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Renal nerves contribute to renal injury, but not hypertension, during chronic inflammatory disease
Author(s) -
Mathis Keisa W.,
VenegasPont Marcia,
Ray William H.,
Masterson Chester W.,
Dwyer Terry M.,
Ryan Michael J.
Publication year - 2011
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.25.1_supplement.1078.5
Subject(s) - medicine , denervation , albuminuria , inflammation , endocrinology , pathogenesis , kidney , blood pressure
Inflammation contributes to the pathogenesis of hypertension and renal disease. Systemic lupus erythematosus (SLE) is an inflammatory disorder with prevalent hypertension and renal injury. Evidence suggests that patients with SLE may have enhanced sympathetic nervous system activity. Using an established hypertensive mouse model of SLE (NZBWF1) we tested whether the renal nerves promote hypertension and renal injury during SLE. Female SLE and control (NZW) mice were subjected to bilateral renal denervation (Dnx) or sham surgery at 32 weeks of age. Successful Dnx was confirmed by measuring renal catecholamines with HPLC. At 34 weeks of age, mean arterial pressure (MAP) was assessed in conscious mice using carotid artery catheters. MAP was increased in sham SLE mice compared to sham controls (135 ± 5 vs. 120 ± 1; p<0.02). Dnx did not alter MAP in control (117 ± 3) or SLE (133 ± 4) mice. None of the SLE Dnx mice had albuminuria (≥100 mg/dL by dipstick) compared with 40% of SLE sham mice. Renal cortex MCP‐1 protein expression was lower in SLE Dnx mice compared to SLE sham mice (p<0.01) and CuZn superoxide dismutase (SOD) was increased in SLE Dnx mice compared to SLE sham mice (p<0.01). These data suggest that the renal nerves promote renal injury during SLE independent of MAP, and possibly by contributing to local inflammation and oxidative stress. Supported by 10POST4350019 (KWM) and HL085907 , HL092284 , and HL085907S1 (MJR).