Neuroendocrine activation after myocardial infarction

An acute myocardial infarction causes a threat to circulatory homoeostasis, and the activation of various neuroendocrine systems is believed to be an attempt to readjust to both myocardial and systemic consequences of the destabilising event.Increased sympathetic nervous tone, enhanced activity of the circulating and local renin-angiotensin systems, and disturbed endocrine or paracrine function of the endothelium may all provoke vasoconstriction in the systemic and coronary vascular beds.Activation of the renin- angiotensin system also serves to induce salt and water retention and to expand circulating blood volume.On the other hand, the effects of an augmented secretion of natriuretic peptides from cardiac myocytes should reduce vasoconstriction and water retention.There is increasing evidence suggesting that pharmaco- logical interventions that modify the neuro- endocrine responses may significantly alter the clinical course of the underlying disease process and even improve the prognosis of patients with myocardial infarction.