ATP regulates sodium channel kinetics in pancreatic islet beta cellsZou, Na (Avtor) Rupnik, Marjan (Avtor) Langerhansovi otočkitrebušna slinavkaPancreatic beta cells act as glucose sensors, in which intracellular ATP ([ATP](i)) are altered with glucose concentration change. The characterization of voltage-gated sodium channels under different [ATP](i) remains unclear. Here, we demonstrated that increasing [ATP](i) within a certain range of concentrations (2-8 mM) significantly enhanced the voltage-gated sodium channel currents, compared with 2 mM cytosolic ATP. This enhancement was attenuated by even high intracellular ATP (12 mM). Furthermore, elevated ATP modulated the sodium channel kinetics in a dose-dependent manner. Increased [ATP](i) shifted both the current-voltage curve and the voltage-dependent inactivation curve of sodium channel to the right. Finally, the sodium channel recovery from inactivation was significantly faster when the intracellular ATP level was increased, especially in 8 mM [ATP](i), which is an attainable concentration by the high glucose stimulation. In summary, our data suggested that elevated cytosolic ATP enhanced the activity of Na(+) channels, which may play essential roles in modulating cell excitability and insulin release when blood glucose concentration increases.20132015-07-10 12:40:51Delo ni kategorizirano50505UDK: 612.349.7COBISS_ID: 512288568ISSN pri članku: 0022-2631NUK URN: URN:SI:UM:DK:8YJ0HDMYsl