ACE inhibitors
Target: Angiotensin-converting enzyme (ACE)
- ~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
GLP-1 receptor agonists
GLP-1 receptor agonists are a class of injectable and oral medications that mimic the incretin hormone GLP-1. Originally developed for type
edPDE5 inhibitors
Phosphodiesterase type 5 (PDE5) inhibitors are the first-line oral treatment for erectile dysfunction. They work by blocking PDE5 from break
hair loss5-alpha reductase inhibitors
5-alpha reductase inhibitors slow the conversion of testosterone to dihydrotestosterone (DHT), the androgen primarily responsible for male-p
skincareTopical retinoids
Topical retinoids are vitamin A derivatives applied to the skin to accelerate cell turnover, reduce comedonal acne, and reverse photodamage.
mental healthSSRIs (selective serotonin reuptake inhibitors)
SSRIs are the first-line pharmacologic treatment for major depressive disorder and most anxiety disorders. They block reuptake of serotonin
cholesterolStatins (HMG-CoA reductase inhibitors)
Statins are the cornerstone of pharmacologic LDL-cholesterol lowering and the most widely prescribed cardiovascular drug class in the world.
Related topics
Sources
Primary sources cited above. FDA labeling, peer-reviewed trials, and specialty-society guidelines only.
- 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
- Effects of an Angiotensin-Converting–Enzyme Inhibitor, Ramipril, on Cardiovascular Events in High-Risk Patients (HOPE) · New England Journal of Medicine, 2000 · PMID 10639539
- The Effect of Angiotensin-Converting–Enzyme Inhibition on Diabetic Nephropathy (Captopril Collaborative) · New England Journal of Medicine, 1993 · PMID 8413456
- 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).