Oxidative stress promotes hypertension and albuminuria during the autoimmune disease systemic lupus erythematosus
| Autor: | C. Warren Masterson, Michael J. Ryan, Nicholas J. Stewart, Marcia Venegas-Pont, Katie L. Wasson, Keisa W. Mathis |
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| Rok vydání: | 2012 |
| Předmět: |
medicine.medical_specialty
Renal cortex Immunoblotting Blood Pressure Autoimmunity medicine.disease_cause Essential hypertension Antioxidants Article Cyclic N-Oxides Mice Internal medicine Internal Medicine medicine Albuminuria Animals Lupus Erythematosus Systemic Autoimmune disease Kidney Proteinuria Lupus erythematosus Mice Inbred NZB business.industry Disease progression Acetophenones Drug Synergism medicine.disease Disease Models Animal Oxidative Stress medicine.anatomical_structure Endocrinology Blood pressure Immunology Hypertension Disease Progression Spin Labels Female medicine.symptom business Oxidative stress Follow-Up Studies Kidney disease |
| Zdroj: | Hypertension (Dallas, Tex. : 1979). 59(5) |
| ISSN: | 1524-4563 |
| Popis: | Several lines of evidence suggest that essential hypertension originates from an autoimmune-mediated mechanism. One consequence of chronic immune activation is the generation of oxygen-derived free radicals, resulting in oxidative stress. Renal oxidative stress has direct prohypertensive actions on renal microvascular and tubular function. Whether oxidative stress contributes to the prevalent hypertension associated with autoimmune disease is not clear. We showed previously that female NZBWF1 mice, an established model of the autoimmune disease systemic lupus erythematosus (SLE), develop hypertension associated with renal oxidative stress. In the present study we tested the hypothesis that oxidative stress contributes to autoimmune-mediated hypertension by treating SLE and control (NZW/LacJ) mice with tempol (2.0 mmol/L) and apocynin (1.5 mmol/L) in the drinking water for 4 weeks. Although the treatment did not alter SLE disease activity (assessed by plasma double-stranded DNA autoantibodies), blood pressure and renal injury (urinary albumin) were reduced in the treated SLE mice. Tempol plus apocynin–treated SLE mice had reduced expression of nitrosylated proteins in the renal cortex, as well as reduced urinary and renal cortical hydrogen peroxide, suggesting that treatment reduced renal markers of oxidative stress. These data suggest that renal oxidative stress plays an important mechanistic role in the development of autoimmune-mediated hypertension. |
| Databáze: | OpenAIRE |
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