Toda N, Okamura T
Department of Pharmacology, Shiga University of Medical Sciences, Ohtsu, Japan.
Hypertension. 1992 Feb;19(2):161-6. doi: 10.1161/01.hyp.19.2.161.
Physiological importance in vasodilator innervation alleviating noradrenergic neurogenic vasoconstriction has not been clarified. Isolated monkey mesenteric artery strips denuded of the endothelium responded to nerve stimulation by electrical pulses or nicotine with a contraction, which was potentiated by Ng-nitro-L-arginine, a nitric oxide synthesis inhibitor, but not by the D-enantiomer. The potentiation was abolished by L-arginine. NG-Nitro-L-arginine did not potentiate the response to exogenous norepinephrine nor did it increase the release of [3H]norepinephrine from adrenergic nerves electrically stimulated. The contraction was reversed by treatment with phentolamine and guanethidine to a relaxation, which was abolished by NG-nitro-L-arginine. The inhibition was reversed by L- but not D-arginine. The relaxant response was not influenced by atropine, timolol, or indomethacin. These findings strongly suggest the importance of reciprocal nitric oxide-related (nitroxidergic) vasodilator and noradrenergic vasoconstrictor innervation in the regulation of monkey arterial tone.
血管舒张神经支配在减轻去甲肾上腺素能神经源性血管收缩中的生理重要性尚未阐明。去除内皮的离体猴肠系膜动脉条对电脉冲或尼古丁刺激神经产生收缩反应，一氧化氮合成抑制剂Nω-硝基-L-精氨酸可增强该反应，而其D-对映体则无此作用。L-精氨酸可消除这种增强作用。Nω-硝基-L-精氨酸既不能增强对外源性去甲肾上腺素的反应，也不能增加电刺激肾上腺素能神经释放[3H]去甲肾上腺素。酚妥拉明和胍乙啶处理可使收缩反应逆转成舒张反应，而Nω-硝基-L-精氨酸可消除该舒张反应。L-精氨酸而非D-精氨酸可逆转这种抑制作用。舒张反应不受阿托品、噻吗洛尔或吲哚美辛的影响。这些发现强烈提示，一氧化氮相关（硝氧能）血管舒张神经和去甲肾上腺素能血管收缩神经的相互支配在调节猴动脉张力中具有重要作用。
