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'''Angiotensin-converting-enzyme inhibitors''' ('''ACE inhibitors''') are a class of [[medication]] used primarily for the treatment of [[hypertension|high blood pressure]] and [[heart failure]].<ref name="Kaplans Essentials of Cardiac Anesthesia 2018 p. ">{{cite book | title=Kaplan's Essentials of Cardiac Anesthesia | publisher=Elsevier | year=2018 | isbn=978-0-323-49798-5 | doi=10.1016/c2012-0-06151-0 | quote=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). }}</ref><ref name="Aronow 2010 pp. 327–337">{{cite book | last=Aronow | first=Wilbert S. | title=Brocklehurst's Textbook of Geriatric Medicine and Gerontology | chapter=Cardiac Arrhythmias | publisher=Elsevier | year=2010 | isbn=978-1-4160-6231-8 | doi=10.1016/b978-1-4160-6231-8.10045-5 | pages=327–337 | quote=Angiotensin-converting enzyme inhibitors ACE inhibitors have been demonstrated to reduce sudden cardiac death in some studies of persons with CHF.24,56}}</ref> 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 [[Enzyme inhibitor|inhibit]] the activity of [[angiotensin-converting enzyme]], an important component of the [[renin–angiotensin system]] which converts [[angiotensin I]] to [[angiotensin II]],<ref name="Byrd Ram Lerma 2019 pp. 477–482">{{cite book | last1=Byrd | first1=James Brian | last2=Ram | first2=C. Venkata S. | last3=Lerma | first3=Edgar V. | title=Nephrology Secrets | chapter=Pharmacologic treatment of hypertension | publisher=Elsevier | year=2019 | isbn=978-0-323-47871-7 | doi=10.1016/b978-0-323-47871-7.00078-2 | pages=477–482 | s2cid=263490929 | quote=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.}}</ref> and hydrolyses [[bradykinin]].<ref name="Kaplans Essentials of Cardiac Anesthesia 2018 p. "/> Therefore, ACE inhibitors decrease the formation of angiotensin II, a [[vasoconstrictor]], and increase the level of [[bradykinin]], a [[peptide]] [[vasodilator]].<ref name="Kaplans Essentials of Cardiac Anesthesia 2018 p. "/><ref name="Byrd Ram Lerma 2019 pp. 477–482"/> This combination is synergistic in lowering blood pressure.<ref name="Kaplans Essentials of Cardiac Anesthesia 2018 p. "/><ref name="Byrd Ram Lerma 2019 pp. 477–482"/>
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]].{{TOC limit}}
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