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A possible role for endogenous opioids in the control of prolactin and luteinizing hormone secretion in the human



A possible role for endogenous opioids in the control of prolactin and luteinizing hormone secretion in the human



Journal of Endocrinological Investigation 4(1): 31-36



The participation by endogenous opioid peptides in the control of prolactin [PRL] and gonadotropin secretion was investigated in 5 normal men and 6 normal women, and in 4 men and 5 women with persisting hyperprolactinemia following transsphenoidal pituitary microsurgery for prolactinomas. Administration [i.v.] of the specific opiate-receptor antagonist, naloxone hydrochloride (0.2 mg/kg bolus), failed to affect serially sampled serum PRL levels in normal male or female subjects. With prolactinoma 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 [LH] 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 1 of 4 hyperprolactinemic male patients manifested a stimulatory response of LH to naloxone. Among all 20 subjects, none exhibited a change in follicle stimulating hormone levels acutely after nalxone. Evidently naloxone will not fulfill is 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.

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Accession: 004609615

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PMID: 7240669


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