L-硝基精氨酸对神经刺激所致大鼠肠系膜动脉反应的影响

目的观察大鼠肠系膜动脉对神经刺激引起的反应及其与NO的关系。方法：采用离体去除内皮血管实验方法，测定肠系膜动脉条的等容张力变化。结果：电刺激和化学（烟碱）刺激明显引起大鼠肠系膜动脉收缩，L－硝基精氨酸（L－NA，NO合成抑制剂）明显增强上述收缩反应，此增强作用可被L一精氨酸（NO供体）取消。L－NA对刺激交感神经末梢去甲肾上腺素的释放及对去甲肾上腺素的血管收缩作用均无明显影响。动脉条用哌唑嗪处理并用PGF(2a)部分收缩后，电刺激和烟碱均可引起血管舒张，此舒张效应可被L－NA抑制，该抑制作用又可为L-精氨酸逆转。结论：电刺激和化学（烟碱）刺激引起的动脉舒张效应为NO所致，并提示在大鼠肠系股动脉可能有与NO有关的血管扩张神经存在。

Modification by N~G-nitro-L-arginine to the response to nerve stimulation in rat mesenteric arteries

To observe the effects ofnerve stimulation on isolated mesenteric arterystrips of rats and their correlation with a nitricoxide. METHODS: The isometric tension of endothelium-denuded isolated mesenteric arterystrips from rats were measured by a forcedisplacement transducer. RESULTS: Rat mesen-teric artery strips responded to transmural elec-trical stimulation and nicotine with a contraction, which was potentiated by N--nitro-L-argi-nine (L-NA), a nitric oxide (NO) synthesis in-hibitor, but not by the D-enantiomer. L-argi-nine, but not D--arginine, reversed the potentia-tion. Release of norepinephrine evoked by adren-ergic nerve stimulation and contractile responseto exogenous norepinephrine were not increasedby L-NA. In the endothelium--denuded arterystrips treated with prazosin. electrical stimulation and nicotine produced a relaxation, whichwere abolished by L-NA. The inhibitions wereantagonized by L-arginine. Stimulation of nervesincreased the level of cGMP in the arteries.CONCLUSIONS: Rat mesenteric arteries are innervated by vasodilator correlating with NO andnoradrenergic vasoconstrictor nerves; the vasodilatation is mediated by NO released possiblyfrom nerves.