Angiotensin converting enzyme (ACE) is a protein that raises your blood pressure by converting an inactive hormone into one of the most powerful blood-pressure-regulating molecules in the body. It sits at the center of a hormonal cascade called the renin-angiotensin-aldosterone system (RAAS), and it is also the target of one of the most widely prescribed classes of blood pressure medication. Understanding what ACE does helps explain how your body controls blood pressure, why certain medications work, and what it means when a doctor orders an ACE blood test.
How ACE Works in the Body
ACE is a zinc-containing enzyme anchored to the surface of cells, primarily in the lining of blood vessels. Its main job is to clip a small, inactive hormone called angiotensin I into a shorter, highly active hormone called angiotensin II. Angiotensin I is itself produced upstream: when your kidneys detect low blood pressure or low blood volume, they release an enzyme called renin, which converts a liver protein into angiotensin I. That molecule is essentially inert until ACE gets to it.
Once ACE creates angiotensin II, a cascade of effects follows. Angiotensin II tightens blood vessel walls, which immediately raises blood pressure. It also signals your adrenal glands to release aldosterone, a hormone that tells your kidneys to hold onto sodium and water. More fluid in the bloodstream means higher pressure. On top of that, angiotensin II stimulates the reabsorption of sodium bicarbonate in the kidneys, further increasing fluid retention. Together, these actions form a tightly coordinated system designed to keep blood pressure from dropping too low.
Where ACE Is Found
ACE is most concentrated in the lungs, specifically in the tiny capillaries surrounding the air sacs. This makes anatomical sense: nearly all of your blood passes through the lungs with every circuit, giving ACE maximum exposure to circulating angiotensin I. Smaller amounts of ACE are found in the kidneys, the lining of blood vessels throughout the body, and other tissues. ACE is mostly fixed to cell membranes rather than floating freely, though a small amount does circulate in the blood, which is what doctors measure in lab tests.
ACE Does More Than Regulate Blood Pressure
Although angiotensin I is the best-known target, ACE is a surprisingly versatile enzyme. It also breaks down bradykinin, a molecule that relaxes blood vessels and lowers blood pressure. By degrading bradykinin, ACE effectively removes a natural counterbalance to its own blood-pressure-raising activity. ACE also breaks down substance P, a peptide involved in pain signaling and inflammation, and a small peptide called Ac-SDKP that helps regulate cell growth. This broad range of targets is why blocking ACE with medication has effects well beyond simple blood pressure control.
ACE vs. ACE2
ACE2 gained widespread attention during the COVID-19 pandemic because the virus uses it to enter human cells, but it is a different enzyme with a nearly opposite function. ACE2 was first identified in 2000 from human heart tissue. While ACE converts angiotensin I into the vessel-constricting angiotensin II, ACE2 trims angiotensin II into a smaller fragment called angiotensin 1-7, which relaxes blood vessels instead. These two enzymes work as counterweights: the ACE pathway raises blood pressure, and the ACE2 pathway lowers it. ACE2 is most heavily expressed in the kidneys and heart rather than the lungs, which is another key distinction.
ACE Inhibitor Medications
Drugs that block ACE are called ACE inhibitors, and they are among the most commonly prescribed medications worldwide. The first, captopril, was approved in 1981. Others you may recognize include lisinopril, enalapril, ramipril, and benazepril. By preventing ACE from producing angiotensin II, these drugs lower blood pressure, reduce strain on the heart, and slow kidney damage in people with chronic kidney disease.
ACE inhibitors are prescribed for high blood pressure, heart failure with reduced pumping capacity, coronary artery disease, and to protect the kidneys in people with diabetes. They have documented survival benefits across several of these conditions, which is why they remain a cornerstone of cardiovascular treatment decades after their introduction.
One of the most recognizable side effects of ACE inhibitors is a persistent dry cough, which affects a significant number of people who take them. The reason traces directly back to ACE’s role in breaking down bradykinin. When the enzyme is blocked, bradykinin and substance P build up in the airways, irritating nerve endings and triggering a cough reflex. A rarer but more serious side effect, angioedema (sudden swelling of the lips, tongue, or throat), also stems from excess bradykinin. In about half of people who develop this reaction, there is an underlying deficiency in other enzymes that would normally help clear bradykinin, making the buildup even more pronounced when ACE is blocked.
The ACE Blood Test
A serum ACE test measures the amount of the enzyme circulating in your blood. The normal adult range is 16 to 85 units per liter (U/L). Children and teenagers typically run 20 to 50 percent higher than adults, so their reference range is different.
Doctors most often order this test when they suspect sarcoidosis, an inflammatory condition in which clusters of immune cells called granulomas form in the lungs, skin, or other organs. The cells that make up these granulomas produce extra ACE, so blood levels rise. Elevated ACE can also appear in other granulomatous diseases, including tuberculosis, histoplasmosis, and silicosis. The test is not specific enough to diagnose sarcoidosis on its own, but it is useful alongside imaging and biopsy results, and it can help track whether the disease is responding to treatment over time.