Hormonal stress response


Epinephrine (adrenal medulla) and norepinephrine (nerve endings) are released by the sympathetic nerve system and result in gluconeogenesis, glycogenolysis, lipolysis, and glucagon release (in addition to their hemodynamic effects). Cortisol (release from the adrenal cortex) also leads to gluconeogenesis, adipocyte sensitization (to growth hormone and catecholamines), blocks the anti-proteolytic actions of insulin, and also has potent antiinflammatory effects. The pancreas releases insulin (beta cells) and glucagon (alpha cells), which act in opposition, as well as somatostatin (D cells) which oppose both

Also note that surgical stress can lead to decreased gonadotropin-releasing hormone release by the hypothalamus (and a consequent hypogonadotropic hypogonadism response). While TSH and free T4 are usually normal, serum T3 concentrations and bound T4 may decrease, and reverse T3 may increase, leading to “sick-euthyroid syndrome

Stress Response

Increased release of

  • Sympathetic Nervous System: norepinephrine (spillover from nerve endings)
  • Adrenal Medulla: epinephrine
  • Adrenal Cortex: cortisol
  • Pancreas: insulin, glucagon, and somatostatin

Decreased release of:

  • Hypothalamus: gonadotropin-releasing hormone (hypogonadotropic hypogonadism)

Changes in:

  • Thyroid hormones: normal TSH and free T4, decreased T3 and bound T3, increased reverse T3, “sick euthyroid syndrome


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Keyword history


See Also:

ABA:Septic shock – stress response mediators