ENDOGENOUS OPIOID MEDIATION OF THE INHIBITORY EFFECT OF ETHANOL ON THE PROLACTIN RESPONSE TO BREAST STIMULATION IN NORMAL WOMEN

The effect of ethanol on the prolactin (PRL) response to breast stimul ation was tested in normal women. The possible role of endogenous opio ids in the control of the PRL response to breast stimulation and ethan ol action was also examined. Eleven normal women were tested four time s on the 22nd day of four consecutive regular menstrual cycles. All wo men underwent mechanical breast stimulation (for 10 min) with the conc omitant administration of normal saline, naloxone (2 mg in an iv bolus plus 10 mg over 75 min, or 4 mg in an iv bolus plus 20 mg over 75 min .), ethanol (50 ml in 110 ml of whiskey p.o.) or the combination of et hanol and naloxone. Serum PRL levels rose significantly after breast s timulation, with a mean peak response (71.4% higher than baseline at 2 0 min). The PRL response to breast stimulation was not changed by the treatment with the lower (2 plus 10 mg) or the higher (4 plus 20 mg) d ose of naloxone, whereas it was strikingly decreased by ethanol (mean peak was 25% higher than baseline). However, when ethanol was given to gether with naloxone, the peak rise induced by breast stimulation was only partially inhibited by ethanol (the mean PRL peak was 46.2% highe r than baseline). At both doses naloxone produced similar effects. The se data demonstrate that ethanol inhibits the PRL response to breast s timulation. Naloxone-sensitive endogenous opioids do not appear to be involved in the control of the PRL rise induced by breast stimulation. In contrast, since naloxone partially reversed the inhibiting effects of ethanol, a partial involvement of opioid peptides in ethanol actio n is supposed.