The zona glomerulosa of the adrenal cortex exclusively produces aldosterone because it expresses aldosterone synthase (CYP11B2) but lacks 17α-hydroxylase (CYP17A1). The consequence of the absence of CYP17A1 in zona glomerulosa is that:

• A Pregnenolone and progesterone cannot be hydroxylated at position 17, preventing production of DHEA, androgens, and cortisol; the pathway proceeds via corticosterone to aldosterone ✓
• B 21-hydroxylation cannot occur in zona glomerulosa, so 17-hydroxyprogesterone cannot be converted to cortisol precursors
• C Cholesterol cannot be converted to pregnenolone in zona glomerulosa, so all aldosterone precursors are imported from zona fasciculata
• D StAR protein is absent in zona glomerulosa, preventing mitochondrial cholesterol uptake and limiting aldosterone to ACTH-independent synthesis

Explanation

In zona glomerulosa, the mineralocorticoid pathway runs: cholesterol → pregnenolone → progesterone → deoxycorticosterone (DOC) via CYP21A2 (21-hydroxylase) → corticosterone → aldosterone via CYP11B2. Because CYP17A1 (17α-hydroxylase/17,20-lyase) is absent, neither 17α-hydroxypregnenolone nor 17α-hydroxyprogesterone can be made, blocking the route to DHEA, androgens, and cortisol. All cortisol synthesis is confined to zona fasciculata (which has CYP17A1 but lacks CYP11B2). This compartmentalization is clinically relevant: ACTH regulates zona fasciculata cortisol, while angiotensin II and K⁺ regulate zona glomerulosa aldosterone via Ca²⁺-calmodulin pathways.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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