Mechanical contractions and electrical activities of the fundic longitudinal and antral circular muscle fibers were investigated in order to elucidate topical differences of gastric motility. K-induced contracture was produced by exposure of muscle strips to high K Tyrode solution. Membrane potential and mechanical contraction were simultaneously recorded by conventional glass microelectrode method and single sucrose-gap technique. All experiments were performed in tris-buffered Tyrode solution which was aerated with 100% O₂ and kept 35℃. The results obtained were as follows: 1) The resting membrane potential of circular muscle cells in the antral region was about 10 mV more negative than that in the fundic region. 2) The membrane potentials decreased almost linearly as the extracellular KCI concentration was increased both in antral circular muscle cells and in fundic longitudinal muscle cells. 3) The thresholdal K concentration of K-contracture was 15 mM (membrane potential, -48 mV) for the antral circular muscle strip and 20 mM for the fundic longitudinal muscle cells. 4) The ratio of membrane permeability coefficient for Na⁺ and K⁺, P_Na/P_K(α) was 0.065 for antral circular muscle cells and was 0.108 for fundic longitudinal muscle cells. 5) K-contracture of antral and fundic smooth muscle strips showed the contracture composed of phasic and tonic components. The amplitude of the phasic component increased sigmoidally in a dose-dependent manner, whereas that of the tonic component was maximal at a concentration of 40 mM KCI and at the concentrations above or below 40 mM KCI the amplitude was reduced. 6) The inverse relationship between the amplitude of tonic component and extracellular KCI concentration in the range of 40 to 150 mM KCI was more prominent in the antral circular muscle strip than in the fundic longitudinal muscle strip, where the amplitude of the tonic component decreased less steeply and was maintained higher at the same high K concentrations. 7) The tonic component was totally dependent on the external Ca²⁺ and completely abolished by verapamil, while tile phasic component was far less dependent on the external Ca²⁺ and partially suppressed by verapamil. From the above results, the following conclusions could be made. 1) The phasic component of K-contracture is produced both by intracellular Ca²⁺ mobilization and by Ca²⁺-influx from outside, while the tonic component is generated and maintained by the Ca²⁺-influx through the potential-dependent Ca²⁺ channel. 2) The mechanism of reducing the free Ca²⁺ concentration in the myoplasm seems to be more developed in the antral circular muscle than in the fundic longitudinal muscle. 3) The lower resting membrane potential of the fundic longitudinal muscle cell reflects a relatively high P_Na/P_K ratio of about 0.108.