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KMID : 0811719980020020133
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Korean Journal of Physiology & Pharmacology
1998 Volume.2 No. 2 p.133 ~ p.145
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Ca2+Signalling in Endothelial Cells : Role of ion Channels
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Bernd Nilius
Felix Viana/Masahiro Kamouchi/Cristina Fasolato/Jan Eggermont/Guy Droogmans
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Abstract
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Ca2+?signals in endothelial cells are determined by release from intracellular stores and entry through the plasma membrane. In this review, the nature of Ca2+ entry and mechanisms of its control are reviewed. The following ion channels play a pivotal role in regulation of the driving force for Ca2+ entry: an inwardly rectifying K+ channel, identified as Kir2.1, a big-conductance, Ca2+?activated K+ channel (hslo) and at least two Cl? channels (a volume regulated Cl? channel, VRAC, and a Ca2+ activated Cl? channel, CaCC). At least two different types of Ca2+-entry channels exist: 1. A typical CRAC-like, highly selective Ca2+ channel is described. Current density for this Ca2+ entry is approximately 0.1pA/pF at 0 mV and thus 10 times smaller than in Jurkat or mast cells. 2. Another entry pathway for Ca2+ entry is a more non-selective channel, which might be regulated by intracellular Ca2+. Although detected in endothelial cells, the functional role of trp1,3,4 as possible channel proteins is unclear. Expression of trp3 in macrovascular endothelial cells from bovine pulmonary artery induced non-selective cation channels which are probably not store operated or failed to induce any current. Several features as well as a characterisation of Ca2+-oscillations in endothelial cells is also presented.
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KEYWORD
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Endothelium-Ca2, -entry channels-potassium channels-Ca2,
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