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Am J Physiol Renal Physiol 286: F298-F306, 2004. First published November 4, 2003; doi:10.1152/ajprenal.00185.2003
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A1 adenosine receptor knockout mice exhibit increased renal injury following ischemia and reperfusion

H. Thomas Lee,1 Hua Xu,1 Samih H. Nasr,2 Jurgen Schnermann,3 and Charles W. Emala1

Departments of 1Anesthesiology and 2Pathology, College of Physicians and Surgeons of Columbia University, New York, New York 10032; and 3National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892

Submitted 13 May 2003 ; accepted in final form 21 October 2003

Controversy exists regarding the effect of A1 adenosine receptor (AR) activation in the kidney during ischemia and reperfusion (I/R) injury. We sought to further characterize the role of A1 ARs in modulating renal function after I/R renal injury using both pharmacological and gene deletion approaches in mice. A1 AR knockout mice (A1KO) or their wild-type littermate controls (A1WT) were subjected to 30 min of renal ischemia. Some A1WT mice were subjected to 30 min of renal ischemia with or without pretreatment with 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) or 2-chrolo-cyclopentyladenosine (CCPA), selective A1 AR antagonist and agonist, respectively. Plasma creatinine and renal histology were compared 24 h after renal injury. A1KO mice exhibited significantly higher creatinines and worsened renal histology compared with A1WT controls following renal I/R injury. A1WT mice pretreated with the A1 AR antagonist or agonist demonstrated significantly worsened or improved renal function, respectively, after I/R injury. In addition, A1WT mice pretreated with DPCPX or CCPA showed significantly increased or reduced markers of renal inflammation, respectively (renal myeloperoxidase activity, renal tubular neutrophil infiltration, ICAM-1, TNF-{alpha}, and IL-1{beta} mRNA expression), while demonstrating no differences in indicators of apoptosis. In conclusion, we demonstrate that endogenous or exogenous preischemic activation of A1 ARs protects against renal I/R injury in vivo via mechanisms leading to decreased necrosis and inflammation.

acute renal failure; inflammation; ischemic-repefusion injury


Address for reprint requests and other correspondence: H. Thomas Lee, Dept. of Anesthesiology, Anesthesiology Research Laboratories, College of Physicians and Surgeons of Columbia Univ., P&S Box 46 (PH-5), 630 W. 168th St., New York, NY 10032-3784 (E-mail: tl128{at}columbia.edu).




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