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Involvement of Ca2+ waves in excitation-contraction coupling of rat atrial cardiomyocytes.

机译:Ca2 +波参与大鼠心房心肌细胞的兴奋-收缩耦合。

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摘要

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.
机译:用快速扫描激光共聚焦显微镜和fluo-3对大鼠心肌细胞的早期Ca2 +瞬变进行二维和线扫描分析,以阐明缺乏C的心房肌细胞从肌浆网释放Ca2 +的激活机制。发达的T形管网络。电刺激心室肌细胞后,Ca 2+浓度最早在Z线水平开始上升,并在约10毫秒内在整个细胞质中变得均匀。相反,在刺激心房肌细胞时,最早的Ca2 +升高发生在细胞周围,然后扩散到细胞内部。超过30毫秒后,细胞质Ca2 +变得均匀。 Ca2 +的上升传播速度为112 +/- 5.1 microm / sec(n = 10),与在心房和心室肌细胞中观察到的自发Ca2 +波相似。在心房肌膜下和中央区域之间,自发的Ca2 +火花的频率,振幅和动力学没有差异。 Ryanodine浓度依赖性地降低了离体大鼠心房和心室组织制剂的收缩力;心房肌细胞的敏感性较高。本研究显示心房而不是心室肌细胞中传播的Ca2 +诱导的Ca +释放机制的参与。这种差异可能是对生理和药理刺激作出反应的一些房室差异的基础。

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