| Class | Prostaglandin agonists |
|---|---|
| Chemistry |
Prostaglandin E1 analogue |
| Routes of administration |
Oral, sublingual, vaginal |
| Absorption |
Well absorbed; bioavailability is 54% |
| Solubility |
pKa 14.68; water-soluble |
| Distribution |
VOD = 13.6L/kg; approximately 90% protein-bound |
| Metabolism |
Misoprosol is rapidly de-esterified in the liver into an active acid metabolite |
| Elimination |
Clearance is almost completely hepatic; the active metabolite is 80% renally cleared |
| Time course of action |
Half-life is approximately 20-40 minutes; duration of action is 2-4 hours mainly because of the active metabolite |
| Target receptor |
Prostaglandin E2 receptors are the main molecular target. For gastric acid suppression, the specific receptors are EP3, which are Gi-coupled receptors. |
| Mechanism of action |
By acting as a PGE2 receptor agonist, misoprostol decreases the secretion of gastric acid by decreasing the expression of proton pumps on the luminal surface of parietal cells. This is the opposite of the effect of NSAIDs. |
| Clinical effects |
Decreased gastric acid production, increased GI and uterine contractility, vasodilation |
| Literature reference |
Walt (1992) |
| CICM details of understanding | Not specifically listed in the CICM syllabus |
| Mentioned around Deranged Physiology | |
| Related SAQs |