The adrenal cortex: zones, hormones and androgens !
- Concept
- Exam priority: medium
The outer layer of each adrenal gland has three zones: one makes the salt hormone, one the stress hormone and one weak male hormones.
Updated 2026-11-01
Also called: Zona glomerulosa, Zona fasciculata, Zona reticularis, DHEA
See it in 3D: Right adrenal gland · Left adrenal gland
What it is
The adrenal cortex comes from mesoderm and has three concentric zones, each with its own enzymes and its own main controller. From outside in, the glomerulosa makes aldosterone under angiotensin II and potassium, the fasciculata makes cortisol under ACTH, and the reticularis makes the androgen precursors DHEA, DHEA-S and androstenedione, also under ACTH. All start from cholesterol; the enzymes present in each zone decide the product, which is why one missing enzyme (congenital adrenal hyperplasia) changes all three outputs at once. The steroid chemistry is on the Biochemistry pages.
Key facts
- Adrenarche (around 6–8 years) is the rise of reticularis androgens; it causes pubic and axillary hair and body odour, independent of puberty.
- In women, adrenal androgens supply a large share of total androgens; in men the testis dominates.
- ACTH keeps the fasciculata and reticularis trophic: long glucocorticoid use atrophies them, but the glomerulosa survives.
- Steroids are not stored: each zone makes and releases them on demand, so the rate-limiting step is moving cholesterol into the mitochondrion (StAR).
Hormone axes and feedback
Hypothalamic–pituitary–adrenal axisLesion None (normal)
Tap a box to see the hormone, or choose a lesion to see the lab pattern.
- Stimulates (+)
- Inhibits / negative feedback (−)
- Level ↑
- Level ↓
The three zones of the adrenal cortex
| Zone | Main product | Main controller | Lost in |
|---|---|---|---|
| Glomerulosa (outer) | Aldosterone | Angiotensin II, K⁺ | Addison disease; hyporeninemic states |
| Fasciculata (middle) | Cortisol | ACTH | Addison and secondary insufficiency |
| Reticularis (inner) | DHEA, DHEA-S, androstenedione | ACTH | Addison and secondary insufficiency |
| Excess: 21-hydroxylase deficiency | Androgens ↑, cortisol ↓, aldosterone ↓ | ACTH ↑ (no feedback) | Congenital (autosomal recessive) |
Clinical notes
- Classic 21-hydroxylase deficiency: ambiguous genitalia in girls and a salt-wasting crisis (hyponatremia, hyperkalemia, shock) in the first weeks of life in both sexes; newborn screening measures 17-OH-progesterone.
- 11β-hydroxylase deficiency: virilization with hypertension, because 11-deoxycorticosterone acts as a mineralocorticoid.
- 17α-hydroxylase deficiency: hypertension and hypokalemia with no sex steroids (undervirilized 46,XY, absent puberty).
- Addison disease: hyperpigmentation (high ACTH and MSH from POMC), hyperkalemia, hypotension and loss of axillary and pubic hair in women.
Test yourself
Think of the answer, then tap the question to see it.
Why does a patient with secondary adrenal insufficiency usually have normal potassium?
The glomerulosa is driven by angiotensin II and potassium, not mainly by ACTH. With the adrenal intact, aldosterone is preserved and potassium is handled normally.
Why does 21-hydroxylase deficiency cause virilization?
Low cortisol removes feedback, so ACTH rises and the cortex grows. The precursors cannot go on to cortisol or aldosterone, so they are diverted to androgens.
Why can 11β-hydroxylase deficiency cause hypertension while 21-hydroxylase deficiency causes salt wasting?
With 11β-hydroxylase missing, 11-deoxycorticosterone accumulates; it is a mineralocorticoid, so sodium is retained. With 21-hydroxylase missing, no mineralocorticoid is made.
Why are adrenal androgens more noticeable clinically in women than in men?
In women they provide a large part of total androgens, so their loss reduces body hair and libido and their excess virilizes; in men testicular testosterone masks both.
See it in 3D
The structures of Durgical's 3D anatomy where it happens.
Related topics
- The HPA axis and its circadian rhythm
- Actions of cortisol
- Aldosterone: actions and control
- The adrenal medulla and catecholamines
- Sex determination and differentiation
- Puberty
Related conditions
- Congenital adrenal hyperplasia due to 21-hydroxylase deficiency
- Congenital adrenal hyperplasia due to 11β-hydroxylase deficiency
- Congenital adrenal hyperplasia due to 17α-hydroxylase deficiency
- Adrenal insufficiency
- Cushing syndrome
- Polycystic ovary syndrome
In Biochemistry
- Adrenal enzymes and congenital adrenal hyperplasia
- Steroid hormone synthesis (overview)
- 21-Hydroxylase (CYP21A2)
- 11β-Hydroxylase (CYP11B1)
- 17α-Hydroxylase/17,20-lyase (CYP17A1)
- 17-Hydroxyprogesterone (17-OHP)
- Cortisol
- Aldosterone
Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.
Sources: 17.6 The Adrenal Glands (OpenStax (Rice University), 2022); Congenital adrenal hyperplasia: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2025); Anatomy, Abdomen and Pelvis: Adrenal Glands (Suprarenal Glands) (StatPearls (NCBI Bookshelf), 2024); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 78). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).
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Representative model, for educational purposes only.