Effects of hypoxia induced by Na2S2O4 on intracellular calcium and resting potential of mouse glomus cells

Isolated and cultured glomus cells, obtained from mouse carotid bodies, were superfused with Ham's F-12 equilibrated with air (mean PO2, 119 Torr; altitude 1350 m). [Ca2+](o) was 3.0 mM. In one experimental series, dual cell penetrations with microelectrodes measured intracellular calcium ([Ca2+](i)) and the resting potential(E-m). In another series, [Ca2+](i) was measured with Indo-1/AM, dissolved in DMSO. Normoxic cells had a mean E-m of -42.4 mV and [Ca2+](i) was about 80 nM (measured with both methods). The calculated calcium equilibrium potential (E-Ca) was 137 +/- 0.74 mV. Hypoxia, induced by Na2SO4 1 mM, reduced pO(2) to 10-14 Torr. This effect was accompanied by cell depolarization to -19.1 mV. Hypoxia increased [Ca2+](i) to 231 nM when detected with Ca-Sensitive microelectrodes. but only to 130.2 nM when measured with Indo-1/AM. Calcium increases were preceded by decreases in [Ca2+](i), which also were more pronounced with microelectrode measurements. CoCl2 1 mM blocked the hypoxic [Ca2+](i) increase and exaggerated the decreases in [Ca2+](i). Correlations between Delta E-m and Delta[Ca2+](i) during hypoxia were significant (p < 0.05) in 19% of the cells. But. in 29% of them significance was at the p < 0.1 level. In the rest (52%), there was no correlation between these parameters. Thus, voltage-gated calcium channels are rare in mouse glomus cells. Their activation by depolarization cannot explain the two to threefold increase in [Ca2+](i) seen during hypoxia. More likely, [Ca2+](i) increase may be due to hypoxic inactivation of a Ca-Mg ATPase transport system across the cell membrane. The blunting of hypoxic [Ca2+](i) increase, seen in Indo-1/AM experiments, is probably due to its solvent (DMSO), which also depresses hypoxic cell depolarization. (C) 1999 Elsevier Science B.V. All rights reserved.