Lauth D, Hertting G, Jackisch R
Institute of Pharmacology, University of Freiburg, Germany.
Eur J Pharmacol. 1993 May 12;236(1):165-6. doi: 10.1016/0014-2999(93)90242-a.
The release of tritiated noradrenaline, evoked by stimulation of rat hippocampus slices with 3,4-diaminopyridine (200 microM, 2 min), was enhanced by the nitric oxide (NO) synthase substrate, L-arginine (but not by D-arginine), by NO donors (sodium nitroprusside, 3-morpholino-sydnonimine), and by 8-Br-cGMP. The effect of L-arginine was stereospecifically antagonized by NG-nitro-L-arginine, which given alone was inhibitory. From these findings we conclude that endogenously formed NO facilitates 3,4-diaminopyridine-evoked noradrenaline release in rat hippocampus.
用3,4 - 二氨基吡啶(200微摩尔,2分钟)刺激大鼠海马切片所诱发的氚标记去甲肾上腺素释放,可被一氧化氮(NO)合酶底物L - 精氨酸(而非D - 精氨酸)、NO供体(硝普钠、3 - 吗啉代 - 西多硝胺)以及8 - 溴 - 环鸟苷酸增强。L - 精氨酸的作用被NG - 硝基 - L - 精氨酸立体特异性拮抗,单独给予NG - 硝基 - L - 精氨酸具有抑制作用。从这些发现我们得出结论,内源性生成的NO促进大鼠海马中3,4 - 二氨基吡啶诱发的去甲肾上腺素释放。