Linked Life Data

11115418

Source:http://linkedlifedata.com/resource/pubmed/id/11115418

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2001-1-26
pubmed:abstractText
Resveratrol has been shown to induce vasorelaxation. In this study, we investigated the mechanism(s) of resveratrol-induced vasorelaxation in resistance mesenteric arteries from male lean and dietary-induced obese rats. Compared with lean rats, arteries from dietary-obese rats showed significant (P<0.001) endothelial dysfunction, as indicated by a decrease (>20%) in maximal acetylcholine-induced vasorelaxation. Resveratrol (5-35 micromol/l) induced concentration-dependent relaxation of mesenteric arteries preconstricted with noradrenaline (8 micromol/l) or KCl (125 mmol/l) from both lean and dietary-obese rats. There were no significant differences between the two groups, achieving a maximum relaxation of >95% at a concentration of 35 micromol/l. In noradrenaline-preconstricted arteries from lean rats, N(G)-nitro-L-arginine methyl ester (L-NAME; 100 and 300 micromol/l) caused a significant (P<0.01) concentration-dependent rightward shift in reseveratrol activity, with no effect on maximal responses. However, L-NAME (100 and 300 micromol/l) did not alter the effects of reseveratrol on arteries from dietary-obese rats, giving superimposed concentration-responses curves. Indomethacin was also ineffective in altering resveratrol activity in arteries from both lean and dietary-obese rats. In noradrenaline-precontracted arteries from dietary-obese rats, responses to resveratrol were not attenuated by endothelial denudation, indicating an action independent of the endothelium. This study indicates that: (a) the maximal effects of resveratrol on resistance arteries from lean and dietary-obese rats are not effected by endothelial dysfunction, and (b) the effects of resveratrol in lean animals (where endothelial function is not impaired), but not in dietary-obese rats, are mediated via NO.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0143-5221
pubmed:author
pubmed:issnType
Print
pubmed:volume
100
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
55-60
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11115418-Acetylcholine, pubmed-meshheading:11115418-Animals, pubmed-meshheading:11115418-Body Weight, pubmed-meshheading:11115418-Dose-Response Relationship, Drug, pubmed-meshheading:11115418-Drug Interactions, pubmed-meshheading:11115418-Endothelium, Vascular, pubmed-meshheading:11115418-Indomethacin, pubmed-meshheading:11115418-Male, pubmed-meshheading:11115418-Mesenteric Arteries, pubmed-meshheading:11115418-NG-Nitroarginine Methyl Ester, pubmed-meshheading:11115418-Norepinephrine, pubmed-meshheading:11115418-Obesity, pubmed-meshheading:11115418-Rats, pubmed-meshheading:11115418-Rats, Wistar, pubmed-meshheading:11115418-Stilbenes, pubmed-meshheading:11115418-Vasoconstrictor Agents, pubmed-meshheading:11115418-Vasodilation, pubmed-meshheading:11115418-Vasodilator Agents
pubmed:year
2001
pubmed:articleTitle
The mechanism of resveratrol-induced vasorelaxation differs in the mesenteric resistance arteries of lean and obese rats.
pubmed:affiliation
Diabetes and Endocrinology Research Unit, Department of Medicine, University of Liverpool, UCD, Daulby Street, Liverpool L69 3GA, UK. naderali@liverpool.ac.uk
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't