• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Life sciences >cGMP stimulates endoplasmic reticulum Ca(2+)-ATPase in vascular endothelial cells.
【24h】

cGMP stimulates endoplasmic reticulum Ca(2+)-ATPase in vascular endothelial cells.

机译：cGMP刺激血管内皮细胞中的内质网Ca（2 +）-ATPase。

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

Calcium is a crucial regulator of many physiological processes such as cell growth, division, differentiation, cell death and apoptosis. In this study, we examined the effect of cGMP on agonist-induced [Ca(2+)](i) transient in isolated rat aortic endothelial cells. 100 microM ATP was applied to the cells bathed in a Ca(2+)-free physiological solution to induce a [Ca(2+)](i) transient that was caused by Ca(2+) release from intracellular stores. cGMP, which was applied after [Ca(2+)](i) reached its peak level, accelerated the falling phase of [Ca(2+)](i) transient. Pre-treatment of the cells with CPA abolished the accelerating effect of cGMP on the falling phase of [Ca(2+)](i) transient. The effect of cGMP was reversed by KT5823, a highly specific inhibitor of protein kinase G. Taken together, these data suggest that cGMP may reduce [Ca(2+)](i) level by promoting Ca(2+) uptake through sarcoplasmic/endoplasmic reticulum ATPase and that the effect of cGMP may be mediated by protein kinase G.
机译：钙是许多生理过程（例如细胞生长，分裂，分化，细胞死亡和细胞凋亡）的重要调节剂。在这项研究中，我们检查了cGMP对激动剂诱导的[Ca（2 +）]（i）瞬变在离体大鼠主动脉内皮细胞中的作用。将100 microM ATP应用于沐浴在无Ca（2+）的生理溶液中的细胞，以诱导由细胞内存储中Ca（2+）释放引起的[Ca（2 +）]（i）瞬变。在[Ca（2 +）]（i）达到其峰值水平后应用的cGMP加速了[Ca（2 +）]（i）瞬态的下降阶段。用CPA预处理细胞消除了cGMP对[Ca（2 +）]（i）瞬态下降阶段的加速作用。蛋白质激酶G的高度特异性抑制剂KT5823逆转了cGMP的作用。总而言之，这些数据表明cGMP可能通过促进通过肌浆/内质网ATPase和cGMP的作用可能是由蛋白激酶G介导的。

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