| Class | Potassium channel activator |
|---|---|
| Chemistry |
benzothiadiazine |
| Routes of administration |
Oral and IV |
| Absorption |
Good bioavailability; rapidly absorbed |
| Solubility |
pKa = 10.43; insoluble in water |
| Distribution |
VOD = 0.33L/kg; 90-95% protein bound |
| Metabolism |
Hepatic metabolism (80%) into inactive metabolites |
| Elimination |
Renal excretion of unchanged drug (20%); half life is long, ~ 26 hours |
| Time course of action |
Duration of effect is much shorter than half life, because it ends up being trapped in a protein-bound form |
| Target receptor |
ATP-sensitive potassium channels |
| Mechanism of action |
The mechanism of action is not entirely clear, but seems to have something to do with ATP-sensitive potassium channels. Activation of these channels inhibits the opening of voltage-dependent calcium channels indirectly, by hyperpolarising the membrane. |
| Clinical effects |
Class effects (arterial vasodilation, reflex tachycardia, RAAS activation). Does not act as a venodilator. Inhibits insulin release from the pancreas. |
| Literature reference |
Thien (1980) |
| CICM details of understanding | Not specifically listed in the CICM syllabus |
| Mentioned around Deranged Physiology | |
| Related SAQs |