Natriuretic peptides and myocardial ischaemia

In both experimental and clinical myocardial ischaemia, release of BNP occurs rapidly from ventricular myocardium, prompting speculation that the early activation of the natriuretic peptide receptor/cGMP signalling system may be an important autocrine/paracrine response to ischaemia. Among the growing list of pleiotropic actions of natriuretic peptides is the attenuation of tissue susceptibility to ischaemic injury. BNP and other natriuretic peptides limit the extent of tissue infarction during ischaemia and reperfusion. The mechanism of cytoprotection is related to cGMP accumulation and opening of ATP-sensitive K+ channels. The effects of longer-term upregulation of natriuretic peptide expression in the heart following myocardial infarction could include the suppression of growth and proliferative responses in myocytes and broblasts. Thus, chronic elevation of natriuretic peptide expression in infarcted myocardium probably represents a negative regulatory system to counter the pro-hypertrophic and pro-brotic signalling activated by other mediators such as angiotensin II and catecholamines. The acute and chronic actions of natriuretic peptides in myocardial ischaemia suggest a prole of activity that may be therapeutically benecial in the management of patients with acute coronary syndromes and for the optimisation of post-infarction remodelling.