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 (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 

Original languageEnglish (US)
Pages (from-to)141-145
Number of pages5
JournalComparative biochemistry and physiology. Part A, Molecular & integrative physiology
Volume201
DOIs
StatePublished - Nov 1 2016

Fingerprint

Grief
Columbidae
Vasodilation
Acetylcholine
Arteries
Glucose
Oxidative stress
Oxidative Stress
Mammals
Endothelium
1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt
Tibial Arteries
Edge detection
Phenylephrine
Superoxides
Hyperglycemia
Osmolar Concentration
Superoxide Dismutase
Software
Antioxidants

Keywords

  • Acetylcholine
  • Artery
  • Avian
  • Hyperglycemia
  • Superoxide
  • Vasodilation

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Physiology

Cite this

High glucose impairs acetylcholine-mediated vasodilation in isolated arteries from Mourning doves (Z. macroura). / Jarrett, Catherine L.; Ahmed, Zoha; Faust, James J.; Sweazea, Karen.

In: Comparative biochemistry and physiology. Part A, Molecular & integrative physiology, Vol. 201, 01.11.2016, p. 141-145.

Research output: Contribution to journalArticle

@article{397d192926214c96991ed0bc01dae8a1,
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 (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 ",
keywords = "Acetylcholine, Artery, Avian, Hyperglycemia, Superoxide, Vasodilation",
author = "Jarrett, {Catherine L.} and Zoha Ahmed and Faust, {James J.} and Karen Sweazea",
year = "2016",
month = "11",
day = "1",
doi = "10.1016/j.cbpa.2016.07.010",
language = "English (US)",
volume = "201",
pages = "141--145",
journal = "Comparative Biochemistry and Physiology - A Physiology",
issn = "1095-6433",
publisher = "Elsevier Inc.",

}

TY - JOUR

T1 - High glucose impairs acetylcholine-mediated vasodilation in isolated arteries from Mourning doves (Z. macroura)

AU - Jarrett, Catherine L.

AU - Ahmed, Zoha

AU - Faust, James J.

AU - Sweazea, Karen

PY - 2016/11/1

Y1 - 2016/11/1

N2 - 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 

AB - 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 

KW - Acetylcholine

KW - Artery

KW - Avian

KW - Hyperglycemia

KW - Superoxide

KW - Vasodilation

UR - http://www.scopus.com/inward/record.url?scp=84979042744&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84979042744&partnerID=8YFLogxK

U2 - 10.1016/j.cbpa.2016.07.010

DO - 10.1016/j.cbpa.2016.07.010

M3 - Article

VL - 201

SP - 141

EP - 145

JO - Comparative Biochemistry and Physiology - A Physiology

JF - Comparative Biochemistry and Physiology - A Physiology

SN - 1095-6433

ER -