...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Involvement of sarcoplasmic reticulum in changing intracellular calcium due to Na+/K+-ATPase inhibition in cardiomyocytes.
【24h】

Involvement of sarcoplasmic reticulum in changing intracellular calcium due to Na+/K+-ATPase inhibition in cardiomyocytes.

机译：由于心肌细胞中Na + / K + -ATPase抑制，肌浆网参与改变细胞内钙。

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

Earlier studies have demonstrated that ouabain-induced increase in [Ca2+]i, as a consequence of sarcolemma (SL) Na+/K+-ATPase inhibition, is associated with activation of both the SL Na+/Ca2+ exchanger and SL Ca2+ channels. In view of the importance of sarcoplasmic reticulum (SR) in the regulation of [Ca2+]i, this study examined the role of SR in ouabain-induced increase in [Ca2+]i in both quiescent and KCl-depolarized cardiomyocytes. For this purpose, adult rat cardiomyocytes were loaded with fura-2 and ouabain-induced changes in [Ca2+]i were monitored upon treatment with or without different agents that are known to influence Ca2+ handling by the intracellular organelles. Ouabain not only increased the basal [Ca2+]i and augmented KCl-induced increase in [Ca2+]i but also produced similar effects on the ATP-induced increase in [Ca2+]i. Treatments of cardiomyocytes with caffeine, ryanodine, or cyclopiazonic acid, which affect SR Ca2+ stores, attenuated the ouabain-induced increase in basal Ca2+ as well as augmentation of the KCl response. Both ryanodine and cyclopiazonic acid produced additional effects, when used in combination with a SL Ca2+ channel inhibitor (verapamil), but not with a Na+/Ca2+ exchange inhibitor (KB-R7943). Inhibitors of Ca2+/calmodulin kinase, protein kinase A, and inositol-3-phosphate receptors were also observed to depress the ouabain-induced increase in [Ca2+]i in cardiomyocytes. On the other hand, mitochondrial Ca2+ transport inhibitors did not exert any effect on the ouabain-induced alterations in [Ca2+]i in cardiomyocytes. Furthermore, ouabain did not show any direct effect on the Ca2+ uptake and Ca2+ release activities of SR or mitochondria. These results suggest an indirect involvement of SR Ca2+ stores in the ouabain-induced increase in [Ca2+]i in cardiomyocytes and indicate the participation of both Ca2+-induced Ca2+ release and regulatory mechanisms in this action.
机译：较早的研究表明，由于肌膜（SL）Na + / K + -ATPase抑制，哇巴因诱导的[Ca2 +] i的增加与SL Na + / Ca2 +交换子和SL Ca2 +通道的激活有关。鉴于肌浆网（SR）在[Ca2 +] i调控中的重要性，本研究探讨了SR在哇巴因诱导的静态和KCl去极化心肌细胞中[Ca2 +] i增加的作用。为此目的，成年大鼠心肌细胞装有fura-2，用或不使用已知会影响细胞内细胞器处理Ca2 +的不同试剂处理时，即可监测哇巴因诱导的[Ca2 +] i变化。瓦巴因不仅增加了基础[Ca2 +] i并增加了KCl诱导的[Ca2 +] i的增加，而且对ATP诱导的[Ca2 +] i的增加产生了类似的影响。用咖啡因，ryanodine或环吡嗪酸处理心肌细胞会影响SR Ca2 +的储存，从而减弱了哇巴因诱导的基础Ca2 +的增加以及KCl反应的增强。当与SL Ca2 +通道抑制剂（维拉帕米）组合使用，但与Na + / Ca2 +交换抑制剂（KB-R7943）组合使用时，ryanodine和环吡唑酸都产生附加效果。还观察到Ca2 + /钙调蛋白激酶，蛋白激酶A和肌醇-3-磷酸酯受体的抑制剂抑制了哇巴因诱导的心肌细胞[Ca2 +] i的增加。另一方面，线粒体Ca2 +转运抑制剂对哇巴因诱导的心肌细胞[Ca2 +] i的改变没有任何作用。此外，哇巴因对SR或线粒体的Ca 2+吸收和Ca 2+释放活性没有直接影响。这些结果表明SR Ca2 +储存间接参与了哇巴因诱导的心肌细胞中[Ca2 +] i的增加，并表明Ca2 +诱导的Ca2 +释放和调节机制均参与了这一动作。

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