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.