Journal of Clinical Endocrinology & Metabolism, Vol 68, 1060-1066, Copyright © 1989 by Endocrine Society

ARTICLES

Naloxone antagonism of corticotropin-releasing hormone stimulation of prolactin secretion in rhesus monkeys

DA Vanvugt, MY Webb and RL Reid
Department of Obstetrics and Gynaecology, Queen's University, Kingston, Ontario, Canada.

The effect of opiate receptor blockade on human CRH-induced PRL secretion was examined in ovariectomized and normal female rhesus monkeys. A bolus iv dose of 100 micrograms CRH acutely stimulated PRL secretion in both normal and ovariectomized animals. The magnitude of the PRL response was greater in ovariectomized monkeys (212% increase; n = 5) than in normal monkeys (56% increase; n = 5). Naloxone pretreatment inhibited CRH-induced PRL release in a dose-dependent fashion, whereas nalmefene did not, in both normal and ovariectomized monkeys. Administration of nalmefene alone significantly stimulated PRL secretion in normal monkeys (57% increase; n = 10), but not in ovariectomized monkeys (10% increase; n = 10). Naloxone alone had no effect. Since nalmefene has a high affinity for both the kappa- and mu- receptors whereas naloxone binds primarily to the mu-receptor, these results suggest that CRH-induced PRL secretion in monkeys is mediated by an endogenous opiate which binds to an opiate receptor other than or in addition to the mu- and kappa-receptors.

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