Аннотация:Background Reactive oxygen species (ROS), including those produced by NADPH oxidase (NOX), play an important vasomotor role, especially at early postnatal period. Mechanisms for regulating vascular tone can change significantly due to neonatal asphyxia and accompanying hypoxia. We tested the hypothesis that normobaric hypoxia (8% O2) for 2 h at the second day of life changes the functional contribution of NOX-derived ROS to the regulation of agonist-induced contraction in early postnatal rats.MethodsWe studied saphenous arteries from 11- to 14-day-old male offspring using isometric myography and Western blotting and assessed the content of biochemical parameters in blood serum.Results The values of main biochemical parameters in blood serum and the protein content of NOXs and superoxide dismutases in arterial tissue did not differ between “Control” and “Hypoxia” pups. The NOX inhibitor VAS2870 equally reduced the contractile responses of arteries to α1-adrenoceptor agonist methoxamine in “Control” and “Hypoxia” pups, but its effect was more pronounced in the arteries from “Hypoxia” pups when vasocontraction was evoked by the agonist of thromboxane A2 receptors U46619.Conclusion Perinatal hypoxia at the second day of life increases procontractile influence of NOX-derived ROS to the regulation of U46619-induced vasocontraction in the systemic arteries at early postnatal ontogenesis.