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Am J Physiol Heart Circ Physiol 280: H1075-H1080, 2001;
0363-6135/01 $5.00
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Vol. 280, Issue 3, H1075-H1080, March 2001

Slow delayed rectifier current and repolarization in canine cardiac Purkinje cells

Wei Han1, Zhiguo Wang2, and Stanley Nattel1,2

1 Department of Pharmacology and Therapeutics, McGill University, Montreal, Quebec H3G 1Y6; and 2 Research Center and Department of Medicine, Montreal Heart Institute, Montreal, Quebec H1T 1C8 and University of Montreal, Montreal, Quebec, Canada H3C 3J7

Although cardiac Purkinje cells (PCs) are believed to be the source of early afterdepolarizations generating ventricular tachyarrhythmias in long Q-T syndromes (LQTS), the ionic determinants of PC repolarization are incompletely known. To evaluate the role of the slow delayed rectifier current (IKs) in PC repolarization, we studied PCs from canine ventricular false tendons with whole cell patch clamp (37°C). Typical IKs voltage- and time-dependent properties were noted. Isoproterenol enhanced IKs in a concentration-dependent fashion (EC50 ~ 30 nM), negatively shifted IKs activation voltage dependence, and accelerated IKs activation. Block of IKs with 293B did not alter PC action potential duration (APD) in the absence of isoproterenol; however, in the presence of isoproterenol, 293B significantly prolonged APD. We conclude that, without beta -adrenergic stimulation, IKs contributes little to PC repolarization; however, beta -adrenergic stimulation increases the contribution of IKs by increasing current amplitude, accelerating IKs activation, and shifting activation voltage toward the PC plateau voltage range. IKs may therefore provide an important "braking" function to limit PC APD prolongation in the presence of beta -adrenergic stimulation.

ventricular arrhythmias; action potential; long Q-T syndrome


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