Ebeigbe A B, Cressier F, Konneh M K, Luu T D, Criscione L
Cardiovascular Research Department, CIBA-GEIGY Limited, Basel, Switzerland.
Biochem Biophys Res Commun. 1990 Jun 29;169(3):873-9. doi: 10.1016/0006-291x(90)91974-w.
Endothelium-dependent relaxation mediated by the formation of nitric oxide (NO) from L-arginine, is prevented by the arginine analog NG-monomethyl L-arginine (L-NMMA) (Palmer et al., Biochem. Biophys. Res. Comm. 153:1251-1256 (1988)). In the rat mesenteric arterial bed, incubation with L-NMMA did not prevent acetylcholine-induced relaxation, which, however, was reversed when L-NMMA was added during its maximum effect. A similar profile of action was observed with methylene blue, an inhibitor of guanylate cyclase. Methylene blue, but not L-NMMA, increased basal perfusion pressure. These data indicate that in the mesenteric arterial bed, NO formation via the L-NMMA-sensitive pathway occurs during stimulation with acetylcholine, but not under basal conditions.
由L-精氨酸生成一氧化氮(NO)介导的内皮依赖性舒张作用,可被精氨酸类似物NG-单甲基-L-精氨酸(L-NMMA)所阻断(Palmer等人,《生物化学与生物物理研究通讯》153:1251 - 1256 (1988))。在大鼠肠系膜动脉床中,与L-NMMA共同孵育并不能阻断乙酰胆碱诱导的舒张作用,然而,当在乙酰胆碱发挥最大效应期间添加L-NMMA时,这种舒张作用会被逆转。用鸟苷酸环化酶抑制剂亚甲蓝观察到了类似的作用情况。亚甲蓝而非L-NMMA会升高基础灌注压。这些数据表明,在肠系膜动脉床中,通过L-NMMA敏感途径生成NO的过程发生于乙酰胆碱刺激期间,而非基础条件下。