Reactive oxygen species are oxygen derivates and play an active role in vascular biology. These compounds are generated within the vascular wall, at the level of endothelial and vascular smooth muscle cells, as well as by adventitial fibroblasts. In healthy conditions, ROS are produced in a controlled manner at low concentrations and function as signaling molecules regulating vascular contraction-relaxation and cell growth. Physiologically, the rate of ROS generation is counterbalanced by the rate of elimination. In hypertension, an enhanced ROS generation occurs, which is not counterbalanced by the endogenous antioxidant mechanisms, leading to a state of oxidative stress. In the present paper, major angiotensin II-induced vascular ROS generation within the vasculature, and relative sources, will be discussed. Recent development of signalling pathways whereby angiotensin II-driven vascular ROS induce and accelerate functional and structural vascular injury will be also considered. 1. Introduction Hypertension is associated with increased peripheral resistance, resulting predominantly from functional, structural, and mechanical alterations at the level of small-resistance arteries. Functional alterations, which include an impaired endothelial function, are mainly assessed as an impaired acetylcholine-induced, endothelium-dependent relaxation. Vascular structural changes include vascular remodeling, secondary to an increased cell growth, cell migration, and low-grade vascular inflammation [1, 2]. In particular, an increased media-to-lumen ratio (M/L) may result from a reduced outer diameter that narrows the lumen without net growth (eutrophic remodeling) or from a thicker media encroaching on the lumen (hypertrophic remodeling) [1, 2]. Another hallmark of hypertension-induced structural abnormalities is represented by changes in the mechanical properties of arteries, with particular regard for increased stiffness [3]. Vascular fibrosis is critically important in the determinism of vascular structural modifications, and it involves changes in extracellular matrix (ECM) components, including collagen type I and III, elastin, and fibronectin. An increase in collagen and fibronectin and a decrease in elastin contents have been shown in the media of small arteries from hypertensive animals [3–5]. It is widely accepted that angiotensin (Ang) II, traditionally involved in modulating blood pressure and electrolyte homeostasis, is also greatly implicated in the pathogenesis of endothelial dysfunction and vascular remodeling [6–8]. This concept is strengthened by
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