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| 2007 JASN IMPACT FACTOR 7.111 | HOME AUTHOR INFO EDITORIAL BOARD SUBSCRIBE FEEDBACK ALERTS HELP | |||
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| 2007 JASN IMPACT FACTOR 7.111 | HOME AUTHOR INFO EDITORIAL BOARD SUBSCRIBE FEEDBACK ALERTS HELP | |||
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BASIC SCIENCE |
Division of Nephrology and Hypertension and Cardiovascular-Kidney Institute, Georgetown University, Washington, DC
Correspondence to Dr. Christopher S. Wilcox, Division of Nephrology and Hypertension, Georgetown University Hospital, 3800 Reservoir Road, NW/PHC, Suite #F6003, Washington, DC 20007. Phone: 202-444-9183; Fax: 202-444-7893;
ABSTRACT. The hypothesis that a high salt (HS) intake increases oxidative stress was investigated and was related to renal cortical expression of NAD(P)H oxidase and superoxide dismutase (SOD). 8-Isoprostane PGF2
and malonyldialdehyde were measured in groups (n = 6 to 8) of conscious rats during low-salt, normal-salt, or HS diets. NADPH- and NADH-stimulated superoxide anion (O2·-) generation was assessed by chemiluminescence, and expression of NAD(P)H oxidase and SOD were assessed with real-time PCR. Excretion of 8-isoprostane and malonyldialdehyde increased incrementally two- to threefold with salt intake (P < 0.001), whereas prostaglandin E2 was unchanged. Renal cortical NADH- and NADPH-stimulable O2·- generation increased (P < 0.05) 30 to 40% with salt intake. Compared with low-salt diet, HS significantly (P < 0.005) increased renal cortical mRNA expression of gp91phox and p47phox and decreased expression of intracellular CuZn (IC)-SOD and mitochondrial (Mn)-SOD. Despite suppression of the renin-angiotensin system, salt loading enhances oxidative stress. This is accompanied by increased renal cortical NADH and NADPH oxidase activity and increased expression of gp91phox and p47phox and decreased IC- and Mn-SOD. Thus, salt intake enhances generation of O2·- accompanied by enhanced renal expression and activity of NAD(P)H oxidase with diminished renal expression of IC- and Mn-SOD. E-mail: wilcoxch@georgetown.edu
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