Thomas G, Ramwell P W
Department of Physiology and Biophysics, Georgetown University Medical Center, Washington, D.C. 20007.
Biochem Biophys Res Commun. 1992 Mar 16;183(2):584-9. doi: 10.1016/0006-291x(92)90522-m.
Using a specific HPLC analysis for guanidines, we find that rat aorta contains guanidino succinate (GS), guanidino acetate (GA), guanidino propionate (GP), guanidino butyrate (GB), methyl guanidine (MG) and guanidine. The concentration of L-arginine (0.05 nmol/mg tissue) is significantly lower than the other guanidines. GS is found to be the most potent vasodilator-guanidine in the rat aorta preparation and this vasodilation depends predominantly on the presence of the endothelium. This effect of GS is antagonized by NG-monomethyl L-arginine (L-NMMA), NW-nitro L-arginine benzyl ester (L-NABA), hemoglobin and by methylene blue, all of which are known to block or attenuate endothelium dependent relaxation. Further, the relaxation mediated by GS is accompanied by the formation of cGMP in the rat aorta. From these results we suggest that GS may be a major endogenous source of EDRF.
通过使用一种针对胍类的特定高效液相色谱分析法，我们发现大鼠主动脉中含有胍基琥珀酸（GS）、胍基乙酸（GA）、胍基丙酸（GP）、胍基丁酸（GB）、甲基胍（MG）和胍。L-精氨酸的浓度（0.05纳摩尔/毫克组织）显著低于其他胍类。在大鼠主动脉制剂中，GS被发现是最有效的血管舒张性胍，且这种血管舒张主要取决于内皮的存在。GS的这种作用可被NG-单甲基-L-精氨酸（L-NMMA）、NW-硝基-L-精氨酸苄酯（L-NABA）、血红蛋白以及亚甲蓝所拮抗，所有这些物质都已知会阻断或减弱内皮依赖性舒张。此外，GS介导的舒张伴随着大鼠主动脉中cGMP的形成。从这些结果我们推测，GS可能是内皮舒张因子（EDRF）的主要内源性来源。
