This study was designed to characterize ureteral smooth muscle motility and also to study the effect of forskolin (FSK) and isoproterenol (ISO) on smooth muscle contractility in murine ureter. High K+ (50 mM) produced tonic contraction by 0.17±0.06 mN (n=19). Neuropeptide and neurotransmitters such as serotonin (5μM), histamine (20μM), and carbarchol (CCh, 10∼50μM) did not produce significant contraction. However, CCh (50μM) produced slow phasic contraction in the presence of 25 mM K+. Cyclopiazonic acid (CPA, 10μM), SR Ca2+-ATPase blocker, produced tonic contraction (0.07 mN). Meanwhile, inhibition of mitochondria by protonophore carbnylcyanide m-chlorophenylhydrazone (CCCP) also produced weak tonic contraction (0.01 mN). The possible involvement of K+ channels was also pursued. Tetraethyl ammonium chloride (TEA, 10 mM), glibenclamide (10μM) and quinidine (20 μM) which are known to block Ca2+-activated K+ channels (KCa channel), ATP-sensitive K+ channels (KATP) and nonselective K+ channel, respectively, did not elicit any significant effect. However, Ba2+ (1∼2 mM), blocker of inward rectifier K+ channels (KIR channel), produced phasic contraction in a reversible manner, which was blocked by 1μM nicardipine, a blocker of dehydropyridine-sensitive voltage-dependent L-type Ca2+ channels (VDCCL) in smooth muscle membrane. This Ba2+-induced phasic contraction was significantly enhanced by 10μM cyclopiazonic acid (CPA) in the frequency and amplitude. Finally, regulation of Ba2+-induced contraction was studied by FSK and ISO which are known as adenylyl cyclase activator and β-adrenergic receptor agonist, respectively. These drugs significantly suppressed the frequency and amplitude of Ba2+-induced contraction (p＜0.05). These results suggest that Ba2+ produces phasic contraction in murine ureteral smooth muscle which can be regulated by FSK and β-adrenergic stimulation.