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Immunoreactive Inhibin Secretion by the Hypophysectomized Female Rat: Demonstration of the Modulating Effect of Gonadotropin-Releasing Hormone and Estrogen Through a Direct Ovarian Site of Action^*

CATHERINE RIVIER and WYLIE VALE

The Clayton Foundation Laboratories for Peptide Biology, The Salk Institute La Jolla, California 92037

Address all correspondence and requests for reprints to: Dr. Catherine Rivier, Clayton Foundation Laboratories for Peptide Biology, The Salk Institute, 10010 North Torrey Pines Road, La Jolla, California 92037.

Abstract

To investigate the possibility that sex steroids and GnRH might act directly at the level of the ovary to modulate the secretion of immunoreactive inhibin, we have administered estradiol benzoate, PMSG, or GnRH analogs to immature (24-day-old) hypophysectomized female rats. The sc injection of 10–100 µg estradiol benzoate markedly (P < 0.01) increased plasma inhibin levels measured 48 h later. Administration of the GnRH agonist [DTrp6,Pro9-NEt]GnRH significantly (P < 0.05) inhibited both spontaneous and PMSGinduced inhibin secretion, while the GnRH antagonist [Ac-D2Nal¹,D4ClPhe²,D3Pal³,Arg⁵,DGlu⁶(AA),DAla¹⁰]GnRH augmented the stimulatory effect of PMSG action on inhibin release. These results suggest a direct ovarian site of action of sex steroids and GnRH analogs in modulating the release of immunoreactive inhibin. They also support the hypothesis that an endogenous GnRH-like peptide of ovarian origin plays a physiological paracrine role in modulating inhibin secretion in the rat (Endocrinology 124: 195–198, 1989)

Footnotes

^* This work was supported by NIH Grant HD-13527, and Award B86.29A/ICCR from The Population Council, and was conducted in part by The Clayton Foundation for Research, California Division.

Clayton Foundation Investigator.

Received August 28, 1988.

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