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Cardiovascular Research 2005 67(4):578-580; doi:10.1016/j.cardiores.2005.06.010
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Copyright © 2005, European Society of Cardiology

Hypoxic modulation of cardiac L-type Ca2+ current: Interaction of reactive oxygen species and β-adrenergic signaling

Robert T. Mallet*

Department of Integrative Physiology, University of North Texas Health Science Center, 3500 Camp Bowie Boulevard, Fort Worth, Texas 76107-2699, USA

* Tel.: +1 817 735 2260; fax: +1 817 735 5084. Email address: malletr@hsc.unt.edu

Received 16 June 2005; accepted 17 June 2005

KEYWORDS calcium channels; hypoxia; isoproterenol; mitochondria; superoxide

The first 10% of the full text of this article appears below.

See article by Hool et al. [5] (pages 624–635) in this issue.


   1. Introduction
 
Sarcolemmal L-type Ca2+ channels are integral components of the excitation–contraction coupling mechanism in cardiomyocytes. Membrane depolarization to –30 mV opens these channels [1], allowing rapid influx of Ca2+ which peaks within 2–3 ms [2]. This inward Ca2+ current (ICa) produces the plateau phase of the cardiomyocyte action potential and triggers a massive release of Ca2+ from the sarcoplasmic reticulum via ryanodine-sensitive Ca2+ channels, arrayed in close proximity to the L-type channels. The resultant cytosolic Ca2+ transient activates crossbridge cycling and mechanical force production by the contractile machinery and inactivates the L-type Ca2+ current [2]. Cardiac L-type channels contain four subunits ({alpha}1C, {alpha}2, β2, {delta}) . . . [Full Text of this Article]


   2. Redox modulation of ICa and hypoxia–β-adrenergic interaction
 

   3. Sources of ·O2– and H2O2 that dampen β-adrenergic activation of ICa
 

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