ACE Inhibitors

Use

  1. Hypertension
  2. CCF
  3. Post infarction to prevent deleterious cardiac remodelling

Presentation

Tablets

Dose

Ramipril 2.5mg BD

Onset

2 hrs

MoA (Mechanism)

  • Inhibits AI \( \xrightarrow{\text{ACE }} \) AII (ramiprilat binds reversibly to ACE so it can’t act & dissoc. very slowly → long t ½)
  • ∴ formation of AII
  • ∴ cardinal effects
    • Vasodilation (arterial & venous)
    • ↓BP, preL, afteRL
    • ↓blood volume
    • ↓symp activity
    • Inhibit cardiac & vascular hypertrophy

PD

CVS – ↓BP & circulating volume

  • ↑[kallikreins] which are also metabolised by ACE compound the VD

CNS – ↓symp outflow

PK

A

60% OBA

D

PPB 70%

M

Hepatic metabolism to RAMIPRILAT

E

t ½ B 20hrs

Metabolites & active drug excreted renally (60%) & faecally (40%)

Adverse Effects

  • Angioedema
  • Dry cough 2° ↑[bradykinin]
  • Hyperkalaemia
  • Headache
  • Dizziness
  • Fatigue
  • Renal impairment
  • C/I in pregnancy
  • C/I in bilateral renal a. stenosis
  • AII constricts eff > aff arteriole
  • ∴ helps maintain glomerular filtration → removing this can cause an abrupt ↓filtration
  • Big problem with bilateral renal a. stenosis