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Article: Tetrandrine, a calcium antagonist of Chinese herbal origin, interacts with vascular muscle α1-adrenoceptor

TitleTetrandrine, a calcium antagonist of Chinese herbal origin, interacts with vascular muscle α1-adrenoceptor
Authors
KeywordsTetrandrine
Plant alkaloid
Adrenoceptor
Vascular smooth muscle
Calcium
Issue Date1996
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/lifescie
Citation
Life Sciences, 1996, v. 59 n. 23, p. PL359-PL364 How to Cite?
AbstractThe effects of tetrandrine (TET) on the contractile responses of rat aortic rings and perfused rat mesenteric arteries to phenylephrine (PE) were investigated. TET inhibited the maximal contraction to PE in a concentration-dependent manner. TET significantly inhibited the transient contraction in Ca2+-free medium presumably due to release of intracellular Ca2+ after activation of α1-adrenoceptors. However, it caused a stronger inhibition of the sustained contraction in Ca2+-containing medium presumably the result of Ca2+ influx. TET has no inhibitory effect on caffeine-induced transient contraction. Radioligand receptor binding study using isolated dog aortic muscle membranes indicated that TET inhibited the binding of 3H-prazosin in a competitive manner, hence showing that TET interacted directly with the α1-adrenoceptors. Thus, TET affected PE-induced aortic contractions by multiple mechanisms, inhibiting interaction of PE with α1-adrenoceptors and interfering with PE-induced responses involving both Ca2+ entry and release.
DescriptionLetter
Persistent Identifierhttp://hdl.handle.net/10722/224100
ISSN
2015 Impact Factor: 2.685
2015 SCImago Journal Rankings: 1.056

 

DC FieldValueLanguage
dc.contributor.authorKwan, CY-
dc.contributor.authorChen, YY-
dc.contributor.authorMa, MF-
dc.contributor.authorDaniel, EE-
dc.contributor.authorHui, SSG-
dc.date.accessioned2016-03-23T08:15:44Z-
dc.date.available2016-03-23T08:15:44Z-
dc.date.issued1996-
dc.identifier.citationLife Sciences, 1996, v. 59 n. 23, p. PL359-PL364-
dc.identifier.issn0024-3205-
dc.identifier.urihttp://hdl.handle.net/10722/224100-
dc.descriptionLetter-
dc.description.abstractThe effects of tetrandrine (TET) on the contractile responses of rat aortic rings and perfused rat mesenteric arteries to phenylephrine (PE) were investigated. TET inhibited the maximal contraction to PE in a concentration-dependent manner. TET significantly inhibited the transient contraction in Ca2+-free medium presumably due to release of intracellular Ca2+ after activation of α1-adrenoceptors. However, it caused a stronger inhibition of the sustained contraction in Ca2+-containing medium presumably the result of Ca2+ influx. TET has no inhibitory effect on caffeine-induced transient contraction. Radioligand receptor binding study using isolated dog aortic muscle membranes indicated that TET inhibited the binding of 3H-prazosin in a competitive manner, hence showing that TET interacted directly with the α1-adrenoceptors. Thus, TET affected PE-induced aortic contractions by multiple mechanisms, inhibiting interaction of PE with α1-adrenoceptors and interfering with PE-induced responses involving both Ca2+ entry and release.-
dc.languageeng-
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/lifescie-
dc.relation.ispartofLife Sciences-
dc.rightsPosting accepted manuscript (postprint): © <year>. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/-
dc.subjectTetrandrine-
dc.subjectPlant alkaloid-
dc.subjectAdrenoceptor-
dc.subjectVascular smooth muscle-
dc.subjectCalcium-
dc.titleTetrandrine, a calcium antagonist of Chinese herbal origin, interacts with vascular muscle α1-adrenoceptor-
dc.typeArticle-
dc.identifier.emailKwan, CY: cykwan@hkucc.hku.hk-
dc.identifier.emailHui, SSG: schui@hkuspace.hku.hk-
dc.identifier.doi10.1016/S0024-3205(96)00552-8-
dc.identifier.hkuros21294-
dc.identifier.volume59-
dc.identifier.issue23-
dc.identifier.spagePL359-
dc.identifier.epagePL364-
dc.publisher.placeUnited States-

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