Nitric oxide and pulmonary circulation.

The aim of this review is to outline the characteristics of pulmonary circulation in health and disease and to define the value of exhaled NO (eNO) as a means to assess the involvement of pulmonary circulation in pathology. The discovery of the endocrine role of the endothelium has generated great interest in its potential role in regulating the vascular tone of the pulmonary vascular bed. Nitric oxide (NO)-mediated, endothelium-dependent relaxation has been demonstrated in the pulmonary arteries of animals and humans. Changes in the NO pathway in pulmonary hypertension are not completely understood. It is clear that NO has an important role in modulating the response to acute hypoxia, increased flow, and shear stress. The amount of exhaled NO (eNO) in different species may be easily measured, reflecting the overall NO metabolism from the lung (thus including epithelial, endothelial and other cell activity). The development of pulmonary hypertension secondary to systemic (systemic sclerosis, chronic heart failure) or pulmonary (COPD) diseases appears to be associated with a decrease in eNO production both at rest and during exercise. Chronic inhalation of NO appears to protect against pulmonary hypertension in animal models. Exhaled NO is attracting interest for its in vivo ability to represent the features of pulmonary circulation in pathology.