| Class | Vasopressor |
|---|---|
| Chemistry |
Ethanolamine derivative |
| Routes of administration |
oral |
| Absorption |
Good oral bioavailabiliy (93%) |
| Solubility |
pKa = 13.77, good water solubility |
| Distribution |
VOD= 5L/kg, less than 30% protein-bound |
| Metabolism |
A prod-drug: metabolised in the liver (by deglycinatio) into the pharmacologically active metabolite, desglymidodrine. Desglymomidodrine is in turn metabolised by hepatic oxidation via the CYP2D6. |
| Elimination |
Minimal free drug is eliminated in the urine |
| Time course of action |
Half-life of the prodrug is 30 minutes; the half-life of desglumidodrine is about 3 hours |
| Target receptor |
Alpha-1 noradrenaline receptors |
| Mechanism of action |
Midodrine is a direct agonist of alpha1 receptors, similar to noradrenaline; it increases the release of a secondary messenger (inositol triphosphate, IP3) which results in the release of calcium into the cytosol, and thus enhanced smooth muscle contractility. |
| Clinical effects |
Apart from increasing peripheral rsistance and blood pressure, midodrine can cause piloerection, diarrhoea and urinary hesitancy |
| Literature reference |
McTavish et al, 1989 |
| CICM details of understanding | Not specifically listed in the CICM syllabus |
| Mentioned around Deranged Physiology | |
| Related SAQs |