Oxidative stress, renal infiltration of immune cells, and salt-sensitive hypertension: all for one and one for all.
Recent evidence indicates that interstitial infiltration of T cells and macrophages plays a role in the pathogenesis of salt-sensitive hypertension. The present review examines this evidence and summarizes the investigations linking the renal accumulation of immune cells and oxidative stress in the development of hypertension. The mechanisms involved in the hypertensive effects of oxidant stress and tubulointerstitial inflammation, in particular intrarenal ANG II activity, are discussed, focusing on their potential for sodium retention. The possibility of autoimmune reactivity in hypertension is raised in the light of the proinflammatory and immunogenic pathways stimulated by the interrelationship between oxidant stress and inflammatory response. Finally, we present some clinical considerations derived from the recognition of this interrelationship.
Servicio de Nefrología, Hospital Universitario, Universidad del Zulia, Instituto de Inmunobiología (Fundacite-Zulia Maracaibo 400-A, Venezuela. bri@iamnet.com
Bernardo
B
Rodríguez-Iturbe
Nosratola D
ND
Vaziri
Jaime
J
Herrera-Acosta
Richard J
RJ
Johnson
D006801:Humans; D006977:Hypertension, Renal / Q000276:immunology* / Q000378:metabolism*; D007668:Kidney / Q000166:cytology / Q000276:immunology / Q000378:metabolism*; D018384:Oxidative Stress / Q000502:physiology*; D017673:Sodium Chloride, Dietary / Q000494:pharmacology; D013601:T-Lymphocytes / Q000276:immunology*
D017673:Sodium Chloride, Dietary