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

# Distal tubule and collecting duct

- Mechanism
- Exam priority: high

The end of the nephron does the fine tuning: how much salt, water, potassium and acid leaves in urine, under hormone control.

Updated 2026-11-01

Also called: Distal nephron, Principal and intercalated cells

**See it in 3D:** [Kidneys](https://durgical.com/en/anatomy/kidney/) · [Left adrenal gland](https://durgical.com/en/anatomy/suprarenal-gland/) · [Right adrenal gland](https://durgical.com/en/anatomy/suprarenal-gland-abdomen/)

## Key points

- Distal tubule: Na⁺-Cl⁻ cotransporter (NCC), ≈ 5% of Na⁺; the thiazide target. Reabsorbs Ca²⁺ under PTH.
- Principal cell: ENaC reabsorbs Na⁺ and ROMK/BK secretes K⁺; aldosterone raises both and ADH inserts AQP2.
- α-intercalated cell: secretes H⁺ (H⁺-ATPase, H⁺/K⁺-ATPase) and reabsorbs HCO₃⁻; the β cell does the opposite (pendrin).
- Na⁺ reabsorption through ENaC makes the lumen negative, which draws K⁺ and H⁺ secretion.
- More flow and Na⁺ reaching the collecting duct = more K⁺ in urine (why loop and thiazide diuretics cause hypokalemia).
- Thiazides lower calcium loss (mild hypercalcemia); loop diuretics raise it.

## What it is

The distal convoluted tubule and collecting duct reabsorb only ≈ 5–10% of filtered sodium, but this is the stretch hormones regulate. Aldosterone sets how much Na⁺ is reabsorbed and how much K⁺ and H⁺ are secreted; ADH sets how much water returns; PTH sets how much calcium. The final composition of urine is decided here.

## How it works, step by step

- In the distal tubule, NCC brings in Na⁺ and Cl⁻; low intracellular Na⁺ favours Ca²⁺ exit across the basolateral side (Na⁺/Ca²⁺ exchanger).
- Aldosterone enters the principal cell, binds the mineralocorticoid receptor and increases ENaC, ROMK and Na⁺/K⁺-ATPase.
- Na⁺ enters through ENaC without an accompanying anion and leaves the lumen negative (≈ −40 mV).
- That voltage and high intracellular K⁺ push K⁺ into the lumen through ROMK and BK.
- In the α-intercalated cell, H⁺-ATPase secretes H⁺, buffered by phosphate and ammonia; the new HCO₃⁻ returns to blood.
- ADH, through the V2 receptor and cAMP, inserts aquaporin 2 into the luminal membrane and water leaves toward the hypertonic medulla.

### The nephron: segments, transporters and diuretics

**Na⁺ reabsorbed** ≈ 5% **Water reabsorbed** 0%

#### Distal convoluted tubule

- **What it does:** Reabsorbs ≈ 5% of Na⁺; impermeable to water (keeps diluting). Actively reabsorbs Ca²⁺, under PTH control, and Mg²⁺.
- **Transporters:** NCC (Na⁺-Cl⁻ cotransporter); TRPV5 (Ca²⁺) with the basolateral Na⁺/Ca²⁺ exchanger; TRPM6 (Mg²⁺).
- **Hormones:** PTH (more Ca²⁺ reabsorption); aldosterone and Ang II in the late part.
- **Drugs:** Thiazides (5): block NCC; lower Ca²⁺ excretion (hypocalciuria) and cause hypokalemia and hyponatremia.
- **Disorders:** Gitelman syndrome (like a thiazide: hypokalemic alkalosis, hypomagnesemia, hypocalciuria). Gordon syndrome (pseudohypoaldosteronism type 2): the opposite, hypertension with hyperkalemia.

- 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.

### 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.

## Regulation

- *+* **Aldosterone**: More ENaC and Na⁺/K⁺-ATPase: retains Na⁺, secretes K⁺ and H⁺.
- *+* **ADH (V2 receptor)**: Inserts AQP2 in the collecting duct: reabsorbs water and concentrates urine.
- *+* **PTH**: Increases Ca²⁺ reabsorption in the distal tubule.
- *−* **Natriuretic peptides**: Inhibit Na⁺ reabsorption in the medullary collecting duct: natriuresis.
- *+* **High tubular flow**: Activates BK channels and increases K⁺ secretion.

## Collecting duct cells

| Cell | Transporters | Does | Hormone |
| --- | --- | --- | --- |
| Principal | ENaC, ROMK/BK, AQP2 | Reabsorbs Na⁺ and water; secretes K⁺ | Aldosterone, ADH |
| α-intercalated | H⁺-ATPase, H⁺/K⁺-ATPase, AE1 | Secretes H⁺; reabsorbs HCO₃⁻ and K⁺ | Aldosterone |
| [β-intercalated](https://durgical.com/en/conditions/metabolic-alkalosis/) | Pendrin | Secretes HCO₃⁻ | Increases in alkalosis |

## Clinical notes

- Primary hyperaldosteronism: hypertension, hypokalemia and metabolic alkalosis with low renin.
- Adrenal insufficiency (no aldosterone): sodium is lost, K⁺ and H⁺ retained: hyponatremia, hyperkalemia and acidosis.
- Gitelman syndrome (NCC): like a thiazide, with hypokalemia, hypomagnesemia and hypocalciuria.
- Liddle syndrome (ENaC always on): hypertension and hypokalemia with low aldosterone.

## Memory aid

'Sodium in, potassium out': every Na⁺ aldosterone rescues in the collecting duct leaves the lumen negative and pushes a K⁺ or H⁺ into urine.

## Test yourself

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

## Why does excess aldosterone cause both hypokalemia and metabolic alkalosis?

It increases Na⁺ entry through ENaC; the lumen becomes more negative and drives K⁺ secretion (principal cells) and H⁺ secretion (α-intercalated cells).

## Why do thiazides reduce urinary calcium while loop diuretics increase it?

Blocking NCC lowers Na⁺ inside the distal cell; the Na⁺/Ca²⁺ exchanger moves more Ca²⁺ into blood, so more is reabsorbed. Loop diuretics instead abolish the voltage that reabsorbs Ca²⁺.

## What does ADH do in the principal cell, and why does it need a hypertonic medulla?

Through the V2 receptor and cAMP it inserts AQP2 into the luminal membrane. Water only leaves if the medullary interstitium is more concentrated than the lumen.

## Why does a patient on a loop diuretic lose more potassium even though the drug acts before the collecting duct?

More flow and Na⁺ reach the collecting duct: more ENaC Na⁺ uptake, a more negative lumen and washout of secreted K⁺, plus aldosterone activated by hypovolemia.

[Add to my cards (4)](https://durgical.app/estudiar/?add=/en/physiology/distal-tubule-and-collecting-duct/)

## See it in 3D

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

- [Kidneys](https://durgical.com/en/anatomy/kidney/)
- [Left adrenal gland](https://durgical.com/en/anatomy/suprarenal-gland/)
- [Right adrenal gland](https://durgical.com/en/anatomy/suprarenal-gland-abdomen/)

## Related topics

- [Potassium balance](https://durgical.com/en/physiology/potassium-balance/)
- [ADH, thirst and water balance](https://durgical.com/en/physiology/adh-thirst-and-water-balance/)
- [Where and how diuretics act](https://durgical.com/en/physiology/where-and-how-diuretics-act/)
- [Aldosterone: actions and control](https://durgical.com/en/physiology/aldosterone-actions-and-control/)
- [Renal handling of H⁺ and bicarbonate](https://durgical.com/en/physiology/renal-handling-of-h-and-bicarbonate/)
- [The renin–angiotensin–aldosterone system](https://durgical.com/en/physiology/the-renin-angiotensin-aldosterone-system/)
- [Transport in the loop of Henle](https://durgical.com/en/physiology/transport-in-the-loop-of-henle/)

## Related conditions

- [Hyperkalaemia](https://durgical.com/en/conditions/hyperkalaemia/)
- [Hypokalaemia](https://durgical.com/en/conditions/hypokalaemia/)
- [Metabolic alkalosis](https://durgical.com/en/conditions/metabolic-alkalosis/)
- [Adrenal insufficiency](https://durgical.com/en/conditions/adrenal-insufficiency/)
- [Hypercalcaemia](https://durgical.com/en/conditions/hypercalcaemia/)

## In Biochemistry

- [Aldosterone](https://durgical.com/en/biochemistry/molecules/aldosterone/)
- [Na⁺/K⁺-ATPase (sodium pump)](https://durgical.com/en/biochemistry/enzymes/na-k-atpase/)

[← 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: [25.6 Tubular Reabsorption](https://openstax.org/books/anatomy-and-physiology-2e/pages/25-6-tubular-reabsorption) (OpenStax (Rice University), 2022); [25.8 Endocrine Regulation of Kidney Function](https://openstax.org/books/anatomy-and-physiology-2e/pages/25-8-endocrine-regulation-of-kidney-function) (OpenStax (Rice University), 2022); [High potassium level: MedlinePlus Medical Encyclopedia](https://medlineplus.gov/ency/article/001179.htm) (MedlinePlus, US National Library of Medicine, 2026); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 28). 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/distal-tubule-and-collecting-duct/