Endothelium-derived nitric oxide (NO) is a powerful pulmonary vasodila
tor which also prevents adhesion and agregation of platelets, controls
growth of smooth muscle and influences the expression of growth promo
ting and vasoactive substances. Impaired endothelial NO production con
tributes to pulmonary vasoconstriction and vascular remodeling in seve
ral forms of pulmonary hypertension, notably neonatal and hypoxic pulm
onary hypertension. While chronic NO inhibition in utero produces pers
istent pulmonary hypertension in newborn lambs, chronic inhalation of
NO in rats exposed to hypoxia opposes development of pulmonary hyperte
nsion. Exogenous NO gas delivered via the airspaces is a selective pul
monary vasodilator now employed as therapy in various lung disorders.