Skip Navigation


Cardiovascular Research Advance Access originally published online on September 13, 2007
Cardiovascular Research 2008 77(2):285-292; doi:10.1093/cvr/cvm009
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
77/2/285    most recent
cvm009v2
cvm009v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (1)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Venetucci, L. A.
Right arrow Articles by Eisner, D. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Venetucci, L. A.
Right arrow Articles by Eisner, D. A.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2007. For permissions please email: journals.permissions@oxfordjournals.org

The sarcoplasmic reticulum and arrhythmogenic calcium release

Luigi A. Venetucci, Andrew W. Trafford, Stephen C. O'Neill and David A. Eisner*

Unit of Cardiac Physiology, University of Manchester, Core Technology Facility, 46 Grafton St, Manchester M13 9NT, UK

* Corresponding author. Tel: +44 161 275 2702; fax: +44 161 275 2703. E-mail address: eisner{at}man.ac.uk

There is much evidence showing that some lethal ventricular arrhythmias arise from waves of Ca2+ release from the sarcoplasmic reticulum (SR) that propagate along cardiac cells. The purpose of this review is to discuss the mechanism of production of these waves and how they depend on the properties of the SR Ca2+ release channel or ryanodine receptor (RyR). The best-known method of producing Ca2+ waves is by increasing the Ca2+ content of the cell by either increasing Ca2+ influx or decreasing efflux. Once SR Ca2+ content reaches a threshold level a Ca2+ wave is produced. Altering the properties of the RyR affects the threshold level of Ca2+ required to produce a wave. Patients with a mutation in the RyR suffer from catecholaminergic polymorphic ventricular tachycardia, and this may be due to a decrease in the SR Ca2+ threshold for wave production. Heart failure has also been suggested to result in Ca2+ waves due to a leak of Ca2+ through the RyR. We review the finding that these changes in RyR function will only result in Ca2+ waves in the steady state if some other mechanism maintains the SR Ca2+ content. The review concludes with a description of potential mechanisms for treating arrhythmias produced by Ca2+ waves.

KEYWORDS Calcium; Wave; Delayed afterdepolarization; Arrhythmia

Time for primary review: 26 days


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Circ. Res.Home page
L. A. Venetucci and D. A. Eisner
Calsequestrin Mutations and Sudden Death: A Case of Too Little Sarcoplasmic Reticulum Calcium Buffering?
Circ. Res., August 1, 2008; 103(3): 223 - 225.
[Full Text] [PDF]

Home page
 Cardiovasc ResHome page
D. Garcia-Dorado, H. M. Piper, and D. A. Eisner
Sarcoplasmic reticulum and mitochondria in cardiac pathophysiology
Cardiovasc Res, January 15, 2008; 77(2): 231 - 233.
[Full Text] [PDF]


Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.