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ACE inhibitors

Target: Angiotensin-converting enzyme (ACE)

Reviewed by the WeighedHealth Editorial Team against primary clinical sources — FDA labeling, peer-reviewed trials, and specialty-society guidelines.
Content current as of June 2026; updated when guidance or availability changes.
Last verified by WeighedHealth Editorial Team against primary sources
~0-15 mmHg
typical systolic BP drop monotherapy
~0-10%
develop persistent dry cough
<0%
angioedema (higher in Black patients)
$0-12/mo
generic cash price floor

What are ace inhibitors?

ACE inhibitors are first-line therapy for hypertension, heart failure with reduced ejection fraction, post-MI, and diabetic nephropathy. They block angiotensin-converting enzyme, reducing angiotensin II production and aldosterone secretion — lowering vascular tone, sodium retention, and ventricular afterload. The class includes lisinopril, enalapril, ramipril, benazepril, captopril, fosinopril, moexipril, perindopril, quinapril, and trandolapril.

How do ace inhibitors work?

ACE converts angiotensin I to angiotensin II, a potent vasoconstrictor and stimulus for aldosterone release. Blocking ACE drops angiotensin II and aldosterone, dilating arterioles and reducing sodium/water retention. The enzyme also degrades bradykinin — accumulation of bradykinin is the mechanism behind the characteristic ACE-inhibitor cough and (rarely) angioedema. Renoprotective effects come from preferential efferent-arteriole vasodilation, reducing intraglomerular pressure.

History of ace inhibitors

Captopril (Capoten, 1981) was the first oral ACE inhibitor, derived from a snake-venom peptide. Enalapril (Vasotec, 1985) introduced once-daily dosing. Lisinopril (1987) became the most prescribed because of its simple pharmacokinetics — not metabolized, renally excreted, no prodrug activation needed. Ramipril (1991) accumulated landmark trial evidence (HOPE, AIRE). All ACE inhibitors are now generic and cost $4-12/month.

Drugs in this class

    Other drug classes

    Related topics

    Sources

    Primary sources cited above. FDA labeling, peer-reviewed trials, and specialty-society guidelines only.

    1. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure · Hypertension, 2018 · PMID 29133356
    2. Effects of an Angiotensin-Converting–Enzyme Inhibitor, Ramipril, on Cardiovascular Events in High-Risk Patients (HOPE) · New England Journal of Medicine, 2000 · PMID 10639539
    3. The Effect of Angiotensin-Converting–Enzyme Inhibition on Diabetic Nephropathy (Captopril Collaborative) · New England Journal of Medicine, 1993 · PMID 8413456
    4. 2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure · European Heart Journal, 2021 · PMID 34447992

    People also ask

    • What's the difference between ACE inhibitors and ARBs?

      ACE inhibitors block angiotensin II production. ARBs block the angiotensin II receptor. Clinical efficacy is similar across hypertension and heart failure. The biggest practical differences: ACE inhibitors cause dry cough in 5-10% (bradykinin accumulation) and have slightly higher angioedema risk; ARBs avoid both. ACE inhibitors have slightly longer outcome-trial pedigree in some indications. ARBs are usually preferred when cough develops.

    • Why does my ACE inhibitor cause a dry cough?

      ACE also degrades bradykinin. When ACE is blocked, bradykinin (and substance P) accumulate in the airways, triggering a dry, persistent, often nighttime cough. It usually starts within weeks of initiation but can appear months in. It resolves within 1-4 weeks of discontinuation. Switching to an ARB is the standard fix.

    • Can ACE inhibitors damage my kidneys?

      Paradoxically, they protect kidneys in diabetic nephropathy and CKD with proteinuria — the efferent-arteriole vasodilation reduces glomerular pressure. A small (up to 30%) creatinine rise after initiation is expected and acceptable. Larger rises suggest bilateral renal artery stenosis or pre-existing severe CKD; recheck and consider stopping.

    • Is ACE inhibitor angioedema dangerous?

      Yes. Swelling of lips, tongue, throat, or bowel can be life-threatening. Risk is ~0.1-0.7%, higher in Black patients (2-4x) and in those with prior angioedema history. Symptoms warrant immediate ED evaluation. The class is contraindicated for life after an episode; ARBs are usually tolerated but with caution.

    • Can I take an ACE inhibitor with potassium supplements or salt substitutes?

      Caution. ACE inhibitors raise serum potassium. Adding potassium supplements, potassium-sparing diuretics, or potassium-based salt substitutes (NoSalt, Morton Lite Salt) can cause hyperkalemia, especially in CKD. Discuss before combining.

    • Are ACE inhibitors safe in pregnancy?

      No — contraindicated in second and third trimesters due to fetal renal damage, oligohydramnios, and skull hypoplasia. Discontinue before conception when possible; switch to pregnancy-compatible antihypertensives (labetalol, nifedipine, methyldopa).

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