Tanaka H, Masumiya H, Sekine T, Kase J, Kawanishi T, Hayakawa T, Miyata S, Sato Y, Nakamura R, Shigenobu K
Department of Pharmacology, Toho University School of Pharmaceutical Sciences, Chiba, Japan.
Life Sci. 2001 Dec 28;70(6):715-26. doi: 10.1016/s0024-3205(01)01436-9.
Two-dimensional and line-scan analyses of the early phase Ca2+ transients in rat cardiomyocytes were performed with a rapid-scanning laser confocal microscope and fluo-3 to elucidate the mechanism of activation of Ca2+ release from the sarcoplasmic reticulum in atrial myocytes which lack a well developed T-tubular network. On electrical stimulation of ventricular myocytes, Ca2+ concentration began to rise earliest at the Z-line level and became uniform throughout the cytoplasm within about 10 msec. In contrast, on stimulation of atrial myocytes, the earliest rise in Ca2+ occurred at the cell periphery and then spread to the cell interior; cytoplasmic Ca2+ became uniform after more than 30msec. The velocity of the propagation of rise in Ca2+ was 112 +/- 5.1 microm/sec (n = 10), which was similar to that of spontaneous Ca2+ waves observed in atrial and ventricular myocytes. No difference in frequency, amplitude and kinetics of spontaneous Ca2+ sparks was observed between the subsarcolemmal and central regions of atrial myocytes. Ryanodine concentration-dependently decreased the contractile force of isolated rat atrial and ventricular tissue preparations; the sensitivity was higher in atrial myocytes. The present study visualized the involvement of a propagated Ca2+-induced-Ca+ release mechanism in atrial but not ventricular myocytes. This difference may underlie some of the atrioventricular difference in response to physiological and pharmacological stimuli.
使用快速扫描激光共聚焦显微镜和Fluo-3对大鼠心肌细胞早期Ca2+瞬变进行二维和线扫描分析，以阐明缺乏发达T小管网络的心房肌细胞中肌浆网Ca2+释放的激活机制。对心室肌细胞进行电刺激时，Ca2+浓度最早在Z线水平开始升高，并在约10毫秒内遍及整个细胞质。相比之下，对心房肌细胞进行刺激时，Ca2+最早在细胞周边升高，然后扩散到细胞内部；超过30毫秒后细胞质Ca2+才变得均匀。Ca2+升高的传播速度为112±5.1微米/秒（n = 10），与在心房和心室肌细胞中观察到的自发Ca2+波速度相似。在心房肌细胞的肌膜下和中央区域之间，未观察到自发Ca2+火花的频率、幅度和动力学存在差异。Ryanodine浓度依赖性地降低了离体大鼠心房和心室组织标本的收缩力；心房肌细胞的敏感性更高。本研究观察到Ca2+诱导的Ca2+释放机制在心房肌细胞而非心室肌细胞中的参与情况。这种差异可能是心房和心室对生理和药理刺激反应存在差异的部分原因。
