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Circulation Research. 2006;99:223-224
doi: 10.1161/01.RES.0000236790.08267.74
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(Circulation Research. 2006;99:223.)
© 2006 American Heart Association, Inc.


Editorials

Life, Sudden Death, and Intracellular Calcium

D.A. Eisner, L.A. Venetucci, A.W. Trafford

From the Unit of Cardiac Physiology, University of Manchester, United Kingdom.

Correspondence to D.A. Eisner, Unit of Cardiac Physiology, University of Manchester, Core Technology Facility, 46 Grafton St, Manchester M13 9NT, U.K. E-mail eisner@man.ac.uk



See related articles, pages 283–291 and 292–298


Key Words: RyR • SR • calcium


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

Since the original studies of Ringer,1 calcium (Ca2+) has become almost synonymous with contraction in the heart. Two papers in the current issue of Circulation Research focus on other roles of this cation.1 Wu and Bers2 show that Ca2+ in the nuclear envelope is in a store that is functionally interconnected with the sarcoplasmic reticulum (SR), a result that may have implications for the role of calcium in controlling gene transcription.2 The other area and the main focus of this editorial is the role of Ca2+ ions in arrhythmogenesis. Liu et al3 present important data concerning the occurrence of arrhythmias in a mouse expressing a mutant SR Ca2+ release channel (ryanodine receptor [RyR]). To discuss this result, we will first briefly summarize current concepts in the area.

It is now known that most of the calcium that activates contraction comes from an intracellular store (the SR) and is released through the RyR. Release occurs through the process of calcium-induced calcium release. This depends on the fact that the probability of the RyR being open is increased by an increase of cytoplasmic Ca2+ concentration ([Ca2+]i). The entry of a small amount of Ca2+ into the cell through the L-type Ca2+ current thereby triggers much more release from the SR. It has been appreciated for a long time that such a Ca2+-induced Ca2+ release mechanism is inherently prone to positive feedback as the Ca2+ released will tend to further activate the RyR. Both theoretical4 and experimental5 studies have . . . [Full Text of this Article]


Related Article:

Sarcoplasmic Reticulum and Nuclear Envelope Are One Highly Interconnected Ca2+ Store Throughout Cardiac Myocyte
Xu Wu and Donald M. Bers
Circ. Res. 2006 99: 283-291. [Abstract] [Full Text] [PDF]



This article has been cited by other articles:


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Am. J. Physiol. Heart Circ. Physiol.Home page
W. T. Clusin
Mechanisms of calcium transient and action potential alternans in cardiac cells and tissues
Am J Physiol Heart Circ Physiol, January 1, 2008; 294(1): H1 - H10.
[Abstract] [Full Text] [PDF]