HYPOXIA-INDUCED BY NA2S2O4 INCREASES [NA- EXPERIMENTS WITH NA+-SELECTIVE MICROELECTRODES AND VOLTAGE-CLAMPING(](I) IN MOUSE GLOMUS CELLS, AN EFFECT DEPRESSED BY COBALT )

The intracellular sodium concentration ([Na+](i)) and resting porentia l (E-m) of cultured mouse glomus cells (clustered and isolated) were s imultaneously measured with intracellular Na+-sensitive and convention al, KCl-filled, microelectrodes. Results obtained in clustered and iso lated cells were similar. During normoxia (PO2 12.2 Torr), [Na+](i) wa s 12-13 mM corresponding to a Na+ equilibrium potential (E-Na) of abou t 58 mV. Em was about - 42 mV. Hypoxia, induced by Na2S2O4 1 mM (PO2 1 0 Torr), depolarized the cells by about 20 mV, [Na+](i) increased by 2 1 mM and E-Na dropped to about 35 mV. One millimolar of CoCl2 depresse d, or blocked, the effects of Na2S2O4 on [Na+](i) but did not affect h ypoxic depolarization. Voltage-clamping at -70 mV, while delivering pu lses of different amplitudes, produced only small (about 10 pA) and sl ow TTX-insensitive inward currents. Fast and large (TTX-sensitive) inw ard currents were not detected. The cell conductance (measured with vo ltage ramps) was less than 1 nS. It was not affected by hypoxia but wa s depressed by cobalt. Voltage ramps elicited small inward currents in control and hypoxic solutions that were much smaller than those induc ed by barium (presumably enhancing calcium currents). Also, normoxic a nd hypoxic currents had lower thresholds and their troughs were at mor e negative voltages than in the presence of Ba2+. All currents were bl ocked by 1 mM CoCl2 suggesting that, at this concentration, cobalt exe rted 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 activati on of voltage-gated channels. (C) 1998 Elsevier Science B.V. All right s reserved.