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Conference Paper: Vitamin D3 does not augment EDHF-mediated relaxations to bradykinin

TitleVitamin D3 does not augment EDHF-mediated relaxations to bradykinin
Authors
KeywordsPharmacy and pharmacology environmental studies
Toxicology and environmental safety
Issue Date2010
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/PTO
Citation
The 16th World Congress on Basic and Clinical Pharmacology (WorldPharma2010), Copenhagen, Denmark, 17-23 July 2010. In Basic & Clinical Pharmacology & Toxicology, 2010, v. 107, suppl. 1, p. 692 How to Cite?
AbstractThe most active metabolite of vitamin D, 1, 25-dihydroxyvitamin D3 acutely reduces endothelium-dependent contractions to acetylcholine by reducing the increase in calcium concentration caused by the muscarinic agonist in the endothelial cells. The release of endothelium-derived hyperpolarizing factor involves calcium-dependent potassium channels. Thus, vitamin D3 may also affect endothelium-dependent relaxations by regulating EDHF-mediated responses. The present experiments were designed to investigate the effect of acute treatment of vitamin D3 on the EDHF pathway. Rings of porcine coronary arteries, with endothelium, were suspended in organ chambers for isometric tension recording. To study the EDHF mediated relaxation, quiescent rings were incubated with L-NAME (nitric oxide synthase inhibitor, 10-4 M) and indomethacin (cyclooxygenase inhibitor, 10-5 M) for 40 minutes. They were contracted with prostaglandin F2α and then relaxed with cumulatively increasing concentrations of bradykinin. The experiments were carried out in the presence or absence of 10-7 M 1,25-dihydroxyvitamin D3. The results show that the relaxation induced by bradykinin was not altered significantly by the prior incubation of 1,25-dihydroxyvitamin D3, suggesting that vitamin D3 does not have an regulatory effect on EDHF-mediated responses. Thus the vascular protective effect of vitamin D is probably due to a reduction of endothelium-dependent contractions.
DescriptionFocused Conference Group: P15 – Endotheliumin Health and Disease. Paper No. 1255
Persistent Identifierhttp://hdl.handle.net/10722/126879
ISSN
2015 Impact Factor: 3.097
2015 SCImago Journal Rankings: 0.539

 

DC FieldValueLanguage
dc.contributor.authorZou, Qen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.date.accessioned2010-10-31T12:53:54Z-
dc.date.available2010-10-31T12:53:54Z-
dc.date.issued2010en_HK
dc.identifier.citationThe 16th World Congress on Basic and Clinical Pharmacology (WorldPharma2010), Copenhagen, Denmark, 17-23 July 2010. In Basic & Clinical Pharmacology & Toxicology, 2010, v. 107, suppl. 1, p. 692en_HK
dc.identifier.issn1742-7835-
dc.identifier.urihttp://hdl.handle.net/10722/126879-
dc.descriptionFocused Conference Group: P15 – Endotheliumin Health and Disease. Paper No. 1255-
dc.description.abstractThe most active metabolite of vitamin D, 1, 25-dihydroxyvitamin D3 acutely reduces endothelium-dependent contractions to acetylcholine by reducing the increase in calcium concentration caused by the muscarinic agonist in the endothelial cells. The release of endothelium-derived hyperpolarizing factor involves calcium-dependent potassium channels. Thus, vitamin D3 may also affect endothelium-dependent relaxations by regulating EDHF-mediated responses. The present experiments were designed to investigate the effect of acute treatment of vitamin D3 on the EDHF pathway. Rings of porcine coronary arteries, with endothelium, were suspended in organ chambers for isometric tension recording. To study the EDHF mediated relaxation, quiescent rings were incubated with L-NAME (nitric oxide synthase inhibitor, 10-4 M) and indomethacin (cyclooxygenase inhibitor, 10-5 M) for 40 minutes. They were contracted with prostaglandin F2α and then relaxed with cumulatively increasing concentrations of bradykinin. The experiments were carried out in the presence or absence of 10-7 M 1,25-dihydroxyvitamin D3. The results show that the relaxation induced by bradykinin was not altered significantly by the prior incubation of 1,25-dihydroxyvitamin D3, suggesting that vitamin D3 does not have an regulatory effect on EDHF-mediated responses. Thus the vascular protective effect of vitamin D is probably due to a reduction of endothelium-dependent contractions.-
dc.languageengen_HK
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/PTO-
dc.relation.ispartofBasic & Clinical Pharmacology & Toxicologyen_HK
dc.rightsThe definitive version is available at www.blackwell-synergy.com-
dc.subjectPharmacy and pharmacology environmental studies-
dc.subjectToxicology and environmental safety-
dc.titleVitamin D3 does not augment EDHF-mediated relaxations to bradykininen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1742-7835&volume=107, suppl. 1&spage=692&epage=&date=2010&atitle=Vitamin+D3+does+not+augment+EDHF-mediated+relaxations+to+bradykinin-
dc.identifier.emailZou, Q: zouqian1112@hotmail.comen_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.hkuros175328en_HK
dc.identifier.volume107, suppl. 1en_HK
dc.identifier.spage692en_HK
dc.identifier.epage692-
dc.description.otherThe 16th World Congress on Basic and Clinical Pharmacology (WorldPharma2010), Copenhagen, Denmark, 17-23 July 2010. In Basic & Clinical Pharmacology & Toxicology, 2010, v. 107, suppl. 1, p. 692-

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