Patients who have severe hypogonadotropic hypogonadism caused by presumed hypothalamic disease often have a subnormal LH response to a bolus dose of gonadotropin-releasing hormone (GnRH). To determine if this subnormal response is the result of lack of exposure of the pituitary gonadotroph cells to GnRH, five such men were given daily infusions of 500 microgram GnRH, for 7 days. A standard 250-microgram bolus test dose of GnRH was administered before and again immediately after the week of GnRH infusions. Five men who had severe hypogonadotropic hypogonadism as a result of presumed pituitary disease also received daily GnRH infusions for 1 week. The mean incremental LH responses (+/- SE) to GnRH of the men with presumed hypothalamic disease were 5.0 +/- 1.9 mIU/ml before and 56.9 mIU/ml after the week of infusions. The mean incremental LH responses of the men with presumed pituitary disease were 2.4 +/- 0.7 mIU/ml before and 3.7 +/- 2.9 mIU/ml after the week of infusions. These data suggest that the normal gonadotroph requires prolonged exposure to GnRH for LH responsiveness to become normal, but that the severely damaged gonadotroph cannot be stimulated to release LH normally even by the same prolonged stimulation with GnRH.
A B S T R A C T The influence of testosterone on gonadotropin-releasing hormone (GnRH) secretion was assessed indirectly by altering the serum testosterone concentration of male rats and measuring GnRH release from their incubated hypothalami 1 wk later.GnRH release from hypothalami ofcastrated rats was 13.4±+1.2 (SE) pg/h, compared to 35.3±3.8 pg/h from hypothalami of intact rats (P < 0.001). GnRH release from the hypothalami of castrated rats treated with testosterone propionate, 100 or 500 ,ug daily, was 25.0±3.4 pg/h and 27.9±3.6 pg/h, which is significantly greater (P < 0.05 and P < 0.01, respectively) than that from hypothalami of castrated rats treated only with sesame oil. A similar decrease in GnRH release from hypothalami of hypophysectomized rats and prevention of this decrease by treating the hypophysectomized rats with testosterone propionate is evidence that the observed effects of testosterone are not mediated via luteinizing hormone and(or) follicle-stinriulating hormone secretion. Treatment of castrated rats with either dihydrotestosterone propionate or estradiol benzoate also prevented the decrease in GnRH release from the hypothalami of castrated rats.We conclude that testosterone, dihydrotestosterone, and estradiol all prevent the decrease in GnRH release from hypothalami of castrated rats treated with these steroids. The possibility exists that these steroids may also maintain GnRH secretion in vivo.
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