Abstract
1. The present article reviews the role of immune-competent cells infiltrating the kidney and their association with oxidative stress and renal angiotensin activity in the development of salt-sensitive hypertension. 2. We discuss changes in the pressure-natriuresis relationship resulting from renal inflammation and its improvement resulting from immunosuppressive treatment. 3. The potential role of T-cell-driven reactivity in sustaining the renal inflammation is examined in the light of accumulating evidence of autoimmune mechanisms in experimental and clinical hypertension.
© 2011 The Authors. Clinical and Experimental Pharmacology and Physiology © 2011 Blackwell Publishing Asia Pty Ltd.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Autoantibodies / analysis
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Autoimmune Diseases / etiology*
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Autoimmune Diseases / immunology*
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Autoimmune Diseases / metabolism
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Autoimmune Diseases / physiopathology
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Autoimmunity*
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HSP70 Heat-Shock Proteins / antagonists & inhibitors
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HSP70 Heat-Shock Proteins / metabolism
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Heat-Shock Proteins / antagonists & inhibitors
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Heat-Shock Proteins / metabolism
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Humans
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Hypertension / etiology*
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Hypertension / immunology*
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Hypertension / metabolism
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Hypertension / physiopathology
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Kidney Tubules / immunology
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Kidney Tubules / physiopathology
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Macrophages / immunology
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Natriuresis
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Nephritis / physiopathology*
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Sodium Chloride, Dietary / adverse effects*
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T-Lymphocytes / immunology
Substances
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Autoantibodies
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HSP70 Heat-Shock Proteins
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Heat-Shock Proteins
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Sodium Chloride, Dietary
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heat-shock protein 65, human