Renal infiltration of immunocompetent cells: cause and effect of sodium-sensitive hypertension.
This review examines the participation of immunocompetent cells that accumulate in tubulointerstitial areas of the kidney in the pathogenesis of sodium-sensitive hypertension. Tubulointerstitial inflammation is a universal feature in experimental models of sodium-sensitive hypertension, and the suppression of inflammation and its constant companions, oxidative stress and renal angiotensin II activity, ameliorates or prevents hypertension. Human studies also support the association between renal inflammation and hypertension. The proinflammatory effects of a high sodium diet and the mechanisms by which renal inflammation induces sodium retention are discussed. It is suggested that autoimmune reactivity may play a role in the development and maintenance of renal inflammation in hypertensive states.
Rodriguez-Iturbe
Bernardo
B
Renal Service, Instituto Venezolano de Investigaciones Científicas (IVIC)-Zulia, Hospital Universitario, Universidad del Zulia, Maracaibo, Venezuela. bernardori@telcel.net.ve
D000328:Adult; D000804:Angiotensin II / Q000378:metabolism; D000818:Animals; D015551:Autoimmunity / Q000502:physiology; D004195:Disease Models, Animal; D006360:Heat-Shock Proteins / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000209:etiology / Q000503:physiopathology*; D007121:Immunocompetence; D007249:Inflammation / Q000503:physiopathology*; D007668:Kidney / Q000166:cytology* / Q000378:metabolism; D008875:Middle Aged; D009393:Nephritis / Q000503:physiopathology; D018384:Oxidative Stress; D051381:Rats; D012964:Sodium / Q000378:metabolism; D012982:Sodium, Dietary / Q000009:adverse effects* / Q000494:pharmacology
D006360:Heat-Shock Proteins; D012982:Sodium, Dietary; D000804:Angiotensin II; D012964:Sodium