Circadian regulation of cardiovascular function: a role for vasoactive intestinal peptide

Oct 19, 2010American journal of physiology. Heart and circulatory physiology

Daily body clock control of heart and blood vessel function may involve a key signaling molecule

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Abstract

VIP-deficient mice exhibited weak circadian rhythms in heart rate and body temperature compared to wild-type controls.

Loss of vasoactive intestinal peptide (VIP) resulted in phase-advanced circadian rhythms in heart rate, body temperature, and activity.
Clock gene expression in the cardiac tissue of VIP-deficient mice was rhythmic but phase advanced compared to wild-type mice.
In constant darkness, VIP-deficient mice lost normal circadian rhythms in heart rate, although some maintained rhythms in body temperature.
The loss of VIP altered autonomic regulation of heart rate but did not lead to cardiac dysfunction or differences in heart size.

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The circadian system, driven by the suprachiasmatic nucleus (SCN), regulates properties of cardiovascular function. The dysfunction of this timing system can result in cardiac pathology. The neuropeptide vasoactive intestinal peptide (VIP) is crucial for circadian rhythms in a number of biological processes including SCN electrical activity and wheel running behavior. Anatomic evidence indicates that SCN neurons expressing VIP are well positioned to drive circadian regulation of cardiac function through interactions with the autonomic centers. In this study, we tested the hypothesis that loss of VIP would result in circadian deficits in heart rate (HR) and clock gene expression in cardiac tissue. We implanted radiotelemetry devices into VIP-deficient mice and wild-type (WT) controls and continuously recorded HR, body temperature, and cage activity in freely moving mice. Under light-dark conditions, VIP-deficient mice displayed weak rhythms in HR, body temperature, and cage activity, with onsets that were advanced in phase compared with WT mice. Similarly, clock gene expression in cardiac tissue was rhythmic but phase advanced in mutant mice. In constant darkness, the normal circadian rhythms in HR were lost in VIP-deficient mice; however, most mutant mice continued to exhibit circadian rhythms of body temperature with shortened free-running period. The loss of VIP altered, but did not abolish, autonomic regulation of HR. Analysis of the echocardiograms did not find any evidence for a loss of cardiac function in VIP-deficient mice, and the size of the hearts did not differ between genotypes. These results demonstrate that VIP is an important regulator of physiological circadian rhythmicity in the heart.

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Circadian regulation of cardiovascular function: a role for vasoactive intestinal peptide

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