Ryanodine Receptor-Mediated Ca2+ Events in Atrial Myocytes of Patients with Atrial FibrillationLiang X.a · Xie H.b · Zhu P.-H.b · Hu J.a, d · Zhao Q.c · Wang C.-S.c · Yang C.c
aBio-X Life Science Research Center, College of Life Science and Biotechnology, Shanghai Jiao Tong University, bUnit of Cell Signal Transduction, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, cDepartment of Cardiac Surgery and Shanghai Institute of Cardiovascular Disease, Zhong Shan Hospital, Fu Dan University, and dShanghai Institute of Applied Physics, Chinese Academy of Sciences, Shanghai, China
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Article / Publication Details
Background: Many alterations in sarcoplasmic reticulum Ca2+ handling proteins in atrial myocytes have been associated with atrial fibrillation (AF) in clinical patients, whereas the functional consequences of these alterations mostly remain unclear. Methods and Results: To know whether or not ryanodine receptor (RyR)-mediated intracellular Ca2+ events in AF atrial myocytes are affected by protein alterations, we investigated spontaneous Ca2+ sparks and Ca2+ waves in intact and permeabilized atrial myocytes of AF patients (npatients = 21) and normal sinus rhythm (NSR) patients (npatients = 22) by laser scanning confocal microscopy. It was found that the frequency, amplitude and rise time of Ca2+ sparks were comparable between AF and NSR groups, while full width and full duration at half maximum intensity significantly increased in the AF group. Along with these changes, the frequency of small and global Ca2+ waves increased in AF atrial myocytes. Conclusions: Our results clearly indicated that the spatiotemporal properties but not the frequency of Ca2+ sparks were affected in AF atrial myocytes. In addition, the frequency of Ca2+ waves increased. This profile of the alterations in RyR-mediated Ca2+ events in AF atrial myocytes was different from previous studies. The underlying mechanisms, as well as possible reasons for this discrepancy, were discussed.
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