HISTAMINE-INDUCED AND STRESS-INDUCED PROLACTIN SECRETION - IMPORTANCEOF VASOPRESSIN V-1-RECEPTORS AND V-2-RECEPTORS

We investigated the involvement of arginine vasopressin (AVP) V-1- and V-2-receptors in the prolactin (PRL) secretory response to histamine (HA) or restraint stress stimulation in conscious male rats by selecti ve blockade of AVP receptors using different antagonists. Histamine (2 70 nmol) administered intracerebroventricularly or 5 min of restraint stress stimulated PRL secretion 10-14-fold. Pretreatment with the sele ctive V-1- receptor antagonists -butyl-beta-mercapto-beta,beta-cyclope ntamethylene propionic acid)-2-(O-methyl)tyrosine-8-D-arginine] vasopr essin or [1-(beta-mercapto-beta,beta-cyclopentamethylene propionic aci d)-2-(O-methyl)tyrosine-8-arginine] vasopressin inhibited the PRL resp onse to HA and restraint stress in a dose-dependent manner with maxima l inhibition of 60%. The effect of the two antagonists was identical w hen equipotent antivasopressor doses were administered. The selective V-2-receptor antagonist [1-(beta-mercapto-beta,beta-cyclopentamethylen e propionic acid)-2-D-isoleucine-4-isoleucine-8-arginine] vasopressin was unable to inhibit the PRL response significantly. Combined adminis tration of the V-1-receptor antagonist -butyl-beta-mercapto-beta,beta- cyclopentamethylene propionic acid)-2-(O-methyl)tyrosine-8-D-arginine] vasopressin and the V-2-receptor antagonist inhibited the PRL respons e to HA to the same extent as that observed when the V-1-antagonist wa s administered alone. None of the antagonists used had any effect on b asal PRL secretion. We conclude that AVP seems to play a role in the m ediation of HA- and restraint stress-induced secretion of PRL, and tha t the AVP receptor involved is primarily of the V-1-type or similar to this.