Reactive oxygen species (ROS), in addition to their known role in the pathogenesis of many diseases, also have regulatory effects in the cardiovascular system including the control of vascular tone [1,2]. Depending on whether the vessel belongs to the pulmonary or systemic circulation, the diameter/branching order of the vessel, concentration of ROS and the compartment of their production within the cell, ROS can increase or decrease vascular tone, which is discussed in detail in previously published reviews [[1], [2], [3]]. It is worth noting, however, that the latter is indicated mainly for a mature vascular system.

The transition from placental to pulmonary respiration at birth is accompanied by a sharp increase in oxygenation of organs and tissues, which can lead to excess production of ROS [4]. Various organs and tissues of the newborn may be damaged as a result of this oxidative stress, which is called “oxygen radical disease in newborn” [5]. For example, in pulmonary circulation of newborns, the influence of ROS limits endothelium-dependent vasorelaxation [[6], [7], [8], [9]] and may contribute to the development of neonatal pulmonary hypertension - one of the leading causes of death among infants [5,10]. At the same time, several important adaptive reactions of the newborn organism are largely realized with the participation of ROS. Thus, it has been shown that the contraction of the ductus arteriosus, necessary for the separation of the two fetal circulations, is largely due to the influence of ROS [11]. In systemic circulation, ROS participate in so-called brain-sparing effect. This is a vital response that redistribute cardiac output to cerebral circulation thereby protecting the fetal brain from acute hypoxia during delivery [12]. Brain-sparing effect matures to the end of fetal development and then ceases in early postnatal ontogenesis [13]. Besides systemic mechanisms, brain-sparing effect is due to the local influence of ROS. Hypoxia leads to ROS generation in peripheral arteries, which reduce the bioavailability of NO produced by the endothelium, and, therefore, induce vasoconstriction [14,15]. However, to the best of our knowledge, nothing is known about the role of ROS in the regulation of the tone in systemic circulation during early postnatal ontogenesis in conditions of sufficient oxygen supply.

NADPH oxidase (NOX) is a key source of ROS in vascular cells [2]. It has been proven that ROS produced by NADPH oxidase take part in the processes of angiogenesis [16,17] and differentiation of arterial smooth muscle cells into a contractile phenotype [18,19]. In other words, NADPH oxidase-derived ROS regulate the processes of development and maturation of vascular system that are actively occurring in the organism during the period of early postnatal ontogenesis. In this regard, it can be assumed, that the production of ROS in the systemic vessels of newborns is greater than in adults, as well as their vasomotor role. Importantly, antioxidant therapy is commonly used for prevention the consequences of oxidative stress in newborn [5], but it does not take into account potential vasoregulatory role of ROS in the systemic vessels at early postnatal period, which indicates the need and significance to address this issue. Therefore, in this study we tested the hypothesis that the functional contribution of ROS produced by NADPH oxidases to the regulation of the tone of peripheral arteries in rats during early postnatal ontogenesis is greater than in adult animals.