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E-book
Author Montezano, Augusto C.

Title Reactive oxygen species and the cardiovascular system / Augusto C. Montezano and Rhian M. Touyz
Published San Rafael, Calif. (1537 Fourth Street, San Rafael, CA 94901 USA) : Morgan & Claypool, ©2012

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Description 1 online resource (viii, 93 pages) : illustrations
Series Colloquium series on integrated systems physiology, 2154-5626 ; # 32
Colloquium series on integrated systems physiology ; # 32. 2154-5626
Contents 1. Introduction
2. Redox molecules -- 2.1 Superoxide and hydrogen peroxide -- 2.2 Reactive nitrogen species (RNS)
3. Production and metabolism of ROS in the cardiovascular system -- 3.1 Xanthine oxidase -- 3.2 Uncoupled nitric oxide synthase -- 3.3 Mitochondrial respiratory enzymes -- 3.4 Nox-family NAD(P)H oxidases -- 3.4.1 Nox1 -- 3.4.2 Nox2 -- 3.4.3 Nox4 -- 3.4.4 Nox5
4. Interactions between mitochondria and Noxs
5. Distribution of Noxes in the vascular wall
6. Regulation of Noxes
7. Protecting against oxidative stress, antioxidant defenses -- 7.1 Enzymatic antioxidants -- 7.2 Non-enzymatic antioxidants
8. How does oxidative stress cause disease?
9. Oxidative stress and hypertension -- 9.1 Production of ROS in the cardiovascular and renal systems in hypertension -- 9.2 ROS and autonomic outflow and hypertension -- 9.3 Oxidative stress in experimental hypertension -- 9.4 Oxidative stress and clinical hypertension
10. Antioxidant therapy and human hypertension
11. NADPH oxidase and Nox isoforms as therapeutic targets, clinical potential
12. Other strategies to reduce oxidative stress
13. Assessing reactive oxygen species in the cardiovascular system -- 13.1 Cytochrome C reduction -- 13.2 Lucigenin-enhanced chemiluminescence -- 13.3 Dihydroethidium and high-performance liquid chromatography -- 13.4 Dichlorofluorescein and amplex red to measure H2O2 -- 13.5 Dihydrorhodamine oxidation to measure ONOO- -- 13.6 Electron spin resonance
14. Assessing ROS in clinical studies
15. Conclusion -- Acknowledgments -- References -- Author biographies
Summary Reactive oxygen species (ROS) influence various physiological processes including host defense, hormone biosynthesis, and cellular signaling. Increased ROS production (oxidative stress) is implicated in many diseases of the cardiovascular system, including hypertension, atherosclerosis, cardiac failure, stroke, diabetes, and kidney disease. ROS are produced throughout the cardiovascular system, in the kidney and central and peripheral nervous system. A major source for cardiovascular, renal, and neural ROS is a family of non-phagocytic NAD(P)H oxidases, including the prototypic Nox2 homologue-based NAD(P)H oxidase, as well as other NAD(P)H oxidases, such as Nox1 and Nox4. Other possible sources include mitochondrial electron transport enzymes, xanthine oxidase, cyclooxygenase, lipoxygenase, and uncoupled nitric oxide synthase (NOS). NAD(P)H oxidasederived ROS is important in regulating endothelial function and vascular tone and oxidative stress is implicated in endothelial dysfunction, inflammation, hypertrophy, apoptosis, migration, fibrosis, angiogenesis and rarefaction, important processes involved in vascular remodeling in cardiovascular disease. These findings have evoked considerable interest because of the possibilities that therapies targeted against non-phagocytic NAD(P)H oxidase to decrease ROS generation and/or strategies to increase nitric oxide (NO) availability and antioxidants may be useful in minimizing vascular injury and thereby prevent or regress target organ damage associated with hypertension and other cardiovascular diseases
Analysis superoxide
hydrogen peroxide
Nox
heart
vascular system
kidneys
blood pressure
vascular remodeling
inflammation
antioxidant
Notes Part of: Colloquium digital library of life sciences
Bibliography Includes bibliographical references (pages 55-91)
Notes Online resource; title from PDF title page (Morgan & Claypool, viewed Sep. 27, 2012)
Subject Active oxygen -- Physiological effect.
Oxidative stress.
Active oxygen.
Reactive Oxygen Species
Oxidative Stress
HEALTH & FITNESS -- Diseases -- Genetic.
MEDICAL -- Genetics.
Active oxygen
Active oxygen -- Physiological effect
Oxidative stress
Form Electronic book
Author Touyz, Rhian M.
ISBN 9781615043637
1615043632