Oxidative stress in Dahl salt-sensitive hypertension

Shumei Meng, Garrick W. Cason, Anthony W. Gannon, Lorraine C. Racusen, R. Davis Manning

Research output: Contribution to journalArticlepeer-review

Abstract

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.

Original languageEnglish (US)
Pages (from-to)1346-1352
Number of pages7
JournalHypertension
Volume41
Issue number6
DOIs
StatePublished - Jun 1 2003

Keywords

  • Arterial pressure
  • Glomerulosclerosis
  • Oxidative stress
  • Renal disease
  • Urine

ASJC Scopus subject areas

  • Internal Medicine

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