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1 Department of Anesthesiology, College of Physicians and Surgeons of Columbia University, New York, NY, USA
2 Department of Pathology, College of Physicians and Surgeons of Columbia University, New York, NY, USA
3 National Institute of Diabetes and Digestive and Kidney Diseases, National Institution of Health, Bethesda, MD, USA
* To whom correspondence should be addressed. E-mail: tl128{at}columbia.edu.
Controversey exists regarding the effect of A1 adenosine receptor (AR) activation in the kidney during ischemia and reperfusion (IR) injury. We sought to further characterize the role of A1 ARs in modulating renal function after IR renal injury utilizing both pharmacologic and gene deletion approaches in mice. A1 adenosine receptor knock-out 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 DPCPX or CCPA (selective A1 AR antagonist or agonist, respectively). Plasma creatinine and renal histology were compared 24 hrs after renal injury. A1KO mice exhibited significantly higher creatinines and
worsened renal histology compared to A1WT controls following renal IR injury. A1WT mice pretreated with the A1 AR antagonist or agonist demonstrated significantly worsened or improved renal function, respectively, after IR 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-
and IL-1
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 IR injury in vivo via mechanisms leading to decreased necrosis
and inflammation.
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