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Am J Physiol Renal Physiol 279: F1060-F1066, 2000;
0363-6127/00 $5.00
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Vol. 279, Issue 6, F1060-F1066, December 2000

Mechanisms of albuminuria in the chronic nitric oxide inhibition model

Michelle Indira Arcos1, Clarice Kazue Fujihara1, Antônio Sesso2, Euthymia Brandão De Almeida Prado1, Maria José Brandão De Almeida Prado1, Gilberto De Nucci3, and Roberto Zatz1

1 Renal Division, Department of Clinical Medicine, and 2 Department of Pathology, Faculty of Medicine, University of São Paulo, São Paulo 01246-903; and 3 Department of Pharmacology, State University of Campinas School of Medicine, Campinas, 13083-970 Brazil

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 Nomega -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 ~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.

kidney glomerulus; kidney physiopathology; capillary permeability; sodium; dietary


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