ARBs — Clinical Use & Key Differences
Mechanism of Action
ARBs block angiotensin II directly at the AT1 receptor instead of inhibiting the converting enzyme. Because the enzyme is left alone, bradykinin does not accumulate — which is why the dry cough and angioedema seen with ACE inhibitors are markedly reduced. Downstream aldosterone suppression is the same, so potassium and renal risks persist.
ACE inhibitor vs ARB
ACE inhibitor (-pril)
- Mechanism
- Blocks ACE enzyme; less angiotensin II + more bradykinin
- Signature effect
- Dry cough + higher angioedema risk (bradykinin)
- Shared risks
- Hyperkalemia, teratogenic, AKI in bilateral RAS
ARB (-sartan)
- Mechanism
- Blocks angiotensin II at AT1 receptor directly
- Signature effect
- Cough rare; used when ACE not tolerated
- Shared risks
- Hyperkalemia, teratogenic, AKI in bilateral RAS
Common Medications
Indications
Side Effects
Contraindications & Interactions
Contraindications
Interactions
Administration & Monitoring
Patient Teaching
Clinical Pearl
An ARB is an ACE inhibitor without the cough — same RAAS family reunion, same pregnancy ban, same potassium watch, just a different seat at the table.