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The cardiac late sodium channel protein, or late INa, is a sustained inward sodium current that persists during the plateau phase of the cardiac action potential. It is primarily mediated by the NaV1.5 voltage-gated sodium channel. While small in amplitude compared to the peak sodium current, late INa contributes to maintaining membrane depolarization and modulating action potential duration. Pathologically increased late INa is implicated in heart failure, arrhythmias, and Long QT Syndrome Type 3, making it a therapeutic target for antiarrhythmic drugs.
Inhibition of late sodium current, reduction of intracellular sodium and calcium overload.
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