Linked Life Data

20935150

Source:http://linkedlifedata.com/resource/pubmed/id/20935150

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2010-12-3
pubmed:abstractText
Myocardial infarction (MI) has been shown to induce endothelial dysfunction in peripheral resistance arteries and thus increase peripheral resistance. This study was designed to investigate the underlying mechanisms of post-MI-related dysfunctional dilatation of peripheral resistance arteries and, furthermore, to examine whether exercise may restore dysfunctional dilatation of peripheral resistance arteries. Adult male Sprague-Dawley rats were divided into three groups: sham-operated, MI, and MI + exercise. Ultrastructure and relaxation function of the mesenteric arteries, as well as phosphatidylinositol-3 kinase (PI3K), Akt kinases (Akt), endothelial nitric oxide synthase (eNOS) activity, and phosphorylation of PI3K, Akt, and eNOS by ACh were determined. Post-MI rats exhibited pronounced ultrastructural changes in mesenteric artery endothelial cells and endothelial dysfunction. In addition, the activities of PI3K, Akt, and eNOS, and their phosphorylation by ACh were significantly attenuated in mesenteric arteries (P < 0.05-0.01). After 8 wk of exercise, not only did endothelial cells appeared more normal in structure, but also ameliorated post-MI-associated mesenteric arterial dysfunction, which were accompanied by elevated activities of PI3K, Akt, and eNOS, and their phosphorylation by ACh (P < 0.05-0.01). Importantly, inhibition of either PI3K or eNOS attenuated exercise-induced restoration of the dilatation function and blocked PI3K, Akt, and eNOS phosphorylation by ACh in the mesenteric arteries. These data demonstrate that MI induces dysfunctional dilation of peripheral resistance arteries by degradation of endothelial structural integrity and attenuating PI3K-Akt-eNOS signaling. Exercise may restore dilatation function of peripheral resistance arteries by protecting endothelial structural integrity and increasing PI3K-Akt-eNOS signaling cascades.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1522-1539
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
299
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H2097-106
pubmed:meshHeading
pubmed-meshheading:20935150-Animals, pubmed-meshheading:20935150-Disease Models, Animal, pubmed-meshheading:20935150-Dose-Response Relationship, Drug, pubmed-meshheading:20935150-Endothelial Cells, pubmed-meshheading:20935150-Enzyme Inhibitors, pubmed-meshheading:20935150-Male, pubmed-meshheading:20935150-Mesenteric Arteries, pubmed-meshheading:20935150-Myocardial Infarction, pubmed-meshheading:20935150-Nitric Oxide Synthase Type III, pubmed-meshheading:20935150-Phosphatidylinositol 3-Kinases, pubmed-meshheading:20935150-Phosphorylation, pubmed-meshheading:20935150-Physical Exertion, pubmed-meshheading:20935150-Proto-Oncogene Proteins c-akt, pubmed-meshheading:20935150-Rats, pubmed-meshheading:20935150-Rats, Sprague-Dawley, pubmed-meshheading:20935150-Recovery of Function, pubmed-meshheading:20935150-Signal Transduction, pubmed-meshheading:20935150-Time Factors, pubmed-meshheading:20935150-Vasodilation, pubmed-meshheading:20935150-Vasodilator Agents
pubmed:year
2010
pubmed:articleTitle
Exercise improves the dilatation function of mesenteric arteries in postmyocardial infarction rats via a PI3K/Akt/eNOS pathway-mediated mechanism.
pubmed:affiliation
Department of Pharmacology, Xi'an Jiaotong University, College of Medicine, Xi'an, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't