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Fractal dynamics in circadian cardiac time series of corticotropin-releasing factor receptor subtype-2 deficient mice

MPG-Autoren
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Stiedl,  Oliver
Molecular neuroendocrinology, Max Planck Institute of Experimental Medicine, Max Planck Society;

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Meyer,  Michael
Fractal physiology, Max Planck Institute of Experimental Medicine, Max Planck Society;

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Zitation

Stiedl, O., & Meyer, M. (2003). Fractal dynamics in circadian cardiac time series of corticotropin-releasing factor receptor subtype-2 deficient mice. Journal of mathematical biology, 47(2), 169-197. doi:10.1007/s00285-003-0197-7.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-0029-2793-C
Zusammenfassung
Non-linear fractal analysis of circadian 24 hr heartbeat interval time series was performed in corticotropin releasing factor receptor-subtype 2 (CRFR2) deficient mice. We hypothesized that, as a result of its central as well as its peripheral expression, CRFR2 would mediate or interfere with the circadian rhythmicity. The dynamical properties of cardiac interbeat intervals were expected to be different between CRFR2 (+/+) and CRFR2 (-/-) mice when studied over an extended circadian 24 hr cycle. The dynamics of neurocardiac control were found to remain remarkably stable throughout the circadian cycle. In disagreement with the initial hypothesis, the dynamical properties underlying the cardiac control process were common to both CRFR2 (+/+) and CRFR2 (-/-) mice suggesting that control of heart rate does not rely on the elaborate interaction of CRFR2-sensor and its intrinsic feedback arrangement. Lack of expression of CRFR2 would not compromise cardiac control and its dynamical output or is subserved by other, unknown mechanisms. Functional integrity of CRFR2 would not constitute an indispensable requirement of physiologic cardiac control. The circadian rhythm of heart rate is generated centrally and is independent of expression of CRFR2. While "normal" strain C57BL/6N mice exhibit a circadian dark/light cycle of heart rate, absence of circadian fluctuations in transgenic CRFR2-mice (both +/+ and -/-) and "normal" strain C57BL/6J mice points at the importance of other deficiencies that may be related to a common genetic background. Mutant mice that share a common 129SvJ- or C57BL/6J-derived genetic background may not present an optimal model for physiological studies of cardiovascular control.