B-type natriuretic peptide expression and cardioprotection is regulated by Akt dependent signaling at early reperfusion

•BNP postconditioning (BNPPost) protects the ex vivo rat heart from reperfusion injuries.•BNPPost elevated Akt and p70s6k phosphorylation at early reperfusion.•Effect of BNPPost abolished by inhibiting RISK or natriuretic peptide receptors.•The myocardial BNP mRNA levels in the area at risk (AA) are elevated in early reperfusion.•Ischemic postconditioning did not elevate the BNP mRNA levels at early reperfusion. Exogenously administered B-type natriuretic peptide (BNP) has been shown to offer cardioprotection through activation of particulate guanylyl cyclase (pGC), protein kinase G (PKG) and KATP channel opening. The current study explores if cardioprotection afforded by short intermittent BNP administration involves PI3K/Akt/p70s6k dependent signaling, and whether this signaling pathway may participate in regulation of BNP mRNA expression at early reperfusion. Isolated Langendorff perfused rat hearts were subjected to 30min of regional ischemia and 120min of reperfusion (IR). Applying intermittent 3×30s infusion of BNP peptide in a postconditioning like manner (BNPPost) reduced infarct size by >50% compared to controls (BNPPost 17±2% vs. control 42±4%, p