## Mechanism of ACE Inhibitor–Induced Cough **Key Point:** ACE (angiotensin-converting enzyme) is identical to kininase II, the enzyme responsible for degrading bradykinin. When ACEIs block ACE, bradykinin accumulates in the lungs, triggering cough via C-fiber stimulation in the respiratory epithelium. ## Incidence and Clinical Features **High-Yield:** - Occurs in 10–20% of ACEI users - Dry, persistent, non-productive cough - Typically develops within weeks of starting therapy - Resolves within 1–4 weeks of drug discontinuation - More common in women, smokers, and those with baseline airway hyperreactivity **Clinical Pearl:** The cough is NOT due to angiotensin II inhibition (ARBs block angiotensin II receptors directly and do not cause cough) but specifically due to bradykinin accumulation. ## Comparison: ACEIs vs ARBs | Feature | ACE Inhibitors | Angiotensin Receptor Blockers | | --- | --- | --- | | Mechanism | Block ACE (kininase II) | Block AT1 receptor | | Bradykinin accumulation | Yes | No | | Dry cough | 10–20% | <2% | | Hyperkalemia risk | Moderate | Moderate | | Pregnancy safety | Contraindicated | Contraindicated | **Mnemonic:** **ACE = Angiotensin-Converting Enzyme = Kininase II** — blocking it causes bradykinin buildup → cough. [cite:KD Tripathi 8e Ch 31]
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