Human Reproduction, Vol. 14, No. 1, 21-26,
January 1999
© 1999 European Society of Human Reproduction and Embryology
FSH inhibits the augmentation by oestradiol of the pituitary responsiveness to GnRH in the female rat
Division of Reproductive Biology, Department of Obstetrics and Gynaecology, University of Groningen, Hanzeplein 1, PO Box 30.001, 9700 RB Groningen, The Netherlands
The effect of follicle stimulating hormone (FSH) treatment on the pituitary response to gonadotrophin-releasing hormone (GnRH) was studied in rats in various reproductive conditions. A 3-day treatment of cycling rats with FSH (Metrodin®; 10 IU/injection) lowered the spontaneous pre-ovulatory LH-surge and suppressed the pituitary luteinizing hormone (LH) response to GnRH. FSH also suppressed the LH response of pseudopregnant (PSP) rats on day 8 of pseudopregnancy, but not that of day-8 PSP rats which had been ovariectomized on day 4 (OVX–PSP rats). GnRH induced self priming in cycling, PSP and OVX–PSP rats. Oestradiol strongly augmented the pituitary LH-response to GnRH injection in PSP and OVX–PSP rats, but not in cycling rats; probably because in these latter animals the LH response to GnRH was already augmented by endogenous oestradiol. FSH suppressed the LH response to GnRH in oestradiol-treated PSP and cycling rats; in these latter rats the suppression of the LH response was as strong as that in cycling rats not treated with oestradiol. FSH did not suppress the LH response of oestradiol-treated OVX–PSP rats. The effect of FSH was not associated with changes in plasma oestradiol and progesterone concentrations. Analysis of the data revealed that FSH specifically suppressed the augmentative effect of oestradiol, but did not affect the GnRH-self priming effect. It is concluded that under the influence of FSH, the ovaries produce a factor which suppresses the augmentative effect of oestradiol on the GnRH-induced LH response of the pituitary gland. It is suggested that this effect of FSH underlies the suppression of the spontaneous LH-surges of FSH-treated cycling rats. As the present putative `oestrogen-antagonizing factor' did not suppress the GnRH-self priming effect, it is suggested that this factor is not identical to gonadotrophin surge inhibiting factor.
Key words: antagonist/GnRH responsiveness/LH/oestradiol
1 To whom correspondence should be addressed
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