Description of Physiology of the Stress Mechanism

The Stress-Response Cycle
The human stress-response cycle is a complex neuroendocrine response triggered by perceived or real threats from the environment or internal stimuli. The sympathetic nervous system and the hypothalamus-pituitary-adrenal (HPA) axis are primarily responsible for the
physiological changes associated with a stressful state (Selye, 1937).  The initial catecholamine response triggered from the sympathetic nervous system involves a rapid release of epinephrine and norepinephrine into the bloodstream and throughout the body, inducing the changes characteristic of the ‘fight or flight’ response—increased heart rate and respiration, pupil dilation, and more blood flow to the skeletal muscles, vigilance, and so forth……

These changes are rapid but readily reversed when the initial danger has
passed. A slower, more profound effect is also produced by the activity of the HPA axis.
Corticotrophin-releasing hormone or factor (CRH) is synthesized in the hypothalamus and
released into the hypothalamic-pituitary portal system, where it flows to the pituitary. In turn, the
pituitary gland releases adrenocorticotropic hormone (ACTH) into the bloodstream and past the
blood-brain barrier. Once this arrives at the adrenal gland, the cortex releases glucocorticoids
into the bloodstream, which have longer lasting effects than the catecholamines released from
the sympathetic nervous system and adrenal medulla. In humans, the main glucocorticoid is
cortisol, a hormone with wide-ranging effects in the body that is derived from cholesterol in the
zona fasciculata of the adrenal cortex. Upon its release, cortisol’s objective is to return the
organism to homeostasis following a stressful event. This adaptive mechanism evolved to
promote survival in early warm-blooded creatures by minimizing loss of bodily resources and
recuperating from damage due to injury or disease (Selye, 1937; Haller, et al., 1998). Cortisol
helps maintain a state of elevated blood pressure by sensitizing catecholamine receptors in the
blood vessels. Blood sugar is increased by reducing glucogenesis and increasing the breakdown
of glycogen, protein, and lipids in the liver. The immune system is disrupted and suppressed in a
variety of ways. Cytokine signaling is also disrupted by the suppression of nuclear factor κβ signaling pathways, which can block the normal inflammatory response and prevent T-cell
proliferation. Histamine production is also
suppressed, and immune cells are redistributed back to the bone marrow (Wiegers & Reul,
1998). Although cortisol is normally released in a pattern corresponding to the circadian rhythm
(lowest around midnight and highest early morning) and is present in the bloodstream at all
times, excessive stimulation of the HPA axis can be detrimental to the organism. The cortisol
response itself has a self-limiting component: the negative feedback loop formed when cortisol is
released inhibits the release of CRH from the hypothalamus.
Animal models of stress-induced diseases and conditions have provided important
insight into the physiological mechanisms. The physiological response to stress—a flood of
catecholamines followed more slowly by the release of glucocorticoids—is found in all mammals,
birds, and some reptiles, with a glucocorticoid-like receptor present in amphibians that is
believed to effect GABA transmission (Haller, et al., 1998). Rat models of the stress response
focus on the release of corticosterone (CORT), the rodent equivalent of the human
glucocorticoid cortisol. Investigating the complex relationship between stress and pain
processing is an important aspect of research with significant clinical implications. The stress
response involves nearly every aspect of an organism’s physiology, and its impact upon sensory
and affective nervous system processes clearly includes the processing of nociceptive stimuli.

from Uhelski 2009

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