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J. Biol. Chem., Vol. 262, Issue 12, 5448-5454, 04, 1987
P Arkhammar, T Nilsson, P Rorsman and PO Berggren
The effects of glucose, diazoxide, K+, and tolbutamide on the activity of
K+ channels, membrane potential, and cytoplasmic free Ca2+ concentration
were investigated in beta-cells from the Uppsala colony of obese
hyperglycemic mice. With [K+]e = [K+]i = 146 mM, it was demonstrated that
the dominating channel at the resting potential is a K+ channel with a
single-channel conductance of about 65 picosiemens and a reversal potential
of about +70 mV (pipette potential). This channel is characterized by
complex kinetics with openings grouped in bursts. The channel was
completely inhibited by 20 mM glucose in intact cells or by intracellularly
applied Mg-ATP (1 mM). The number of active channels was markedly reduced
already by 5 mM glucose. However, the single channel current of the
channels remaining active was unaffected, indicating no major
depolarization. To evoke a substantial depolarization of the membrane and
thereby action potentials, a total block in channel activity was necessary.
This could be achieved either by increasing the concentration of glucose to
20 mM or by combining 5 mM glucose with 100 microM tolbutamide. In both
cases, the effect was counteracted by the hyperglycemic sulfonamide
diazoxide. The effects on single channel activity were paralleled by
changes in membrane potential and cytoplasmic free Ca2+ concentration, also
when the latter measurements were performed at room temperature. The
transient increase in the number of active channels and the resulting
hyperpolarization observed after raising the glucose concentration to 20 mM
probably reflected a drop in cytoplasmic ATP concentration. It is suggested
that ATP works as a key regulator of the beta-cell membrane potential and
thereby the opening of voltage-activated Ca2+ channels.
Inhibition of ATP-regulated K+ channels precedes depolarization-induced increase in cytoplasmic free Ca2+ concentration in pancreatic beta- cells
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