Norlund L, Lindström P, Sehlin J
Naunyn Schmiedebergs Arch Pharmacol. 1985 Oct;331(1):104-7. doi: 10.1007/BF00498858.
Potassium transport was measured in beta-cell-rich islets from ob/ob-mice using the K+-analogue 86Rb+. Both tetracaine (0.1 mM) and glibenclamide (0.1 microM) reduced the ouabain-resistant 86Rb+ influx but did not significantly affect the ouabain-sensitive portion (Na+/K+ pump). Tetracaine (0.5 - 1 mM) or glibenclamide (0.2 mM) decreased the 86Rb+ equilibrium content and glibenclamide (1 microM) transiently reduced the 86Rb+ efflux rate but 0.1 mM tetracaine had only a slight effect on this flux rate. The results suggest that a change in ouabain-resistant (passive) K+ fluxes, but not the Na+/K+ pump, is involved in stimulation of insulin secretion by glibenclamide and tetracaine. Both drugs may exert similar effects on the beta-cell plasma membrane.
使用钾离子类似物86Rb+,在来自ob/ob小鼠的富含β细胞的胰岛中测量钾转运。丁卡因(0.1 mM)和格列本脲(0.1 μM)均降低了哇巴因抗性的86Rb+流入,但对哇巴因敏感部分(Na+/K+泵)无显著影响。丁卡因(0.5 - 1 mM)或格列本脲(0.2 mM)降低了86Rb+平衡含量,格列本脲(1 μM)短暂降低了86Rb+流出速率,但0.1 mM丁卡因对该通量速率仅有轻微影响。结果表明,格列本脲和丁卡因刺激胰岛素分泌涉及哇巴因抗性(被动)钾通量的变化,而非Na+/K+泵。两种药物可能对β细胞质膜发挥相似作用。