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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Veröffentlicht in:Hypertension (Dallas, Tex. 1979) Tex. 1979), 2010-09, Vol.56 (3), p.498-504
Hauptverfasser: Luo, Zaiming, Teerlink, Tom, Griendling, Kathy, Aslam, Shakil, Welch, William J, Wilcox, Christopher S
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Sprache:eng
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Zusammenfassung: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