Hypoxia induced by Na2S2O4 increases [Na+]i in mouse glomus cells, an effect depressed by cobalt. Experiments with Na+-selective microelectrodes and voltage-clamping.

The intracellular sodium concentration ([Na+]i) and resting potential (Em) of cultured mouse glomus cells (clustered and isolated) were simultaneously measured with intracellular Na+-sensitive and conventional, KCl-filled, microelectrodes. Results obtained in clustered and isolated cells were similar. During normoxia (PO2 122 Torr), [Na+]i was 12-13 mM corresponding to a Na+ equilibrium potential (ENa) of about 58 mV. Em was about -42 mV. Hypoxia, induced by Na2S2O4 1 mM (PO2 10 Torr), depolarized the cells by about 20 mV, [Na+]i increased by 21 mM and ENa dropped to about 35 mV. One millimolar of CoCl2 depressed, or blocked, the effects of Na2S2O4 on [Na+]i but did not affect hypoxic depolarization. Voltage-clamping at -70 mV, while delivering pulses of different amplitudes, produced only small (about 10 pA) and slow TTX-insensitive inward currents. Fast and large (TTX-sensitive) inward currents were not detected. The cell conductance (measured with voltage ramps) was less than 1 nS. It was not affected by hypoxia but was depressed by cobalt. Voltage ramps elicited small inward currents in control and hypoxic solutions that were much smaller than those induced by barium (presumably enhancing calcium currents). Also, normoxic and hypoxic currents had lower thresholds and their troughs were at more negative voltages than in the presence of Ba2+. All currents were blocked by 1 mM CoCl2 suggesting that, at this concentration, cobalt exerted a nonspecific effect on glomus membrane channels. Hypoxia induced a large [Na+]i increase (presumably through inflow), but very small voltage-gated inward currents. Thus, Na+ increases (inflow) probably occurred by disturbing a Na+/K+ exchange mechanism and not by activation of voltage-gated channels.