dc.contributor.author | Demuth, D.G. | |
dc.contributor.author | Gkoumassi, E. | |
dc.contributor.author | Droege, M.J. | |
dc.contributor.author | Dekkers, B.G.J. | |
dc.contributor.author | Esselink, H.J. | |
dc.contributor.author | Vanree, R.M. | |
dc.contributor.author | Parsons, M. | |
dc.contributor.author | Zaagsma, J. | |
dc.contributor.author | Molleman, A. | |
dc.contributor.author | Nelemans, S.A. | |
dc.date.accessioned | 2008-10-28T09:51:25Z | |
dc.date.available | 2008-10-28T09:51:25Z | |
dc.date.issued | 2005 | |
dc.identifier.citation | Demuth , D G , Gkoumassi , E , Droege , M J , Dekkers , B G J , Esselink , H J , Vanree , R M , Parsons , M , Zaagsma , J , Molleman , A & Nelemans , S A 2005 , ' Arachidonic Acid Mediates Non-Capacitative Calcium Entry Evoked by CB1-Cannabinoid Receptor Activation in DDT1MF-2 Smooth Muscle Cells ' , Journal of Cellullar Physiology , vol. 205 , no. 1 , pp. 58-67 . https://doi.org/10.1002/jcp.20390 | |
dc.identifier.issn | 0021-9541 | |
dc.identifier.other | dspace: 2299/2478 | |
dc.identifier.uri | http://hdl.handle.net/2299/2478 | |
dc.description | ‘The definitive version is available at www3.interscience.wiley.com '. Copyright Wiley-Liss, Inc. DOI: 10.1002/jcp.20390 [Full text of this article is not available in the UHRA] | |
dc.description.abstract | Cannabinoid CB1-receptor stimulation in DDT1 MF-2 smooth muscle cells induces a rise in [Ca2+]i, which is dependent on extracellular Ca2+ and modulated by thapsigargin-sensitive stores, suggesting capacitative Ca2+ entry (CCE), and by MAP kinase. Non-capacitative Ca2+ entry (NCCE) stimulated by arachidonic acid (AA) partly mediates histamine H1-receptor-evoked increases in [Ca2+]i in DDT1 MF-2 cells. In the current study, both Ca2+ entry mechanisms and a possible link between MAP kinase activation and increasing [Ca2+]i were investigated. In the whole-cell patch clamp configuration, the CB-receptor agonist CP 55, 940 evoked a transient, Ca2+-dependent K+ current, which was not blocked by the inhibitors of CCE, 2-APB, and SKF 96365. AA, but not its metabolites, evoked a transient outward current and inhibited the response to CP 55,940 in a concentration-dependent manner. CP 55,940 induced a concentration-dependent release of AA, which was inhibited by the CB1 antagonist SR 141716. The non-selective Ca2+ channel blockers La3+ and Gd3+ inhibited the CP 55,940-induced current at concentrations that had no effect on thapsigargin-evoked CCE. La3+ also inhibited the AA-induced current. CP 55,940-induced AA release was abolished by Gd3+ and by phospholipase A2 inhibition using quinacrine; this compound also inhibited the outward current. The CP 55,940-induced AA release was strongly reduced by the MAP kinase inhibitor PD 98059. The data suggest that in DDT1 MF-2 cells, AA is an integral component of the CB1 receptor signaling pathway, upstream of NCCE and, via PLA2, downstream of MAP kinase. © 2005 Wiley-Liss, Inc. | en |
dc.language.iso | eng | |
dc.relation.ispartof | Journal of Cellullar Physiology | |
dc.title | Arachidonic Acid Mediates Non-Capacitative Calcium Entry Evoked by CB1-Cannabinoid Receptor Activation in DDT1MF-2 Smooth Muscle Cells | en |
dc.contributor.institution | Department of Human and Environmental Sciences | |
dc.description.status | Peer reviewed | |
rioxxterms.versionofrecord | 10.1002/jcp.20390 | |
rioxxterms.type | Journal Article/Review | |
herts.preservation.rarelyaccessed | true | |