| Class | ACE-inhibitor |
|---|---|
| Chemistry |
L-proline derivative with sulfhydryl(-SH) group |
| Routes of administration |
Oral |
| Absorption |
75% oral bioavailability |
| Solubility |
pKa 9.8 |
| Distribution |
2L/kg |
| Metabolism |
60% hepatic metabolism |
| Elimination |
40% renally excreted unchanged |
| Time course of action |
Effects are maximal very shortly (15min) following oral administration, but the effect is short-lived (~ 6 hrs) |
| 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 |
FDI PI booklet |
| CICM details of understanding | Not specifically listed in the CICM syllabus |
| Mentioned around Deranged Physiology | |
| Related SAQs |