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Conference Paper: Chronic treatment of vitamin D derivatives reduce endothelium-dependent contractions in the aorta of the spontaneously hypertensive rat

TitleChronic treatment of vitamin D derivatives reduce endothelium-dependent contractions in the aorta of the spontaneously hypertensive rat
Authors
Issue Date2009
PublisherHong Kong College of Cardiology. The Journal's web site is located at http://www.hkcchk.com/journals.php#3
Citation
The 13th Annual Scientific Meeting of the Institute of Cardiovascular Science and Medicine, Hong Kong, 12 December 2009. In Journal of the Hong Kong College of Cardiology, 2009, v. 17 n. 2, p. 53, abstract no. OC8 How to Cite?
AbstractThe available evidences suggest that vitamin D has cardiovascular effects besides regulating calcium homeostasis. Previous studies demonstrated that 1,25-dihydroxyvitamin D3, the major metabolite of vitamin D, acutely reduce endothelium-dependent contractions induced by acetylcholine. To examine the chronic effect of 1,25-dihydroxyvitamin D3, rats were treated with the vitamin D derivative for 6 weeks. The serum 1,25-dihydroxyvitamin D3 level was significantly higher than the control while the mean arterial blood pressure was significantly lower. Aortic rings with or without endothelium were used for organ bath experiments. The release of prostacyclin and thromboxane A2 after acetylcholine or A23187 stimulation were measured. The cytosolic-free calcium concentration was measured by confocal microscopy with the fluorescent dyes Fluo-4. Real time PCR was used to compare the mRNA level of COX-1, prostacyclin synthase, thromboxane synthase and eNOS between the control and treated groups. Both acetylcholine- and A23187-induced endothelium-dependent contractions were reduced significantly in the treated group. The acetylcholine-induced release of prostacyclin and the A23187-induced thromboxane A2 was reduced in the treated group. There was no significant difference in cytosolic free calcium concentration caused by acetylcholine or A23187 between control and treated groups. COX-1 mRNA level was significantly inhibited in the treated SHR. These results demonstrate that chronic treatment of 1,25-dihydroxyvitamin D3 modulates vascular tone by inhibiting the expression level of COX-1 mRNA which is a completely different mechanism as in the acute treatment. This chronic effect to EDCF may account for one of the factors that reducing the mean arterial blood pressure in the SHR rats.
Persistent Identifierhttp://hdl.handle.net/10722/106684
ISSN
2015 SCImago Journal Rankings: 0.102

 

DC FieldValueLanguage
dc.contributor.authorWong, MSKen_HK
dc.contributor.authorMan, RYKen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.date.accessioned2010-09-25T23:26:08Z-
dc.date.available2010-09-25T23:26:08Z-
dc.date.issued2009en_HK
dc.identifier.citationThe 13th Annual Scientific Meeting of the Institute of Cardiovascular Science and Medicine, Hong Kong, 12 December 2009. In Journal of the Hong Kong College of Cardiology, 2009, v. 17 n. 2, p. 53, abstract no. OC8en_HK
dc.identifier.issn1027-7811-
dc.identifier.urihttp://hdl.handle.net/10722/106684-
dc.description.abstractThe available evidences suggest that vitamin D has cardiovascular effects besides regulating calcium homeostasis. Previous studies demonstrated that 1,25-dihydroxyvitamin D3, the major metabolite of vitamin D, acutely reduce endothelium-dependent contractions induced by acetylcholine. To examine the chronic effect of 1,25-dihydroxyvitamin D3, rats were treated with the vitamin D derivative for 6 weeks. The serum 1,25-dihydroxyvitamin D3 level was significantly higher than the control while the mean arterial blood pressure was significantly lower. Aortic rings with or without endothelium were used for organ bath experiments. The release of prostacyclin and thromboxane A2 after acetylcholine or A23187 stimulation were measured. The cytosolic-free calcium concentration was measured by confocal microscopy with the fluorescent dyes Fluo-4. Real time PCR was used to compare the mRNA level of COX-1, prostacyclin synthase, thromboxane synthase and eNOS between the control and treated groups. Both acetylcholine- and A23187-induced endothelium-dependent contractions were reduced significantly in the treated group. The acetylcholine-induced release of prostacyclin and the A23187-induced thromboxane A2 was reduced in the treated group. There was no significant difference in cytosolic free calcium concentration caused by acetylcholine or A23187 between control and treated groups. COX-1 mRNA level was significantly inhibited in the treated SHR. These results demonstrate that chronic treatment of 1,25-dihydroxyvitamin D3 modulates vascular tone by inhibiting the expression level of COX-1 mRNA which is a completely different mechanism as in the acute treatment. This chronic effect to EDCF may account for one of the factors that reducing the mean arterial blood pressure in the SHR rats.-
dc.languageengen_HK
dc.publisherHong Kong College of Cardiology. The Journal's web site is located at http://www.hkcchk.com/journals.php#3-
dc.relation.ispartofJournal of the Hong Kong College of Cardiologyen_HK
dc.titleChronic treatment of vitamin D derivatives reduce endothelium-dependent contractions in the aorta of the spontaneously hypertensive raten_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1027-7811&volume=17&issue=2&spage=53, abstract no. OC8&epage=&date=2009&atitle=Chronic+treatment+of+Vitamin+D+derivatives+reduce+endothelium-dependent+contractions+in+the+aorta+of+the+spontaneously+hypertensive+rat-
dc.identifier.emailWong, MSK: mikwong@hkusua.hku.hken_HK
dc.identifier.emailMan, RYK: rykman@hkucc.hku.hken_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.authorityMan, RYK=rp00236en_HK
dc.identifier.hkuros169813en_HK
dc.identifier.volume17en_HK
dc.identifier.issue2en_HK
dc.identifier.spage53en_HK
dc.identifier.epage53-
dc.description.otherThe 13th Annual Scientific Meeting of the Institute of Cardiovascular Science and Medicine, Hong Kong, 12 December 2009. In Journal of the Hong Kong College of Cardiology, 2009, v. 17 n. 2, p. 53, abstract no. OC8-

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