For the pharmacological treatment of frequency, urgency and/or urge incontinence due to bladder overactivity, anticholinergics have been used as first-choice drugs. However, these drugs can exert severe side effects (accommodation paralysis, constipation, tachycardia, dry mouth and blurred vision) and some patients are refractory to their actions. Thus there is a need for new drug therapies with novel mechanisms of action. β-Adrenoceptors are found in the body of the bladder, where they mediate relaxation of the detrusor muscle. It has been reported that β3-adrenoceptor subtypes are predominantly present in the smooth muscles of bladder and urethra in the pig and human. Recently, β3-adrenoceptors have been reported to predominantly mediate relaxation of the bladder smooth muscle. However, the relaxant effects of β3-adrenoceptor agonists are half of those of (±)isoproterenol, a non-selective - adrenoceptor agonist, and the antagonist affinity of β3-adrenoceptor antagonists varies according to the drugs tested. It has also been suggested that both β2-, and β3-adrenoceptors are involved in relaxation of the human bladder, but the involvement of the β3-adrenoceptor may be greater than that of β2-adrenoceptor. Another possibility is that other -adrenoceptors, possibly β4-adrenoceptor and/or atypical β-adrenoceptors, may coexist and play a functional role in mediating the relaxation of the bladder.