Intrarenal renin-angiotensin system is upregulated in experimental model of progressive renal disease induced by chronic inhibition of nitric oxide synthesis

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dc.contributor.authorGraciano, Miguel Luis
dc.contributor.authorCavaglieri, Rita de Cassia
dc.contributor.authorDelle, Humberto
dc.contributor.authorDominguez, Wagner Vasques
dc.contributor.authorCasarini, Dulce Elena [UNIFESP]
dc.contributor.authorMalheiros, Denise Maria Avancini Costa
dc.contributor.authorNoronha, Irene Lourdes
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.date.accessioned2016-01-24T12:37:16Z
dc.date.available2016-01-24T12:37:16Z
dc.date.issued2004-07-01
dc.description.abstractLocally generated angiotensin II (AngII) may be involved in the pathogenic mechanisms of chronic renal diseases. Renal expression of AngII and other components of the renin-angiotensin system (RAS) were analyzed by immunohistochemistry and Western blot in a model of chronic progressive nephropathy induced by inhibition of nitric oxide synthesis. Renal injury was evaluated by histology and albumin excretion. Systemic RAS status was evaluated through plasma renin activity (PRA) and plasma AngII concentration. in addition, the effects of enalapril, losartan, and mycophenolate mofetil (MMF) on AngII expression in animals with chronic renal disease was also analyzed. Plasma renin activity and plasma AngII were not different between rats with nephropathy and controls (2.08 +/- 0.7 versus 2.03 +/- 0.5 ng/ml/h and 94.3 +/- 18 versus 78.9 +/- 16 fmol/ml, respectively). However, rats with chronic progressive nephropathy showed augmented renal content of angiotensinogen protein (13.5 +/- 3.5 versus 2.2 +/- 0.4 pixels in control rats; P < 0.05), enhanced expression of cathepsin D-a renin-like enzyme-in cortical collecting tubules (103.5 +/- 27.0 versus 66.2 +/- 3.6 cells/mm(2) in controls; P < 0.01), and increased expression of AT, receptor in interstitium (54.7 +/- 7.8 versus 1.3 +/- 0.4 cells/mm(2) in controls; P < 0.001). Kidney angiotensin-converting enzyme content did not differ among the groups. Notably, an increased number of interstitial cells expressing AngII was detected in the renal interstitium (9.5 +/- 1.6 versus 1.7 +/- 0.6 cells/mm(2) in controls; P < 0.05). Rats treated with Nomega-nitro-L-arginine-methyl-esther and losartan presented a decreased local AngII formation, in contrast to its known effect on plasma AngII. Moreover, mycophenolate mofetil lowered interstitial AngII expression, suggesting that inflammatory signaling may be involved in interstitial AngII generation. This study demonstrates the upregulation of local RAS in the kidney in a model of chronic progressive nephropathy.en
dc.description.affiliationUniv São Paulo, Renal Pathophysiol Lab, Div Nephrol, Fac Med, BR-01246903 São Paulo, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Div Nephrol, Kidney Hormones Lab, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Div Nephrol, Kidney Hormones Lab, São Paulo, Brazil
dc.description.sourceWeb of Science
dc.format.extent1805-1815
dc.identifierhttps://doi.org/10.1097/01.ASN.0000131528.00773.A9
dc.identifier.citationJournal of the American Society of Nephrology. Philadelphia: Lippincott Williams & Wilkins, v. 15, n. 7, p. 1805-1815, 2004.
dc.identifier.doi10.1097/01.ASN.00000131528.00773.A9
dc.identifier.issn1046-6673
dc.identifier.urihttps://repositorio.unifesp.br/handle/11600/27830
dc.identifier.wosWOS:000222275600015
dc.language.isoeng
dc.publisherLippincott Williams & Wilkins
dc.relation.ispartofJournal of the American Society of Nephrology
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.titleIntrarenal renin-angiotensin system is upregulated in experimental model of progressive renal disease induced by chronic inhibition of nitric oxide synthesisen
dc.typeinfo:eu-repo/semantics/article
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