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Naloxone Antagonism of Corticotropin-Releasing Hormone Stimulation of Prolactin Secretion in Rhesus Monkeys^*

Division of Reproductive Endocrinology, Departments of Obstetrics and Gynaecology (DA. V., M. Y. W., R.L.R.) and Physiology (D.A.V.) Queen's University Kingston, Ontario, Canada K7L 3N6

Address all correspondence and requests for reprints to: Dean A. VanVugt, Ph.D., Department of Obstetrics and Gynecology, Etherington Hall, Queen's University, Kingston, Ontario, Canada K7L 3N6.

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 µg 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 dosedependent 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 - and µ-receptors whereas naloxone binds primarily to the µ-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 µ- and -receptors.

^* Presented in part at the Annual Meeting of the Canadian Fertility and Andrology Society, October 5–8, 1988. This work was supported by grants from the Medical Research Council of Canada (to D.A.V. and R.L.R.).

Received November 2, 1988.

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