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Systematic (IUPAC) name
Clinical data
Trade names Midamor
AHFS/ monograph
  • US: B
Pharmacokinetic data
Bioavailability Readily absorbed
Metabolism none
Half-life 6 to 9 hours
Excretion unchanged in urine
2016-88-8 YesY
PubChem CID 16231
IUPHAR ligand 2421
DrugBank DB00594 YesY
ChemSpider 15403 YesY
UNII 7M458Q65S3 YesY
KEGG D07447 YesY
Chemical data
Formula C6H8ClN7O
229.627 g/mol
 YesY (what is this?)  (verify)

Amiloride is a potassium-sparing diuretic, first approved for use in 1967 (then known as MK 870), used in the management of hypertension and congestive heart failure. Amiloride was also tested as treatment of cystic fibrosis, but it was revealed inefficient in vivo due to its short time of action, therefore longer-acting epithelial sodium channel (ENaC) inhibitors may prove more effective, e.g. Benzamil.[1]

It is on the World Health Organization's List of Essential Medicines, a list of the most important medication needed in a basic health system.[2]


Amiloride is a guanidinium group containing pyrazine derivative.

Mechanism of action[edit]

Amiloride works by directly blocking the epithelial sodium channel (ENaC) thereby inhibiting sodium reabsorption in the late distal convoluted tubules, connecting tubules, and collecting ducts in the kidneys (this mechanism is the same for triamterene).[3] This promotes the loss of sodium and water from the body, but without depleting potassium. The drug is often used in conjunction with thiazide (e.g. co-amilozide) or loop diuretics (e.g. co-amilofruse). Due to its potassium-sparing capacities, hyperkalemia (high blood potassium levels) is occasionally observed in patients taking amiloride. The risk is high in concurrent use of ACE inhibitors or spironolactone. Patients are also advised not to use potassium-containing salt replacements.[4] Amiloride also carries the risk of developing an acidosis.

A fraction of the effects of amiloride is inhibition of cyclic GMP-gated cation channels in the inner medullary collecting duct.[5]

Amiloride has a second action on the heart, blocking Na+/H+ exchangers Sodium-hydrogen antiporter 1 or NHE-1. This minimizes reperfusion injury in ischemic attacks.

Amiloride also blocks the Na+/H+ antiporter on the apical surface of the proximal tubule cells, in the kidney, abolishing more than 80% of the action of angiotensin II on the secretion of hydrogen ions in proximal tubule cells.[6]

Acid-sensing ion channels (ASICs) are also sensitive to inhibition by amiloride. ASICs are involved in nociceptor responses to pH.[7]

Formulations and trade names[edit]

  • co-amilozide (amiloride hydrochloride with hydrochlorothiazide)

See also[edit]


  1. ^ (Review)Pharmacological treatment of the biochemical defect in cystic fibrosis airways, H.C. Rodgers, A.J. Knox
  2. ^ "WHO Model List of EssentialMedicines". World Health Organization. October 2013. Retrieved 22 April 2014. 
  3. ^ Loffing, Johannes and Kaissling, Brigitte (2003). "Sodium and calcium transport pathways along the mammalian distal nephron: from rabbit to human". Am J Physiol Renal Physiol 284 (4): F628–F643. doi:10.1152/ajprenal.00217.2002. PMID 12620920. 
  4. ^ LoSalt Advisory Statement (PDF)
  5. ^ Walter F., PhD. Boron. Medical Physiology: A Cellular And Molecular Approaoch. Elsevier/Saunders. ISBN 1-4160-2328-3.  page 875
  6. ^ M G Cogan, Angiotensin II: a powerful controller of sodium transport in the early proximal tubule, Hypertension. 1990;15:451-458, doi: 10.1161/01.HYP.15.5.451,
  7. ^ Hunt and Koltzenburg 2005 'The neurobiology of pain'