Linked Life Data

17964568

Source:http://linkedlifedata.com/resource/pubmed/id/17964568

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-3
pubmed:dateCreated
2008-1-8
pubmed:abstractText
Culture of intact arteries is a frequently employed experimental model for investigating the mechanisms governing the regulation of vascular endothelin receptors. Endothelin type A (ET(A)) and type B (ET(B)) receptors on vascular smooth muscle cells are up-regulated in organ culture and the enhanced vasoconstriction mimics the changes that occur in cardiovascular disease. The effect of organ culture on endothelial dilatory endothelin ET(B) receptors is not known. We hypothesize that organ culture decreases the endothelin receptor-mediated dilatation and that this is one possible mechanism by which the effects of the endothelin in blood vessels are altered during culture. Porcine coronary arteries were studied before and after 24 h of culture, using in vitro pharmacology and immunofluorescence. Sarafotoxin 6c and endothelin-1 were used to examine the endothelin ET(A) and ET(B) receptor effects, and the antagonists, Nomega-nitro-l-arginine (l-NOARG) for nitric oxide (NO), indomethacin for prostaglandins and charybdotoxin in combination with apamin for endothelium-derived hyperpolarizing factor (EDHF), were used to study the endothelium-derived dilatory mediators. Organ culture induced up-regulation of the sarafotoxin 6c (ET(B) receptor agonist) and endothelin-1 (ET(A) receptor agonist) elicited vasoconstriction. The sarafotoxin 6c contraction was stronger after endothelium denudation, suggesting endothelium-dependent dilatation. The endothelin-1 contraction was not affected by endothelium denudation. The increase in sarafotoxin 6c contraction after removal of the endothelium was more pronounced before than after organ culture, suggesting down-regulated endothelial endothelin ET(B) receptors. Also, the immunofluorescence staining intensities for endothelial endothelin ET(B) receptors were higher before than after organ culture. Pre-incubation with inhibitors for dilatory mediators suggested that both NO and EDHF play a vasodilatory role, while prostaglandins are not involved. In conclusion, endothelial endothelin ET(B) receptors induce NO and EDHF mediated vasodilatation in porcine coronary arteries. In organ culture, endothelial endothelin ET(B) receptors are down-regulated, mimicking the changes that occur in cardiovascular disease. Down-regulation of endothelial endothelin ET(B) receptors may in part explain the increased endothelin ET(B) receptor-mediated vasoconstriction frequently studied in organ culture.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0014-2999
pubmed:author
pubmed:issnType
Print
pubmed:day
28
pubmed:volume
579
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
233-40
pubmed:meshHeading
pubmed-meshheading:17964568-Animals, pubmed-meshheading:17964568-Biological Factors, pubmed-meshheading:17964568-Coronary Vessels, pubmed-meshheading:17964568-Down-Regulation, pubmed-meshheading:17964568-Endothelin-1, pubmed-meshheading:17964568-Endothelium, Vascular, pubmed-meshheading:17964568-Female, pubmed-meshheading:17964568-Fluorescent Antibody Technique, pubmed-meshheading:17964568-Male, pubmed-meshheading:17964568-Muscle, Smooth, Vascular, pubmed-meshheading:17964568-Nitric Oxide, pubmed-meshheading:17964568-Organ Culture Techniques, pubmed-meshheading:17964568-Receptor, Endothelin A, pubmed-meshheading:17964568-Receptor, Endothelin B, pubmed-meshheading:17964568-Swine, pubmed-meshheading:17964568-Up-Regulation, pubmed-meshheading:17964568-Vasoconstriction, pubmed-meshheading:17964568-Vasodilation, pubmed-meshheading:17964568-Viper Venoms
pubmed:year
2008
pubmed:articleTitle
Endothelin receptor-mediated vasodilatation: effects of organ culture.
pubmed:affiliation
Department of Medicine, Lund University Hospital, Lund, Sweden.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't