Angiotensin II and NADPH Oxidase Increase ADMA in Vascular Smooth Muscle Cells

Asymmetrical dimethylarginine inhibits nitric oxide synthase, cationic amino acid transport, and endothelial function. Patients with cardiovascular risk factors often have endothelial dysfunction associated with increased plasma asymmetrical dimethylarginine and markers of reactive oxygen species. W...

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Bibliographic Details
Published in:Hypertension (Dallas, Tex. 1979) Tex. 1979), 2010-09, Vol.56 (3), p.498-504
Main Authors: Luo, Zaiming, Teerlink, Tom, Griendling, Kathy, Aslam, Shakil, Welch, William J, Wilcox, Christopher S
Format: Article
Language:English
Subjects:
Analysis of Variance
Angiotensin II - metabolism
Angiotensin II - pharmacology
Animals
Arginine - analogs & derivatives
Arginine - genetics
Arginine - metabolism
Arterial hypertension. Arterial hypotension
Benzimidazoles - pharmacology
Biological and medical sciences
Blood and lymphatic vessels
Blood vessels and receptors
Blotting, Western
Cardiology. Vascular system
Cells, Cultured
Fundamental and applied biological sciences. Psychology
Medical sciences
Muscle, Smooth, Vascular - cytology
Muscle, Smooth, Vascular - drug effects
Muscle, Smooth, Vascular - metabolism
Myocytes, Smooth Muscle - drug effects
Myocytes, Smooth Muscle - metabolism
NADPH Oxidases - genetics
NADPH Oxidases - metabolism
Rats
Reactive Oxygen Species - metabolism
Reverse Transcriptase Polymerase Chain Reaction
Tetrazoles - pharmacology
Vertebrates: cardiovascular system
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Summary:Asymmetrical dimethylarginine inhibits nitric oxide synthase, cationic amino acid transport, and endothelial function. Patients with cardiovascular risk factors often have endothelial dysfunction associated with increased plasma asymmetrical dimethylarginine and markers of reactive oxygen species. We tested the hypothesis that reactive oxygen species, generated by nicotinamide adenine dinucleotide phosphate oxidase, enhance cellular asymmetrical dimethylarginine. Incubation of rat preglomerular vascular smooth muscle cells with angiotensin II doubled the activity of nicotinamide adenine dinucleotide phosphate oxidase but decreased the activities of dimethylarginine dimethylaminohydrolase by 35% and of cationic amino acid transport by 20% and doubled cellular (but not medium) asymmetrical dimethylarginine concentrations (P
ISSN:0194-911X
1524-4563
DOI:10.1161/HYPERTENSIONAHA.110.152959