Engling R, Föhr K J, Kemmer T P, Gratzl M
Abteilung Anatomie und Zellbiologie der Universität Ulm, FRG.
Cell Calcium. 1991 Jan;12(1):1-9. doi: 10.1016/0143-4160(91)90079-t.
The effects of Ca2+ and GTP on the release of Ca2+ from the inositol 1,4,5-trisphosphate (IP3) sensitive Ca2+ compartment were investigated with digitonin permeabilized rat pancreatic acinar cells. The amount of Ca2+ released due to IP3 directly correlated with the amount of stored Ca2+ and was found to be inversely proportional to the medium free Ca2+ concentration. Ca2+ release induced by 0.18 microM IP3 was half maximally inhibited at 0.5 microM free Ca2+, i.e. at concentrations observed in the cytosol of pancreatic acinar cells. GTP did not cause Ca2+ release on its own, but a single addition of GTP (20 microM) abolished the apparent desensitization of the Ca2+ release which was observed during repeated IP3 applications. This effect of GTP was reversible. GTP gamma S could not replace GTP. Desensitization still occurred when GTP gamma S was added prior to GTP. The reported data indicate that GTP, stored Ca2+ and cytosolic free Ca2+ modulate the IP3 induced Ca2+ release.
利用洋地黄皂苷通透的大鼠胰腺腺泡细胞，研究了Ca2+和GTP对肌醇1,4,5-三磷酸（IP3）敏感的Ca2+区室释放Ca2+的影响。IP3诱导释放的Ca2+量与储存的Ca2+量直接相关，且发现其与细胞外游离Ca2+浓度成反比。0.18微摩尔IP3诱导的Ca2+释放在游离Ca2+浓度为0.5微摩尔时受到最大抑制的一半，即处于在胰腺腺泡细胞胞质溶胶中观察到的浓度。GTP自身不会引起Ca2+释放，但单次添加GTP（20微摩尔）可消除在重复施加IP3期间观察到的Ca2+释放的明显脱敏现象。GTP的这种作用是可逆的。GTPγS不能替代GTP。在添加GTP之前添加GTPγS时仍会发生脱敏现象。所报道的数据表明，GTP、储存的Ca2+和胞质游离Ca2+调节IP3诱导的Ca2+释放。
