• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cell and Tissue Research >Reactive oxygen radicals and gaseous transmitters in carotid body activation by intermittent hypoxia
【24h】

Reactive oxygen radicals and gaseous transmitters in carotid body activation by intermittent hypoxia

机译：间歇性缺氧的反应性氧自由基和颈动脉体激活中的气态发射器

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

Sleep apnea is a prevalent respiratory disease characterized by periodic cessation of breathing during sleep causing intermittent hypoxia (IH). Sleep apnea patients and rodents exposed to IH exhibit elevated sympathetic nerve activity and hypertension. A heightened carotid body (CB) chemoreflex has been implicated in causing autonomic abnormalities in IH-treated rodents and in sleep apnea patients. The purpose of this article is to review the emerging evidence showing that interactions between reactive oxygen species (ROS) and gaseous transmitters as a mechanism cause hyperactive CB by IH. Rodents treated with IH exhibit markedly elevated ROS in the CB, which is due to transcriptional upregulation of pro-oxidant enzymes by hypoxia-inducible factor (HIF)-1 and insufficient transcriptional regulation of anti-oxidant enzymes by HIF-2. ROS, in turn, increases cystathionine γ-lyase (CSE)-dependent H~(2)S production in the CB. Blockade of H~(2)S synthesis prevents IH-evoked CB activation. However, the effects of ROS on H~(2)S production are not due to direct effects on CSE enzyme activity but rather due to inactivation of heme oxygenase-2 (HO-2), a carbon monoxide (CO) producing enzyme. CO inhibits H~(2)S production through inactivation of CSE by PKG-dependent phosphorylation. During IH, reduced CO production resulting from inactivation of HO-2 by ROS releases the inhibition of CO on CSE thereby increasing H~(2)S. Inhibiting H~(2)S synthesis prevented IH-evoked sympathetic activation and hypertension.
机译：睡眠呼吸暂停是一种普遍存在的呼吸系统疾病，其特征在于睡眠期间呼吸期间的周期性停止，导致间歇性缺氧（IH）。暴露于IH的睡眠呼吸暂停患者和啮齿动物表现出升高的交感神经活动和高血压。提高的颈动脉体（CB）化学速度均涉及引起IH处理的啮齿动物和睡眠呼吸暂停患者的自主异常。本文的目的是审查新兴的证据，表明反应性氧物质（ROS）和气态变送器之间的相互作用，作为机制，使IH的过度增长。用IH处理的啮齿动物在CB中表现出明显升高的RO，这是由于缺氧诱导因子（HIF）-1的促氧化剂酶的转录上调，并且HIF-2的抗氧化剂酶的转录调节不足。反过来，ROS增加了CB中的胱硫氨酸氨酰γ-裂解酶（CSE） - 依赖性H〜（2）S生产。阻断H〜（2）S合成可防止IH诱发的CB激活。然而，ROS对H〜（2）S产生的影响不是由于对CSE酶活性的直接影响，而是由于血红素氧酶-2-2（HO-2）的灭活，产生一氧化碳（CO）生产酶。 CO通过PKG依赖性磷酸化灭活CSE来抑制H〜（2）S产生。在IH期间，由ROS的HO-2失活导致的CO生产释放了CO在CSE上的抑制，从而增加H〜（2）。抑制h〜（2）的合成阻止了IH诱发的交感神经激活和高血压。

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