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Article: Epigallocatechin gallate elicits contractions of the isolated aorta of the aged spontaneously hypertensive rat

TitleEpigallocatechin gallate elicits contractions of the isolated aorta of the aged spontaneously hypertensive rat
Authors
Issue Date2011
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/PTO
Citation
Basic And Clinical Pharmacology And Toxicology, 2011, v. 109 n. 1, p. 47-55 How to Cite?
AbstractThe present study examined the effect of the green tea catechin epigallocatechin gallate (EGCG) on endothelium-dependent responses in the aorta of 36-week-old spontaneously hypertensive rats (SHR). Isometric tension was measured in isolated aortic rings. The release of prostanoid end products was determined using enzyme immunoassay kits and the intracellular reactive oxygen species (ROS) concentration using confocal microscopy. EGCG did not improve endothelium-dependent relaxations evoked by acetylcholine, except in the presence of indomethacin. EGCG did not inhibit endothelium-dependent contractions induced by acetylcholine or ATP. At 10 -6M and higher concentrations, EGCG caused increases in tension in the SHR aorta. The EGCG-induced contractions were accompanied by an increased production of ROS. The amount of prostanoid end products was increased significantly by EGCG, indicating that their production followed the activation of cyclooxygenase (COX). These prostanoids in turn stimulated thromboxane-prostanoid (TP) receptors and caused contractions. EGCG induced significantly smaller contractions in aortae of normotensive Wistar-Kyoto rats (WKY), accompanied with a lower production of ROS and a lesser release of prostanoids. These observations suggest that EGCG-induced contractions occur more readily in blood vessels of hypertensive than normotensive animals. The present findings indicate that the increased oxidative stress in the ageing hypertensive animals contributes to the loss of the beneficial effects and the enhancement of the adverse effects of EGCG. © 2011 The Authors. Basic & Clinical Pharmacology & Toxicology © 2011 Nordic Pharmacological Society.
Persistent Identifierhttp://hdl.handle.net/10722/133645
ISSN
2015 Impact Factor: 3.097
2015 SCImago Journal Rankings: 0.539
ISI Accession Number ID
Funding AgencyGrant Number
Hong Kong Research Grant Council (University of Hong Kong)777208
Research Centre of Heart, Brain, Hormone and Healthy Aging of the University of Hong Kong
Funding Information:

Z. Li thanks Dr Marcel W.L. Koo for his advice and for reading the manuscript. This study was supported by the Hong Kong Research Grant Council (University of Hong Kong, No. 777208) and by Research Centre of Heart, Brain, Hormone and Healthy Aging of the University of Hong Kong.

References

 

DC FieldValueLanguage
dc.contributor.authorLi, Zen_HK
dc.contributor.authorWang, Yen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.date.accessioned2011-05-24T02:13:06Z-
dc.date.available2011-05-24T02:13:06Z-
dc.date.issued2011en_HK
dc.identifier.citationBasic And Clinical Pharmacology And Toxicology, 2011, v. 109 n. 1, p. 47-55en_HK
dc.identifier.issn1742-7835en_HK
dc.identifier.urihttp://hdl.handle.net/10722/133645-
dc.description.abstractThe present study examined the effect of the green tea catechin epigallocatechin gallate (EGCG) on endothelium-dependent responses in the aorta of 36-week-old spontaneously hypertensive rats (SHR). Isometric tension was measured in isolated aortic rings. The release of prostanoid end products was determined using enzyme immunoassay kits and the intracellular reactive oxygen species (ROS) concentration using confocal microscopy. EGCG did not improve endothelium-dependent relaxations evoked by acetylcholine, except in the presence of indomethacin. EGCG did not inhibit endothelium-dependent contractions induced by acetylcholine or ATP. At 10 -6M and higher concentrations, EGCG caused increases in tension in the SHR aorta. The EGCG-induced contractions were accompanied by an increased production of ROS. The amount of prostanoid end products was increased significantly by EGCG, indicating that their production followed the activation of cyclooxygenase (COX). These prostanoids in turn stimulated thromboxane-prostanoid (TP) receptors and caused contractions. EGCG induced significantly smaller contractions in aortae of normotensive Wistar-Kyoto rats (WKY), accompanied with a lower production of ROS and a lesser release of prostanoids. These observations suggest that EGCG-induced contractions occur more readily in blood vessels of hypertensive than normotensive animals. The present findings indicate that the increased oxidative stress in the ageing hypertensive animals contributes to the loss of the beneficial effects and the enhancement of the adverse effects of EGCG. © 2011 The Authors. Basic & Clinical Pharmacology & Toxicology © 2011 Nordic Pharmacological Society.en_HK
dc.languageengen_US
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/PTOen_HK
dc.relation.ispartofBasic and Clinical Pharmacology and Toxicologyen_HK
dc.rightsThe definitive version is available at http://onlinelibrary.wiley.com/-
dc.titleEpigallocatechin gallate elicits contractions of the isolated aorta of the aged spontaneously hypertensive raten_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1742-7835&volume=109&issue=1&spage=47&epage=55&date=2011&atitle=Epigallocatechin+gallate+elicits+contractions+of+the+isolated+aorta+of+the+aged+spontaneously+hypertensive+rat-
dc.identifier.emailWang, Y: yuwanghk@hku.hken_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.authorityWang, Y=rp00239en_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1742-7843.2011.00683.xen_HK
dc.identifier.pmid21310006-
dc.identifier.scopuseid_2-s2.0-79958839643en_HK
dc.identifier.hkuros185127en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79958839643&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume109en_HK
dc.identifier.issue1en_HK
dc.identifier.spage47en_HK
dc.identifier.epage55en_HK
dc.identifier.isiWOS:000292474600008-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLi, Z=54397452700en_HK
dc.identifier.scopusauthoridWang, Y=34973733700en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK
dc.identifier.citeulike9429766-

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