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A Role For TNF‐α in Hypertension During Systemic Lupus Erythematosus
Author(s) -
VenegasPont Marcia,
Glover Porter H.,
LaMarca Babbette D.,
Jones Allison V.,
Ryan Michael J.
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.968.3
Subject(s) - oxidative stress , medicine , tumor necrosis factor alpha , endocrinology , kidney , etanercept , albuminuria , cytokine , immunology , blood pressure , inflammation
Systemic Lupus Erythematosus (SLE) is an independent risk factor for developing hypertension. The inflammatory cytokine TNF‐α has been implicated in the pathology of hypertension and SLE, perhaps through increased oxidative stress. We tested whether the TNF‐α antagonist etanercept (ETAN) reduces mean arterial pressure (MAP) and protects the kidney in a female mouse model of SLE (NZBWF1). Thirty week old SLE and control mice (NZW/LacJ) received ETAN (0.8mg/kg SC weekly x 4 weeks) or vehicle. Mice with SLE were hypertensive compared to controls. Treatment with ETAN reduced MAP in SLE but not control mice. Treatment with ETAN also reduced the albuminuria associated with SLE. Renal cortex NADPH oxidase activity was higher in SLE mice compared to controls and lowered in SLE mice treated with ETAN. Interestingly, the pathognomonic Anti‐dsDNA antibodies were increased in ETAN treated SLE mice. These data suggest that TNF‐α, through increasing renal oxidative stress, is an important factor in the development of SLE hypertension. (Supported by HL 08597 MJR) *p< 0.05 vs. Ctrl †p<0.05 vs. SLE+Veh