Differential modulation of pancreatic β‐cell bursting by intracellular pH in the presence and absence of a K‐ATP channel blocker

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Abstract
The study of the influence of intracellular pH (pHi) changes on the mechanism underlying pancreatic β‐cell bursting has been hampered by concomitant effects on the activity of background ATP‐dependent K+ (K‐ATP) channels. β‐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 pH; shift (exposure to 20 mM NH4C1) 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 β‐cell ion channels to pHi and the prevalent role of K‐ATP channels as electrical transducers of cytoplasmic pH changes under regular physiological conditions.