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Am J Physiol Heart Circ Physiol 284: H491-H500, 2003; doi:10.1152/ajpheart.00576.2002
0363-6135/03 $5.00
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Vol. 284, Issue 2, H491-H500, February 2003

Regional upregulation of Kv2.1-encoded current, IK,slow2, in Kv1DN mice is abolished by crossbreeding with Kv2DN mice

Jun Zhou1,*, Sodikdjon Kodirov1,*, Mitsunobu Murata1, Peter D. Buckett1, Jeanne M. Nerbonne2, and Gideon Koren1

1 Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115; and 2 Department of Molecular Biology and Pharmacology, Washington University School of Medicine, St. Louis, Missouri 63110

Overexpression of a truncated Kv1.1 channel transgene in the heart (Kv1DN) resulted in mice with a prolonged action potential duration due to marked attenuation of a rapidly activating, slowly inactivating potassium current (IK,slow1) in ventricular myocytes. Optical mapping and programmed electrical stimulation revealed inducible ventricular tachycardia due to spatial dispersion of repolarization and refractoriness. Here we show that a delayed rectifier with slower inactivation kinetics (IK,slow2) was selectively upregulated in Kv1DN cardiocytes. This electrical remodeling was spatially restricted to myocytes derived from the apex of the left ventricle. Biophysical and pharmacological studies of IK,slow2 indicate that it resembles Kv2-encoded currents. Northern blot analyses and real-time PCR revealed upregulation of Kv2.1 transcript in Kv1DN mice. Crossbreeding of Kv1DN mice with mice expressing a truncated Kv2.1 polypeptide (Kv2DN) eliminated IK,slow2. In summary, our data indicate that the spatially restrictive upregulation of Kv2.1-encoded currents underlies the increased dispersion of the repolarization observed in Kv1DN mice.

cardiac arrhythmia; electrophysiology; potassium channels; long QT syndrome

* J. Zhou and S. Kodirov contributed equally to this work.




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