A patient with severe diarrhoea develops plasma osmolality of 272 mOsm/kg yet shows intense vasoconstriction and a plasma ADH level far above the level expected for that osmolality. The dominant stimulus responsible is:

• A Angiotensin II acting on the subfornical organ to inhibit ADH release
• B Direct stimulation of hypothalamic osmoreceptors by sodium concentration below threshold
• C Baroreceptor unloading from reduced arterial filling, relayed via the vagus and glossopharyngeal nerves to the medulla and then the magnocellular nuclei ✓
• D Reduced atrial natriuretic peptide causing secondary osmoreceptor sensitisation

Explanation

Hypovolaemia unloads carotid sinus and aortic arch baroreceptors; reduced vagal and glossopharyngeal afferent firing disinhibits magnocellular PVN and SON neurons, releasing ADH powerfully even when osmolality is low. This non-osmotic volume stimulus can override osmotic regulation, explaining hyponatraemia in volume depletion. Angiotensin II actually stimulates ADH release via the subfornical organ, so option A states the wrong direction, and low sodium would inhibit rather than trigger osmoreceptors.

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

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