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Effects of ₁-Adrenergic Blockade on Pulsatile Luteinizing Hormone, Follicle-Stimulating Hormone, and Prolactin Secretion in Polycystic Ovary Syndrome^*

Institute of Reproductive Physiology and Pathology (R.P., S. V., M.S., O.M., E.P., R.F., C.F.) and Central Laboratory (M.C., M.E.G.), University of Bologna 1-40138 Bologna, Italy

Address requests for reprints to: Dr. Roberto Paradisi, Institute of Reproductive Physiology and Pathology, S. Orsola Hospital, University of Bologna, Massarenti 13, I-40138 Bologna, Italy.

Central noradrenergic mechanisms may participate in the regulation of pulsatile gonadotropin secretion in women with the polycystic ovary syndrome (PCO). To examine this possibility we measured serum LH, FSH, and PRL concentrations at 10-min intervals and total testosterone and 17β-estradiol at 60-min intervals for 8 h basally and during the infusion of the ₁-adrenoceptor antagonist thymoxamine (10 µg/kgmin) in 10 young women with PCO. Mean and integrated serum LH concentrations as well as LH pulse frequency were not significantly altered (P = NS) during the thymoxamine infusion. However, we found an increase in LH pulse amplitude as both net (P < 0.002) and percent (P < 0.002) increment, as well as mean LH peak values (P < 0.05) during ₁-adrenergic blockade. There were no significant changes in pulsatile FSH and PRL secretion or gonadal sex steroids during these experimental conditions. These data suggest that in PCO patients, 1) brain noradrenergic mechanisms do not play a stimulatory role in regulating the frequency of pulsatile LH secretion, 2) central noradrenergic activity inhibits LH pulse amplitude, and 3) PRL and FSH pulsatility are not altered by central noradrenergic blockade.

^* This work was supported in part by a grant from the University of Bologna.

Received February 19, 1987.

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