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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1994-6-2
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pubmed:abstractText |
The vasoactive peptides endothelin-1 (ET-1) and angiotensin-II (AII) have been implicated in chronic hypertension and may play important roles in related vascular diseases such as restenosis and atherosclerosis. Using a rat aortic smooth muscle (RASM) cell model, both ET-1 and AII induced concentration-dependent delayed increases in DNA synthesis relative to that in the serum-deprived controls. Stimulation of DNA synthesis was maximal at 100 nM for each peptide. All treatment of RASM cells resulted in a greater mitogenic effect (4- to 7-fold) than that observed for ET-1 (3-fold). When added in the presence of AII, ET-1 had a supplemental effect on DNA synthesis (5- to 10-fold above control). Although RASM cells expressed both ETA and AT1 receptors, radioligand binding experiments indicated that approximately 10-fold as many AT1 receptors as ETA receptors were present. In signal transduction studies, ET-1 and AII each elicited concentration-dependent increases in the intracellular Ca2+ concentration. ET-1 and AII also stimulated phosphoinositide metabolism and phosphorylation of a specific substrate for protein kinase-C. The release of total inositol phosphates in response to ET-1 and AII was concentration dependent and inhibited by the ETA receptor-selective antagonist BQ-123 and the AT1 receptor-selective antagonist losartan, respectively. In addition, tyrosine phosphorylation of 120- and 75-kilodalton proteins as well as the mitogen-activated protein kinases p44mapk and p42mapk was observed within 5 min of the addition of either ET-1 or AII. Taken together, these data indicate that ET-1 and AII may promote smooth muscle cell growth through common intracellular signaling mechanisms.
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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/Angiotensin II,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/DNA,
http://linkedlifedata.com/resource/pubmed/chemical/Endothelins,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Angiotensin,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Endothelin
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0888-8809
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
8
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
148-58
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:8170471-Angiotensin II,
pubmed-meshheading:8170471-Animals,
pubmed-meshheading:8170471-Calcium,
pubmed-meshheading:8170471-Cells, Cultured,
pubmed-meshheading:8170471-DNA,
pubmed-meshheading:8170471-Endothelins,
pubmed-meshheading:8170471-Mitosis,
pubmed-meshheading:8170471-Models, Biological,
pubmed-meshheading:8170471-Muscle, Smooth, Vascular,
pubmed-meshheading:8170471-Phosphorylation,
pubmed-meshheading:8170471-Protein Kinases,
pubmed-meshheading:8170471-Rats,
pubmed-meshheading:8170471-Receptors, Angiotensin,
pubmed-meshheading:8170471-Receptors, Endothelin,
pubmed-meshheading:8170471-Signal Transduction,
pubmed-meshheading:8170471-Time Factors
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pubmed:year |
1994
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pubmed:articleTitle |
Endothelin-1 and angiotensin-II stimulate delayed mitogenesis in cultured rat aortic smooth muscle cells: evidence for common signaling mechanisms.
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pubmed:affiliation |
Department of Cardiovascular Biochemistry, Bristol-Myers Squibb Pharmaceutical Research Institute, Princeton, New Jersey 08543.
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pubmed:publicationType |
Journal Article
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