In the present study, we tried to determine what effects were induced by β-adrenoceptor agonists on 40mM KCl-induced rhythmic contraction and to clarify which β-adrenoceptor subtypes are involved in the regulation of ureter motility in the guinea pig by using in vitro functional analysis. 40mM KCl-induced rhythmic contraction was abolished by papaverine (10^-6M), nicardipine (10^-5M) and cromakalim (10^-5M), but was not influenced by atropine (10^-6M). Isoprenaline decreased the amplitude, and changed the pattern of 40mM KCl-induced rhythmic contraction in concentration-dependent manner. These results suggest the posslbility that the stimulation of β-adrenoceptors may regulate the ureteral peristalsis. Salbutamol (selective β₂-AR agonist) and CGP12177 (β_{1, 2}-AR antagonist and β₃-AR partial agonist) were also effective in decreasing the amplitude and changing the pattern of the rhythmic contraction. The pD₂ values of agonists were 7.57 (isoprenaline), 5.80 (CGP12177) and 7.63 (salbutamol), respectively. The concentration-response curves of isoprenaline and salbutamol were rightward shifted by the presence of propranolol, and the apparent pA₂ values for propranolol against isoprenaline and salbutamol were 7.12 and 6.29, respectively. These results suggest that inhibition for 40mM KCl-induced rhythmic contraction of the ureter by isoprenaline and salbutamol mediated mainly via atypical β-adrenoceptor subtype.