Effects of Exogenous LH or FSH on Endogenous FSH, Progesterone and Estradiol Secretion1

Abstract
In 1 set of experiments, an ovulatory dose of ovine LH [luteinizing hormone] or FSH [follicle stimulating hormone] was injected, on the afternoon of proestrus, into rats which had received pentobarbital (PB). Serum FSH was elevated over noninjected controls at 1000 h estrus. The adrenal glands were not necessary for this response. Ovariectomy, performed shortly before the gonadotropin injection, caused and elevation in serum FSH the following morning, which was not further increased by the injection of LH or FSH. Serum LH was not elevated nor was pituitary LH content decreased at 1000 h estrus in any treatment group. In a 2nd set of experiments, the time course of LH, FSH, estradiol (E2) and progesterone (P4) was investigated, between proestrous afternoon (1630 h) and estrous morning (1000 h), in 3 treatment groups: saline controls (no PB), PB controls (no LH), PB + LH (8 .mu.g i.v. at 1530 h). Saline controls showed a maximum LH and FSH primary surge at 1830 h; LH returned to baseline by 2300 h, while FSH fell slowly through the night. P4 was elevated at 1830 h and 2300 h, then fell to baseline; E2 fell abruptly between 1630 h and 1830 h. In PB controls, serum LH and P were continuously low, but a small rise in FSH occurred at 2300 h and 0400 h (estrus). E2 fell significantly also, but not as low as in the saline controls. LH, superimposed on PB, raised LH at 1630 h, but no further rises occurred, while FSH rose gradually to peak at 0400 h and then fell part way to saline control levels by 1000 h estrus. FSH appeared to be released independently of LH. The injected LH also induced a rise in P4 at 1630 h and 1830 h, with E2 falling, as in saline controls, between 1630 h and 1830 h. In a 3rd experiment, P4 injection was tested, superimposed on PB blockade. P4 failed to increase LH or FSH (in a manner resembling LH injection), but did cause E2 to fall. The primary LH (and/or FSH) surge, as well as exogenous LH or FSH superimposed on PB blockade, can induce a release of FSH independently of changes in measured steriods (serum P4, E2) and in the absence of concomitant LH release. The induction of FSH release could not be detected in the absence of the ovary, but ovariectomy by itself increased FSH release without LH release. The data suggest that gonadotropins, as well as ovariectomy, may induce FSH release by altering a nonsteroidal feedback from the ovaries.