Renal inflammation, autoimmunity and salt-sensitive hypertension

Clin Exp Pharmacol Physiol. 2012 Jan;39(1):96-103. doi: 10.1111/j.1440-1681.2011.05482.x.

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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Autoantibodies / analysis
  • Autoimmune Diseases / etiology*
  • Autoimmune Diseases / immunology*
  • Autoimmune Diseases / metabolism
  • Autoimmune Diseases / physiopathology
  • Autoimmunity*
  • HSP70 Heat-Shock Proteins / antagonists & inhibitors
  • HSP70 Heat-Shock Proteins / metabolism
  • Heat-Shock Proteins / antagonists & inhibitors
  • Heat-Shock Proteins / metabolism
  • Humans
  • Hypertension / etiology*
  • Hypertension / immunology*
  • Hypertension / metabolism
  • Hypertension / physiopathology
  • Kidney Tubules / immunology
  • Kidney Tubules / physiopathology
  • Macrophages / immunology
  • Natriuresis
  • Nephritis / physiopathology*
  • Sodium Chloride, Dietary / adverse effects*
  • T-Lymphocytes / immunology

Substances

  • Autoantibodies
  • HSP70 Heat-Shock Proteins
  • Heat-Shock Proteins
  • Sodium Chloride, Dietary
  • heat-shock protein 65, human