Vanhoutte P M
Institut de Recherches Internationales Servier, Courbevoie, France.
Verh K Acad Geneeskd Belg. 1998;60(3):251-66.
The endothelium plays an obligatory role in a number of relaxations of isolated arteries. These endothelium-dependent relaxations are due to the release by the endothelial cells of potent vasodilator substances [endothelium-derived relaxing factors (EDRF)]. The best characterized EDRF is nitric oxide (NO). Nitric oxide is formed by the metabolism of L-arginine by the constitutive NO synthase of endothelial cells. In arterial smooth muscle, the relaxations evoked by EDRF are explained best by the stimulation by NO of soluble guanylate cyclase that leads to the accumulation of cyclic GMP. The endothelial cells also release an unidentified substance that causes hyperpolarization of the cell membrane (endothelium-derived hyperpolarizing factor, EDHF). The release of EDRF from the endothelium can be mediated by both pertussis toxin-sensitive (alpha2-adrenergic activation, serotonin, thrombin, aggregating platelets) and insensitive (adenosine diphosphate, bradykinin) G-proteins. In blood vessels from animals with regenerated endothelium, and/or atherosclerosis, there is a selective loss of the pertussis-toxin sensitive mechanism of EDRF-release which favors the occurrence of vasospasm, thrombosis and cellular growth.
内皮细胞在离体动脉的多种舒张反应中起重要作用。这些内皮依赖性舒张反应是由于内皮细胞释放强效血管舒张物质[内皮源性舒张因子（EDRF）]所致。目前研究最为深入的EDRF是一氧化氮（NO）。一氧化氮由内皮细胞的组成型一氧化氮合酶催化L-精氨酸代谢生成。在动脉平滑肌中，EDRF引起的舒张反应最好的解释是NO刺激可溶性鸟苷酸环化酶，导致环磷酸鸟苷（cGMP）积聚。内皮细胞还释放一种不明物质，可引起细胞膜超极化（内皮源性超极化因子，EDHF）。内皮细胞释放EDRF可由百日咳毒素敏感的G蛋白（α2肾上腺素能激活、5-羟色胺、凝血酶、聚集的血小板）和不敏感的G蛋白（二磷酸腺苷、缓激肽）介导。在具有再生内皮和/或动脉粥样硬化的动物血管中，EDRF释放的百日咳毒素敏感机制存在选择性丧失，这有利于血管痉挛、血栓形成和细胞生长的发生。
