Abrahamsson H, Berggren P O, Rorsman P
FEBS Lett. 1985 Oct 7;190(1):21-4. doi: 10.1016/0014-5793(85)80418-x.
The effects of the hypoglycemic sulfonylureas tolbutamide and glibenclamide on free cytoplasmic Ca2+, [Ca2+]i, were compared with that of a depolarizing concentration of K+ in dispersed and cultured pancreatic beta-cells from ob/ob mice. [Ca2+]i was measured with the fluorescent Ca2+-indicator quin2. The basal level corresponded to 150 nM and increased to 600 nM after exposure to 30.9 mM K+. The corresponding levels after stimulation with 1 microM glibenclamide and 100 microM tolbutamide were 390 and 270 nM respectively. K+ depolarization increased [Ca2+]i more rapidly than either of the sulfonylureas. It is suggested that the increased [Ca2+]i obtained after stimulation by sulfonylureas is due to depolarization of the beta-cells with subsequent entry of Ca2+ through voltage-dependent channels.
将降血糖磺酰脲类药物甲苯磺丁脲和格列本脲对游离细胞质钙离子浓度（[Ca2+]i）的影响，与能使ob/ob小鼠分离培养的胰岛β细胞发生去极化的钾离子浓度的影响进行了比较。用荧光钙离子指示剂喹啉-2测量[Ca2+]i。基础水平相当于150 nM，暴露于30.9 mM钾离子后增加到600 nM。用1 microM格列本脲和100 microM甲苯磺丁脲刺激后的相应水平分别为390 nM和270 nM。钾离子去极化使[Ca2+]i升高的速度比任何一种磺酰脲类药物都快。提示磺酰脲类药物刺激后[Ca2+]i升高是由于β细胞去极化，随后钙离子通过电压依赖性通道进入细胞所致。
