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      • Record: found
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      Increased Store-Operated Ca 2+ Entry into Contractile Vascular Smooth Muscle following Organ Culture

      , ,

      Journal of Vascular Research

      S. Karger AG

      Ca2+ channels, Ca2+ stores, Artery, Phenotype, Organ culture

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          Abstract

          Ca<sup>2+</sup> inflow via store-operated Ca<sup>2+</sup> channels was investigated in rings of rat tail and basilar arteries kept in serum-free organ culture, which is known to preserve the contractility of the vascular smooth muscle. After culture for 3–4 days, Ca<sup>2+</sup> release from intracellular stores in response to caffeine (20 m M) was augmented 2- to 4-fold. Following depletion of intracellular Ca<sup>2+</sup> stores by caffeine and thapsigargin (10 µ M), addition of Ca<sup>2+</sup> (2.5 m M) caused an increase in the intracellular Ca<sup>2+</sup> concentration which was 2–3 times greater in cultured than in freshly dissected rings, and was not affected by verapamil (10 µ M). In contrast, L-type Ca<sup>2+</sup> channel currents were decreased by 20% after culture. While freshly dissected rings developed no or very little force in response to the addition of Ca<sup>2+</sup> after store depletion, cultured rings developed 42% (tail artery) and 60% (basilar artery) of the force of high-K<sup>+</sup>-induced contractions. These contractions in cultured vessels were insensitive to verapamil but could be completely relaxed by SKF-96365 (30 µ M). Store depletion by caffeine increased the Mn<sup>2+</sup> quench rate 3- to 4-fold in freshly dissected as well as cultured tail artery, while there was no increase in freshly dissected basilar artery, but a 3-fold increase in cultured basilar artery. Uptake of Ca<sup>2+</sup> into intracellular stores was twice as rapid in cultured as in freshly dissected tail artery. This study shows that organ culture of vascular smooth muscle tissue causes changes in Ca<sup>2+</sup> handling, resembling the pattern seen in dedifferentiating smooth muscle cells in culture, although contractile properties are maintained.

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          Most cited references 5

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          • Abstract: found
          • Article: not found

          On the molecular basis and regulation of cellular capacitative calcium entry: roles for Trp proteins.

           M Jiang,  D Platano,  G Boulay (1996)
          During the last 2 years, our laboratory has worked on the elucidation of the molecular basis of capacitative calcium entry (CCE) into cells. Specifically, we tested the hypothesis that CCE channels are formed of subunits encoded in genes related to the Drosophila trp gene. The first step in this pursuit was to search for mammalian trp genes. We found not one but six mammalian genes and cloned several of their cDNAs, some in their full length. As assayed in mammalian cells, overexpression of some mammalian Trps increases CCE, while expression of partial trp cDNAs in antisense orientation can interfere with endogenous CCE. These findings provided a firm connection between CCE and mammalian Trps. This article reviews the known forms of CCE and highlights unanswered questions in our understanding of intracellular Ca2+ homeostasis and the physiological roles of CCE.
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            What drives calcium entry during [Ca2+]i oscillations?--challenging the capacitative model.

            An increased entry of Ca2+ across the plasma membrane plays a key role in the generation and maintenance of the [Ca2+]i signals seen in cells following activation of receptors coupled to the PLC/InsP3 signaling pathway. In recent years, considerable efforts have been made to define the nature and control of this agonist-enhanced Ca2+ entry. To date, these studies have largely focussed on the so-called 'capacitative' or store-operated model and, although many important details remain unclear, the critical role this mechanism plays in maintaining the sustained elevated 'plateau' type of [Ca2+]i response seen at high agonist concentrations is now well established. Far less well understood is the nature of the enhanced Ca2+ entry associated with the more complex [Ca2+]i signals typical of stimulation at more physiological levels of agonist. Where such entry has been considered, it too has generally been assumed to result from a capacitative or 'store-operated' mechanism. Significantly, however, direct evidence in support of this assumption is lacking. This review attempts to critically examine this assumption and presents the argument that several key characteristics of capacitative or store-operated mechanisms of agonist-activated Ca2+ entry are incompatible with its operation during these types of [Ca2+]i signal.
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              • Record: found
              • Abstract: found
              • Article: not found

              Ca2+ entry channels in rat thoracic aortic smooth muscle cells activated by endothelin-1.

               S Miwa,  Y Iwamuro,  X. Zhang (1999)
              The contraction of the rat aorta induced by endothelin-1 (ET-1) requires entry of extracellular Ca2+, but involvement of voltage-operated Ca2+ channel is minor. Using whole-cell recordings of patch-clamp and monitoring of the intracellular free Ca2+ concentration ([Ca2+]i), we characterized Ca2+ entry channels in A7r5 cells activated by ET-1. ET-1 activates three types of voltage-independent Ca2+ entry channels: two types of Ca2+-permeable nonselective cation channels (designated NSCC-1 and NSCC-2) and a store-operated Ca2+ channel (SOCC). Furthermore, it was found that these channels can be pharmacologically discriminated using Ca2+ channel blockers such as SK&F 96365 and LOE 908. NSCC-1 is resistant to SK&F 96365, but sensitive to LOE 908, whereas NSCC-2 is sensitive to both SK&F 96365 and LOE 908. SOCC is sensitive to SK&F 96365, but resistant to LOE 908. Using these channel blockers, we analyzed Ca2+ entry channels involved in the ET-1-induced contractions of rat thoracic aorta and increases in [Ca2+]i of single smooth muscle cells. The responses to lower concentrations of ET-1 ( or = 1 nM) were suppressed by SK&F 96365 or LOE 908 to about 10% and 35% of controls, respectively, and abolished by combined treatment with SK&F 96365 and LOE 908. These results show that the responses of rat aorta to lower concentrations of ET-1 involve only one Ca2+ channel that is sensitive to SK&F 96365 and LOE 908 (NSCC-2), whereas those to higher concentrations of ET-1 involve NSCC-1, NSCC-2 and SOCC, contributing 10%, 55% and 35%, respectively, to total Ca2+ entry.
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                Author and article information

                Journal
                JVR
                J Vasc Res
                10.1159/issn.1018-1172
                Journal of Vascular Research
                S. Karger AG
                1018-1172
                1423-0135
                2001
                August 2001
                11 July 2001
                : 38
                : 4
                : 324-331
                Affiliations
                Department of Physiological Sciences, Lund University, Lund, Sweden
                Article
                51063 J Vasc Res 2001;38:324–331
                10.1159/000051063
                11455203
                © 2001 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 5, Tables: 2, References: 28, Pages: 8
                Categories
                Research Paper

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