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Interplay of Ryanodine Receptor Distribution and Calcium Dynamics

Leighton T. Izu ^*, Shawn A. Means , John N. Shadid , Ye Chen-Izu ^* and C. William Balke ^*

^* Department of Internal Medicine, University of Kentucky, School of Medicine, Lexington, Kentucky; and Sandia National Laboratories, Albuquerque, New Mexico

Correspondence: Address reprint requests to Leighton T. Izu, PhD, University of Kentucky School of Medicine, Biological and Biomedical Sciences Research Bldg., Rm. B257, 741 South Limestone Rd., Lexington, KY 40536-0509. Tel.: 859-323-6882; Fax: 859-257-3235; E-mail: leightonizu{at}uky.edu.

Spontaneously generated calcium (Ca²⁺) waves can trigger arrhythmias in ventricular and atrial myocytes. Yet, Ca²⁺ waves also serve the physiological function of mediating global Ca²⁺ increase and muscle contraction in atrial myocytes. We examine the factors that influence Ca²⁺ wave initiation by mathematical modeling and large-scale computational (supercomputer) simulations. An important finding is the existence of a strong coupling between the ryanodine receptor distribution and Ca²⁺ dynamics. Even modest changes in the ryanodine receptor spacing profoundly affect the probability of Ca²⁺ wave initiation. As a consequence of this finding, we suggest that there is information flow from the contractile system to the Ca²⁺ control system and this dynamical interplay could contribute to the increased incidence of arrhythmias during heart failure.

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