The hypothesis that changes in environmental 02 tension (pOi) could
affect the ionic conductances of dissociated type I cells of the carotid body was
tested. Cells were subjected to whole-cell patch clamp and ionic currents were
recorded in a control solution with normal pO 2 (pO~ = 150 mmHg) and 3-5 min
after exposure to the same solution with a lower pO,. Na and Ca currents were
unaffected by lowering pO, to 10 mmHg, however, in all cells studied (n = 42)
exposure to hypoxia produced a reversible reduction of the K current. In 14 cells
exposed to a pO 2 of 10 mmHg peak K current amplitude decreased to 35 +_ 8% of
the control value. The effect of low pO2 was independent of the internal Ca 2+
concentration and was observed in the absence of internal exogenous nucleotides.
Inhibition of K channel activity by hypoxia is a graded phenomenon and in the
range between 70 and 120 mmHg, which includes normal pO, values in arterial
blood, it is directly correlated with pO 2 levels. Low pO2 appeared to slow down the
activation time course of the K current but deactivation kinetics seemed to be
unaltered. Type I cells subjected to current clamp generate large Na- and Cadependent
action potentials repetitively. Exposure to low pO~ produces a 4-10
mV increase in the action potential amplitude and a faster depolarization rate of
pacemaker potentials, which leads to an increase in the firing frequency. Repolarization
rate of individual action potentials is, however, unaffected, or slightly
increased. The selective inhibition of K channel activity by low pO, is a phenomenon
without precedents in the literature that explains the chemoreceptive properties
of type I cells. The nature of the interaction of molecular O, with the K channel
protein is unknown, however, it is argued that a hemoglobin-like O, sensor,
perhaps coupled to a G protein, could be involved.
