title: Impaired pressure natriuresis is associated with interstitial inflammation in salt-sensitive hypertension.
abstract: OBJECTIVE
  Impairment of the pressure natriuresis relationship is a central event in the pathogenesis of hypertension. Renal tubulointerstitial inflammation results in salt-sensitive hypertension and, until recently, the changes in pressure natriuresis induced by renal inflammation received little attention.
  
  
  RESULTS
  Oxidative stress and increased intrarenal angiotensin II activity, in association with rarefaction and loss of peritubular vascular network, may be involved in the inflammation-induced blunting of the natriuresis resulting from increments in renal perfusion pressure.
  
  
  CONCLUSIONS
  Here, we review the mechanisms for the impairment in pressure natriuresis resulting from renal tubulointerstitial inflammation in reference to the normal physiologic mechanisms involved in this response.
authors.affiliation: The Renal Service, Hospital Universitario, Universidad del Zulia, Maracaibo, Venezuela. brodrigueziturbe@gmail.com
authors.forename: Bernardo
authors.initials: B
authors.lastname: Rodriguez-Iturbe
authors.forename: Martha
authors.initials: M
authors.lastname: Franco
authors.forename: Richard J
authors.initials: RJ
authors.lastname: Johnson
mesh_terms: D000804:Angiotensin II / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D007684:Kidney Tubules / Q000098:blood supply; D055806:Microvessels / Q000503:physiopathology; D009318:Natriuresis / Q000502:physiology*; D009395:Nephritis, Interstitial / Q000378:metabolism / Q000503:physiopathology*; D018384:Oxidative Stress; D017673:Sodium Chloride, Dietary / Q000009:adverse effects
chemical_list: D017673:Sodium Chloride, Dietary; D000804:Angiotensin II