Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/53525
Type: Artigo de periódico
Title: Mechanisms of albuminuria in the chronic nitric oxide inhibition model
Author: Arcos, MI
Fujihara, CK
Sesso, A
Prado, EBD
Brandao, MJ
Prado, D
De Nucci, G
Zatz, R
Abstract: Chronic 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.
Subject: kidney glomerulus
kidney physiopathology
capillary permeability
sodium
dietary
Country: EUA
Editor: Amer Physiological Soc
Rights: embargo
Date Issue: 2000
Appears in Collections:Artigos e Materiais de Revistas Científicas - Unicamp

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