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Role of oxidative stress reduction on AT 1 receptor‐dependent cardiovascular alterations in renovascular hypertension
Author(s) -
Nishi Erika Emy,
Bergamaschi Cassia T,
Almeida Vitor R,
OliveiraSales Elizabeth B,
Giorgi Fran C,
Simon Karin A,
Campos Ruy R
Publication year - 2011
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.25.1_supplement.1027.11
Subject(s) - oxidative stress , medicine , endocrinology , renovascular hypertension , tbars , baroreflex , losartan , glutathione , blood pressure , angiotensin ii , chemistry , lipid peroxidation , heart rate , biochemistry , enzyme
Renovascular hypertension is associated with increased renal sympathetic nerve activity (rSNA), baroreflex dysfunction and oxidative stress. We tested whether AT 1 receptor blockade would produce systemic antioxidant effects and, comparatively, whether oxidative stress reduction with an antioxidant would produce cardiovascular alterations. Losartan (Lo, 30mg/kg/day) or vitC (vC,150mg/kg/day) were orally administered for 1 week by the 6th week after left renal artery clipping (2K1C). Systemic oxidative stress was evaluated by the balance of blood concentrations of TBARS and glutathione (GSH). Both Lo and vC significantly (p<0.05) normalized TBARS (from 1.6±0.1 to 1.0±0.1 and 1.1±0.1nmol/ml, respectively) and GSH (from 3.4±0.4 to 5.2±0.3 and 5.2±0.2μmol/g Hb) in the 2K1C group. Hypertension (172±3mmHg) and rSNA (162±4spikes/s) were significantly reduced after Lo (115±9 and 96±8) and vC (133±6 and 118±12). Both Los and vC increased renal baroreflex sensitivity for pressor (67% and 105%,) and depressor responses (140% and 120%,) in the 2K‐1C rats. Thus, our data suggest that AT 1 ‐dependent cardiovascular dysfunctions in the 2K1C model are largely mediated by systemic oxidative stress. Supported by FAPESP