|Systematic (IUPAC) name|
|Biological half-life||6 to 9 hours|
|Excretion||unchanged in urine|
|ATC code||C03DB01 (WHO)|
|Molar mass||229.627 g/mol[[Script error: No such module "String".]]|
|Script error: No such module "collapsible list".|
Mechanism of action
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). 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) are 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. Amiloride also carries the risk of developing an acidosis.
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.
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|30px||This drug article relating to the cardiovascular system is a stub. You can help ssf by expanding it.|
- 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: F628–F643. PMID 12620920.
- LoSalt Advisory Statement (PDF)
- Walter F., PhD. Boron. Medical Physiology: A Cellular And Molecular Approaoch. Elsevier/Saunders. ISBN 1-4160-2328-3. page 875