• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Nitrite enhances RBC hypoxic ATP synthesis and the release of ATP into the vasculature: a new mechanism for nitrite-induced vasodilation.
【24h】

Nitrite enhances RBC hypoxic ATP synthesis and the release of ATP into the vasculature: a new mechanism for nitrite-induced vasodilation.

机译：亚硝酸盐增强了RBC低氧ATP的合成，并增强了ATP向血管系统的释放：亚硝酸盐诱导的血管舒张的新机制。

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

A role for nitric oxide (NO) produced during the reduction of nitrite by deoxygenated red blood cells (RBCs) in regulating vascular dilation has been proposed. It has not, however, been satisfactorily explained how this NO is released from the RBC without first reacting with the large pools of oxyhemoglobin and deoxyhemoglobin in the cell. In this study, we have delineated a mechanism for nitrite-induced RBC vasodilation that does not require that NO be released from the cell. Instead, we show that nitrite enhances the ATP release from RBCs, which is known to produce vasodilation by several different methods including the interaction with purinergic receptors on the endothelium that stimulate the synthesis of NO by endothelial NO synthase. This mechanism was established in vivo by measuring the decrease in blood pressure when injecting nitrite-reacted RBCs into rats. The observed decrease in blood pressure was not observed if endothelial NO synthase was inhibited by N(omega)-nitro-L-arginine methyl ester (L-NAME) or when any released ATP was degraded by apyrase. The nitrite-enhanced ATP release was shown to involve an increased binding of nitrite-modified hemoglobin to the RBC membrane that displaces glycolytic enzymes from the membrane, resulting in the formation of a pool of ATP that is released from the RBC. These results thus provide a new mechanism to explain nitrite-induced vasodilation.
机译：有人提出在脱氧红细胞（RBC）还原亚硝酸盐过程中产生的一氧化氮（NO）在调节血管扩张中的作用。然而，尚未令人满意地解释该NO如何在不首先与细胞中大量的氧合血红蛋白和脱氧血红蛋白反应的情况下从RBC中释放出来。在这项研究中，我们描述了亚硝酸盐诱导的RBC血管舒张的机制，该机制不需要从细胞中释放NO。取而代之的是，我们表明亚硝酸盐增强了RBC的ATP释放，已知通过多种不同的方法产生血管舒张作用，包括与内皮上嘌呤能受体的相互作用，刺激内皮一氧化氮合酶合成一氧化氮。通过测量将亚硝酸盐反应的RBC注射到大鼠中时血压的降低，在体内建立了这种机制。如果内皮型NO合酶被N（ω）-硝基-L-精氨酸甲酯（L-NAME）抑制，或者任何释放的ATP被腺苷三磷酸双磷酸酶降解，则未观察到血压降低。已显示出亚硝酸盐增强的ATP释放涉及亚硝酸盐修饰的血红蛋白与RBC膜的结合增加，从而取代了膜上的糖酵解酶，导致形成了从RBC释放的ATP池。因此，这些结果提供了解释亚硝酸盐诱导的血管舒张的新机制。

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