ABSTRACT
Overactive bladder (OAB) is characterized by the urinary symptoms of frequency, urgency, and
urge incontinence as a result of involuntary detrusor contractions during bladder filling. Such
contractions are predominantly under the control of the parasympathetic nervous system.
Acetylcholine released from the parasympathetic nerve endings activates the M3 muscarinic
receptors on the detrusor smooth muscles and modulates bladder contractility. Antimuscarinic
agents inhibit the binding of acetylcholine to the muscarinic receptors and suppress involuntary
detrusor contraction (1). Immediate-release oxybutynin was the gold standard in pharmacologic
treatment of OAB for almost three decades. Its antimuscarinic (M3) activity is nonselective for
the urinary bladder, resulting in significant systemic side effects, particularly dry mouth, that
limit its clinical utility (2,3). Even though alternative routes of administration of oxybutynin,
such as intravesical instillation (4-6), intravesical implant (7), and rectal suppository (8), are
available, oral agents remain the mainstay in treatment of OAB. Newer pharmacologic agents,
e.g., tolterodine, and modified drug delivery mechanisms for oxybutynin (e.g., extended-release
oxybutynin) have revolutionized the treatment of OAB (4,5).
