Document Detail

Deoxycorticosterone acetate salt hypertension in apolipoprotein E-/- mice results in accelerated atherosclerosis: the role of angiotensin II.
MedLine Citation:
PMID:  18158357     Owner:  NLM     Status:  MEDLINE    
Previous studies have shown that administration of angiotensin II to atherosclerosis-prone animal models results in an increase in the extent of atherosclerosis and that this effect may be independent of changes in blood pressure. We sought to determine whether atherosclerosis was increased in the setting of a low renin model of hypertension. Apolipoprotein E-deficient mice were made hypertensive using the deoxycorticosterone acetate salt model. We found that this resulted in a dramatic increase in the atherosclerotic lesion area in the setting of either a low- or high-fat diet. In the hypertensive animals, we observed an increase in angiotensin II staining that was localized to the adventitial macrophages. The increase in atherosclerosis was inhibited by administration of an angiotensin receptor antagonist, an angiotensin-converting enzyme inhibitor, or a renin inhibitor. In addition, blood pressure reduction, with either a calcium channel blocker or hydralazine, reduced the extent of atherosclerosis indicating an important contribution of the mechanical effects of elevated blood pressure. These data suggest that, even in the setting of hypertension that is not associated with activation of the systemic renin-angiotensin system, local generation of angiotensin II within the arterial wall may be of pathophysiological relevance to the development of atherosclerosis.
Daiana Weiss; W Robert Taylor
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2007-12-24
Journal Detail:
Title:  Hypertension     Volume:  51     ISSN:  1524-4563     ISO Abbreviation:  Hypertension     Publication Date:  2008 Feb 
Date Detail:
Created Date:  2008-01-24     Completed Date:  2008-02-26     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7906255     Medline TA:  Hypertension     Country:  United States    
Other Details:
Languages:  eng     Pagination:  218-24     Citation Subset:  IM    
Division of Cardiology, Department of Medicine, Emory University School of Medicine, 1639 Pierce Dr, Suite 319 WMB, Atlanta, GA 30322, USA.
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MeSH Terms
Angiotensin II / metabolism*
Aorta / pathology
Apolipoproteins E / deficiency*
Atherosclerosis / etiology*,  pathology
Blood Vessels / metabolism
Hypertension / chemically induced*,  complications*,  metabolism
Mice, Knockout
Renin-Angiotensin System
Sodium Chloride*
Time Factors
Grant Support
Reg. No./Substance:
0/Apolipoproteins E; 11128-99-7/Angiotensin II; 64-85-7/Desoxycorticosterone; 7647-14-5/Sodium Chloride
Comment In:
Hypertension. 2008 Feb;51(2):175-6   [PMID:  18158343 ]

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