ACE inhibitor
An ACE inhibitor blocks the enzyme that manufactures one of the body's most powerful vessel-tightening hormones. Picture a factory along an assembly line: angiotensin-converting enzyme (ACE) takes an inactive precursor and converts it into angiotensin II, a hormone that clamps arteries shut and tells the kidneys to hold onto salt and water. Jam that factory step and the clamp loosens, so blood pressure falls.
Mechanistically, ACE converts angiotensin I to angiotensin II within the renin–angiotensin–aldosterone system, and it also breaks down bradykinin, a vasodilator. By inhibiting ACE, these drugs lower angiotensin II (less vasoconstriction and less aldosterone-driven fluid retention) and let bradykinin accumulate (extra vasodilation). Members share the suffix -pril, such as captopril, enalapril, lisinopril and ramipril, and are widely used for hypertension, heart failure and protecting the kidneys in diabetes.
The accumulation of bradykinin explains the characteristic side effect: a persistent dry cough in some patients. Rarely it causes angioedema, a dangerous swelling of the face and airway. ACE inhibitors can raise blood potassium and reduce kidney filtration, so they are avoided in pregnancy and in bilateral renal artery stenosis, and renal function and potassium are checked after starting.
Ramipril, started at a low dose and titrated upward, is a standard ACE inhibitor for a patient with heart failure and reduced ejection fraction, slowing disease progression.
ACE inhibitors do more than lower pressure; they protect the failing heart and diabetic kidney.
If a dry cough becomes intolerable, patients are usually switched to an angiotensin receptor blocker, which achieves a similar effect without raising bradykinin.