Role of Adenosine in Renal Protection Induced by a Brief Episode of Ischemic Preconditioning in Rats

Abstract

ABSTRACT-The protective effect of a brief episode of ischemic preconditioning was examined at an early phase of ischemic-reperfusion injury in the rat kidney. Rats were subjected to 50 min of left renal artery occlusion followed by 120 min of reperfusion. Ischemic preconditioned rats were subjected to preconditioning with two cycles of 3-min ischemia and 5-min reperfusion (IPC). Ischemic-reperfusion injury led to a low recovery of the glomerular filtration rate (GFR). Overt morphological changes, consisting of blood trapping and tubular collapse, were seen. IPC improved the recovery of GFR and renal morphology. The IPC effect was not blocked by 8-(p-sulfophenyl)-theophylline (SPT), a non-selective adenosine receptor antagonist, by 1,3-dipropyl-8-cyclopentylxanthine (DPCPX), a selective A 1-receptor antagonist, or by 3,7-dimethyl-1-propargylxanthine (DMPX), a selective A2-receptor antagonist. Intravenous infusion of adenosine (30 mg/min per rat, for 5 min) prior to the 50-min occlusion improved the recovery of GFR, and this protection of GFR was blocked by SPT. Thus, both IPC and exogenous adenosine attenuated ischemicreperfusion injury of the kidney. However, because three adenosine receptor antagonists failed to abolish the protective effect of IPC, there is no evidence to indicate that activation of adenosine receptors contributes to the IPC effect in the kidney.

Gentamicin-induced preconditioning of proximal tubular LLC-PK1 cells stimulates nitric oxide production but not the synthesis of heat shock protein

“…The mechanisms involved in preconditioning are not fully understood, but may depend on the release of endog-Preconditioning with gentamicin of LLC-PK1 cells www.bjournal.com.br enous protective mediators such as adenosine (13), prostacyclin (14), bradykinin (15), nitric oxide (NO) (9), opening of K ATP channels (16), endothelin 1 decrease (17), and heat shock protein (HSP) synthesis (18). The protective effect of the initial preconditioning stress may involve the ability of tissue to induce HSP synthesis (19,20) and to increase NO production (21).…”

Pretreatment with adenosine and adenosine A1 receptor agonist protects against intestinal ischemia-reperfusion injury in rat

“…The endogenous adenosine or selective pharmacological agonists activate A1ARs. Preischemic activation of A1ARs has been demonstrated to prevent from I/R damage in various organs including heart [15][16][17][18]25] , kidney [26,27] and brain [28,29] . In these studies, the activation of A1ARs has been strongly implicated in the mediation of IPC.…”

“…Administration of adenosine either prior to ischemia or during reperfusion has been shown to attenuate myocardial injury [23,24] . Treatment with adenosine A1AR agonist initiates preconditioning not only in heart [15][16][17][18]25] but also in tissues such as kidney [26,27] and brain [28,29] , resulting in attenuation of ischemic injury. One of the underlying mechanisms suggested for adenosine receptor-mediated preconditioning in the heard is through involvement of protein kinase C (PKC) in heart [11,12,30] .…”

Visualisation of the Effects of Dilazep on Rat Afferent and Efferent Arterioles In Vivo

“…An equivalent volume of saline was administered as a control. To investigate the effects of dilazep further, three adenosine receptor antagonists were administered as pre-treatments: 8-p-sulfophenyl theophylline (8-sPT, 10 mg/kg), a nonselective adenosine receptor antagonist, was administered intravenously; 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 1 mg/kg), a selective A1 receptor antagonist, was administered intraperitoneally; and 3,7-dimethyl-1-propargylxanthine (DMPX, 1 mg/kg), a selective adenosine A2 receptor antagonist was administered intraperitoneally (17). These agonists, 8-sPT, DPCPX and DMPX, were purchased from the Sigma-Aldrich Corporation (St. Louis, USA), and dilazep was donated by Kowa Co., Ltd.…”