The urinary bladder has physiological functions of urine storage and voluntary micturition. These functions are regulated through by complex interaction between neural and myogenic mechanisms. Alterations in these mechanisms may cause dysfunction of bladder such as overactive bladder. Overactive bladder is a common condition characterised by the symptoms of urinary frequency, urgency and incontinence. Acetylcholine, a cholinergic agent, causes the initiation of micturition via muscarinic receptors, especially M3 receptors and to some extent M2. Antimuscarinic drugs are generally thought to exert their therapeutic action on detrusor overactivity by reducing the ability of the detrusor muscle to contract. Although atropin can almost completely block parasympathetic-nerve mediated contraction of human detrusor muscle, there is still atropine-resistant response resulted from purinergic signaling in human detrusor muscle. There is also evidence that abnormal purinergic transmission in patients with detrusor instability. It was also shown that abnormal purinergic transmission may cause the symptoms seen in overactive bladder and urothelial ATP release is augmented under pathophysiogical conditions. Also, in recent years, there is further evidence that a third subtype, beta3-adrenergic receptor, mediates relaxation in human detrusor muscle and discusses the potential use of beta3-adrenergic receptor agonists for the treatment of overactive bladder. It was also shown that phosphodiesterase inhibitors such as rolipram induced a significant decrease on the cyclophosphamid-induced spontaneous contractions. Thiols also may play a differential role in regulating bladder contractility depending on age. Based on these recent advances, ATP, purinergic receptors, beta3 adrenergic receptors, phosphodiesterase and thiols are become to be new therapeutic targets to management of detrusor dysfunction.