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Effect of Hypophysectomy, Prolactin, and Prostaglandin F₂ on Gonadotropin Binding in Vivo and in Vitro in the Corpus Luteum^*

HAROLD R. BEHRMAN, DANIEL L. GRINWICH, MARTIN HICHENS and GORDON J. MACDONALD

Reproductive Biology Section, Departments of Obstetrics and Gynecology and Pharmacology, Yale University School of Medicine New Haven, Connecticut 06510
the Merck Institute for Therapeutic Research West Point, Pennsylvania 19485
the Department of Anatomy, CMDNJ-Rutgers Medical School Piscataway, New Jersey 08854

Address requests for reprints to: Dr. Harold R. Behrman, Yale University, School of Medicine, Department of Obstetrics and Gynecology, 333 Cedar Street, New Haven, Connecticut 06510.

Abstract

The present studies focus on the mechanism of the early action of prostaglandin F₂ (PGF₂) on the corpus luteum. In pseudopregnant rats with an intact pituitary, PGF₂ produced a significant decrease in accumulation of [^l25I]iodo-CG by corpora lutea (-40%; P < 0.01) and plasma progesterone (-56%; P < 0.05) within 2 h. These effects of PGF₂ were prevented in animals treated with PRL 6 h before PGF₂ injection. Luteal membrane-binding capacity for LH was unchanged within 2 h of PGF₂ treatment. Hypophysectomy markedly reduced luteal membrane-binding capacity for LH, accumulation of [¹²⁵I]iodo-CG by corpora lutea in vivo, and plasma progesterone within 48 h; these effects were prevented by PRL replacement injections. In hypophysectomized control animals, PGF₂ did not significantly change [¹²⁵I]iodo-CG and [¹²⁵I]iodo-PRL accumulation by corpora lutea in vivo, or plasma progesterone levels. In hypophysectomized PRL-treated animals, PGF₂ caused a significant decrease in both [¹²⁵I]iodo-CG (-69%; P < 0.001) and [¹²⁵I]iodo-PRL (-38%; P < 0.05) accumulation by corpora lutea as well as a significant decrease in the concentration of plasma progesterone (-60%; P < 0.01). From these studies, it seems that the rapid drop in plasma progesterone levels produced by PGF₂ was associated with a decrease in labeled gonadotropin uptake by corpora lutea but not from a loss of gonadotropin receptors.

Footnotes

^* This work was supported in part by PHS Research Grant HD-10718.

Present address: Department of Physiology, University of Manitoba, 770 Bannatyne Avenue, Winnipeg, Canada R3E 0W3

Received November 22, 1976.