Hypertension. 2003;41:1346-1352
Published online before print April 28, 2003, doi: 10.1161/01.HYP.0000070028.99408.E8
Published online before print April 28, 2003, doi: 10.1161/01.HYP.0000070028.99408.E8
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(Hypertension. 2003;41:1346.)
© 2003 American Heart Association, Inc.
Scientific Contributions |
Oxidative Stress in Dahl Salt-Sensitive Hypertension
From the Department of Physiology and Biophysics, University of Mississippi Medical Center (S.M., G.W.C., A.W.G., R.D.M.), Jackson, and the Department of Pathology, Johns Hopkins Medical Institute (L.C.R.), Baltimore, Md.
Correspondence to R. Davis Manning, Jr, Department of Physiology and Biophysics, 2500 N State St, Jackson, MS 39216. E-mail dmanning{at}physiology.umsmed.edu
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 µmol · 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 mm Hg (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 O2·- release increased significantly in the high-Na group when compared with the low-Na group. Tempol decreased both renal cortical and medullary O2·- release in the high- and low-Na rats, but the decrease in O2·- release was greater in high-Na rats. The data suggest that oxidative stress contributes to Dahl salt-sensitive hypertension and the accompanying renal damage.
Key Words: arterial pressure • renal disease • urine • glomerulosclerosis • oxidative stress
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