Nitric oxide and asthma

Nitric oxide (NO) is both a free radical derived from oxygen and a paracrine factor playing a fundamental role in the mechanisms causing relaxation of smooth muscle cells. The complexity of physiological and physiopathological effects of NO in respiratory disease is partly due to the highly variable types of response with regards to : (i) expression of different isoforms of NO synthase, (ii) cellular source and molecular target of NO and (iii) the amount of NO produced. It is, however, demonstrated that NO synthesis is increased during bronchial inflammation, hence providing the rationale for measuring exhaled NO in patients with airways inflammatory disease such as asthma and bronchiectasis. It is also likely that inhibition of endogenous NO synthesis worsens a pre-existing bronchial hyperreactivity. However, inhaling exogenous NO does not seem to have clearcut beneficial effects in patients with asthma, as shown by the marginal increase in expiratory flow rates seen after Inhaled NO as compared with inhaled beta 2-agonists. Therefore, the ambivalence of the effects of NO, on one hand, and the relative lack of insight into its mechanisms, on the other hand, still as yet hamper the pharmacological use of NO in asthma.