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Articles in PresS, published online ahead of print September 19, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00661.2002
Submitted on July 26, 2002
Accepted on September 12, 2002
1 Department of Pharmacology, Columbia University, College of Physicians and Surgeons, New York, New York, USA
2 Department of Pharmacology, Columbia University, College of Physicians and Surgeons, New York, New York, USA; Center for Molecular Therapeutics, Columbia University, College of Physicians and Surgeons, New York, New York, USA
3 Department of Medicine, Columbia University, College of Physicians and Surgeons, New York, New York, USA
* To whom correspondence should be addressed. E-mail: alw4{at}columbia.edu.
We expressed human IKs channels in the murine heart which lacks native IKs, to determine its 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 to 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.
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