Linked Life Data

15764840

Source:http://linkedlifedata.com/resource/pubmed/id/15764840

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2005-3-23
pubmed:abstractText
In canine ventricular myocardium, endothelin-1 (ET-1) alone induced only a weak transient negative inotropic effect (NIE). However, ET-1 induced a marked sustained positive inotropic effect (PIE) subsequent to a transient NIE in the presence of norepinephrine (NE) at low concentrations (0.1 - 1 nM) and elicited a pronounced sustained NIE in the presence of NE at high concentrations (around 100 nM). Thus, the extent of beta-adrenoceptor stimulation induced by NE played a crucial role in determining the characteristics of the inotropic effects of ET-1. The characteristics of ET receptor subtypes involved in contractile regulation and Ca(2+) signaling induced by ET-1 were determined. The ET-1-induced transient NIE and decrease in Ca(2+) transients were abolished by the selective ET(A)-receptor antagonist FR319317, but not by the selective ET(B)-receptor antagonist BQ-788. The sustained PIE and the increase in Ca(2+) transients induced by ET-1 were abolished by FR319317, but not inhibited by BQ-788. In contrast, the sustained NIE of ET-1 was abolished by the non-selective ET antagonist TAK-044, markedly attenuated by FR319317, and partially inhibited by BQ-788. ET-1 alone elicited a PIE in the presence of BQ-788, which indicates that the activation of ET(B)-receptors counteracts the development of the PIE of ET-1. The current findings indicate that both ET(A) and ET(B) receptors are involved in the regulation of Ca(2+) signaling and contractility in canine ventricular myocardium.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1347-8613
pubmed:author
pubmed:issnType
Print
pubmed:volume
97
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
417-28
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:15764840-Animals, pubmed-meshheading:15764840-Azepines, pubmed-meshheading:15764840-Calcium Signaling, pubmed-meshheading:15764840-Dogs, pubmed-meshheading:15764840-Dose-Response Relationship, Drug, pubmed-meshheading:15764840-Endothelin-1, pubmed-meshheading:15764840-Female, pubmed-meshheading:15764840-Heart Ventricles, pubmed-meshheading:15764840-Indoles, pubmed-meshheading:15764840-Kinetics, pubmed-meshheading:15764840-Male, pubmed-meshheading:15764840-Myocardial Contraction, pubmed-meshheading:15764840-Myocytes, Cardiac, pubmed-meshheading:15764840-Norepinephrine, pubmed-meshheading:15764840-Oligopeptides, pubmed-meshheading:15764840-Peptides, Cyclic, pubmed-meshheading:15764840-Piperidines, pubmed-meshheading:15764840-Receptor Cross-Talk, pubmed-meshheading:15764840-Receptors, Endothelin
pubmed:year
2005
pubmed:articleTitle
Receptor subtypes mediating the inotropic effects and Ca(2+) signaling induced by endothelin-1 through crosstalk with norepinephrine in canine ventricular myocardium.
pubmed:affiliation
Department of Cardiovascular Pharmacology, Yamagata University School of Medicine, Yamagata.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't