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On the Mechanism of the Positive Feedback Action of Estradiol on Luteinizing Hormone Secretion in the Rhesus Monkey¹

Laboratory for Neuroendocrinology and Department of Integrative Biology and Pharmacology, The University of Texas-Houston Medical School, Houston, Texas 77225

Address all correspondence and requests for reprints to: Dr. Ernst Knobil, Laboratory for Neuroendocrinology, The University of Texas- Houston Medical School, P.O. Box 20708, Houston, Texas 77225. E-mail: eknobil{at}girch1.med.uth.tmc.edu

In women and rhesus monkeys, both the negative and positive feedback actions of estradiol (E₂) on gonadotropin secretion (inhibition followed by a surge) can be exerted directly at the level of the pituitary gland. We have tested the hypothesis that the positive feedback action of E₂ represents but an "escape" from its negative feedback inhibition of gonadotropin secretion consequent to a desensitization of the gonadotropes occasioned by sustained exposure to elevated concentrations of the steroid. We have attempted to replicate such a desensitization by blocking the negative feedback action of E₂ by the administration of a potent estrogen receptor antagonist devoid of any agonistic properties (ZM 182,780) to rhesus monkeys in the midfollicular phase of the menstrual cycle (n = 14). The estrogen antagonist, administered at a dose that in separate experiments completely blocked both the negative and the positive feedback effect of exogenous E₂ on pituitary LH secretion, failed to produce a surge-like increase in serum LH concentrations. The present results do not support the hypothesis that the LH surge is the consequence of the removal of the negative feedback action of E₂. Evidence is presented that ZM 182,780, in contrast to its inhibition of E₂-induced LH surges, cannot block the inhibition of hypothalamic GnRH pulse generator activity by E₂.

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