Abstract
Angiotensin II (AngII) has well-characterized effects on blood pressure and fluid balance that adversely affect atherosclerotic cardiovascular disease. More recently, there is a realization that AngII exerts direct effects on arterial wall cells to influence atherosclerotic lesion formation. Several groups have shown that infusion of AngII into hyperlipidemic mice rapidly and profoundly augments lesion formation. The increase in lesions from AngII was not attributable to elevated blood pressure. The lesions formed from AngII infusion are overtly similar to those formed during hypercholesterolemia, with infiltration of macrophages and T lymphocytes. Unexpectedly, AngII infusion into these mice also led to the development of abdominal aortic aneurysms. These aneurysms exhibit many aspects of the human disease including medial degeneration, inflammation, thrombus, and rupture. The definition of the cellular mechanisms by which Ang II promotes these vascular pathologies may provide new therapeutic strategies.
Original language | English |
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Pages (from-to) | 117-120 |
Number of pages | 4 |
Journal | Trends in Cardiovascular Medicine |
Volume | 14 |
Issue number | 3 |
DOIs | |
State | Published - Apr 2004 |
Bibliographical note
Funding Information:Work on these projects was supported by the National Institutes of Health (HL62846 and HL 70239). The authors thank Debra Rateri for her editorial assistance.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine