Role of gonadotropins and progesterone in determining the preovulatory estradiol rise in the ewe

Abstract

The contributions of the follicular phase increase in LH and the decrease in progesterone to the determination of the preovulatory estradiol rise in the ewe were examined by mimicking these changes, separately or in combination, in seasonally anestrous animals. Prior to this test, each ewe was pretreated for 15 days with Silastic implants containing progesterone to produce an artificial luteal phase. The implants were then either removed or left in place, and purified ovine LH was infused to simulate the progressive increase in mean serum LH concentrations seen during the follicular phase of the estrous cycle. If LH was not given, the concentration of estradiol remained low and constant, whether or not progesterone was withdrawn. When LH was infused after progesterone withdrawal (n=8), a significant increase in serum estradiol from 1 to 5 pg/ml resulted. Four of these ewes had an LH surge, which induced ovulation and formation of functional corpora lutea. In these ewes, estradiol fell precipitously within 4 h of the LH peak. In the other four animals, no LH surge occurred and estradiol remained elevated until the end of the infusion. When a luteal phase progesterone concentration was maintained, LH infusion produced an elevation in serum estradiol, but the response was significantly less (P<0.01) than that produced by LH when progesterone was withdrawn. These data suggest that, in the ewe, the follicular phase estradiol rise is driven by the sustained increase in tonic LH secretion and is terminated by the preovulatory LH surge. The fall in progesterone at luteolysis probably contributes to the estradiol rise in 2 ways: 1) it allows the requisite increase in tonic LH secretion; and 2) it increases the response of the follicle to this LH increase. Finally, by demonstrating that the ovary of the anestrous ewe can produce an estradiol rise in response to a follicular phase increment in LH, these studies provide important support for the hypothesis that a primary cause of seasonal anestrus is the absence of a sustained rise in tonic LH secretion.