Pharmacology · single question

What is the mechanism of action of ACE inhibitors?

  1. Prevent the conversion of Angiotensin I to Angiotensin II
  2. Block angiotensin II receptors
  3. Inhibit renin release
  4. Block calcium channels in vascular smooth muscle
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Correct answer: A. Prevent the conversion of Angiotensin I to Angiotensin II

Prevent conversion of Angiotensin I to Angiotensin II (A). ACE (Angiotensin Converting Enzyme) inhibitors (e.g., lisinopril, enalapril, captopril) block the ACE enzyme in the lungs:
• Angiotensin I → (normally ACE) → Angiotensin II (potent vasoconstrictor)
• With ACE inhibited → Angiotensin II NOT formed → vasodilation → lower blood pressure

• Bonus mechanism: ACE also breaks down bradykinin. When ACE is inhibited, bradykinin accumulates → causes the classic dry, non-productive cough (ACE inhibitor cough in 10-15% of patients).
• Bradykinin accumulation also causes ANGIOEDEMA — swelling of lips/tongue/throat — a serious dental office emergency!
• ARBs (B): block AT1 receptors — no bradykinin accumulation → no cough/angioedema.
• Dental significance: ACE inhibitor angioedema can be confused with dental allergy.
  • A. ACE inhibitors indirectly decrease aldosterone (by preventing Ang II from stimulating aldosterone release) — but the direct mechanism is blocking ACE.
  • B. ACE inhibitors (lisinopril, enalapril, captopril) block the ACE enzyme, preventing conversion of angiotensin I → angiotensin II. Without Ang II: no vasoconstriction, no aldosterone release, no sodium/water retention → BP decreases. Side effect: dry cough (bradykinin accumulation).
  • C. ACE inhibitors actually INCREASE renin (via feedback) as a side effect — but increased renin is not the mechanism of action.
  • D. Blocking Ang II RECEPTORS is the mechanism of ARBs (losartan, valsartan) — NOT ACE inhibitors. ACE inhibitors prevent Ang II formation; ARBs block its action.

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