A novel oxygen‐sensitive potassium current in rat carotid body type I cells.

Abstract

1. Hypoxic stimuli depolarize carotid body type I cells causing voltage‐gated calcium influx. This study investigates the cause of this membrane depolarization. Isolated type I cells from neonatal (11‐16 day) rat carotid bodies were used in the experiments. 2. Tetraethylammonium (TEA; 10 mM), 1 and 5 mM 4‐aminopyridine (4‐AP) and 20 nM charybdotoxin all failed to evoke a significant rise in [Ca2+]i. Similarly, in perforated patch whole‐cell recordings, a combination of 10 mM TEA and 5 mM 4‐AP failed to depolarize type I cells. 3. In type I cells voltage clamped at ‐70 mV, anoxia evoked a small inward current under control conditions, but had no effect in the absence of pipette and extracellular K+. 4. Anoxia decreased resting membrane conductance from 322 to 131 pS. The anoxia‐sensitive current (measured using voltage ramps from ‐100 to ‐40 mV) had a reversal potential of ‐89 mV in 4.5 mM Ko+ and ‐66 mV in 20 mM Ko+, indicating that this current was carried principally by potassium ions. In contrast, 10 mM TEA + 5 mM 4‐AP had little effect on the current‐voltage relationship of the cells over the same range. 5. This O2‐sensitive K+ conductance showed only mild outward rectification over the range ‐90 to +30 mV, which could be approximated by the Goldman‐Hodgkin‐Katz current equation. In addition, there was no time‐dependent activation or inactivation of membrane currents elicited by voltage steps in the range ‐100 to ‐30 mV. 6. The O2‐sensitive K+ conductance was inhibited by graded reductions in PO2 to 40 Torr and below, with a K1/2 of about 12 Torr. 7. The data suggest that hypoxia depolarizes type I cells principally through the inhibition of a small voltage‐insensitive resting (or background) K+ conductance, and not through the inhibition of voltage‐gated TEA and 4‐AP‐sensitive K+ channels (e.g. maxi‐K or KO2 channels), as has been previously suggested.