Source:http://linkedlifedata.com/resource/pubmed/id/11146410
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
6
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| pubmed:dateCreated |
2001-1-26
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| pubmed:abstractText |
Previous studies demonstrated that maintenance of steady-state myogenic tone requires Ca(2+)-dependent myosin phosphorylation. The present studies furthered these observations by examining temporal relationships among Ca(2+), myosin phosphorylation and vessel diameter during acute increases in intraluminal pressure and norepinephrine stimulation. Rat cremaster muscle arterioles were cannulated and loaded with the Ca(2+)-sensitive indicator fura-2. The extent of myosin phosphorylation was measured using two-dimensional gel electrophoresis. Acute increases in intraluminal pressure caused a biphasic increase in intracellular Ca(2+) ([Ca(2+)](i)), characterized by a transient peak followed by a decline to a steady-state level which remained significantly higher than control values. Peak [Ca(2+)](i) was significantly related to vessel distension and increased with the change in wall tension. Increased intraluminal pressure resulted in a monophasic increase in myosin phosphorylation that was significantly correlated with instantaneous wall tension. In general, norepinephrine induced larger [Ca(2+)](i) transients and a biphasic myosin phosphorylation pattern. The results demonstrate: (a) major roles for Ca(2+) and myosin phosphorylation in arteriolar myogenic and norepinephrine-induced responses; (b) that changes in Ca(2+) and phosphorylation during a myogenic response are related to changes in wall tension, and (c) differences in Ca(2+) and phosphorylation patterns between the two modes of contraction reflect possible differences in underlying signaling mechanisms. The data further emphasize that spontaneous arteriolar tone represents a state of maintained smooth muscle activation that requires increases in [Ca(2+)](i) and myosin light-chain phosphorylation.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:issn |
1018-1172
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| pubmed:author | |
| pubmed:copyrightInfo |
Copyright 2000 S. Karger AG, Basel
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| pubmed:issnType |
Print
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| pubmed:volume |
37
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
556-67
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| pubmed:dateRevised |
2009-11-19
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| pubmed:meshHeading |
pubmed-meshheading:11146410-Animals,
pubmed-meshheading:11146410-Arterioles,
pubmed-meshheading:11146410-Blood Pressure,
pubmed-meshheading:11146410-Calcium Signaling,
pubmed-meshheading:11146410-Electrophoresis, Gel, Two-Dimensional,
pubmed-meshheading:11146410-Male,
pubmed-meshheading:11146410-Muscle, Smooth, Vascular,
pubmed-meshheading:11146410-Muscle Tonus,
pubmed-meshheading:11146410-Myosin-Light-Chain Kinase,
pubmed-meshheading:11146410-Myosins,
pubmed-meshheading:11146410-Norepinephrine,
pubmed-meshheading:11146410-Phosphorylation,
pubmed-meshheading:11146410-Pressure,
pubmed-meshheading:11146410-Protein Processing, Post-Translational,
pubmed-meshheading:11146410-Rats,
pubmed-meshheading:11146410-Rats, Sprague-Dawley,
pubmed-meshheading:11146410-Time Factors,
pubmed-meshheading:11146410-Vasoconstriction,
pubmed-meshheading:11146410-Vasoconstrictor Agents
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| pubmed:articleTitle |
Temporal aspects of Ca(2+) and myosin phosphorylation during myogenic and norepinephrine-induced arteriolar constriction.
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| pubmed:affiliation |
Department of Physiology, Eastern Virginia Medical School, Norfolk, Va., USA.
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| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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