Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
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Drug
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Target Concepts:
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Query: UMLS:C0406810 (
NAME
)
13,345
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The purpose of the present study was to examine renal functional changes caused by chronic blockade of nitric oxide (NO) synthesis in young rats. Two types of NO synthase inhibitor were used: NG-nitro-L-arginine methyl ester (L-
NAME
) as a non-selective inhibitor and aminoguanidine (AG) as a selective inhibitor of the inducible isoform. Oral administration of L-
NAME
(20-80 mg/dL of drinking water), not AG (400 mg/dL), for 4 weeks induced systemic hypertension in the treated rats. Both inhibitors caused a significant reduction in urinary excretion of NO2-/NO3-. Rats treated with L-
NAME
developed proteinuria and tubular enzymuria (high excretion of
N-acetyl-beta-D-glucosaminidase
) in a dose-dependent fashion, with normal serum levels of creatinine, albumin and cholesterol. Chronic AG administration did not alter the urinary levels of protein and
N-acetyl-beta-D-glucosaminidase
or serum laboratory values. Overall, these observations highlight the importance of the continuous generation of NO by the constitutive isoform in the control of vascular tone and the maintenance of renal glomerular and tubular function. Oral administration of L-
NAME
may serve as a model of chronic NO-deficient hypertension with renal injury in young rats.
...
PMID:Renal functional measurements in young rats with chronic inhibition of nitric oxide synthase. 900 96
Urinary
N-acetyl-beta-D-glucosaminidase
(
NAG
) had been shown to be a useful early marker of renal injury such as lead nephrotoxicity. This study investigated the effect of lead acetate on nephrotoxicity and its correlation with the nitric oxide (NO) system by determining the
NAG
release in perfused rat kidney. Lead acetate caused a time and concentration-dependent increase in enzymuria. The effect of concurrent perfusion with lead and L-arginine (L-arg) or L-N(G)-nitro arginine methyl ester (L-
NAME
) [substrate and inhibitor of NO synthase respectively] in the perfusion fluid was also studied by measuring
NAG
activity in the perfusate kidney rat. L-arg (2 mM) has significantly decreased the lead-induced
NAG
release (P < 0.001), and L-
NAME
(0.1 mM) has significantly increased the lead-induced enzyme release in a time-dependent manner (P < 0.001). Moreover, histological studies using light microscope showed that some of the epithelial cells of the proximal convoluted tubules are degenerated or necrotic and desquamated into the lumens in rat treated with lead acetate. This change occurs at 50 microg/dl of lead acetate and was increased by addition of L-
NAME
to lead acetate. However, addition of L-arg had no effect on histology of lead nephrotoxicity. This may suggest that lead may interfere with the NO system in rat kidney.
...
PMID:Increase by NO synthase inhibitor of lead-induced release of N-acetyl-beta-D-glucosaminidase from perfused rat kidney. 1043 75
This study was designed to evaluate the role of nitric oxide (NO) in FK506-induced nephrotoxicity by administering an inhibitor of NO synthesis, N omega-nitro-L-arginine methyl ester (L-
NAME
) to rats treated with FK506. After one week of treatment with FK506 (3.2 mg/kg/day, intramuscularly) and/or L-
NAME
(5 mg/100 mL of L-
NAME
in the drinking water), the arterial pressure, urinary NOx, and parameters for renal function were measured, and histological analysis of the kidney was made. In the L-
NAME
without FK506 group, L-
NAME
administration effectively inhibited urinary NOx excretion and increased mean arterial pressure (MAP) without any change in renal function. In the FK506 without L-
NAME
group, FK506 treatment showed increase in urinary NOx excretion and mild renal dysfunction. In the FK506 with L-
NAME
group, urinary NOx excretion was decreased by L-
NAME
administration and renal function was significantly worsened than FK506 without L-
NAME
group. The plasma creatinine, BUN and urinary
N-acetyl-beta-D-glucosaminidase
increased 2-, 3-, and 3-fold, respectively and the creatinine clearance was reduced by 50% as compared with that in the FK506 without L-
NAME
group. Histological analysis revealed severe interstitial fibrosis and tubular atrophy in the FK506 + L-
NAME
treatment group. Thus, results suggest that NO synthesis is enhanced in the kidney during FK506-induced nephrotoxicity and that NO synthesis inhibition aggravates FK506-induced nephrotoxicity. NO may play a protective role attributable to the balance of vasoactive substances in FK506-induced nephrotoxicity.
...
PMID:Effects of nitric oxide synthesis inhibition on FK506-induced nephrotoxicity in rats. 1125 20
