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stress can induce modifications in the central nervous(CNS), autonomic nervous and neuroendocrine system. thus, the stress response has long been measured in laboratory experiments by biochemical changes in the hormone system that are referred to as the sympathetic nervous system(SNS) and potuitary-adrenocortical axes(HPA). these axes react to acute stress of chronic stress. the activation of these two particular pathways result in elevated serum levels of catecholamine, cortisol, ACTH, dopamine, and others hormones. but there is considerable debate about the relevance of traditional laboratory stress findings to real-life situation. the neurobiology of stress is a key step to the understanding of stress-induced changes of immune functions. the immune system operates in communication with brain and endocrine system. because of this extensive communication, the immune system can influence how we feel and behave. the stress are associated with endocrine and autonomic changes that can inhibit immune system fuction. the concept of neurocardiology renders plausible the various theoretical constructs of stress as they relate to circulatory vascular disease. detailed reviews of the anatomic connections between the brain and the heart and of experimental and clinical data on the role of the CNS in cardiac dysfunction can be found elsewhere. in this study, we reviewed that stress was associated with cardiovascular disease mortality through the known cardiovascular risk factors(hypertension, heart rate variability, homocycteine, and clotting system).
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