The inward rectifier current (IK1) controls cardiac excitability and is involved in arrhythmogenesis.

The cardiac inwardly rectifying potassium current (I(K1)) stabilizes the resting membrane potential and is responsible for shaping the initial depolarization and final repolarization of the action potential. The inwardly rectifying potassium channel (Kir2.x) subfamily members primarily mediate cardiac I(K1), but other inward rectifiers, including the acetylcholine-sensitive (Kir3.x) and ATP-sensitive (Kir6.x) inward rectifiers, also may modulate cardiac excitability. Studies suggest I(K1) plays a role in ventricular arrhythmias, highlighted by the recently described Andersen's syndrome and studies in the guinea pig heart model of ventricular fibrillation. This article describes the salient properties of cardiac I(K1) and discusses the role of this current in the cardiac action potential and in underlying regional differences in cardiac excitability. The mechanism of channel block, assembly, and structure are reviewed. The article discusses the role of I(K1) in ventricular fibrillation and speculates on modulation of I(K1) as a preventative antiarrhythmic mechanism.