Ca(2+)‐activated K+ channels in isolated type I cells of the neonatal rat carotid body.

1. Ca(2+)‐activated K+ (K+Ca) channels in neonatal rat type I carotid body cells were studied using single channel patch clamp techniques. In outside‐out patches, using symmetrical 120 mM [K+] solutions, channels were observed with a slope conductance of 190 pS and a reversal potential of 0 mV. Reducing [K+]o to 5 mM shifted the reversal potential as expected for a K(+)‐selective channel. 2. With 100 nM Ca2+ bathing the cytosolic aspect of patches, channel activity (number of active channels in a patch x open probability, NPo) increased with depolarization. NPo also increased with increasing ‘cytosolic’ [Ca2+] at a fixed membrane potential (0 mV). Using outside‐out patches, bath application of 20 or 100 nM charybdotoxin reduced NPo by > 85%. These data indicate the presence of K+Ca channels in type I cells. 3. At 0 mV, using solutions of identical composition (1 microM Ca2+ bathing the cytosolic aspect of the channels), NPo was higher in outside‐out patches than in inside‐out patches. NPo was greatest in recordings using the perforated‐vesicle technique. 4. Hypoxia and anoxia were without effect on K+Ca channels in outside‐out patches, but caused significant, reversible reductions of NPo in channels recorded in perforated vesicles. 5. The whole‐cell perforated‐patch technique was used to record membrane potential at 35‐37 degrees C. Hypoxia, anoxia and charybdotoxin all depolarized type I cells. 6. Our results suggest an important role for K+Ca channels in type I carotid body cells, and their activity in relation to a model for chemotransduction is discussed.