| Class | Potassium channel activator |
|---|---|
| Chemistry |
pyrimidine N-oxide |
| Routes of administration |
Oral, IV, topical |
| Absorption |
Well absorbed (95%); |
| Solubility |
pKa 4.61; slightly water-solible |
| Distribution |
VOD = 200L/kg; minimally protein bound |
| Metabolism |
90% is metabolised in the liver |
| Elimination |
10% is excreted unchanged in the kidneys; half-life is about 3 hours |
| Time course of action |
Therapeutic effect can last significantly longer then the half life (up to 72 hours) |
| 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. Causes hypertrichosis, which may be desirable, ...or not. |
| Literature reference |
Campese (1981) |
| CICM details of understanding | Not specifically listed in the CICM syllabus |
| Mentioned around Deranged Physiology | |
| Related SAQs |