ALPHA-MELANOCYTE-STIMULATING HORMONE ANTAGONIZES THE INHIBITORY EFFECT OF CORTICOTROPIN-RELEASING HORMONE ON LUTEINIZING-HORMONE SECRETION DURING THE LUTEAL-PHASE IN NORMAL WOMEN

CRH inhibits the secretion of gonadotropins by activating endogenous o pioids, whereas alpha MSH, which displays various behavioral and neuro endocrine effects contrary to those of the opioids, stimulates their r elease. To evaluate the possible interaction of CRH and alpha MSH, eig ht women in the luteal phase underwent the following tests: 1) ovine C RH infused at 100 mu g/h for 3 h, 2) alpha MSH (2.5 mg as an iv bolus 60 min after the start of saline infusion), 3) CRH plus alpha MSH (inj ected 60 min after the start of CRH infusion), and 4) placebo. LH, FSH , PRL, ACTH, and cortisol were determined every 15 min for 180 min. CR H significantly (P < 0.001) reduced serum LH. alpha MSH alone signific antly (P < 0.001) increased LH to a peak within 15-30 min (baseline, 3 .3 +/- 0.7 mIU/mL; maximum increase, 3.5 +/- 0.9 mIU/mL) and induced a n even greater rise when injected during the CRH infusion (baseline, 2 .8 +/- 03 mIU/mL; maximum increase 7.5 +/- 1.6 mIU/mL; P < 0.05 us. al pha MSH alone). FSH was always unaffected. ACTH and cortisol increased (P < 0.001) during the CRH infusion and fell significantly (P < 0.001 ) during the placebo infusion. alpha MSH had no effect on these change s. PRL fell during the placebo infusion (P < 0.001). No changes were i nduced by CRH or alpha MSH. In conclusion, alpha MSH antagonizes CRH i nhibition of LH secretion. This finding lends support to the view that differential posttranslational processing of POMC contributes to the regulation of LH secretion. Further investigation is needed to clarify the mechanism of the antagonism between alpha MSH and CRH.