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哇巴因对豚鼠主动脉肌肉张力和细胞内钙离子水平的影响。

Effects of ouabain on muscle tension and intracellular Ca2+ level in guinea-pig aorta.

作者信息

Iwamoto T, Harada K, Nakajima F, Sukamoto T

机构信息

Department of Pharmacology, Kanebo Ltd., Osaka, Japan.

出版信息

Eur J Pharmacol. 1992 Nov 24;224(1):71-6. doi: 10.1016/0014-2999(92)94820-l.

Abstract

The effects of ouabain on muscle tension and the intracellular Ca2+ level ([Ca2+]i) were examined in guinea-pig aorta loaded with fura-2. Ouabain caused a gradual and sustained increase in both [Ca2+]i and muscle tension. There was a positive correlation between these two parameters. In Ca(2+)-free solution, ouabain did not affect either [Ca2+]i or muscle tension, suggesting that the ouabain-induced increase in [Ca2+]i was not due to Ca2+ release from storage sites. The ouabain-induced increase in [Ca2+]i and muscle tension was inhibited by Ni2+, which inhibits the Na+/Ca2+ exchanger, but not by verapamil. Furthermore, anionic and cationic amphiphiles were used as modulators of the Na+/Ca2+ exchanger. Sodium dodecyl sulfate accelerated the responses to ouabain, whereas dodecyltrimethylammonium bromide inhibited them. These results suggest that in the guinea-pig aorta, ouabain induces contraction by increasing the Ca2+ influx through the Na+/Ca2+ exchanger on the plasma membrane, but not through verapamil-sensitive Ca2+ channels.

摘要

在装载了fura - 2的豚鼠主动脉中研究了哇巴因对肌肉张力和细胞内钙离子水平([Ca2+]i)的影响。哇巴因导致[Ca2+]i和肌肉张力逐渐且持续增加。这两个参数之间存在正相关。在无钙溶液中,哇巴因对[Ca2+]i或肌肉张力均无影响,这表明哇巴因诱导的[Ca2+]i增加并非由于储存位点释放钙离子。哇巴因诱导的[Ca2+]i和肌肉张力增加被抑制钠离子/钙离子交换体的Ni2+所抑制,但未被维拉帕米抑制。此外,阴离子和阳离子两亲分子被用作钠离子/钙离子交换体的调节剂。十二烷基硫酸钠加速了对哇巴因的反应,而十二烷基三甲基溴化铵则抑制了这些反应。这些结果表明,在豚鼠主动脉中,哇巴因通过增加质膜上钠离子/钙离子交换体的钙离子内流来诱导收缩,而不是通过维拉帕米敏感的钙离子通道。

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