title: Recent developments in the management of detrusor overactivity.
abstract: OBJECTIVE
  Detrusor overactivity is a relatively common yet embarrassing symptom complex with significant impact on quality of life. The mainstay of current pharmacological treatment involves use of muscarinic receptor antagonists, but their therapeutic efficacy is limited by their troublesome side effects resulting in the non-continuance of treatment in a significant number of patients. Therefore, the development of new drugs can proceed by targeting alternative pathways affecting detrusor overactivity. In this article, the pharmacological basis for the current therapeutic alternatives for managing detrusor overactivity and possible future developments are discussed.
  
  
  RESULTS
  It is clear that far from being a passive container for urine, the urothelium is a crucial part of the bladder. Its functions are complex, dynamic and important, and only now becoming understood. The release of ATP from urothelium in response to distension and its action on P2X receptors resulting in activating both motor and sensory neurons is being increasingly recognised. In the normal bladder, muscarinic receptor stimulation produces the main part of detrusor contraction. However, in functionally abnormal bladders, a non-cholinergic activation via the purinergic receptors may occur. The central nervous mechanisms controlling the micturition reflex have also recently attracted attention.
  
  
  CONCLUSIONS
  Recent research has suggested that several transmitters may modulate voiding. However, few drugs with clinical benefits have been developed so far. Present treatments for overactive bladders have significant non-compliance rates. Hopefully, future research will lead to drugs with greater therapeutic benefits and better tolerance.
authors.affiliation: Department of Urology, Royal Hallamshire Hospital, Sheffield, UK.
authors.forename: Vivek
authors.initials: V
authors.lastname: Kumar
authors.forename: Lucy
authors.initials: L
authors.lastname: Templeman
authors.forename: Christopher R
authors.initials: CR
authors.lastname: Chapple
authors.forename: Russell
authors.initials: R
authors.lastname: Chess-Williams
mesh_terms: D000318:Adrenergic beta-Agonists / Q000627:therapeutic use; D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D019274:Botulinum Toxins, Type A / Q000627:therapeutic use; D002211:Capsaicin / Q000627:therapeutic use; D004224:Diterpenes / Q000627:therapeutic use; D005260:Female; D006801:Humans; D018727:Muscarinic Antagonists / Q000627:therapeutic use; D015221:Potassium Channels / Q000187:drug effects; D015320:Tachykinins / Q000627:therapeutic use; D001743:Urinary Bladder / Q000187:drug effects / Q000294:innervation / Q000503:physiopathology*; D001750:Urinary Bladder, Neurogenic / Q000188:drug therapy* / Q000503:physiopathology; D014554:Urination / Q000502:physiology
chemical_list: D000318:Adrenergic beta-Agonists; D000319:Adrenergic beta-Antagonists; D004224:Diterpenes; D018727:Muscarinic Antagonists; D015221:Potassium Channels; D015320:Tachykinins; C024353:resiniferatoxin; D019274:Botulinum Toxins, Type A; D002211:Capsaicin