Dihydropyridine calcium antagonists depress the amplitude of the plasma melatonin cycle in baboons

Meyer, A. C.; Nieuwenhuis, Jacobus J.; Kociszewska, V.J.; Joubert, W. S.; Meyer, Barbara J.

doi:10.1016/0024-3205(86)90388-7

Cited by 15 publications

(5 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Verapamil may well have increased the renal excretion of MT, by improving renal blood flow. Meyer et al [39] treated baboons with intraperitoneal injections of the calcium antagonists verapamil, nifedipine, nitrendipine and nisoldipine. If verapamil increases the renal excretion of MT, this could in turn mask a 'true' stimulatory effect of the drug on the pinealocytes.…”

Section: Discussionmentioning

confidence: 99%

“…On the contrary, other research groups have found decreased NAT activity (N-acetyltransferase, the rate-limiting enzyme step in MT biosynthesis) [36][37][38] when testing the effects of calcium channel blockers in other species. Meyer et al [39] treated baboons with intraperitoneal injections of the calcium antagonists verapamil, nifedipine, nitrendipine and nisoldipine. The three dihydropyridine calcium antagonists depressed the nocturnal plasma MT peak levels by up to 40%, whereas verapamil did not affect the MT peak level.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Does hypercalcaemia or calcium antagonism affect human melatonin secretion or renal excretion?

Wikner

Wetterberg

Röjdmark

1997

Eur J Clin Investigation

View full text Add to dashboard Cite

Patients with primary hyperparathyroidism have higher serum melatonin concentrations during active disease than after surgical cure. Whether this is caused by hypercalcaemia per se, increased parathyroid hormone secretion or other mechanisms is unknown. We decided to elucidate whether exogenous hypercalcaemia influences melatonin secretion. For this purpose, eight healthy volunteers were infused with calcium and saline on separate days and in random order (experiment A). Hypercalcaemia inhibited nocturnal melatonin secretion by 20% but left urinary melatonin excretion unaffected. If exogenous hypercalcaemia inhibits melatonin secretion, it is reasonable to assume that calcium channel blockers such as verapamil might have the opposite effect. This was investigated in experiment B, in which eight healthy subjects were treated on separate occasions with oral verapamil and placebo. Verapamil did not affect nocturnal melatonin secretion but increased melatonin excretion by 145%. As 6-sulphatoxy-melatonin is the main melatonin metabolite excreted by the kidneys, it was considered important to find out whether verapamil would also influence the excretion of 6-sulphatoxy-melatonin. This was investigated in experiment C, in which eight healthy volunteers were treated, on separate occasions, with oral verapamil and placebo. In this experiment also, verapamil increased urinary melatonin excretion significantly (by 67%), but left excretion of 6-sulphatoxy-melatonin unaffected. These findings imply that verapamil influences the renal and/or hepatic handling of melatonin.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Does hypercalcaemia or calcium antagonism affect human melatonin secretion or renal excretion?

Wikner

Wetterberg

Röjdmark

1997

Eur J Clin Investigation

View full text Add to dashboard Cite

show abstract

“…At the end of the DG studies, blood was obtained to assess circulating melatonin concentrations to determine if day-night differences in melatonin were apparent, as described in humans, baboons, and other monkeys (36,38,39). In all animals, we found that levels were very low (0-1.4 pg͞ml) including those animals studied in darkness at night.…”

Section: Resultsmentioning

confidence: 99%

Newborn primate infants are entrained by low intensity lighting

Rivkees

Hofman

Fortman

1997

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

At the present time we do not know when the circadian timing system of human infants becomes responsive to light. Because of human study limitations, it is not currently possible to address this issue in clinical studies. Therefore, to provide insights into when the circadian system of humans becomes responsive to light, baboons were studied. We first assessed if the biological clock located in suprachiasmatic nuclei (SCN) is responsive to light at birth. When term newborn infants were exposed to bright light at night (5000 lux), SCN metabolic activity and c-fos mRNA expression increased, indicating the presence of photic responsiveness. When photic entrainment of developing rhythmicity was examined in infants, low intensity (200 lux) cycled lighting was sufficient to entrain circadian phase. However, low intensity lighting was not sufficient to induce changes in SCN metabolic activity or c-fos mRNA expression. Phase-response studies indicated that light exposure (200 lux) before the onset of activity most effectively shifted circadian phase. These data provide direct evidence that the SCN are responsive to visually mediated light information in a primate at birth. Further consideration of lighting conditions that infants are exposed to is therefore warranted.

show abstract

“…In addition to involvement of calcium in the modulation of synthetic activity of the pineal gland, there is a growing body of information suggesting a role for calcium in the release of melatonin (20,21,23,24). Dihydropyridine calcium channel antagonists have been shown to reduce the amplitude of the nocturnal rise in plasma melatonin in baboons.…”

Section: Pinealocyte Calcium Channelsmentioning

confidence: 99%

Involvement of Calcium in Pineal Gland Function

Morton¹,

Reíter²

1991

Experimental Biology and Medicine

View full text Add to dashboard Cite

he pineal gland functions as a neurohumoral transducer, accepting photic information from T the retinae and converting this neural message into chemical mediators, the best documented of which is melatonin (N-acetyl-5-methoxytryptamine) ( 1). The onset of darkness causes information to travel from the suprachiasmatic nuclei of the hypothalamus via the superior cervical ganglia to postganglionic sympathetic nerves that end in the pineal, where they release norepinephrine. The resultant stimulation of B-adrenergic receptors, possibly augmented by a-adrenergic stimulation, leads to an increased activity of N-acetyltransferase (NAT) (2), the rate-limiting enzyme involved in synthesis of melatonin ( 3 ) . Serotonin, derived from dietary tryptophan taken up by pinealocytes from the blood, is N-acetylated by NAT, which is subsequently 0-methylated by hydroxyindole-0-methyltransferase (HIOMT) to form melatonin, which is then released into the general circulation. Being a small lipophilic molecule, melatonin is generally considered to be released rapidly and passively following synthesis, although there is some evidence that short-term storage of melatonin by the pineal gland might occur (4).Melatonin's lipophilicity also ensures that it distributes widely to target tissues, which, therefore, receive photoperiodic information and can subsequently act with appropriate physiological responses ( 5 ) .The multiplicity of extracellular and intracellular ' Fullbright Fellow on leave from Department of Preclinical Veterinary Studies,

show abstract

Dihydropyridine calcium antagonists depress the amplitude of the plasma melatonin cycle in baboons

Cited by 15 publications

References 24 publications

Does hypercalcaemia or calcium antagonism affect human melatonin secretion or renal excretion?

Does hypercalcaemia or calcium antagonism affect human melatonin secretion or renal excretion?

Newborn primate infants are entrained by low intensity lighting

Involvement of Calcium in Pineal Gland Function

Contact Info

Product

Resources

About