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Adrenal cortex — zona fasciculata and zona reticularis

Target gland or tissue · MC2R StAR 21-hydroxylase

ACTH raises cAMP through MC2R, and its rate-limiting action is StAR-mediated transport of cholesterol into mitochondria. The fasciculata makes cortisol; the reticularis makes DHEA, DHEAS and androstenedione.

Traced from the start

  1. Corticotrophin-releasing hormone (paraventricular nucleus)
  2. Corticotroph — ACTH cleaved from pro-opiomelanocortin
  3. Adrenal cortex — zona fasciculata and zona reticularis

Detail

Layer order
Glomerulosa (aldosterone), fasciculata (cortisol), reticularis (androgens), from outer to inner
Independent layer
Aldosterone answers to angiotensin II and potassium, so it survives pituitary failure entirely
Trophic effect
ACTH excess causes bilateral hyperplasia; prolonged absence causes atrophy over several weeks
Key enzymes
21-hydroxylase and 11-beta-hydroxylase for cortisol; 17-alpha-hydroxylase and 17,20-lyase for androgens

When it goes wrong

21-hydroxylase deficiency, over 90% of congenital adrenal hyperplasia

Cortisol and aldosterone fail, ACTH rises and precursors shunt into androgens: virilisation of a female newborn and a salt-wasting crisis at 1-2 weeks with vomiting, hyponatraemia, hyperkalaemia and raised 17-hydroxyprogesterone

Autoimmune adrenalitis (primary Addison disease)

Both cortisol and aldosterone lost: postural hypotension, hyponatraemia with hyperkalaemia, pigmentation, high ACTH and no cortisol rise on the short synacthen test

Weeks of suppression by exogenous glucocorticoid

The atrophic cortex fails a short synacthen test even though the adrenal gland itself is healthy

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