Source:http://linkedlifedata.com/resource/pubmed/id/11842020
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
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| pubmed:dateCreated |
2002-2-13
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| pubmed:abstractText |
The purpose of this study was to test the hypothesis that endothelium-dependent dilation (flow-induced dilation and ACh-induced dilation) in rat soleus muscle arterioles is impaired by hindlimb unweighting (HLU). Male Sprague-Dawley rats (approximately 300 g) were exposed to HLU or weight-bearing control (Con) conditions for 14 days. Soleus first-order (1A) and second-order (2A) arterioles were isolated, cannulated, and exposed to step increases in luminal flow at constant pressure. Flow-induced dilation was not impaired by HLU in 1A or 2A arterioles. The cyclooxygenase inhibitor indomethacin (Indo; 50 microM) did not alter flow-induced dilation in 1As or 2As. Inhibition of nitric oxide synthase (NOS) with N(omega)-nitro-L-arginine (L-NNA; 300 microM) reduced flow-induced dilation by 65-70% in Con and HLU 1As. In contrast, L-NNA abolished flow-induced dilation in 2As from Con rats but had no effect in HLU 2As. Combined treatment with L-NNA + Indo reduced tone in 1As and 2As from Con rats, but flow-induced dilation in the presence of L-NNA + Indo was not different from responses without inhibitors in either Con or HLU 1As or 2As. HLU also did not impair ACh-induced dilation (10(-9)-10(-4) M) in soleus 2As. L-NNA reduced ACh-induced dilation by approximately 40% in Con 2As but abolished dilation in HLU 2As. Indo did not alter ACh-induced dilation in Con or HLU 2As, whereas combined treatment with L-NNA + Indo abolished ACh-induced dilation in 2As from both groups. We conclude that flow-induced dilation (1As and 2As) was preserved after 2 wk HLU, but HLU decreased the contribution of NOS in mediating flow-induced dilation and increased the contribution of a NOS- and cyclooxygenase-independent mechanism (possibly endothelium-derived hyperpolarizing factor). In soleus 2As, ACh-induced dilation was preserved after 2-wk HLU but the contribution of NOS in mediating ACh-induced dilation was increased.
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| pubmed:grant | |
| pubmed:keyword | |
| 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:month |
Mar
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| pubmed:issn |
8750-7587
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
92
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
901-11
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| pubmed:dateRevised |
2007-11-14
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| pubmed:meshHeading |
pubmed-meshheading:11842020-Acetylcholine,
pubmed-meshheading:11842020-Animals,
pubmed-meshheading:11842020-Arterioles,
pubmed-meshheading:11842020-Endothelium, Vascular,
pubmed-meshheading:11842020-Hindlimb Suspension,
pubmed-meshheading:11842020-Male,
pubmed-meshheading:11842020-Muscle, Skeletal,
pubmed-meshheading:11842020-Nitric Oxide Synthase,
pubmed-meshheading:11842020-Prostaglandin-Endoperoxide Synthases,
pubmed-meshheading:11842020-Rats,
pubmed-meshheading:11842020-Rats, Sprague-Dawley,
pubmed-meshheading:11842020-Regional Blood Flow,
pubmed-meshheading:11842020-Stress, Mechanical,
pubmed-meshheading:11842020-Vasodilation,
pubmed-meshheading:11842020-Vasodilator Agents
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| pubmed:year |
2002
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| pubmed:articleTitle |
Mechanisms of flow and ACh-induced dilation in rat soleus arterioles are altered by hindlimb unweighting.
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| pubmed:affiliation |
Department of Physiology, University of Missouri, Columbia, Missouri 65211, USA.
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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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