Linked Life Data

9495850

Source:http://linkedlifedata.com/resource/pubmed/id/9495850

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1998-4-9
pubmed:abstractText
The purpose of this study was to investigate the role of extracellular Ca++ influx via L-type and non-L-type Ca++ channels in thromboxane A2 receptor-mediated contraction. In intact rat aorta, U46619, a selective thromboxane A2 receptor agonist, induced concentration-dependent increases in intracellular Ca++ ([Ca++]i) and contraction (EC50 values of 5.5 and 6.1 nM, respectively). U46619 (10 nM) induced approximately 60 to 70% of maximal [Ca++]i elevation and contraction. Treatment with verapamil, an L-type Ca++ channel blocker, before 10 nM U46619 challenge, or during the plateau [Ca++]i elevation and contraction, decreased these parameters by approximately 50%. Ni++, a nonselective blocker of cation channels, or SKF96365, a purported blocker of receptor-operated Ca++ channels, further decreased the contraction and abolished the [Ca++]i elevation that remained after verapamil treatment of 10 nM U46619-challenged vessels. Pretreatment with verapamil and Ni++ to prevent Ca++ influx and with cyclopiazonic acid to deplete [Ca++]i stores also partially prevented U46619-induced contraction, whereas [Ca++]i elevation was abolished. These results suggest that thromboxane A2 receptor-mediated contraction of vascular smooth muscle partly depends on the influx of extracellular Ca++ via both L-type and non-L-type Ca++ channels, as well as a mechanism independent of [Ca++]i elevation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0022-3565
pubmed:author
pubmed:issnType
Print
pubmed:volume
284
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
921-8
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Role of extracellular Ca++ influx via L-type and non-L-type Ca++ channels in thromboxane A2 receptor-mediated contraction in rat aorta.
pubmed:affiliation
Department of Pharmacology and Cell Biophysics, University of Cincinnati, Ohio, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't