原创力文档selective deletion of the a1 adenosine receptor abolishes heart-rate slowing effects of intravascular adenosine in vivo腺苷a1受体的选择性删除废除心率减缓体内血管内腺苷的影响.pdfVIP
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selective deletion of the a1 adenosine receptor abolishes heart-rate slowing effects of intravascular adenosine in vivo腺苷a1受体的选择性删除废除心率减缓体内血管内腺苷的影响
Selective Deletion of the A1 Adenosine Receptor
Abolishes Heart-Rate Slowing Effects of Intravascular
Adenosine In Vivo
Michael Koeppen1., Tobias Eckle1., Holger K. Eltzschig1,2*
1 Mucosal Inflammation Program, Department of Anesthesiology and Perioperative Medicine, University of Colorado Denver, Aurora, Colorado, United States of America,
¨ ¨
2 Department of Anesthesiology and Critical Care Medicine, Tubingen University Hospital, Tubingen, Germany
Abstract
Objective: Intravenous adenosine induces temporary bradycardia. This is due to the activation of extracellular adenosine
receptors (ARs). While adenosine can signal through any of four ARs (A1AR, A2AAR, A2BAR, A3AR), previous ex vivo studies
implicated the A1AR in the heart-rate slowing effects. Here, we used comparative genetic in vivo studies to address the
contribution of individual ARs to the heart-rate slowing effects of intravascular adenosine.
Methods and Results: We studied gene-targeted mice for individual ARs to define their in vivo contribution to the heart-
rate slowing effects of adenosine. Anesthetized mice were treated with a bolus of intravascular adenosine, followed by
measurements of heart-rate and blood pressure via a carotid artery catheter. These studies demonstrated dose-dependent
slowing of the heart rate with adenosine treatment in wild-type, A2AAR 2/ 2, A2BAR 2/ 2, or A3AR 2/ 2 mice. In contrast,
adenosine-dependent slowing of the heart-rate was completely abolished in A1AR 2/ 2 mice. Moreover, pre-treatment with a
specific A1AR antagonist (DPCPX) attenuated the heart-rate slowing effects of adenosine in wild-type, A2AAR 2/ 2, or
A2BAR 2/ 2 mice, but did not alter hemodynamic responses of A1AR 2/ 2 mice.
Conclusions: The present
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