{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1361137045657487360.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1152/ajpheart.00903.2001"}},{"identifier":{"@type":"URI","@value":"https://www.physiology.org/doi/pdf/10.1152/ajpheart.00903.2001"}}],"dc:title":[{"@value":"Gap junction-dependent and -independent EDHF-type relaxations may involve smooth muscle cAMP accumulation"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:p> We have compared the mechanisms that contribute to endothelium-derived hyperpolarizing factor (EDHF)-type responses induced by ACh and the Ca<jats:sup>2+</jats:sup> ionophore A-23187 in the rabbit iliac artery. Relaxations to both agents were associated with ∼1.5-fold elevations in smooth muscle cAMP levels and were attenuated by the adenylyl cyclase inhibitor 2′,5′-dideoxyadenosine (DDA) and potentiated by the cAMP phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX). Mechanical responses were inhibited by coadministration of the Ca<jats:sup>2+</jats:sup>-activated K<jats:sup>+</jats:sup>channel blockers apamin and charybdotoxin, both in the absence and presence of IBMX, but were unaffected by blockade of ATP-sensitive K<jats:sup>+</jats:sup> channels with the sulphonylurea glibenclamide. Relaxations and elevations in cAMP evoked by ACh were abolished by 18α-glycyrrhetinic acid, which disrupts gap junction plaques, whereas the corresponding responses to A-23187 were unaffected by this agent. Consistently, in “sandwich” bioassay experiments, A-23187, but not ACh, elicited extracellular release of a factor that evoked relaxations that were inhibited by DDA and potentiated by IBMX. These findings provide evidence that EDHF-type relaxations of rabbit iliac arteries evoked by ACh and A-23187 depend on cAMP accumulation in smooth muscle, but involve signaling via myoendothelial gap junctions and the extracellular space, respectively. </jats:p>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1381137045657487361","@type":"Researcher","foaf:name":[{"@value":"Andrew T. Chaytor"}],"jpcoar:affiliationName":[{"@value":"Department of Diagnostic Radiology, Wales Heart Research Institute, University of Wales College of Medicine, Cardiff CF14 4XN, United Kingdom"}]},{"@id":"https://cir.nii.ac.jp/crid/1381137045657487362","@type":"Researcher","foaf:name":[{"@value":"Hannah J. Taylor"}],"jpcoar:affiliationName":[{"@value":"Department of Diagnostic Radiology, Wales Heart Research Institute, University of Wales College of Medicine, Cardiff CF14 4XN, United Kingdom"}]},{"@id":"https://cir.nii.ac.jp/crid/1381137045657487360","@type":"Researcher","foaf:name":[{"@value":"Tudor M. Griffith"}],"jpcoar:affiliationName":[{"@value":"Department of Diagnostic Radiology, Wales Heart Research Institute, University of Wales College of Medicine, Cardiff CF14 4XN, United Kingdom"}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"03636135"},{"@type":"EISSN","@value":"15221539"}],"prism:publicationName":[{"@value":"American Journal of Physiology-Heart and Circulatory Physiology"}],"dc:publisher":[{"@value":"American Physiological Society"}],"prism:publicationDate":"2002-04-01","prism:volume":"282","prism:number":"4","prism:startingPage":"H1548","prism:endingPage":"H1555"},"reviewed":"false","url":[{"@id":"https://www.physiology.org/doi/pdf/10.1152/ajpheart.00903.2001"}],"createdAt":"2015-03-03","modifiedAt":"2019-09-08","relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1390001206127103616","@type":"Article","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"ja","@value":"糖尿病性血管合併症における内皮由来過分極因子の重要性と治療戦略へのアプローチ"},{"@language":"en","@value":"A Therapeutic Target for Endothelium-derived Hyperpolarizing Factor Signaling in Diabetic Vascular Complication"},{"@language":"ja-Kana","@value":"トウニョウビョウセイ ケッカン ガッペイショウ ニ オケル ナイヒ ユライ カブンキョク インシ ノ ジュウヨウセイ ト チリョウ センリャク エ ノ アプローチ"},{"@value":"ChemInform Abstract: A Therapeutic Target for Endothelium‐Derived Hyperpolarizing Factor Signaling in Diabetic Vascular Complication"}]},{"@id":"https://cir.nii.ac.jp/crid/1390282680155233280","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Endothelium-Derived Relaxing Factor–Mediated Vasodilation in Mouse Mesenteric Vascular Beds"}]},{"@id":"https://cir.nii.ac.jp/crid/2051714792004250240","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Glomerular expression of connexin 40 and connexin 43 in rat experimental glomerulonephritis"}]}],"dataSourceIdentifier":[{"@type":"CROSSREF","@value":"10.1152/ajpheart.00903.2001"},{"@type":"CROSSREF","@value":"10.1254/jphs.11197fp_references_DOI_BeTj2m1t4ba4KLlC0sSRywfIwpu"},{"@type":"CROSSREF","@value":"10.1007/s10157-012-0687-2_references_DOI_BeTj2m1t4ba4KLlC0sSRywfIwpu"},{"@type":"CROSSREF","@value":"10.1248/yakushi.130.777_references_DOI_BeTj2m1t4ba4KLlC0sSRywfIwpu"}]}