Abstract
Overactive bladder (OAB) syndrome, which is characterized by a complex of storage symptoms (urinary urgency, frequency, nocturia and urgency incontinence) is highly prevalent in the general population; it causes significant distress to patients in terms of their psychosocial and physical functioning. Muscarinic receptors of bladder smooth muscles are involved in both normal and involuntary detrusor contraction (detrusor overactivity). Up-regulation of the muscarinic receptor function may contribute to the pathophysiology of OAB. In addition, several reports have suggested that various stimulations release many substances (ATP, prostaglandins, nitric oxide and acetylcholine) from bladder urothelium, which contribute to the pathophysiology of the increased bladder sensation, OAB symptoms and detrusor overactivity. The bladder urothelium also prossesses the non-neuronal cholinergic system and high density of muscarinic receptors. The roles and functions of the non-neuronal cholinergic system in OAB are currently under evaluation. Furthermore, new action sites of anticholinergic drugs have also been proposed. In this review, in addition to the pathophysiology of detrusor overactivity and OAB, the pharmacotherapy for OAB is discussed.
