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Neuronal sodium channels: emerging components of the nano‐machinery of cardiac calcium cycling
Author(s) -
Veeraraghavan Rengasayee,
Györke Sándor,
Radwański Przemysław B.
Publication year - 2017
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jp273058
Subject(s) - sarcolemma , biophysics , calcium , endoplasmic reticulum , contraction (grammar) , chemistry , sodium calcium exchanger , cardiac muscle , context (archaeology) , microbiology and biotechnology , neuroscience , myocyte , homeostasis , gene isoform , cardiac action potential , electrophysiology , biology , endocrinology , biochemistry , repolarization , organic chemistry , paleontology , gene
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.