stress responses

stress

• reactions/responses to internal and external stimuli that require acute and/or chronic adaptations for survival

• comprides of endocrine, neural, and immune responses to stressors

allostasis

• maintaining this stability through change, coordinated physiological reactions to anticipate, regulate and adapt to stressors

• allostatic responses are necessary (and healthy) when orchestrated/balanced, and when turned off efficiently

chronic activation

allostatic state that can cause long term physiological changes (accumulation of abdominal adiposity or hypertension); can contribute to disease

stress signals

• CRH, glucocorticoids, catecholamines influence CNS centers like the mesocorticolimbic dopaminergic system (reward system), amygala/hippocampus complex (fear related behaviour), thermoregulatory and appetite satiety centers

• corticotropin releasing hormone also suppresses GnRH neurons

physical adaptation includes redirection of energy resources

• increases in the cardiovascular tone, respiratory rate and some energy mobilizing metabolic processes (gluconeogensis and lipolysis)

• oxygen and nutrients primarily shunted to the central nervous system and to specific tissues (muscles) where they are needed to respond to stressor

• non essential energy consuming functions (digestion, reproduction, growth, and immunity) are temporarily suppressed

autonomic nervous system response to stress

• rapidly responsive, regulating cardiovasular, respiratory, renal, gastrointestinal, endocrine, & other systems (via PNS and/or SNS)

• postganglionic sympathetic neurons innervate smooth muscle cells of vasculature, skeletal muscles, heart, kidneys, gut, adipose tissue (mostly via norepinephrine as a neurotransmitter)

• the sympathetic nervous system activity is supplemented by circulating epinephrine (And some norepinephrine) from adrenal medulla, a “modified sympathetic ganglion”

• catecholamines = among the shortest lived signaling molecules in plasma: circulating half life between 10-100s (half in circulation bound to albumin)

stress rapid response

• catecholamine release: rapid (nervous system = fast)

• catecholamine signaling: rapid second messenger cascades

stress long term

• cortisol helps coordinate metabolism (Nutrient mobilization) with daily activity and sleep patterns; also has central nervous system functions (MRs & GRs widely expressed in brain) including effects on neurogenesis, learning & memory

• glucocoticoids also exert effects that can prepare for subsequent stressors, permissive actions that prime the faster initiating stress mechanisms

• some glucocorticoid effects allow for continued enhancement of stress responses (if responses still required 1 hr past onset of stressor)
  other glucocorticoid effects suppress or rein in the stress activated defense mechanisms

stress coordinated responses

• in addition to regulating adrenocorticotropic hormone ACTH, cortiocotropin releasing hormone CRH also mediates activation of sympathetic nervous system (leads to increased plasma catecholamine concentrations)

• norepinephrine (neurotransmitter): also a potent stimulant of CRH release; noadrenergic neurons from hindbrain project to the hypothalamic paraventricular nucleus

permissive effects

• phenylethanolamine N-methyltransferase enzyme converts norepinephrine to epinephrine (Almost exclusively in adrenal medulla): gene expression is induced by cortisol

• cortisol prolongs catecholamine actions by decreasing levels of degrading enzymes (e.g. in neuromuscular junctions)

• cortisol prolongs epinephrine-induced rise in blood glucose (by increasing expression of gluconeogenic enzymes that are activated by epinephrine)