Hopkins W F, Fatherazi S, Cook D L
Department of Physiology and Biophysics, University of Washington School of Medicine, Seattle.
FEBS Lett. 1990 Dec 17;277(1-2):101-4. doi: 10.1016/0014-5793(90)80818-4.
U-56324, a hypoglycemic agent derived from nicotinic acid, inhibited the activity of ATP-sensitive potassium channels in excised patches from mouse pancreatic B-cells. The effect of U-56324 on channel activity was reversible and concentration-dependent while it had no effect on single channel conductance. The positional isomer, U-59588, which has relatively little hypoglycemic activity, had no effect on channel properties. U-56324, at the same concentrations, had no effect on calcium-activated potassium channels. The basis for the potentially antidiabetic properties of U-56324 may therefore be due to direct and specific inhibition of ATP-sensitive potassium channels.
U - 56324是一种源自烟酸的降血糖药物，它抑制了从小鼠胰腺β细胞分离的膜片中ATP敏感性钾通道的活性。U - 56324对通道活性的影响是可逆的且呈浓度依赖性，而对单通道电导没有影响。位置异构体U - 59588的降血糖活性相对较小，对通道特性没有影响。相同浓度下，U - 56324对钙激活钾通道没有影响。因此，U - 56324潜在的抗糖尿病特性可能是由于其对ATP敏感性钾通道的直接和特异性抑制作用。
