Mechanisms of albuminuria in the chronic nitric oxide inhibition model

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...

Full description

Saved in:
Bibliographic Details
Published in:American journal of physiology. Renal physiology 2000-12, Vol.279 (6), p.F1060-F1066
Main Authors: Arcos, M I, Fujihara, C K, Sesso, A, de Almeida Prado, E B, de Almeida Prado, M J, de Nucci, G, Zatz, R
Format: Article
Language:English
Subjects:
Albuminuria - metabolism
Animals
Electrophoresis, Polyacrylamide Gel
Enzyme Inhibitors - pharmacology
Kidney - enzymology
Kidney - pathology
Kidney - ultrastructure
Kidney Function Tests
Kidney Glomerulus - drug effects
Kidney Glomerulus - ultrastructure
Male
NG-Nitroarginine Methyl Ester - pharmacology
Nitric Oxide - antagonists & inhibitors
Nitric Oxide Synthase - antagonists & inhibitors
Permeability
Proteinuria - urine
Rats
Rats, Wistar
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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.
ISSN:1931-857X
1522-1466
DOI:10.1152/ajprenal.2000.279.6.f1060