Collecting duct
Tubulus renalis colligens
Also known as: collecting tubule, collecting duct system, papillary duct, duct of Bellini
The final, hormonally regulated segment of the urine-forming system, receiving fluid from several nephrons and running from cortex to papilla; principal cells adjust Na⁺, K⁺ and water (aldosterone, ADH) and intercalated cells adjust acid–base.
Overview
Connecting tubules from several nephrons join a cortical collecting duct, which descends in a medullary ray, through the outer medullary and inner medullary collecting ducts, fusing repeatedly to form the large papillary ducts (of Bellini) that open at the area cribrosa of the papilla. Collecting ducts arise from the ureteric bud, not the metanephric mesenchyme.
Two cell types: principal cells (≈60–70%) reabsorb Na⁺ through ENaC and secrete K⁺ through ROMK/BK channels under aldosterone control, and reabsorb water through AQP2 inserted under ADH control; intercalated cells — α (type A) secrete H⁺ and reabsorb HCO₃⁻ and K⁺; β (type B) secrete HCO₃⁻ (pendrin).
The collecting duct reabsorbs only ≈2–5% of filtered Na⁺ but determines the final urine: its water permeability ranges from almost nil (no ADH → dilute urine) to very high (maximal ADH → urine equilibrates with the ≈1200 mOsm/kg papillary interstitium). In the inner medulla, ADH also opens UT-A1/UT-A3 urea transporters, which drives urea recycling.
- Location
From the cortex (medullary rays) through the medulla to the renal papilla.
Parts & subdivisions
- ENaC, ROMK, AQP2 — Na⁺ reabsorption, K⁺ secretion, water reabsorption.
- α: H⁺ secretion; β: HCO₃⁻ secretion.
- Papillary ducts (of Bellini)Large terminal ducts opening on the papilla.
Anatomy
- Histology
Simple cuboidal (cortex) becoming tall columnar (papillary ducts) epithelium with distinct lateral cell borders; light-staining principal cells and darker, mitochondria-rich intercalated cells.
Function
- Final regulation of water reabsorption (ADH) — urine concentration
- Na⁺ reabsorption and K⁺ secretion (aldosterone)
- H⁺ or HCO₃⁻ secretion (acid–base fine-tuning)
- Urea recycling (inner medulla)
- Regulation
ADH (V2 → AQP2, UT-A1), aldosterone (ENaC, ROMK, Na⁺/K⁺-ATPase), ANP (inhibits ENaC/CNG channels in the inner medullary CD), acidosis/aldosterone (α-intercalated H⁺-ATPase).
Clinical significance
Potassium-sparing diuretics
Spironolactone/eplerenone antagonise the mineralocorticoid receptor; amiloride/triamterene block ENaC. Both reduce K⁺ (and H⁺) secretion → risk of hyperkalaemia. Amiloride treats Liddle syndrome and lithium-induced nephrogenic DI.
Liddle syndrome
Autosomal dominant gain-of-function of ENaC (reduced degradation) → hypertension, hypokalaemia, metabolic alkalosis with low renin and aldosterone; responds to amiloride, not spironolactone.
Diabetes insipidus and SIADH
No ADH effect (central or nephrogenic DI) → large volumes of dilute urine; excess ADH (SIADH) → inappropriately concentrated urine and dilutional hyponatraemia, treated with fluid restriction or vaptans (V2 antagonists).
Test yourself
Antidiuretic hormone increases water reabsorption in the collecting duct mainly by:
- Inserting aquaporin-2 into the apical membrane of principal cells via V2 receptors and cAMP
- Inserting aquaporin-1 into the thin descending limb
- Opening ENaC channels in intercalated cells
- Constricting the efferent arteriole via V1 receptors
Answer: Inserting aquaporin-2 into the apical membrane of principal cells via V2 receptors and cAMP
ADH binds V2 receptors on the basolateral membrane of principal cells → Gs → cAMP → PKA → fusion of AQP2-containing vesicles with the apical membrane. Water exits basolaterally via AQP3/AQP4. AQP1 in the PCT and descending limb is constitutive.
During water deprivation, which mechanism contributes about half of the osmolality of the inner medullary interstitium?
- Active NaCl transport by the thin ascending limb
- Urea recycling via ADH-regulated UT-A1/UT-A3 transporters in the inner medullary collecting duct
- Secretion of K⁺ by principal cells
- Reabsorption of glucose in the loop of Henle
Answer: Urea recycling via ADH-regulated UT-A1/UT-A3 transporters in the inner medullary collecting duct
ADH increases urea permeability of the inner medullary collecting duct, so urea concentrated by upstream water reabsorption diffuses into the interstitium, where it contributes ≈50% of the ≈1200 mOsm/kg at the papilla.
A child has a normal anion gap metabolic acidosis, urine pH persistently >5.5, hypokalaemia and nephrocalcinosis. Which cells are most likely defective?
- Podocytes
- Principal cells of the collecting duct
- Proximal tubule cells
- α-intercalated cells of the collecting duct
Answer: α-intercalated cells of the collecting duct
Distal (type 1) renal tubular acidosis results from failure of α-intercalated cells to secrete H⁺ (H⁺-ATPase, H⁺/K⁺-ATPase, AE1), so urine cannot be acidified below ≈5.5. Proximal (type 2) RTA is a HCO₃⁻ reclamation defect; type 4 is hypoaldosteronism with hyperkalaemia.
Compiled from standard anatomy and physiology references — see the Urinary System sources. For education only; not medical advice.