• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>The journal of clinical hypertension. >Impaired Vasodilation in the Pathogenesis of Hypertension: Focus on Nitric Oxide, Endothelial-Derived Hyperpolarizing Factors, and Prostaglandins
【24h】

Impaired Vasodilation in the Pathogenesis of Hypertension: Focus on Nitric Oxide, Endothelial-Derived Hyperpolarizing Factors, and Prostaglandins

机译：高血压发病机制中血管舒张受损：集中于一氧化氮，内皮源性超极化因子和前列腺素。

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

Under resting conditions the arterial vasculature exists in a vasoconstricted state referred to as vascular tone. Physiological dilatation in response to increased flow, a function of normal endothelium is necessary to maintain normal blood pressure. Endothelial dysfunction in vascular smooth muscle cells thus results in loss of normal vasorelaxant function and the inability of arteries to appropriately dilate in response to increased blood flow in either a systemic or regional vascular bed, resulting in increased blood pressure, a sequence that may represent a common pathway to hypertension. Normal vasorelaxation is mediated by a number of endothelial systems including nitric oxide (NO), prostaglandins (PGI 2 and PGE 2), and a family of endothelial-derived hyperpolarizing factors (EDHF). In response to hemodynamic shear stress, endothelium continuously releases NO, EDHF, and PGI 2 to provide vasodilatation. EDHF, not a single molecule but rather a group of molecules that includes epoxyeicosatrienoic acids, hydrogen peroxide, carbon monoxide, hydrogen sulfide, C-natriuretic peptide, and K + itself, causes vasodilatation by activation of vascular smooth muscle cell K + channels, resulting in hyperpolarization and thus vasorelaxation. The understanding and effective management of blood pressure requires an understanding of both physiologic and pathophysiologic regulation of vascular tone. This review describes molecular mechanisms underlying normal endothelial regulation and pathological states, such as increased oxidative stress, which cause loss of vasorelaxation. Possible pharmacological interventions to restore normal function are suggested.
机译：在静止状态下，动脉脉管系统处于血管收缩状态，称为血管张力。响应于流量增加的生理扩张，维持正常血压是正常内皮功能所必需的。因此，血管平滑肌细胞的内皮功能障碍会导致正常血管舒张功能的丧失，以及动脉无法响应全身或局部血管床中血流量的增加而适当扩张，从而导致血压升高，该序列可能代表了常见的高血压途径。正常的血管舒张由许多内皮系统介导，包括一氧化氮（NO），前列腺素（PGI 2和PGE 2）以及一系列内皮衍生的超极化因子（EDHF）。响应血流动力学切应力，内皮细胞持续释放NO，EDHF和PGI 2以提供血管舒张作用。 EDHF不是单个分子，而是包括环氧二十碳三烯酸，过氧化氢，一氧化碳，硫化氢，C-利钠肽和K +本身的一组分子，它通过激活血管平滑肌细胞K +通道而引起血管舒张。在超极化，从而血管舒张。对血压的理解和有效管理需要对血管紧张度的生理和病理生理调节的理解。这篇综述描述了正常的内皮调节和病理状态（例如增加的氧化应激）的分子机制，这些氧化机制导致血管舒张丧失。建议采取可能的药理干预措施以恢复正常功能。

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