Mechanisms of albuminuria in the chronic nitric oxide inhibition model

dc.creatorArcos, MI
dc.creatorFujihara, CK
dc.creatorSesso, A
dc.creatorPrado, EBD
dc.creatorBrandao, MJ
dc.creatorPrado, D
dc.creatorDe Nucci, G
dc.creatorZatz, R
dc.date2000
dc.dateDEC
dc.date2014-12-02T16:30:09Z
dc.date2015-11-26T17:39:02Z
dc.date2014-12-02T16:30:09Z
dc.date2015-11-26T17:39:02Z
dc.date.accessioned2018-03-29T00:20:40Z
dc.date.available2018-03-29T00:20:40Z
dc.identifierAmerican Journal Of Physiology-renal Physiology. Amer Physiological Soc, v. 279, n. 6, n. F1060, n. F1066, 2000.
dc.identifier1931-857X
dc.identifierWOS:000165545100010
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/53525
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/53525
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/53525
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1286359
dc.descriptionChronic nitric oxide (NO) inhibition causes hypertension and renal injury. Concomitant salt overload promotes massive albuminuria. We investigated the mechanisms whereby these treatments impair glomerular permselectivity. Adult male Munich-Wistar rats received either a standard-salt (SS; 0.5% Na) or high-salt (HS; 3.1% Na) diet and either no treatment or the NO inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME). At 30 days, albuminuria was moderate, the density of fixed anionic sites at the glomerular basement membrane (GBM), estimated by cationic ferritin binding, declined by similar to 35%, and the fractional clearance of 70-kDa neutral dextran (phi) rose moderately in rats receiving L-NAME and SS. Rats given L-NAME and HS exhibited massive albuminuria, whereas phi was nearly tripled. Depletion of GBM anionic sites was also seen in these rats. The GBM was thickened in both L-NAME-treated groups. These abnormalities were largely reversed after cessation of treatments. These results indicate that chronic L-NAME treatment promotes reversible albuminuria by impairing both glomerular size and charge selectivity. These effects likely reflect functional rather than structural disruption of the glomerular wall.
dc.descriptiono TEXTO COMPLETO DESTE ARTIGO, ESTARÁ DISPONÍVEL À PARTIR DE AGOSTO DE 2015.
dc.description279
dc.description6
dc.descriptionF1060
dc.descriptionF1066
dc.languageen
dc.publisherAmer Physiological Soc
dc.publisherBethesda
dc.publisherEUA
dc.relationAmerican Journal Of Physiology-renal Physiology
dc.relationAm. J. Physiol.-Renal Physiol.
dc.rightsembargo
dc.sourceWeb of Science
dc.subjectkidney glomerulus
dc.subjectkidney physiopathology
dc.subjectcapillary permeability
dc.subjectsodium
dc.subjectdietary
dc.subjectGlomerular-basement-membrane
dc.subjectVascular-permeability
dc.subjectArterial-hypertension
dc.subjectLeukocyte Adhesion
dc.subjectSlit Diaphragm
dc.subjectRat
dc.subjectSclerosis
dc.subjectInjury
dc.subjectPermselectivity
dc.subjectBarrier
dc.titleMechanisms of albuminuria in the chronic nitric oxide inhibition model
dc.typeArtículos de revistas


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