Linked Life Data

7509953

Source:http://linkedlifedata.com/resource/pubmed/id/7509953

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1994-4-4
pubmed:abstractText
The mechanism for the endothelin (ET)-induced vasodilatation of the endothelium-intact rat coronary vascular bed was investigated. Continuous infusion (0.1-1 nM) or bolus injection (1-100 pmol) of ET-1 or ET-3 elicited a dose-related transient decrease, followed by a slight sustained increase, in the coronary perfusion pressure (CPP). The decrease in CPP induced by an injection (10 pmol) of ET-1 or ET-3 was not modified by indomethacin (5 microM). However, oxyhemoglobin (5 mM) shortened the duration of the ET-induced decrease in CPP, although it did not affect the magnitude. The ET-induced decrease in CPP was abolished by raising K+ in the perfusing solution from 5.9 to 16.9 mM. These findings suggest that the ET-induced dilatation of the rat coronary vascular beds may not be mediated by cyclooxygenase products. The ET-induced vasorelaxation may be mediated, at least in part, by endothelium-derived relaxing factor and may be related to opening of K+ channels.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0160-2446
pubmed:author
pubmed:issnType
Print
pubmed:volume
22 Suppl 8
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
S232-4
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Possible contribution of potassium channels to the endothelin-induced dilatation of rat coronary vascular beds.
pubmed:affiliation
Department of Cardiovascular Medicine, School of Medicine, Hokkaido University, Sapporo, Japan.
pubmed:publicationType
Journal Article, In Vitro