Gylfe E, Hellman B, Arvidson G, Sandblom J
Biochem Med. 1984 Apr;31(2):246-53. doi: 10.1016/0006-2944(84)90029-2.
Black lipid membranes and liposomes loaded with Ca2+ or 5,6-carboxyfluorescein were used for exploring the mechanism of action of insulin-releasing sulfonylureas. Unlike the Ca2+/H+ exchanging ionophore A-23187, tolbutamide did not stimulate the net efflux of Ca2+ from the liposomes. Glibenclamide caused a sustained release of Ca2+, but this effect could be attributed to labilization of the liposomal membrane as indicated by a quantitatively similar loss of the stability marker 5,6-carboxyfluorescein. Unlike the neutral ionophore nonactin or the channel forming quasi-ionophore gramicidin A, the sulfonylureas did not alter the conductance of black lipid membranes in medium containing Na+, K+, Ca2+, Mg2+, and Cl-. It is concluded that the sulfonylureas tested lack ionophore properties but that glibenclamide can labilize membranes.
负载Ca2+或5,6 - 羧基荧光素的黑色脂质膜和脂质体被用于探究胰岛素释放磺脲类药物的作用机制。与Ca2+/H+交换离子载体A - 23187不同，甲苯磺丁脲不会刺激脂质体中Ca2+的净流出。格列本脲会引起Ca2+的持续释放，但这种效应可归因于脂质体膜的不稳定，这由稳定性标记物5,6 - 羧基荧光素类似的定量损失所表明。与中性离子载体缬氨霉素或形成通道的准离子载体短杆菌肽A不同，磺脲类药物在含有Na+、K+、Ca2+、Mg2+和Cl-的培养基中不会改变黑色脂质膜的电导。结论是，所测试的磺脲类药物缺乏离子载体特性，但格列本脲可使膜不稳定。
