As arterial O₂ (PaO₂) is reduced during systemic hypoxia, right ventricular (RV)work and O₂ consumption (MVO₂) increase. Mechanisms responsible for maintaining RV O₂ demand/supply balance during hypoxia have not been delineated. To address this problem, right coronary (RC) blood flow and RV O₂ extraction were measured in nine conscious, instrumented dogs exposed to normobaric hypoxia. Catheters were implanted in the right ventricle for measuring pressure, in the ascending aorta for measuring arterial pressure and for sampling arterial blood, and in a RC vein. A flow transducer was placed around the RC artery. After recovery from surgery, the dogs were exposed to hypoxia in a chamber ventilated with N₂, and blood samples and hemodynamic data were collected as chamber O₂ was reduced progressively to 8-10 %. Following control measurements, the chamber was opened, and the dog was allowed to recover. N-nitro-L-arginine (LNA) was then administered (35 mg/kg, via RV catheter) to inhibit nitric oxide (NO) production, and the hypoxia protocol was repeated. RC blood flow increased during hypoxia due to coronary vasodilation since RC conductance increased from 0.65 ± 0.05 to 1.32 ± 0.12 ml/min/100 g. LNA blunted the hypoxia-induced increase in RC conductance. RV O₂ extraction remained constant at 64 ± 4 % as PaO₂ was decreased, but after LNA, extraction increased to 70 ± 3 % during normoxia, and then to 78 ± 3% during hypoxia. RV MVO₂ increased during hypoxia, but after LNA, MVO₂ was lower at any respective PaO₂. The relationship between heart rate times RV systolic pressure (rate-pressure product) and RV MVO₂was not altered by LNA. To account for LNAmediated decreases in RV MVO₂, O₂ demand/supply variables were plotted as functions of MVO₂. The slope of the conductance/MVO₂ relationship was depressed by LNA (P=0.03), whereas the slope of the extraction/MVO₂ relationship increased (P=0.003). In summary, increases in RV MVO₂ during hypoxia are met normally by increasing RC blood flow. When NO synthesis is blocked, the large RV O₂extraction reserve is mobilized to maintain RV O₂ demand/supply balance. We conclude that NO contributes to RC vasodilation during systemic hypoxia.