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Conference Paper: Activation of n-AChRs contributes to endothelium-dependent relaxations in the rat aorta

TitleActivation of n-AChRs contributes to endothelium-dependent relaxations in the rat aorta
Authors
Issue Date2011
PublisherChinese Journal of Pharmacology and Toxicology Editorial Board.
Citation
2011年中国药理学会第十一次全国学术大会'药物临床研究与评价专题研讨会', 山东省济南市, 2011年9月22-25日. In Chinese Journal of Pharmacology and Toxicology, 2011, v. 25 增刊, p. 140 How to Cite?
AbstractOBJECTIVE: Muscarinic (mAChRs) and nicotinic (nAChRs) acetylcholine receptors are both expressed in endothelial cells. It is generally accepted that mAChRs are responsible for both endothelium-dependent relaxations and contractions evoked by acetylcholine. The present study was designed to study whether or not nAChRs are also involved in endothelium-dependent relaxations. METHODS: Rat aortic rings with or without endothelium were suspended in organ chambers for isometric tension recording. Quiescent rings were incubated with vehicle, mecamylamine (nAChRs inhibitor),atropine (mAChRs inhibitor,),mecamylamine plus atropine, L-NAME (NO synthase inhibitor) or TRAM-34 plus UCL-1684 (inhibitors of EDHF-mediated responses). All rings were incubated with indomethacin(non-selective cyclooxygenase inhibitor) to prevent endothelium - dependent contractions. After 40 minutes of incubation, they were contracted with phenylephrine and then relaxed with cumulatively increasing concentrations of acetylcholine or nicotine. RESULTS: (1) In both SHR and WKY aortae, cetylcholine-induced relaxations were similar in control and mecamyl-amine -treated rings, while the relaxations were significantly reduced in atropine-treated preparations. In rings of 36 weeks old SHRs, the remaining response in the presence of atropine approximated 50%of those observed in untreated control preparations, and was prevented by mecamylamine. In both 36 weeks and 64 weeks old WKY aortae the remaining response in atropine-treated preparations was minimal. (2) In both SHR and WKY aortae, nicotine induced up to 60% endothelium-dependent relaxation and the relaxations were abolished by L-NAME.TRAM-34 plus UCL-1684 partially inhibited the nicotine-induced relaxations in WKY but not in SHR aorta. CONCLUSION: In the SHR and WKY aorta, mAChRs are mainly responsible for endothelium - dependent relaxations under control conditions. However, when mAChRs are inhibited by atropine, nAChRs mediate relaxations to the cholinergic transmitter in the SHR but not the WKY aorta.
DescriptionHKPS / CPS Joint Meeting (中国药理学会-香港药理学会双边学术交流)
Persistent Identifierhttp://hdl.handle.net/10722/149239
ISSN
2015 SCImago Journal Rankings: 0.119

 

DC FieldValueLanguage
dc.contributor.authorVanhoutte, PMGR-
dc.date.accessioned2012-06-22T06:32:03Z-
dc.date.available2012-06-22T06:32:03Z-
dc.date.issued2011-
dc.identifier.citation2011年中国药理学会第十一次全国学术大会'药物临床研究与评价专题研讨会', 山东省济南市, 2011年9月22-25日. In Chinese Journal of Pharmacology and Toxicology, 2011, v. 25 增刊, p. 140-
dc.identifier.issn1000-3002-
dc.identifier.urihttp://hdl.handle.net/10722/149239-
dc.descriptionHKPS / CPS Joint Meeting (中国药理学会-香港药理学会双边学术交流)-
dc.description.abstractOBJECTIVE: Muscarinic (mAChRs) and nicotinic (nAChRs) acetylcholine receptors are both expressed in endothelial cells. It is generally accepted that mAChRs are responsible for both endothelium-dependent relaxations and contractions evoked by acetylcholine. The present study was designed to study whether or not nAChRs are also involved in endothelium-dependent relaxations. METHODS: Rat aortic rings with or without endothelium were suspended in organ chambers for isometric tension recording. Quiescent rings were incubated with vehicle, mecamylamine (nAChRs inhibitor),atropine (mAChRs inhibitor,),mecamylamine plus atropine, L-NAME (NO synthase inhibitor) or TRAM-34 plus UCL-1684 (inhibitors of EDHF-mediated responses). All rings were incubated with indomethacin(non-selective cyclooxygenase inhibitor) to prevent endothelium - dependent contractions. After 40 minutes of incubation, they were contracted with phenylephrine and then relaxed with cumulatively increasing concentrations of acetylcholine or nicotine. RESULTS: (1) In both SHR and WKY aortae, cetylcholine-induced relaxations were similar in control and mecamyl-amine -treated rings, while the relaxations were significantly reduced in atropine-treated preparations. In rings of 36 weeks old SHRs, the remaining response in the presence of atropine approximated 50%of those observed in untreated control preparations, and was prevented by mecamylamine. In both 36 weeks and 64 weeks old WKY aortae the remaining response in atropine-treated preparations was minimal. (2) In both SHR and WKY aortae, nicotine induced up to 60% endothelium-dependent relaxation and the relaxations were abolished by L-NAME.TRAM-34 plus UCL-1684 partially inhibited the nicotine-induced relaxations in WKY but not in SHR aorta. CONCLUSION: In the SHR and WKY aorta, mAChRs are mainly responsible for endothelium - dependent relaxations under control conditions. However, when mAChRs are inhibited by atropine, nAChRs mediate relaxations to the cholinergic transmitter in the SHR but not the WKY aorta.-
dc.languageeng-
dc.publisherChinese Journal of Pharmacology and Toxicology Editorial Board.-
dc.relation.ispartofChinese Journal of Pharmacology and Toxicology-
dc.relation.ispartof中国药理学与毒理学杂誌-
dc.titleActivation of n-AChRs contributes to endothelium-dependent relaxations in the rat aorta-
dc.typeConference_Paper-
dc.identifier.emailVanhoutte, PMGR: vanhoutt@hku.hk-
dc.identifier.authorityVanhoutte, PMGR=rp00238-
dc.identifier.hkuros200021-
dc.identifier.volume25-
dc.identifier.issue增刊-
dc.identifier.spage140-
dc.identifier.epage140-
dc.publisher.placeBeijing, China-

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