Attenuation of the serotonin-induced increase in intracellular calcium in rat aortic smooth muscle cells by sarpogrelate

Simple item page
dc.contributor.authorSaini, HK
dc.contributor.authorSharma, SK
dc.contributor.authorZahradka, P
dc.contributor.authorKumamoto, H
dc.contributor.authorTakeda, N
dc.contributor.authorDhalla, NS
dc.date.accessioned2007-10-05T15:39:04Z
dc.date.available2007-10-05T15:39:04Z
dc.date.issued2003-11-30
dc.description.abstractAlthough serotonin (5-HT) induced proliferation of vascular smooth muscle cells is considered to involve changes in intracellular Ca2+ ([Ca2+](i)), the mechanism of Ca2+ mobilization by 5-HT is not well defined. In this study, we examined the effect of 5-HT on rat aortic smooth muscle cells (RASMCs) by Fura-2 microfluorometry for [Ca2+](i) measurements. 5-HT was observed to increase the [Ca2+](i) in a concentration- and time-dependent manner. This action of 5-HT was dependent upon the extracellular concentration of Ca2+ ([Ca2+](e)) and was inhibited by both Ca2+ channel antagonists (verapamil and diltiazem) and inhibitors of sarcoplasmic reticular Ca2+ pumps (thapsigargin and cyclopiazonic acid). The 5-HT-induced increase in [Ca2+](i) was blocked by sarpogrelate, a 5-HT2A-receptor antagonist, but not by different agents known to block other receptor sites. 5-HT-receptor antagonists such as ketanserin, cinanserin, and mianserin, unlike methysergide, were also found to inhibit the 5-HT-induced Ca2+ mobilization, but these agents were less effective in comparison to sarpogrelate. On the other hand, the increase in [Ca2+](i) in RASMCs by ATP, angiotensin II, endothelin-1, or phorbol ester was not affected by sarpogrelate. These results indicate that Ca2+ mobilization in RASMCs by 5-HT is mediated through the activation of 5-HT2A receptors and support the view that the 5-HT-induced increase in [Ca2+](i) involves both the extracellular and intracellular sources of Ca2+.en
dc.format.extent336505 bytes
dc.format.mimetypeapplication/pdf
dc.identifier.citation0008-4212; CAN J PHYSIOL PHARMACOL, NOV 2003, vol. 81, no. 11, p.1056 to 1063.en
dc.identifier.doi10.1139/Y03-108
dc.identifier.urihttp://hdl.handle.net/1993/2893
dc.language.isoengen_US
dc.rightsNo part of the NRC Research Press electronic journals may be reproduced, stored, or transmitted in any form or by any means, without the written permission of the publisher, except as stated below. Under the Canadian Copyright Act, individuals may download or print single copies of articles for personal research or study. Any person may reproduce short excerpts from articles in the journals for any purpose that respects the moral rights of authors, provided that the source is fully acknowledged. As a courtesy, the consent of authors of such material should be obtained directly from the author. Authorization to reproduce items for other than personal research or study, as stated above, may be obtained via Access © upon payment of the copyright fee of $10.00 per copy. NRC Research Press also extends certain additional rights to authors. The above rights do not extend to copying or reproduction for general distribution, for advertising or promotional purposes, for creating new collective works, or for resale. For such copying or reproduction, arrangements must be made with NRC Research Press.en
dc.rightsopen accessen_US
dc.statusPeer revieweden
dc.subjectsarpogrelateen
dc.subjectserotoninen
dc.subjectvascular smooth muscle cellsen
dc.subjectintracellular Ca2+en
dc.subjectPROTEIN-KINASE-Cen
dc.subjectANGIOTENSIN-IIen
dc.subjectDNA-SYNTHESISen
dc.subjectRECEPTOR ANTAGONISTen
dc.subjectANTIPLATELET AGENTen
dc.subjectPROLIFERATION; 5-HYDROXYTRYPTAMINEen
dc.subjectEXPRESSIONen
dc.subjectMECHANISMSen
dc.subjectARTERIESen
dc.titleAttenuation of the serotonin-induced increase in intracellular calcium in rat aortic smooth muscle cells by sarpogrelateen
dc.typejournal articleen_US
Files
Collections
University of Manitoba Scholarship (login required)