Wakabayashi I, Groschner K
Institut Für Pharmakologie und Toxikologie, Karl-Franzens-Universität Graz, Austria.
Biochem Biophys Res Commun. 1996 Apr 25;221(3):762-7. doi: 10.1006/bbrc.1996.0670.
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.
在ECV304内皮细胞中研究了酸中毒对储存耗竭激活的Ca2+内流的调节作用。将细胞外pH从7.4降至6.9可显著抑制由毒胡萝卜素（100 nM）直接耗竭Ca2+储存所引发的Ca2+内流，但对漏出性Ca2+内流无显著影响。在细胞外Ca2+浓度为2.5 mM时，酸中毒使毒胡萝卜素诱导的Ca2+内流减少了53.7±7.8%。在由高细胞外K+（100 mM）去极化的细胞中也观察到了类似程度的抑制作用。细胞外pH从7.4降至6.9与细胞内pH从7.23±0.01降至7.01±0.03相关。丙酸盐（20 mM）使细胞内pH降至6.97±0.02，但在细胞外Ca2+浓度为2.5 mM时未能显著抑制储存耗竭激活的Ca2+内流。我们的结果表明，细胞外质子浓度的增加通过对质膜Ca2+通道的直接、不依赖膜电位的作用来抑制储存耗竭激活的Ca2+内流。
