Tiger G, Fowler C J
Department of Pharmacology, University of Umeå, Sweden.
Cell Signal. 1991;3(3):209-13. doi: 10.1016/0898-6568(91)90046-w.
The effects of ouabain and monensin upon basal and carbachol-stimulated inositol phospholipid breakdown in rat cerebral cortical miniprisms have been investigated. Basal inositol phospholipid breakdown was increased by both compounds at both 6 and 18 mM K+. Enhancement of the carbachol response at 6 mM, but not at 18 mM K+, was found with high concentrations of ouabain. On the other hand, monensin blocked the response to carbachol. Monensin also inhibited the specific binding of [3H]pirenzepine to cerebral cortical membranes, but this was found only at concentrations higher than required to affect the basal and carbachol-stimulated inositol phospholipid breakdown responses. Ouabain did not affect [3H] pirenzepine binding at any of the concentrations tested (6-600 muM). It is concluded that agents that increase the intracellular sodium ion concentration affect the inositol phospholipid breakdown response to carbachol, but that the modulation can be both to potentiate and to inhibit the response.
研究了哇巴因和莫能菌素对大鼠大脑皮质微小切片中基础和卡巴胆碱刺激的肌醇磷脂分解的影响。在6 mM和18 mM K⁺浓度下，两种化合物均增加了基础肌醇磷脂分解。高浓度哇巴因在6 mM K⁺时增强了卡巴胆碱反应，但在18 mM K⁺时未增强。另一方面，莫能菌素阻断了对卡巴胆碱的反应。莫能菌素还抑制了[³H]哌仑西平与大脑皮质膜的特异性结合，但仅在高于影响基础和卡巴胆碱刺激的肌醇磷脂分解反应所需的浓度时才发现这种情况。在所测试的任何浓度（6 - 600 μM）下，哇巴因均不影响[³H]哌仑西平的结合。得出的结论是，增加细胞内钠离子浓度的药物会影响对卡巴胆碱的肌醇磷脂分解反应，但这种调节既可以增强也可以抑制该反应。
