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Luteinizing hormone (LH) and prolactin are released in pulses which are relatively synchronous in the luteal phase of the menstrual cycle in women. The concordance of LH and prolactin pulses in normal men has not been reported. The objectives of this study were firstly to determine whether LH and prolactin pulses are synchronous in men, and secondly to examine the effects of naloxone and a new orally active opiate antagonist, nalmefene, on LH and prolactin release in men. Three groups of normal male subjects received saline infusion (control n = 5), naloxone infusion (2 mg/h; n = 5) or nalmefene (10 mg p.o.; n = 6). Blood samples were collected every 15 min for 2 h before and 6 h after study medication for determination of LH, prolactin and testosterone by radioimmunoassay. Both naloxone and nalmefene resulted in a significant increase in LH pulse frequency and in mean serum LH and testosterone concentrations with no change in LH pulse amplitude, prolactin pulse frequency or amplitude. In controls, 61% of LH pulses were synchronous with prolactin pulses. There was a decrease in concomitance of LH and prolactin pulses with naloxone (48%) and nalmefene (24%; P < 0.025) administration. In contrast, 52% of prolactin pulses were concomitant with LH pulses in controls, while naloxone (100%) but not nalmefene (67%) resulted in a significant (P < 0.01) increase in pulse synchrony. The difference observed between naloxone and nalmefene on prolactin--LH pulse synchrony is probably due to differential opioid receptor activity at the pituitary and hypothalamic level.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood samples were taken every 5 min for a 3-h period from ovariectomized (OVX) adult rats bearing chronic venous catheters. After 1 h of sampling, an experimental drug was injected through the sampling catheter. The neuroleptics, chlorpromazine and haloperidol, blocked pulsatile discharges of luteinizing hormone (LH) in some animals, for periods of 65-120 min, as did the alpha-adrenergic receptor blockers, phenoxybenzamine and phentolamine. Pimozide, a more specific dopaminergic blocking agent, had less effect, while neither the beta-adrenergic receptor blocker, propranolol, nor the control treatments had any influence on the pulsatile LH patterns. The temporal pattern of inhibition of pulsatile discharges of LH by these drugs is more rapid than the inhibition caused by estrogen treatment in the OVX rat. These results suggest the presence of alpha, but not beta, adrenergic elements in the pulsatile mode of LH release in the OVX rat. They do not support the presence of dopaminergic elements, but neither do they conclusively deny it.