Linked Life Data

15585195

Source:http://linkedlifedata.com/resource/pubmed/id/15585195

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2004-12-8
pubmed:abstractText
Angiotensin converting enzyme (ACE) inhibitors prevent a wide variety of key events underlying atherogenesis. Whether these actions depend solely on reduction of angiotensin II (Ang II) generation is still to be determined. This study was undertaken to determine whether enalapril, an ACE inhibitor, prevents atherosclerosis and vascular inflammation induced by Ang II in apolipoprotein E-deficient (apoE-KO) mice. Subcutaneous infusion of Ang II (1.44 mg/(kg day)) for 4 weeks increased blood pressure and accelerated atherosclerosis development in the carotid arteries. The expression of the endothelial adhesion molecules E-selectin, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), as well as the chemokines monocyte chemotactic protein-1 (MCP-1) and macrophage-colony stimulating factor (M-CSF) was up-regulated in the aortas of Ang II-treated mice. Enalapril co-treatment (25 mg/(kg day), in drinking water) prevented the development of atherosclerosis without affecting blood pressure or circulating cholesterol. In addition to preventing the Ang II-induced over-expression of adhesion molecules and chemokines in the aorta, enalapril up-regulated the expression of peroxisome proliferator-activated receptors (PPARs)-alpha and -gamma, potential anti-inflammatory transcription factors. In the aortic arch, a lesion-prone site, the co-treatment with enalapril reduced the percentage of arterial wall occupied by macrophages and foam cells, medial sclerosis and elastin reduplication. Together, these data suggest an important role for Ang II-independent mechanisms in the antiatherogenic and anti-inflammatory effects of ACE inhibitors.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0021-9150
pubmed:author
pubmed:issnType
Print
pubmed:volume
178
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
9-17
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:15585195-Angiotensin II, pubmed-meshheading:15585195-Angiotensin-Converting Enzyme Inhibitors, pubmed-meshheading:15585195-Animals, pubmed-meshheading:15585195-Aorta, pubmed-meshheading:15585195-Aortic Aneurysm, pubmed-meshheading:15585195-Apolipoproteins E, pubmed-meshheading:15585195-Arteriosclerosis, pubmed-meshheading:15585195-Cell Adhesion Molecules, pubmed-meshheading:15585195-Chemokines, pubmed-meshheading:15585195-Enalapril, pubmed-meshheading:15585195-Endothelium, pubmed-meshheading:15585195-Gene Expression, pubmed-meshheading:15585195-Male, pubmed-meshheading:15585195-Mice, pubmed-meshheading:15585195-Mice, Knockout, pubmed-meshheading:15585195-PPAR alpha, pubmed-meshheading:15585195-PPAR gamma, pubmed-meshheading:15585195-RNA, Messenger, pubmed-meshheading:15585195-Up-Regulation, pubmed-meshheading:15585195-Vasculitis
pubmed:year
2005
pubmed:articleTitle
Enalapril attenuates angiotensin II-induced atherosclerosis and vascular inflammation.
pubmed:affiliation
Department of Pharmacology, Berlex Biosciences, 2600 Hilltop Drive, PO Box 4099, Richmond, CA 94806, USA. valdeci_da_cunha@berlex.com
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't