A 30-year-old man with acute haemorrhage of 1500 mL has a plasma osmolality of 284 mOsm/kg (normal). His plasma ADH concentration is markedly elevated. Which mechanism explains ADH secretion despite normal osmolality?

• A Haemorrhage lowers haematocrit, increasing oxygen delivery to magnocellular neurons
• B Renin-mediated conversion of angiotensinogen directly releases ADH from the posterior pituitary
• C Reduced glomerular filtration rate raises tubular sodium, stimulating osmoreceptors centrally
• D Unloading of arterial baroreceptors and atrial low-pressure receptors disinhibits ADH neurons ✓

Explanation

Severe hypovolaemia unloads both arterial baroreceptors and atrial low-pressure volume receptors, reducing their tonic vagal and glossopharyngeal input to the nucleus tractus solitarius and thereby removing inhibition from magnocellular ADH neurons. This non-osmotic drive can override osmotic regulation entirely, so ADH rises even at low-normal osmolality, prioritising volume over tonicity. Angiotensin II does potentiate ADH but does not act as described in option B.

Reference: Ganong's Review of Medical Physiology, 26th ed.

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