ACE inhibitor
Angiotensin-converting enzyme inhibitor
ACE inhibitor — mechanism card
- Blocks angiotensin I → angiotensin II
- Vasodilation → ↓ BP
- Renal protection
- Bradykinin accumulation → dry cough/angioedema
- ↓ aldosterone → hyperkalemia
- Contraindicated in pregnancy
Drugs with this mechanism (10)
- Benazeprilat — Active ACE-inhibiting metabolite of benazepril; lowers blood pressure but can raise potassium and creatinine.
- Captopril — The first ACE inhibitor; short-acting, sulfhydryl-related dysgeusia.
- Enalaprilat — Only intravenous ACE inhibitor; for when oral antihypertensive therapy is impossible.
- Fosinoprilat — Active ACE-inhibiting metabolite of fosinopril; combined renal and hepatic elimination distinguishes it from most ACE inhibitors.
- Lisinopril — Active ACE inhibitor for hypertension and heart failure; cough and angioedema.
- Moexipril — Older ACE-inhibitor prodrug for hypertension; food markedly reduces absorption.
- Perindoprilat — Active ACE-inhibiting metabolite of perindopril; renally cleared, with hyperkalemia and kidney-function risks.
- Quinaprilat — Active ACE-inhibiting metabolite of quinapril; renal impairment prolongs exposure, increasing hypotension and hyperkalemia risks.
- Ramiprilat — Active ACE-inhibiting metabolite of ramipril; prolonged ACE binding sustains effects, while renal impairment increases exposure.
- Trandolaprilat — Active ACE-inhibiting metabolite of trandolapril; prolonged ACE binding supports sustained blood-pressure lowering.
Self-check
- What accumulated mediator causes ACE-inhibitor cough and angioedema?
Bradykinin. - Why can ACE inhibitors raise potassium?
They lower aldosterone.
All mechanisms · Open ACE inhibitor in the interactive console ↗