Gibson A, Brave S R, McFadzean I, Tucker J F, Wayman C
Biomedical Sciences Division, King's College London, U.K.
Arch Int Pharmacodyn Ther. 1995 Jan-Feb;329(1):39-51.
Nonadrenergic noncholinergic (NANC) relaxations of the anococcygeus muscle are reduced by inhibitors of nitric oxide synthase (NOS). Since NOS can be detected within 6-hydroxydodpamine-resistant nerve tracts running through the muscle, it seems clear that these NANC relaxations result from activation of the L-arginine/NO pathway within the prejunctional nerve terminal, an example of so-called "nitrergic" transmission. However, a number of substances (hydroquinone, superoxide anions, hydroxocobalamin) profoundly reduce relaxations to exogenous NO but do not affect those to nitrergic field stimulation; such observations have raised questions over the nature of the substance actually released from the nitrergic nerves. Several possible explanations are discussed: (1) NO is released attached to a carrier molecule, perhaps in the form of a nitrosothiol; (2) NO is released in a modified redox form; (3) NO is released as a free radical, but is protected within the neuroeffector junction by other substances which preferentially interact with scavenger molecules; and (4) NO is released as a free radical and, because of a rapid and unhindered rate of diffusion over short distances (100-200 microM), it is less susceptible than exogenous NO to scavenger molecules. As yet, there is insufficient experimental evidence to decide which, if any, of these explanations is correct.
一氧化氮合酶（NOS）抑制剂可降低肛门尾骨肌的非肾上腺素能非胆碱能（NANC）舒张作用。由于在贯穿该肌肉的对6-羟基多巴胺耐药的神经束中可检测到NOS，因此很明显这些NANC舒张是由节前神经末梢内L-精氨酸/一氧化氮途径的激活所致，这是所谓“氮能”传递的一个例子。然而，一些物质（对苯二酚、超氧阴离子、羟钴胺素）可显著降低对外源性一氧化氮的舒张反应，但不影响对氮能场刺激的舒张反应；这些观察结果引发了关于从氮能神经实际释放的物质性质的疑问。文中讨论了几种可能的解释：（1）一氧化氮以附着于载体分子的形式释放，可能是以亚硝基硫醇的形式；（2）一氧化氮以修饰的氧化还原形式释放；（3）一氧化氮以自由基形式释放，但在神经效应器接头内受到其他优先与清除剂分子相互作用的物质的保护；（4）一氧化氮以自由基形式释放，并且由于在短距离（100 - 200微摩尔）内快速且不受阻碍的扩散速率，它比外源性一氧化氮更不易受到清除剂分子的影响。迄今为止，尚无足够的实验证据来确定这些解释中哪一个（如果有的话）是正确的。
