Amiloride
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| Amiloride
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| Systematic (IUPAC) name | |
| 3,5-diamino-6-chloro-N- (diaminomethylidene)pyrazine-2-carboxamide | |
| Identifiers | |
| CAS number | |
| ATC code | C03 |
| PubChem | |
| DrugBank | |
| Chemical data | |
| Formula | C6H8ClN7O |
| Mol. mass | 229.627 g/mol |
| Pharmacokinetic data | |
| Bioavailability | Readily absorbed |
| Metabolism | none |
| Half life | 6 to 9 hours |
| Excretion | unchanged in urine |
| Therapeutic considerations | |
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| Legal status | |
| Routes | oral |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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.
Structure
Amiloride is a guanidinium group containing pyrazine derivative.
Mode of action
Amiloride works by directly blocking the epithelial sodium channel (ENaC) thereby inhibiting sodium reabsorption in the distal convoluted 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.[1]
A fraction of the effects of amiloride is inhibition of cyclic GMP-gated cation channels in the inner medullary collecting duct.[2]
References
- ↑ LoSalt Advisory Statement (PDF)
- ↑ Walter F., PhD. Boron. Medical Physiology: A Cellular And Molecular Approaoch. Elsevier/Saunders. ISBN 1-4160-2328-3. page 875
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