Angiotensin receptor blockers (ARBs) are less likely to cause angioedema and cough than ACE inhibitors because

• A. ARBs do not contain a sulfhydryl group
• B. ACE inhibitors are more specific for inhibiting the production of Angiotensin II
• C. ARBs are pseudo-irreversible antagonists
• D. ARBs do not inhibit the breakdown of bradykinin

Answer: (D)

The main idea is that cough and angioedema with ACE inhibitors come from increased bradykinin levels. ACE not only helps form angiotensin II but also breaks down bradykinin. When ACE is inhibited, bradykinin accumulates, leading to vasodilation and heightened vascular permeability, which can trigger a persistent cough or angioedema. ARBs, on the other hand, block the AT1 receptor for angiotensin II but don’t inhibit the enzyme that degrades bradykinin. So bradykinin levels aren’t raised, reducing these bradykinin-mediated adverse effects. The presence of a sulfhydryl group isn’t the driving factor here.