Hypertension. 2003;42:1075-1081
Published online before print October 27, 2003, doi: 10.1161/01.HYP.0000100443.09293.4F
Published online before print October 27, 2003, doi: 10.1161/01.HYP.0000100443.09293.4F
(Hypertension. 2003;42:1075.)
© 2003 American Heart Association, Inc.
Brief Reviews |
Reactive Oxygen Species in the Vasculature
Molecular and Cellular Mechanisms
From the Department of Medicine, Division of Cardiology, Emory University School of Medicine, Atlanta, Ga.
Correspondence to Kathy K. Griendling, Emory University, Division of Cardiology, 319 WMB, 1639 Pierce Drive, Atlanta, GA 30322. E-mail kgriend{at}emory.edu
Accumulating evidence indicates that reactive oxygen species (ROS) play major roles in the initiation and progression of cardiovascular dysfunction associated with diseases such as hyperlipidemia, diabetes mellitus, hypertension, ischemic heart disease, and chronic heart failure. ROS produced by migrating inflammatory cells as well as vascular cells (endothelial cells, vascular smooth muscle cells, and adventitial fibroblasts) have distinct functional effects on each cell type. These include cell growth, apoptosis, migration, inflammatory gene expression, and matrix regulation. ROS, by regulating vascular cell function, can play a central role in normal vascular physiology, and can contribute substantially to the development of vascular disease.
Key Words: antioxidants • vascular disease • muscle, smooth, vascular • endothelium • free radicals • macrophages • oxidative stress
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 L. C. Santarelli, J. Chen, S. H. Heinemann, and T. Hoshi The {beta}1 Subunit Enhances Oxidative Regulation of Large-Conductance Calcium-activated K+ Channels J. Gen. Physiol., September 27, 2004; 124(4): 357 - 370. [Abstract] [Full Text] [PDF]
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R. M. Touyz Reactive Oxygen Species, Vascular Oxidative Stress, and Redox Signaling in Hypertension: What Is the Clinical Significance? Hypertension, September 1, 2004; 44(3): 248 - 252. [Abstract] [Full Text] [PDF]
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D. H. Endemann and E. L. Schiffrin Endothelial Dysfunction J. Am. Soc. Nephrol., August 1, 2004; 15(8): 1983 - 1992. [Abstract] [Full Text] [PDF]
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E. L. Schiffrin and R. M. Touyz From bedside to bench to bedside: role of renin-angiotensin-aldosterone system in remodeling of resistance arteries in hypertension Am J Physiol Heart Circ Physiol, August 1, 2004; 287(2): H435 - H446. [Full Text] [PDF]
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G. S. Jose, M. U. Moreno, S. Olivan, O. Beloqui, A. Fortuno, J. Diez, and G. Zalba Functional Effect of the p22phox -930A/G Polymorphism on p22phox Expression and NADPH Oxidase Activity in Hypertension Hypertension, August 1, 2004; 44(2): 163 - 169. [Abstract] [Full Text] [PDF]
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 G. Wang, J. Anrather, J. Huang, R. C. Speth, V. M. Pickel, and C. Iadecola NADPH Oxidase Contributes to Angiotensin II Signaling in the Nucleus Tractus Solitarius J. Neurosci., June 16, 2004; 24(24): 5516 - 5524. [Abstract] [Full Text] [PDF]
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G. Ceolotto, M. Bevilacqua, I. Papparella, E. Baritono, L. Franco, C. Corvaja, M. Mazzoni, A. Semplicini, and A. Avogaro Insulin Generates Free Radicals by an NAD(P)H, Phosphatidylinositol 3'-Kinase-Dependent Mechanism in Human Skin Fibroblasts Ex Vivo Diabetes, May 1, 2004; 53(5): 1344 - 1351. [Abstract] [Full Text] [PDF]
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M. S. Wolin Subcellular Localization of Nox-Containing Oxidases Provides Unique Insight Into Their Role in Vascular Oxidant Signaling Arterioscler. Thromb. Vasc. Biol., April 1, 2004; 24(4): 625 - 627. [Full Text] [PDF]
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