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Altered K+ Channel Expression in the Hypertrophied and Failing Heart

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Potassium Channels in Cardiovascular Biology

Abstract

Hypertrophied and failing hearts display abnormal electrophysiological properties. Commonly, myocytes from these diseased hearts exhibit a prolongation of action potential duration. The most consistently detected change in ionic currents that could produce this property is a decrease in the transient outward K+ current (I to). Recent studies have revealed that two Kv4 subfamily channel subunits, Kv4.2 and Kv4.3, constitute cardiac I to channels. Furthermore, expression of these subunits is decreased in hypertrophied and failing hearts. In this chapter, we will summarize these electrophysiological and molecular biological findings. Possible mechanisms leading to the downregulation of I to channels and consequences of the altered I to channel expression in arrthythmogenesis also will be discussed.

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Authors and Affiliations

  1. Department of Pharmacology, University of Pittsburgh, Pittsburgh, Pennsylvania, 15261, USA

    Koichi Takimoto & Edwin S. Levitan

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  1. Koichi Takimoto
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  2. Edwin S. Levitan
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Editors and Affiliations

  1. Walter McKenzie Health Science Centre, University of Alberta Hospital, Edmonton, Alberta, Canada

    Stephen L. Archer

  2. Medical College of Wisconsin, Milwaukee, Wisconsin, USA

    Nancy J. Rusch

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© 2001 Springer Science+Business Media New York

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Takimoto, K., Levitan, E.S. (2001). Altered K+ Channel Expression in the Hypertrophied and Failing Heart. In: Archer, S.L., Rusch, N.J. (eds) Potassium Channels in Cardiovascular Biology. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1303-2_37

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  • DOI: https://doi.org/10.1007/978-1-4615-1303-2_37

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4613-5487-1

  • Online ISBN: 978-1-4615-1303-2

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