The urinary bladder is a storage vessel for most of the time, when intravesical pressure remains low and the outflow resistance high. During voiding the reverse occurs when intravesical pressure rises and the outflow relaxes. The initiation and control of this change of function are carried out by a complex interplay between sensory mechanisms in the bladder, coordination of responses in the brain and sacral spinal cord and control over bladder and outflow muscle tone. Lower urinary tract (LUT) function can become disorganized and manifests commonly as overactive bladder (OAB) symptoms of urgency and frequency, with or without incontinence. The causes may be associated with neurogenic disorders, outflow tract obstruction or be idiopathic in the majority of cases. Several pharmaceutical approaches to manage OAB are possible which rely predominantly on manipulating mechanisms that generate detrusor contraction or reduce the magnitude of outflow obstruction. The introduction of successful agents requires knowledge of the mechanisms that generate contraction in LUT tissues both in the normal and overactive bladder. Several other potential approaches, such as reducing sensations from the urinary tract or modulating central nervous system pathways, are also briefly described.