INVOLVEMENT OF VASOPRESSIN V(1)-RECEPTOR AND V(2)-RECEPTOR IN HISTAMINE-INDUCED AND STRESS-INDUCED SECRETION OF ACTH AND BETA-ENDORPHIN

Arginine-vasopressin (AVP) seems to be involved in the histamine (HA)- and stress-induced release of ACTH and beta-endorphin (beta-END). We studied the effect of selective AVP V1- or V2-receptor blockade on the ACTH and beta-END response to HA or restraint stress in conscious male rats. HA (270 nmol) administered intracerebroventricularly or 5 min of restraint stress caused a 3- to 7-fold increase in the plasma levels of ACTH and beta-END immunoreactivity (beta-ENDir). Pretreatment of the animals with the nonselective V1+2-receptor antagonist[I-Pmp-2-D-Phe-4-Ile-8-Arg]vasopressin, which was administered intravenously in a low (23 nmol) or a high dose (90 nmol) inhibited the HA- or restraint stress-induced secretion of ACTH and beta-ENDir 60 and 25-70%, respectively. Pretreatment with equipotent doses of the selective V1-receptor antagonist[1-(p-tBu)Pmp-2-Tyr(O-Me)-8-D-Arg]vasopressin (25 nmol) and/or the selective V2-receptor antagonist [I-Pmp-2-D-Ile-4-Ile-8-Arg]vasopressin (7.0 nmol) attenuated the response of ACTH and beta-ENDir to HA or restraint stress by 60-80 and 40-60%, respectively. In general, these doses of antagonists had no effect on basal hormone levels. We conclude that AVP takes part in the mediation of HA- and restraint stress-induced ACTH and beta-END secretion. This effect seems to be mediated via both AVP V1- and V2-receptors or a less selective receptor with ligand specificity for both V1- and V2-receptor antagonists.