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1 Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi, United States
2 Pathology, University of Mississippi Medical Center, Jackson, Mississippi, United States
3 Dept. of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi, United States
* To whom correspondence should be addressed. E-mail: dmanning{at}physiology.umsmed.edu.
The goal of this study was to test the hypothesis that increases in oxidative stress in Dahl S rats on a high salt diet help to stimulate renal nuclear factor kappa B (NFκB), renal proinflammatory cytokines and chemokines thus contributing to hypertension, renal damage and dysfunction. We specifically studied whether antioxidant treatment of Dahl S rats on high Na intake would decrease renal inflammation and thus attenuate the hypertensive and adverse renal responses. Sixty-four 7-to 8-week old Dahl S or R/Rapp strain rats were maintained for 5 weeks on a high sodium (8%) or high sodium+ vitamins C (1g/l in drinking H2O) and E (5000IU/kg in food). Arterial and venous catheters were implanted at day 21. By day 35 in the high Na S rats, antioxidant treatment significantly increased the renal reduced-to-oxidized glutathione ratio, and decreased renal cortical H2O2 and O2.-release, and renal NF
B. Antioxidant treatment with vitamins C and E in high Na S rats also decreased renal monocytes/macrophages in the glomeruli, cortex and medulla, tumor necrosis factor alpha by 39%, and monocyte chemoattractant protein-1 by 38%. Vitamin-treated, high Na S rats also experienced decreases in arterial pressure, urinary protein excretion, renal tubulointerstitial damage, and glomerular necrosis and increases in glomerular filtration rate, and renal plasma flow. In conclusion, antioxidant treatment of high Na Dahl S rats decreased renal inflammatory cytokines and chemokines, renal immune cells, NFB, and arterial pressure and improved renal function and damage.
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