| Class | Calcium channel blocker |
|---|---|
| Chemistry |
1,4-dihydropyridine |
| Routes of administration |
Oral |
| Absorption |
oral bioavailability 45% |
| Solubility |
pKa 3.93, excellent lipid solubility |
| Distribution |
Basically insoluble in water, 96-98% protein bound. VOD =13 L/kg |
| Metabolism |
Mainly hepatic clearance, by CYP3A4 |
| Elimination |
Time to peak effect = 0.5 hrs; elimination half-life 2 hrs |
| Time course of action |
Clinical effects persist for longer than the half life would suggest, because they are mainly determined by drug-receptor affinity |
| Target receptor |
α1c subunit of the L-type calcium channel (selective for the smooth muscle isoform) |
| Mechanism of action |
Modulates the opening of voltage-gated calcium channels, which prevents intracellular calcium influx during depolarisation. This decreases the availability of intracellular calcium for vascular smooth muscle cells, decreasing their resting tone. |
| Clinical effects |
Relaxation of vascular smooth muscle, thereby decreasing peripheral vascular resistance and afterload. Side effects include flushing and constipation. |
| Literature reference |
Abernethy & Schwartz (1999) |
| CICM details of understanding | Not specifically listed in the CICM syllabus |
| Mentioned around Deranged Physiology | |
| Related SAQs |