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Title:
Oxidative Stress and Vascular Function: Implications for Pharmacologic Treatments | Current Hypertension Reports
Description:
Production of considerable amounts of reactive oxygen species (ROS) eventually leads to oxidative stress. A key role of oxidative stress is evident in the pathologic mechanisms of endothelial dysfunction and associated cardiovascular diseases. Vascular enzymes such as NADPH oxidases, xanthine oxidase, and uncoupled endothelial nitric oxide synthase are involved in the production of ROS. The question remains whether pharmacologic approaches can effectively combat the excessive ROS production in the vasculature. Interestingly, existing registered cardiovascular drugs can directly or indirectly act as antioxidants, thereby preventing the damaging effects of ROS. Moreover, new compounds targeting NADPH oxidases have been developed. Finally, food-derived compounds appear to be effective inhibitors of oxidative stress and preserve vascular function.
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Keywords {🔍}
article, google, scholar, pubmed, cas, vascular, nadph, antioxidant, ros, nox, stress, endothelial, oxidative, oxidase, enos, cardiovascular, activity, xanthine, oxidases, function, role, production, oxygen, drugs, cells, flavonoids, pphox, dysfunction, effects, effect, larginine, disease, factor, protein, domain, inhibition, hypertension, pharmacologic, enzymes, action, molecules, enzyme, growth, pharmacol, heart, molecular, cellular, binding, electron, access,
Topics {✒️}
transforming growth factor-β pdgf—platelet-derived growth factor platelet-derived growth factor mono-o-methylated flavanols nerve-derived growth factor α1-adrenoceptor-blocking pharmacophore competitively displaces l-arginine l-arg—l-arginine metal-responsive transcription factor n-hydroxy-l-arginine article download pdf calmodulin-dependent kinase ii l-arginine levels fall reactive oxygen species l-cit—l-citrulline medical-chemical approach nadph-oxidase-derived ros intracellular l-arginine concentrations protein-coupled receptor signaling long-established cardiovascular drugs makes life finite short biological half-lives α-tocopherol-thiazolidinedione hybrid successful drugs possess endothelial-bound xo increases registered cardiovascular drugs hypertension-induced cardiovascular damage ros-generating nadph oxidases heart infarct size including akt/protein kinase fad—flavin adenine dinucleotide post-myocardial infarction patients mammalian xanthine oxidoreductase—mechanisms food-derived compounds ace—angiotensin-converting enzyme epidermal growth factor privacy choices/manage cookies antiarrhythmic-α-tocopherol hybrids [37] β-adrenergic receptors l-arginine lies inhibiting nadph oxidases biologically inactive products amino acids mimic ligand-induced oxidants specific carbazole moiety weseler & aalt bast design antioxidant drugs substrate l-arginine membrane-bound units tumor necrosis factor
Questions {❓}
- Harrison R: Structure and function of xanthine oxidoreductase: where are we now?
- How do flavanols improve vascular function?
- ROS in Atherosclerosis: What We Know?
- De Leeuw PW, Bast A: Tomato extract for hypertension?
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headline:Oxidative Stress and Vascular Function: Implications for Pharmacologic Treatments
description:Production of considerable amounts of reactive oxygen species (ROS) eventually leads to oxidative stress. A key role of oxidative stress is evident in the pathologic mechanisms of endothelial dysfunction and associated cardiovascular diseases. Vascular enzymes such as NADPH oxidases, xanthine oxidase, and uncoupled endothelial nitric oxide synthase are involved in the production of ROS. The question remains whether pharmacologic approaches can effectively combat the excessive ROS production in the vasculature. Interestingly, existing registered cardiovascular drugs can directly or indirectly act as antioxidants, thereby preventing the damaging effects of ROS. Moreover, new compounds targeting NADPH oxidases have been developed. Finally, food-derived compounds appear to be effective inhibitors of oxidative stress and preserve vascular function.
datePublished:2010-04-22T00:00:00Z
dateModified:2010-04-22T00:00:00Z
pageStart:154
pageEnd:161
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keywords:
Hypertension
Vasculature
Antioxidant
NADPH oxidase
Xanthine oxidase
eNOS
NO
Reactive oxygen species
ROS
Oxidative stress
Flavonoids
Polyphenols
Antihypertensive drugs
NOX
Oxygen radicals
Internal Medicine
Cardiology
Metabolic Diseases
Nephrology
Primary Care Medicine
General Practice / Family Medicine
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headline:Oxidative Stress and Vascular Function: Implications for Pharmacologic Treatments
description:Production of considerable amounts of reactive oxygen species (ROS) eventually leads to oxidative stress. A key role of oxidative stress is evident in the pathologic mechanisms of endothelial dysfunction and associated cardiovascular diseases. Vascular enzymes such as NADPH oxidases, xanthine oxidase, and uncoupled endothelial nitric oxide synthase are involved in the production of ROS. The question remains whether pharmacologic approaches can effectively combat the excessive ROS production in the vasculature. Interestingly, existing registered cardiovascular drugs can directly or indirectly act as antioxidants, thereby preventing the damaging effects of ROS. Moreover, new compounds targeting NADPH oxidases have been developed. Finally, food-derived compounds appear to be effective inhibitors of oxidative stress and preserve vascular function.
datePublished:2010-04-22T00:00:00Z
dateModified:2010-04-22T00:00:00Z
pageStart:154
pageEnd:161
license:https://creativecommons.org/licenses/by-nc/2.0
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keywords:
Hypertension
Vasculature
Antioxidant
NADPH oxidase
Xanthine oxidase
eNOS
NO
Reactive oxygen species
ROS
Oxidative stress
Flavonoids
Polyphenols
Antihypertensive drugs
NOX
Oxygen radicals
Internal Medicine
Cardiology
Metabolic Diseases
Nephrology
Primary Care Medicine
General Practice / Family Medicine
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