Involvement of Ca2+ waves in excitation-contraction coupling of rat atrial cardiomyocytes.
Involvement of Ca2+ waves in excitation-contraction coupling of rat atrial cardiomyocytes.
复制标题
Ca2 波参与大鼠心房心肌细胞的兴奋-收缩耦合。
DOI：
10.1016/s0024-3205(01)01436-9
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发表时间：
2001
期刊：
影响因子：
6.1
通讯作者：
K. Shigenobu
中科院分区：
文献类型：
--
作者：
H. Tanaka;H. Masumiya;T. Sekine;J. Kase;T. Kawanishi;T. Hayakawa;S. Miyata;Y. Sato;R. Nakamura;K. Shigenobu
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钙瞬变进行二维和线扫描分析，以阐明缺乏发达T-管网络的心房肌细胞肌浆网钙释放激活的机制。电刺激心室肌细胞时，Ca ~（2+）浓度最早在Z线水平开始升高，并在约10毫秒内在整个细胞质中变得均匀。相反，刺激心房肌细胞时，最早的Ca 2+升高发生在细胞周边，然后扩散到细胞内部;细胞质Ca 2+在超过30毫秒后变得均匀。Ca ~（2+）上升的传播速度为112 ± 5.1 μm/sec（n=10），与心房和心室肌细胞自发Ca ~（2+）波的传播速度相似。心房肌细胞膜下区和中央区自发性钙火花的频率、幅度和动力学无差异。Ryanodine浓度依赖性地降低离体大鼠心房和心室组织制备物的收缩力;心房肌细胞的敏感性较高。本研究可视化的参与传播的Ca 2+诱导的Ca 2+释放机制，在心房，而不是心室肌细胞。这种差异可能是对生理和药理刺激的反应的一些房室差异的基础。
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 10msec. 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 μm/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-Ca2+release mechanism in atrial but not ventricular myocytes. This difference may underlie some of the atrio-ventricular difference in response to physiological and pharmacological stimuli.