Levin R M, Hypolite J, Broderick G A
Division of Urology, University of Pennsylvania School of Medicine, Philadelphia.
J Androl. 1994 Jan-Feb;15(1):36-40.
Erectile function (erection and detumescence) involves the complex interaction of direct neuronal stimulation of corporal smooth muscle, neurohumoral release of specific endothelial contractile and relaxant factors, and secondary modulation by a variety of putative neuropeptides and vasoactive modulators including nitric oxide. The specific aim of the current study was to determine the relative contribution of nitric oxide, adrenergic, purinergic, and cholinergic stimulation in the relaxant response to field stimulation. The results demonstrate that virtually all of the inhibitory effects of field-stimulated relaxation could be explained by the release of nitric oxide. L-NAME (L-NG-nitro arginine methyl ester, a competitive inhibitor of NO synthase) reduced field-stimulated relaxation by over 95% at all frequencies. Neither atropine nor propranolol (or the combination of the two) had any significant effect on field-stimulated relaxation. L-NAME blocked both field-stimulated relaxation and bethanechol-stimulated relaxation. However, methylene blue (a guanyl cyclase inhibitor) was significantly more potent at blocking bethanechol-stimulated relaxation than field-stimulated relaxation. Neither L-NAME nor methylene blue had any effect on nitroprusside (a direct liberator of NO) nor ATP-stimulated relaxation. Isoproterenol had only a minor inhibitory effect on phenylephrine-contracted tissue. These data suggest that 1) Methylene blue, which inhibits guanyl cyclase, is a relatively poor inhibitor of field-stimulated relaxation. 2) L-NAME is a potent inhibitor of NO synthesis and can in a dose-dependent fashion inhibit over 95% of field-stimulated relaxation. 3) Equipotent relaxation of corporal smooth muscle can be effected through pharmacologic stimulation with ATP (2 mM), nitroprusside (200 microM), and field stimulation (32 Hz).(ABSTRACT TRUNCATED AT 250 WORDS)
勃起功能（勃起与消肿）涉及海绵体平滑肌的直接神经刺激、特定内皮收缩和舒张因子的神经体液释放，以及包括一氧化氮在内的多种假定神经肽和血管活性调节剂的次级调节之间的复杂相互作用。本研究的具体目的是确定一氧化氮、肾上腺素能、嘌呤能和胆碱能刺激在对场刺激的舒张反应中的相对贡献。结果表明，场刺激舒张的几乎所有抑制作用都可以用一氧化氮的释放来解释。L-NAME（L-NG-硝基精氨酸甲酯，一种一氧化氮合酶的竞争性抑制剂）在所有频率下均使场刺激舒张减少超过95%。阿托品和普萘洛尔（或两者联合使用）对场刺激舒张均无显著影响。L-NAME阻断场刺激舒张和氨甲酰甲胆碱刺激的舒张。然而，亚甲蓝（一种鸟苷酸环化酶抑制剂）在阻断氨甲酰甲胆碱刺激的舒张方面比场刺激舒张更有效。L-NAME和亚甲蓝对硝普钠（一种一氧化氮的直接释放剂）和ATP刺激的舒张均无影响。异丙肾上腺素对去氧肾上腺素收缩的组织只有轻微的抑制作用。这些数据表明：1）抑制鸟苷酸环化酶的亚甲蓝是场刺激舒张的相对较弱的抑制剂。2）L-NAME是一氧化氮合成的有效抑制剂，并且可以以剂量依赖的方式抑制超过95%的场刺激舒张。3）通过用ATP（2 mM）、硝普钠（200 microM）和场刺激（32 Hz）进行药理刺激，可以实现海绵体平滑肌的等效舒张。（摘要截断于250字）
