[K]o can be increased under a variety of conditions including subarachnoid hemorrhage. The increase of [K]o in the range of 5∼15 mM may affect tensions of blood vessels and cause relaxation of agonist-induced precontracted vascular smooth muscle (K-induced relaxation). In this study, effect of the increase in extracellular K concentration on the agonist-induced contractions of various arteries including resistant arteries of rabbit was examined, using home-made Mulvany-type myograph. Extracellular K was increased in three different ways; from initial 1 to 3 mM, from initial 3 to 6 mM, or from initial 6 to 12 mM. In superior mesenteric arteries, the relaxation induced by extracellular K elevation from initial 6 to 12 mM was the most prominent among the relaxations induced by the elevations in three different ways. In cerebral arteries, the most prominent relaxation was produced by the elevation of extracellular K from initial 1 to 3 mM and a slight relaxation was provoked by the elevation from initial 6 to 12 mM. In superior mesenteric arteries, K-induced relaxation by the elevation from initial 6 to 12 mM was blocked by Ba2 (30 μM) and the relaxation by the elevation from 1 to 3 mM or from 3 to 6 mM was not blocked by Ba2. In cerebral arteries, however, K-induced relaxation by the elevation from initial 3 to 6 mM was blocked by Ba2, whereas the relaxation by the elevation from 1 to 3 mM was not blocked by Ba2. Ouabain inhibited all of the relaxations induced by the extracellular K elevations in three different ways. In cerebral arteries, when extracellular K was increased to 14 mM with 2 or 3 mM increments, almost complete relaxation was induced at 1 or 3 mM of initial K concentration and slight relaxation occurred at 6 mM. TEA did not inhibit Ba2-sensitive relaxation at all and NMMA or endothelial removal did not inhibit K-induced relaxation. Most conduit arteries such as aorta, carotid artery, and renal artery were not relaxed by the elevation of extracellular K. Among conduit arteries, trunk of superior mesenteric artery and basilar artery were relaxed by the elevations of [K]o. These data suggest that K-induced relaxation has two independent components, Ba2-sensitive and Ba2-insensitive one and there are different mechanisms for K-induced relaxation in various arteries.