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Cardiovascular Research 2001 52(2):246-254; doi:10.1016/S0008-6363(01)00378-9
© 2001 by European Society of Cardiology
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Copyright © 2001, European Society of Cardiology

Spatial alterations of Kv channels expression and K+ currents in post-MI remodeled rat heart

B Huang, D Qin and N El-Sherif*

Cardiology Division, Department of Medicine, Box 1199, State University of New York Health Science Center and Veterans Affairs Medical Center, 450 Clarkson Avenue, Brooklyn, NY 11203, USA

* Corresponding author. Tel.: +1-718-270-4147; fax: +1-718-630-3740 nelsherif{at}aol.com

Objective: The hypothesis being tested in the present study is that increased anisotropic properties occurs in the remodeled post-infarction heart due to spatial alterations in Kv channels expression and K+ currents of the remodeled myocardium. Methods: Three to 4 weeks post myocardial infarction (MI) in the rat, we measured the two components of the outward K+ current, Ito-fast (f) and Ito-slow(s) in the epicardium (epi) and endocardium (endo) of noninfarcted remodeled left ventricle (LV) using patch clamp techniques. Alterations in mRNA and/or protein levels of potassium channel genes Kv1.4, Kv1.5, Kv2.1, Kv4.2 and Kv4.3 were measured in epi, midmyocardium (mid), and endo regions of LV and in the right ventricle (RV). Results: In sham operated rat heart, the density of Ito-f was 2.3 times greater in epi compared to endo myocytes. In post-MI heart, the density of Ito-f and Ito-s decreased to a similar degree in LV epi and endo but the difference in Ito-f density between epi and endo persisted. The mRNA and/or protein levels of Kv1.4, Kv2.1, Kv4.2 and Kv4.3 but not Kv1.5 decreased to a varying extent in different regions of LV but not in RV of post-MI heart. Conclusions: Our results suggest that regional downregulation of Kv channels expression and density of K+ currents can be a significant determinant of increased spatial electrophysiological heterogeneity and contribute to increased electrical instability of the post-MI heart.

KEYWORDS Gap junctions; Gene expression; Infarction; K-channel; Remodeling


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