ACE inhibitors are a class of blood pressure medications used primarily to treat hypertension, heart failure, and kidney disease. They work by blocking an enzyme that produces a hormone responsible for tightening blood vessels, which lets arteries relax and reduces the workload on your heart. Beyond lowering blood pressure, these drugs play a protective role for the heart and kidneys, making them one of the most widely prescribed medication classes in cardiovascular medicine.
How ACE Inhibitors Work
Your body has a built-in system for regulating blood pressure called the renin-angiotensin system. A key player in this system is angiotensin II, a powerful hormone that constricts blood vessels, triggers the release of a salt-retaining hormone called aldosterone, and promotes water retention. All of these actions raise blood pressure.
ACE inhibitors block the enzyme (angiotensin-converting enzyme) that creates angiotensin II. With less of this hormone circulating, your blood vessels relax and your body holds onto less salt and water. At the same time, blocking this enzyme causes levels of bradykinin to rise. Bradykinin is a substance that stimulates the production of nitric oxide and other natural vasodilators, further helping blood vessels open up. This dual action, reducing a constrictor while boosting a dilator, is what makes ACE inhibitors effective.
High Blood Pressure
Treating hypertension is the most common use for ACE inhibitors. The 2025 joint guidelines from the American Heart Association and American College of Cardiology list them as one of four first-line drug classes for high blood pressure, alongside ARBs, calcium channel blockers, and thiazide diuretics. They can be used alone or combined with other blood pressure medications when a single drug isn’t enough.
For people with diabetes and high blood pressure, any of these four first-line classes is appropriate. But ACE inhibitors get a specific recommendation when kidney damage is also present, because they offer benefits beyond blood pressure control alone.
Heart Failure
ACE inhibitors are a cornerstone of treatment for heart failure with reduced ejection fraction, a condition where the heart can’t pump blood as forcefully as it should. When used as part of a multi-drug regimen, the survival benefits are substantial. A large network analysis published by the American Heart Association found that ACE inhibitors alone were associated with a 16% reduction in mortality compared to placebo. When combined with beta-blockers and a mineralocorticoid receptor antagonist, the three-drug combination was linked to a 56% reduction in death.
These medications reduce the strain on the heart by lowering blood pressure and decreasing fluid retention. Over time, this helps prevent the heart from enlarging further and can slow the progression from mild to severe heart failure.
Recovery After a Heart Attack
Starting an ACE inhibitor within the first 24 to 36 hours after a heart attack improves survival. A major overview of randomized trials found that early treatment reduced 30-day mortality from 7.6% to 7.1%, translating to about 5 lives saved per 1,000 patients treated. That benefit appeared quickly: 40% of the survival advantage was seen within the first two days, and roughly 85% within the first week.
ACE inhibitors also reduced the incidence of nonfatal heart failure after a heart attack. For patients who develop signs of heart failure in the days following an attack, these drugs lower the risk of death (primarily from cardiovascular causes) and reduce the chance of hospitalization for worsening heart failure. Treatment typically begins during the hospital stay and continues for at least four to six weeks, often longer depending on how the heart is recovering.
Kidney Protection
ACE inhibitors have a specific protective effect on the kidneys that goes beyond their blood pressure benefits. In the kidney, angiotensin II constricts the small blood vessel leaving the filtering unit, which raises pressure inside the filter and damages it over time. By blocking angiotensin II, ACE inhibitors reduce this internal pressure and slow the progression of kidney disease.
This is especially important for people with diabetes. Protein leaking into the urine (proteinuria) is both a sign of kidney damage and a driver of further decline. ACE inhibitors reduce proteinuria significantly. In one study, an ACE inhibitor alone cut protein in the urine by about 33%, and combining it with a certain type of calcium channel blocker achieved a 62% reduction. Current guidelines recommend an ACE inhibitor (or ARB) as the first choice for treating high blood pressure in people with chronic kidney disease who have moderate or severe levels of protein in their urine.
Cardiovascular Risk Reduction
For people aged 55 and older who are at high risk of cardiovascular events, ACE inhibitors can reduce the chance of heart attack, stroke, or cardiovascular death even when blood pressure isn’t the primary concern. This applies to people with a history of coronary artery disease, stroke, peripheral vascular disease, or diabetes combined with at least one additional risk factor such as smoking, high cholesterol, low HDL cholesterol, or high blood pressure. This broader protective role is one reason ACE inhibitors are prescribed to some patients who don’t have a traditional blood pressure diagnosis.
Common ACE Inhibitors
There are ten ACE inhibitors approved in the United States. The most frequently prescribed include lisinopril, enalapril, and ramipril. The full list:
- Lisinopril (Zestril, Prinivil)
- Enalapril (Vasotec)
- Ramipril (Altace)
- Benazepril (Lotensin)
- Captopril (Capoten)
- Fosinopril (Monopril)
- Quinapril (Accupril)
- Perindopril (Aceon)
- Moexipril (Univasc)
- Trandolapril (Mavik)
All work through the same mechanism. Differences between them mostly come down to how long they last in the body (some are taken once daily, others twice) and how they’re processed by the liver and kidneys.
Side Effects and Risks
The most well-known side effect is a persistent dry cough, caused by the buildup of bradykinin in the lungs. It affects roughly 5% to 20% of people taking ACE inhibitors and is the most common reason patients switch to an ARB, which works through a related but different pathway and rarely causes cough.
A rarer but more serious risk is angioedema, a sudden swelling of the face, lips, tongue, or throat that can obstruct breathing. The overall incidence is low, but it varies significantly by race. Research published in CHEST found the incidence among Black Americans was 5%, compared to 0.7% among white Americans, a sevenfold difference. If you experience any facial or throat swelling while taking an ACE inhibitor, it requires immediate medical attention.
Other possible side effects include elevated potassium levels, dizziness from blood pressure dropping too low, and, less commonly, changes in kidney function. Your doctor will typically check blood work within a few weeks of starting treatment to monitor potassium and kidney markers.
Pregnancy
ACE inhibitors are contraindicated after the 12th week of pregnancy. Use during the second and third trimesters has been linked to serious harm to the developing baby, including kidney failure, underdeveloped lungs, bone malformations, dangerously low blood pressure, and in some cases, neonatal death. Women who are planning to become pregnant should switch to a pregnancy-safe blood pressure medication beforehand. If pregnancy is discovered while taking an ACE inhibitor during the first trimester, the risk from early exposure appears lower, but the medication should be stopped promptly and an alternative started.