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Am J Physiol Heart Circ Physiol 285: H1797-H1818, 2003; doi:10.1152/ajpheart.00407.2003
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Acute adenosinergic cardioprotection in ischemic-reperfused hearts

John P. Headrick, Ben Hack, and Kevin J. Ashton

Heart Foundation Research Center, School of Health Science, Griffith University, Southport, Queensland 4217, Australia

Cells of the cardiovascular system generate and release purine nucleoside adenosine in increasing quantities when constituent cells are "stressed" or subjected to injurious stimuli. This increased adenosine can interact with surface receptors in myocardial, vascular, fibroblast, and inflammatory cells to modulate cellular function and phenotype. Additionally, adenosine is rapidly reincorporated back into 5'-AMP to maintain the adenine nucleotide pool. Via these receptor-dependent and independent (metabolic) paths, adenosine can substantially modify the acute response to ischemic insult, in addition to generating a more sustained ischemia-tolerant phenotype (preconditioning). However, the molecular basis for acute adenosinergic cardioprotection remains incompletely understood and may well differ from more widely studied preconditioning. Here we review current knowledge and some controversies regarding acute cardioprotection via adenosine and adenosine receptor activation.

adenosine; adenosine receptor activation; ischemia; reperfusion injury


Address for reprint requests and other correspondence: J. Headrick, Heart Foundation Research Centre, Griffith Univ., Southport QLD 4217, Australia (E-mail: J.Headrick{at}griffith.edu.au).




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