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Wakabayashi, I; Groschner, K.
Evidence for a direct inhibitory effect of extracellular H+ on store depletion-activated Ca2+ entry in vascular endothelial cells.
Biochem Biophys Res Commun. 1996; 221(3):762-767 Doi: 10.1006/bbrc.1996.0670
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Co-authors Med Uni Graz
Groschner Klaus
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Abstract:
Modulation of store depletion-activated Ca2+ entry by acidosis was investigated in ECV304 endothelial cells. Lowering extracellular pH from 7.4 to 6.9 markedly suppressed Ca2+ entry elicited by direct depletion of Ca2+ stores with thapsigargin (100 nM), but did not significantly affect leak Ca2+ entry. Acidosis diminished thapsigargin-induced Ca2+ entry by 53.7 +/- 7.8% at 2.5 mM extracellular Ca2+. A similar degree of inhibition was observed in cells depolarized by high extracellular K+ (100 mM). Reduction of extracellular pH from 7.4 to 6.9 was associated with a decrease in intracellular pH from 7.23 +/- 0.01 to 7.01 +/- 0.03. Propionate (20 mM) caused a reduction of intracellular pH to 6.97 +/- 0.02, but failed to suppress store depletion-activated Ca2+ entry at 2.5 mM extracellular Ca2+ significantly. Our results suggest that an increase in extracellular proton concentration inhibits store depletion-activated Ca2+ entry through a direct, membrane potential-independent effect on the plasmalemmal Ca2+ channel.
Find related publications in this database (using NLM MeSH Indexing)
Calcium - metabolism
Cell Line -
Cell Membrane Permeability -
Endothelium, Vascular - cytology Endothelium, Vascular - drug effects Endothelium, Vascular - metabolism
Humans -
Hydrogen - metabolism
Hydrogen-Ion Concentration -
Membrane Potentials -
Potassium - metabolism
Terpenes - pharmacology
Thapsigargin -

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