Toda N, Yoshida K, Okamura T
Department of Pharmacology, Shiga University of Medical Sciences, Ohtsu, Japan.
Naunyn Schmiedebergs Arch Pharmacol. 1991 Feb;343(2):221-4. doi: 10.1007/BF00168614.
Dog temporal artery strips without endothelium responded to transmural electrical stimulation with a contraction which was potentiated by NG-nitro-L-arginine (L-NNA). The noradrenaline-induced contraction and the release of 3H-noradrenaline were not affected. The stimulation-induced contraction was reversed to a relaxation by phentolamine. The relaxation was not influenced by timolol and atropine but inhibited by L-NNA; L-arginine abolished the inhibition. Transmural stimulation released NOx from the arteries, the release being abolished by L-NNA. Potentiation by L-NNA of the neurally-induced contraction appears to be due to elimination of NO produced by non-adrenergic, non-cholinergic vasodilator nerve activation.
无内皮的犬颞动脉条对跨壁电刺激产生收缩反应，该反应可被NG-硝基-L-精氨酸（L-NNA）增强。去甲肾上腺素诱导的收缩和3H-去甲肾上腺素的释放不受影响。酚妥拉明可使刺激诱导的收缩转变为舒张。该舒张不受噻吗洛尔和阿托品影响，但被L-NNA抑制；L-精氨酸可消除这种抑制作用。跨壁刺激可使动脉释放NOx，L-NNA可消除这种释放。L-NNA对神经诱导收缩的增强作用似乎是由于消除了非肾上腺素能、非胆碱能血管舒张神经激活产生的NO。
