Key result
Angiotensin II, the principal effector of the renin-angiotensin cascade, can be synthesized by pathways that do and do not require angiotensin-converting enzyme.
Provides an overview of angiotensin receptors and their antagonists, including the pathways of angiotensin synthesis.
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Non-ACE angiotensin II pathways persist despite ACE inhibition; leaves open optimal RAS inhibitor selection in cardiovascular disease.
Angiotensins are peptide hormones derived from the protein precursor angiotensinogen by the sequential actions of proteolytic enzymes (Figure 1). The classic pathway of angiotensin synthesis includes a reaction catalyzed by angiotensin-converting enzyme (ACE), which occurs not only in plasma but also in the kidneys, brain, adrenal glands, ovaries, and possibly other tissues.1 The intrarenal renin–angiotensin system affects glomerular filtration, as discussed below, but the importance of angiotensin synthesis in other tissues is not known. Angiotensin II, the principal effector of the renin–angiotensin cascade, can also be synthesized by a pathway that does not require ACE.2 Angiotensin II stimulates a variety . . .
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Goodfriend et al. (1996) reported a review. Angiotensin Receptors and Their Antagonists was evaluated. Angiotensin II, the principal effector of the renin-angiotensin cascade, can be synthesized by pathways that do and do not require angiotensin-converting enzyme.
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