Bradykinin B2Receptor is Involved in the Late Phase of Preconditioning in Rabbit Heart

Abstract

C. Kositprapa, R. A. Ockaili and R. C. Kukreja. Bradykinin B2Receptor is Involved in the Late Phase of Preconditioning in Rabbit Heart. Journal of Molecular and Cellular Cardiology (2001) 33, 0000–0000. Activation of bradykinin B2receptor has been shown to confer short-term cardioprotection against a prolonged ischemic insult. The present study was designed to delineate the role of B2receptor in the late phase of ischemic preconditioning. Anesthetized, open chest, male rabbits were assigned to 1 of 6 groups (n=8/group). Ischemic preconditioning was elicited by four 5-min occlusion periods interspersed with 10 min of reperfusion. To test the role of B2receptors, rabbits were pretreated with specific receptor antagonist, HOE-140 (1 μ gm/kg IV bolus), 15 min prior to ischemic preconditioning. Additionally, two separate groups of animals were treated by intra-atrial infusion with either bradykinin (0.05 μ g/kg/min for 15 min) or saline. Twenty-four hours later, the animals were subjected to 30 min of ischemia and 3 h of reperfusion. Infarct size was determined by tetrazolium staining. Ischemic preconditioning reduced infarct size from 43.09±4.66 to 20.65±1.87 (% risk area, P<0.05), which was blocked by HOE-140 as indicated by increase in infarct size (36.72±4.04%, P<0.05). HOE-140 treatment had no significant effect on infarct size in the sham group. Similarly, intra-atrial infusion of bradykinin caused decrease in the infarct size from 52.36±2.17% in the saline control group to 22.83±1.71% (P<0.05). The degree of infarct limitation with bradykinin was comparable to ischemic preconditioning (20.65±1.87%v 22.83±1.71%, P>0.05). For the first time, these results provide evidence for the involvement of B2receptor in the genesis of late phase of ischemic preconditioning.