论文部分内容阅读
在二氧化酶作用下,L-精氨酸转变为 L-胍氨酸和 NO,此 NO 显示 EDRF 样的重要的生物活性。N~G-nitro-L-arginine 在体外和体内都抑制 EDRF 的生物合成,是 EDRF 有效拮抗剂。本文研究结果表明 N~G-nitro-L-arginine 和 HCl·N~GO~2-NO_2-L-Arg-OCH_3在体外有血管舒张作用,但是这两个化合物在体内对动脉血压具有剂量依赖的增加效应。在体外 HCl·N~(G-)NO_2-L-Arg-N_G-NO_2-L-Arg-OCH_3对 NE 收缩的鼠动脉肌条有舒张作用,而在体内它具有两向性。例如低剂量时可使大鼠平均动脉血压(MAP)降低,而高剂量时使 MAP 增高。N~G-Tos-L-Arg-N~G-Tos-L-Arg-OH 具有剂量依赖关系的舒血管作用和降低血压的活性。
Under the action of dioxygenase, L-arginine is converted to L-guanine and NO, which shows significant EDRF-like biological activity. N ~ G-nitro-L-arginine inhibits EDRF biosynthesis both in vitro and in vivo and is a potent antagonist of EDRF. The results of this study showed that vasodilatory effects of N ~ G-nitro-L-arginine and HCl · N ~ GO ~ 2-NO_2-L-Arg-OCH_3 were observed in vitro, but the two compounds were dose- Increase effect. In vitro, HCl · N ~ (G-) NO_2-L-Arg-N_G-NO_2-L-Arg-OCH_3 has a diastolic effect on NE-contracted murine arterial muscle strips and has biodism in vivo. For example, low mean arterial pressure (MAP) in rats can be reduced, while high doses of MAP increased. N ~ G-Tos-L-Arg-N ~ G-Tos-L-Arg-OH had a dose-dependent vasodilatory and antihypertensive activity.