| Class | Potassium channel activator |
|---|---|
| Chemistry |
pyrimidinecarboxamide |
| Routes of administration |
Oral only |
| Absorption |
Well absorved; bioavailability is > 75% |
| Solubility |
pKa = 3.18; reasonably amphoteric |
| Distribution |
VOD = 1.0-1.4L/kg; about 24% protein bound |
| Metabolism |
Mainly hepatic metabolism by denitration and then introduction into the nicotinamide metabolism |
| Elimination |
Inactive metabolites are eliminated in urine. Half life is about 2 hrs. |
| Time course of action |
Long-acting, duration of effect is close to 12 hrs |
| 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). Unlike the other members of this class, nicorandil DOES act as a venodilator, because it has some nitrate-like nitric oxide donor properties. |
| Literature reference |
Markham (2000) |
| CICM details of understanding | Not specifically listed in the CICM syllabus |
| Mentioned around Deranged Physiology | |
| Related SAQs |