## Mechanism of Cough: ACE Inhibitors vs ARBs **Key Point:** The dry cough associated with ACE inhibitors is caused by inhibition of angiotensin-converting enzyme, which also degrades bradykinin. Accumulation of bradykinin stimulates vagal C-fibres in the respiratory tract, triggering a dry, persistent cough. ARBs do not inhibit ACE and therefore do not cause bradykinin accumulation or cough. ### Comparative Pharmacology | Feature | ACE Inhibitors | ARBs | |---------|----------------|------| | **Mechanism** | Block ACE enzyme (inhibits both Ang II formation AND bradykinin degradation) | Block AT1 receptor (selective Ang II blockade) | | **Bradykinin Effect** | Accumulation → cough (10–20% incidence) | No accumulation → no cough | | **Cough Incidence** | 10–20% | < 2% | | **Mortality Benefit (HF)** | Established in systolic HF | Similar to ACE-I | | **K^+^ Effect** | Hyperkalemia risk (via aldosterone ↓) | Hyperkalemia risk (via aldosterone ↓) | **Clinical Pearl:** When a patient on an ACE inhibitor develops an intractable dry cough, switching to an ARB (which provides equivalent Ang II blockade without bradykinin accumulation) is the standard approach. **High-Yield:** The cough is a class effect of ACE inhibitors — it occurs with all members (lisinopril, enalapril, ramipril, etc.) and is NOT a sign of drug toxicity but a predictable pharmacological consequence. [cite:Harrison 21e Ch 297]
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