Stress-induced activation of the sympathetic nervous system.
Discrepancies between perceptions of internal or external circumstances and innate or acquired expectations lead to patterned stress responses involving several homeostatic systems, of which the sympathoadrenomedullary system (SAMS) is one. Severe, generalized threats such as hypoglycaemia, hypoxia, haemorrhage, circulatory collapse, and fight/flight situations elicit generalized SAMS activation, including cardiac stimulation, splanchnic, cutaneous, and renal vasoconstriction, and usually preserved skeletal muscle blood flow. Patterned sympathetic neural responses, resulting in redistribution of blood volume or changes in glandular activity, occur during orthostasis, exercise, altered environmental temperature, the postprandial state, and performance of attention-requiring tasks. In all these situations, SAMS activity is co-ordinated with that of the parasympathetic nervous system, the pituitary-adrenocortical system, and probably several neuropeptide systems. Although acute stress-induced SAMS activation can be a health hazard, the role of chronically repeated, stress-induced SAMS activation in the development of cardiovascular disease remains unclear. Benzodiazepines, beta-adrenoceptor blockers, and alpha 2-adrenoceptor agonists can attenuate effects of stress-induced SAMS activation, but pressor responses often are maintained.
Goldstein
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D000818:Animals; D005075:Biological Evolution; D001921:Brain / Q000503:physiopathology; D006801:Humans; D013116:Spinal Cord / Q000503:physiopathology; D013312:Stress, Physiological / Q000503:physiopathology*; D013315:Stress, Psychological / Q000503:physiopathology*; D013564:Sympathetic Nervous System / Q000502:physiology / Q000503:physiopathology*