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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
- Endothelial dysfunction is the result of the effects of ACE in two distinct and parallel systems.
- In the renin angiotensin system, ACE converts Ang I to Ang II, which has multiple, well described vasoconstrictive and proliferative actions.
- Increases in Ang II lead to increased production of superoxide ions via the NADH/NADPH oxidase system. The increase in oxidative stress leads to endothelial dysfunction through direct actions, and through actions that reduce NO, PG2, and endothelial hyperpolarizing factor.
- In the kallikrein-kinin system, ACE acts by degrading bradykinin into active peptides. This promotes endothelial dysfunction through reductions in the vasodilating and antiproliferating substances, including NO, PG2, and endothelial hyperpolarizing factor.
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