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Cardiovascular Drugs Quiz
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Which mechanism best explains why some patients develop a persistent dry cough when treated with an ACE inhibitor for hypertension?
- A Direct irritation of airway smooth muscle by angiotensin II You picked ✕
- B Accumulation of bradykinin in the lungs due to reduced breakdown You picked ✓
- C Accumulation of adenosine in the airways due to reduced breakdown You picked ✕
- D Accumulation of angiotensin I in the lungs due to reduced conversion You picked ✕
- E Immune-mediated hypersensitivity reaction to the drug You picked ✕
Correct!
Incorrect
The answer is B: Accumulation of bradykinin in the lungs due to reduced breakdown
Explanation
Why B is correct
See Anti-Hypertensive Drugs. Option B is correct. Angiotensin-converting enzyme (ACE) converts angiotensin I to angiotensin II, which narrows blood vessels and raises blood pressure, and ACE inhibitors such as ramipril lower blood pressure by blocking this step. ACE also breaks down bradykinin, a peptide that causes vasodilation and can irritate nerve endings in the airway. When ACE is inhibited, bradykinin breakdown is reduced, so it accumulates. The result is a persistent dry cough, which is a common or very common side-effect of the whole class. The exact mechanism is not fully understood, but bradykinin is considered the most likely culprit, and the same mediator is linked to the rare but dangerous side-effect of angioedema (swelling of the face and throat). The cough is a class effect, so it can occur with any ACE inhibitor. NICE advises that if an ACE inhibitor is not tolerated, for example because of cough, an angiotensin receptor blocker (ARB) is offered instead. Memory aid: ACE inhibitor: bradykinin up, cough up.
- Mechanism: ACE inhibition reduces the breakdown of bradykinin, so it accumulates.
- Side-effect: A persistent dry cough, which is a class effect of ACE inhibitors.
- Management: If an ACE inhibitor is not tolerated, NICE advises offering an angiotensin receptor blocker instead.
Why the other options are incorrect
- A. Direct irritation of airway smooth muscle by angiotensin II: ACE inhibitors reduce angiotensin II rather than raising it, and angiotensin II is not known to irritate the airway directly. This option does not explain the cough. Your answer
- C. Accumulation of adenosine in the airways due to reduced breakdown: Angiotensin-converting enzyme does not break down adenosine, and adenosine accumulation is not the mechanism of ACE inhibitor cough; the symptom is linked to bradykinin rather than adenosine. Your answer
- D. Accumulation of angiotensin I in the lungs due to reduced conversion: ACE inhibitors block the conversion of angiotensin I to angiotensin II, so angiotensin I can accumulate, but angiotensin I is not the mediator that triggers the cough; the cough is due to bradykinin. Your answer
- E. Immune-mediated hypersensitivity reaction to the drug: The cough is not an allergic or immune-mediated reaction. It occurs through the drug's pharmacological effect and is not a hypersensitivity response, so it is not treated as an allergy. Your answer
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