Paper Information

Title:  REDUCTION OF PROTEINURIA BY INHIBITION OF INDUCIBLE NITRIC OXIDE SYNTHASE IN RAT RENAL ISCHEMIA-REPERFUSION INJURY
Type: SPEECH
Author(s): KADKHODAEI M.,ZAHMATKESH M.
 
 
 
Name of Seminar: IRANIAN CONGRESS OF PHYSIOLOGY AND PHARMACOLOGY
Type of Seminar:  CONGRESS
Sponsor:  PHYSIOLOGY AND PHARMACOLOGY SOCIETY, MASHHAD UNIVERSITY OF MEDICAL SCIENCE
Date:  2007Volume 18
 
 
Abstract: 

Introduction: In recent years, there are some reports on the involvement of iNOS (inducible form of nitric oxide synthase) in proteinuria associated with renal disease. Studies in models of acute renal failure (ARF) have yielded convincing evidence that iNOS can be induced during ischemia-reperfusion (IR) conditions and acute renal allograft rejection. The present study was designed to investigate the effect of L-Nil (N6-(1-Iminoethyl)-L- lysine hydrochloride), a selective inhibitor of iNOS, in prevention of renal proteinuria in IR injury.
Methods: Rats were randomly assigned in four groups of Sham-operated, Sham+L-Nil, IR and IR+L-Nil. Ischemic acute renal failure (ARF) was induced by 40-min clamping of the renal arteries followed by 6 h reperfusion. Rats were administered either L-Nil (3 mg kg-1 I.V. bolus followed by infusion of 1 mg kg-1 h-1) or saline. To monitor glomerular & tubular functional changes before and after treatment, BUN, plasma creatinine (Cr) and urinary NAG (N-Acetyl-
b-D-glucosaminidase) activity were measured. Total protein, albumin, low and high molecular weight protein excretion rates were determined by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) of urine samples.
Results: Renal IR resulted in significant low and high molecular weight proteinuria. L-Nil significantly prevented the IR-induced increases in total protein, albumin and
a1-microglobulin excretion.
Conclusion: This study suggests that iNOS inhibition reduces IR-mediated renal proteinuria.

 
Keyword(s): 
 
Yearly Visit 12  
 
Latest on Blog
Enter SID Blog