Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1999-11-24
pubmed:abstractText
Angiotensin II (AngII) generation in response to vascular injury has long been assumed to influence neointimal proliferation contributing to restenosis. This concept has been supported by evidence that ACE inhibition and AT1 receptor blockade effectively limits restenosis in the rat. On the other hand, ACE inhibition has proven ineffective in clinical trails. The present study examines the response of the porcine coronary artery after angioplasty in vitro and compares the actions of an ACE inhibitor to AngII receptor antagonists.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0008-6363
pubmed:author
pubmed:issnType
Print
pubmed:volume
42
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
761-72
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:10533617-Analysis of Variance, pubmed-meshheading:10533617-Angioplasty, Balloon, Coronary, pubmed-meshheading:10533617-Angiotensin II, pubmed-meshheading:10533617-Angiotensin Receptor Antagonists, pubmed-meshheading:10533617-Angiotensin-Converting Enzyme Inhibitors, pubmed-meshheading:10533617-Animals, pubmed-meshheading:10533617-Antihypertensive Agents, pubmed-meshheading:10533617-Captopril, pubmed-meshheading:10533617-Cell Division, pubmed-meshheading:10533617-Coronary Disease, pubmed-meshheading:10533617-Coronary Vessels, pubmed-meshheading:10533617-Culture Techniques, pubmed-meshheading:10533617-Imidazoles, pubmed-meshheading:10533617-Losartan, pubmed-meshheading:10533617-Muscle, Smooth, Vascular, pubmed-meshheading:10533617-Pyridines, pubmed-meshheading:10533617-Recurrence, pubmed-meshheading:10533617-Swine, pubmed-meshheading:10533617-Tetrazoles
pubmed:year
1999
pubmed:articleTitle
Angiotensin II receptor antagonists prevent neointimal proliferation in a porcine coronary artery organ culture model.
pubmed:affiliation
Department of Physiology, University of Manitoba, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't