pubmed-article:11842020 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:11842020 | lifeskim:mentions | umls-concept:C0034721 | lld:lifeskim |
pubmed-article:11842020 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
pubmed-article:11842020 | lifeskim:mentions | umls-concept:C0003847 | lld:lifeskim |
pubmed-article:11842020 | lifeskim:mentions | umls-concept:C0242694 | lld:lifeskim |
pubmed-article:11842020 | lifeskim:mentions | umls-concept:C1522391 | lld:lifeskim |
pubmed-article:11842020 | lifeskim:mentions | umls-concept:C0012359 | lld:lifeskim |
pubmed-article:11842020 | lifeskim:mentions | umls-concept:C0806140 | lld:lifeskim |
pubmed-article:11842020 | lifeskim:mentions | umls-concept:C0205349 | lld:lifeskim |
pubmed-article:11842020 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
pubmed-article:11842020 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:11842020 | pubmed:dateCreated | 2002-2-13 | lld:pubmed |
pubmed-article:11842020 | 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. | lld:pubmed |
pubmed-article:11842020 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11842020 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11842020 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11842020 | pubmed:keyword | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11842020 | pubmed:keyword | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11842020 | pubmed:language | eng | lld:pubmed |
pubmed-article:11842020 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11842020 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:11842020 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11842020 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11842020 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11842020 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11842020 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:11842020 | pubmed:month | Mar | lld:pubmed |
pubmed-article:11842020 | pubmed:issn | 8750-7587 | lld:pubmed |
pubmed-article:11842020 | pubmed:author | pubmed-author:LaughlinM... | lld:pubmed |
pubmed-article:11842020 | pubmed:author | pubmed-author:SchrageWillia... | lld:pubmed |
pubmed-article:11842020 | pubmed:author | pubmed-author:WoodmanChrist... | lld:pubmed |
pubmed-article:11842020 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:11842020 | pubmed:volume | 92 | lld:pubmed |
pubmed-article:11842020 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:11842020 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:11842020 | pubmed:pagination | 901-11 | lld:pubmed |
pubmed-article:11842020 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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pubmed-article:11842020 | pubmed:year | 2002 | lld:pubmed |
pubmed-article:11842020 | pubmed:articleTitle | Mechanisms of flow and ACh-induced dilation in rat soleus arterioles are altered by hindlimb unweighting. | lld:pubmed |
pubmed-article:11842020 | pubmed:affiliation | Department of Physiology, University of Missouri, Columbia, Missouri 65211, USA. | lld:pubmed |
pubmed-article:11842020 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:11842020 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:11842020 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |