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Theodore Cooper Lecture: Tissue angiotensin and pathobiology of vascular disease: a unifying hypothesis.

Publication ,  Journal Article
Dzau, VJ
Published in: Hypertension
April 2001

There is increasing evidence that direct pathobiological events in the vessel wall play an important role in vascular disease. An important mechanism involves the perturbation of the homeostatic balance between NO and reactive oxygen species. Increased reactive oxygen species can inactivate NO and produce peroxynitrite. Angiotensin II is a potent mediator of oxidative stress and stimulates the release of cytokines and the expression of leukocyte adhesion molecules that mediate vessel wall inflammation. Inflammatory cells release enzymes (including ACE) that generate angiotensin II. Thus, a local positive-feedback mechanism could be established in the vessel wall for oxidative stress, inflammation, and endothelial dysfunction. Angiotensin II also acts as a direct growth factor for vascular smooth muscle cells and can stimulate the local production of metalloproteinases and plasminogen activator inhibitor. Taken together, angiotensin II can promote vasoconstriction, inflammation, thrombosis, and vascular remodeling. In this article, we propose a model that unifies the interrelationship among cardiovascular risk factors, angiotensin II, and the pathobiological mechanisms contributing to cardiovascular disease. This model may also explain the beneficial effects of ACE inhibitors on cardiovascular events beyond blood pressure reduction.

Duke Scholars

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Published In

Hypertension

DOI

EISSN

1524-4563

Publication Date

April 2001

Volume

37

Issue

4

Start / End Page

1047 / 1052

Location

United States

Related Subject Headings

  • Risk Factors
  • Reactive Oxygen Species
  • Peptidyl-Dipeptidase A
  • Nitric Oxide
  • Models, Biological
  • Inflammation
  • Humans
  • Homeostasis
  • Enzyme Activation
  • Endothelium, Vascular
 

Citation

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Dzau, V. J. (2001). Theodore Cooper Lecture: Tissue angiotensin and pathobiology of vascular disease: a unifying hypothesis. Hypertension, 37(4), 1047–1052. https://doi.org/10.1161/01.hyp.37.4.1047
Dzau, V. J. “Theodore Cooper Lecture: Tissue angiotensin and pathobiology of vascular disease: a unifying hypothesis.Hypertension 37, no. 4 (April 2001): 1047–52. https://doi.org/10.1161/01.hyp.37.4.1047.
Dzau, V. J. “Theodore Cooper Lecture: Tissue angiotensin and pathobiology of vascular disease: a unifying hypothesis.Hypertension, vol. 37, no. 4, Apr. 2001, pp. 1047–52. Pubmed, doi:10.1161/01.hyp.37.4.1047.

Published In

Hypertension

DOI

EISSN

1524-4563

Publication Date

April 2001

Volume

37

Issue

4

Start / End Page

1047 / 1052

Location

United States

Related Subject Headings

  • Risk Factors
  • Reactive Oxygen Species
  • Peptidyl-Dipeptidase A
  • Nitric Oxide
  • Models, Biological
  • Inflammation
  • Humans
  • Homeostasis
  • Enzyme Activation
  • Endothelium, Vascular