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Am J Physiol Regul Integr Comp Physiol 294: R76-R83, 2008. First published November 7, 2007; doi:10.1152/ajpregu.00466.2007
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INFLAMMATION AND CYTOKINES

TNF-{alpha} inhibition reduces renal injury in DOCA-salt hypertensive rats

Ahmed A. Elmarakby,1 Jeffrey E. Quigley,1 John D. Imig,1,3 Jennifer S. Pollock,1,4 and David M. Pollock1,2,3,4

1Vascular Biology Center and Departments of 2Surgery, 3Physiology, and 4Pharmacology and Toxicology, Medical College of Georgia, Augusta, Georgia

Submitted 29 June 2007 ; accepted in final form 29 October 2007

Studies suggest that the inflammatory cytokine TNF-{alpha} plays a role in the prognosis of end-stage renal diseases. We previously showed that TNF-{alpha} inhibition slowed the progression of hypertension and renal damage in angiotensin II salt-sensitive hypertension. Thus, we hypothesize that TNF-{alpha} contributes to renal inflammation in a model of mineralocorticoid-induced hypertension. Four groups of rats (n = 5 or 6) were studied for 3 wk with the following treatments: 1) placebo, 2) placebo + TNF-{alpha} inhibitor etanercept (1.25 mg·kg–1·day–1 sc), 3) deoxycorticosterone acetate + 0.9% NaCl to drink (DOCA-salt), or 4) DOCA-salt + etanercept. Mean arterial blood pressure (MAP) measured by telemetry increased in DOCA-salt rats compared with baseline (177 ± 4 vs. 107 ± 3 mmHg; P < 0.05), and TNF-{alpha} inhibition had no effect in the elevation of MAP in these rats (177 ± 8 mmHg). Urinary protein excretion significantly increased in DOCA-salt rats compared with placebo (703 ± 76 vs. 198 ± 5 mg/day); etanercept lowered the proteinuria (514 ± 64 mg/day; P < 0.05 vs. DOCA-salt alone). Urinary albumin excretion followed a similar pattern in each group. Urinary monocyte chemoattractant protein (MCP)-1 and endothelin (ET)-1 excretion were also increased in DOCA-salt rats compared with placebo (MCP-1: 939 ± 104 vs. 43 ± 7 ng/day, ET-1: 3.30 ± 0.29 vs. 1.07 ± 0.03 fmol/day; both P < 0.05); TNF-{alpha} inhibition significantly decreased both MCP-1 and ET-1 excretion (409 ± 138 ng/day and 2.42 ± 0.22 fmol/day, respectively; both P < 0.05 vs. DOCA-salt alone). Renal cortical NF-{kappa}B activity also increased in DOCA-salt hypertensive rats, and etanercept treatment significantly reduced this effect. These data support the hypothesis that TNF-{alpha} contributes to the increase in renal inflammation in DOCA-salt rats.

deoxycorticosterone acetate; renal inflammation; blood pressure; tumor necrosis factor-{alpha}; etanercept; nuclear factor-{kappa}B


Address for reprint requests and other correspondence: D. M. Pollock, Vascular Biology Center, Medical College of Georgia, Augusta, GA 30912-2500 (e-mail: dpollock{at}mcg.edu)




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