The effect of testosterone and other adrenal steroids on PMS-induced ovulation in the immature rat

Abstract

17 alpha-hydroxyprogesterone (up to 200 mug/day) and 11 beta-hydroxyandrostenedione (up to 500 mug) had no effect on PMS-induced ovulation in intact immature rats. 10 mug/day of testosterone propoinate (TP) on days 28-30 of life decreased the percent of animals ovulating and the number of ova produced; this effect persisted in adrenalectomized animals with or without corticosterone replacement. Three daily doses of 10 mug TP increased the electrical threshold of the medial preoptic area in pentobarbital-blocked, PMS-stimulated animals. And TP decreased the rate of release and synthesis of FSH during the ovulatory surge, and the storage and rate of release of LH; it also inhibited the response to HCG in the PMS-primed animal, suggesting a direct target-organ effect.

PIP: The ability of testosterone propionate and other adrenal steroids to inhibit ovulation induced by pregnant mare's serum (PMS) was studied in immature rats. As much as 200 mcg/day of 17alpha-hydroxyprogesterone and 500 mcg of 11beta-hydroxyandrostenedione had no effect on PMS-induced ovulation. Both 7 and 10 mcg/day of TP, administered on Days 28-30 of life, significantly reduced the percentage of rats ovulating (p less than .06; p less than .01, respectively), and decreased the number of ova. A similar effect was observed in adrenalectomized animals, with or without cortisone replacement. 10 mcg TP, administered 3 times a day to pentobarbital-blocked, PMS-stimulated animals, caused an increase in the electrical threshold of the medial preoptic area. TP diminished the rate of release and synthesis of follicle-stimulating hormone during the ovulatory surge, and decreased the storage and rate of release of luteinizing hormone. The response to human chorionic gonadotropin was also inhibited by TP. The results suggest that TP may have a direct inhibitory action at the target organ.