Effects of sodium on beta-cell electrical activity.

The present studies, designed to evaluate the contribution of Na+ to the mouse pancreatic beta-cell membrane potential, were performed utilizing intracellular microelectrodes. Complete removal of external sodium, in the presence of glucose, did not significantly affect spike peak potential. However, it caused a negative shift of the resting membrane potential, both in the presence and absence of glucose. After this initial hyperpolarization, the membrane gradually depolarized, the rate of depolarization being slower in the absence of glucose. This two-phase hyperpolarization-depolarization pattern remained when ouabain was added, both in the presence and absence of glucose. An increase of input resistance was associated with the slow depolarization. During this depolarization the maximum rate of rise (dV/dtmax) of the action potential ("spike") decreased. There was no direct relationship between dV/dtmax and [Na]0. Readdition of low [Na]0 (14 mM) to a glucose medium reactivated the postburst hyperpolarization (PBH), even in the presence of ouabain. These observations indicate that there is a significant resting sodium permeability (PNa). However, the action potential (spike) is not generated by activation of a voltage-dependent (gated) sodium channel. The membrane depolarization after Na+ removal reflects concomitant inhibition of the Na+-K+ pump and decrease of potassium permeability (PK). The blockage of PBH in the absence of Na+ is not related to the inhibition of an oscillatory Na+-K+ pump but to the inactivation of a PK. Aside from its effect on the Na+-K+ pump, ouabain may stimulate PNa.