Cardiovascular Drugs Quiz

See Anti-Hypertensive Drugs. ACE normally helps break down bradykinin, a peptide that can stimulate airway sensory nerves. An ACE inhibitor reduces that breakdown, allowing bradykinin to accumulate and contribute to a persistent dry cough (B). This cough is a pharmacological adverse effect rather than evidence that the drug has failed to lower blood pressure. The cough mechanism is separate from reduced angiotensin II formation, which accounts for much of the therapeutic effect. When cough makes an ACE inhibitor intolerable, an angiotensin receptor blocker may preserve treatment of the same hormonal pathway without inhibiting ACE itself.

Direct angiotensin II airway irritation (A) is not the recognised cough mechanism, and ACE inhibition reduces formation of that hormone. Reduced aldosterone (D) changes renal sodium and potassium handling rather than causing the proposed bronchoconstriction. Sympathetic suppression causing airway collapse (C) is not a recognised explanation for this side effect. An immune-mediated reaction (E) would be a different process; the usual isolated ACE-inhibitor dry cough follows altered peptide breakdown.