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(Circulation Research. 2002;91:451.)
© 2002 American Heart Association, Inc.

Editorials

L-Type Ca²⁺ Channels Gaining Respect in Heart Failure

Timothy J. Kamp, Jia-Qiang He

From the Departments of Medicine and Physiology, University of Wisconsin–Madison.

Correspondence to Timothy J. Kamp, H6/343 Clinical Science Center, Box 3248, 600 Highland Ave, Madison, WI 53792. E-mail tjk@medicine.wisc.edu

Key Words: heart ventricle • myocardium • congestive heart failure • L-type calcium channels • patch-clamp techniques

An extract of the first 250 words of the full text is provided, because this article has no abstract.

L-type Ca²⁺ channels are essential for the initiation and regulation of excitation-contraction (EC) coupling in adult cardiac muscle.¹ The rapid influx of Ca²⁺ through these channels triggers release of intracellular Ca²⁺ from the sarcoplasmic reticulum (SR) stores, and the resulting Ca²⁺ transient activates the myofilaments and thus contraction. Given that failing ventricular myocytes exhibit impaired contractility and abnormal Ca²⁺ transients, the L-type Ca²⁺ channel makes for a good suspect as a contributor to the derangement of EC coupling. However, most initial studies of whole-cell currents through L-type Ca²⁺ channels (I_Ca) in both human heart failure and animal models did not show a significant difference between nonfailing and failing myocytes.² In the meantime, important changes in the abundance and/or function of other Ca²⁺ cycling proteins including the sarcoplasmic reticulum Ca²⁺-ATPase (SERCA2a), Na⁺-Ca²⁺ exchanger (NCX), and ryanodine receptors (RyRs) took the spotlight as the bad actors in heart failure.³ The L-type Ca²⁺ channel was left behind as a boring, obligatory participant in EC coupling.

Times may be changing for the status of the L-type Ca²⁺ channel in the world of failing hearts. The article by Chen et al,⁴ in this issue of Circulation Research, unmasks important changes in the density as well as regulation of L-type Ca²⁺ channels in failing human ventricular myocytes. And, perhaps most encouragingly, the authors show that these changes can be partly reversed in patients with left ventricular assist devices (LVADs). This article adds more evidence to recent publications suggesting significant changes in . . . [Full Text of this Article]

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