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近年发现内皮衍生舒张因子(EDRF)是一氧化氮(NO),而内皮细胞可通过NO合酶从L-精氨酸合成NO,后者弥散至邻近平滑肌,或与血小板接触,激活可溶性鸟苷酸环化酶而形成cGMP,抑制血小板活性。在内皮细胞中NO的合成引起cGMP的升高,其中高浓度瓜氨酸增强NO的合成。NO的作用与持续血管舒张的张力有关,后者是调节血流的重要因素,这里存在L-精氨酸:NO通路,硝基血管舒张剂就是根据这个原理,用以释放NO,在临床上已应用近150年。至于L-精氨酸:NO通路调节血小板功能方面,NO激活血小板中的可溶性鸟苷酸环化酸而抑制血小板聚集和粘附。胶原、二磷酸腺甙和凝血酶等聚集剂可增高血小板细胞内Ca~(++),后者也可激活血小板内NO合酶。不论来自血小板本身或内皮的NO均表示控制血小板聚集和粘附的强大机制。
In recent years, it has been found that endothelial-derived relaxing factor (EDRF) is nitric oxide (NO), and endothelial cells synthesize NO from L-arginine by NO synthase, which diffuses to adjacent smooth muscle or to platelets and activates soluble guanosine Acid cyclase to form cGMP, inhibit platelet activity. The synthesis of NO in endothelial cells causes an increase in cGMP, with high concentrations of citrulline enhancing NO synthesis. The role of NO is associated with sustained diastolic tension, which is an important factor in the regulation of blood flow. There is L-arginine: NO pathway here, and nitro-vasodilator is used to release NO according to this principle, clinically Has been used for nearly 150 years. As for the L-arginine: NO pathway regulates platelet function, NO activates soluble guanylate cyclic acid in platelets to inhibit platelet aggregation and adhesion. Collagen, adenosine diphosphate and thrombin and other aggregates can increase platelet intracellular Ca ~ (++), which can also activate platelet NO synthase. NO from platelets themselves or from the endothelium represents a powerful mechanism for controlling platelet aggregation and adhesion.