The alpha-1-adrenergic neuronal system is involved in the pulsatile release of luteinizing hormone-releasing hormone in the ovariectomized female rhesus monkey.

It has been postulated that catecholamines are integral to the control of LHRH release. In the present study, the roles of adrenergic and dopaminergic receptors in the control of pulsatile LHRH release are examined. The effects of prazosin (an alpha 1-antagonist), rauwolscine (an alpha 2-antagonist), propranolol (a beta-antagonist), haloperidol (a dopamine antagonist), SCH23390 (a D1 antagonist), and LY163502 (a D2 agonist), on in vivo LHRH release in the stalk-median eminence were tested in ovariectomized female rhesus monkeys using push-pull perfusion. Prazosin caused a significant suppression of the LHRH release. This was primarily due to a significant suppression of LHRH pulse amplitude, but not pulse frequency, i.e. the interpulse interval was not affected by the administration of prazosin. In contrast to prazosin, none of the other adrenergic or dopaminergic drugs had significant effects on LHRH release. We conclude from these results that (1) the stimulatory effects of norepinephrine (NE) and/or epinephrine on pulsatile LHRH release are mediated by alpha 1-adrenergic receptors but not alpha 2- or beta-adrenergic receptors, and (2) dopaminergic receptors do not appear to be involved in pulsatile LHRH release in ovariectomized rhesus monkeys.