Source:http://linkedlifedata.com/resource/pubmed/id/12060103
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
7
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pubmed:dateCreated |
2002-6-12
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pubmed:abstractText |
1. Acetylcholine (ACh) evokes endothelium-dependent hyperpolarization in arterial cells, presumably through endothelium-derived hyperpolarizing factor (EDHF). The identity of EDHF is still elusive; however, several recent studies suggest the possible involvement of myoendothelial gap junctions in the EDHF response. 2. To elucidate the role of gap junctions in endothelium-dependent hyperpolarization, we examined the effects of the gap junction inhibitors 18 alpha-glycyrrhetinic acid (18 alpha-GA; 10(-4) mol/L) and carbenoxolone (3 x 10(-4) mol/L), a water-soluble form of 18 beta-GA, on hyperpolarization and relaxation to ACh in rat proximal and distal mesenteric arteries. Experiments were performed in the presence of indomethacin (10(-5) mol/L) and N(G)-nitro-L-arginine (10(-4) mol/L). 3. In both proximal and distal mesenteric arteries, ACh-induced hyperpolarization and relaxation were partially inhibited by 18 alpha-GA and abolished by carbenoxolone. 4. Endothelium-independent hyperpolarization to levcromakalim, an ATP-sensitive K+ channel opener, were unaffected by 18 alpha-GA or carbenoxolone in both arteries. 5. Relaxations to levcromakalim were unaffected by 18 alpha-GA, but were inhibited somewhat by carbenoxolone in proximal mesenteric arteries. 6. These findings suggest that myoendothelial gap junctions play a critical role in EDHF-mediated responses in both proximal and distal mesenteric arteries of the rat.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/18alpha-glycyrrhetinic acid,
http://linkedlifedata.com/resource/pubmed/chemical/Acetylcholine,
http://linkedlifedata.com/resource/pubmed/chemical/Biological Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Carbenoxolone,
http://linkedlifedata.com/resource/pubmed/chemical/Glycyrrhetinic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/endothelium-dependent...
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0305-1870
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
29
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
595-602
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:12060103-Acetylcholine,
pubmed-meshheading:12060103-Animals,
pubmed-meshheading:12060103-Biological Factors,
pubmed-meshheading:12060103-Carbenoxolone,
pubmed-meshheading:12060103-Endothelium, Vascular,
pubmed-meshheading:12060103-Gap Junctions,
pubmed-meshheading:12060103-Glycyrrhetinic Acid,
pubmed-meshheading:12060103-Male,
pubmed-meshheading:12060103-Membrane Potentials,
pubmed-meshheading:12060103-Mesenteric Arteries,
pubmed-meshheading:12060103-Muscle, Smooth, Vascular,
pubmed-meshheading:12060103-Rats,
pubmed-meshheading:12060103-Rats, Wistar,
pubmed-meshheading:12060103-Vasodilation
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pubmed:year |
2002
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pubmed:articleTitle |
Critical role of gap junctions in endothelium-dependent hyperpolarization in rat mesenteric arteries.
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pubmed:affiliation |
Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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