Abstract
Three interacting peripheral stress effector systems are activated during exposure of humans and other animals to acute as well as chronic stressors. They include the sympathetic-adrenal medullary (SAM) system, the hypothalamic-pituitary-adrenocortical (HPA) axis, and the innate immune system. The SAM system includes the release of norepinephrine from sympathetic nerve terminals and epinephrine from the adrenal medulla. Plasma levels of norepinephrine and epinephrine have been utilized as an index of SAM activity under basal conditions and following exposure to stress. The HPA axis involves release of corticotropin-releasing factor from neurons in the paraventricular nucleus of the hypothalamus, which stimulates adrenocorticotrophic hormone (ACTH) release from the anterior pituitary, followed by cortisol or corticosterone release from the adrenal cortex. The HPA axis is regulated in part by a system of negative feedback loops. The chemical messengers of the innate immune system include proinflammatory (IL-1β, IL-6, and TNF-α) and anti-inflammatory cytokines (IL-4 and IL-10).
Published Version
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