ISSN:
1432-0428
Keywords:
Keywords Nitric oxide
;
nitrite
;
nitrate
;
l-arginine
;
N-omega-nitro-l-arginine
;
ischaemic acute renal failure
;
diabetes mellitus
;
streptozotocin
;
rats.
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Summary Changes in nitric oxide (NO) levels were determined in ischaemic acute renal failure in streptozotocin-induced diabetes mellitus rats. Two weeks after streptozotocin administration and immediately after right nephrectomy, the left renal artery was occluded for 60 min. Similar procedures were carried out in non-diabetic rats. The nitrite (NO2) + nitrate (NO3) levels were measured in plasma and urine. The effects of chronic oral supplementation with l-arginine and an NO synthase inhibitor (N-omega-nitro-l-arginine) were also studied in both diabetic and non-diabetic rats before and after renal artery clamping. The rats with diabetic acute renal failure had a much lower creatinine clearance (90 ± 22 μl · min−1· 100 g body weight −1, p 〈 0.005), and higher fractional excretion of sodium (FENa)% (10.90 ± 4.2, p 〈 0.001) and protein excretion (2078 ± 69 μg/ml creatinine clearance, p 〈 0.001) compared with the respective values in the non-diabetic groups (163 ± 30; 1.46 ± 86; 453.3 ± 31). The plasma and urine NO2 + NO3 levels were significantly higher in the untreated diabetic rats compared with the untreated normal rats before ischaemia (p 〈 0.001). The ischaemic acute renal failure in non-diabetic rats increased the plasma and urinary NO2 + NO3 excretion after ischaemia. The urinary excretion of these metabolites decreased significantly and their plasma levels remained unchanged in the ischaemic diabetic rats. The l-arginine administration resulted in a small but significantly higher creatinine clearance after clamping in the non-diabetic rats. The NO synthase inhibitor caused deterioration in renal function in all ischaemic and non-ischaemic groups. In summary, the greater vulnerability to ischaemia of the diabetic kidney seems to be associated with both impaired response to and impaired production of NO. [Diabetologia (1996) 39: 1036–1040]
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00400651
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