Reactive Oxygen Species Influence Vascular Structure and are Proinflammatory

In hypertension, oxidative stress promotes vascular smooth muscle cell proliferation and hypertrophy, collagen deposition, and alterations in activity of matrix metalloproteinases (MMP), which lead to arterial remodeling (Fig. 4.3). Superoxide anion and H2O2 stimulate growth factor-like cellular responses, such as intracellular alkalinization, MAP kinase phosphorylation, and tyrosine kinase activation. H2O2 induces vascular smooth muscle cell DNA synthesis, increases expression of protooncogenes, and promotes cell growth.7,99 During vascular damage in hypertension when oxidative stress is increased redox-sen-sitive growth actions may lead to accelerated proliferation and hypertrophy, further contributing to vascular injury and remodeling.3,7 ROS also modulate vascular structure in hypertension by increasing deposition of extracellular matrix proteins, such as collagen and fibronectin. Superoxide anion and H2O2 influence activity of vascular MMP2 and MMP9, which promote degradation of basement membrane and elastin, respectively.112 Redox-sensitive inflammatory processes, including expression of proinflammatory molecules, such as vascular cell adhesion molecule-1 (VCAM-1) and monocyte chemotactic protein-1 (MCP-1), lipid peroxidation, and cell migration, further contribute to vascular remodeling in hypertension.113-115

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