For the lungs to perform their gas-exchange function efficiently, the pulmonary circulation must maintain low pulmonary arterial and capillary pressure while accommodating the entire cardiac output (QT). In addition perfusion (&) must be distributed among the ventilated units so that local & is appropriate for local ventilation (V) and so that the blood spends an adequate amount of time in close apposition to alveolar gas. To a large extent these conditions are achieved as a result of the anatomical and passive mechanical properties of the normal pulmonary vascular bed. These properties are reasonably well optimized within the context of the normal right and left heart function in spite of the large variations in QT, the difference in density between blood and air, and the inherent difficulties involved in distributing & evenly among the elements of a complex parallel network. The pulmonary vascular bed also has the machinery for active control of vessel tone. Vasomotor tone is low in the normal lung. Thus, in contrast to systemic vascular beds, in which vasodilation in response to the need for increased & has received much of the attention, the mechanisms and consequences of vasoconstriction have been of major concern in the studies of pulmonary circulation. With the possible exception of the vasoconstriction resulting