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高血压、内皮与慢性血管疾病的发病机制

Hypertension, the endothelium and the pathogenesis of chronic vascular disease.

作者信息

Haller H

机构信息

Franz Volhard Klinik, Virchow-Klinkum, Humboldt Universität, Berlin Germany.

出版信息

Kidney Blood Press Res. 1996;19(3-4):166-71. doi: 10.1159/000174066.

Abstract

The endothelium lines all vessels of the body and is the most important structure for communication between the flowing blood and the vessel wall. Healthy endothelium has antiadhesive and antithrombotic properties and is crucial for maintaining blood flow. It serves as a permeability barrier and prevents noxious agents from entering the vessel wall. Endothelial cells have secretory functions and secrete vasorelaxant substances. Therefore, functioning endothelium sustains the homoeostasis of the vessel wall. Endothelial functions are impaired by risk factors for cardiovascular disease such as hypertension, hyperlipidemia and hyperglycemia. Hypertension leads to decreased generation of nitric oxide in endothelial cells, thereby diminishing their vasorelaxant properties. Hypertension also contributes to an increase in endothelial cell permeability leading to intimal edema. Thirdly, hypertension increases the expression of adhesion molecules and increases the adherence of leukocytes to the vessel wall. Hence, hypertension directly contributes to the pathological alterations of the endothelium and it seems that these effects initiate and accelerate the pathogenesis of chronic vascular disease.

摘要

内皮细胞衬于身体所有血管的内表面,是流动的血液与血管壁之间进行交流的最重要结构。健康的内皮细胞具有抗黏附及抗血栓形成特性,对维持血流至关重要。它作为一道通透性屏障,可防止有害物质进入血管壁。内皮细胞具有分泌功能,能分泌血管舒张物质。因此,正常功能的内皮细胞维持着血管壁的稳态。心血管疾病的危险因素,如高血压、高脂血症和高血糖,会损害内皮功能。高血压导致内皮细胞中一氧化氮生成减少,从而削弱其血管舒张特性。高血压还会导致内皮细胞通透性增加,引发内膜水肿。第三,高血压会增加黏附分子的表达,增加白细胞与血管壁的黏附。因此,高血压直接导致内皮细胞的病理改变,而且这些影响似乎启动并加速了慢性血管疾病的发病机制。

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