On the Role of Calcium in the Regulatory Volume Decrease (RVD) Response in Ehrlich Mouse Ascites Tumor Cells |
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Authors: | NK Jørgensen S Christensen H Harbak AM Brown IH Lambert EK Hoffmann LO Simonsen |
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Institution: | Biochemical Department, The August Krogh Institute, University of Copenhagen, Universitetsparken 13, DK-2100 Copenhagen ?, Denmark, DK Department of Cellular and Molecular Physiology, The August Krogh Institute, University of Copenhagen, Universitetsparken 13, DK-2100 Copenhagen ?, Denmark, DK Department of Physiology and Pharmacology, University of Nottingham, Nottingham, U.K., GB
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Abstract: | The putative role for Ca2+ entry and Ca2+ mobilization in the activation of the regulatory volume decrease (RVD) response has been assessed in Ehrlich cells. Following
hypotonic exposure (50% osmolarity) there is: (i) no increase in cellular Ins(1,4,5)P3 content, as measured in extracts from 2-3H]myoinositol-labeled cells, a finding at variance with earlier reports from our group; (ii) no evidence of Ca2+-signaling recorded in a suspension of fura-2-loaded cells; (iii) Ca2+-signaling in only about 6% of the single, fura-2-loaded cells at 1-mm Ca2+ (1% only at 0.1-mm Ca2+ and in Ca2+-free medium), as monitored by fluorescence-ratio imaging; (iv) no effect of removing external Ca2+ upon the volume-induced K+ loss; (v) no significant inhibition of the RVD response in cells loaded with the Ca2+ chelator BAPTA when the BAPTA-loading is performed in K+ equilibrium medium; (vi) an inhibition of the swelling-induced K+ loss (about 50%) at 1-mm Ba2+, but almost no effect of charybdotoxin (100 nm) or of clotrimazole (10 μm), reported inhibitors of the K+ loss induced by Ca2+-mobilizing agonists. Thus, Ca2+signaling by Ca2+ release or Ca2+ entry appears to play no role in the activation mechanism for the RVD response in Ehrlich cells.
Received: 8 December 1996/Revised: 14 January 1997 |
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Keywords: | : Volume regulation — Phosphoinositidase C — Ins(1 4 5)P3— Ca2+signaling — K+ channels — Charybdotoxin — Clotrimazole |
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