pubmed-article:3366477 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:3366477 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
pubmed-article:3366477 | lifeskim:mentions | umls-concept:C0003842 | lld:lifeskim |
pubmed-article:3366477 | lifeskim:mentions | umls-concept:C0042401 | lld:lifeskim |
pubmed-article:3366477 | lifeskim:mentions | umls-concept:C0683598 | lld:lifeskim |
pubmed-article:3366477 | lifeskim:mentions | umls-concept:C0857121 | lld:lifeskim |
pubmed-article:3366477 | pubmed:issue | 5 | lld:pubmed |
pubmed-article:3366477 | pubmed:dateCreated | 1988-6-15 | lld:pubmed |
pubmed-article:3366477 | pubmed:abstractText | The endothelium-dependent and presumed endothelium-independent vasodilators acetylcholine and sodium nitroprusside, respectively, were used to characterize relaxation responses of mesenteric resistance arteries from stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar-Kyoto rats (WKY). Vessels were preconstricted using concentrations of norepinephrine or 5-hydroxytryptamine, which reduced their diameters by 50 to 60%. Relaxation responses to acetylcholine (10(-8) - 10(-7) M) were significantly smaller (p less than 0.05) in vessel segments from SHRSP, but the maximal relaxations at higher concentrations were the same in both strains. However, SHRSP vessels relaxed to a greater extent than did those of the WKY at all concentrations of sodium nitroprusside. Endothelium removal significantly enhanced sodium nitroprusside-induced dilations in both rat strains, and the dilations were significantly greater in segments from SHRSP in the concentration range of 3 X 10(-8) to 10(-6) M. The decreased relaxation to acetylcholine in resistance arteries from adult hypertensive rats compared with those from the normotensive strain suggests that functional alterations in the endothelium may play a role in hypertensive disease. | lld:pubmed |
pubmed-article:3366477 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:3366477 | pubmed:language | eng | lld:pubmed |
pubmed-article:3366477 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:3366477 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:3366477 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:3366477 | pubmed:month | May | lld:pubmed |
pubmed-article:3366477 | pubmed:issn | 0194-911X | lld:pubmed |
pubmed-article:3366477 | pubmed:author | pubmed-author:HalpernWW | lld:pubmed |
pubmed-article:3366477 | pubmed:author | pubmed-author:TesfamariamBB | lld:pubmed |
pubmed-article:3366477 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:3366477 | pubmed:volume | 11 | lld:pubmed |
pubmed-article:3366477 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:3366477 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:3366477 | pubmed:pagination | 440-4 | lld:pubmed |
pubmed-article:3366477 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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pubmed-article:3366477 | pubmed:meshHeading | pubmed-meshheading:3366477-... | lld:pubmed |
pubmed-article:3366477 | pubmed:year | 1988 | lld:pubmed |
pubmed-article:3366477 | pubmed:articleTitle | Endothelium-dependent and endothelium-independent vasodilation in resistance arteries from hypertensive rats. | lld:pubmed |
pubmed-article:3366477 | pubmed:affiliation | Department of Physiology and Biophysics, University of Vermont, College of Medicine, Burlington. | lld:pubmed |
pubmed-article:3366477 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:3366477 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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