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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 26 |
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Mechanisms of cardiac RAS activation in cardiac remodeling
- This diagram by Dzau summarizes the mechanisms that activate the renin-angiotensin system (RAS) in the heart and lead to cardiac remodeling.
- It is now known that there are two RAS, the circulatory RAS and the tissue RAS. The tissue RAS is present in cardiac tissue, vascular walls, the central nervous system, lungs, etc. It produces more than 90% of all ACE in the body. The tissue RAS exerts long-term effects on vascular structure and function.26
- Increased pressure overload in the heart, associated with left ventricular hypertrophy (LVH) and hypertension, results in an adaptive ventricular response in which gene expression of ACE is increased. Resulting intracardiac activation of Ang II contributes to myocardial remodeling, to an adaptive response to overload, and ultimately to increased diastolic stiffness that is charactertic of left LVH.
- Long-term treatment with ACE inhibitors blocks Ang II production and thereby limits progression of cardiac remodeling. This explains the well-documented benefits of ACE inhibition in preventing or reducing LVH.
- The next slides discuss the role of the endothelium in heart failure.
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