Abstract
The high pulmonary vascular resistance (PVR) of atelectatic, hypoxic, fetal lungs limits intrauterine pulmonary blood flow (PBF) to less than 10% of combined right and left ventricular output. At birth, PVR decreases precipitously to accommodate the entire cardiac output. The present review focuses on the role of endothelium-derived nitric oxide (NO), prostacyclin, and vascular smooth muscle potassium channels in mediating the decrease in PVR that occurs at birth, and in maintaining reduced pulmonary vasomotor tone during the neonatal period. The contribution of vasodilator and vasoconstrictor modulator activity to the pathophysiology of neonatal pulmonary hypertension is also addressed.