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Cardiovascular Research Advance Access [Accepted Manuscript] published online on November 10, 2007
Cardiovascular Research, doi:10.1093/cvr/cvm063
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Crosstalk between L-type Ca2+ channels and the sarcoplasmic reticulum - alterations during cardiac remodeling

Virginie Bito1, Frank R. Heinzel1,2, Liesbeth Biesmans1, Gudrun Antoons3 and Karin R. Sipido1,

1 Department of Cardiovascular Medicine, Division of Experimental Cardiology, University of Leuven, Leuven, Belgium
2 Division of Cardiology, University Hospital Graz, Austria
3 Department of Medical Physiology, University Medical Center, Utrecht, the Netherlands

Address for correspondence Karin R. Sipido, MD, PhD, Lab. of Experimental Cardiology, KUL Campus Gasthuisberg O/N 7th floor, Herestraat 49, B-3000 Leuven, Belgium. Tel. ++32 16 347153, FAX ++32 16 345844, E-mail: Karin.Sipido{at}med.kuleuven.be

In the cardiac dyad, sarcolemmal L-type Ca2+ channels (LCC) and sarcoplasmic reticulum (SR) Ca2+ release channels (RyR) are structurally in close proximity. This organization provides for an efficient functional coupling, tuning SR Ca2+ release for optimal contraction of the myocyte. Given that LCC are regulated by the prevailing [Ca2+], this structural organization is the setting for feedback mechanisms and crosstalk. A defective coupling of Ca2+ influx via LCC to activation of RyR and SR Ca2+ release has been implicated in reduced release in heart failure. Both functional changes in LCC properties and structural re-organization of LCC in T-tubules could be involved. LCC are regulated by cytosolic Ca2+ , and crosstalk with SR Ca2+ handling occurs on a long-term basis, i.e. during steady-state changes in heart rate, on an intermediate-term basis, i.e. on a beat-to-beat basis during sudden rate changes, and on a very short- or immediate-term basis, i.e. during a single heartbeat. We review the properties and consequences of these different feedback mechanisms and the changes in heart failure and cardiac hypertrophy that have thus far been studied.

KEYWORDS cardiac hypertrophy; heart failure; calcium channel; sarcoplasmic reticulum; excitation-contraction coupling; arrhythmias

Time for primary review: 6


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