Effect of an increase in FSH on the production of gonadotrophin-surge-attenuating factor in women

Gonadotrophin-surge-attenuating factor (GnSAF) is a putative nonsteroidal ovarian factor that is produced by FSH and that attenuates the LH surge in superovulated women. To study further the role of FSH in the production of GnSAF, 12 normally ovulating women were divided into two groups and investigated during two cycles: a cycle treated with placebo (control) and a cycle treated with FSH. In group 1 (n = 6), placebo (2 ml 0.9% normal saline) or FSH (450 iu) was injected i.m. on day 2 of the cycle (09:00 h). In group 2 (n = 6), placebo (2 ml 0.9% normal saline) or FSH (225 iu) was injected on the day (09:00 h) on which the dominant follicle was 14–15 mm in diameter, as measured by ultrasound (i.e. after the pituitary had been primed by endogenous oestrogen for several days). The response of LH over 30 min (ALH) to an injection of 10 μg LHRH i.v. (bioassay for GnSAF in vivo) was investigated once a day in group 1, and 4, 8, 12 and 24 h after the injection of placebo or FSH in group 2. In group 1, ALH was significantly attenuated 12 h after treatment with FSH compared with the control cycles, while serum oestradiol concentrations increased 24 h after the injection of FSH. The decrease in ALH lasted for the period when the FSH concentation was increased (3 days). A significant decrease in the basal concentration of LH was correlated with the increase in the oestradiol concentration. In group 2, ALH increased significantly between 4 and 8 h after treatment (LHRH self-priming effect) in both cycles. However, ALH was significantly attenuated in the FSH-treated cycles compared with the control cycles after 8, 12 and 24 h. At the same time, serum concentrations of oestradiol and immunoreactive inhibin did not change significantly. These results suggest that GnSAF is a nonsteroidal ovarian substance, different from inhibin, the production of which is dependent on FSH and which exerts potent antagonistic effects on the oestradiol-induced self-priming action of LHRH.