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Free radicals enhance Na+/Ca2+ exchange in ventricular myocytes

, : Free radicals enhance Na+/Ca2+ exchange in ventricular myocytes. American Journal of Physiology 271(3 Pt 2): H823-H833

Oxygen-derived free radicals (OFR) have been implicated in the pathogenesis of intracellular Ca-2+ overload and the arrhythmias that characterize cardiac reperfusion. These arrhythmias may in large part be due to activation of the pathological transient inward current (I-TI). However, the identity of the I-TI generated by OFR is uncertain. We previously found that H-2O-2, an OFR-generating compound, markedly stimulated the I-TI elicited by brief caffeine pulses in patch-clamped guinea pig ventricular myocytes. In the present study, using patch-clamped rabbit ventricular myocytes loaded with the Ca-2+-sensitive indicator fura 2, we have further characterized this I-TI and have identified its major component to be Na+/Ca-2+ exchange, based on its dependence on extracellular Na+ and sarcoplasmic reticulum Ca-2+ release, its sensitivity to Ni-2+, and the effects of its inhibition on relaxation. The effect on I-TI was not unique to H-2O-2, because another free radical-generating system, xanthine + xanthine oxidase, produced a similar response. We hypothesize that enhancement of Na+/Ca-2+ exchange by OFR during reperfusion, when intracellular Na+ is elevated, may promote intracellular Ca-2+ overload and triggered arrhythmias.


PMID: 8853314

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