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Am J Physiol Heart Circ Physiol 284: H168-H175, 2003. First published September 19, 2002; doi:10.1152/ajpheart.00661.2002
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Vol. 284, Issue 1, H168-H175, January 2003

Electrophysiological consequences of human IKs channel expression in adult murine heart

Christine Chiello Tracy1, Candido Cabo1, James Coromilas2, Junko Kurokawa1, Robert S. Kass1,3, and Andrew L. Wit1,3

1 Departments of Pharmacology and 2 Medicine and 3 Center for Molecular Therapeutics, Columbia University, College of Physicians and Surgeons, New York, New York 10032

We expressed human delayed rectifier K+ cardiac current (IKs) channels in the murine heart, which lacks native IKs, to determine their electrophysiological role. Mice expressing human IKs channels were anesthetized, and an electrocardiogram and monophasic action potentials (MAP) recorded from the left ventricle. Sinus rate was not different between wild-type mice (WT) and transgenic mice (TG). Infusion of isoproterenol accelerated WT heart rate but not TG. Lack of TG sinus rate responsiveness may have resulted from accumulated outward current in IKs channels in sinus node. Ventricular MAP duration of TG mice to 50% repolarization (APD50) during ventricular pacing was shorter than WT, likely resulting from outward current through IKs channels. TG APD50 showed enhanced responsiveness (shortening) to isoproterenol compared with WT. Ventricular tachyarrhythmias were initiated in TG mice by programmed stimulation but not in WT and were accelerated by isoproterenol. IKs channels impart beta -adrenergic sensitivity to the ventricles and may be responsible for ventricular tachyarrhythmias.

arrhythmia; beta -adrenergic; repolarization; heart rate; delayed rectifier K+ cardiac current


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