The study was undertaken to examine the possibility of the involvement of K<sup>+</sup> channels in the mechanism of relaxant-action of imipramine on the isolated canine detrusor muscle strips. Canine urinary bladder were isolated, and smooth muscle strips of 15 mm long and 2 mm wide from the mid-portion of anterior wall were made in the Tyrode solution of 0 ~ 4˚C. The strips were prepared for isometric myography in Biancani s isolated muscle chamber containing 1 ml of Tyrode solution, which was maintained with pH 7.4 by aeration with 95% O<Sub>2</sub>/5%CO<sub>2</sub> at 37˚C. RP 52891, a non-specific K<sup>+</sup> channel opener, concentration-dependently suppressed the spontaneous phasic contractions of the detrusor strips. Imipramine, a tricyclic antidepressant, also reduced the spontaneous contractions in a concentration-dependent manner. RP 52891 was more potent than imipramine(p<0.05), and Imipramine was more efficient than RP 52891(p<0.05).Procaine, a voltage-dependent K<sup>+</sup> channel blocker, glibenclamide, an ATP-dependent K<sup>+</sup> channel blocker, and apamin, a calcium-dependent K<sup>+</sup> channel blocker antagonized the relaxant effect of RP 52891, but not of imipramine. Imipramine reduced the electric field stimulation (EFS) -induced contractions concentration-dependently. None of the K<sup>+</sup> channel blockers employed for this study, procaine, glibenclamide or apamin antagonized the inhibitory action of imipramine on the EFS-induced contraction. These results suggest that in canine detrusor, the K<sup>+</sup> channels of the characteristics of voltage-dependent, ATP-dependent and/or calcium-dependent are exist, and the inhibitory action of imipramine on the contractility of the detrusor is independent from the K<sup>+</sup> channels.