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Nitric oxide and pulmonary hypertension.

The constitutive release of NO by the endothelium plays a key role in maintaining normal low basal pulmonary vascular tone and countering hypoxic vasoconstrictive tone in many mammals and in humans. Many, but not all, studies have suggested that reduced availability of NO contributes to the increased pulmonary vascular resistance that occurs in experimental models and in humans with pulmonary hypertension. Potential mechanisms limiting the activity of NO include L-arginine deficiency and a reduction in eNOS expression or message stability. Inhaled NO therapy may overcome some of these abnormalities, improving oxygenation and reducing pulmonary artery pressure in patients with primary and secondary forms of pulmonary hypertension.