Pediatric hypertension is increasingly recognized as a complex condition shaped by both systemic and cellular factors, with oxidative stress emerging as a key driver of vascular dysfunction. In both their primary and secondary forms, reactive oxygen species (ROS) disrupt redox homeostasis, impair endothelial signaling, and promote inflammation and tissue remodeling. Metabolic dysregulation, renal pathology, and early-life stressors contribute to the accumulation of ROS through pathways involving NADPH oxidases, mitochondrial dysfunction, xanthine oxidase activity, and altered arginine metabolism. These mechanisms converge on the vasculature, diminishing nitric oxide bioavailability and promoting hypertensive phenotypes. Beyond disease initiation, redox imbalance influences the response to treatment, surgical outcomes, and long-term cardiovascular risk. By further elucidating these mechanisms, the complex relationship between oxidative stress, vascular biology, and blood pressure regulation in children may be more clearly defined and more effectively targeted in clinical management.