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Cardiovascular Research 2007 75(1):7-9; doi:10.1016/j.cardiores.2007.04.029
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Copyright © 2007, European Society of Cardiology

Sarcoplasmic reticulum Ca2+ release channel complex and automatism: A matter of fine tuning

José W.M. Bassani* and Rosana A. Bassani

Centro de Engenharia Biomédica and Dept. Engenharia Biomédica/FEEC, Universidade Estadual de Campinas, Campinas SP, Brazil

* Centro de Engenharia Biomédica/UNICAMP, Caixa Postal 6040, 13084-971 Campinas, SP, Brazil. Tel.: +55 19 3521 9287; fax: +55 19 3289 3346. bassani@ceb.unicamp.br

Received 15 April 2007; accepted 26 April 2007

The first 10% of the full text of this article appears below.

See article by Dirksen et al. [10] (pages 69–78) and Faber and Rudy [15] (pages 79–88) in this issue.

In heart muscle, excitation contraction coupling (ECC) relies on proper release of Ca2+ from the sarcoplasmic reticulum (SR), which is accomplished by the activation of SR Ca2+ release channels (also known as ryanodine receptors, RyR) upon Ca2+ binding, a process termed calcium-induced calcium release [1]. The spontaneous activation of a cluster of RyRs produces local Ca2+ release seen under confocal fluorescence microscopy as minuscule flashes of light called Ca2+ sparks, the elementary Ca2+ release events [2].

SR release units are never totally quiescent. They keep on releasing Ca2+ randomly even during diastole, when sparks are rare in time and spatially separable [3]. During ECC, thousands of intracellular release events are synchronized by Ca2+ influx during the action potential, which . . . [Full Text of this Article]


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