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Article: Plant alkaloids, tetrandrine and hernandezine, inhibit calcium-depletion stimulated calcium entry in human and bovine endothelial cells

TitlePlant alkaloids, tetrandrine and hernandezine, inhibit calcium-depletion stimulated calcium entry in human and bovine endothelial cells
Authors
KeywordsCa2+ antagonist caecum
endothelial cells
fura-2
hernandezine
SK and F 96365
tetrandrine
Issue Date1996
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/lifescie
Citation
Life Sciences, 1996, v. 58, p. 2327-2335 How to Cite?
AbstractDepletion of internal Ca*+ stores causes capacitative Ca*’ entry which occurs through non-selective cation channels sensitive to blockade by SK&F 96365. Recently, alkaloids of Chinese herbal medicinal origin, tetrandrine and hemandezine, have been shown to possess actions including inhibition of Ca2+ channels in non-excitable cell types. In this study, we compared the actions of these novel inhibitors to those of SK&F 96365 in fura-Zloaded endothelial cells from human umbilical vein and bovine pulmonary artery. Depletion of Ca*+ from the internal stores was accomplished in Ca*+-free medium using an endoplasmic reticulum Ca*+ pump inhibitor, cyclopiazonic acid (CPA) or receptor agonists, histamine and bradykinin. Stimulation with histamine or bradykinin caused a marked and rapid transient increase in Ca*+ signal whereas CPA caused a smaller amplitude increase of longer duration. Restoring Ca*’ to the medium caused marked and sustained increases in the fluorescence indicating movement of Ca*’ into the cytosol presumably stimulated by the emptied Ca*’ stores. SK&F 96365 as well as tetrandrine and hemandezine antagonized depletion-induced Ca*’ entry. The results suggest that these putative inhibitors interact with Ca*+ entry triggered by depletion of the internal Ca*+ stores and their action is presumed to be on the non-selective cation channels. Their effectiveness may be enhanced by the mechanisms which lead to the opening of the Ca*+ influx channel.
Persistent Identifierhttp://hdl.handle.net/10722/224102
ISSN
2023 Impact Factor: 5.2
2023 SCImago Journal Rankings: 1.257
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLow, AM-
dc.contributor.authorBerdik, M-
dc.contributor.authorSormaz, L-
dc.contributor.authorGatience, S-
dc.contributor.authorBuchanan, MR-
dc.contributor.authorKwan, CY-
dc.contributor.authorDaniel, EE-
dc.date.accessioned2016-03-23T08:38:39Z-
dc.date.available2016-03-23T08:38:39Z-
dc.date.issued1996-
dc.identifier.citationLife Sciences, 1996, v. 58, p. 2327-2335-
dc.identifier.issn0024-3205-
dc.identifier.urihttp://hdl.handle.net/10722/224102-
dc.description.abstractDepletion of internal Ca*+ stores causes capacitative Ca*’ entry which occurs through non-selective cation channels sensitive to blockade by SK&F 96365. Recently, alkaloids of Chinese herbal medicinal origin, tetrandrine and hemandezine, have been shown to possess actions including inhibition of Ca2+ channels in non-excitable cell types. In this study, we compared the actions of these novel inhibitors to those of SK&F 96365 in fura-Zloaded endothelial cells from human umbilical vein and bovine pulmonary artery. Depletion of Ca*+ from the internal stores was accomplished in Ca*+-free medium using an endoplasmic reticulum Ca*+ pump inhibitor, cyclopiazonic acid (CPA) or receptor agonists, histamine and bradykinin. Stimulation with histamine or bradykinin caused a marked and rapid transient increase in Ca*+ signal whereas CPA caused a smaller amplitude increase of longer duration. Restoring Ca*’ to the medium caused marked and sustained increases in the fluorescence indicating movement of Ca*’ into the cytosol presumably stimulated by the emptied Ca*’ stores. SK&F 96365 as well as tetrandrine and hemandezine antagonized depletion-induced Ca*’ entry. The results suggest that these putative inhibitors interact with Ca*+ entry triggered by depletion of the internal Ca*+ stores and their action is presumed to be on the non-selective cation channels. Their effectiveness may be enhanced by the mechanisms which lead to the opening of the Ca*+ influx channel.-
dc.languageeng-
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/lifescie-
dc.relation.ispartofLife Sciences-
dc.subjectCa2+ antagonist caecum-
dc.subjectendothelial cells-
dc.subjectfura-2-
dc.subjecthernandezine-
dc.subjectSK and F 96365-
dc.subjecttetrandrine-
dc.subject.meshAlkaloids - pharmacology-
dc.subject.meshBenzylisoquinolines-
dc.subject.meshCalcium - deficiency - metabolism-
dc.subject.meshCalcium Channel Blockers - pharmacology-
dc.subject.meshEndothelium, Vascular - cytology - drug effects - metabolism-
dc.titlePlant alkaloids, tetrandrine and hernandezine, inhibit calcium-depletion stimulated calcium entry in human and bovine endothelial cells-
dc.typeArticle-
dc.identifier.emailKwan, CY: cykwan@hkucc.hku.hk-
dc.identifier.doi10.1016/0024-3205(96)00233-0-
dc.identifier.pmid8649222-
dc.identifier.scopuseid_2-s2.0-0029904215-
dc.identifier.hkuros26908-
dc.identifier.volume58-
dc.identifier.spage2327-
dc.identifier.epage2335-
dc.identifier.isiWOS:A1996UL98700007-
dc.identifier.issnl0024-3205-

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