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Am J Physiol Renal Physiol 279: F809-F818, 2000;
0363-6127/00 $5.00
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Vol. 279, Issue 5, F809-F818, November 2000

A2A adenosine receptor-mediated inhibition of renal injury and neutrophil adhesion

Mark D. Okusa1, Joel Linden1,2, Liping Huang1, Jayson M. Rieger3, Timothy L. Macdonald3, and Long P. Huynh1

Departments of 1 Medicine, 2 Molecular Physiology and Biological Physics, and 3 Chemistry, University of Virginia, Charlottesville, Virginia 22908

We sought to determine the mechanisms responsible for the reduced renal tissue injury by agonists of A2A adenosine receptors (A2A-ARs) in models of ischemia-reperfusion (I/R) injury. DWH-146e, a selective A2A-AR agonist, was administered subcutaneously to Sprague-Dawley rats and C57BL/6 mice via osmotic minipumps, and animals were subjected to I/R. I/R led to an increase in plasma creatinine and kidney neutrophil infiltration. Infusion of DWH-146e at 10 ng · kg-1 · min-1 produced a 70% reduction in plasma creatinine as well as a decrease in neutrophil density in outer medulla and cortex and myeloperoxidase activity in the reperfused kidney. Myeloperoxidase activity in kidney correlated with the degree of renal injury. P-selectin and intercellular adhesion molecule 1 (ICAM-1) immunoreactivity were most prominent in endothelial cells of peritubular capillaries and interlobular arteries of cortex and outer and inner medulla of vehicle-treated mice whose kidneys were subjected to I/R. DWH-146e treatment led to a pronounced decrease in P-selectin- and ICAM-1-like immunoreactivity. These data are consistent with our hypothesis that A2A-AR agonists limit I/R injury due to an inhibitory effect on neutrophil adhesion.

acute renal failure; neutrophil-endothelial cell interaction; intercellualr adhesion molecule 1; P-selectin


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