Activation of NADPH Oxidase During Progression of Cardiac Hypertrophy to Failure

ABSTRACT—Increased reactive oxygen species (ROS) production is implicated in the pathophysiology of left ventricular (LV) hypertrophy and heart failure. However, the enzymatic sources of myocardial ROS production are unclear. We examined the expression and activity of phagocyte-type NADPH oxidase in...

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Bibliographic Details
Published in:Hypertension (Dallas, Tex. 1979) Tex. 1979), 2002-10, Vol.40 (4), p.477-484
Main Authors: Li, Jian-Mei, Gall, Nick P, Grieve, David J, Chen, Mingyou, Shah, Ajay M
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Cardiology. Vascular system
Disease Progression
Enzyme Activation
Guinea Pigs
Heart
Heart Failure - enzymology
Heart Failure - etiology
Hypertrophy, Left Ventricular - enzymology
Hypertrophy, Left Ventricular - etiology
Male
Medical sciences
Mitogen-Activated Protein Kinases - metabolism
Myocarditis. Cardiomyopathies
Myocardium - enzymology
NADPH Oxidases - metabolism
Phosphorylation
Protein Subunits
Reactive Oxygen Species - metabolism
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Summary:ABSTRACT—Increased reactive oxygen species (ROS) production is implicated in the pathophysiology of left ventricular (LV) hypertrophy and heart failure. However, the enzymatic sources of myocardial ROS production are unclear. We examined the expression and activity of phagocyte-type NADPH oxidase in LV myocardium in an experimental guinea pig model of progressive pressure-overload LV hypertrophy. Concomitant with the development of LV hypertrophy, NADPH-dependent O2 production in LV homogenates, measured by lucigenin (5 μmol/L) chemiluminescence or cytochrome c reduction assays, significantly and progressively increased (by ≈40% at the stage of LV decompensation;P
ISSN:0194-911X
1524-4563
DOI:10.1161/01.hyp.0000032031.30374.32