第一个Robert Furchgott讲座:从内皮依赖性松弛到l -精氨酸:NO途径。

Blood vessels Pub Date : 1990-01-01 DOI:10.1159/000158812
S Moncada
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引用次数: 46

摘要

一氧化氮(NO)从血管内皮细胞和新鲜血管组织中释放,其数量足以解释内皮源性松弛因子的生物作用。它是由l-精氨酸的末端胍基氮原子合成的,该过程被ng -单甲基- l-精氨酸(L-NMMA)抑制。使用L-NMMA的研究表明,血管壁不断产生NO以维持血管舒张剂的张力。l -精氨酸:NO途径现已在许多其他细胞和组织中被发现,在许多细胞和组织中,它作为刺激可溶性鸟苷酸环化酶的转导机制。
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The first Robert Furchgott lecture: from endothelium-dependent relaxation to the L-arginine:NO pathway.

Nitric oxide (NO) is released from vascular endothelial cells and fresh vascular tissue in amounts sufficient to account for the biological actions of endothelium-derived relaxing factor. It is synthesized from the terminal guanidino nitrogen atom(s) of L-arginine, a process that is inhibited by NG-monomethyl-L-arginine (L-NMMA). Studies using L-NMMA have shown that NO is constantly generated by the vessel wall to maintain vasodilator tone. The L-arginine:NO pathway has now been identified in a number of other cells and tissues, in many of which it acts as the transduction mechanism for stimulation of the soluble guanylate cyclase.

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