pubmed-article:7491898 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:7491898 | lifeskim:mentions | umls-concept:C0031330 | lld:lifeskim |
pubmed-article:7491898 | lifeskim:mentions | umls-concept:C0034493 | lld:lifeskim |
pubmed-article:7491898 | lifeskim:mentions | umls-concept:C1135918 | lld:lifeskim |
pubmed-article:7491898 | lifeskim:mentions | umls-concept:C0025465 | lld:lifeskim |
pubmed-article:7491898 | lifeskim:mentions | umls-concept:C0521116 | lld:lifeskim |
pubmed-article:7491898 | pubmed:issue | 5 Pt 1 | lld:pubmed |
pubmed-article:7491898 | pubmed:dateCreated | 1996-1-4 | lld:pubmed |
pubmed-article:7491898 | pubmed:abstractText | The inference that ATP-sensitive K+ (KATP) channels are involved in arterial responses to the synthetic K+ channel openers, hypoxia, adenosine, and calcitonin gene-related peptide, has relied on the sensitivity of these responses to the sulfonylureas glibenclamide and tolbutamide and to tetraethylammonium (TEA+). The inhibition of KATP currents by glibenclamide, tolbutamide, and TEA+ was investigated in single smooth muscle cells from rabbit mesenteric artery by use of the whole cell patch-clamp technique. The synthetic K+ channel openers pinacidil (half-activation 0.6 microM), cromakalim (half-activation 1.9 microM), and diazoxide (half-activation 37.1 microM) activated K(+)-selective currents that were blocked by glibenclamide. Elevation of pipette (intracellular) ATP concentration decreased K+ currents induced by pinacidil. Half-inhibition of KATP currents by glibenclamide and tolbutamide occurred at 101 nM and 351 microM, respectively. KATP currents were also inhibited by external TEA+, with half-inhibition at 6.2 mM. The results indicate that glibenclamide is an effective inhibitor of KATP channels in arterial smooth muscle and that tolbutamide and TEA+ are much less effective. Furthermore, these results support numerous functional studies that have demonstrated that the vasorelaxations to K+ channel openers are inhibited by < 10 microM glibenclamide but not by < 1 mM TEA+. | lld:pubmed |
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pubmed-article:7491898 | pubmed:language | eng | lld:pubmed |
pubmed-article:7491898 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7491898 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:7491898 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7491898 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:7491898 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:7491898 | pubmed:month | Nov | lld:pubmed |
pubmed-article:7491898 | pubmed:issn | 0002-9513 | lld:pubmed |
pubmed-article:7491898 | pubmed:author | pubmed-author:BraydenJ EJE | lld:pubmed |
pubmed-article:7491898 | pubmed:author | pubmed-author:NelsonM TMT | lld:pubmed |
pubmed-article:7491898 | pubmed:author | pubmed-author:QuayleJ MJM | lld:pubmed |
pubmed-article:7491898 | pubmed:author | pubmed-author:BonevA DAD | lld:pubmed |
pubmed-article:7491898 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:7491898 | pubmed:volume | 269 | lld:pubmed |
pubmed-article:7491898 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:7491898 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:7491898 | pubmed:pagination | C1112-8 | lld:pubmed |
pubmed-article:7491898 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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pubmed-article:7491898 | pubmed:year | 1995 | lld:pubmed |
pubmed-article:7491898 | pubmed:articleTitle | Pharmacology of ATP-sensitive K+ currents in smooth muscle cells from rabbit mesenteric artery. | lld:pubmed |
pubmed-article:7491898 | pubmed:affiliation | Department of Pharmacology, University of Vermont Medical Research Facility, Colchester 05446, USA. | lld:pubmed |
pubmed-article:7491898 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:7491898 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:7491898 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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