• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Brief rapid pacing depresses contractile function via Ca(2+)/PKC-dependent signaling in cat ventricular myocytes.
【24h】

Brief rapid pacing depresses contractile function via Ca(2+)/PKC-dependent signaling in cat ventricular myocytes.

机译：短暂的快速起搏通过猫心室肌细胞中的Ca（2 +）/ PKC依赖性信号传导抑制了收缩功能。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

The purpose of this study is to determine the effects of brief rapid pacing (RP; approximately 200-240 beats/min for approximately 5 min) on contractile function in ventricular myocytes. RP was followed by a sustained inhibition of peak systolic cell shortening (-44 +/- 4%) that was not due to changes in diastolic cell length, membrane voltage, or L-type Ca(2+) current (I(Ca,L)). During RP, baseline and peak intracellular Ca(2+) concentration ([Ca(2+)](i)) increased markedly. After RP, Ca(2+) transients were similar to control. The effects of RP on cell shortening were not prevented by 1 microM calpain inhibitor I, 25 microM L-N(5)-(1-iminoethyl)-orthinthine, or 100 microM N(G)-monomethyl-L-arginine. However, RP-induced inhibition of cell shortening was prevented by lowering extracellular [Ca(2+)] (0.5 mM) during RP or exposure to chelerythrine (2-4 microM), a protein kinase C (PKC) inhibitor, or LY379196 (30 nM), a selective inhibitor of PKC-beta. Exposure to phorbol ester (200 nM phorbol 12-myristate13-acetate) inhibited cell shortening (-46 +/- 7%). Western blots indicated that cat myocytes express PKC-alpha, -delta, and -epsilon as well as PKC-beta. These findings suggest that brief RP of ventricular myocytes depresses contractility at the myofilament level via Ca(2+)/PKC-dependent signaling. These findings may provide insight into the mechanisms of contractile dysfunction that follow paroxysmal tachyarrhythmias.
机译：这项研究的目的是确定短暂的快速起搏（RP;约200-240次/分钟，持续约5分钟）对心室肌细胞收缩功能的影响。 RP后持续抑制峰值收缩期细胞缩短（-44 +/- 4％），这不是由于舒张期细胞长度，膜电压或L型Ca（2+）电流（I（Ca， L））。在RP期间，基线和峰值细胞内Ca（2+）浓度（[Ca（2 +）]（i））明显增加。 RP后，Ca（2+）瞬变类似于控件。 1 microM钙蛋白酶抑制剂I，25 microM L-N（5）-（1-亚氨基乙基）-鸟氨酸或100 microM N（G）-单甲基-L-精氨酸不能阻止RP对细胞缩短的影响。但是，通过在RP期间降低细胞外[Ca（2+）]（0.5 mM）或暴露于白屈菜红碱（2-4 microM），蛋白激酶C（PKC）抑制剂或LY379196（ 30 nM），PKC-β的选择性抑制剂。暴露于佛波醇酯（200 nM佛波醇12-肉豆蔻酸酯13-乙酸酯）可抑制细胞缩短（-46 +/- 7％）。 Western印迹表明，猫心肌细胞表达PKC-α，δ和ε以及PKC-β。这些发现表明，短暂的心室肌RP通过Ca（2 +）/ PKC依赖性信号传导降低了肌丝水平的收缩力。这些发现可能提供对阵发性快速性心律失常后收缩功能障碍机制的见解。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号