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Am J Physiol Heart Circ Physiol (September 9, 2005). doi:10.1152/ajpheart.00589.2005
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Submitted on June 3, 2005
Accepted on August 26, 2005

Endogenous adenosine protects the preconditioned heart during the early minutes of reperfusion by activating Akt

Nataliya V Solenkova1, Viktoriya Solodushko1, Michael V Cohen2, and James M Downey1*

1 Physiology, University of South Alabama, Mobile, AL, USA
2 Physiology, University of South Alabama, Mobile, AL, USA; Medicine, University of South Alabama, Mobile, AL, USA

* To whom correspondence should be addressed. E-mail: jdowney{at}usouthal.edu.

Ischemic preconditioning (IPC) is thought to protect by activating survival kinases during reperfusion. We tested whether binding of adenosine receptors is also required during reperfusion and, if so, how long these receptors must be populated. Isolated rabbit hearts were subjected to 30 min of regional ischemia and 2 h of reperfusion. IPC reduced infarct size from 32.1±4.6% of the risk zone in control hearts to 7.3±3.6%. IPC's protection was blocked by a 20-min pulse of the non-selective adenosine receptor blocker 8-(p-sulfophenyl) theophylline when started either 5 min before or 10 min after the onset of reperfusion, but not when started after 30 min of reperfusion. Protection was also blocked by either 1,3-dipropyl-8-cyclopentylxanthine, an adenosine A1-selective receptor antagonist, or MRS1754, an A2B-selective antagonist, but not by 8-(3-chlorostyryl)caffeine, an A2A-selective antagonist. Blockade of phosphatidylinositol 3-OH kinase (PI3K) with a 20-min pulse of wortmannin started either 5 min before or 10 or 30 min after the onset of reperfusion also aborted protection, but failed when started after 60 min of reflow. U0126, an antagonist of extracellular signal-regulated kinases (ERK) 1/2, blocked protection when started 5 min before reperfusion but not when started after only 10 min of reperfusion. These studies reveal that A1 and/or A2B receptors initiate the protective signal transduction cascade during reperfusion. While PI3K activity must continue long into the reperfusion phase, adenosine receptor occupancy is no longer needed by 30 min of reperfusion, and ERK activity is only required in the first few minutes of reperfusion.




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