Ionic currents on type-I cells of the rabbit carotid body measured by voltage-clamp experiments and the effect of hypoxia.

Type-I cells (from rabbit embryos) in primary culture were studied in voltage-clamp experiments using the whole cell arrangement of the patch-clamp technique. With a pipette solution containing 130 mM K+ and 3 mM Mg-ATP, large outward currents were obtained positive to a threshold of about -30 mV by clamping cells from -50 mV to different test pulses (-80 to 50 mV). Negative to -30 mV, the slope conductance was low (outward rectification). The outward currents were blocked by external Cs+ (5 mM) and partially blocked by TEA (5 mM) and Co2+ (1 mM). The initial part of the outward currents during depolarizing voltage pulses exhibited a transient Ca2+ inward component partially superimposed to a Ca2+-dependent outward current. Inward currents were further characterized by replacing K+ with Cs+ in the intra- and extracellular solution in order to minimize the outward component and by using 1.8 mM Ca2+, 10.8 mM Ca2+ or 10.8 mM Ba2+ as charge carrier. Slow-inactivating inward currents were recorded at test potentials ranging from -50 to 40 mV (holding potential -80 mV). The maximal amplitude, measured at 10 mV in the U-shaped I-V curve, amounted to 247 +/- 103 pA (n = 3). This inward current was insensitive to 3 microM TTX, but blocked by 1 mM Co2+ and partially reduced by 10 microM D600 and 3 microM PN 200-100. In contrast to outward currents, the inward currents exhibited a 'run-down' within about 10 min. Lowering the pO2 from the control of 150 Torr (air-gassed medium) to 28 Torr had no apparent effect on inward currents, but depressed reversibly outward currents by 28%. In conclusion, it is suggested that type-I cells possess voltage-activated K+ and Ca2+ channels which might be essential for chemoreception in the carotid body.