B-type natriuretic peptide limits reperfusion injury via opening of ATP-sensitive potassium channels

Abstract

B-type natriuretic peptide (BNP) and other natriuretic peptides given pre-ischaemia, limit infarction both in in-vivo and ex-vivo models of ischaemia–reperfusion injury. Furthermore, many studies have implicated the opening of the mitochondrial and sarcolemmal ATP-sensitive potassium (KATP) channels to be an important trigger of this protection. However, fewer studies have solely examined the role of natriuretic peptides in attenuating the extent of myocardial reperfusion injury. We hypothesise that BNP salvages the myocardium when given at reperfusion, and that this protection is dependent on the opening of KATP channels.