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Division of Nephrology and Hypertension, Georgetown University, Washington, District of Columbia
Submitted 22 March 2005 ; accepted in final form 31 May 2005
Renal oxygen tension is substantially lower in the medulla than in the cortex and is reduced in hypertensive rats, a model of oxidative stress. Expression of NADPH oxidase, the primary source for superoxide anion (O2–·) in the kidney, is elevated in hypertension. Because molecular oxygen (O2) is required for O2–· formation, we tested the hypothesis that renal NADPH oxidase activity is limited by low O2. O2–· production by rat kidney tissue or cultured cells exposed to levels of PO2 that mimics those in the kidney was assessed by lucigenin-enhanced chemiluminescence. NADPH-dependent O2–· production by kidney homogenates decreased reversibly by 60–90% after graded reductions of ambient O2 from 10 to 0% (76 to 2 mmHg PO2). The NADPH-dependent O2–· production by the kidney homogenate was reduced by decreasing PO2 below 
30 mmHg. The response of tissue homogenates to low PO2 was not different between normotensive and hypertensive rats. Similarly, NADPH-dependent O2–· production was lower during 2% O2 compared with 10% O2 in rat proximal tubule cells (–57 ± 1%), vascular smooth muscle (–42 ± 5%), cardiomyocytes (–57 ± 1%), and mouse inner medulla collecting duct cells (–58 ± 3%). We conclude that O2–· production by NADPH oxidase is dependent on availability of O2. Therefore, O2–· generation may be limited in the kidney, both in the normal renal medulla and in the cortex of hypertensive kidneys.
reactive oxygen species; hypertension; hypoxia
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