Acute adenosinergic cardioprotection in ischemic-reperfused hearts

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

Research output: Contribution to journalReview articleResearchpeer-review

147 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)H1797-H1818
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume285
Issue number5
DOIs
Publication statusPublished - Nov 2003
Externally publishedYes

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Adenosine
Purine Nucleosides
Phenotype
Purinergic P1 Receptors
Adenine Nucleotides
Adenosine Monophosphate
Cardiovascular System
Blood Vessels
Ischemia
Fibroblasts

Cite this

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Acute adenosinergic cardioprotection in ischemic-reperfused hearts. / Headrick, John P.; Hack, Ben; Ashton, Kevin J.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 285, No. 5 , 11.2003, p. H1797-H1818.

Research output: Contribution to journalReview articleResearchpeer-review

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AU - Ashton, Kevin J.

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