Linked Life Data

15655118

Source:http://linkedlifedata.com/resource/pubmed/id/15655118

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2005-2-25
pubmed:abstractText
In essential hypertension, conduit arteries present hypertrophic remodeling (increased cross-sectional area), whereas small arteries undergo eutrophic remodeling. The involvement of matrix metalloproteinases (MMPs) and de-adhesion proteins, such as tenascin-C and thrombospondin, has been relatively well characterized in large artery remodeling, but their contribution is not known in small artery remodeling. Rats received N(omega)-nitro-L-arginine methyl ester (L-NAME; 50 mg/kg per day) in their drinking water on days 1, 3, 7, 14, and 28. Arterial MMP-2 activity was measured by ELISA, whereas levels of tenascin-C and thrombospondin were assessed by Western blotting. To determine the involvement of MMPs, additional L-NAME rats received the nonselective MMP inhibitor doxycycline (30 mg/kg per day) on days 7, 14, and 28. Already, at day 1, pressure was elevated. Media/lumen ratio of mesenteric arteries and the aorta increased gradually to reach significance at 28 days. However, the cross-sectional area increased only in the aorta, confirming the heterogeneous remodeling process. In small arteries, MMP-2 activity increased after 7 and 14 days of treatment and returned to baseline at 28 days, whereas the elevation was more progressive but sustained in the aorta. The level of thrombospondin paralleled that of MMP-2 in small arteries, whereas tenascin-C levels declined rapidly and stayed below control values. Doxycycline blunted large artery remodeling but had no influence on the development of eutrophic remodeling despite elevation of MMP-2 activity in the process. Thus, in contrast to large artery hypertrophic remodeling, in which the contributions of cellular de-adhesion and matrix breakdown is manifest, the contribution of MMPs in eutrophic remodeling appears less crucial.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1524-4563
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
45
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
432-7
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:15655118-Animals, pubmed-meshheading:15655118-Aorta, pubmed-meshheading:15655118-Arteries, pubmed-meshheading:15655118-Blotting, Western, pubmed-meshheading:15655118-Doxycycline, pubmed-meshheading:15655118-Enzyme Activation, pubmed-meshheading:15655118-Enzyme Inhibitors, pubmed-meshheading:15655118-Enzyme-Linked Immunosorbent Assay, pubmed-meshheading:15655118-Extracellular Matrix, pubmed-meshheading:15655118-Hypertension, pubmed-meshheading:15655118-Male, pubmed-meshheading:15655118-Matrix Metalloproteinase 2, pubmed-meshheading:15655118-Mesenteric Arteries, pubmed-meshheading:15655118-NG-Nitroarginine Methyl Ester, pubmed-meshheading:15655118-Nitric Oxide Synthase, pubmed-meshheading:15655118-Rats, pubmed-meshheading:15655118-Rats, Wistar, pubmed-meshheading:15655118-Tenascin, pubmed-meshheading:15655118-Thrombospondins
pubmed:year
2005
pubmed:articleTitle
Different involvement of extracellular matrix components in small and large arteries during chronic NO synthase inhibition.
pubmed:affiliation
Faculty of Pharmacy, Université de Montréal, Quebec, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't