| Class | Angiotensin receptor blocker |
|---|---|
| Chemistry |
Imidazole analogue |
| Routes of administration |
Oral |
| Absorption |
60-80 oral bioavailability |
| Solubility |
pKa 4.1 |
| Distribution |
0.7L/kg |
| Metabolism |
75% hepatic metabolism |
| Elimination |
25% is renally excreted in an unchanged form |
| Time course of action |
Effects are maximal ~ 1 hour following oral administration |
| Target receptor |
AT1 receptor |
| Mechanism of action |
By interfering with the binding of Angiotensin-II and its receptor (by competitive inhibition), tthis drug interrupts the effects of renin-angiotensin-aldosterone system activation, which are mainly mediated by Angiotensin II via the AT1 receptor. |
| Clinical effects |
Vasodilation (without reflex tachycardia), increased natriuresis, increased sensitivity to diuretics, decreased glomerular filtration. Positive effects of vascular and myocardial remodelling in CCF. angioedema. |
| Literature reference |
Miura et al (2011) |
| CICM details of understanding | Not specifically listed in the CICM syllabus |
| Mentioned around Deranged Physiology | |
| Related SAQs |