title: High glucose impairs acetylcholine-mediated vasodilation in isolated arteries from Mourning doves (Z. macroura).
abstract: 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 (20mM vs. 30mM) for 1h 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, 5min 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 20mM d-glucose and 10mM 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 (10mM) 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.
authors.affiliation: School of Nutrition and Health Promotion, Arizona State University, Phoenix, AZ, USA.
authors.forename: Catherine L
authors.initials: CL
authors.lastname: Jarrett
authors.affiliation: School of Life Sciences, Arizona State University, Tempe, AZ, USA.
authors.forename: Zoha
authors.initials: Z
authors.lastname: Ahmed
authors.affiliation: School of Life Sciences, Arizona State University, Tempe, AZ, USA.
authors.forename: James J
authors.initials: JJ
authors.lastname: Faust
authors.affiliation: School of Nutrition and Health Promotion, Arizona State University, Phoenix, AZ, USA; School of Life Sciences, Arizona State University, Tempe, AZ, USA. Electronic address: Karen.Sweazea@asu.edu.
authors.forename: Karen L
authors.initials: KL
authors.lastname: Sweazea
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001158:Arteries / Q000187:drug effects / Q000502:physiology; D010856:Columbidae / Q000502:physiology*; D005260:Female; D005947:Glucose / Q000378:metabolism*; D006943:Hyperglycemia / Q000503:physiopathology; D066298:In Vitro Techniques; D008297:Male; D018384:Oxidative Stress; D013482:Superoxide Dismutase / Q000378:metabolism; D013481:Superoxides / Q000378:metabolism; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology*
chemical_list: D013481:Superoxides; D013482:Superoxide Dismutase; D005947:Glucose; D000109:Acetylcholine
keywords: Acetylcholine; Artery; Avian; Hyperglycemia; Superoxide; Vasodilation