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Published on: July 10, 2017
Adrenomedullary, adrenocortical, and sympathoneural responses to stressors: a meta-analysis
David S Goldstein1, Irwin J Kopin
1Clinical Neurocardiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892-1620, USA. goldsteind@ninds.nih.gov
Objective:
Exposure to stressors alters activities of the adrenomedullary hormonal system (AHS), hypothalamic-pituitary-adrenocortical (HPA) axis, and sympathetic nervous system (SNS). Here we report results of a meta-analysis of the literature, examining inter-relationships among AHS, HPA, and SNS responses to stressors, as measured by plasma epinephrine (EPI), corticotrophin (ACTH), and norepinephrine (NE) levels.
Methods:
The medical scientific literature was culled by PubMed searches, to retrieve publications describing original data about plasma EPI, ACTH, and NE levels measured before and during or after exposure to stressors. Magnitudes of responses were graded from a score of 0 for no response to 4 for a massive increase to >or=10 times the baseline value.
Results:
A total of 15 stressors were identified for which at least 2 publications reported data for EPI, ACTH, and NE responses. A total of 60 reports were included. Mean EPI responses were strongly positively correlated with mean ACTH responses (r=0.93) and less strongly with NE responses (r=0.40). Plasma EPI responses were disproportionately larger than NE responses during hypoglycemia and smaller than NE responses during cold exposure without hypothermia, orthostasis, and active escape/avoidance. Plasma NE responses were disproportionately larger than ACTH responses during cold exposure without hypothermia and severe/exhausting exercise and smaller than ACTH responses during hypoglycemia.
Discussion:
The results of this meta-analysis indicate a close association between adrenomedullary and hypothalamic-pituitary-adrenocortical responses across a variety of stressors. This association seems to be if anything stronger than that between adrenomedullary and sympathetic noradrenergic responses.
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