Which clinical feature best distinguishes ACE inhibitors from angiotensin II receptor blockers (ARBs) in the management of hypertension?

Explanation

## Distinguishing Feature: Dry Cough ### Mechanism of Cough in ACE Inhibitors **Key Point:** ACE inhibitors cause a dry, persistent cough in 10–20% of patients due to **inhibition of bradykinin degradation**. ACE (angiotensin-converting enzyme) is identical to kininase II, which normally breaks down bradykinin. When ACE is inhibited, bradykinin accumulates in the lungs, triggering cough via C-fiber stimulation in the respiratory tract. ### Why ARBs Do Not Cause Cough **High-Yield:** ARBs block the angiotensin II type 1 (AT1) receptor directly and do **not inhibit ACE or kininase II**. Bradykinin metabolism proceeds normally, so cough is rare (<2% incidence). ### Comparison Table: ACE-I vs ARB Adverse Effects | Feature | ACE Inhibitors | ARBs | | --- | --- | --- | | **Dry cough** | 10–20% (bradykinin-mediated) | <2% (rare) | | **Hyperkalemia** | Yes (both block aldosterone) | Yes (both block aldosterone) | | **Angioedema** | Yes (bradykinin-mediated, 0.1–0.2%) | Rare (<0.1%) | | **Proteinuria reduction** | Yes (both reduce glomerular pressure) | Yes (both reduce glomerular pressure) | | **Renal protection in DM** | Yes | Yes | **Clinical Pearl:** If a patient on an ACE inhibitor develops a troublesome dry cough, switching to an ARB is the standard approach — efficacy is maintained without the cough. **Mnemonic:** **BACK** — **B**radykinin accumulation causes **A**CE-inhibitor **C**ough; **K**ininase II is blocked. ### Why Cough Is the Best Discriminator While both classes share hyperkalemia risk, angioedema risk, and proteinuria reduction, the **dry cough is pathognomonic for ACE inhibitors** and virtually absent in ARBs. This makes it the single best clinical feature to distinguish the two drug classes.