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The posterior pituitary: ADH and oxytocin !

  • Regulation
  • Exam priority: medium

The posterior pituitary releases two hypothalamic hormones: ADH, which makes the kidney save water, and oxytocin, for birth and milk.

Updated 2026-11-01

Also called: Vasopressin, Antidiuretic hormone, Oxytocin

See it in 3D: Hypothalamus · Pituitary gland

What it is

ADH and oxytocin are made in neurons of the supraoptic and paraventricular nuclei, travel down the axons bound to neurophysins and are released in the posterior pituitary. ADH responds mainly to plasma osmolality and, more strongly but less sensitively, to falling volume. Oxytocin responds to neuroendocrine reflexes: nipple suckling and stretch of the cervix.

How it works, step by step

  1. Plasma osmolality rises: osmoreceptor neurons shrink and activate the ADH-producing neurons.
  2. Action potentials run down the stalk and release ADH into posterior pituitary capillaries; thirst is also triggered.
  3. In the collecting-duct principal cell, ADH activates V2 → cAMP → PKA, which inserts aquaporin 2 into the luminal membrane.
  4. Water moves into the hypertonic medullary interstitium and urine concentrates; ADH also adds urea transporters.
  5. Osmolality falls and ADH drops; within minutes the aquaporins are pulled back by endocytosis.

Guide values

ParameterValueNote
Plasma osmolality≈275–295 mOsm/kg
ADH release threshold≈280–285 mOsm/kg
Possible urine osmolality≈50–1200 mOsm/kgfrom maximal dilution to maximal concentration
Plasma sodium≈135–145 mEq/L

Approximate values for a healthy adult at rest; each laboratory sets its own ranges.

Disorders of water and ADH

DisorderPlasma sodiumUrineAfter water deprivation and ADH analog
Central diabetes insipidusHigh-normal or ↑Dilute, large volumeNo concentration with deprivation; concentrates with the analog
Nephrogenic diabetes insipidusHigh-normal or ↑Dilute, large volumeConcentrates with neither
Primary polydipsiaLow-normalDilute, large volumeConcentrates with deprivation
SIADH↓Concentrated, high urine sodiumNot applicable: the problem is too much ADH

Clinical notes

  • SIADH: typical causes are small cell lung carcinoma, central nervous system disease, pneumonia and drugs.
  • Lithium is a classic cause of nephrogenic diabetes insipidus; hypercalcemia and hypokalemia also blunt the response to ADH.
  • Correcting chronic hyponatremia too fast can cause osmotic demyelination.

Test yourself

Think of the answer, then tap the question to see it.

Why does SIADH cause hyponatremia without edema?

The retained water spreads through all compartments, and the mild volume expansion increases sodium excretion (natriuretic peptide, less aldosterone); extracellular volume stays near normal.

How does the water deprivation test separate central from nephrogenic diabetes insipidus?

In both, urine stays dilute with deprivation. After an ADH analog, central DI concentrates the urine (the kidney responds) and nephrogenic DI does not.

Why does a large hemorrhage release ADH even with normal osmolality?

Falling volume and pressure reduce baroreceptor firing; this stimulus is less sensitive than the osmotic one but far more powerful, and it puts volume ahead of osmolality.

Why does nipple suckling cause milk ejection within seconds?

It is a neuroendocrine reflex: sensory nerves from the nipple activate paraventricular neurons that release oxytocin, which contracts the myoepithelial cells of the alveoli.

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In Biochemistry

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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: 17.3 The Pituitary Gland and Hypothalamus (OpenStax (Rice University), 2022); Syndrome of inappropriate antidiuretic hormone secretion: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2024); Diabetes insipidus: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2024); Antidiuretic hormone blood test: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2024); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 76). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).

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