in rats given daily one-hour access to ETOH. Daily subcutaneous treatment with AVP or DGAVP had no effect on ETOH consumption at doses ranging from 2 to 200 micrograms/kg (SC). Blood pressure was substantially elevated following a single 20 microgram/kg injection of AVP, indicating that AVP was biologically active at doses which failed to alter ethanol consumption. These findings indicate the VP does not affect established ETOH drinking and furthermore is not likely a critical factor in the reduction of ETOH intake by the RAS.