Cardiac voltage-gated potassium channels (Kv channels)

Cardiac voltage-gated potassium (Kv) channels are essential transmembrane proteins that regulate the flow of potassium ions across the cardiac cell membrane in response to changes in membrane potential [1]. These channels play a fundamental role in the repolarization phase of the cardiac action potential, effectively determining the duration of the electrical impulse and the refractory period of the heart [2]. Major subtypes include the rapid (Ikr) and slow (Iks) delayed rectifier channels, the transient outward (Ito) channel, and the ultra-rapid (Ikur) channel, each contributing to different phases of the cardiac cycle [1, 2]. Dysregulation or genetic mutations in these channels are linked to various cardiac pathologies, including Long QT syndrome, Short QT syndrome, and atrial fibrillation [3]. Pharmacologically, these channels are the primary targets for Class III antiarrhythmic agents, which aim to prolong the action potential to prevent re-entrant arrhythmias [4]. However, unintended inhibition of certain Kv channels, particularly the hERG channel (KCNH2), is a significant safety concern in drug development due to the risk of drug-induced proarrhythmia and Torsades de Pointes [3, 5].

Other names

Voltage-gated K+ channelsCardiac Kv channelsVoltage-dependent potassium channelshERG (KCNH2)Kv1.5 (KCNA5)KvLQT1 (KCNQ1)Kv4.3 (KCND3)IkrIksItoIkur

Blockade of potassium ion efflux during the repolarization phase of the cardiac action potential, leading to prolongation of the action potential duration (APD) and the effective refractory period (ERP).