NDLI: Decreased connexin43 expression in the mouse heart potentiates pacing-induced remodeling of repolarizing currents

Content Provider	PubMed Central
Author	Kontogeorgis, Andrianos Li, Xiaodong Kang, Eunice Y. Feig, Jonathan E. Ponzio, Marc Kang, Guoxin Kaba, Riyaz A. Wit, Andrew L. Fisher, Edward A. Morley, Gregory E. Peters, Nicholas S. Coetzee, William A. Gutstein, David E.
Abstract	Gap junction redistribution and reduced expression, a phenomenon termed gap junction remodeling (GJR), is often seen in diseased hearts and may predispose toward arrhythmias. We have recently shown that short-term pacing in the mouse is associated with changes in connexin43 (Cx43) expression and localization but not with increased inducibility into sustained arrhythmias. We hypothesized that short-term pacing, if imposed on murine hearts with decreased Cx43 abundance, could serve as a model for evaluating the electrophysiological effects of GJR. We paced wild-type (normal Cx43 abundance) and heterozygous Cx43 knockout (Cx43+/−; 66% mean reduction in Cx43) mice for 6 h at 10–15% above their average sinus rate. We investigated the electrophysiological effects of pacing on the whole animal using programmed electrical stimulation and in isolated ventricular myocytes with patch-clamp studies. Cx43+/− myocytes had significantly shorter action potential durations (APD) and increased steady-state (I ss) and inward rectifier (I K1) potassium currents compared with those of wild-type littermate cells. In Cx43+/− hearts, pacing resulted in a significant prolongation of ventricular effective refractory period and APD and significant diminution of I ss compared with unpaced Cx43+/− hearts. However, these changes were not seen in paced wild-type mice. These data suggest that Cx43 abundance plays a critical role in regulating currents involved in myocardial repolarization and their response to pacing. Our study may aid in understanding how dyssynchronous activation of diseased, Cx43-deficient myocardial tissue can lead to electrophysiological changes, which may contribute to the worsened prognosis often associated with pacing in the failing heart.
Related Links	http://dx.doi.org/10.1152/ajpheart.590.2008
Starting Page	1905
File Format	PDF
ISSN	15221539
e-ISSN	15221539
Journal	American Journal of Physiology - Heart and Circulatory Physiology
Issue Number	5
Volume Number	295
Language	English
Publisher	American Physiological Society
Publisher Date	2008-11-01
Access Restriction	Open
Rights Holder	American Physiological Society
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Cardiology and Cardiovascular Medicine

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