Emotional Stress-induced Oxidative Stress Response in the Cardiovascular System

Abstract

Catecholamine intoxication and disturbance of coronary microcirculation, both of which may be responsible for the pathogenesis of takotsubo cardiomyopathy, could trigger the oxidation stress response in the cardiovascular system. We investigated expression and localization of inducible hemeoxygenase 1 (HO-1) and inducible cyclooxygenase 2 (COX-2), one of the oxidative stress-related factors in the heart and the aorta of immobilization stressed (IMO) rats, an animal model of takotsubo cardiomyopathy. In response to IMO, the levels of HO-1m RNA and COX-2m RNA were increased at 3h in the heart and at 1h in the aorta, respectively. The signals for HO-1m RNA were expressed in the scatted cells in the myocardium and the aortic adventitia. The signals for COX-2m RNA were expressed in the scatted cells in the myocardium and in the spindle cells in the aortic media. Blocking of α or β-adrenoceptor significantly attenuated up-regulation of HO-1m RNA levels in the heart. Blocking of α-adrenoceptor completely abolished the up-regulation of COX-2m RNA levels in the aorta, while blocking of β-adrenoceptor completely abolished the up-regulation of COX-2m RNA levels in the heart. Thus, emotional stress and surge of catecholamine up-regulate HO-1 and COX-2 in the heart and in the aorta.