Investigating the effect of CoCl2 administration on diabetic nephropathy and associated aortic dysfunction

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.

We examined the effect of CoCl(2) (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.

A significant attenuation of the augmented responses to angiotensin II was observed in CoCl(2)-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.

Chronic hypoxia augments angiotensin II responses in the thoracic aorta of uninephrectomized diabetic control rats. CoCl(2) 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.