Pathophysiology of the urothelium and detrusor

Authors

  • Pradeep Tyagi Associate Professor, William Beaumont School of Medicine, Royal Oak, MI

DOI:

https://doi.org/10.5489/cuaj.709

Abstract

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.

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Author Biography

Pradeep Tyagi, Associate Professor, William Beaumont School of Medicine, Royal Oak, MI

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How to Cite

Tyagi, P. (2013). Pathophysiology of the urothelium and detrusor. Canadian Urological Association Journal, 5(5-S2), S128-S130. https://doi.org/10.5489/cuaj.709

Issue

Vol. 5 No. 5-S2 (2011): October

Section

Review

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