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

Normal cardiac action potential repolarization is dependent on activation o f several K+ currents, including I-Kr and I-Ks I-Kr activates rapidly at po sitive potentials, exhibits inward rectification caused by C-type inactivat ion, and is potently blocked by methanesulfonanilide antiarrhythmic drugs a nd several other common medications. I-Ks activates very slowly, does not i nactivate and is blocked by some benzodiazepines and a chromanol. HERG enco des subunits that form channels that mediate I-Kr. KVLQT1 and minK encode s ubunits that coassemble to form channels that mediate I-Ks Mutations in any of these genes cause long QT syndrome, a disorder of cardiac repolarizatio n that predisposes individuals to lethal arrhythmias. In this review, we su mmarize recent studies of the biophysical and pharmacological properties of HERG and KvLOT1/minK K+ channels. Copyright (C) 1999 S. Karger AG, Basel.