| Class | Alpha-2 agonist |
|---|---|
| Chemistry |
Imidazoline derivative |
| Routes of administration |
Oral only |
| Absorption |
Well absorbed orally, 88% bioavailability |
| Solubility |
pKa is ~ 7.4; moderately lipophilic |
| Distribution |
VOD is 1.83L/kg; about 10% protein-bound |
| Metabolism |
Undergoes minimal hepatic metabolism; most of the dose is excreted unchanged in the urine |
| Elimination |
Half-life is only 2.2 hours |
| Time course of action |
Duration fo effect is quite prolonged, something in the order of 24 hours, |
| Target receptor |
Mainly affects imidazoline receptors (where it acts as an agonist), rather than alpha-2 receptors (40:1 selectivity). |
| Mechanism of action |
Like clonidine and methyldopa, moxonidine decreases sympathetic outflow by a presynaptic alpha-2 effect, but it also acts on the rostral ventrolateral medulla to downregulate sympathetic activity. |
| Clinical effects |
Because of the mainly imidzoline agonist effect, this drug produces a decrease in blood pressure without much bradycardia or sedation. |
| Literature reference |
Morris & Reid (1997) |
| CICM details of understanding | Not specifically listed in the CICM syllabus |
| Mentioned around Deranged Physiology | |
| Related SAQs |