• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Life sciences >Hydrogen sulfide decreases adenosine triphosphate levels in aortic rings and leads to vasorelaxation via metabolic inhibition.
【24h】

Hydrogen sulfide decreases adenosine triphosphate levels in aortic rings and leads to vasorelaxation via metabolic inhibition.

机译：硫化氢降低主动脉环中三磷酸腺苷的水平，并通过代谢抑制导致血管舒张。

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

AIMS: Hydrogen sulfide (H(2)S) at low concentrations serves as a physiological endogenous vasodilator molecule, while at higher concentrations it can trigger cytotoxic effects. The aim of our study was to elucidate the potential mechanisms responsible for the effects of H(2)S on vascular tone. MAIN METHODS: We measured the vascular tone in vitro in precontracted rat thoracic aortic rings and we have tested the effect of different oxygen levels and a variety of inhibitors affecting known vasodilatory pathways. We have also compared the vascular effect of high concentrations of H(2)S to those of pharmacological inhibitors of oxidative phosphorylation. Furthermore, we measured adenosine triphosphate (ATP)-levels in the same vascular tissues. KEY FINDINGS: We have found that in rat aortic rings: (1) H(2)S decreases ATP levels; (2) relaxations to H(2)S depend on the ambient oxygen concentration; (3) prostaglandins do not take part in the H(2)S induced relaxations; (4) the 3':5'-cyclic guanosine monophosphate (cGMP)-nitric oxide (NO) pathway does not have a role in the relaxations (5) the role of K(ATP) channels is limited, while Cl(-)/HCO(3)(-) channels have a role in the relaxations. (6): We have observed that high concentrations of H(2)S relax the aortic rings in a fashion similar to sodium cyanide, and both agents reduce cellular ATP levels to a comparable degree. SIGNIFICANCE: H(2)S, a new gasotransmitter of emerging importance, leads to relaxation via Cl(-)/HCO(3)(-) channels and metabolic inhibition and the interactions of these two factors depend on the oxygen levels of the tissue.
机译：目的：低浓度的硫化氢（H（2）S）可以作为生理性内源性血管扩张分子，而高浓度的硫化氢可以触发细胞毒性作用。我们研究的目的是阐明造成H（2）S对血管张力影响的潜在机制。主要方法：我们在体外测量了预收缩大鼠胸主动脉环的血管紧张度，并测试了不同氧水平和各种抑制剂对已知血管舒张途径的影响。我们还比较了高浓度H（2）S的血管作用与氧化磷酸化的药理抑制剂的作用。此外，我们测量了相同血管组织中的三磷酸腺苷（ATP）水平。主要发现：我们发现在大鼠主动脉环中：（1）H（2）S降低ATP水平; （2）H（2）S的弛豫取决于周围的氧气浓度; （3）前列腺素不参与H（2）S诱导的弛豫; （4）3'：5'-环鸟苷一磷酸（cGMP）-一氧化氮（NO）途径在弛豫中不起作用（5）K（ATP）通道的作用有限，而Cl（-） / HCO（3）（-）通道在松弛中起作用。 （6）：我们已经观察到高浓度的H（2）S以类似于氰化钠的方式使主动脉环松弛，并且这两种药物都会将细胞的ATP水平降低到相当的程度。重要性：H（2）S是一种新兴的新兴气体递质，可通过Cl（-）/ HCO（3）（-）通道引起舒张并抑制代谢，这两个因素的相互作用取决于组织中的氧气水平。

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