What is the site of action of antidiuretic hormone (ADH)?

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Site of Action of Antidiuretic Hormone

The site of action of antidiuretic hormone (ADH) is the collecting ducts of the kidney. 1, 2, 3

Mechanism of Action

ADH (also known as vasopressin) acts specifically on the collecting ducts through the following mechanism:

  • Binds to vasopressin V2 receptors (V2R) expressed on the basolateral membrane of collecting duct cells 1
  • Initiates a signaling cascade involving:
    • G protein activation
    • Adenylyl cyclase stimulation
    • cAMP production
    • Protein kinase A (PKA) activation 1, 3
  • Results in the exocytic insertion of aquaporin-2 (AQP2) water channels into the apical membrane of collecting duct cells 1, 4
  • Water then flows from the tubule lumen to the hypertonic medullary interstitium through:
    • AQP2 in the apical membrane
    • AQP3 and AQP4 (constitutive water channels) in the basolateral membrane 1, 4

Evidence Supporting Collecting Ducts as the Primary Site

The collecting ducts are definitively established as the primary site of ADH action based on several lines of evidence:

  • The FDA drug label for desmopressin (synthetic ADH analog) explicitly states: "The antidiuretic effects of desmopressin acetate are mediated by stimulation of vasopressin 2 (V2) receptors, thereby increasing water re-absorption in the kidney" 3

  • Consensus statements from the European Reference Network on Rare Kidney Diseases specifically illustrate the mechanism of "vasopressin-regulated water reabsorption in the distal collecting duct" 1

  • Clinical guidelines note that ADH's action enables "the formation of concentrated urine" through its effects on collecting duct water permeability 1, 2

Clinical Implications

Understanding ADH's site of action is crucial for managing several clinical conditions:

  • In nephrogenic diabetes insipidus (NDI), there is resistance to ADH at the collecting ducts, leading to inability to concentrate urine despite normal ADH secretion 1

  • In syndrome of inappropriate ADH secretion (SIADH), excessive ADH causes increased water reabsorption at the collecting ducts, leading to hyponatremia 2

  • Therapeutic agents like tolvaptan work by antagonizing vasopressin receptors in the collecting ducts, making them useful for treating conditions with excess ADH activity 2

Physiological Regulation

The collecting duct response to ADH is dynamically regulated:

  • When ADH is present: AQP2 water channels are inserted into the apical membrane, increasing water permeability
  • When ADH is withdrawn: AQP2 channels are retrieved by endocytosis, decreasing water permeability 4, 5
  • Flow rate through the collecting duct can affect the degree of osmotic equilibration between urine and renal papilla, even in the presence of maximal ADH 6

Therefore, based on the most current and authoritative evidence, the correct answer is (a) collecting ducts.

References

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Guideline

Regulation of Antidiuretic Hormone Secretion

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Research

The mechanisms of aquaporin control in the renal collecting duct.

Reviews of physiology, biochemistry and pharmacology, 2000

Research

Antidiuretic hormone moves membranes.

The American journal of physiology, 1988

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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