High glucose impairs acetylcholine-mediated vasodilation in isolated arteries from Mourning doves (Z. macroura)

Normal avian plasma glucose levels are 1.5–2 times greater than mammals of similar size. In mammals, hyperglycemia induces oxidative stress and impaired endothelium-dependent vasodilation. Prior work has shown that mourning doves have high levels of antioxidants and isolated vessels have low endogenous oxidative stress. Therefore, the hypothesis was that endothelium-dependent vasodilation of isolated avian arteries would not be impaired following acute exposure to high glucose. Isolated small resistance cranial tibial arteries (c. tibial) were cannulated and pressurized in a vessel chamber then incubated with either normal or high glucose (20 mM vs. 30 mM) for 1 h at 41 °C. Vessels were then pre-constricted to 50% of resting inner diameter with phenylephrine (PE) followed by increasing doses of acetylcholine (ACh; 10^− 9 to 10^− 5 M, 5 min per step). Percent vasodilation was measured by tracking the inner diameter with edge-detection software. Contrary to our hypothesis, ACh-induced vasodilation was impaired with acute exposure to high glucose (p = 0.013). The impairment was not related to increased osmolarity since vasodilation of arteries exposed to an equimolar combination of 20 mM D-glucose and 10 mM L-glucose was not different from controls (p = 0.273). Rather, the impaired vasodilation was attributed to oxidative stress since superoxide levels were elevated 168 ± 42% (p = 0.02) and pre-exposure of arteries to the superoxide dismutase mimetic tiron (10 mM) improved vasodilation (p < 0.05). Therefore, isolated arteries from doves do not have endogenous mechanisms to prevent impaired vasodilation resulting from high glucose-mediated increases in oxidative stress.