Pathophysiology of the urothelium and detrusor

Conventional wisdom now agrees that symptoms of overactivebladder (OAB) seem to emanate from an aberration in the voidingreflex, leading to involuntary detrusor contractions of eitherneurogenic or myogenic origin. Furthermore, emerging evidencealso encourages us to adopt a new paradigm, in which bladderurothelium is not just a simple barrier but an active contributor tobladder function. In this paradigm, aberration in sensory mechanismsemanating from the urothelium can also contribute to OABsymptoms through altered excitability of afferents in the bladderleading to increased bladder sensation. The high density of muscarinicreceptors expressed on urothelium can not only mediaterelease of urothelium-derived inhibitory factor, but can also be seenas an alternative site of action for antimuscarinic drugs. Urotheliumalso expresses a host of other receptors such as TRPV1 and TRPM8,whose functional role is yet to be confirmed.