A client with long-standing hypertension reports a new persistent dry cough after starting a medication two weeks ago. Which drug is the most likely cause?

A persistent dry cough is the classic and well-documented adverse effect of angiotensin-converting enzyme (ACE) inhibitors, occurring in approximately 10–15% of patients. ACE inhibitors block the breakdown of bradykinin and substance P in the lungs, causing accumulation of these mediators in the bronchial mucosa, which triggers the nonproductive cough. The cough begins days to weeks after initiation, consistent with the two-week time frame described in this scenario, and resolves only upon discontinuing the drug. Angiotensin receptor blockers (ARBs) work downstream and do not block bradykinin degradation, so they do not cause this cough — this is why ARBs are used as an alternative for patients who cannot tolerate ACE inhibitors. Dihydropyridine calcium channel blockers such as amlodipine act on vascular smooth muscle and are not associated with cough; their main adverse effects include peripheral edema and reflex tachycardia. Thiazide diuretics promote sodium and water excretion and may cause hypokalemia and hyperuricemia but do not cause a dry cough. Identifying this drug-class adverse effect is critical because it is a common reason for non-adherence to antihypertensive therapy.