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Cardiovascular Research Advance Access originally published online on August 14, 2007
Cardiovascular Research 2008 77(2):237-244; doi:10.1093/cvr/cvm002
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2007. For Permissions please e-mail: journals.permissions@oxfordjournals.org

t-tubules and sarcoplasmic reticulum function in cardiac ventricular myocytes

Clive Orchard1,* and Fabien Brette2

1 Department of Physiology, University of Bristol, Bristol, BS8 1TD, UK
2 Faculty of Life Sciences, University of Manchester, Manchester, M13 9NT, UK

* Corresponding author. Tel: +44 117 331 2228; fax: +44 117 331 2228. E-mail: clive.orchard{at}bristol.ac.uk

Although the existence of t-tubules in mammalian cardiac ventricular myocytes has been recognized for a long time, it now appears that their structure and function are more complex than previously believed. Recent work has provided evidence that many of the key proteins underlying excitation–contraction coupling are located predominantly at the t-tubules. L-type Ca2+ current (ICa) flowing across the t-tubule membrane provides a rapidly inactivating Ca2+ influx that triggers Ca2+ release from the sarcoplasmic reticulum (SR), thereby allowing rapid and synchronous Ca2+ release throughout the cell; ICa at the t-tubules also appears to be more sensitive than that at the surface membrane to regulation by beta-adrenergic stimulation and intracellular Ca2+. In contrast, although its density is lower, ICa flowing across the surface membrane inactivates slowly, and thus may help load the SR with Ca2+. There is also increasing evidence that many of the mechanisms that remove Ca2+ from the cytoplasm are located predominantly at the t-tubules, which therefore play an important role in determining cellular, and hence SR, Ca2+ content. Thus, the t-tubules appear to play a central role in the increase and subsequent decrease of Ca2+ during the systolic Ca2+ transient. Remodelling of the t-tubules has been reported in cardiac pathologies, and may play a role in the altered cellular, and hence cardiac, function observed in such conditions.

KEYWORDS Cardiac muscle; t-tubules; Calcium; Excitation–contraction coupling; Sarcoplasmic reticulum; Heart failure

Time for primary review: 23 days


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