EFFECT OF AN INCREASE IN FSH ON THE PRODUCTION OF GONADOTROPIN-SURGE-ATTENUATING FACTOR IN WOMEN

Gonadotrophin-surge-attenuating factor (GnSAF) is a putative nonsteroi dal 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 place bo (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 (Delta LH) to an inject ion of 10 mu g 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 p lacebo or FSH in group 2. In group 1, Delta LH was significantly atten uated 12 h after treatment with FSH compared with the control cycles, while serum oestradiol concentrations increased 24 h after the injecti on of FSH. The decrease in Delta LH lasted for the period when the FSH concentation was increased (3 days). A significant decrease in the ba sal concentration of LH was correlated with the increase in the oestra diol concentration. In group 2, Delta LH increased significantly betwe en 4 and 8 h after treatment (LHRH self-priming effect) in both cycles . However, Delta LH was significantly attenuated in the FSH-treated cy cles compared with the control cycles after 8, 12 and 24 h. At the sam e time, serum concentrations of oestradiol and immunoreactive inhibin did not change significantly. These results suggest that GnSAF is a no nsteroidal ovarian substance, different from inhibin, the production o f which is dependent on FSH and which exerts potent antagonistic effec ts on the oestradiol-induced self-priming action of LHRH.