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Reduced Nitric Oxide Concentration in the Renal Cortex of Streptozotocin-Induced Diabetic Rats
Journal article   Open access   Peer reviewed

Reduced Nitric Oxide Concentration in the Renal Cortex of Streptozotocin-Induced Diabetic Rats

Fredrik Palm, Donald G. Buerk, Per-Ola Carlsson, Peter Hansell and Per Liss
Diabetes (New York, N.Y.), v 54(11), pp 3282-3287
01 Nov 2005
PMID: 16249456
url
https://doi.org/10.2337/diabetes.54.11.3282View
Published, Version of Record (VoR)Maybe Open Access (Publisher Bronze) Open

Abstract

Nitric oxide (NO) regulates vascular tone and mitochondrial respiration. We investigated the hypothesis that there is reduced NO concentration in the renal cortex of diabetic rats that mediates reduced renal cortical blood perfusion and oxygen tension (Po2). Streptozotocin-induced diabetic and control rats were injected with l-arginine followed by Nω-nitro-l-arginine-metyl-ester (l-NAME). NO and Po2 were measured using microsensors, and local blood flow was recorded by laser-Doppler flowmetry. Plasma arginine and asymmetric dimethylarginine (ADMA) were analyzed by high-performance liquid chromatography. l-Arginine increased cortical NO concentrations more in diabetic animals, whereas changes in blood flow were similar. Cortical Po2 was unaffected by l-arginine in both groups. l-NAME decreased NO in control animals by 87 ± 15 nmol/l compared with 45 ± 7 nmol/l in diabetic animals. l-NAME decreased blood perfusion more in diabetic animals, but it only affected Po2 in control animals. Plasma arginine was significantly lower in diabetic animals (79.7 ± 6.7 vs. 127.9 ± 3.9 mmol/l), whereas ADMA was unchanged. A larger increase in renal cortical NO concentration after l-arginine injection, a smaller decrease in NO after l-NAME, and reduced plasma arginine suggest substrate limitation for NO formation in the renal cortex of diabetic animals. This demonstrates a new mechanism for diabetes-induced alteration in renal oxygen metabolism and local blood flow regulation.

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Endocrinology & Metabolism
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