Published online before print September 8, 2008, doi: 10.1161/HYPERTENSIONAHA.108.117234
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(Hypertension. 2008;52:797.)
© 2008 American Heart Association, Inc.
Editorial Commentaries |
Circadian Clocks, Autonomic Rhythms, and Blood Pressure Dipping
From the Division of Clinical Pharmacology, Department of Medicine and Pharmacology, Vanderbilt University School of Medicine, Nashville, Tenn.
Correspondence to Italo Biaggioni, MD, Professor of Medicine and Pharmacology, 556 RRB, Vanderbilt University, Nashville, TN 37232. E-mail Italo.biaggioni@vanderbilt.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Blood pressure does not fluctuate in random fashion but follows characteristic rhythmic patterns. A blood pressure rhythm of 
0.1 Hz (6 cycles/min) is easily recognizable when blood pressure is monitored continuously and was first independently recognized in the late 1800s by Traube, Hering, and Mayer. This pattern can be analyzed using spectral analysis of the low-frequency range in the frequency domain. There is controversy about the genesis of this rhythm. Two theories have been proposed. The pacemaker theory suggests that the rhythm is generated from oscillators within the central nervous system, either located in discrete pacemaker neurons or originating in neuronal networks. Alternatively, this rhythm may result from a resonance phenomenon because the baroreflex inhibits sympathetic tone after every increase in blood pressure. There is some disagreement about the utility of using the power of the low-frequency blood pressure variability as a measurement of sympathetic modulation of vascular tone. However, there is little doubt that information modulating rhythmic blood pressure fluctuation is transmitted through efferent autonomic nerves because it is greatly reduced in patients with pure autonomic failure and is abolished by blockade of autonomic ganglia neurotransmission.1 It has been argued that rhythmic sympathetic discharge is beneficial because it provides a more effective mechanism to regulated cardiovascular tone.2 In this regard, it is important to note that increasing the frequency of sympathetic activation much above 0.1 Hz would not translate into more effective neurovascular coupling because of the relatively low-frequency response of vascular contraction.
Blood pressure also fluctuates with
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