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| Slide Lecture Programs |
| 2000 Core Curriculum |
| The endothelium: New insights into the origins and treatment of CAD |
August 31, 2000
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| II: |
Interactions of the RAS: ACE and the angiotensin II and bradykinin pathways |
Slide 20 |
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Components and major actions of the renin angiotensin system
- The slide lists components and major actions of the tissue renin-angiotensin and kallikrein-kinin systems. As shown, ACE is uniquely positioned to regulate the balance between pressor/profilerative effects and depressor/antiproliferative effects.
- The cardiovascular actions of bradykinin are mediated through B2 receptors. By stimulating synthesis and release of nitric oxide, prostacyclin, and endothelium derived hyperpolarizing factor, bradykinin can also cause vasodilation, inhibition of platelet adhesion, and inhibition of smooth muscle cell proliferation.15
- Four Ang II receptors have been identified.16 The AT1 receptor is the best characterized. The AT2 receptor may counteract the effects of the AT1 receptor, while the AT3 receptor may stimulate endothelial release of PAI-1.
- The biological actions of Ang-(1-7) have only recently begun to receive attention. Like bradykinin, Ang-(1-7) produces a variety of vasodilatory, natriuretic, and antiproliferative responses to counterbalance many of the effects of Ang II.17
- Ang-(1-7) is formed from Ang I by the action of several tissue-specific endopeptidases, principally neprilysin, which is located on the surface of endothelial and epithelial cells.18 It is converted to the inactive peptide Ang-(1-5) by ACE. The accumulating evidence suggests that much of the effects of Ang-(1-7) are mediated by an endothelial receptor subtype distinct from AT1 and AT2.17 AT1 receptor blockers (ARBs) do not appear to have a major effect on Ang-(1-7) activity.
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