ACE inhibitor therapy is the use of angiotensin converting enzyme inhibitors, a class of medication used primarily for the treatment of cardiovascular and kidney diseases, which work by causing relaxation of blood vessels and a decrease in blood volume, leading to lower blood pressure and decreased oxygen demand from the heart. ACE inhibitors inhibit the activity of angiotensin converting enzyme, a component of the renin angiotensin system that converts angiotensin I to angiotensin II and breaks down bradykinin, so that ACE inhibitors decrease the formation of angiotensin II, a vasoconstrictor, while increasing the level of bradykinin, a peptide vasodilator, a combination that acts together to lower blood pressure. This same mechanism, by allowing increased levels of bradykinin that would normally be broken down, explains the two most common side effects of ACE inhibitors, angioedema and cough. Frequently prescribed ACE inhibitors include benazepril, zofenopril, perindopril, trandolapril, captopril, enalapril, lisinopril, and ramipril.
Facts
Disputed
Origin YearCaptopril, the first orally active ACE inhibitor, was synthesized in 1975. This fact records 1981, the year the United States Food and Drug Administration approved captopril, the point ACE inhibitor therapy became clinically available rather than an experimental compound. Sources
1. Wikipedia
Wikipedia contributors, Wikimedia FoundationACE inhibitor - History section
Captopril was approved by the United States Food and Drug Administration in 1981.
- Clinical use status
View the Source Frequently Asked Questions
Why do ACE inhibitors cause a cough and angioedema?
Raised bradykinin levels cause both side effects.
The same mechanism that lowers blood pressure explains them. ACE inhibitors block the enzyme that breaks down bradykinin, a peptide vasodilator, so bradykinin levels rise. That increase is what accounts for the two most common side effects, angioedema and cough.
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