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rdf:type |
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lifeskim:mentions |
umls-concept:C0003009,
umls-concept:C0006675,
umls-concept:C0010453,
umls-concept:C0020291,
umls-concept:C0031621,
umls-concept:C0178719,
umls-concept:C0220781,
umls-concept:C0221464,
umls-concept:C0442805,
umls-concept:C0596981,
umls-concept:C1637379,
umls-concept:C1883254
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pubmed:issue |
24
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pubmed:dateCreated |
1985-2-21
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pubmed:abstractText |
Smooth muscle cells were cultured from rat thoracic aorta and labeled to a stable specific activity with 45Ca2+, myo-[2-3H]inositol, or 32Pi. The efflux of 45Ca2+ was monitored over 10-sec intervals. Angiotensin II (AII) increased the amount of 45Ca2+ lost by 5-fold in the first 10-sec interval after the addition of AII and by 10-fold in the second 10-sec interval. AII-stimulated 45Ca2+ release was blocked by the angiotensin antagonist [1-sarcosine, 8-leucine]AII and by La3+. The removal of external Ca2+ had no effect on AII-stimulated 45Ca2+ release. Depolarization with high external K+ only slightly increased 45Ca2+ efflux and had no effect on AII-induced 45Ca2+ release. AII had no effect on the initial rate of 45Ca2+ influx. These results indicate that the rapid 45Ca2+ efflux evoked by AII is probably due to the release of 45Ca2+ sequestered intracellularly rather than to an increase in the Ca2+ permeability of the plasma membrane. AII provoked rapid increases in the levels of phosphatidic acid and phosphoinositides in the cells. These increases in phospholipids were associated with increases in phospholipase C-generated inositol phosphates (tri-, di-, and mono-). It appears that AII simultaneously increases phosphoinositide hydrolysis and synthesis in vascular smooth muscle, and both phospholipid effects may contribute to inositol triphosphate generation, which was sufficiently rapid to have a role in intracellular Ca2+ mobilization.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/6096858-13732018,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6096858-14907713,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6096858-17788298,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6096858-189844,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6096858-190404,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6096858-221461,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6096858-4188409,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6096858-4367920,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6096858-4684128,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6096858-5044754,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6096858-6136270,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6096858-6143700,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6096858-6248553,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6096858-6269920,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6096858-6277961,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6096858-6280182,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6096858-6295182,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6096858-6297743,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6096858-6300146,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6096858-6309146,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6096858-6311519,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6096858-6317349,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6096858-6325926,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6096858-6373768,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6096858-6605482,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6096858-6607924,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6096858-6891617,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6096858-7132555,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6096858-7260047,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6096858-82969
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0027-8424
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
81
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
7812-6
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pubmed:dateRevised |
2010-9-13
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pubmed:meshHeading |
pubmed-meshheading:6096858-Angiotensin II,
pubmed-meshheading:6096858-Animals,
pubmed-meshheading:6096858-Aorta, Thoracic,
pubmed-meshheading:6096858-Calcium,
pubmed-meshheading:6096858-Cells, Cultured,
pubmed-meshheading:6096858-Hydrolysis,
pubmed-meshheading:6096858-Kinetics,
pubmed-meshheading:6096858-Muscle, Smooth, Vascular,
pubmed-meshheading:6096858-Phosphatidic Acids,
pubmed-meshheading:6096858-Phosphatidylinositols,
pubmed-meshheading:6096858-Rats,
pubmed-meshheading:6096858-Rats, Inbred Strains
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pubmed:year |
1984
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pubmed:articleTitle |
Angiotensin II rapidly increases phosphatidate-phosphoinositide synthesis and phosphoinositide hydrolysis and mobilizes intracellular calcium in cultured arterial muscle cells.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.
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