Resumen

RUEDA, Angélica; DE ALBA-AGUAYO, David R.  y  VALDIVIA, Héctor H.. Ryanodine receptor, calcium leak and arrhythmias. Arch. Cardiol. Méx. [online]. 2014, vol.84, n.3, pp.191-201. ISSN 1665-1731.  https://doi.org/10.1016/j.acmx.2013.12.008.

The participation of the ionic Ca²⁺ release channel/ryanodine receptor in cardiac excitation-contraction coupling is well known since the late '80s, when various seminal papers communicated its purification for the first time and its identity with the "foot" structures located at the terminal cisternae of the sarcoplasmic reticulum. In addition to its main role as the Ca²⁺ channel responsible for the transient Ca²⁺ increase that activates the contractile machinery of the cardiomyocytes, the ryanodine receptor releases Ca²⁺ during the relaxation phase of the cardiac cycle, giving rise to a diastolic Ca²⁺ leak. In normal physiological conditions, diastolic Ca²⁺ leak regulates the proper level of luminal Ca²⁺, but in pathological conditions it participates in the generation of both, acquired and hereditary arrhythmias. Very recently, several groups have focused their efforts into the development of pharmacological tools to control the altered diastolic Ca²⁺ leak via ryanodine receptors. In this review, we focus our interest on describing the participation of cardiac ryanodine receptor in the diastolic Ca²⁺ leak under physiological or pathological conditions and also on the therapeutic approaches to control its undesired exacerbated activity during diastole.

Palabras llave : Ryanodine receptor; Heart; Arrhythmia; Calcium leak; Calcium sparks; Mexico.

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