Chapter

Angiotensin receptor blockers

John J.V. McMurray

in Oxford Textbook of Heart Failure

Published on behalf of Oxford University Press

ISBN: 9780199577729
Published online July 2011 | e-ISBN: 9780199697809 | DOI: http://dx.doi.org/10.1093/med/9780199577729.003.0040

Series: Oxford Textbooks

Angiotensin receptor blockers

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Angiotensin receptor blockers (ARBs) were developed to providean alternative approach to interrupting the renin–angiotensin system(RAS), which was pharmacologically distinct from that ofangiotensin converting enzyme (ACE) inhibitors. By selectivelyblocking the angiotensin II type 1 (AT1) receptor, ARBs werethought to offer the potential for more complete blockade of theRAS. Evidence had accumulated that angiotensin II could be generatedthrough enzymes other than ACE (e.g. chymase) and ARBsblock the action of angiotensin II, regardless of its source, at thereceptor level. Another fundamental difference betweenthe two approaches is the lack of effect of ARBs on bradykininwhich is metabolized by ACE (also known as kininase II).Accumulation of bradykinin with ACE inhibitors is responsible forcough and angioedema. Consequently, it was hoped that ARBswould be better tolerated than ACE inhibitors. Bradykinin, however, may also have beneficial effects, including vasodilatation,antithrombotic activity, and inhibition of pathological tissueremodelling. This latter perspective, that bradykinin might have beneficial actions, underpinned the hypothesis that the combinationof an ACE inhibitor and ARB might be better than an ACEinhibitor alone in heart failure (HF). In other words, the ARBwould maximize RAS inhibition and the ACE inhibitor wouldaugment bradykinin.

Chapter.  6432 words.  Illustrated.

Subjects: Cardiovascular Medicine

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