Journal
HYPERTENSION
Volume 41, Issue 6, Pages 1346-1352Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/01.HYP.0000070028.99408.E8
Keywords
arterial pressure; renal disease; urine; glomerulosclerosis; oxidative stress
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Funding
- NHLBI NIH HHS [HL-51971] Funding Source: Medline
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The role of oxidative stress in the long-term regulation of arterial pressure, renal hemodynamics, and renal damage was studied in Dahl salt-sensitive rats. Twenty-eight Dahl S/Rapp strain rats, equipped with indwelling arterial and venous catheters, were subjected to a 3-week intravenous infusion of either low Na (0.9 mmol/d) or high Na (20.6 mmol/d) or the superoxide dismutase mimetic, 4-hydroxyl-2,2,6,6-tetramethylpiperidine-1-oxyl (Tempol), at 125 mumol.kg(-1).h(-1) plus low Na or high Na. After 21 days, mean arterial pressure was 140+/-3 mm Hg in the high-Na group, 118+/-1 mmHg (P<0.05) in the high-Na/Tempol group, and unchanged in the low-Na/Tempol and low-Na groups. Tempol did not change renal blood flow, glomerular filtration rate, or glomerular cross-sectional area in rats subjected to the high-Na intake but did decrease urinary protein excretion, the percentage of sclerotic glomeruli, and the kidney weight to body weight ratio. In 15 additional Dahl S rats subjected to high or low Na intake for 3 weeks, renal cortical and medullary O-2(is approximately equal to) release increased significantly in the high-Na group when compared with the low-Na group. Tempol decreased both renal cortical and medullary O-2(is approximately equal to) release in the high- and low-Na rats, but the decrease in O-2(is approximately equal to) release was greater in high- Na rats. The data suggest that oxidative stress contributes to Dahl salt-sensitive hypertension and the accompanying renal damage.
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