We investigated the participation by endogenous opioid peptides in the control of prolactin and gonadotropin secretion in 5 normal men and 6 normal women and in 4 men and 5 women with persisting hyperprolactinemia following transsphenoidal pituitary microsurgery for prolactinomas. Iv administration of the specific opiate-receptor antagonist, naloxone hydrochloride (0.2 mg/kg bolus), failed to affect serially sampled serum prolactin levels in normal male or female subjects. With prolactinemia patients, naloxone suppressed hyperprolactinemia to 37% and 32% of mean control values in 2 of 4 males, but in none of 6 females. When luteinizing hormone was serially sampled under the same conditions, 5 of 5 normal males (but no female, normal or abnormal) demonstrated a monophasic increase in serum LH concentrations after injection of the antagonist. The LH peak was 55% ± 4% above basal levels (p<0.01). In contrast to normal men, only one of 4 hyperprolactinemic male patients manifested a stimulatory response of LH to naloxone. Among all 20 subjects, none exhibited a change in FSH levels acutely after naloxone. These data suggest that: naloxone will not fulfill its postulated role as an ideal therapy for hyperprolactinemia and hypogonadotropism, at least in women; endogenous opioids may participate in the neuroendocrine regulation of LH secretion in the normal human; male-female differences may modify the role of endogenous opioids; and some male patients with hyperprolactinemia exhibit defective opioid-related neuroregulation of LH secretion.
|Original language||English (US)|
|Number of pages||6|
|Journal||Journal of Endocrinological Investigation|
|State||Published - 1981|
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