Reactive oxygen species in vascular biology: implications in hypertension

• Published in: Histochemistry and cell biology 2004-10, Vol.122 (4), p.339-352
• Main Authors: Touyz, R M, Schiffrin, E L
• Format: Article
• Language: English
• Subjects: Arteriosclerosis - complications; Arteriosclerosis - metabolism; Arteriosclerosis - pathology; Blood Vessels - metabolism; Blood Vessels - pathology; Cell Movement - physiology; Cell Proliferation; Endothelial Cells - metabolism; Endothelial Cells - pathology; Fibroblasts - metabolism; Fibroblasts - pathology; Humans; Hypertension - etiology; Hypertension - metabolism; Hypertension - pathology; Myocytes, Smooth Muscle - metabolism; Myocytes, Smooth Muscle - pathology; NADPH Oxidases - metabolism; Reactive Oxygen Species - metabolism
• ISSN: 0948-6143; 1432-119X
• DOI: 10.1007/s00418-004-0696-7

Reactive oxygen species (ROS), including superoxide (*O2-), hydrogen peroxide (H2O2), and hydroxyl anion (OH-), and reactive nitrogen species, such as nitric oxide (NO) and peroxynitrite (ONOO-), are biologically important O2 derivatives that are increasingly recognized to be important in vascular biology through their oxidation/reduction (redox) potential. All vascular cell types (endothelial cells, vascular smooth muscle cells, and adventitial fibroblasts) produce ROS, primarily via cell membrane-associated NAD(P)H oxidase. Reactive oxygen species regulate vascular function by modulating cell growth, apoptosis/anoikis, migration, inflammation, secretion, and extracellular matrix protein production. An imbalance in redox state where pro-oxidants overwhelm anti-oxidant capacity results in oxidative stress. Oxidative stress and associated oxidative damage are mediators of vascular injury and inflammation in many cardiovascular diseases, including hypertension, hyperlipidemia, and diabetes. Increased generation of ROS has been demonstrated in experimental and human hypertension. Anti-oxidants and agents that interrupt NAD(P)H oxidase-driven *O2- production regress vascular remodeling, improve endothelial function, reduce inflammation, and decrease blood pressure in hypertensive models. This experimental evidence has evoked considerable interest because of the possibilities that therapies targeted against reactive oxygen intermediates, by decreasing generation of ROS and/or by increasing availability of antioxidants, may be useful in minimizing vascular injury and hypertensive end organ damage. The present chapter focuses on the importance of ROS in vascular biology and discusses the role of oxidative stress in vascular damage in hypertension.