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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
N
-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 (
) rose moderately in
rats receiving L-NAME and SS. Rats given L-NAME and HS exhibited massive albuminuria,
whereas 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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