ACE INBIHITORS

1. ACE-I

1. Functions to inhibit ACE. Therefore,
   • Reduced conversion of AT-I to AT-II. This means less vasoconstriction and less aldosterone release.
   • Reduced breakdown of bradykinin, therefore leading to increased prostaglandin synthesis and vasodilation.

Overall effect is to reduce PVR and reduce BP.

1. PO. Captopril has 95% bioavailability that is reduced by food.

1. Metabolized by the liver. Note that all ACE-I are prodrugs, except captopril and Lisinopril.

1. Renal – 50% unchanged.

1. Management of HTN
   • Useful in treating HTN with IHD as a single agent, as there is no rebound tachycardia.
   • Useful in treating HTN with CKD – it reduces proteinuria and stabilizes GFR.

1. Pregnancy – especially in 2nd and 3rd trimester. It causes hydronephrosis and renal failure in the fetus.
2. AKI

1. Renal impairment

1. K+ sparing drugs/K+ supplements (Anything that increased K+)
   • May cause hyperkalemia
2. NSAIDs
   • NSAIDs will reduce prostaglandin synthesis – this overall reduces the anti-hypertensive effect of ACE-I.

1. Hypotension – especially first dose hypotension, and especially if there is concomitant salt restriction/patient in hypovolemic state.
2. AKI
3. Cough/angioedema
4. Hyperkalemia
5. Teratogenicity