Background: This study was designed to investigate whether the activation of calcium-activated potassium (KCa) or adenosine triphosphate sensitive potassium (KATP) channels are required for bradykinin-induced microvascular preconditioning. Methods: Isolated rabbit hearts underwent retrograde perfusion with Krebs-Henseleit buffer (KHB) followed by 60 minutes of ischemic arrest with cold crystalloid cardioplegia (CCCP). Eight CCCP hearts received no pretreatment. Six bradykinin-preconditioned hearts received a 10-minute coronary infusion of 10-8 mol/L bradykinin-enriched KHB followed by a 5-minute recovery period before CCCP. Six hearts received both 10-8 mol/L charybdotoxin (a KCa channel blocker) and bradykinin preconditioning. Finally, 6 other hearts received 10-5° mol/L glibenclamide (a KATP channel blocker) to bradykinin-enriched KHB. All hearts were reperfused for 30 minutes with KHB. Results: Bradykinin preconditioning significantly improved the recovery of left ventricular and microvascular function, as compared with control. On the other hand, bradykinin preconditioning significantly reduced the contractile responses to U46619, a thromboxane A2 analogue. Charybdotoxin significantly inhibited the improved recovery of bradykinin-induced left ventricular and microvascular function. Glibenclamide tended to diminish the bradykinin preconditioning-enhanced recovery of left ventricular function, but failed to affect bradykinin preconditioning-improved recovery of microvascular function. Conclusion: Both KCa and KATP channels were involved partially in bradykinin-induced myocardial preconditioning. However, bradykinin induces microvascular preconditioning through the opening of KCa channels rather than KATP channels.
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