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Endocrinology. 1982 Jul;111(1):231-7.

The contribution of gonadostatin (inhibin-F) to the control of gonadotropin secretion in a simulated estrous cycle in steroid-treated ovariectomized rats.

Abstract

We have examined the contribution of gonadostatin to the control of gonadotropin secretion throughout the rat estrous cycle. The estrous cycle was simulated in rats ovariectomized on diestrus-1, designated day 1 (D-1) by use of low or high level estradiol and progesterone Silastic implants. The steroid implant regimen simulated the major changes of these hormones in the blood during the course of the estrous cycle. Injections of porcine follicular fluid (pFF) were superimposed on this steroid regimen. Four treatment combinations of steroid and pFF or their controls were tested: 1) steroid implants only, 2) pFF only at a constant dose level, 3) steroid implants and pFF injections at a constant dose level, and 4) steroid implants and pFF injections with reduced levels on simulated proestrus. In group 1 both basal and surge release of LH were similar to those in the intact rat, but both basal and surge release of FSH were significantly elevated above levels observed in the intact rat for the respective periods. In group 2 FSH was suppressed to diestrous levels throughout the course of the experiment, with no surge occurring on D-3. Serum LH levels were slightly elevated above diestrous levels (50-150 ng/ml) with no surge. In group 3 serum levels of both gonadotropins were suppressed to diestrous levels on D-1 and D-2, and a steroid-induced, pFF-attenuated surge occurred on the afternoon of D-3. Group 4 had, with a minor variation, proestrous-like FSH and LH surges on D-3 and basal (diestrous) gonadotropin levels during simulated D-1, D-2, and early proestrus. This study supports previous evidence for estradiol and progesterone control of LH secretion and elaborates the control of FSH secretion. The role of gonadostatin and steroids is demonstrated in the negative feedback regulation of FSH secretion.

PMID:
6806075
DOI:
10.1210/endo-111-1-231
[Indexed for MEDLINE]

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