Diurnal Rhythms, the Renin-Angiotensin System and Antihypertensive Therapy

Michael Schachter


Br J Cardiol. 2004;11(4) 

In This Article

Regulatory Mechanisms

The master pacemaker for human circadian rhythms is located in the suprachiasmatic nucleus in the anterior hypothalamus.[7] The main regulatory input is light, while the pineal hormone melatonin seems to be the most important endocrine messenger so far described. It is interesting that melatonin levels decline with age and that cardiovascular circadian rhythms appear to be flattened in the elderly, as noted above. It has recently been reported that exogenous melatonin may lower blood pressure,[8] but the relevance and reproducibility of this have yet to be established.

Much more work has focused on the roles of the autonomic nervous system, and latterly also the renin-angiotensin-aldosterone system, in modulating cardiovascular circadian rhythms. It has been shown that sympathetic activity increases during the day, from or before waking, while the parasympathetic system follows the opposite pattern, with greater activity during sleep.[9] The renin-angiotensin system also appears to follow a rhythm which largely parallels sympathetic activity although this has been somewhat controversial, with some suggestions that the pattern of hormone secretion was driven by blood pressure change rather than helping to initiate it. Although the relevant data are neither as extensive as one might expect, nor as recent, it seems that there is an early morning rise in plasma renin activity, with a peak at around 8 am with similar or slightly delayed peaks in angiotensin II and aldosterone levels. The increase in renin activity actually precedes waking and the possible morning surge in blood pressure, which would be plausible if part of that rise were driven by angiotensin II or even aldosterone. There are also fluctuations in renin level during sleep, with maximal levels during slow wave, non-rapid eye movement sleep.[10,11] It is not clear whether these mechanisms are disturbed in essential hypertension.