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Effect of Angiotensin II on Oxidative Stress in Female Borderline Hypertensive Rats
Author(s) -
Zimmerman Margaret Ann,
Sullivan Jennifer
Publication year - 2010
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.24.1_supplement.701.10
Subject(s) - oxidative stress , endocrinology , medicine , catalase , angiotensin ii , kidney , urine , western blot , chemistry , blood pressure , biochemistry , gene
Oxidative stress is a contributing factor to cardiovascular tissue injury. Angiotensin II (Ang II) produces oxidative stress in male animals, but it's effect in females in unknown. The focus of this study was to determine the effect of chronic Ang II on oxidative stress levels in the kidneys of female Borderline Hypertensive Rats (BHR). Following two weeks of Ang II infusion (200ng/kg/min), BHR mean arterial pressure rose from 111±3 to 135±7 mmHg. Protein levels in the urine, which corresponds to kidney tissue damage, increased by 17±3 mg/day in Ang II‐treated BHRs. Whole body oxidative stress was assessed through observations of H 2 O 2 levels in urine. Ang II treated animals showed a 72±29 mg/ml increase in H 2 O 2 in urine as compared to control animals. Protein expression of NOX 4 , gp91, p22, p67, CuSOD, MnSOD, ECSOD and catalase was determined by western blot. Ang‐II treated BHRs renal tissue showed a decrease in MnSOD and catalase, and no significant differences in NOX 4 , gp91, p22, p67, CuSOD, and ECSOD protein levels. We found that chronic Ang II treatment resulted in hypertension, kidney tissue damage and elevation in whole body oxidative stress. Research was supported by funds from grant number 1 RO1 HL093271‐O1A1.