Molecular mechanism of emotional stress-induced and catecholamine-induced heart attack.

Emotional or physical stress triggers 'tako-tsubo' cardiomyopathy or 'transient left ventricular apical ballooning', but the pathogenesis is unclear. In response to the immobilization stress of rats, a useful model of emotional stress, rapid activation of p44/p42 mitogen-activated protein kinase was observed in the heart, followed by a transient upregulation of immediate early genes in the smooth muscle cells of coronary arteries, the endothelial cells and the myocardium. Heat shock protein 70 was induced in the aortic and coronary arterial smooth muscle cells and in the myocardium. Natriuretic peptide genes were also upregulated in the myocardium. Sequential gene expression can be considered as an adaptive response to emotional stress. Blocking of both α-adrenoceptors and β-adrenoceptors eliminated the upregulation of immediate early genes induced by stress, while α-agonists and β-agonists upregulated immediate early genes in the perfused heart. Activation of α-adrenoceptors and β-adrenoceptors is the primary trigger of emotional stress-induced molecular changes in the heart.