Background: 

The influence and importance of B-type natriuretic peptide in acute myocardial infarction has for many years been ignored, and BNP has been underestimated as only a predictor of heart failure. Since it has recently been shown that exogenously administered BNP can reduce infarct size when delivered before, during and after ischemia, a study of BNPpostconditioning and mechanism in the ischemic myocardium was investigated.

Aim: 

Determine whether postconditioning with BNP reduced infarct size compared to ischemic reperfused hearts and determine if natriuretic peptide receptor A (NPR-A) and/or the RISK pathway is necessary for the protection.

Methods: 

The Langendorff perfused rat heart subjected to 30 min of regional ischemia (RI) and 120 min of reperfusion were exposed to Ischemic Postconditioning (IPost) by 3 x 30 s of global ischemia and 3 x 30 s infusion of recombinant BNP as a postconditioning mimetic (BNPPost). Inhibitors of the RISK pathway (wortmannin (Wi), SH-6 and rapamycin (Rap) and NPR-A (isatin) were employed in order determine whether the activation of these pathways are required for BNP induced cardioprotection.

Results: 

Compared to ischemia reperfusion, BNP postconditioning reduced infarct sizes by more than 50% (BNPPost 17 ±2% vs. Ctr 42 ±4%, p< 0.05). Co-administation of inhibitors the RISK pathway (Wi, SH-6 and Rap) or the NPR receptor (isatin) abrogated the cardioprotection, while the inhibitors by themselves had no effect on the size of infarct.

Conclusion: 

BNP is protective as a postconditioning mimetic and relies on both NPR binding and RISK signalling.