Modulation by stress in cross-talk between glucocorticoid receptor, sintase nitric oxide and beta adrenoceptors signalling pathways in rats cardiac tissue

Abstract

Since the definition of the term "stress" given by the endocrinologist Hans Selye in 1936, to understand the mechanisms related to its response, has been occupied the attention of scientists and doctors. It is believed that at least one third of the diseases are related to stress. The lifestyle in the West, represents the major cause of stress in humans, and is called "psycho-social stress", caused by the accelerated process of urbanization and lifestyles changing. They also affect economic interest aspect (conditioning by environments and unusual situations) and wild species (by changes in habitat and imbalance of eco-systems). The endocrine response to stress in humans and animals include the activation of the hypothalamic-pituitary-adrenal axis (HPA), which stimulates the secretion of glucocorticoids by the adrenal cortex, and activation of the sympathetic nervous system-adrenal medulla, which stimulates the release of catecholamines. The relationship between these two systems is of great physiological importance. In general, steroid hormones induce the refinement or the regulation of processes mediated by catecholamines. The experimental models of foot-shock stress have been used to investigate adaptive mechanisms, mainly in the cardiovascular system. In this model there is increased secretion of glucocorticoids, which interact with their receptors and regulate the expression of genes, including beta adrenoceptors genes. NO is a signaling molecule capable of regulating a variety of cardiovascular functions and its concentration is closely related to the expression of nitric oxide synthases (NOS). The aim of this study is to clarify the relationship between glucocorticoid, beta adrenergic signaling pathways and expression of NOS. (AU)