Idiopathic pulmonary arterial hypertension (IPAH) is associated with lower levels of the pulmonary vasodilator nitric oxide (NO) and its biochemical reaction products (NO2-, NO3-) in part due to reduction of pulmonary endothelial NO synthesis. However, NO levels are also determined by consumptive reactions, such as with superoxide to form peroxynitrite that subsequently may generate stable products of nitrotyrosine (Tyr-NO2) and/or NO3-. In this context, superoxide dismutase (SOD) preserves NO in vivo by scavenging superoxide and preventing consumptive reactions. Here, we hypothesized that reactive oxygen species (ROS) consumption of NO may contribute to the low NO and development of pulmonary hypertension. To test this, nitrotyrosine and antioxidants glutathione [GSH], glutathione peroxidase [GPx], catalase and superoxide dismutase [SOD] were evaluated in IPAH and healthy controls. SOD and GPx activities were decreased in IPAH lungs [all p<0.05] while catalase and GSH were similar among the groups [all p>0.2]. SOD activity was related to exhaled NO [R =0.72, p=0.002], and inversely related to bronchoalveolar lavage (BAL) NO3- [-0.73; p=0.04]. Pulmonary artery pressure could be predicted by a regression model incorporating SOD, GPx, and NO3- values (R2 = 0.96, p=0.01). These findings suggest that SOD and GPx are associated with alterations of NO and pulmonary artery pressure in IPAH.