Emotional Stress- and Catecholamine-Induced Molecular and Electrocardiographic Responses in the Heart

Abstract

Emotional stress, and associated activation of the sympatho-adrenergic system underlie cardiac accidents. Immobilization (IMO) of rats is a useful model of emotional stress, since it activates the sympatho-adrenergic system and hypothalamo-pituitaryadrenocortical axis.¹ When cells are confronted with the change of their environment, a set of genes and their proteins are rapidly induced. Immediate early genes (IEGs)/proto-oncogenes such as c-fos and c-jun ² and heat shock proteins .(HSP)³ are the typical stress-induced substances. Fos family and Jun family proteins form hetero-(Fos-Jun) or homo-(Jun–Jun) dimers (AP-1), which may elicit expression of target genes and contribute to the cellular response to the primary stimulus. HSPs are also important since they act as molecular chaperones to prevent the misfolding of cellular proteins. In situ hybridization histochemistry (ISH) is a very effective method to detect discrete cells activated by stress. Monitoring mRNAs for IEGs or HSPs has demonstrated the spatial and temporal spread of excitation from the whole body to the intracellular molecules² (Fig. 1). By use of ISH and IMO models, we demonstrated the molecular and electrocardiographic changes, which are mediated by activation of α- and β- adrenoceptors in the heart.