Ovarian steroid modulation of gonadotropin secretion and pituitary responsiveness to luteinizing hormone-releasing hormone in the female hamster.

The significance of ovarian estradiol (E2) and progesterone secretion in the regulation of pituitary LH and FSH secretion and pituitary responses to LHRH was investigated in the hamster. Cycling females showed increased LH and FSH responses to LHRH on the morning of proestrus as compared to the responses observed on diestrus day 2. Pituitary responsiveness to LHRH declined on the evening of proestrus, after the preovulatory LH/FSH release. The secondary increase in serum FSH concentration on the morning of estrus was accompanied by a selective increase in the pituitary FHS response to exogenous LHRH. Hamsters ovariectomized (ovx) on diestrus day 2 exhibited daily afternoon LH surges but not FSH surges for at least 10 days after ovx. The magnitude of the LH surges in ovx hamsters was approximately 30-50% of that observed in proestrous females. The pituitary LH response to exogenous LHRH in ovx animals was about 25% as great as in proestrus hamsters. Serum FSH concentrations in ovx females increased by only 30% after LHRH injection, while similar treatment with LHRH resulted in 3- to 4-fold increments in serum FSH in proestrous hamsters. Implantation of E2 capsules in ovx hamsters resulted in increased gonadotropin responses to exogenous LHRH. Serum LH concentrations in the E2-implanted, LHRH-injected animals were as great as those observed after LHRH injection in proestrous females. Administration of LHRH, LH, or progesterone on the morning of proestrus failed to detectably alter the timing or magnitude of the proestrus afternoon FSH surge. The present results suggest that the increasing serum titers of estrogen on diestrus and early proestrus result in increased pituitary sensitivity to LHRH, and this increased sensitivity probably contributes to the magnitude of the preovulatory LH surge. The increases in LH and progesterone which occur during the afternoon do not seem to be responsible for triggering the proestrous FSH surge.