Abstract
In excitable tissues, voltage-dependent Na+ current (INa) is best known for supporting autoregenerative depolarization and impulse propagation. Its transient component (INaT), which is large and terminated within several milliseconds by channel inactivation, fulfils this role. Nevertheless, INa also includes a smaller sustained component, i.e. one persisting during prolonged membrane depolarization, which contributes to repolarization course. Sustained INa implies slow or incomplete inactivation of a proportion of the Na+ channels activated during the action potential upstroke. Several mechanisms may underlie this phenomenon and contribute to arrhythmogenesis in different conditions.
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