• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Modulation of the Ca2+ sensitivity of airway smooth muscle cells in murine lung slices.
【24h】

Modulation of the Ca2+ sensitivity of airway smooth muscle cells in murine lung slices.

机译：鼠肺切片中气道平滑肌细胞对Ca2 +敏感性的调节。

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

To investigate the phenomenon of Ca(2+) sensitization, we developed a new intact airway and arteriole smooth muscle cell (SMC) "model" by treating murine lung slices with ryanodine-receptor antagonist, ryanodine (50 microM), and caffeine (20 mM). A sustained elevation in intracellular Ca(2+) concentration ([Ca(2+)](i)) was induced in both SMC types by the ryanodine-caffeine treatment due to the depletion of internal Ca(2+) stores and the stimulation of a persistent influx of Ca(2+). Arterioles responded to this sustained increase in [Ca(2+)](i) with a sustained contraction. By contrast, airways responded to sustained high [Ca(2+)](i) with a transient contraction followed by relaxation. Subsequent exposure to methacholine (MCh) induced a sustained concentration-dependent contraction of the airway without a change in the [Ca(2+)](i). During sustained MCh-induced contraction, Y-27632 (a Rho-kinase inhibitor) and GF-109203X (a protein kinase C inhibitor) induced a concentration-dependent relaxation withoutchanging the [Ca(2+)](i). The cAMP-elevating agents, forskolin (an adenylyl cyclase activator), IBMX (a phosphodiesterase inhibitor), and caffeine (also acting as a phosphodiesterase inhibitor), exerted similar relaxing effects. These results indicate that 1) ryanodine-caffeine treatment is a valuable tool for investigating the contractile mechanisms of SMCs while avoiding nonspecific effects due to cell permeabilization, 2) in the absence of agonist, sustained high [Ca(2+)](i) has a differential time-dependent effect on the Ca(2+) sensitivity of airway and arteriole SMCs, 3) MCh facilitates the contraction of airway SMCs by inducing Ca(2+) sensitization via the activation of Rho-kinase and protein kinase C, and 4) cAMP-elevating agents contribute to the relaxation of airway SMCs through Ca(2+) desensitization.
机译：为了研究Ca（2+）致敏现象，我们通过使用鼠李糖碱受体拮抗剂，鼠李糖碱（50 microM）和咖啡因（20毫米）。由于内部Ca（2+）的消耗和刺激的原因，通过ryanodine-caffeine处理在两种SMC类型中诱导了细胞内Ca（2+）浓度（[Ca（2 +）]（i）的持续升高。 Ca（2+）持续涌入的原因。小动脉对这种持续增加的[Ca（2 +）]（i）具有持续收缩的反应。相比之下，气道响应持续高[Ca（2 +）]（i）短暂收缩，然后放松。随后暴露于乙酰甲胆碱（MCh）导致气道持续浓度依赖性收缩而[Ca（2 +）]（i）不变。在持续的MCh诱导的收缩过程中，Y-27632（一种Rho激酶抑制剂）和GF-109203X（一种蛋白激酶C抑制剂）诱导了浓度依赖性的松弛，而没有改变[Ca（2 +）]（i）。 cAMP增强剂福司可林（腺苷酸环化酶激活剂），IBMX（磷酸二酯酶抑制剂）和咖啡因（也用作磷酸二酯酶抑制剂）发挥了类似的松弛作用。这些结果表明：1）莱丹定-咖啡因治疗是研究SMC收缩机制同时避免由于细胞通透性引起的非特异性作用的有价值的工具，2）在不存在激动剂的情况下持续维持高[Ca（2 +）]（i）对气道和小动脉SMC的Ca（2+）敏感性具有不同的时间依赖性影响，3）MCh通过激活Rho激酶和蛋白激酶C诱导Ca（2+）致敏，促进气道SMC的收缩，和4）cAMP提升剂有助于通过Ca（2+）脱敏作用来放松气道SMC。

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