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Preserving postischemic reperfusion in the kidney: a role for extracellular adenosine
Joel M Weinberg1, Manjeri A Venkatachalam
1Division of Nephrology, Department of Internal Medicine, Veterans Affairs Ann Arbor Healthcare System, University of Michigan, Ann Arbor, Michigan, USA. wnberg@umich.edu
Abstract:
Several adenosine receptor subtypes on endothelial, epithelial, mesangial, and inflammatory cells have been implicated in ischemic acute kidney injury, a life-threatening condition that frequently complicates the care of hospitalized patients. In this issue of the JCI, Grenz and coworkers provide novel insight into how preservation of postischemic renal perfusion by endothelial cell adenosine A2B receptors is antagonized by adenosine reuptake into proximal tubule cells by equilibrative nucleotide transporter 1, which can be inhibited by dipyridamole. The work suggests that adenosine A2B receptor agonists and inhibition of equilibrative nucleoside transporters by dipyridamole may have therapeutic potential in ischemic acute kidney injury, a condition for which there are currently no specific therapeutic interventions.
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