Does activation of alpha- or beta-adrenoceptors trigger emotional stress-induced cardiac changes in a rat model of Tako-tsubo cardiomyopathy?
In a rat model, emotional stress-induced Tako-tsubo cardiomyopathy is primarily triggered by alpha- and beta-adrenoceptor activation, leading to specific molecular and functional cardiac changes.
Emotional or physical stress triggers Tako-tsubo cardiomyopathy in postmenopausal females, which is characterized by an elevation of the ST segment in the electrocardiogram (ECG) and left ventricular apical ballooning in the left ventriculogram (LVG). Immobilization stress (IMO) of rats can reproduce these ECG and LVG changes, both of which are normalized by combined blockade of alpha- and beta-adrenoceptors. An increase of serum estrogen partially attenuated these cardiac changes. IMO induced a rapid activation of p44/p42 mitogen-activated protein kinase, followed by a transient upregulation of immediate early genes (IEG) in the coronary artery and myocardium. Blocking of both alpha- and beta-adrenoceptors eliminated the upregulation of IEG induced by stress, while alpha- or beta-agonists upregulated IEG in the perfused heart. Heat shock protein 70 was induced in the aorta, coronary artery, and the myocardium. Natriuretic peptide genes (ANP and BNP) were also upregulated in the myocardium. Sequential gene expression can be considered as an adaptive response to stress. Activation of alpha- or beta-adrenoceptors is the primary trigger of emotional stress-induced cardiac changes.
Takashi Ueyama (2004) studied this question.