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Abstract Excitation–contraction coupling is the bridge between cardiac electrical activation and mechanical contraction. It is driven by the influx of Ca 2+ across the sarcolemma triggering Ca 2+ release from the sarcoplasmic reticulum (SR) – a process termed Ca 2+ ‐induced Ca 2+ release (CICR) – followed by re‐sequestration of Ca 2+ into the SR. The Na + /Ca 2+ exchanger inextricably couples the cycling of Ca 2+ and Na + in cardiac myocytes. Thus, influx of Na + via voltage‐gated Na + channels (Na V ) has emerged as an important regulator of CICR both in health and in disease. Recent insights into the subcellular distribution of cardiac and neuronal Na V isoforms and their ultrastructural milieu have important implications for the roles of these channels in mediating Ca 2+ ‐driven arrhythmias. This review will discuss functional insights into the role of neuronal Na V isoforms vis‐à‐vis cardiac Na V s in triggering such arrhythmias and their potential as therapeutic targets in the context of the aforementioned structural observations. image
Veeraraghavan et al. (Tue,) studied this question.