Biophysical properties and molecular basis of cardiac rapid and slow delayed rectifier potassium channels

Normal cardiac action potential repolarization is dependent on activation of several K(+) currents, including I(Kr) and I(Ks). I(Kr) activates rapidly at positive potentials, exhibits inward rectification caused by C-type inactivation, and is potently blocked by methanesulfon-anilide antiarrhythmic drugs and several other common medications. I(Ks) activates very slowly, does not inactivate and is blocked by some benzodiazepines and a chromanol. HERG encodes subunits that form channels that mediate I(Kr). KVLQT1 and minK encode subunits that coassemble to form channels that mediate I(Ks). Mutations in any of these genes cause long QT syndrome, a disorder of cardiac repolarization that predisposes individuals to lethal arrhythmias. In this review, we summarize recent studies of the biophysical and pharmacological properties of HERG and KvLQT1/minK K(+) channels.