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Endocrinology, doi:10.1210/endo-128-2-710
Endocrinology Vol. 128, No. 2 710-716
Copyright © 1991 by the Endocrine Society.
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Interrelationship between the Actions of Testosterone and Primate Sertoli Cell Inhibin in the Control of Gonadotropin Secretion by Cultured Pituitary Cells*

SATOSHI KITAHARA, FUMIKAZU KOTSUJI, HUGH S. KEEPING, HIROYUKI OSHIMA, PHILIP TROEN and STEPHEN J. WINTERS

Department of Medicine, Montefiore Hospital, and University of Pittsburgh School of Medicine Pittsburgh, Pennsylvania, 15213

Abstract

There is accumulating evidence that the differential regulation of LH and FSH secretion in the male is partly accomplished by the direct actions of testosterone (T) and inhibin on the pituitary. The present study was designed to examine the interaction between T and inhibin, in the presence and absence of GnRH, using dispersed pituitary cells in monolayer culture and cells perifused with pulses of GnRH from intact, 2-week castrated, and castrated T-replaced young adult male rats. The effect of partially purified inhibin from primate Sertoli cell culture medium (pSCI) to suppress basal FSH secretion was similar with pituitary cells from intact and castrated rats. T increased basal FSH secretion in the presence or absence of pSCI but did not alter the dose-dependent suppression of FSH by pSCI with cells from either intact or castrate rats. Castration increased basal FSH and LH secretion, whereas only basal FSH release was increased with cells from T-replaced castrates. T pretreatment increased the action of pSCI to suppress GnRH-stimulated FSH and LH release from perifused pituitary cells. These data indicate that T and inhibin exert opposite but independent effects on basal FSH release. The action of inhibin to suppress basal FSH secretion is not impaired by the absence of T and inhibin subsequent to castration. By contrast, the actions of T and inhibin to suppress GnRHstimulated gonadotropin secretion are coordinated and interrelated. (Endocrinology 128: 710–716, 1991)

Footnotes

* This work was supported in part by NIH Grants R01-HD-19546 (to S.J.W.) and R01-HD-25272 (to H.S.K.) Portions of this work were published in abstract form in J Androl 10(l):23, 1989, and in the Program of the Eighth International Congress of Endocrinology, Kyoto, 1988, Abstract 03-19-067.

Received September 27, 1990.




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