Key result
Angiotensin II-driven vascular reactive oxygen species generation induces and accelerates functional and structural vascular injury in hypertension.
This review highlights the mechanisms by which angiotensin II-driven oxidative stress contributes to vascular damage in hypertension.
May inform ROS-targeted therapies in hypertension; leaves open clinical validation in prospective trials.
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.
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Virdis et al. (2011) conducted a review in Hypertension. Angiotensin II was evaluated. Angiotensin II-driven vascular reactive oxygen species generation induces and accelerates functional and structural vascular injury in hypertension.
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