异紫堇定的扩血管作用与环核苷酸的关系(英文)

应用血管平滑肌等张收缩和放射免疫测定环核苷酸水平等方法研究了异紫堇定扩血管作用及其机理 .结果表明 ,异紫堇定浓度依赖性地松弛去甲肾上腺素 (NE ,1μmol·L- 1)和KCl(30mmol·L- 1)预收缩的兔胸主动脉螺旋条 ,EC50 分别为 (12 .6± 4 .4 )和 (447± 38) μmol·L- 1,对NE的作用比对KCl强 36倍 .亚甲蓝 (10 μmol·L- 1)可部分抑制异紫堇定的扩血管作用 ,但不受格列本脲 ,吲哚美辛 ,普萘洛尔或N L 硝基精氨酸影响 .异紫堇定还可促进cGMP生成增加 ,并可被亚甲蓝完全阻断 .异紫堇定对cAMP的生成无影响 .结果提示 ,异紫堇定的扩血管作用至少部分通过激活鸟苷酸环化酶 ,促进cGMP的生成实现

Relation of vasodilative action of isocorydine to cyclic nucleotides

The vasodilative mechanism of isocorydine in isolated rabbit aorta was studied by recording the isotonic contraction and radioimmunoassaying the levels of cyclic nucleotides. Isocorydine induced a relaxation with a concentration dependent manner in the isolated rabbit aortic strips precontracted by norepinephrine (NE, 1 μmol·L -1 ) or KCl (30 mmol·L -1 ), the EC 50 was (12.6±4.4) and (447±38)μmol·L -1 , respectively. The effect of isocorydine on the precontraction induced by NE was 36 times as strong as that by KCl. The relaxing effect of isocorydine on the strip of rabbit aorta precontracted by NE was partially inhibited by methylene blue (10 μmol·L -1 ), but was not affected by glibenclamide, indomethacin, propranolol or N L nitro arginine. Furthermore, isocorydine (10, 100 μmol·L -1 ) increased the levels of cGMP, and the effect were inhibited by methylene blue. The results suggest that the vasodilative mechanism of isocorydine be related to accumulation of cGMP by activating guanylate cyclase.