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Alteration of Feedback Mechanism of Estrogen on Gonadotropin by Sulpiride-Induced Hyperprolactinemia^*

Human Reproduction Research Unit, Department of Gynecology and Obstetrics, Free University of Brussels Brussels, Belgium

Address requests for reprints to: Dr. M. L'Hermite, Service de Gynecologie, Hopital St. Pierre, rue Haute 322, B-1000 Bruxelles, Belgium.

Four normally cycling women received an iv injection of 20 mg Premarin (conjugated estrogens equivalent to 20 mg estrone sulfate) on the seventh day of two consecutive cycles; the second experiment was performed under sulpiride-induced hyperprolactinemia (mean PRL level = 906 µU MRC standard 71/222 per ml; significantly 7.8 times greater than mean control level of 115 µU MRC standard 71/222 per ml, P < 0.001). In comparison to the control experiment, sulpiride-induced hyperprolactinemia prevented the occurrence of any gonadotropin peak within the 84 h of estrogen administration; the negative feedback effect of estrogen on gonadotropin secretion was maintained and was even potentiated. These alterations of feedback mechanisms of estrogen were considered to be related to hyperprolactinemia itself rather than to sulpiride.

Five other normally cycling women received iv injections of 100 µg LRH on the 22nd day of a cycle under sulpiride-induced hyperprolactinemia since the onset of menstruation. Their mean LH response was somewhat greater (although not statistically significant) and their mean FSH response was considerably greater (P < 0.001 at all times) than those of a control group of 10 women tested in their luteal phase. The results of these LRH tests under sulpiride-induced hyperprolactinemia give some support to the concept that hyperprolactinemia interferes at the hypothalamic or higher level with cyclic release of endogenous LRH.

^* This work was supported by grants from the Ford Foundation and the Fonds de la Recherche Scientifique Medicale (Belgium). It was presented at the Eleventh Acta Endocrinologica Congress (1).

Received August 12, 1976.