Risk of endothelial dysfunction in streptozotocin-induced diabetic Sprague-Dawley rats: Nitric oxide in focus

Abstract

Endothelial dysfunction in diabetes manifests in part as  reduction of nitric oxide (NO) bioavailability, which leads to inadequate relaxation of the vascular smooth muscle and a disparity between the vasoconstrictive and vasorelaxant intracellular pathways which favours a rise in vasoconstriction. In this current work, we evaluated serum Nitric oxide (NO) concentration and the activity of Nitric oxide synthase (NOS) in streptozotocin-induced diabetic male and female rats' serum. Our results showed initial and final fasting blood glucose concentration 5.30±0.16mmol/l and 5.24±.015mmol/l versus 5.68±0.18mmol/l and 5.43±0.15mmol/l in male and female controls. Among the diabetic rats, the initial and final fasting blood glucose concentration was 17.50±1.91mmol/l and 15.68±2.84mmol/l versus 20.50±4.76mmol/l and 19.40±4.13mmol/l in male and female rats respectively. NO concentration was 106.12±7.23μmol/l and 131.81±12.54 μmol/l in male and female control rats compared to 52.38±3.01μmol/l and 65.29±16.19 μmol/l in male and female diabetic rats respectively. Serum activity of NOS were 133.72±10.92μIU/l and 156.06±18.22 μIU/l in control male and female rats compared to 98.01±1.48 μIU/l, 78.89±8.39μIU/l in diabetic male and female rats respectively. The difference in both NO concentration and NOS activity was significant between diabetics and non-diabetic rats as well as between male and female diabetics rats (p< 0.05). The endothelial dysfunction in diabetic animals regardless of gender may be an initial pointer to upcoming pathogenesis and we recommend routine evaluation of NO concentration and NOS activities among diabetics.