Linked Life Data

11282220

Source:http://linkedlifedata.com/resource/pubmed/id/11282220

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2001-4-3
pubmed:abstractText
Relaxations to acetylcholine and contractions to acetylcholine in the presence of the nitric oxide (NO) synthesis inhibitor (L-N(G)-nitroarginine methyl ester, L-NAME) were studied in aortic rings from rabbits fed either a control or a diet containing 0.5% cholesterol+14% coconut oil for 14 weeks and treated or not with atorvastatin (2.5 mg kg(-1) day(-1)). Rings were incubated with the endothelin (ET(A)) receptor antagonist BQ123, and/or the thromboxane A(2) (TXA(2))/prostaglandin H(2) (PGH(2)) receptor antagonist ifetroban. In rabbits, high cholesterol and triglyceride plasma levels were associated with intimal thickening and blunted acetylcholine-relaxation as compared with controls. By contrast, acetylcholine+L-NAME response was higher. Incubation with either ifetroban or BQ123 increased acetylcholine-relaxation in both diet groups and it reduced the constrictor response only in dyslipidemic rabbits. Removal of endothelium reduced acetylcholine+L-NAME contraction in dyslipidemic rabbits, although increased it in control animals. Atorvastatin treatment reduced plasma lipid levels and lesion size in dyslipidemic animals. Likewise, it prevented acetylcholine-relaxation reduction. In addition, atorvastatin reduced constrictor response in dyslipidemic rabbits but only in rings with endothelium. Incubation with either ifetroban or BQ123 did not further modify these responses in atorvastatin-treated animals in any group. These data suggest that ET and TXA(2) availabilities seem to participate in the endothelial dysfunction associated with dyslipidemia. Atorvastatin treatment reduces intimal thickening and improves endothelial dysfunction in rabbits. This effect seems to be a consequence of its ability to act on ET and TXA(2) systems.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0306-3623
pubmed:author
pubmed:issnType
Print
pubmed:volume
34
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
263-72
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11282220-Animals, pubmed-meshheading:11282220-Anticholesteremic Agents, pubmed-meshheading:11282220-Aorta, pubmed-meshheading:11282220-Drug Interactions, pubmed-meshheading:11282220-Endothelins, pubmed-meshheading:11282220-Endothelium, Vascular, pubmed-meshheading:11282220-Enzyme Inhibitors, pubmed-meshheading:11282220-Heptanoic Acids, pubmed-meshheading:11282220-Hyperlipidemias, pubmed-meshheading:11282220-Male, pubmed-meshheading:11282220-NG-Nitroarginine Methyl Ester, pubmed-meshheading:11282220-Pyrroles, pubmed-meshheading:11282220-Rabbits, pubmed-meshheading:11282220-Receptor, Endothelin A, pubmed-meshheading:11282220-Receptors, Endothelin, pubmed-meshheading:11282220-Receptors, Prostaglandin, pubmed-meshheading:11282220-Receptors, Thromboxane A2, Prostaglandin H2, pubmed-meshheading:11282220-Vasoconstriction
pubmed:year
2000
pubmed:articleTitle
Effect of atorvastatin on endothelium-dependent constrictor factors in dyslipidemic rabbits.
pubmed:affiliation
Department of Physiology, School of Medicine, Universidad Complutense, Madrid 28040, Spain.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't