title: Proinflammatory role of angiotensin II in a rat nephrosis model induced by adriamycin.
abstract: BACKGROUND
  Nephrotic syndrome induced by adriamycin (ADR) is an experimental model of glomerulosclerosis in humans. The AT(1) receptor for angiotensin II (Ang II) is involved in the renal expression of the nuclear factor-kappa B (NF-ΚB) during this nephrosis. NF-ΚB is a transcription factor for proinflammatory effects of Ang II; however, there is no information about the role of this receptor in the renal proinflammatory events in ADR nephrosis.
  
  
  METHODS
  To determine the role of Ang II in ADR nephrosis, Sprague-Dawley rats were treated with ADR (6 mg/kg iv). One ADR group received oral losartan treatment (15 mg/kg gavage) 3 days before ADR injection and then daily for 4 weeks, and the other group water. Animals were sacrificed at week 4 and renal macrophage infiltration, ICAM-1, superoxide anion (O(2(-))) and Ang II expressions were analysed by indirect immunofluorescence and histochemical techniques.
  
  
  RESULTS
  ADR rats showed increased expression of ICAM-1, Ang II, O(2(-)) and macrophage infiltration, events that were diminished by losartan treatment. Ang II expression remained unaltered after antagonist treatment. Proteinuria was reduced after 3 weeks of treatment.
  
  
  CONCLUSIONS
  These data suggest that Ang II plays a role in the inflammatory events during ADR-induced nephrosis, probably mediated by AT(1) receptors.
authors.affiliation: Instituto de Investigaciones Clínicas Dr. Américo Negrette, Facultad de Medicina, Universidad del Zulia, Maracaibo, Venezuela.
authors.forename: Maydelin
authors.initials: M
authors.lastname: Muñoz
authors.forename: Jaimar
authors.initials: J
authors.lastname: Rincón
authors.forename: Adriana
authors.initials: A
authors.lastname: Pedreañez
authors.forename: Ninoska
authors.initials: N
authors.lastname: Viera
authors.forename: Juan P
authors.initials: JP
authors.lastname: Hernández-Fonseca
authors.forename: Jesús
authors.initials: J
authors.lastname: Mosquera
mesh_terms: D000804:Angiotensin II / Q000378:metabolism*; D000818:Animals; D002784:Cholesterol / Q000097:blood; D004195:Disease Models, Animal; D004317:Doxorubicin; D019332:Endothelin-1 / Q000378:metabolism; D005455:Fluorescent Antibody Technique; D007249:Inflammation / Q000150:complications / Q000473:pathology; D018836:Inflammation Mediators / Q000378:metabolism*; D007668:Kidney / Q000187:drug effects / Q000473:pathology; D019808:Losartan / Q000494:pharmacology; D008297:Male; D009401:Nephrosis / Q000097:blood / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology*; D011507:Proteinuria / Q000097:blood / Q000150:complications / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors; D014280:Triglycerides / Q000097:blood; D015430:Weight Gain / Q000187:drug effects
chemical_list: D019332:Endothelin-1; D018836:Inflammation Mediators; D014280:Triglycerides; D000804:Angiotensin II; D004317:Doxorubicin; D002784:Cholesterol; D019808:Losartan