The effect of atenolol, a p!-adrenergic antagonist, on nocturnal plasma melatonin secretion: Evidence for a dose-response relationship in humans
Article first published online: 30 JAN 2007
Journal of Pineal Research
Volume 23, Issue 3, pages 131–135, October 1997
How to Cite
Nathan, P. J., Maguire, K. R., Burrows, G. D. and Norman, T. R. (1997), The effect of atenolol, a p!-adrenergic antagonist, on nocturnal plasma melatonin secretion: Evidence for a dose-response relationship in humans. Journal of Pineal Research, 23: 131–135. doi: 10.1111/j.1600-079X.1997.tb00345.x
- Issue published online: 30 JAN 2007
- Article first published online: 30 JAN 2007
- April 18,1997; June 23,1997.
- β1-adrenergic receptor;
- pineal gland
Nathan PJ, Maguire KP, Burrows GD, Norman T.R. The effect of atenolol, a β1-adrenergic antagonist, on nocturnal plasma melatonin secretion: Evidence for a dose-response relationship in humans. J. Pineal Res. 1997; 23:131–135. © Munksgaard, Copenhagen
Pineal β1-adrenergic receptors are involved in the regulation of melatonin secretion. The involvement of β1adrenergic receptors has been demonstrated by the ability of acute administration ofβ-antagonists to suppress the nocturnal rise of circulating melatonin and its urinary metabolite 6-sulphatoxymelatonin (aMT6s). The present study was undertaken to examine the relationship between increasing doses of atenolol and nocturnal plasma melatonin concentrations. Six healthy subjects participated in the study for a period of 5 weeks. Subjects were administered placebo, 12.5, 25, 37.5, and 50 mg doses of atenolol in a randomized single blind design. Each dose was separated by a 1 week washout period. Blood samples were collected at regular intervals from 19.00 hr to 06.00 hr. Repeated measures analysis of variance showed a dose-dependent decrease in plasma melatonin concentrations (P < 0.01). A Student Newman-Keuls post hoc test indicated significant differences between placebo and all doses of atenolol (P < 0.05). The results demonstrate a dose-dependent relationship between β1-receptor blockade and suppression of nocturnal plasma melatonin in humans.