On the role of calcium in the regulatory volume decrease (RVD) response in Ehrlich mouse ascites tumor cells

• Published in: The Journal of membrane biology Vol. 157; no. 3; pp. 281 - 299
• Main Authors: Jorgensen, N K, Christensen, S, Harbak, H, Brown, A M, Lambert, I H, Hoffmann, E K, Simonsen, L O
• Format: Journal Article
• Language: English
• Published: United States 01.06.1997
• Subjects: Animals; Calcium - metabolism; Carcinoma, Ehrlich Tumor - metabolism; Carcinoma, Ehrlich Tumor - pathology; Cell Size; Mice; Signal Transduction; Tumor Cells, Cultured
• ISSN: 0022-2631; 1432-1424
• DOI: 10.1007/s002329900236

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 microM), 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.