ACE Inhibitors — MOA & Clinical Use

ACE inhibitors (lisinopril, enalapril, captopril, ramipril — the "-pril" drugs) block angiotensin-converting enzyme, which normally converts angiotensin I to angiotensin II. Angiotensin II is a potent vasoconstrictor that also triggers aldosterone release, causing sodium and water retention. By blocking this conversion, ACE inhibitors produce vasodilation, reduce preload and afterload, and decrease aldosterone-driven fluid retention. This mechanism makes them first-line therapy for hypertension, heart failure with reduced ejection fraction (HFrEF), and diabetic nephropathy. In heart failure, they reduce cardiac workload and slow ventricular remodeling — the progressive chamber dilation that worsens outcomes. In diabetic kidney disease, they dilate the efferent arteriole of the glomerulus, reducing intraglomerular pressure and slowing proteinuria progression. ACE inhibitors also raise bradykinin levels (because ACE normally degrades bradykinin), which contributes to vasodilation but also explains the characteristic dry cough — a side effect covered in the sibling atom, not here.