Molecular physiology of cardiac delayed rectifier K+ channels

Abstract

Delayed rectifier K+ current in cardiac myocytes is the sum of two distinct currents, IKr and IKs. The molecular basis of these channels has recently been defined. HERG subunits coassemble to form IKr channels. KvLQT1 and minK subunits coassemble to form IKs channels. Mutations in HERG or KVLQT1 genes predispose affected individuals to ventricular arrhythmias and sudden death.