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2004 CARDIOVASCULAR AND KIDNEY INVESTIGATORS MEETING

Angiotensin-induced defects in renal oxygenation: role of oxidative stress

Division of Nephrology and Hypertension and Cardiovascular Kidney Institute, Georgetown University, Washington, DC

Submitted 24 June 2004 ; accepted in final form 18 August 2004

We tested the hypothesis that superoxide anion (O₂^–·) generated in the kidney by prolonged angiotensin II (ANG II) reduces renal cortical PO₂ and the use of O₂ for tubular sodium transport (T_Na:Q_O2). Groups (n = 8–11) of rats received angiotensin II (ANG II, 200 ng·kg^–1·min^–1 sc) or vehicle for 2 wk with concurrent infusions of a permeant nitroxide SOD mimetic 4-hydroxy-2,2,6,6-tetramethylpiperidine 1-oxyl (Tempol, 200 nmol·kg^–1·min^–1) or vehicle. Rats were studied under anesthesia with measurements of renal oxygen usage and PO₂ in the cortex and tubules with a glass electrode. Compared with vehicle, ANG II increased mean arterial pressure (107 ± 4 vs. 146 ± 6 mmHg; P < 0.001), renal vascular resistance (42 ± 3 vs. 65 ± 7 mmHg·ml^–1·min^–1·100 g^–1; P < 0.001), renal cortical NADPH oxidase activity (2.3 ± 0.2 vs. 3.6 ± 0.4 nmol O₂^–··min^–1·mg^–1 protein; P < 0.05), mRNA and protein expression for p22^phox (2.1- and 1.8-fold respectively; P < 0.05) and reduced the mRNA for extracellular (EC)-SOD (–1.8 fold; P < 0.05). ANG II reduced the PO₂ in the proximal tubule (39 ± 1 vs. 34 ± 2 mmHg; P < 0.05) and throughout the cortex and reduced the T_Na:Q_O2 (17 ± 1 vs. 9 ± 2 µmol/µmol; P < 0.001). Tempol blunted or prevented all these effects of ANG II. The effects of prolonged ANG II to cause hypertension, renal vasoconstriction, renal cortical hypoxia, and reduced efficiency of O₂ usage for Na⁺ transport, activation of NADPH oxidase, increased expression of p22^phox, and reduced expression of EC-SOD can be ascribed to O₂^–· generation because they are prevented by an SOD mimetic.

reactive oxygen species: superoxide dismutase; TEMPOL; nitroxides; NADPH oxidase; hypertension

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