抄録
Emotional stress triggers takotsubo cardiomyopathy in postmenopausal women. Immobilization stress (IMO) of rats, a conventional animal model of emotional stress, can reproduce the ECG and LVG changes that occur in takotsubo cardiomyopathy, both of which are prevented by combined blockade of α- and β-adrenoceptors. IMO induces a rapid activation of p44/p42 mitogen-activated protein kinase, followed by a transient up-regulation of immediate early genes such as c-fos mRNA in the coronary artery and myocardium. Blocking of both α- and β-adrenoceptors eliminates these molecular changes induced by stress. These data suggest that activation of α- or β-adrenoceptors is the primary trigger of emotional stress-induced cardiac changes. Estrogen supplementation partially attenuates these cardiac changes. Estrogen supplementation attenuates the IMO-induced increase of c-Fos immunoreactivity in medial amygdaloid nucleus, paraventricular hypothalamic nucleus; these regions contain central sympathetic neurons and neurons with immunoreactive estrogen receptors. It also down-regulates c-fos mRNA expression in the adrenal gland and the heart, suggesting an increase of estrogen attenuates the stress-induced hypothalamo-sympatho-adrenal outflow from the central nervous system to the target organs. In addition, estrogen treatment up-regulates ANP and HSP70 in the heart. These data suggest that reduction of estrogen following menopause might be involved in the primary cause of takotsubo cardiomyopathy both by indirect action on the nervous system and by direct action on the heart [J Physiol Sci. 2007;57 Suppl:S53]
