Although overactive bladder (OAB) and detrusor overactivity(DO) are not synonyms, they share therapeutic optionsand partially underlying physiopathological mechanisms.The aim of this overview is to give insight into new potentialtargets for the treatment of OAB and DO. A narrative reviewwas done in order to reach this goal. Ageing, pelvic floordisorders, hypersensitivity disorders, morphologic bladderchanges, neurological diseases, local inflammations, infections,tumors and bladder outlet obstruction may alter thenormal voluntary control of micturition, leading to OAB andDO. The main aim of pharmacotherapy is to restore normalcontrol of micturition, inhibiting the emerging pathologicalinvoluntary reflex mechanism. Therapeutic targets can befound at the levels of the urothelium, detrusor muscles, autonomicand afferent pathways, spinal cord and brain. Increasedexpression and/or sensitivity of urothelial-sensorymolecules that lead to afferent sensitization have been documentedas a possible pathogenesis of OAB. Targeting afferent pathways and/or bladder smooth muscles by modulatingactivity of ligand receptors and ion channels could beeffective to suppress OAB

Insight into New Potential Targets for the Treatment ofOveractive Bladder and Detrusor Overactivity. Urol Int. 2012 Jun 26:1-8

CERRUTO, Maria Angela;ARTIBANI, Walter;
2012

Abstract

Although overactive bladder (OAB) and detrusor overactivity(DO) are not synonyms, they share therapeutic optionsand partially underlying physiopathological mechanisms.The aim of this overview is to give insight into new potentialtargets for the treatment of OAB and DO. A narrative reviewwas done in order to reach this goal. Ageing, pelvic floordisorders, hypersensitivity disorders, morphologic bladderchanges, neurological diseases, local inflammations, infections,tumors and bladder outlet obstruction may alter thenormal voluntary control of micturition, leading to OAB andDO. The main aim of pharmacotherapy is to restore normalcontrol of micturition, inhibiting the emerging pathologicalinvoluntary reflex mechanism. Therapeutic targets can befound at the levels of the urothelium, detrusor muscles, autonomicand afferent pathways, spinal cord and brain. Increasedexpression and/or sensitivity of urothelial-sensorymolecules that lead to afferent sensitization have been documentedas a possible pathogenesis of OAB. Targeting afferent pathways and/or bladder smooth muscles by modulatingactivity of ligand receptors and ion channels could beeffective to suppress OAB
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11562/435049
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