Properties of a transient K+ current in chemoreceptor cells of rabbit carotid body.

1. Adult rabbit carotid body chemoreceptor cells, enzymatically dispersed and short‐term cultured, exhibit an inactivating outward K+ current that is reversibly inhibited by low PO2. In the present work we have characterized the biophysical and pharmacological properties of this current using the whole‐cell voltage clamp recording technique. 2. Inactivating current was recorded after blockage of Ca2+ currents with extracellular Co2+, Cd2+, or after complete washing out of Ca2+ channels. 3. The threshold of activation of this inactivating current was about ‐40 mV. Current activated very quickly (mean rise time 4.8 +/‐ 0.42 ms at +60 mV) but inactivated more slowly. Inactivation was well fitted by two exponentials with time constants of 79.7 +/‐ 6.6 and 824 +/‐ 42.8 ms (at +40 mV). The inactivation process showed a little voltage dependence. 4. The steady‐state inactivation was well fitted by a Boltzman function. Inactivation was fully removed at potentials negative to ‐80 mV and was complete at voltages near ‐10 mV; 50% inactivation occurred at ‐41 mV. 5. Recovery from inactivation had several components and was voltage dependent. Initial recovery was fast, but full recovery, even at ‐100 mV, required more than 30 s. 6. Inactivating current was selectively blocked by 4‐aminopyridine (4‐AP), in a dose‐dependent manner (IC50, 0.2 mM). The duration of chemoreceptor cells action potentials was augmented by 1 mM 4‐AP from 2.3 +/‐ 0.36 to 7.0 +/‐ 0.25 ms at 0 mV. Tetraethylamonium (TEA), at concentrations above 5 mM, blocked inactivating and non‐inactivating components of the whole K+ current. 7. Inactivating current was modulated by cyclic AMP (cAMP). Bath application of 2 mM dibutyryl cAMP reduced peak amplitude by 18.7 +/‐ 2.9% (at +30 mV) and slowed down the rise time of the current. The effect was not voltage dependent. Forskolin (10‐20 microM) also affected inactivating current, by accelerating the inactivation process. In the same preparations neither dibutyryl cAMP nor forskolin affected Ca2+ currents. 8. It is concluded that modulation of K+ channels by cAMP might play a physiological role potentiating the low PO2 inhibition of K+ channels.