Acute adenosinergic cardioprotection in ischemic-reperfused hearts.
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.
Headrick
John P
JP
Heart Foundation Research Centre, Griffith University, Southport, Queensland 4217, Australia. J.Headrick@griffith.edu.au
Hack
Ben
B
Ashton
Kevin J
KJ
D000208:Acute Disease; D000241:Adenosine / Q000502:physiology*; D000818:Animals; D006801:Humans; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology*; D018047:Receptors, Purinergic P1 / Q000502:physiology*
D018047:Receptors, Purinergic P1; D000241:Adenosine