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Crosstalk between L-type Ca2+ channels and the sarcoplasmic reticulum: alterations during cardiac remodelling Bito V; Heinzel FR; Biesmans L; Antoons G; Sipido KRCardiovasc Res 2008[Jan]; 77 (2): 315-24In the cardiac dyad, sarcolemmal L-type Ca(2+) channels (LCCs) and sarcoplasmic reticulum (SR) Ca(2+) release channels (RyR) are structurally in close proximity. This organization provides for an efficient functional coupling, tuning SR Ca(2+) release for optimal contraction of the myocyte. Given that LCC are regulated by the prevailing [Ca(2+)], this structural organization is the setting for feedback mechanisms and crosstalk. A defective coupling of Ca(2+) influx via LCC to activation of RyR has been implicated in reduced SR Ca(2+) 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 Ca(2+), and crosstalk with SR Ca(2+) 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.|Animals[MESH]|Arrhythmias, Cardiac/etiology[MESH]|Calcium Channels, L-Type/*physiology[MESH]|Calcium/metabolism[MESH]|Cardiomegaly/*metabolism[MESH]|Feedback, Physiological[MESH]|Heart Failure/*metabolism[MESH]|Heart Rate[MESH]|Humans[MESH]|Myocardial Contraction[MESH]|Ryanodine Receptor Calcium Release Channel/physiology[MESH]|Sarcoplasmic Reticulum/*physiology[MESH] |
