Linked Life Data

11020487

Source:http://linkedlifedata.com/resource/pubmed/id/11020487

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2000-12-15
pubmed:abstractText
We have used preconstricted rings of rabbit superior mesenteric artery to investigate the contribution of phospholipase A(2) and gap junctional communication to endothelium-derived hyperpolarizing factor (EDHF)-type relaxations evoked by melittin, a polypeptide toxin known to mobilize arachidonic acid from the cell membrane. Arachidonyl trifluoromethyl ketone (30 microM), an inhibitor of the Ca(2+)-dependent phospholipase A(2), and Gap 27 (300 microM), a connexin-mimetic peptide which attenuates intercellular communication via gap junctions, both abolished the endothelium-dependent component of EDHF-type responses evoked by melittin in the presence of the NO synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME, 300 microM) and the cyclooxygenase inhibitor indomethacin (10 microM). By contrast, the sulfhydryl agent thimerosal (300 nM), which amplifies EDHF activity, potentiated nitric oxide (NO)/prostanoid-independent relaxations induced by melittin. Neither arachidonyl trifluoromethyl ketone nor thimerosal modulated relaxations evoked by the peptide toxin in the absence of L-NAME and indomethacin. We conclude that melittin evokes EDHF-type relaxations through activation of the endothelial Ca(2+)-dependent phospholipase A(2) followed by the transmission of a chemical and/or electrical signal via myoendothelial gap junctions. This mechanism of vasorelaxation may be negatively regulated by NO.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0014-2999
pubmed:author
pubmed:issnType
Print
pubmed:day
13
pubmed:volume
406
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
239-45
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Role of phospholipase A(2) and myoendothelial gap junctions in melittin-induced arterial relaxation.
pubmed:affiliation
Department of Diagnostic Radiology, Wales Heart Research Institute, University of Wales College of Medicine, Health Park, CF14 4XN, Cardiff, UK.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't