Conventional wisdom now agrees that symptoms of overactive bladder (OAB) seem to emanate from an aberration in the voiding reflex, leading to involuntary detrusor contractions of either neurogenic or myogenic origin. Furthermore, emerging evidence also encourages us to adopt a new paradigm, in which bladder urothelium is not just a simple barrier but an active contributor to bladder function. In this paradigm, aberration in sensory mechanisms emanating from the urothelium can also contribute to OAB symptoms through altered excitability of afferents in the bladder leading to increased bladder sensation. The high density of muscarinic receptors expressed on urothelium can not only mediate release of urothelium-derived inhibitory factor, but can also be seen as an alternative site of action for antimuscarinic drugs. Urothelium also expresses a host of other receptors such as TRPV1 and TRPM8, whose functional role is yet to be confirmed.