Angiotensin-converting-enzyme inhibitor | |
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Drug class | |
Class identifiers | |
Use | Hypertension |
ATC code | C09A |
Biological target | Angiotensin-converting enzyme |
Clinical data | |
Drugs.com | Drug Classes |
Consumer Reports | Best Buy Drugs |
WebMD | MedicineNet RxList |
External links | |
MeSH | D000806 |
Legal status | |
In Wikidata |
Angiotensin-converting-enzyme inhibitors (ACE inhibitors) are a class of medication used primarily for the treatment of high blood pressure and heart failure.[1][2] This class of medicine works by causing relaxation of blood vessels as well as a decrease in blood volume, which leads to lower blood pressure and decreased oxygen demand from the heart.
ACE inhibitors inhibit the activity of angiotensin-converting enzyme, an important component of the renin–angiotensin system which converts angiotensin I to angiotensin II,[3] and hydrolyses bradykinin.[1] Therefore, ACE inhibitors decrease the formation of angiotensin II, a vasoconstrictor, and increase the level of bradykinin, a peptide vasodilator.[1][3] This combination is synergistic in lowering blood pressure.[1][3]
As a result of inhibiting the ACE enzyme in the bradykinin system, the ACE inhibitor drugs allow for increased levels of bradykinin which would normally be degraded. Bradykinin produces prostaglandin. This mechanism can explain the two most common side effects seen with ACE Inhibitors: angioedema and cough.
Frequently prescribed ACE inhibitors include benazepril, zofenopril, perindopril, trandolapril, captopril, enalapril, lisinopril, and ramipril.
Mechanisms of Action:ACE inhibitors act by inhibiting one of several proteases responsible for cleaving the decapeptide Ang I to form the octapeptide Ang II. Because ACE is also the enzyme that degrades bradykinin, ACE inhibitors increase circulating and tissue levels of bradykinin (Fig. 8.4).
Angiotensin-converting enzyme inhibitors ACE inhibitors have been demonstrated to reduce sudden cardiac death in some studies of persons with CHF.24,56
ACE inhibitors inhibit the conversion of angiotensin I to angiotensin II, thereby producing vasodilation and lowering BP. Because the hydrolysis of bradykinin is also inhibited by these drugs, cough (7% to 12%) can occur.