ACTHutskillelse

ACTHutskillelse, or ACTH secretion, is the process by which the anterior pituitary gland releases adrenocorticotropic hormone (ACTH) into the bloodstream. ACTH is produced by corticotroph cells in the pars distalis in response to corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP) released from the hypothalamus. Once secreted, ACTH stimulates the adrenal cortex, particularly the zona fasciculata, to synthesize and release glucocorticoids, mainly cortisol. ACTH acts on the melanocortin 2 receptor (MC2R) on adrenal cortical cells and has a trophic effect on the adrenal cortex, helping to maintain adrenal gland size and function.

Secretion is regulated by the hypothalamic-pituitary-adrenal (HPA) axis. ACTH release is pulsatile and exhibits a pronounced circadian rhythm, typically higher in the morning and lower at night, with acute stressors (physical or psychological) increasing secretion. Cortisol provides negative feedback at both the hypothalamus and pituitary, suppressing CRH and ACTH production when cortisol levels are elevated.

Abnormal ACTHutskillelse has clinical significance. Excess ACTH, from a pituitary adenoma (Cushing disease) or ectopic ACTH-secreting tumors, leads to hypercortisolism. ACTH deficiency can cause secondary adrenal insufficiency. ACTH levels are measured clinically to assess pituitary or adrenal function, and the cosyntropin (ACTH1-24) stimulation test evaluates adrenal responsiveness when ACTH deficiency or insufficiency is suspected.

Biochemically, ACTH is synthesized from the precursor pro-opiomelanocortin (POMC) and is released as a 39-amino-acid peptide. Its primary biological role is to stimulate cortisol production rather than to exert direct metabolic actions.