cholecalciferol and Urinary-Bladder--Neurogenic

Overactive bladder (OAB) signifies the presence of urinary urgency and can have major effects on quality of life and social functioning. Standard antimuscarinic drugs have good initial response rates but substantial adverse effects and long-term compliance problems.. To review the complexities of the mechanisms underlying OAB and the current drugs available for treating its symptoms.. The literature was reviewed to define current therapies and drugs in clinical trials. Articles were identified by means of a computerised PubMed and Cochrane Library search (using the following keywords: overactive bladder, detrusor overactivity, urgency and bladder), supported by a search of the PharmaProjects database.. New drug classes, such as beta-3 adrenergic agonists, may work by reducing contractility or excitability of bladder muscle. Moderation of afferent activity may allow improved OAB symptoms, with lower risk of affecting voiding function. Agents acting on the CNS could influence OAB favourably, but target selection and adverse effects are an issue. The recognition of the functional contribution of the urothelium and the diversity of nerve transmitters has sparked interest in both peripheral and central modulation of OAB pathophysiology.

Topics: Adrenergic alpha-Antagonists; Adrenergic beta-Agonists; Botulinum Toxins, Type A; Calcium Channel Blockers; Cholecalciferol; Electric Stimulation Therapy; Humans; Muscarinic Antagonists; Parasympatholytics; Potassium Channels; Serotonin Antagonists; Urinary Bladder, Neurogenic; Urinary Bladder, Overactive