ABSTRACT
The lower urinary tract (lut) is controlled by a complex interplay between the central (cns) and peripheral nervous systems and local regulatory factors [1]. Malfunction at various levels may result in micturition disorders, which roughly can be classified as disturbances of storage or emptying. Failure to store urine may lead to various forms of incontinence (mainly urgency and stress incontinence), and failure to empty to urinary retention. Lower urinary tract symptoms (luts) include storage, voiding, and postmicturition symptoms. Storage symptoms (urgency, frequency with and without incontinence, nocturia) form the overactive bladder (oab) syndrome, which may or may not be associated with involuntary detrusor contractions demonstrated by cystometry (detrusor overactivity [DO]). Pharmacological treatment of urinary incontinence (ui) is a main option, and several drugs with different modes and sites of action have been tried [2–4]. However, to be able to optimize existing therapies and to identify suitable new targets for treatment, knowledge about the mechanisms of micturition is necessary.
