| Class | ENaC channel blocker |
|---|---|
| Chemistry |
Pyrazinoylguanidine |
| Routes of administration |
Oral only |
| Absorption |
50% bioavailability, which is reduced when it is taken with food |
| Solubility |
pKa 8.67; sparingly soluble in water |
| Distribution |
VOD = 5L/kg; 23% protein-bound |
| Metabolism |
Does not undergo any hepatic metabolism |
| Elimination |
All of the administered dose is cleared renally; half-life is about 6-9 hours |
| Time course of action |
Peak activity is about 2 hours after administration; effect last about 24 hours |
| Target receptor |
Amiloride and triamterene both bind to and inhibit the ENaC sodium channel in the collecting duct |
| Mechanism of action |
By decreasing the reabsorption of sodium via the ENaC channel, amiloride and triamterene increase the loss of sodium. The increased sodium concentration in the lumen of the collecting duct creates a positive charge which repels potassium ions and therefore leads to potassium retention. |
| Clinical effects |
Hyperkalemia, hyponatremia |
| Literature reference |
TGA PI data sheet |
| CICM details of understanding | Not specifically listed in the CICM syllabus |
| Mentioned around Deranged Physiology | |
| Related SAQs |