PROLACTIN STIMULATES THE RELEASE OF OXYTOCIN IN LACTATING RATS - EVIDENCE FOR A PHYSIOLOGICAL-ROLE VIA AN ACTION AT THE NEURAL LOBE

The present studies were designed to investigate whether prolactin (PRL) influences the secretion of oxytocin (OT) in lactating rats, and to test whether the previously reported inhibitory and stimulatory effects of dopamine-2 (D-2) agonists and antagonists, respectively, on OT release might be secondary to their respective inhibitory and stimulatory effects on the release of PRL. Intravenous administration of either rat (r) or ovine (o) PRL to lactating, nonsuckled rats increased basal plasma concentrations of OT. rGH was ineffective, but administration of oGH did produce some stimulation of OT release. Both oPRL and rPRL significantly enhanced the electrical stimulation-induced release of OT from isolated stalk-neurointermediate lobes, in vitro, without affecting the basal release of the peptide. oGH was ineffective on basal or stimulated in vitro OT release, and neither hormone altered basal or stimulation-induced release of vasopressin from these tissues. Both rPRL and oPRL reversed the inhibitory effect of the D-2 dopamine agonist bromocriptine. Immunoneutralization of circulating PRL with a highly specific antiserum abolished the increases in OT in response to either suckling or to administration of the D-2 dopamine antagonist domperidone. These findings suggest that (1) an action of PRL released by suckling may be of physiological importance in promoting the release of OT in lactating rats; (2) that PRL may increase OT release, at least in part, through a stimulatory action on the neural lobe, and perhaps directly on OT-containing neurosecretory nerve endings, and (3) that the previously reported inhibitory effect of D-2 dopamine receptor stimulation, and the stimulatory effect of a D-2 dopamine antagonist on OT release may be secondary to their analogous actions on the release of PRL.