Toda N, Ayajiki K, Yoshida K, Kimura H, Okamura T
Department of Pharmacology, Shiga University of Medical Sciences, Ohtsu, Japan.
Circ Res. 1993 Jan;72(1):206-13. doi: 10.1161/01.res.72.1.206.
Histochemical study revealed that transcutaneous injection of ethanol into the vicinity of the pterygopalatine ganglion greatly decreased the positive staining for NADPH diaphorase activity after 1 week in the ipsilateral ganglion of a dog and abolished the staining of perivascular nerves in the middle and posterior cerebral arteries. Transmural electrical stimulation or nicotine produced a relaxation in middle and posterior cerebral arteries isolated from the side with the nontreated ganglion (control side), whereas the relaxation was abolished or reversed to a contraction in the arteries from the side with the ethanol-treated ganglion. Nitric oxide-induced relaxations did not differ in the arteries from both sides. The response to nerve stimulation of the control arteries was suppressed by treatment with NG-nitro-L-arginine (L-NA), an inhibitor of nitric oxide synthase, and the inhibition was reversed by L-arginine. Nicotine produced a contraction followed by a relaxation in central retinal arterial strips obtained from the control side; the relaxation was abolished and the contraction was potentiated in the arteries from the treated side. The nicotine-induced relaxation was abolished by L-NA, and the contraction was suppressed by phentolamine. On the other hand, the nicotine-induced relaxation in superficial temporal arteries, susceptible to L-NA, was not attenuated by treatment with ethanol. The findings obtained so far support our hypothesis that nitric oxide released from the vasodilator nerve acts as a transmitter to produce arterial smooth muscle relaxation and suggest that the nerve fibers to the cerebral and retinal arteries arise from the pterygopalatine ganglion.
组织化学研究显示，经皮向翼腭神经节附近注射乙醇，1周后犬同侧神经节中烟酰胺腺嘌呤二核苷酸磷酸黄递酶（NADPH diaphorase）活性的阳性染色显著减少，大脑中动脉和后动脉血管周围神经的染色消失。透壁电刺激或尼古丁可使取自未处理神经节侧（对照侧）的大脑中动脉和后动脉舒张，而取自乙醇处理神经节侧的动脉，其舒张作用消失或转为收缩。一氧化氮诱导的舒张在两侧动脉中无差异。对照动脉对神经刺激的反应可被一氧化氮合酶抑制剂NG-硝基-L-精氨酸（L-NA）抑制，L-精氨酸可逆转这种抑制作用。尼古丁可使取自对照侧的视网膜中央动脉条先收缩后舒张；取自处理侧的动脉，其舒张作用消失，收缩作用增强。尼古丁诱导的舒张被L-NA消除，收缩作用被酚妥拉明抑制。另一方面，对L-NA敏感的颞浅动脉中，尼古丁诱导的舒张未因乙醇处理而减弱。目前的研究结果支持我们的假说，即血管舒张神经释放的一氧化氮作为递质产生动脉平滑肌舒张，并提示支配大脑和视网膜动脉的神经纤维起源于翼腭神经节。
