Analysis of molecular response in the heart to emotional stress

情绪压力和相关的肾上腺素能系统激活是心脏事故的基础。大鼠制动应激引起交感-肾上腺髓质系统激活，引起缺血性心电图改变。与这些变化相对应，即刻早期基因/转录因子（IEGs）在冠状动脉平滑肌细胞、内皮细胞和心肌中表达。此外，热休克蛋白70的mRNA诱导的主动脉和冠状动脉平滑肌细胞从30分钟至3小时后开始的应激。利钠肽基因（ANP和BNP）也上调。这些基因的顺序表达可以被认为是对压力的适应性反应。不是一个单一的，但协同阻断α和β肾上腺素受体阻断IEGs的表达引起的压力。α或β激动剂上调灌注心脏中的IEGs。α或β肾上腺素受体的激活是心脏中应激诱导的分子和电生理变化的主要触发因素。在这些心脏细胞中的α和β肾上腺素受体的下游之间的信号转导的串扰也被建议。

Emotional stress, and associated activation of adrenergic system underlie cardiac accidents. Immobilization stress of rats, which produces activation of the sympatho-adrenal medullary system, induced ischemic electrocardiographic changes. Corresponding to these changes, immediate early genes/transcriptional factors (IEGs) were expressed in the smooth muscle cells of coronary arteries, enodothelial cells and myocardium. Furthermore, mRNA for heat shock protein 70 was induced in the aortic and coronary smooth muscles cells from 30min to 3h after onset of stress. Natriuretic peptide genes (ANP and BNP) were also upregulated. Sequential expression of these genes can be considered as an adaptive response to stress. Not a single but synergistic blocking of alpha and beta adrenoceptors blocked the IEGs expressions elicited by stress. Either alpha or beta agonist upregulated IEGs in the perfused heart. Activation of alpha or beta adrenoceptors is the primary trigger of stress-induced molecular and electrophysiological changes in the heart. Crosstalk of signal transduction between downstream of alpha and beta adrenoceptors in these cardiac cells is also suggested.