Bevan C, Theiss C, Kinne R K
Max-Planck-Institut fuer Systemphysiologie, Dortmund, West Germany.
Biochem Biophys Res Commun. 1990 Jul 31;170(2):563-8. doi: 10.1016/0006-291x(90)92128-m.
The role of Ca2+ was studied in the release of the organic osmolyte sorbitol from rat IMCD cells in response to hypoosmotic stress. When cells were exposed to hypoosmotic media, sorbitol release was greatly reduced in Ca-free media which, on readmission of Ca2+, returned to control values. Under isoosmotic conditions, the ionophore A23187 stimulated sorbitol release without any effect on cell volume. Addition of trifluoperazine, a calmodulin inhibitor, but not the protein kinase C inhibitor H-7, inhibited the osmotically-activated sorbitol release. These results suggest that sorbitol release is a calmodulin-dependent event, possibly activated by a rise in intracellular calcium as a result of cell swelling.
研究了钙离子（Ca2+）在大鼠内髓集合管（IMCD）细胞因低渗应激而释放有机渗透剂山梨醇过程中的作用。当细胞暴露于低渗培养基时，在无钙培养基中山梨醇释放量大幅降低，而再加入Ca2+后，释放量恢复到对照值。在等渗条件下，离子载体A23187刺激山梨醇释放，对细胞体积无任何影响。添加钙调蛋白抑制剂三氟拉嗪可抑制渗透激活的山梨醇释放，但蛋白激酶C抑制剂H-7则无此作用。这些结果表明，山梨醇释放是一个依赖钙调蛋白的事件，可能是由于细胞肿胀导致细胞内钙升高而激活的。
