Premium
KIDNEY FIBROSIS IN HYPERTENSIVE RATS: Role of Oxidative Stress
Author(s) -
Zhao Wenyuan,
Chen Sue S,
Ahokas Robert A,
sun Yao
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.803.13
Subject(s) - oxidative stress , nadph oxidase , kidney , endocrinology , medicine , apocynin , fibrosis , angiotensin ii , nox4 , population , kidney disease , myofibroblast , blood pressure , chemistry , environmental health
Renal fibrosis occurs in patients with hypertension. Oxidative stress appears in hypertensive kidney disease. Herein, we tested the hypothesis that oxidative stress contributes to the development of renal fibrosis during hypertension. SD rats were treated with angiotensin (Ang)II (9ug/h sc) for 4 wks with/without co‐treatment of antioxidants, apocynin and tempol (120mg/kg/day each). Appearance of renal oxidative stress and its effect on the expression of TGF‐b1, population of myofibroblasts, collagen synthesis/degradation and fibrosis in kidneys were examined. Chronic AngII infusion elevated systemic blood pressure, which was accompanied with extensive renal fibrosis and oxidative stress represented as upregulated NADPH oxidase and suppressed SOD. Antioxidants led to: 1) markedly decreased renal NADPH oxidase; 2) significantly attenuated gene expression of TGF‐b1, type‐I collagen, and TIMP‐I/‐II in the kidney; 3) largely reduced population of myofibroblasts in both the cortex and medulla; 4) significantly reduced renal collagen; 5) and partially suppressed blood pressure. Thus, AngII‐induced hypertension leads to renal oxidative stress by increasing NADPH oxidase and reducing SOD in the kidney. Renal oxidative stress upregulates collagen synthesis, while suppresses collagen degradation, thereby promoting the development of fibrosis in kidneys of hypertensive rats.