Angiotensin II-Dependent Chronic Hypertension and Cardiac Hypertrophy Are Unaffected by gp91phox-Containing NADPH Oxidase
- 1 April 2005
- journal article
- research article
- Published by Wolters Kluwer Health in Hypertension
- Vol. 45 (4) , 530-537
- https://doi.org/10.1161/01.hyp.0000158845.49943.5e
Abstract
The gp91phox-containing NADPH oxidase is the major source of reactive oxygen species (ROS) in the cardiovascular system and inactivation of gp91phox has been reported to blunt hypertension and cardiac hypertrophy seen in angiotensin (Ang) II-infused animals. In the current study, we sought to determine the role of gp91phox-derived ROS on cardiovascular outcomes of chronic exposure to Ang II. The gp91phox-deficient mice were crossed with transgenic mice expressing active human renin in the liver (TTRhRen). TTRhRen mice exhibit chronic Ang II–dependent hypertension and frank cardiac hypertrophy by age 10 to 12 weeks. Four genotypes of mice were generated: control, TTRhRen trangenics (TTRhRen), gp91phox-deficient (gp91−), and TTRhRen transgenic gp91phox-deficient (TTRhRen/gp91−). Eight to 10 mice/group were studied. ROS levels were significantly reduced (P<0.05) in the heart and aorta of TTRhRen/gp91− and gp91−mice compared with control counterparts, and this was associated with reduced cardiac, aortic, and ...Keywords
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