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Am J Physiol Heart Circ Physiol 278: H806-H817, 2000;
0363-6135/00 $5.00
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Vol. 278, Issue 3, H806-H817, March 2000

Characterization and functional consequences of delayed rectifier current transient in ventricular repolarization

Gary A. Gintant

Cardiology Division, Department of Internal Medicine, and Department of Pharmacology, Wayne State University School of Medicine, Detroit, Michigan 48201

Although inactivation of the rapidly activating delayed rectifier current (IKr) limits outward current on depolarization, the role of IKr (and recovery from inactivation) during repolarization is uncertain. To characterize IKr during ventricular repolarization (and compare with the inward rectifier current, IK1), voltage-clamp waveforms simulating the action potential were applied to canine ventricular, atrial, and Purkinje myocytes. In ventricular myocytes, IKr was minimal at plateau potentials but transiently increased during repolarizing ramps. The IKr transient was unaffected by repolarization rate and maximal after 150-ms depolarizations (+25 mV). Action potential clamps revealed the IKr transient terminating the plateau. Although peak IKr transient density was relatively uniform among myocytes, potentials characterizing the peak transients were widely dispersed. In contrast, peak inward rectifier current (IK1) density during repolarization was dispersed, whereas potentials characterizing IK1 defined a narrower (more negative) voltage range. In summary, rapidly activating IKr provides a delayed voltage-dependent (and functionally time-independent) outward transient during ventricular repolarization, consistent with rapid recovery from inactivation. The heterogeneous voltage dependence of IKr provides a novel means for modulating the contribution of this current during repolarization.

arrhythmias; Purkinje fibers; human ether-à-go-go-related gene; atrial myocytes; canine myocardium


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