This study was carried out to define some of the cellular ionic mechanisms controlling cerebral arterial muscle. Muscle cells were enzymatically dispersed from cat cerebral arteries. Cells were dialyzed and voltage-clamped using patch pipettes and whole-cell currents measured. Using pipette solutions allowing us to record K + currents we identified an outward current elicited by depolarizing voltage steps beyond -20 inV. This outward current exhibited properties of delayed outward rectification having a peak macroscopic current at +90 mV of 504+_236 pA. The current was sensitive to 4-aminopyridine, but was sensitive to tetraethylammonium only at very high doses. When CsC1 was in the recording pipette, macroscopic outward currents could not be recorded. Variations in the extracellular Ca 2+ concentration from 0.5 to 5.0 mM had no effect on current amplitude or voltage dependence; similarly the Ca 2+ channel blockers nifedipine and Mn 2+ were without effect on this outward current. The current inactivated slowly with no decay seen even with 3-s command pulses. Repetitive voltage pulses from -60 to + 90 mV at a frequency of 1 Hz resulted in "cumulative reduction", depressing peak current by 60% after ten pulses. Upon reduction of pH from 7.43 to 7.20 we observed a 350~ increase in peak outward current in 7 of 12 cells studied in this regard. Thus, the cellular mechanism responsible for cerebral vascular dilation to acidosis and/or hypercapnia may involve an increase in outward K Β§ current.