• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Life sciences >Inhibitory effect of tetrabutylammonium ions on endotheliumitric oxide-mediated vasorelaxation.
【24h】

Inhibitory effect of tetrabutylammonium ions on endotheliumitric oxide-mediated vasorelaxation.

机译：四丁基铵离子对内皮/一氧化氮介导的血管舒张作用的抑制作用。

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

Apart from the well-described K+ channel blocking effects in vascular smooth muscle cells, monovalent quaternary ammonium ions may also interact with endothelial cells in the endothelium-intact mammalian arteries. The present study was aimed to examine the effect of tetrabutylammonium ions on endothelium-dependent and -independent relaxation in the rat isolated aortic rings. Pretreatment with tetrabutylammonium concentration dependently reduced the endothelium-dependent relaxation induced by acetylcholine, cyclopiazonic acid and ionomycin. Tetrabutylammonium also inhibited endothelium-independent relaxation induced by hydroxylamine or nitroprusside. Pretreatment of endothelium-denuded rings with tetrabutylammonium did not affect relaxation induced by NS1619 or by diltiazem. In contrast, tetrabutylammonium significantly reduced the pinacidil- or cromakalim-induced relaxation. Tetrabutylammonium also inhibited the acetylcholine- but not nitroprusside-induced increase of tissue content of cyclic GMP in the aortic rings. The present study indicates that tetrabutylammonium ions could inhibit endothelial and exogenous nitric oxide-mediated aortic relaxation while it had no effect on relaxation induced by activation of Ca2+-activated K+ channels (by NS1619) or by inhibition of voltage-gated Ca2+ channels (by diltiazem). The inhibitory effect on pinacidil- and cromakalim-induced relaxation suggests that tetrabutylammonium ions also inhibit ATP-sensitive K+ channels in aortic smooth muscle cells.
机译：除了在血管平滑肌细胞中众所周知的K +通道阻滞作用外，单价季铵离子还可能与完整内皮细胞的哺乳动物动脉中的内皮细胞相互作用。本研究旨在检查四丁基铵离子对大鼠离体主动脉环中内皮依赖性和非依赖性松弛的影响。用四丁基铵浓度预处理可减少乙酰胆碱，环吡唑酸和离子霉素诱导的内皮依赖性舒张。四丁基铵还抑制羟胺或硝普钠诱导的内皮依赖性舒张。用四丁基铵预处理内皮剥落的环不会影响NS1619或地尔硫卓引起的松弛。相反，四丁基铵显着降低了吡那地尔或克罗卡林引起的松弛。四丁基铵也抑制乙酰胆碱，但不抑制硝普钠诱导的主动脉环中GMP组织含量的增加。本研究表明，四丁基铵离子可以抑制内皮和外源性一氧化氮介导的主动脉舒张，而对Ca2 +激活的K +通道的激活（通过NS1619）或电压门控的Ca2 +通道的抑制（地尔硫卓）没有影响）。对吡那地尔和克罗卡林诱导的松弛的抑制作用表明，四丁基铵离子还抑制主动脉平滑肌细胞中的ATP敏感K +通道。

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