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Negative Feedback Action of Progesterone on Tonic Luteinizing Hormone Secretion in the Ewe: Dependence on the Ovaries¹

Reproductive Endocrinology Program, Departments of Pathology, Physiology, Biological Sciences, and Obstetrics and Gynecology, The University of Michigan Ann Arbor, Michigan 48109

Abstract

The ability of physiological increments in circulating progesterone to inhibit tonic LH secretion in the ewe was investigated in several experimental settings. Progesterone was administered sc by means of Silastic implants containing the steroid. The implants maintained circulating progesterone at levels which were similar to those observed during the mid-luteal phase of the estrous cycle. In long-term ovariectomized ewes, a sustained elevation in circulating progesterone effected a significant reduction in serum LH concentrations, but mean LH levels during progesterone treatment remained more than 20-fold greater than those observed during the mid-luteal phase of the estrous cycle. In other ewes in which this treatment was initiated immediately following ovariectomy, physiological increments in circulating progesterone prevented the typical post-castration rise in serum LH concentrations and maintained circulating LH at midluteal phase levels. This response was shortlived, however, as circulating LH increased, within 2–7 days after ovariectomy, to levels intermediate to those observed in intact ewes and ovariectomized ewes not treated with progesterone. In long-term ovariectomized ewes in which serum LH concentrations had been suppressed by chronic treatment with estradiol implants during the anestrous season, physiological increments in circulating progesterone were effective in maintaining low, mid-luteal phase LH concentrations when the estradiol implants were removed. These findings lead to the conclusion that progesterone can exert a potent inhibition of tonic LH secretion in the ewe. Full manifestation of this effect appears to require the action of another ovarian hormone, perhaps estradiol.

Footnotes

¹ Supported by grants from NIH (HD-07689, HD-09071, HD-08333) and The University of Michigan.

² Postdoctoral Fellow supported by the Ford Foundation.

Received June 18, 1976.

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