© 1998 by European Society of Cardiology
Copyright © 1998, European Society of Cardiology
Sarcoplasmic reticulum in heart failure: central player or bystander?
aDepartment of Medical Biochemistry, Ohio State University Medical Center, 333 Hamilton Hall, 1645 Neil Avenue, Columbus, OH 43210-1218, USA
bDepartments of Molecular Biology and Biophysics and Physiology, University of Maryland School of Medicine, Baltimore, MD 21201, USA
cKrannert Institute of Cardiology and Department of Medicine, Indiana University School of Medicine, Indianapolis, IN 46202, USA
* Corresponding author. Tel. (+1-614) 292 1158; Fax (+1-614) 292 4118; E-mail: altschuld.2@osu.edu
Received 9 September 1997; accepted 17 October 1997
| The first 150 words of the full text of this article appear below. |
| 1 Introduction |
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Myocardial excitation-contraction coupling begins with membrane depolarization, a process that activates voltage-sensitive Ca2+ channels in the sarcolemma and allows a small amount of Ca2+ to enter the cell. This Ca2+ serves as a trigger to activate Ca2+-release channels in the adjacent junctional sarcoplasmic reticulum (SR) [1]: the ensuing efflux of stored SR Ca2+ increases the cytosolic free Ca2+ ion concentration ([Ca2+]i) and initiates contraction. The amount of Ca2+ released by the SR depends on the size of its Ca2+ load and on the size and duration of the initial Ca2+ trigger. This allows [Ca2+]i transient amplitudes to be graded [2]— an important feature in cardiac muscle, where all cells contract with each beat. Modulation of the [Ca2+]i transient amplitude provides one mechanism to vary the force of contraction and thereby match cardiac output to the body's metabolic demands.
Myocardial relaxation occurs when Ca2+
| 2 SR function in heart failure |
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| 3 SERCA2 and SR Ca2+ uptake in failing hearts |
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| 4 The SR Ca2+ release channel, or ryanodine receptor, in failing hearts |
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| 5 Calsequestrin in failing hearts |
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| 6 Phospholamban in failing hearts |
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| 7 Local control and excitation-contraction uncoupling in heart failure |
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| 8 Frequency-dependent phenomena in failing hearts |
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| 9 Is the SR a central player or a bystander in heart failure? |
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