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Several studies have indicated a potential role for SCN10A/Na V 1.8 in modulating cardiac electrophysiology and arrhythmia susceptibility. However, by which mechanism SCN10A/Na V 1.8 impacts on cardiac electrical function is still a matter of debate. To address this, we here investigated the functional relevance of Na V 1.8 in atrial and ventricular cardiomyocytes (CMs), focusing on the contribution of Na V 1.8 to the peak and late sodium current (I Na ) under normal conditions in different species.

Absence of Functional Nav1.8 Channels in Non-diseased Atrial and Ventricular Cardiomyocytes