...
首页> 外文期刊>Japanese Journal of Pharmacology >Mechanisms Mediating the Vasorelaxing Action of Eugenol, a Pungent Oil, on Rabbit Arterial Tissue
【24h】

Mechanisms Mediating the Vasorelaxing Action of Eugenol, a Pungent Oil, on Rabbit Arterial Tissue

机译:丁香油丁香酚对兔动脉组织介导血管松弛作用的机制

获取原文

摘要

References(25) Cited-By(23) The inhibitory actions of eugenol on intracellular Ca2+ concentration ([Ca2+]i) and the contractions induced by excess extracellular K+ concentration ([K+]o) in rabbit thoracic aorta were investigated. Application of excess [K+]o solution (30 - 90 mM) produced contraction and increased the intensity of the Ca2+ fluorescence signal. Pretreatment with eugenol (≥0.1 mM) reduced both the amplitude of contraction and the intensity of the Ca2+ fluorescence signal, but the contraction was more strongly affected than the [Ca2+]i. Application of eugenol (0.3 mM) to tissue precontracted by 90 mM [K+]o solution (immediately after the removal of the 90 mM [K+]o solution) slowed the decay of the [Ca2+]i signal, but it did not change the rate of relaxation. Carbonyl cyanide m-chlorophenylhydrozone (10 μM), a mitochondrial metabolic inhibitor, produced a reduction in tension despite a slight increase in [Ca2+]i when applied to muscle precontracted by 90 mM [K+]o solution. These results indicate that eugenol relaxes the rabbit thoracic aorta while suppressing the Ca2+-sensitivity and both the uptake and extrusion mechanisms for Ca2+. To judge from the similarities between its actions and those of metabolic inhibitors, eugenol may produce its actions at least partly through metabolic inhibition.
机译:参考文献(25)被引-By(23)研究了丁香酚对兔胸主动脉内细胞内Ca2 +浓度([Ca2 +] i)和细胞外K +浓度过高([K +] o)引起的收缩的抑制作用。过量的[K +] o溶液(30-90 mM)的施加产生了收缩,并增加了Ca2 +荧光信号的强度。丁子香酚(≥0.1mM)预处理可同时降低收缩幅度和Ca2 +荧光信号强度,但收缩比[Ca2 +] i更强烈。在90 mM [K +] o溶液预紧的组织上(在去除90 mM [K +] o溶液后立即使用)丁香酚(0.3 mM)减慢了[Ca2 +] i信号的衰减,但并没有改变放松率。线粒体代谢抑制剂羰基氰基间氯苯基氢酮(10μM)产生张力降低,尽管将[Ca2 +] i略微增加到90mM [K +] o溶液预收缩的肌肉上。这些结果表明丁子香酚可放松兔胸主动脉,同时抑制Ca2 +敏感性以及Ca2 +的吸收和挤出机制。从其作用与代谢抑制剂的相似性来判断,丁子香酚可以至少部分通过代谢抑制产生其作用。

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