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We hypothesized that increased superoxide contributes to mean arterial pressure (MAP) regulation in male Sprague-Dawley rats fed a high-salt diet and/or during endothelin (ET(B)) receptor blockade. Four groups on either a normal- or a high-salt diet were studied for 1 week: (1) control; (2) tempol, a superoxide dismutase mimetic, in their drinking water (1 mmol/L); (3) A-192621, an ET(B) antagonist, in their food (10 mg/kg daily); or (4) both tempol and A-192621. Without ET(B) blockade, tempol had no effect on MAP (telemetry) in rats on the normal-salt diet but significantly reduced MAP in rats on the high-salt diet (100+/-3 vs 112+/-2 mm Hg, P&lt;0.05). On the normal-salt diet, A-192621 increased MAP with or without tempol. Under high-salt conditions, tempol attenuated the increase in MAP produced by A-192621, but only during the initial days of treatment. Plasma 8-isoprostanes were increased in all rats on the high-salt diet and were further increased after 3 days of A-192621 but not after 7 days; tempol inhibited the increase produced by A-192621 but had no influence on the increase produced by high salt. H2O2 excretion was significantly higher in rats on a high-salt diet for the 7-day drug treatment compared with those on a normal-salt diet. Tempol further increased H2O2 excretion in rats on a high-salt diet, an effect accelerated in A-192621-treated rats. These data suggest that blood pressure lowering by tempol in rats on a high-salt diet may be unrelated to reductions in superoxide and that renal H2O2 may account for the limited ability of tempol to attenuate hypertension produced by ET(B) receptor blockade.

Arterial Pressure Response to the Antioxidant Tempol and ET B Receptor Blockade in Rats on a High-Salt Diet

Arterial Pressure Response to the Antioxidant Tempol and ET _B Receptor Blockade in Rats on a High-Salt Diet