| Abstract: | K+ depolarization evokes phosphatidylinositol response, i.e. the increased 32P orthophosphate labelling of phosphatidylinositol in frog sartorii muscles. The phosphatidylinositol response seems to be closely related to K+ depolarization and not to the transient Ca2+ release at the beginning of depolarization. It ceases as soon as the muscles depolarized by 90 mmol/l KCl for a short period of time are repolarized, while it continues when the depolarization is maintained. When the muscles are depolarized with 20 mmol/l KCl, the phosphatidylinositol response is also observed. This response is not suppressed by drugs that block Ca2+ mobilization. Other agents like caffeine, azide or EGTA which induce some effects similar to that of K+ depolarization, do not evoke phosphatidylinositol response. Rather, they simply cause a decrease in the labelling of phospholipids, phosphatidylinositol being the least affected. In muscles derived from frogs maintained under healthy conditions Ca2+ release in the early phase of K+ depolarization does not cause significant changes in phospholipid labelling. However, in muscles from frogs starving for many months, a large decrease in the labelling of phospholipids is observed in the early phase of K+ depolarization. It is postulated that the changes in the physicochemical state of the membrane and not Ca2+ gating mechanism or free cell Ca2+ level are crucial in the phosphatidylinositol response in the frog sartorii muscles depolarized by high K+. |
