Endogenous opiates participate in the regulation of pulsatile luteinizing hormone release in an unopposed estrogen milieu: studies in estrogen-replaced, gonadectomized patients with testicular feminization.
Administration of opiate receptor antagonists augmented pulsatile LH release in six estrogen-treated, orchidectomized individuals with testicular feminization. In response to an opiate antagonist, LH pulse frequency increased from 3.0 +/- 0.55 (+/- SE) to 5.0 +/- 0.45 pulses/8 h (P = 0.034). Since these patients have inborn target tissue resistance to androgens, we infer that sustained androgen action is not obligatory to the emergence of endogenous inhibitory opiate tone in man. Rather, these observations document that the suppressive effects of opiates on gonadotropin secretion can be unmasked in the presence of an unopposed estrogen milieu.
D000293:Adolescent; D000328:Adult; D013734:Androgen-Insensitivity Syndrome / Q000097:blood* / Q000628:therapy; D002369:Castration; D004723:Endorphins / Q000502:physiology*; D004958:Estradiol / Q000008:administration & dosage; D004967:Estrogens / Q000502:physiology*; D005260:Female; D006801:Humans; D007986:Luteinizing Hormone / Q000378:metabolism*; D009270:Naloxone; D009271:Naltrexone
D004723:Endorphins; D004967:Estrogens; D009270:Naloxone; D004958:Estradiol; D009271:Naltrexone; D007986:Luteinizing Hormone