Since the discovery of
nitric oxide (NO), an intracellular signal transmitter, the role of NO has been investigated in various organs. In the respiratory system, NO derived from the constitutive type of
NO synthase (cNOS, NOS1, NOS3) induces bronchodilation and pulmonary vasodilatation to maintain homeostasis. In contrast, the roles of excessive NO derived from the inducible type of NOS (iNOS, NOS2) in airway and
lung inflammation in inflammatory
lung diseases including
bronchial asthma and
chronic obstructive pulmonary disease (
COPD) are controversial. In these inflammatory
lung diseases, excessive nitrosative stress has also been observed. In
asthma, some reports have shown that nitrosative stress causes airway
inflammation,
airway hyperresponsiveness, and
airway remodeling, which are the features of
asthma, whereas others have demonstrated the anti-inflammatory role of NO derived from NOS2. In the case of refractory
asthma, more nitrosative stress has been reported to be observed in such airways compared with that in well-controlled asthmatics. In
COPD,
reactive nitrogen species (RNS), which are NO and NO-related molecules including
nitrogen dioxide and
peroxynitrite, cause
lung inflammation, oxidative stress, activation of
matrix metalloproteinase, and inactivation of
antiprotease, which are involved in the pathophysiology of the disease. In the present paper, we review the physiological and pathophysiological effects of NO and NO-related molecules in the respiratory system and in inflammatory
lung diseases.