Source:http://linkedlifedata.com/resource/pubmed/id/10478630
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1999-11-1
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pubmed:abstractText |
We investigated the relationship between tension development and the cytosolic free Ca2+ level ([Ca2+]i) on exposure of the endothelium-denuded isolated rat aorta to palmitoyl-L-alpha-lysophosphatidylcholine. Lysophosphatidylcholine concentration-dependently induced a gradual increase in [Ca2+]i. Application of 10(-4) M lysophosphatidylcholine induced a large and sustained tonic increase in [Ca2+]i (the peak [Ca2+]i was 125.2 +/- 11.5% of the 80 mM K+-induced response) but only a small contraction (4.0 +/- 1.4% of the 80 mM K+ induced contraction). The sustained increase in [Ca2+]i was attenuated when extracellular Ca2+ was removed but it was unaffected by verapamil or 1-(5-isoquinolinesulphonyl)-2-methylpiperazine dihydrochloride (H-7). Digitonin also produced a gradual increase in [Ca2+]i but with a pronounced contraction. Triton X-100 (0.1%) produced a marked elevation in [Ca2+]i with no detectable contraction. Triton X-100, however, caused a rapid leakage of fura PE-3. Treatment with 10(-4) M lysophosphatidylcholine for 1 or 2 h did not affect the contractile response induced by 80 mM K+ and this treatment did not release lactate dehydrogenase from the rat aorta. Treatment with lysophosphatidylcholine did not affect either the cyclic AMP level or the cyclic GMP level in endothelium-denuded aortic tissues. These results show that in the rat aorta lysophosphatidylcholine produces a large increase in [Ca2+]i (possibly in a non-contractile compartment) which does not induce contraction. Thus, the increase in [Ca2+]i induced by lysophosphatidylcholine (i) requires external Ca2+ but is not due to an increased Ca2+ influx through voltage-dependent L-type Ca2+ channels, (ii) is not primarily due to protein kinase C activation and (iii) is probably not due to a detergent action (like those of digitonin and triton X-100). The relative lack of a contractile response to lysophosphatidylcholine is not due to formation of cyclic AMP or cyclic GMP.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic GMP,
http://linkedlifedata.com/resource/pubmed/chemical/Lysophosphatidylcholines,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase C
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0014-2999
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
6
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pubmed:volume |
378
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
177-86
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:10478630-Animals,
pubmed-meshheading:10478630-Aorta, Thoracic,
pubmed-meshheading:10478630-Calcium,
pubmed-meshheading:10478630-Cyclic AMP,
pubmed-meshheading:10478630-Cyclic GMP,
pubmed-meshheading:10478630-Dose-Response Relationship, Drug,
pubmed-meshheading:10478630-Isometric Contraction,
pubmed-meshheading:10478630-Lysophosphatidylcholines,
pubmed-meshheading:10478630-Male,
pubmed-meshheading:10478630-Muscle, Smooth, Vascular,
pubmed-meshheading:10478630-Muscle Contraction,
pubmed-meshheading:10478630-Nitric Oxide,
pubmed-meshheading:10478630-Protein Kinase C,
pubmed-meshheading:10478630-Rats,
pubmed-meshheading:10478630-Rats, Wistar
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pubmed:year |
1999
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pubmed:articleTitle |
Marked dissociation between intracellular Ca2+ level and contraction on exposure of rat aorta to lysophosphatidylcholine.
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pubmed:affiliation |
Department of Physiology and Morphology, Institute of Medicinal Chemistry, Hoshi University, Tokyo, Japan.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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