repolarization

Repolarization is the process by which a cell’s membrane potential returns to its resting level after depolarization. In excitable cells, repolarization terminates the action potential and helps reset ion gradients essential for subsequent excitability. This phase follows the depolarizing surge of current and prepares the cell for another potential impulse.

In neurons and many muscle cells, repolarization is mainly achieved by the outward flow of potassium ions through voltage-gated K+ channels, while sodium channels inactivate to stop inward current. The Na+/K+ ATPase and other ion pumps restore the resting ionic gradients over longer time scales, contributing to long-term stability of excitability.

In cardiac tissue, repolarization is a key part of the ventricular action potential. The cardiac action potential comprises phases 0 to 4; repolarization corresponds to phase 3. It is driven by outward K+ currents, including rapid and slow delayed rectifier channels and inward rectifier channels. The plateau phase (phase 2), caused by a balance between Ca2+ influx through L-type calcium channels and K+ efflux, delays full repolarization. When calcium channels inactivate and potassium currents dominate, the membrane potential returns toward the resting level.

Clinical relevance includes the electrocardiographic representation of ventricular repolarization as the T wave; the QT interval reflects the duration of ventricular depolarization and repolarization. Prolongation of repolarization, as seen in long QT syndromes or drug-induced IKr blockade, increases the risk of ventricular arrhythmias such as torsades de pointes. Electrolyte disturbances and antiarrhythmic drugs can modulate repolarization by affecting potassium or calcium channel function. Refractory periods during repolarization influence the cell’s readiness for subsequent impulses.