犬鼻黏膜中的一氧化氮能血管舒张神经。

Nitroxidergic vasodilator nerve in the canine nasal mucosa.

作者信息

Watanabe H, Tsuru H, Kawamoto H, Yajin K, Sasa M, Harada Y

机构信息

Department of Otorhinolaryngology, Hiroshima University School of Medicine, Japan.

出版信息

Life Sci. 1995;57(10):PL109-12. doi: 10.1016/0024-3205(95)02038-k.

DOI:10.1016/0024-3205(95)02038-k

PMID:7643713

Abstract

The canine nasal mucosa was studied by in vitro bioassay. Non-adrenergic, non-cholinergic (NANC) vasodilator response to transmural electrical stimulation was observed in the presence of guanethidine and atropine. This vasodilator response was abolished by NG-nitro-L-arginine (L-NA) which is an inhibitor of nitric oxide (NO) formation but not by NG-nitro-D-arginine. The inhibitory effect of L-NA was partially reversed by treatment with L-arginine but not with D-arginine. The vasodilator response was significantly suppressed by tetrodotoxin. The present results indicate that NO may mediate neurogenic vasodilation in the canine nasal mucosa.

摘要

通过体外生物测定法对犬鼻黏膜进行了研究。在胍乙啶和阿托品存在的情况下，观察到对跨壁电刺激的非肾上腺素能、非胆碱能（NANC）血管舒张反应。这种血管舒张反应被一氧化氮（NO）形成抑制剂NG-硝基-L-精氨酸（L-NA）消除，但不被NG-硝基-D-精氨酸消除。L-精氨酸处理可部分逆转L-NA的抑制作用，而D-精氨酸则不能。河豚毒素可显著抑制血管舒张反应。目前的结果表明，NO可能介导犬鼻黏膜的神经源性血管舒张。