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The Effect of Glucocorticoids on Estrogen-Dependent Luteinizing Hormone Release in the Ovariectomized Rat and on Gonadotropin Secretion in the Intact Female Rat^*

Department of Physiology, University of Cincinnati College of Medicine Cincinnati, Ohio 45267

Address requests for reprints to: Dr. David M. Baldwin, Department of Physiology, University of Cincinnati Medical Center, 231 Bethesda Avenue, Cincinnati, Ohio 45267.

Abstract

The effects of glucocorticoids on estrogen-induced changes in LH secretion in the ovariectomized rat and on the estrous cycle and gonadotropin levels in the intact female rat were studied. Preliminary experiments showed that multiple injections of dexamethasone or triamcinolone acetonide (TA) inhibited the estradiol benzoate (EB)-induced elevation of LH in the ovariectomized rat. In subsequent experiments, a single injection of TA was found to inhibit the EB-induced elevation in LH in a dose-dependent manner (minimal effective dose, 200 µg) when given 2–8 h after EB but not at times before EB. Single injections of dexamethasone, cortisol, or progesterone given at this time did not alter LH release. TA given 8 h after EB also blocked the estrogen-dependent increase in pituitary responsiveness to LHRH and the priming effect of multiple injections of LHRH. The pituitary response in oil controls given TA was not altered.

Cortisol implants which maintained continuously elevated levels of plasma cortisol were found to disrupt the normal 4-day estrous cycle for periods of 16-52 days, depress basal plasma LH concentrations but not FSH, inhibit plasma levels of both LH and FSH on the expected afternoon of proestrus (1700 h), and increase pituitary FSH content without altering LH content. Similar implants containing corticosterone were less effective in disrupting the 4-day estrous cycle.

The results indicate: 1) that various glucocorticoids will suppress LH secretion when administered under appropriate conditions, and this suppression appears to be directly related to the glucocorticoid potency of the steroid; 2) at least part of the inhibitory action of the glucocorticoids is at the level of the pituitary by antagonizing estrogen-dependent changes in responsiveness to LHRH, but suppression of endogenous LHRH secretion by actions at the central nervous system may exist; and 3) basal FSH secretion does not appear to be altered by glucocorticoids.

Footnotes

^* This work was supported by Grant HD-11160 from the NIH and the University Research Council, University of Cincinnati. A preliminary report of this work has been presented (Fed Proc 37: 371, 1978

Received December 11, 1978.

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