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NOX2 deficiency prevents angiotensin II‐induced hypertrophy and inward remodeling in cerebral arterioles
Author(s) -
Chan Siu Lung,
Baumbach Gary
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.613.11
Subject(s) - medicine , endocrinology , angiotensin ii , arteriole , chemistry , superoxide , renin–angiotensin system , muscle hypertrophy , blood pressure , circulatory system , biochemistry , enzyme
We examined the role of NAD(P)H oxidase subunit NOX2 on structural alterations in cerebral arterioles induced by angiotensin II (Ang II). NOX2‐deficient (NOX2‐/‐) and wild‐type (WT) mice were infused with a pressor or a sub‐pressor dose of Ang II (1000 or 200 ng/kg/day) or saline via osmotic minipumps for 4 weeks. Systolic arterial pressure (SAP) was measured by a tail‐cuff method. Pressure and diameter of cerebral arterioles were measured via an open cranial window in anesthetized mice. In WT and NOX2‐/‐ mice, the pressor, but not the sub‐pressor, dose of Ang II increased SAP (135±5 vs 106±3 mmHg). Superoxide levels in cerebral arterioles (hydroethidine staining) were increased by both doses of Ang II in WT (staining density: 41±5 and 32±2 vs 18±5 %), but not in NOX2‐/‐ mice. The sub‐pressor, as well as the pressor, dose of Ang II significantly reduced external diameter of maximally dilated cerebral arterioles in WT mice (51±3 and 52±3 vs 58±2 μm at 30 mmHg), but not in NOX2‐/‐ mice. Cross‐sectional area (CSA) of the arteriolar wall was significantly increased in WT mice (497±58 vs 388±50 μm 2 ) by the pressor, but not the sub‐pressor, dose of Ang II. In contrast, the pressor dose of Ang II did not increase CSA in NOX2‐/‐ mice. These findings suggest that generation of superoxide may play an important role in Ang II‐induced hypertrophy and inward remodeling in cerebral arterioles.