Lüscher T F, Tanner F C
Department of Medicine, University Hospital, Basel, Switzerland.
Am J Hypertens. 1993 Jul;6(7 Pt 2):283S-293S. doi: 10.1093/ajh/6.7.283s.
The endothelium regulates vascular tone by releasing factors involved in relaxation and contraction, in coagulation and thrombus formation, and in growth inhibition and stimulation. Endothelium-dependent relaxations are elicited by transmitters, hormones, platelet substances, and the coagulation system, and by physical stimuli such as the shear stress from circulating blood. They are mediated by the endothelium-derived relaxing factor, recently identified as nitric oxide, which causes vasodilation and platelet deactivation. Other proposed endothelium-derived relaxing factors include a hyperpolarizing factor, lipooxygenase products, and the cytochrome P450 pathway. Endothelium-derived contracting factors are produced by the cyclooxygenase pathway and by endothelial cells, which produce the peptide endothelin-1, a potent vasoconstrictor that under normal conditions circulates at low levels. The endothelium produces both growth inhibitors--normally dominant--and growth stimuli. Denuded or dysfunctional endothelium leads to a proliferative response and intimal hyperplasia in the vessel wall; moreover, platelets adhere to the site and release potent growth factors. Endothelial dysfunction has numerous causes: Aging is associated with increased formation of contracting factor and decreased relaxing factor; denudation, such as by coronary angioplasty, impairs the capacities of regenerated endothelial cells; oxidized low-density lipoproteins and hypercholesterolemia interfere with nitric oxide production; hypertension morphologically and functionally alters the endothelium; and atherosclerosis markedly attenuates some endothelium-dependent relaxations. For patients with coronary bypass grafts, differences in endothelium-derived vasoactive factors between the internal mammary artery and the saphenous vein may be important determinants of graft function, with the mammary artery having more pronounced relaxations than the saphenous vein and thus a higher patency rate.
内皮细胞通过释放参与舒张和收缩、凝血和血栓形成以及生长抑制和刺激的因子来调节血管张力。内皮依赖性舒张由递质、激素、血小板物质、凝血系统以及诸如循环血液的剪切应力等物理刺激引发。它们由内皮源性舒张因子介导，最近被确定为一氧化氮，一氧化氮可引起血管舒张和血小板失活。其他被认为的内皮源性舒张因子包括超极化因子、脂氧合酶产物和细胞色素P450途径。内皮源性收缩因子由环氧化酶途径和内皮细胞产生，内皮细胞产生肽内皮素-1，这是一种强效血管收缩剂，在正常情况下以低水平循环。内皮细胞既产生生长抑制剂（通常占主导），也产生生长刺激因子。内皮剥脱或功能障碍会导致血管壁的增殖反应和内膜增生；此外，血小板会黏附于该部位并释放强效生长因子。内皮功能障碍有多种原因：衰老与收缩因子形成增加和舒张因子减少有关；诸如冠状动脉成形术导致的内皮剥脱会损害再生内皮细胞的能力；氧化型低密度脂蛋白和高胆固醇血症会干扰一氧化氮的产生；高血压会在形态和功能上改变内皮；动脉粥样硬化会明显减弱一些内皮依赖性舒张。对于接受冠状动脉搭桥术的患者，乳内动脉和大隐静脉之间内皮源性血管活性因子的差异可能是移植物功能的重要决定因素，乳内动脉的舒张比大隐静脉更明显，因此通畅率更高。
