Endothelial function - General considerations
Endothelial function - General considerations
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DOI：
10.2165/00003495-199700531-00003
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发表时间：
1997-01-01
期刊：
影响因子：
11.5
通讯作者：
Haller, H
中科院分区：
文献类型：
--
作者：
Haller, H
内皮参与血管张力的生理调节和病理条件下血管的结构转化。在生理条件下，内皮细胞持续分泌一氧化氮（NO），其松弛平滑肌细胞并确保血管通畅。受损或过度活化的内皮细胞也可以分泌血管收缩因子，其中最著名的是内皮素-1（ET-1），以及影响血管平滑肌细胞分化和生长的因子。在病理条件下，内皮细胞损伤如何导致血管疾病可以在糖尿病患者中得到最好的说明，内皮细胞的结构和功能发生了明显的变化。内皮细胞也与血流中的细胞相互作用。ET-1和其他因子从内皮细胞释放到血流中，在那里它们的趋化作用可以诱导白细胞和血小板迁移到内皮壁。内皮细胞通过表达可与白细胞和血小板上的配体相互作用的特异性表面粘附分子（选择素、整合素和免疫球蛋白的超基因家族）诱导粘附。在动脉粥样硬化危险因素慢性损伤的内皮细胞中粘附分子的表达增加。糖尿病和/或糖尿病患者的内皮层渗透性紊乱导致物质从循环流入血管壁的增加。此外，内皮细胞功能障碍可导致血管内血液凝固加速，很明显，内皮细胞在动脉粥样硬化的许多早期病理生理过程中起着核心作用。因此，研究抗动脉粥样硬化治疗对内皮细胞功能和细胞间相互作用的影响非常重要。直到最近，人们对钙拮抗剂对内皮细胞功能的直接影响知之甚少。最近的研究，包括两项临床研究，表明钙拮抗剂主要影响内皮细胞、平滑肌细胞、单核细胞和血小板的相互作用，这些细胞在动脉粥样硬化发展的早期阶段起着核心作用，而这些药物对血管系统的保护作用在后期阶段似乎很低。
The endothelium is involved in both the physiological regulation of vascular tone and the structural transformation of the vessel under pathological conditions. Under physiological conditions, endothelial cells continuously secrete nitric oxide (NO), which relaxes smooth muscle cells and ensures vessel patency. Damaged or excessively activated endothelial cells can also secrete vasoconstrictor factors, the best known of which is endothelin-1 (ET-1), as well as factors that affect the differentiation and growth of vascular smooth muscle cells.How endothelial cell damage contributes, under pathological conditions, to vascular disease can best be illustrated in patients with diabetes mellitus, in whom there are pronounced changes in endothelial cell structure and function.Endothelial cells also interact with cells in the bloodstream. ET-1 and other factors are released from endothelial cells into the bloodstream, where their chemotactic action can induce leucocytes and platelets to migrate to the endothelial wall. Endothelial cells induce adhesion by expression of specific surface adhesion molecules (selectins, integrins and a supergene family of immunoglobulins) that can interact with Ligands on the leucocytes and platelets. The expression of adhesion molecules is increased in endothelial cells chronically damaged by risk factors for atherosclerosis. The disturbed permeability of the endothelial layer in patients with diabetes mellitus and/or hyperlipidaemia leads to an increased influx of substances from the circulation into the vessel wall. In addition, endothelial cell dysfunction can lead to accelerated intravessel blood coagulation.It is evident that the endothelium plays a central role in many of the early pathophysiological processes involved in atherosclerosis. It is therefore important to investigate the effects of antiatherosclerotic therapy on endothelial cell function and cell-to-cell interactions. Until recently, little was known about the direct effects of calcium antagonists on endothelial cell function. Recent studies, including two clinical studies, indicate that calcium antagonists primarily affect interactions of endothelial cells, smooth muscle cells, monocytes and platelets, which play a central role in the early phases of the development of atherosclerosis, whereas the protective effect of these agents on the vascular system appears to be low at later stages.