Hypoxic pulmonary vasoconstriction (HPV) is modulated by interaction of nitric oxide (NO) production and release of reactive oxygen species (ROS). It is known that antioxidant Tempol inhibits HPV. This can be caused by two possible ways: 1.As reaction of superoxide and NO produces potent vasoconstrictor -peroxinitrite, direct inhibition of superoxide production by Tempol reduces vascular tonus. 2.Inhibition of superoxide production decreases consumption of NO for peroxinitrite production. Increase in NO concentration diminishes HPV. In isolated salt solution perfused lungs we compared pulmonary vasoconstriction before and after administration of Tempol (50mg/kg) into perfusate. To investigate the effect of NO on the intensity of hypoxic pulmonary vasoconstriction, we inhibited the NO production by adding L-NAME into the perfusate. We found significant decrease of vasoconstriction response induced by hypoxia and angiotensin II after administration of Tempol. We didn't find any differences in HPV inhibition caused by L-NAME administration. Conclusion: SOD mimetic Tempol inhibits Angiotensin II and acute hypoxia induced vasoconstriction by reduction of ROS concentration. This effect does not depend on actual release of NO.