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Am J Physiol Renal Physiol (October 15, 2002). doi:10.1152/ajprenal.00271.2002
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Articles in PresS, published online ahead of print October 15, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00271.2002
Submitted on July 24, 2002
Accepted on October 8, 2002

A3 adenosine receptor knock-out mice are protected against ischemic- and myoglobinuric-induced renal failure

H. Thomas Lee1*, Ayuko Ota-Setlik1, Hua Xu1, Vivette D. D'Agati2, Marlene A. Jacobson3, and Charles W. Emala1

1 Department of Anesthesiology, Columbia University, New York, NY, USA
2 Department of Pathology, Columbia University, New York, NY, USA
3 Department of Pharmacology, Merck Research Laboratories, West Point, PA, USA

* To whom correspondence should be addressed. E-mail: tl128{at}columbia.edu.

A3 adenosine receptor (AR) activation and inhibition worsens and improves, respectively, renal function after ischemic reperfusion (IR) injury in rats. We sought to further characterize the role of A3 ARs in modulating renal function after either IR or myoglobinuric renal injury. A3 knockout mice had significantly lower plasma creatinines compared to C57 controls 24 hrs after IR or myoglobinuric renal injury. C57 control mice pretreated with the A3 AR antagonist (MRS-1191) or agonist (IB-MECA, 0.125 mg/kg) demonstrated improved or worsened renal function, respectively, after IR or myoglobinuric renal injury. Higher doses of IB-MECA were lethal in C57 mice subjected to renal ischemia. H1 but not H2 histamine receptor antagonist prevented death in mice pretreated with IB-MECA before renal ischemia. Improvement in renal function was associated with significantly improved renal histology. In conclusion, pre-ischemic A3 AR activation (0.125 mg/kg IB-MECA) exacerbated renal IR injury in mice. Mice lacking A3 ARs or blocking A3 ARs in wild type mice resulted in significant renal protection from ischemic or myoglobinuric renal failure.




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