We sought to find out the mechanism of vascular relaxation by extracellular K⁢ concentration ([K⁢]o) in the cerebral resistant arteriole from rabbit. Single cells were isolated from the cerebral resistant arteriole, and using voltage-clamp technique barium-sensitive K⁢ currents were recorded, and their characteristics were observed. Afterwards, the changes in membrane potential and currents through the membrane caused by the change in [K⁢]o was observed. In the smooth muscle cells of cerebral resistant arteriole, ion currents that are blocked by barium, 4-aminopyridine (4-AP), and tetraethylammonium (TEA) exist. Currents that were blocked by barium showed inward rectification. When the [K⁢]o were 6, 20, 60, and 140 mM, the reversal potentials were ⁣82.7⁑1.0, ⁣49.5⁑1.86, ⁣26⁑1.14, ⁣5.18⁑1.17 mV, respectively, and these values were almost identical to the calculated K⁢ equilibrium potential. The inhibition of barium-sensitive inward currents by barium depended on the membrane potential. At the membrane potentials of ⁣140, ⁣100, and ⁣60 mV, Kd values were 0.44, 1.19, and 4.82 μM, respectively. When [K⁢]o was elevated from 6 mM to 15 mM, membrane potential hyperpolarized to ⁣50 mV from ⁣40 mV. Hyperpolarization by K⁢ was inhibited by barium but not by ouabain. When the membrane potential was held at resting membrane potential and the [K⁢]o was elevated from 6 mM to 15 mM, outward currents increased; when elevated to 25 mM, inward currents increased. Fixing the membrane potential at resting membrane potential and comparing the barium-sensitive outward currents at [K⁢]o of 6 and 15 mM showed that the barium- sensitive outward current increased at 15 mM K⁢. From the above results the following were concluded. Barium-sensitive K⁢ channel activity increased when [K⁢]o is elevated and this leads to an increase in K⁢-outward current. Consequently, the membrane potential hyperpolarizes, leading to the relaxation of resistant arteries, and this is thought to contribute to an increase in the local blood flow of brain.