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Article: Endothelium-removal decreases relaxations of canine coronary arteries caused by β-adrenergic agonists and adenosine

TitleEndothelium-removal decreases relaxations of canine coronary arteries caused by β-adrenergic agonists and adenosine
Authors
Issue Date1985
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/
Citation
Journal Of Cardiovascular Pharmacology, 1985, v. 7 n. 1, p. 139-144 How to Cite?
AbstractExperiments were designed to investigate the importance of the endothelium in relaxation of isolated coronary arteries caused by β-adrenoceptor agonists or adenosine. Rings of canine left circumflex coronary arteries were suspended for isometric tension recording in organ chambers filled with physiological salt solution. Norepinephrine, isoproterenol, adenosine, acetylcholine, and sodium nitroprusside caused relaxations of control rings contracted with prostaglandin F(2α) or KCl. The relaxations to all substances tested were relatively smaller during contractions evoked by KCl than those caused by prostaglandin F(2α). Mechanical removal of the endothelium abolished the relaxations caused by acetylcholine, reduced those caused by the catecholamines and adenosine, and did not affect the relaxations to sodium nitroprusside during contractions to prostaglandin F(2α). Endothelium-removal did not affect relaxations to β-adrenergic agonists or adenosine during contractions to KCl or after pretreatment of the arteries with indomethacin. Indomethacin did not affect responses to acetylcholine or sodium nitroprusside, but augmented those in response to β-adrenoceptor stimulation and adenosine. These results suggest that the endothelial cells of the canine coronary artery produce a signal in response to β-adrenergic agonists and adenosine, which facilitates the direct inhibitory action of these substances on vascular smooth muscle.
Persistent Identifierhttp://hdl.handle.net/10722/170780
ISSN
2015 Impact Factor: 2.462
2015 SCImago Journal Rankings: 0.962
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorRubanyi, Gen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:10:49Z-
dc.date.available2012-10-30T06:10:49Z-
dc.date.issued1985en_US
dc.identifier.citationJournal Of Cardiovascular Pharmacology, 1985, v. 7 n. 1, p. 139-144en_US
dc.identifier.issn0160-2446en_US
dc.identifier.urihttp://hdl.handle.net/10722/170780-
dc.description.abstractExperiments were designed to investigate the importance of the endothelium in relaxation of isolated coronary arteries caused by β-adrenoceptor agonists or adenosine. Rings of canine left circumflex coronary arteries were suspended for isometric tension recording in organ chambers filled with physiological salt solution. Norepinephrine, isoproterenol, adenosine, acetylcholine, and sodium nitroprusside caused relaxations of control rings contracted with prostaglandin F(2α) or KCl. The relaxations to all substances tested were relatively smaller during contractions evoked by KCl than those caused by prostaglandin F(2α). Mechanical removal of the endothelium abolished the relaxations caused by acetylcholine, reduced those caused by the catecholamines and adenosine, and did not affect the relaxations to sodium nitroprusside during contractions to prostaglandin F(2α). Endothelium-removal did not affect relaxations to β-adrenergic agonists or adenosine during contractions to KCl or after pretreatment of the arteries with indomethacin. Indomethacin did not affect responses to acetylcholine or sodium nitroprusside, but augmented those in response to β-adrenoceptor stimulation and adenosine. These results suggest that the endothelial cells of the canine coronary artery produce a signal in response to β-adrenergic agonists and adenosine, which facilitates the direct inhibitory action of these substances on vascular smooth muscle.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/en_US
dc.relation.ispartofJournal of Cardiovascular Pharmacologyen_US
dc.subject.meshAcetylcholine - Pharmacologyen_US
dc.subject.meshAdenosine - Pharmacologyen_US
dc.subject.meshAdrenergic Beta-Agonists - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCoronary Vessels - Drug Effectsen_US
dc.subject.meshDinoprosten_US
dc.subject.meshDogsen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshEndothelium - Physiologyen_US
dc.subject.meshIndomethacin - Pharmacologyen_US
dc.subject.meshIsoproterenol - Pharmacologyen_US
dc.subject.meshMuscle Contraction - Drug Effectsen_US
dc.subject.meshMuscle Relaxation - Drug Effectsen_US
dc.subject.meshNitroprusside - Pharmacologyen_US
dc.subject.meshNorepinephrine - Pharmacologyen_US
dc.subject.meshPotassium Chloride - Pharmacologyen_US
dc.subject.meshProstaglandins F - Pharmacologyen_US
dc.titleEndothelium-removal decreases relaxations of canine coronary arteries caused by β-adrenergic agonists and adenosineen_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.doi10.1097/00005344-198501000-00023-
dc.identifier.pmid2580134-
dc.identifier.scopuseid_2-s2.0-0021987792en_US
dc.identifier.volume7en_US
dc.identifier.issue1en_US
dc.identifier.spage139en_US
dc.identifier.epage144en_US
dc.identifier.isiWOS:A1985ABC5100023-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridRubanyi, G=7005517991en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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