Vanhoutte P M
Institut de Recherches Internationales Servier, Courbevoie, France.
Eur Heart J. 1998 Sep;19 Suppl J:J7-15.
Endothelial cells control the tone of the underlying vascular smooth muscle by secreting vasodilator substances (prostacyclin, nitric oxide and endothelium-derived hyperpolarizing factor). These vasodilator substances also contribute to the antithrombogenicity of the normal endothelium, and inhibit cellular growth. In coronary vascular disease, the ability of the endothelium to secrete vasodilator substances is reduced, while the propensity to release endothelium-derived contracting factors is increased. In particular, the reduced release of nitric oxide in response to aggregating platelets, thrombin and circulating catecholamines favours the occurrence of thrombosis and vasospasm, and plays a key role in the initiation of the atherosclerotic process. From the therapeutic point of view, the best available way to enhance the release of endothelium-derived nitric oxide and hyperpolarizing factor is to inhibit converting enzyme. This will protect endogenous bradykinin from breakdown and prolong its action on endothelial receptors.
内皮细胞通过分泌血管舒张物质（前列环素、一氧化氮和内皮衍生超极化因子）来控制其下方血管平滑肌的张力。这些血管舒张物质也有助于正常内皮的抗血栓形成，并抑制细胞生长。在冠状动脉疾病中，内皮细胞分泌血管舒张物质的能力降低，而释放内皮衍生收缩因子的倾向增加。特别是，对聚集的血小板、凝血酶和循环儿茶酚胺反应时一氧化氮释放减少，有利于血栓形成和血管痉挛的发生，并在动脉粥样硬化过程的起始中起关键作用。从治疗角度来看，增强内皮衍生一氧化氮和超极化因子释放的最佳可用方法是抑制转化酶。这将保护内源性缓激肽不被分解，并延长其对内皮受体的作用。
