Ito Y, Fujisawa K
Department of Pharmacology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Nihon Yakurigaku Zasshi. 1998 Apr;111(4):205-15. doi: 10.1254/fpj.111.205.
In the lung, there is increasing evidence that endogenous nitric oxide (NO) plays multiple roles in physiological control of airway functions, immune responses and host defense against infection, and it is also implicated in inflammatory disease of the airways. As elsewhere, it is generally accepted that NO derived from constitutive NO synthase (cNOS) is involved in physiological regulation of airway function, whereas NO derived from inducible NO synthase (iNOS) is involved in immune responses and inflammatory diseases of the airway. In this mini review, first we describe evidence showing the possible roles of NO and NO-related compounds in nonadrenergic noncholinergic (NANC) relaxation and inhibitory action on excitatory neuro-effector transmission, thereby indicating that NO derived from neuronal cNOS plays a role to provide "double braking" in bronchoconstrictions. Secondly, we will discuss the possible involvement of epithelial damage due to excessive NO production through iNOS in the genesis of airway hyperreactivity and airway inflammation.
在肺中，越来越多的证据表明内源性一氧化氮（NO）在气道功能的生理控制、免疫反应以及宿主抗感染防御中发挥多种作用，并且它也与气道炎症性疾病有关。与其他地方一样，人们普遍认为，由组成型一氧化氮合酶（cNOS）产生的NO参与气道功能的生理调节，而由诱导型一氧化氮合酶（iNOS）产生的NO则参与气道的免疫反应和炎症性疾病。在这篇小型综述中，首先我们描述证据表明NO及与NO相关的化合物在非肾上腺素能非胆碱能（NANC）舒张以及对兴奋性神经效应器传递的抑制作用中可能发挥的作用，从而表明神经元cNOS产生的NO在支气管收缩中起到“双重制动”的作用。其次，我们将讨论通过iNOS产生的过量NO导致的上皮损伤可能参与气道高反应性和气道炎症的发生。
