Human Reproduction, Vol. 16, No. 2, 209-214,
February 2001
© 2001 European Society of Human Reproduction and Embryology
Opinions |
Is GnRH self-priming an obligatory feature of the reproductive cycle?
1 Division of Medical Pharmacology, Leiden/Amsterdam Center for Drug Research, Sylvius Laboratories, University of Leiden, PO Box 9503, 2300 RA Leiden, 2 Research Institute for Endocrinology, Reproduction and Metabolism, Division of Reproductive Endocrinology and Fertility, Division of Obstetrics and Gynaecology, University Hospital Vrije Universiteit, Amsterdam, 3 Department of Obstetrics, Gynaecology and Reproductive Medicine, Leiden University Medical Center, Leiden, and 4 Department of Gynaecology, University Hospital Groningen, The Netherlands
Abstract
Insufficient suppression of LH (premature elevation) and FSH (prolonged release) give rise to blood concentrations which may cause damaging effects on oocyte viability and too many follicles respectively. During the surge, LH rises from low to high threshold values to initiate processes from initiation of the resumption of oocyte meiosis to the induction of ovulation. In general, it is thought that a dramatic increase in LH concentration is required to attain the high threshold for ovulation. A self-priming mechanism, by which gonadotrophin-releasing hormone (GnRH) enhances the LH (and FSH) responses to its own action, was thought to be responsible. However, normal LH surges in rats consist of <2–7% of the maximal pituitary releasing capacity. The physiological roles of LH and FSH favour a control mechanism that restrains their blood concentrations during most of the cycle. Ovarian proteins, e.g. inhibin and putative gonadotrophin-surge-inhibiting factor/attenuating factor (GnSIF/AF), are involved in this process. We argue that the increased pituitary LH responsiveness during the mid-cycle surge is not the result of a self-priming process that `dramatically' increases the LH releasing capacity of the pituitary gland. This is probably due to elimination by GnRH of the inhibitory action of the putative ovarian proteins GnSIF/AF.
Key words: functional antagonism/GnSAF/GnSIF/gonadotrophins/LH hypersecretion
Notes
5 To whom correspondence should be addressed. E-mail: j.koning{at}lacdr.leidenuniv.nl
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