rdf:type |
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lifeskim:mentions |
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pubmed:dateCreated |
1998-6-26
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pubmed:abstractText |
1. The contribution of gap junctions to endothelium-dependent relaxation was investigated in isolated rabbit conduit artery preparations pre-constricted by 10 microM phenylephrine (PhE). 2. Acetylcholine (ACh) relaxed the thoracic aorta by approximately 60 % and the superior mesenteric artery (SMA) by approximately 90 %. A peptide possessing sequence homology with extracellular loop 2 of connexin 43 (Gap 27, 300 microM) inhibited relaxation by approximately 40 % in both artery types. Gap 27 also attenuated the endothelium-dependent component of the relaxation induced by ATP in thoracic aorta but did not modify force development in response to PhE. 3. NG-nitro-L-arginine methyl ester (L-NAME, 300 microM), an inhibitor of NO synthase, attenuated ACh-induced relaxation by approximately 90 % in the aorta but only by approximately 40 % in SMA (P < 0.05). Residual L-NAME-insensitive relaxations were almost abolished by 300 microM Gap 27 in aorta and inhibited in a concentration-dependent fashion in SMA (approximately 50 % at 100 microM and approximately 80 % at 10 mM). Gap 27 similarly attenuated the endothelium-dependent component of L-NAME-insensitive relaxations to ATP in aorta. 4. Responses to cyclopiazonic acid, which stimulates endothelium-dependent relaxation through a receptor-independent mechanism, were also attenuated by Gap 27, whereas this peptide exerted no effect on the NO-mediated relaxation induced by sodium nitroprusside in preparations denuded of endothelium. 5. ACh-induced relaxation of 'sandwich' mounts of aorta or SMA were unaffected by Gap 27 but completely abolished by L-NAME. 6. We conclude that direct heterocellular communication between the endothelium and smooth muscle contributes to endothelium-dependent relaxations evoked by both receptor-dependent and -independent mechanisms. The inhibitory effects of Gap 27 peptide do not involve homocellular communication within the vessel wall or modulation of NO release or action.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/9508817-1320430,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9508817-1690612,
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0022-3751
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
508 ( Pt 2)
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
561-73
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:9508817-Acetylcholine,
pubmed-meshheading:9508817-Adenosine Triphosphate,
pubmed-meshheading:9508817-Animals,
pubmed-meshheading:9508817-Aorta, Thoracic,
pubmed-meshheading:9508817-Cell Communication,
pubmed-meshheading:9508817-Connexin 43,
pubmed-meshheading:9508817-Endothelium, Vascular,
pubmed-meshheading:9508817-Enzyme Inhibitors,
pubmed-meshheading:9508817-Gap Junctions,
pubmed-meshheading:9508817-Indoles,
pubmed-meshheading:9508817-Male,
pubmed-meshheading:9508817-Mesenteric Artery, Superior,
pubmed-meshheading:9508817-Muscle, Smooth, Vascular,
pubmed-meshheading:9508817-Muscle Relaxation,
pubmed-meshheading:9508817-NG-Nitroarginine Methyl Ester,
pubmed-meshheading:9508817-Nitric Oxide Synthase,
pubmed-meshheading:9508817-Phenylephrine,
pubmed-meshheading:9508817-Rabbits,
pubmed-meshheading:9508817-Vasoconstrictor Agents
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pubmed:year |
1998
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pubmed:articleTitle |
Central role of heterocellular gap junctional communication in endothelium-dependent relaxations of rabbit arteries.
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pubmed:affiliation |
Department of Diagnostic Radiology, Cardiovascular Sciences Research Group, University of Wales College of Medicine, Heath Park, Cardiff CF4 4XN, UK.
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