Curriculum Update #5

• Interactions of lipids and RAS: Mechanisms for risk reduction

Hypertension and hypercholesterolemia, the major risk factors for atherosclerotic disease, are frequently associated. Accumulating data suggest the existence of lipoprotein-neurohormonal interactions that may adversely affect vascular structure and reactivity. The attached slide program Interactions of lipids and RAS: Mechanisms for risk reduction examines angiotensin II, atherosclerosis, and the newly recognized parallel pathways to vascular disease. These mechanisms extend our understanding of the potential antiatherosclerotic effects of ACE inhibitors and statins.


This Curriculum Update addresses the interplay of pathways leading to increased cardiovascular risk. In particular, data suggest that the effects of angiotensin II (Ang II) and lipoproteins on cardiovascular risk are not independent. The following topics are covered in this Curriculum Update:

  • Role of Ang II in formation of oxidized LDL (ox-LDL)
  • Evidence for AT 1 receptor upregulation by ox-LDL
  • Role of the ox-LDL receptor (LOX-1) in mediating ox-LDL effects
  • Effects of lipid lowering on blood pressure and vascular reactivity
  • Renin-angiotensin system (RAS) and responses to lipid-lowering agents

Published by Medical Education Consultants, Inc. (MEDCON), on behalf of the University of Florida College of Medicine. Supported by an unrestricted educational grant from Pfizer Inc.

©2001 MEDCON

The editorial content of this program expresses the views of the individual contributors and does not necessarily reflect the views or recommendations of the University of Florida College of Medicine, Pfizer Inc, or the publisher. The indications and dosages of drugs discussed in this program may vary from those approved by the Food and Drug Administration (FDA). The reader is advised to consult the full prescribing information for each medication prior to use.

Interactions of lipids and RAS: Mechanisms for risk reduction

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Interactions of lipids and RAS: Mechanisms for risk reduction Section 1: Interactions of lipids and RAS:Potential molecular mechanisms Effect of ACE inhibition on LDL oxidation in apo E deficient mice Effect of ACE inhibition, AT1 receptor blockade, and hydralazine on LDL oxidation Ang II and atherosclerosis in apo E deficient mice Effect of Ang II and ACE inhibition on cholesterol biosynthesis Role of AT1 receptor in cholesterol biosynthesis ACE and Ang II in the aorta following a high-cholesterol diet (6 months) Antiatherosclerotic effect of ACE inhibition and AT1 receptor blockade Superoxide release in hyperlipidemic rabbit aortas: Effects of endothelium removal Effect of AT1 receptor blockade on superoxide production and NADH oxidase activity Potential interaction of LOX-1 and Ang II in endothelial cells Section 2: Interactions of lipids and RAS: Clinical perspectives Cholesterol lowering reduces blood pressure response to mental stress Combined and distinct vascular effects of ACE inhibitor and statin: Effect on blood pressure Combined and distinct vascular effects of ACE inhibitor and statin: Total regional (forearm) hemodynamic reactivity Hypercholesterolemia-induced AT1 receptor regulation TREND: Effects of ACE inhibition in endothelial response according to LDL-C level QUIET: Effect of quinapril on CAD progression according to LDL-C level ACE genotype determines LDL-C response to statin Hypertension and hypercholesterolemia: Interactions and potential mechanisms


Related at vwbg.org

Lipids and RAS: Interactions that increase cardiovascular risk

Hypertension and hypercholesterolemia frequently coexist, and over the past decade, provocative data have emerged suggesting the existence of neurohormonal interactions between lipoproteins and the renin-angiotensin system (RAS).

ASCOT-LLA: Extending benefits of statins to hypertensive patients

Hypertension and hypercholesterolemia frequently coexist and the interaction of these important risk factors increases cardiovascular risk considerably.

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