Abstract

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 CoCl<sub>2</sub> (10 mg/kg, i.p., OD = once a day) treatment on contractile responses to angiotensin II (10<sup>–10</sup> to 10<sup>–6</sup><smlcap>M</smlcap>) 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 CoCl<sub>2</sub>-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. CoCl<sub>2</sub> 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.

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