The Role of Oxidative Stress in Dahl Salt-Sensitive Hypertension
High sodium intake in the Dahl salt-sensitive (S) rat causes hypertension and renal damage. Our goal was to determine if long-term iv infusion of Tempol, a superoxide dismutase mimetic, would ameliorate the hypertension and reduce renal damage in Dahl S rats subjected to high sodium intake. Dahl S/Rapp rats with indwelling arterial and venous catheters were maintained by iv infusion for 3 weeks on either high Na(20.6 mEq/day)(HN), high Na + Tempol(125μmol/kg/h)(HNT)or low Na(0.9 mEq/day) + Tempol(LNT). Arterial pressure was measured 24 hours/day, and as seen in the figure, was significantly decreased in high Na S rats by Tempol. † -P<.05 compared to HNT,* -P<.05 compared to LNT. At the end of 3 weeks, rats were anesthetized with isoflurane, and kidneys were removed for histological examination. At this time, the percentage of glomeruli with either focal or global sclerosis in HN, HNT and LNT rats was 3.4±0.8*†,1.4±0.4† and0.6±0.08,respectively, and glomerular cross-sectional area (mm2) was 14.3±0.4,12.9±0.5 and 12.2±0.6. Therefore, Tempol significantly reduced arterial pressure and indices of renal damage, glomerular sclerosis and glomerular cross-sectional area. These data suggest that oxidative stress significantly increases arterial pressure and exacerbates renal damage in salt-sensitive Dahl rats during increased sodium intake.