File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Melatonin potentiates contractile responses to serotonin in isolated porcine coronary arteries

TitleMelatonin potentiates contractile responses to serotonin in isolated porcine coronary arteries
Authors
KeywordsNitric oxide
Sodium nitroprusside
Vascular smooth muscle
Vasoconstriction
Issue Date2001
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/
Citation
American Journal Of Physiology - Heart And Circulatory Physiology, 2001, v. 280 n. 1 49-1, p. H76-H82 How to Cite?
AbstractThe present study was designed to determine the effects of melatonin on coronary vasomotor tone. Porcine coronary arteries were suspended in organ chambers for isometric tension recording. Melatonin (10 10-10 5 M) itself caused neither contraction nor relaxation of the tissues. Serotonin (10 9-10 5 M) caused concentration-dependent contractions of coronary arteries, and in the presence of melatonin (10 7 M) the maximal response to serotonin was increased in rings with but not without endothelium. In contrast, melatonin had no effect on contractions produced by the thromboxane A2 analog U-46619 (10 10-10 7 M). The melatonin-receptor antagonist S-20928 (10 6 M) abolished the potentiating effect of melatonin on serotonin-induced contractions in endothelium-intact coronary arteries, as did treatment with 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (10 5 M), methylene blue (10 5 M), or NG-nitro-L-arginine (3 × 10 5 M). In tissues contracted with U-46619, serotonin caused endothelium-dependent relaxations that were inhibited by melatonin (10 7 M). Melatonin also inhibited coronary artery relaxation induced by sodium nitroprusside (10 9-10 5 M) but not by isoproterenol (10 9-10 5 M). These results support the hypothesis that melatonin, by inhibiting the action of nitric oxide on coronary vascular smooth muscle, selectively potentiates the vasoconstrictor response to serotonin in coronary arteries with endothelium.
Persistent Identifierhttp://hdl.handle.net/10722/171263
ISSN
2023 Impact Factor: 4.1
2023 SCImago Journal Rankings: 1.452
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYang, Qen_US
dc.contributor.authorScalbert, Een_US
dc.contributor.authorDelagrange, Pen_US
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorO'rourke, STen_US
dc.date.accessioned2012-10-30T06:13:02Z-
dc.date.available2012-10-30T06:13:02Z-
dc.date.issued2001en_US
dc.identifier.citationAmerican Journal Of Physiology - Heart And Circulatory Physiology, 2001, v. 280 n. 1 49-1, p. H76-H82en_US
dc.identifier.issn0363-6135en_US
dc.identifier.urihttp://hdl.handle.net/10722/171263-
dc.description.abstractThe present study was designed to determine the effects of melatonin on coronary vasomotor tone. Porcine coronary arteries were suspended in organ chambers for isometric tension recording. Melatonin (10 10-10 5 M) itself caused neither contraction nor relaxation of the tissues. Serotonin (10 9-10 5 M) caused concentration-dependent contractions of coronary arteries, and in the presence of melatonin (10 7 M) the maximal response to serotonin was increased in rings with but not without endothelium. In contrast, melatonin had no effect on contractions produced by the thromboxane A2 analog U-46619 (10 10-10 7 M). The melatonin-receptor antagonist S-20928 (10 6 M) abolished the potentiating effect of melatonin on serotonin-induced contractions in endothelium-intact coronary arteries, as did treatment with 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (10 5 M), methylene blue (10 5 M), or NG-nitro-L-arginine (3 × 10 5 M). In tissues contracted with U-46619, serotonin caused endothelium-dependent relaxations that were inhibited by melatonin (10 7 M). Melatonin also inhibited coronary artery relaxation induced by sodium nitroprusside (10 9-10 5 M) but not by isoproterenol (10 9-10 5 M). These results support the hypothesis that melatonin, by inhibiting the action of nitric oxide on coronary vascular smooth muscle, selectively potentiates the vasoconstrictor response to serotonin in coronary arteries with endothelium.en_US
dc.languageengen_US
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/en_US
dc.relation.ispartofAmerican Journal of Physiology - Heart and Circulatory Physiologyen_US
dc.subjectNitric oxide-
dc.subjectSodium nitroprusside-
dc.subjectVascular smooth muscle-
dc.subjectVasoconstriction-
dc.subject.mesh15-Hydroxy-11 Alpha,9 Alpha-(Epoxymethano)Prosta-5,13-Dienoic Acid - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCoronary Vessels - Drug Effects - Physiologyen_US
dc.subject.meshDrug Synergismen_US
dc.subject.meshEnzyme Inhibitors - Pharmacologyen_US
dc.subject.meshIsoproterenol - Pharmacologyen_US
dc.subject.meshMelatonin - Antagonists & Inhibitors - Pharmacologyen_US
dc.subject.meshMuscle Contraction - Drug Effectsen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effects - Physiologyen_US
dc.subject.meshNaphthalenes - Pharmacologyen_US
dc.subject.meshNitric Oxide Donors - Pharmacologyen_US
dc.subject.meshNitric Oxide Synthase - Antagonists & Inhibitorsen_US
dc.subject.meshNitric Oxide Synthase Type Iiien_US
dc.subject.meshNitroprusside - Pharmacologyen_US
dc.subject.meshReceptors, Cell Surface - Antagonists & Inhibitorsen_US
dc.subject.meshReceptors, Cytoplasmic And Nuclear - Antagonists & Inhibitorsen_US
dc.subject.meshReceptors, Melatoninen_US
dc.subject.meshSerotonin - Pharmacologyen_US
dc.subject.meshSwineen_US
dc.subject.meshVasoconstrictor Agents - Pharmacologyen_US
dc.subject.meshVasodilator Agents - Pharmacologyen_US
dc.subject.meshOmega-N-Methylarginine - Pharmacologyen_US
dc.titleMelatonin potentiates contractile responses to serotonin in isolated porcine coronary arteriesen_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.pmid11123220-
dc.identifier.scopuseid_2-s2.0-0035001412en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035001412&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume280en_US
dc.identifier.issue1 49-1en_US
dc.identifier.spageH76en_US
dc.identifier.epageH82en_US
dc.identifier.isiWOS:000165948500010-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridYang, Q=37025903300en_US
dc.identifier.scopusauthoridScalbert, E=7003716133en_US
dc.identifier.scopusauthoridDelagrange, P=7007022477en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.scopusauthoridO'Rourke, ST=7005313078en_US
dc.identifier.issnl0363-6135-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats