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Mechanisms of albuminuria in the chronic nitric oxide inhibition model.

Authors
  • Arcos, M I
  • Fujihara, C K
  • Sesso, A
  • de Almeida Prado, E B
  • de Almeida Prado, M J
  • de Nucci, G
  • Zatz, R
Type
Published Article
Journal
American Journal of Physiology - Renal Physiology
Publisher
American Physiological Society
Publication Date
Dec 01, 2000
Volume
279
Issue
6
Identifiers
PMID: 11097624
Source
Medline
License
Unknown

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 approximately 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.

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