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| 2007 JASN IMPACT FACTOR 7.111 | HOME AUTHOR INFO EDITORIAL BOARD SUBSCRIBE FEEDBACK ALERTS HELP | |||
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BASIC SCIENCE |
Departments of *Anesthesiology and Pathology, College of Physicians and Surgeons of Columbia University, New York, New York.
Correspondence to Dr. H. Thomas Lee, Department of Anesthesiology, Anesthesiology Research Laboratories, Columbia University, P&S Box 46 (PH-5), 630 West 168th Street, New York, NY 10032-3784. Phone: 212-305-4716; Fax: 212-305-8980;
ABSTRACT. It was previously demonstrated that preischemic A1 adenosine receptor (AR) activation protects renal function after ischemia-reperfusion (IR) injury in rats. The role of the A1 AR in modulating inflammation, necrosis, and apoptosis in the kidney after IR renal injury was further characterized. C57BL/6 mice were subjected to 30 min of renal ischemia, with or without pretreatment with 1,3-dipropyl-8-cyclopentylxanthine or 2- chlorocyclopentyladenosine (selective A1 AR antagonist and agonist, respectively). Plasma creatinine levels and renal inflammation, necrosis, and apoptosis were compared 24 h after renal injury. C57BL/6 mice that had been pretreated with the A1 AR agonist demonstrated significantly improved renal function and reduced expression of inflammatory markers, necrosis, and apoptosis 24 h after IR injury. In contrast, C57BL/6 mice that had been pretreated with the A1 AR antagonist demonstrated significantly worsened renal function and increased expression of inflammatory markers, necrosis, and apoptosis. In conclusion, it was demonstrated that endogenous and exogenous preischemic activation of the A1 AR protects against IR injury in vivo, through mechanisms that reduce inflammation, necrosis, and apoptosis. E-mail: tl128@columbia.edu
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