© 1998 by European Society of Cardiology
Copyright © 1998, European Society of Cardiology
Calcium sequestration by the sarcoplasmic reticulum in heart failure
aSalt Lake City VA Medical Center, Internal Medicine and Pharmacology, University of Utah School of Medicine, Salt Lake City, Utah, USA
bLaboratory of Muscle Research and Molecular Cardiology, Clinic III of Internal Medicine, University of Cologne, Cologne, Germany
* Corresponding author. Cardiology Division, 4A-100 SOM, University of Utah Health Sciences Center, 50 North Medical Drive, Salt Lake City, UT 84132, USA. Tel. (+1-801) 581 7715; Fax (+1-801) 581 7735; E-mail:matthew.movsesian@hsc.utah.edu
Received 4 July 1997; accepted 29 October 1997
KEYWORDS Sarcoplasmic reticulum; Heart failure; Ca2+-transporting ATPase; Phospholamban; Human; Ventricle
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1 Introduction |
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Myocardial contraction and relaxation are dependent upon the rise and fall of cytosolic [Ca2+] in cardiac myocytes. The release and sequestration of Ca2+ by the sarcoplasmic reticulum are the principal mechanisms through which this occurs. During relaxation, Ca2+ is actively transported from the cytosol into the sarcoplasmic reticulum; during contraction, this sequestered Ca2+ is passively released into the cytosol through ryanodine-sensitive Ca2+ channels.
Because of the dependence of contraction and relaxation upon ATP-dependent Ca2+ sequestration by the sarcoplasmic reticulum, the possibility that an impairment in this process contributes to the pathophysiology of heart failure has been the focus of a large body of research over the past two decades. While there seems to be a general agreement that ATP-dependent Ca2+ sequestration by the sarcoplasmic reticulum is impaired in failing human myocardium, there remains a fairly intense controversy regarding the molecular aetiology of this impairment. In this review, the rationale
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2 Molecular mechanisms of Ca2+ transport and its regulation |
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3 The hypothesis and its rationale |
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4 Experimental results in animal models and human tissue |
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5 Conclusions |
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