Abnormalities in intracellular Ca(2+) handing are believed to contribute to arrhythmogenesis during atrial fibrillation (AF). Ca(2+)/calmodulin-dependent protein kinaseII δ (CaMKIIδ) overexpression was detected in atrial myocytes from patients and animal models with persistent AF. In the present study, we found that rapid electrical field stimulation applied to primary atrial myocytes altered the CaMKIIδ activity, not expression level, resulting in Ca(2+) disorder. By lentivirus mediated delivery of CaMKIIδ gene or siRNA into atrial myocytes, cells with different CaMKIIδ expression were generated. Changes of CaMKIIδ expression altered the sarcoplasmic reticulum (SR) Ca(2+) release and L-type Ca(2+) channels current (I(Ca)) in both steady and electrical stimulating state. These results revealed the important role of CaMKIIδ in Ca(2+) disorder caused by electrical field stimulation. It also provided a potential method to improve Ca(2+) disorder in AF by modulating CaMKIIδ expression level.
Copyright © 2011 Elsevier Inc. All rights reserved.