Abstract

Under physiological conditions, LH and FSH are stimulated by LHRH from the hypothalamus and are released from the gonadotrophs in a pulsatile manner. Gonadotrophin pulsation is required for adequate control of ovarian function. It has been well documented that acute and repetitive administrations of potent LHRH agonists have paradoxical antifertility effects. In female animals of several species various treatments cause inhibition of ovulation, induce luteolysis and terminate pregnancy (Balmaceda and Asch, 1981; Corbin and Bex, 1981; Vickery and McRae, 1984). In normal women daily administration of LHRH agonist inhibits ovulation (Nillius et al., 1978; Schmidt-Gollwitzer et al., 1981). Acute and short-term dosing have also been shown to interfere with follicular maturation when administered in the early follicular phase of the menstrual cycle (Sheehan et al., 1982; Skarin et al., 1982a) and with corpus luteum function when administered after ovulation (Koyama et al., 1978; Casper and Yen, 1979; Lemay et al., 1979; Bergquist et al., 1980; Lemay et al., 1982, 1983c).

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