作者: ZACHARY C BERWICK , GREGORY A PAYNE , BRANDON LYNCH , GREGORY M DICK , MICHAEL STUREK
DOI: 10.1111/J.1549-8719.2010.00054.X
关键词: Adenosine receptor 、 Dilator 、 Adenosine 、 Internal medicine 、 Vasodilation 、 Coronary circulation 、 Glibenclamide 、 Receptor antagonist 、 Reactive hyperemia 、 Endocrinology 、 Chemistry
摘要: This study was designed to elucidate the contribution of adenosine A(2A) and A(2B) receptors coronary reactive hyperemia downstream K(+) channels involved. Coronary blood flow measured in open-chest anesthetized dogs. Adenosine dose-dependently increased from 0.72 ± 0.1 2.6 0.5 mL/minute/g under control conditions. Inhibition with SCH58261 (1 μm) attenuated adenosine-induced dilation by ∼50%, while combined administration receptor antagonist alloxazine (3 produced no additional effect. significantly reduced response a transient 15 second occlusion; debt/repayment ratio decreased 343 63 232 44%. Alloxazine alone increases ∼30% but failed alter hyperemia. agonist CGS21680 (10 μg bolus) 3.08 0.31 mL/minute/g. dilator 0.76 0.14 inhibition K(V) 4-aminopyridine (0.3mm) 0.11 K(ATP) glibenclamide mg/kg). Combined abolished vasodilation CGS21680. These data indicate that contribute cardiac ischemia via activation channels.