Cardiac sodium channel protein type 5 subunit alpha (NaV1.5) (NaV1.5)

The cardiac sodium channel protein type 5 subunit alpha (NaV1.5), encoded by the SCN5A gene, forms the primary ion channel responsible for the rapid upstroke (phase 0) of the cardiac action potential, enabling rapid electrical conduction across the heart muscle[3][5]. In addition to the large, transient early sodium current, a small fraction of these channels either fail to inactivate or reopen during the plateau phase, generating a sustained or "late" sodium current (I_Na,late)[1][2][3]. This late current, although much smaller in magnitude, significantly influences action potential duration and intracellular sodium and calcium levels, with overactivity implicated in various cardiac pathologies such as arrhythmias and heart failure[2][3]. Drugs targeting this late current are used as antiarrhythmic agents and are under investigation for other cardiac indications[2][3].

Other names

Cardiac sodium channelVoltage-gated sodium channel subunit alpha Nav1.5SCN5A (gene)Late sodium current (I_Na,late)

Inhibition of the late sodium current to reduce prolonged action potential duration and decrease intracellular sodium and calcium overload Blockade of voltage-gated sodium channels to suppress abnormal electrical activity