Nocturnal Elevation of Plasma Melatonin and Urinary 5-Hydroxyindoleacetic Acid in Young Men: Attempts at Modification by Brief Changes in Environmental Lighting and Sleep and by Autonomic Drugs

Abstract

In order to determine whether the human pattern of circulating melatonin resembles that previously described in lower animals, men 19-32 years old were exposed to a light-dark cycle with 14 hours of light per day (L:D 14:10). In whites and blacks, nocturnal (dark phase, sleeping) melatonin levels were almost always elevated to 0.05-0.1 ng/ml plasma compared with lower or undetectable levels during the day, measured by the tadpole bioassay. Thin-layer migration of bioactive material was identical to that for melatonin standard. A rhythm with nocturnal elevation of urinary 5-hydroxyindoleacetic acid (5-HIAA) was observed. Nocturnal (sleep phase) rise in blood melatonin (but not urinary 5-HIAA) continued during 21/2 day-night cycle lengths after the onset of constant light. Though the dark phase plasma melatonin rise was less marked after reversal of the sleep-wake cycle (no change in the light cycle), dark phase rise in urinary 5-HIAA continued. Though marked cardiovascular and other effects were produced by intravenous isoproterenol or scopolamine, no definite effect on melatonin levels was observed after either drug during the light phase in waking subjects.

Norepinephrine or Isoproterenol Stimulation of Pineal N-Acetyltransferase Activity and Melatonin Content in the Syrian Hamster Is Restricted to the Second Half of the Daily Dark Phase

“…The infusion o f isoproterenol into humans during the day is not followed by a commensurate rise in circulating melatonin levels [27], Perhaps the human pineal is similar to the hamster pineal, i.e., it may only possess the necessary receptors during the dark period.…”

Annual Review of Chronopharmacology. Volume 7. Biological Rhythms and Medications. Proceedings of the Conference of Chronopharmacology Held in Nice, France on 12-15 March 1990

“…( such as hippocampus and limbic system ) (Sapolsky et al, 1986) ; or they may stem from the imbalance among different neurotransmit= ters in the C.N.S., due to the selective impairment of noradrenergic pathways in aging (Hornykiewicz,1983). A clinically reliable tool to investigate the central noradrenergic tonus may be the study of melatonin circadian pattern, since the critica: melatonin secretion during the night is mediated by noradrenaline through the P -receptors (Reiter, 1976) and may bq selectively inhibited by f-adrenergic blociing drugs (Vaughan et al, 1976;Cowen et al, 1983). Our experience in this field concerns a croup of 14 clinically healthy women aged 66-90 y., in whom we simultaneously studied the circadian rhythm of plasma melato= nin, ACTH and cortisol, in order to investf;ate the relationships between melato= nin secretion and pituitary-adrenal axis in physiological aging.…”

Melatonin, Light and Circadian Cycles

“…Vaughan et al, (1976) and Weinberg et al, (1979) reported that having subjects sleep during the usual light period did not cause an increase in melatonin. However, lights were on during sleep in "those studies.…”

“…Both light and sleep seemed to contribute, but light was more important. As the melatonin cycle can be shifted by alterations in the light/ dark cycle but does not shift if light/dark is held constant and wake/sleep is shifted (Vaughan et al, 1976), melatonin cannot be the only controller of corticosteroid rhythm.…”