Nocturnal increase of plasma testosterone in men: relation to gonadotropins and prolactin.

The nocturnal increase of plasma testosterone (T) in adult men has been well established. Luteinizing hormone (LH) does not show a similar increase throughout the night, whereas prolactin (PRL) does, suggesting the possibility of other hormone influence on T secretion. To investigate this possibility, 8 young adult men were studied for 4 consecutive nights in the sleep laboratory (2 nights adaptation, 2 nights blood sampling), by blood samples taken every 30 min during the 8-h sleep period, for measurement of LH, follicle stimulating hormone (FSH), PRL, and T. LH and FSH were secreted episodically, with little or no change in baseline levels during the night. PRL and T also were secreted episodically, but their baseline levels increased as the night progressed. Both LH and PRL had maximum within-subject correlations (averages equal +0.35 and +0.48 respectively) with T when they led T by 60 min. Within-subject correlations done on first differences (to remove the effect of slow trends) were near zero. LH and PRL had larger correlations with T than did FSH, for both calculations. These data suggest that both LH and PRL levels precede T levels by about 60 min. PRL thus may participate in the regulation of nocturnal T secretion in adult men.

Periodic limb movement disorder is associated with normal motor conduction latencies when studied by central magnetic stimulation--successful use of a new technique.

This study prospectively tested the hypothesis that patients with periodic limb movement disorder (PLMD) have longer motor conduction latencies than normals. Six healthy adults, 13 patients with PLMD, and 8 patients with long-term multiple sclerosis (MS) had recordings of motor conduction latencies during wake and sleep. MS subjects were included only to show that we could detect prolongation of central conduction; nonMS subjects were used to test the hypothesis. Subjects had no other medical or sleep problems. A novel magnetic stimulator, the Cadwell MES-10, was discharged over the vertex and the C7 cervical spine. It triggered compound muscle action potentials that were recorded in the abductor digiti minimi in the hand. The conduction latencies were the total conduction time (TCT), measured vertex to hand, and the peripheral conduction time (PCT), measured C7 to hand. The difference was the central conduction time (CCT). Only TCT could be obtained during sleep. Supporting the use of TCT as an indirect measure of central conduction was that, in all waking subjects, TCT correlated with CCT (r = 0.91, p = 0.001) but not with PCT. Reliabilities during wake and sleep were 0.95 or higher for TCT and PCT measurements. Waking CCT was greater in MS subjects (13.77 milliseconds) than those without MS (9.21 milliseconds), p = 0.001. Sleeping TCT was much less impressive in distinguishing MS subjects [27.08 milliseconds in nonrapid eye movement (NREM) sleep; 28.64 milliseconds in rapid eye movement (REM) sleep] from nonMS subjects (24.45 milliseconds in NREM; 24.84 milliseconds for REM), p = 0.07 for NREM and p = 0.04 for REM.(ABSTRACT TRUNCATED AT 250 WORDS)

Secretion of hormones influencing water and electrolyte balance (antidiuretic hormone, aldosterone, prolactin) during sleep in normal adult men.

Renal conservation of electrolytes and water occurs normally during sleep. Antidiuretic hormone (ADH), aldosterone (ALDO), and prolactin (PRL) are hormones that may have interactive effects on kidney function. The availability of a radioimmunoassay for ADH as well as for ALDO and PRL permitted the study of the simultaneous secretion patterns of these three hormones during all-night sleep in eight normal young adult men, by blood sampling every 20 min from 2300 to 0700 on two consecutive night. ADH, ALDO, and PRL all appeared to be secreted episodically. The pulsatile release of ADH was random, and average plasma ADH levels were unchanged during the night. ALDO and PRL, on the other hand, had an approximately 90-min secretion rhythm, and average plasma concentrations of both hormones consistently increased during the hours of sleep. Average plasma sodium concentration was constant throughout the night. The nocturnal increase in plasma ALDO may be responsible for the normal reduction of urine sodium excretion during the night. The concomitant increase in plasma PRL might synergize with ALDO in influencing the renal retention of sodium, but PRL alone has little apparent effect on human kidney function. REM sleep-related decreases in urine flow have been noted both in humans and in monkeys, but ADH secretion was not REM related in out subjects. Autonomic activation during REM is one possible explanation for decreased urine flow during this stage of sleep.

Selective neuroendocrine effects of low-dose haloperidol in normal adult men.

The neuroendocrine effects of haloperidol, usually reported as side effects of this drug when given in antipsychotic doses, have not been systematically investigated. In the present study five normal adult men were administered saline and two doses of of haloperidol (0.25 mg, 0.5 mg) intramuscularly in a double-blind randomized block design. The anterior pituitary hormones GH, LH, FSH, and PRL were measured in blood samples taken every 20 min for several hours thereafter. The low doses of haloperidol used have been shown by others to alter the human EEG; in our subjects these doses produced no objective or subjective clinical effects. There were no drug related changes in GH, LH, or FSH. PRL, however, showed a prompt, statistically significant, dose-related increase in plasma levels, with a return to baseline with 5 h. Haloperidol has strong dopamine-blocking effects, and the hypothalamic inhibitory mechanism for PRL release is believed to be dopamine-mediated. The results of this study suggest that haloperidol may have utility in low doses primarily for its hypothalamic neuroendocrine effects, and that dose-related PRL release may be a useful paradigm for comparing dopamine-blocking antipsychotic agents in humans.