Angiotensin‑converting enzyme (ACE) converts inactive angiotensin I into angiotensin II by removing two amino acids. Angiotensin II is a potent vasoconstrictor that raises blood pressure, stimulates aldosterone release to increase sodium and water retention, and enhances sympathetic activity. ACE also breaks down bradykinin, a vasodilator, so ACE activity raises vascular tone and reduces vasodilation.

Common ACE inhibitors include lisinopril, enalapril, ramipril, perindopril, captopril, benazepril, quinapril, fosinopril, moexipril and trandolapril. They’re prescribed for high blood pressure, heart failure and after heart attacks. Side effects may include cough, dizziness and high potassium; they’re avoided in pregnancy. Monitoring kidney function and electrolytes is important when taking them.

When angiotensin‑converting enzyme (ACE) is high, it often signals increased production by activated macrophages—commonly seen with granulomatous diseases such as sarcoidosis, certain infections (e.g., tuberculosis), and some inflammatory or neoplastic conditions. Elevated ACE is a supportive, non‑specific finding used with clinical and imaging data; levels can vary with genetics and medications, and false positives/negatives occur, so further evaluation is required.

In the lungs, angiotensin‑converting enzyme (ACE) on pulmonary endothelium converts angiotensin I to angiotensin II, promoting vasoconstriction and increasing blood pressure, and breaks down bradykinin, reducing vasodilation. These actions regulate pulmonary vascular tone, systemic blood pressure, and fluid balance. ACE activity in lung capillaries is therefore central to cardiovascular homeostasis and influences pulmonary circulation.

Angiotensin‑converting enzyme (ACE) is produced mainly by vascular endothelial cells, especially in the pulmonary (lung) capillary endothelium. Membrane‑bound ACE is abundant on endothelial surfaces; a soluble form circulates in blood. ACE is also expressed in other tissues — kidney, heart, brain, testes, and placenta — where it contributes locally to regulation of blood pressure and fluid balance.

Several hormones raise blood pressure: adrenaline (epinephrine) and noradrenaline cause vasoconstriction and increased heart rate; angiotensin II powerfully constricts vessels; aldosterone promotes sodium and water retention; vasopressin (antidiuretic hormone) increases vascular tone and water reabsorption; cortisol and thyroid hormones can raise vascular reactivity and cardiac output. Renin acts indirectly via the angiotensin pathway.