Opioid control of luteinizing hormone secretion in humans.

The observation that heroin-addicted subjects are amenorrheic and/or hypogonadic suggested a possible role of endogenous opioid peptides (EOP) in the regulation of the hypothalamus-pituitary-gonodal axis. Because EOP are localized all through the axis, they may influence the reproductive function acting at various levels. The injection of morphine decreases plasma LH levels, abolishing the pulsatile pattern of secretion. The evidence that naloxone, an opiate receptor blockade, increases LH levels suggests a tonic inhibitory action of EOP. The naloxone-induced LH increase is not observed before pubertal maturation, in both sexes, and is absent in children with delayed or precocious puberty and in those with Klinefelter's or Turner's syndrome, suggesting a role of gonadal function on the opioid control of LH secretion. In adult women this LH response to naloxone is present during the periovulatory and the luteal phase of the menstrual cycle, suggesting a permissive role of estradiol and mainly of progesterone on the action of EOP on the LH secretion. Indeed, in amenorrheic subjects naloxone lacks to stimulate plasma LH levels and the treatment for the induction of ovulation restores this activity. An increased inhibitory action of EOP on GnRH release may explain the inefficacy of naloxone to stimulate LH secretion in hypogonadotropinic patients, while a decreased action has been hypothesized in postmenopausal women. The clinical implications of EOP in reproductive medicine appear to be promising