Dokita S, Morgan W R, Wheeler M A, Yoshida M, Latifpour J, Weiss R M
Section of Urology, Yale University School of Medicine, New Haven, Connecticut 06510.
Life Sci. 1991;48(25):2429-36. doi: 10.1016/0024-3205(91)90377-n.
Electrical field stimulation induced a relaxation response in female rabbit urethral smooth muscle strips precontracted with phenylephrine. The relaxation response was inhibited by tetrodotoxin, but not by atropine, propranolol, or hexamethonium. The relaxation response thus results from stimulation of inhibitory non-adrenergic, non-cholinergic nerves. The electrically induced relaxation response was inhibited by an inhibitor of nitric oxide biosynthesis, NG-nitro-L-arginine. This inhibition was overcome by addition of a precursor of nitric oxide, L-arginine. An inhibitor of soluble guanylate cyclase, methylene blue, reduced the relaxation response, and a selective cyclic GMP phosphodiesterase inhibitor, M & B 22948, potentiated the relaxation response. These data indicate that agents which affect the biosynthesis of nitric oxide are associated with the urethral relaxation response evoked by electrical field stimulation, and that cyclic GMP may mediate the relaxation response.
电场刺激可诱导预先用去氧肾上腺素预收缩的雌性兔尿道平滑肌条产生舒张反应。该舒张反应可被河豚毒素抑制,但不受阿托品、普萘洛尔或六甲铵抑制。因此,该舒张反应是由抑制性非肾上腺素能、非胆碱能神经的刺激所致。电诱导的舒张反应可被一氧化氮生物合成抑制剂NG-硝基-L-精氨酸抑制。添加一氧化氮前体L-精氨酸可克服这种抑制作用。可溶性鸟苷酸环化酶抑制剂亚甲蓝可降低舒张反应,而选择性环鸟苷酸磷酸二酯酶抑制剂M&B 22948可增强舒张反应。这些数据表明,影响一氧化氮生物合成的药物与电场刺激引起的尿道舒张反应有关,且环鸟苷酸可能介导该舒张反应。