Schwanstecher M, Mnner K, Panten U
Institute of Pharmacology and Toxicology, University of Göttingen, FRG.
Pharmacology. 1994 Aug;49(2):105-11. doi: 10.1159/000139222.
In isolated pancreatic islets of mice, the relationships between free glimepiride concentration and membrane binding or inhibition of ATP-sensitive K+ channels were examined. Microsomal membrane binding and K+ channel inhibition were half-maximal at 0.7 and 0.3 nmol/l glimepiride, respectively. The corresponding concentrations for glibenclamide were 0.4 and 0.6 nmol/l. Administration of glimepiride (10 nmol/l) or glibenclamide (10 nmol/l) to isolated mouse islets perifused with albumin-containing media induced a slow increase in insulin secretion. The kinetics of the secretory responses to glimepiride and glibenclamide were identical. Determination of albumin binding revealed that the free glimepiride and glibenclamide concentrations applied in our investigation were in the range of therapeutic serum concentrations of the free drugs. It is concluded that the effects of glimepiride and glibenclamide are very similar in mouse beta-cells.
在分离的小鼠胰岛中，研究了游离格列美脲浓度与膜结合或ATP敏感性钾通道抑制之间的关系。微粒体膜结合和钾通道抑制在格列美脲浓度分别为0.7和0.3 nmol/l时达到半数最大效应。格列本脲的相应浓度分别为0.4和0.6 nmol/l。向灌注含白蛋白培养基的分离小鼠胰岛中给予格列美脲（10 nmol/l）或格列本脲（10 nmol/l），可使胰岛素分泌缓慢增加。对格列美脲和格列本脲分泌反应的动力学相同。白蛋白结合测定表明，我们研究中应用的游离格列美脲和格列本脲浓度处于游离药物治疗性血清浓度范围内。得出的结论是，格列美脲和格列本脲在小鼠β细胞中的作用非常相似。
