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  • Title: Naloxone-induced prolactin secretion in women: evidence against a direct prolactin stimulatory effect of endogenous opioids.
    Author: Cetel NS, Quigley ME, Yen SS.
    Journal: J Clin Endocrinol Metab; 1985 Jan; 60(1):191-6. PubMed ID: 3964791.
    Abstract:
    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.
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