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Underlying Mechanisms of Detrusor Overactivity Following Bladder Outlet Obstruction
Author(s) -
KIM Joon Chul
Publication year - 2009
Publication title -
luts: lower urinary tract symptoms
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.451
H-Index - 15
eISSN - 1757-5672
pISSN - 1757-5664
DOI - 10.1111/j.1757-5672.2009.00020.x
Subject(s) - urothelium , bladder outlet obstruction , overactive bladder , trpv1 , purinergic receptor , pathophysiology , urinary bladder , receptor , detrusor muscle , transient receptor potential channel , endocrinology , neuroscience , medicine , chemistry , microbiology and biotechnology , biology , pathology , prostate , alternative medicine , cancer
Several studies have demonstrated that many pathophysiological mechanisms can contribute to the development of detrusor overactivity associated with bladder outlet obstruction (BOO). BOO induces a rapid hypertrophy characterized by increased bladder mass and collagen deposition, which play an important role in the intercellular transmission of active force. Detrusor overactivity may be attributed to an increase in afferent activation and neuroplasticity, and nerve growth factor and transient receptor potential vanilloid 1 (TRPV1) are involved in this process. The change in the urothelium and urothelial signaling can also lead to increased afferent nerve activity and contribute to irritative symptoms accompanying outlet obstruction. This is because afferent neuronal fibers are located near the urothelium, and urothelial cells release neurotransmitters in response to bladder wall stretching, as a neuron‐like property. Recently, it has been reported that intercellular communication through gap junctions might participate in the pathophysiology of detrusor overactivity associated with BOO, and these gap junction proteins are differentially regulated during BOO. In addition, the changes in several receptors, such as the muscarinic and purinergic receptors, could have a role in mediating the afferent sensory responses and development of detrusor overactivity following BOO.