IMR Press / FBL / Volume 7 / Issue 4 / DOI: 10.2741/gyorke

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
Regulation of sarcoplasmic reticulum calcium release by luminal calcium in cardiac muscle
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1 Department of Physiology, Texas Tech University Health Sciences Center, Lubbock, Texas 79430-6551, 2 Department of Chemical Engineering, Texas Tech University, Lubbock, TX, USA
Academic Editor:Hector Valdivia
Front. Biosci. (Landmark Ed) 2002, 7(4), 1454–1463;
Published: 1 June 2002
(This article belongs to the Special Issue The structure and function of calcium release channels)

The amount of Ca2+ released from the sarcoplasmic reticulum (SR) is a principal determinant of cardiac contractility. Normally, the SR Ca2+ stores are mobilized through the mechanism of Ca2+-induced Ca2+ release (CICR). In this process, Ca2+ enters the cell through plasmalemmal voltage-dependent Ca2+ channels to activate the Ca2+ release channels in the SR membrane. Consequently, the control of Ca2+ release by cytosolic Ca2+ has traditionally been the main focus of cardiac excitation-contraction (EC) coupling research. Evidence obtained recently suggests that SR Ca release is controlled not only by cytosolic Ca2+, but also by Ca2+ in the lumen of the SR. The presence of a luminal Ca2+ sensor regulating release of SR luminal Ca2+ potentially has profound implications for our understanding of EC coupling and intracellular Ca2+ cycling. Here we review evidence, obtained using in situ and in vitro approaches, in support of such a luminal Ca2+ sensor in cardiac muscle. We also discuss the role of control of Ca2+ release channels by luminal Ca2+ in termination and stabilization of CICR, as well as in shaping the response of cardiac myocytes to various inotropic influences and diseased states such as Ca2+ overload and heart failure.

Excitation-Contraction Coupling
Ryanodine Receptor
Sarcoplasmic Reticulum
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