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1 NO的基本特性及作用 1980年Furchgott和Zawadzki报告内皮细胞(endothelial cell,EC)可产生一种因子,作用于平滑肌引起血管扩张,并命名为内皮源性舒张因子(endothelial derived relaxing factor,EDRF),进一步的研究表明EDRF就是一氧化氮(nitric oxide,NO)。基础状态下,EC可分别通过NADPH、Ca~(2+)/钙调素依赖的NO合成酶使L-精氨酸(Larginine,L-Arg)氨基端胍基脱氨氧化生成NO和L-瓜氨酸(L-citrulline,L-Cit),并在乙酰胆碱、缓激肽、A_(23187)等作用下通过增加细胞内钙离子浓度进一步增加NO的合成和释放。 EDRF的扩血管作用可能是通过平滑肌细胞(SMC)内环磷酸鸟苷酸(cGMP)含量增加来介导的,即EC释放EDRF,后者弥散到SMC,激活鸟苷酸环化酶,使细胞内cGMP含量升高,再经蛋白激酶G引起蛋白质磷酸化,介导平滑肌的松弛反应。外源性NO合成酶抑制剂N~G-monomethyl-L-arginine(L-NMMA)、N~G-nitro-L-arginine-methylester(L-NAME)可抑制NO的合成和释放,引起平滑肌收缩,补充合成NO所需的底物L-Arg或给予体内生理条件下自发特异形成NO的NO供体——硝普
1 The basic characteristics of NO and its role In 1980, Furchgott and Zawadzki reported that endothelial cells (ECs) produce a factor that acts on smooth muscle to cause vasodilation and is named endothelial derived relaxing factor (EDRF) Further studies show that EDRF is nitric oxide (NO). Under the basal conditions, EC could deaminate the amino-terminal guanidine group of L-arginine (L-Arginine) to form NO and L-Arg through NADPH and Ca2 + / calmodulin- Citrulline (L-Cit), and further increase the synthesis and release of NO by increasing intracellular calcium concentration under the action of acetylcholine, bradykinin, A_ (23187) and the like. The vasodilator effect of EDRF may be mediated through an increase in the content of cyclic guanosine monophosphate (cGMP) in smooth muscle cells (SMCs). That is, ED releases EDRF, which diffuses into SMCs to activate guanylate cyclase, Within the cGMP content increased, and then caused by protein kinase G protein phosphorylation, mediating the relaxation of smooth muscle response. N-G-monomethyl-L-arginine (N-GMA) and N-G-nitro-L-arginine methylester (L-NAME) can inhibit the synthesis and release of NO and induce smooth muscle contraction , To supplement the substrate L-Arg required for the synthesis of NO, or to give NO donor, nitroprusside, which spontaneously and specifically forms NO under physiological conditions in vivo