File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Endothelium-dependent inhibition of ergonovine-induced contraction is impaired in porcine coronary arteries with regenerated endothelium

TitleEndothelium-dependent inhibition of ergonovine-induced contraction is impaired in porcine coronary arteries with regenerated endothelium
Authors
Issue Date1989
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://circ.ahajournals.org
Citation
Circulation, 1989, v. 80 n. 3, p. 643-650 How to Cite?
AbstractThe inhibitory effects of the endothelium against ergonovine-induced contraction were examined in isolated porcine coronary arteries under normal conditions and after endothelial regeneration. Endothelium-dependent responses were examined in vitro in normal Yorkshire pigs (n = 16) and in pigs that had undergone balloon endothelium removal of the left anterior descending coronary artery (LAD) 4 weeks before the study (n = 10). The presence of a complete endothelial lining was confirmed histologically. In rings from normal arteries contracted with prostaglandin F(2α) in the presence of indomethacin and ketanserin (a 5-HT2-serotonergic blocker), ergonovine caused endothelium-dependent relaxations. They were attenuated by rauwolscine (an α2-adrenergic blocker), inhibited by methiothepin (a combined 5-HT1- and 5-HT2-serotonergic blocker) or by pertussis toxin (an inhibitor of several G proteins) and abolished by oxyhemoglobin (a selective inactivator of endothelium-derived relaxing factor). In quiescent rings from normal arteries, ergonovine caused contractions that were inhibited by the presence of the endothelium; this endothelium-dependent inhibition was ablished by oxyhemoglobin. The direct contractions were not affected by prazosin (an α1-adrenergic blocker), rauwolscine, 6-hydroxydopamine (an agent causing chemical sympathectomy), or diphenhydramine (an H1-histaminergic blocker) but were inhibited by ketanserin. In rings with regenerated endothelium contracted with prostaglandin F(2α), the endothelium-dependent relaxations to ergonovine were reduced significantly and were not inhibited by pertussis toxin. In quiescent rings with regenerated endothelium, the endothelium-dependent inhibition of ergonovine-induced contraction was less. Oxyhemoglobin caused endothelium-dependent contractions in quiescent rings (an indirect index of basally released endothelium-derived relaxing factor) that were reduced significantly in quiescent rings with regenerated endothelium. These results indicate that 1) the endothelium exerts its inhibitory action against ergonovine-induced contractioins by the release of endothelium-derived relaxing factor under basal conditions and upon stimulation by ergonovine, 2) endothelium-dependent relaxations to ergonovine are mediated mainly by 5-HT1-serotonergic receptors, whereas the direct contractions are mediated by 5-HT2-serotonergic receptors with little contribution of α-adrenoceptors, 3) the inhibitory role of the endothelium is impaired significantly in the regenerated state because of the reduced ability to release the relaxing factor, and 4) endothelial pertussis toxin-sensitive G protein may be involved in the synthesis of the relaxing factor upon stimulation by ergonovine, and dysfunction of the G protein may account partly for the dysfunction of regenerated endothelium.
Persistent Identifierhttp://hdl.handle.net/10722/170940
ISSN
2015 Impact Factor: 17.047
2015 SCImago Journal Rankings: 7.853
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorShimokawa, Hen_US
dc.contributor.authorFlavahan, NAen_US
dc.contributor.authorShepherd, JTen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:11:31Z-
dc.date.available2012-10-30T06:11:31Z-
dc.date.issued1989en_US
dc.identifier.citationCirculation, 1989, v. 80 n. 3, p. 643-650en_US
dc.identifier.issn0009-7322en_US
dc.identifier.urihttp://hdl.handle.net/10722/170940-
dc.description.abstractThe inhibitory effects of the endothelium against ergonovine-induced contraction were examined in isolated porcine coronary arteries under normal conditions and after endothelial regeneration. Endothelium-dependent responses were examined in vitro in normal Yorkshire pigs (n = 16) and in pigs that had undergone balloon endothelium removal of the left anterior descending coronary artery (LAD) 4 weeks before the study (n = 10). The presence of a complete endothelial lining was confirmed histologically. In rings from normal arteries contracted with prostaglandin F(2α) in the presence of indomethacin and ketanserin (a 5-HT2-serotonergic blocker), ergonovine caused endothelium-dependent relaxations. They were attenuated by rauwolscine (an α2-adrenergic blocker), inhibited by methiothepin (a combined 5-HT1- and 5-HT2-serotonergic blocker) or by pertussis toxin (an inhibitor of several G proteins) and abolished by oxyhemoglobin (a selective inactivator of endothelium-derived relaxing factor). In quiescent rings from normal arteries, ergonovine caused contractions that were inhibited by the presence of the endothelium; this endothelium-dependent inhibition was ablished by oxyhemoglobin. The direct contractions were not affected by prazosin (an α1-adrenergic blocker), rauwolscine, 6-hydroxydopamine (an agent causing chemical sympathectomy), or diphenhydramine (an H1-histaminergic blocker) but were inhibited by ketanserin. In rings with regenerated endothelium contracted with prostaglandin F(2α), the endothelium-dependent relaxations to ergonovine were reduced significantly and were not inhibited by pertussis toxin. In quiescent rings with regenerated endothelium, the endothelium-dependent inhibition of ergonovine-induced contraction was less. Oxyhemoglobin caused endothelium-dependent contractions in quiescent rings (an indirect index of basally released endothelium-derived relaxing factor) that were reduced significantly in quiescent rings with regenerated endothelium. These results indicate that 1) the endothelium exerts its inhibitory action against ergonovine-induced contractioins by the release of endothelium-derived relaxing factor under basal conditions and upon stimulation by ergonovine, 2) endothelium-dependent relaxations to ergonovine are mediated mainly by 5-HT1-serotonergic receptors, whereas the direct contractions are mediated by 5-HT2-serotonergic receptors with little contribution of α-adrenoceptors, 3) the inhibitory role of the endothelium is impaired significantly in the regenerated state because of the reduced ability to release the relaxing factor, and 4) endothelial pertussis toxin-sensitive G protein may be involved in the synthesis of the relaxing factor upon stimulation by ergonovine, and dysfunction of the G protein may account partly for the dysfunction of regenerated endothelium.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://circ.ahajournals.orgen_US
dc.relation.ispartofCirculationen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCoronary Vessels - Drug Effects - Physiologyen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshDrug Interactionsen_US
dc.subject.meshEndothelium, Vascular - Drug Effects - Physiologyen_US
dc.subject.meshErgonovine - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMyocardial Contraction - Drug Effectsen_US
dc.subject.meshOrgan Culture Techniquesen_US
dc.subject.meshRegeneration - Drug Effectsen_US
dc.subject.meshSwineen_US
dc.titleEndothelium-dependent inhibition of ergonovine-induced contraction is impaired in porcine coronary arteries with regenerated endotheliumen_US
dc.typeArticleen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1161/01.CIR.80.3.643-
dc.identifier.pmid2766515-
dc.identifier.scopuseid_2-s2.0-0024447397en_US
dc.identifier.volume80en_US
dc.identifier.issue3en_US
dc.identifier.spage643en_US
dc.identifier.epage650en_US
dc.identifier.isiWOS:A1989AP70600025-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridShimokawa, H=16684837100en_US
dc.identifier.scopusauthoridFlavahan, NA=7006398882en_US
dc.identifier.scopusauthoridShepherd, JT=7401742522en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats