Journal
KIDNEY & BLOOD PRESSURE RESEARCH
Volume 35, Issue 6, Pages 694-697Publisher
KARGER
DOI: 10.1159/000343888
Keywords
Chronic hypoxia; Hypoxia inducible factor-1 alpha; Prolyl hydroxylase; Oxidative stress; Nitric oxide; Angiotensin II; Endothelial dysfunction
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Aim: Endothelial dysfunction appears to be a consistent finding in diabetic nephropathy. The study aimed to investigate the effect of cobalt chloride in the amelioration of endothelial dysfunction in uninephrectomized diabetic rats. Methods: We examined the effect of CoCl2 (10 mg/kg, i.p., OD = once a day) treatment on contractile responses to angiotensin II (10(-10) to 10(-6) M) in an aortic preparation of control rats and uninephrectomized diabetic control rats. Blood glucose, plasma urea, creatinine, uric acid, aortic endothelial nitric oxide synthase (eNOS), nitrate/nitrite (NOx), superoxide dismutase, catalase and reduced glutathione levels were checked in the different groups. Results: A significant attenuation of the augmented responses to angiotensin II was observed in CoCl2-treated animals along with a fall in plasma urea, creatinine and uric acid levels. A significant reduction in blood glucose and an increase in aortic eNOS and NOx levels along with antioxidants levels were observed. Conclusion: Chronic hypoxia augments angiotensin II responses in the thoracic aorta of uninephrectomized diabetic control rats. CoCl2 attenuates these enhanced vascular responses with a significant decrease in blood glucose signifying stabilization of the hypoxia-inducible factor in the alleviation of endothelial dysfunction in diabetic nephropathy. Copyright (C) 2013 S. Karger AG, Basel
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