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[Physiology](https://durgical.com/en/physiology/) · [Renal, fluids and acid–base](https://durgical.com/en/physiology/#s-renal)

# ADH, thirst and water balance

- Regulation
- Exam priority: high

The brain senses how concentrated the blood is. If it rises, you get thirsty and ADH tells the kidney to keep water. Blood sodium mirrors that balance.

Updated 2026-11-01

Also called: Vasopressin, Antidiuretic hormone, Osmoregulation

**See it in 3D:** [Hypothalamus](https://durgical.com/en/anatomy/hypothalamus/) · [Pituitary gland](https://durgical.com/en/anatomy/pituitary-gland/) · [Kidneys](https://durgical.com/en/anatomy/kidney/)

## Key points

- Normal plasma osmolality ≈ 285–295 mOsm/kg; ADH starts rising near ≈ 280 and thirst a little higher (≈ 290–295).
- ADH is made in the supraoptic and paraventricular nuclei and released from the posterior pituitary.
- V2 receptor (collecting duct): cAMP → AQP2 → water reabsorption; V1 receptor (vessels): vasoconstriction.
- A large drop in volume or pressure (≈ 5–10%) releases ADH even when osmolality is low: volume beats osmolality.
- Hyponatremia or hypernatremia = a water problem; extracellular volume tells you about total sodium.
- Nausea, pain, mechanical ventilation, drugs and tumours (lung) release ADH without an osmotic stimulus: SIADH.

## What it is

Body water is regulated through plasma osmolality, which depends mostly on sodium. Osmoreceptors in the anterior hypothalamus detect ≈ 1% changes and adjust two outputs: ADH (vasopressin), which makes the kidney reabsorb water, and thirst, which drives drinking. That is why serum sodium is a marker of water, not of total sodium.

## How it works, step by step

- Water is lost (sweat, breathing, low intake) and plasma osmolality rises.
- Osmoreceptor neurons in the anterior hypothalamus (circumventricular organs) shrink and fire.
- They drive the supraoptic and paraventricular nuclei: the posterior pituitary releases ADH and thirst appears.
- ADH binds the V2 receptor in the collecting duct, cAMP rises and AQP2 channels are inserted into the luminal membrane.
- Water leaves the collecting duct toward the hypertonic medulla; urine concentrates and its volume falls.
- With what is drunk and what is retained, osmolality returns to normal and ADH falls (negative feedback).

### The nephron: segments, transporters and diuretics

**Na⁺ reabsorbed** ≈ 2–5% **Water reabsorbed** variable (ADH)

#### Collecting tubule and duct

- **What it does:** Fine tuning: reabsorbs ≈ 2–5% of Na⁺, secretes K⁺ and H⁺ and reabsorbs water as ADH allows (urine from ≈ 50 to ≈ 1200 mOsm/kg). Principal cells handle Na⁺, K⁺ and water; intercalated cells handle acid–base.
- **Transporters:** Principal: ENaC, ROMK and BK (K⁺ secretion; BK is flow-driven), apical AQP2 (ADH) and basolateral AQP3/4. α-intercalated: H⁺-ATPase and H⁺/K⁺-ATPase (secrete acid). β-intercalated: pendrin (secrete HCO₃⁻). Inner medulla: urea transporters (ADH).
- **Hormones:** Aldosterone (more ENaC, ROMK, Na⁺/K⁺-ATPase and H⁺-ATPase); ADH via the V2 receptor → cAMP → AQP2 insertion; atrial natriuretic peptide curbs Na⁺ reabsorption.
- **Drugs:** ENaC blockers (6) and mineralocorticoid receptor antagonists (7): K⁺-sparing (risk of hyperkalemia). V2 receptor antagonists (8, vaptans): aquaretics.
- **Disorders:** Liddle syndrome (overactive ENaC: hypertension, hypokalemia, low renin and aldosterone); nephrogenic diabetes insipidus (V2 or AQP2, lithium); type 1 distal renal tubular acidosis (H⁺ secretion fails: urine pH > 5.5, hypokalemia, stones) and type 4 (hypoaldosteronism: hyperkalemia); SIADH (excess ADH).

- Glomerulus and arterioles
- Proximal tubule
- Thin descending limb
- Thin ascending limb
- Thick ascending limb
- Distal convoluted tubule
- Collecting tubule and duct
- Juxtaglomerular apparatus (macula densa)
- Cortex
- Medulla
- Interstitial osmolality (≈ 300 → 1200 mOsm/kg)

Illustrative schematic drawn by Durgical (a long-loop juxtamedullary nephron); proportions and percentages are approximate and not for clinical decisions.

## Equations

**Calculated plasma osmolality**Osm ≈ 2 × Na⁺ + glucose/18 + BUN/2.8

**Na⁺**
in mEq/L

**glucose, BUN**
in mg/dL

Sodium and its anions supply almost all osmolality; urea does not change tonicity because it crosses membranes.

## Regulation

- *+* **High plasma osmolality**: The most sensitive stimulus: releases ADH and causes thirst.
- *+* **Hypovolemia or hypotension (baroreceptors)**: Releases ADH even with low osmolality if the drop is large.
- *+* **Angiotensin II**: Stimulates thirst and ADH release.
- *+* **Nausea, pain, stress, nicotine**: Release ADH without an osmotic stimulus.
- *−* **Low osmolality or volume expansion**: Suppresses ADH: dilute urine (down to ≈ 50 mOsm/kg).
- *−* **Alcohol**: Inhibits ADH release: water diuresis.

## ADH: too little or too much

| Situation | ADH | Urine | Plasma sodium |
| --- | --- | --- | --- |
| Dehydration | ↑ (appropriate) | Concentrated, scant | Normal or ↑ |
| [Central diabetes insipidus](https://durgical.com/en/conditions/hypernatraemia/) | ↓ | Dilute, copious | ↑ if not drinking |
| [Nephrogenic diabetes insipidus](https://durgical.com/en/conditions/hypernatraemia/) | ↑ (no effect) | Dilute, copious | ↑ if not drinking |
| [SIADH](https://durgical.com/en/conditions/syndrome-of-inappropriate-antidiuretic-hormone-secretion/) | ↑ (inappropriate) | Concentrated | ↓ with normal volume |
| [Primary polydipsia](https://durgical.com/en/conditions/hyponatraemia/) | ↓ (appropriate) | Very dilute | Normal or ↓ |

## Clinical notes

- SIADH: hyponatremia with inappropriately concentrated urine (> 100 mOsm/kg), high urine sodium and clinically normal volume.
- Diabetes insipidus after pituitary surgery or trauma; the nephrogenic form is linked to lithium, hypercalcemia and hypokalemia.
- Correcting chronic hyponatremia too fast can cause osmotic demyelination, because neurons had already adapted.

## Memory aid

'Sodium is water's mirror': high sodium means too little water; low sodium means too much water. To learn about total sodium, look at volume.

## Test yourself

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

## Why can a patient with severe hypovolemia have hyponatremia even when osmolality is already low?

A large fall in circulating volume releases ADH through baroreceptors, overriding the osmotic signal: the kidney retains free water and sodium is diluted.

## What physiologically separates central from nephrogenic diabetes insipidus?

In central DI ADH is missing; in nephrogenic DI ADH is high but the collecting duct does not respond (V2 receptor or AQP2). Urine stays dilute in both.

## Why does SIADH cause hyponatremia without edema?

Retained water spreads into all compartments and the mild expansion triggers natriuresis (natriuretic peptides, less aldosterone): Na⁺ is lost and extracellular volume stays near normal.

## Why doesn't a high urea cause thirst even though measured osmolality rises?

Urea crosses cell membranes, so it does not pull water out of cells or stimulate osmoreceptors: osmolality rises but tonicity does not.

[Add to my cards (4)](https://durgical.app/estudiar/?add=/en/physiology/adh-thirst-and-water-balance/)

## See it in 3D

The structures of Durgical's 3D anatomy where it happens.

- [Hypothalamus](https://durgical.com/en/anatomy/hypothalamus/)
- [Pituitary gland](https://durgical.com/en/anatomy/pituitary-gland/)
- [Kidneys](https://durgical.com/en/anatomy/kidney/)

## Related topics

- [The countercurrent mechanism, urea recycling and urine concentration](https://durgical.com/en/physiology/the-countercurrent-mechanism-urea-recycling-and-urine-concentration/)
- [Urine dilution, free water and osmotic diuresis](https://durgical.com/en/physiology/urine-dilution-free-water-and-osmotic-diuresis/)
- [The posterior pituitary: ADH and oxytocin](https://durgical.com/en/physiology/the-posterior-pituitary-adh-and-oxytocin/)
- [Sodium and extracellular volume regulation (with natriuretic peptides)](https://durgical.com/en/physiology/sodium-and-extracellular-volume-regulation/)
- [Fluid shifts between compartments](https://durgical.com/en/physiology/fluid-shifts-between-compartments/)
- [Osmosis, osmolarity and tonicity](https://durgical.com/en/physiology/osmosis-osmolarity-and-tonicity/)

## Related conditions

- [Syndrome of inappropriate antidiuretic hormone secretion (SIADH)](https://durgical.com/en/conditions/syndrome-of-inappropriate-antidiuretic-hormone-secretion/)
- [Hyponatraemia](https://durgical.com/en/conditions/hyponatraemia/)
- [Hypernatraemia](https://durgical.com/en/conditions/hypernatraemia/)

## In Biochemistry

- [Serum osmolality and osmolar gap](https://durgical.com/en/biochemistry/topics/serum-osmolality-and-osmolar-gap/)

[← All of physiology](https://durgical.com/en/physiology/)

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: [26.2 Water Balance](https://openstax.org/books/anatomy-and-physiology-2e/pages/26-2-water-balance) (OpenStax (Rice University), 2022); [Syndrome of inappropriate antidiuretic hormone secretion: MedlinePlus Medical Encyclopedia](https://medlineplus.gov/ency/article/000314.htm) (MedlinePlus, US National Library of Medicine, 2026); [Antidiuretic hormone blood test: MedlinePlus Medical Encyclopedia](https://medlineplus.gov/ency/article/003702.htm) (MedlinePlus, US National Library of Medicine, 2026); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 29). 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.

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License: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Cite as: DurgiPedia (durgical.com), https://durgical.com/en/physiology/adh-thirst-and-water-balance/