Aim:To investigate the effects of renal ischemic preconditioning(IPC)on bothrenal hemodynamics and the renal interstitial concentrations of adenosine andadenine nucleotides induced by ischemia-reperfusion injury.Methods:Renalhemodynamics responses to ischemia-reperfusion injury in mongrel dog modelswere determined with or without multiple brief renal ischemic preconditioningtreatments,as well as the adenosine A_1 receptor antagonist(KW-3902),respectively.The renal interstitial concentrations of adenosine and adenine nucle-otides in response to ischemia-reperfusion injury,either following 1-3 cycles ofIPC or not,were measured simultaneously using microdialysis samplingtechnology.Results:One 10-min IPC,adenosine A_1 receptor antagonist(KW-3902)also shortened the recovery time of renal blood flow(RBF)and urine flow(UF),as well as mean blood pressure(BP).Advanced renal IPC attenuated theincrement of adenosine and adenine nucleotides,as well as recovery time duringthe 60-rain reperfusion which followed the 60-min renal ischemia.All of theserecovery times were dependent on the cycles of 10-min IPC.The renal interstitialconcentrations of adenosine and adenine nucleotides increased and decreasedduring renal ischemia and reperfusion,respectively.Conclusion:A significantrelativity in dog models exists between the cycles of 10-min renal IPC and therecovery time of BP,UF,and RBF during the 60-min renal reperfusion following60-min renal ischemia,respectively.Renal IPC can protect against ischemia-reperfusion injury and the predominant effect of endogenous adenosine inducedby prolonged renal ischemia;renal adenosine A_1 receptor activation during therenal ischemia-reperfusion injury is detrimental to renal function. Aim: To investigate the effects of renal ischemic preconditioning (IPC) on both renal hemhemics and the renal interstitial concentrations of adenosine and adenine nucleotides induced by ischemia-reperfusion injury. Methods: Renalhemodynamics responses to ischemia-reperfusion injury in mongrel dog models are determined with or without multiple brief renal ischemic preconditioning sites, as well as the adenosine A_1 receptor antagonist (KW-3902), respectively. The renal interstitial concentrations of adenosine and adenine nucleotides in response to ischemia-reperfusion injury, either following 1-3 cycles of IPC or not, (KW-3902) also shortened the recovery time of renal blood flow (RBF) and urine flow (UF), as well as mean blood pressure ( BP) .Advanced renal IPC attenuated theincrement of adenosine and adenine nucleotides, as well as recovery time during the 60-rain reperfusion wh ich followed the 60-min renal ischemia. All of these recovered times were dependent on the cycles of 10-min IPC. The renal interstitial components of adenosine and adenine nucleotides increased and decreased during renal ischemia and reperfusion, respectively. Confluence: A significant relationship in dog models exists between the cycles of 10-min renal IPC and therecovery time of BP, UF, and RBF during the 60-min renal reperfusion following 60-min renal ischemia, respectively. Renal IPC can protect against ischemia-reperfusion injury and the predominant effect of endogenous adenosine inducedby prolonged renal ischemia; renal adenosine A_1 receptor activation during therenal ischemia-reperfusion injury is detrimental to renal function.