Naloxone-induced prolactin secretion in women: evidence against a direct prolactin stimulatory effect of endogenous opioids.

Because both opioids and ovarian steroids influence PRL secretion, the relationship between these inputs to PRL control was investigated. Infusion of the opiate receptor antagonist naloxone (1.6 mg/h for 4-8 h) failed to alter serum PRL levels in hypogonadal women or normal women in the early follicular or late luteal phase. In contrast, a prompt and sustained naloxone-induced release of PRL was found in the late follicular and midluteal phases of the cycle, with maximum increments (mean +/- SE) of 16.9 +/- 5.3 and 9.7 +/- 3.2 ng/ml, respectively. In the luteal phase women, the number of PRL pulses was significantly (P less than 0.001) greater during naloxone than during saline infusion (3.4 vs. 1.6 pulses/8 h), and a positive linear correlation was found between the integrated PRL response to naloxone and the levels of circulating estradiol (r = 0.62) and progesterone (r = 0.95). When serum LH concentrations were determined in the same samples, a significantly (P less than 0.001) greater synchrony of PRL with LH pulses during naloxone infusion (96%) compared to that during saline infusion (36%) was found in the luteal phase women. Thus, naloxone infusion induced an increase in pulsatile PRL release which was synchronized with LH pulses. These findings, not previously reported, suggest that a common neuroendocrine mechanism is involved in the opioidergic control of PRL and LH secretion and that this effect of naloxone is manifested only during high ovarian steroid environments.