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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2-3
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pubmed:dateCreated |
1998-4-3
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pubmed:abstractText |
Prostaglandin F2alpha was tested to determine (a) whether its effect on intracellular Ca2+ levels ([Ca2+]i) and force in vascular smooth muscle was mediated through activation of the thromboxane A2 and/or prostaglandin receptor, and (b) the relative roles of Ca2+ influx via L-type and non-L-type Ca2+ channels in prostaglandin receptor-mediated contraction. [Ca2+]i and force were measured simultaneously in fura-2-loaded rat aortic strips. The thromboxane A2 receptor antagonist, SQ29548 ([1S]-1a,2b(5Z),3b,4a-7-(3-[2-[(phenylamino)carbonyl] hydrazinomethyl)-7-oxobicyclo-[2.2.1]hept-2-yl-5-heptenoic acid), prevented the prostaglandin F2alpha-induced plateau [Ca2+]i elevation and force by 80-90%, while abolishing these responses due to the thromboxane A2 receptor agonist, U46619 (9,11-dideoxy-9alpha,11alpha-methanoepoxy prostaglandin F2alpha). Prostaglandin F2alpha (+ SQ29548)-induced plateau [Ca2+]i elevation and force were not inhibited by verapamil. Ni2+, a non-selective cation channel blocker, in the presence of verapamil, abolished the prostaglandin F2alpha (+ SQ29548)-elevated [Ca2+]i, while the contraction was only partially inhibited. These results suggest that, in rat aorta, (1) elevated [Ca2+]i and force due to high prostaglandin F2alpha concentrations largely results from thromboxane A2 receptor activation, and (2) the prostaglandin component of the prostaglandin F2alpha-induced contraction is dependent on Ca2+ influx via non-L-type channels.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/15-Hydroxy-11 alpha,9...,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channel Blockers,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Dinoprost,
http://linkedlifedata.com/resource/pubmed/chemical/Hydrazines,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Thromboxane,
http://linkedlifedata.com/resource/pubmed/chemical/SQ 29548,
http://linkedlifedata.com/resource/pubmed/chemical/Thromboxane A2,
http://linkedlifedata.com/resource/pubmed/chemical/Verapamil
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0014-2999
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
11
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pubmed:volume |
340
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
203-8
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:9537816-15-Hydroxy-11 alpha,9...,
pubmed-meshheading:9537816-Animals,
pubmed-meshheading:9537816-Aorta, Thoracic,
pubmed-meshheading:9537816-Calcium,
pubmed-meshheading:9537816-Calcium Channel Blockers,
pubmed-meshheading:9537816-Calcium Channels,
pubmed-meshheading:9537816-Dinoprost,
pubmed-meshheading:9537816-Hydrazines,
pubmed-meshheading:9537816-Male,
pubmed-meshheading:9537816-Muscle, Smooth, Vascular,
pubmed-meshheading:9537816-Muscle Contraction,
pubmed-meshheading:9537816-Rats,
pubmed-meshheading:9537816-Rats, Sprague-Dawley,
pubmed-meshheading:9537816-Receptors, Thromboxane,
pubmed-meshheading:9537816-Thromboxane A2,
pubmed-meshheading:9537816-Verapamil
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pubmed:year |
1997
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pubmed:articleTitle |
Intracellular Ca2+ elevation and contraction due to prostaglandin F2alpha in rat aorta.
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pubmed:affiliation |
Department of Pharmacology and Cell Biophysics, University of Cincinnati, OH 45267-0575, USA.
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pubmed:publicationType |
Journal Article,
In Vitro,
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
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