Barbosa R M, Salgado A P, Santos R M, Rosário L M
Department of Zoology, University of Coimbra, Portugal.
FEBS Lett. 1993 Oct 11;332(1-2):9-13. doi: 10.1016/0014-5793(93)80471-6.
The study of the influence of intracellular pH (pHi) changes on the mechanism underlying pancreatic beta-cell bursting has been hampered by concomitant effects on the activity of background ATP-dependent K+ (K-ATP) channels. beta-cells were made to burst in the absence of active K-ATP channels by raising external Ca2+ in the presence of 11 mM glucose and tolbutamide. An alkalinizing pHi shift (exposure to 20 mM NH4Cl) increased the burst active phase duration. Conversely, an acidifying shift (NH4Cl withdrawal) suppressed the electrical activity. This is the mirror image of the effects recorded in the absence of tolbutamide. Glibenclamide and quinine suppressed the alkalinization-evoked hyperpolarization. This study emphasizes the differential sensitivity of different beta-cell ion channels to pHi and the prevalent role of K-ATP channels as electrical transducers of cytoplasmic pH changes under regular physiological conditions.
细胞内pH（pHi）变化对胰腺β细胞爆发机制的影响研究，因对背景ATP依赖性钾离子（K-ATP）通道活性的伴随效应而受阻。在11 mM葡萄糖和甲苯磺丁脲存在的情况下，通过提高细胞外Ca2+浓度，使β细胞在无活性K-ATP通道时爆发。碱化pHi变化（暴露于20 mM NH4Cl）增加了爆发活跃期的持续时间。相反，酸化变化（撤去NH4Cl）则抑制了电活动。这与在无甲苯磺丁脲时记录到的效应相反。格列本脲和奎宁抑制了碱化引起的超极化。本研究强调了不同β细胞离子通道对pHi的敏感性差异，以及在正常生理条件下K-ATP通道作为细胞质pH变化的电转换器的普遍作用。
