| Class | ACE-inhibitor |
|---|---|
| Chemistry |
L-proline derivative with dicarboxylate (-COOH) group |
| Routes of administration |
Oral |
| Absorption |
25% oral bioavailability |
| Solubility |
pKa 2.5 |
| Distribution |
124L |
| Metabolism |
No hepatic metabolism |
| Elimination |
100% of the dose is excreted unchanged by the kidneys |
| Time course of action |
Effects are maximal ~ 1 hour following oral administration |
| Target receptor |
ACE enzyme |
| Mechanism of action |
By interfering with a zinc moiety on the ACE enzyme, this drug nterrupts the conversion of Angiotensin-I into Angiotensin-II, thereby interrupting 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. Also, dry irritating cough and a chance of random angioedema. |
| Literature reference |
Regulski et al (2015) |
| CICM details of understanding | Not specifically listed in the CICM syllabus |
| Mentioned around Deranged Physiology | |
| Related SAQs |