Studies revealed both structural and functional alterations in bladders from patients with LUTS symptoms or animals with experimentally induced bladder dysfunction .
In particular , the urothelium and the suburothelial space , containing afferent nerve fibres and interstitial cells , have been found to form a functional unit that is essential in the process of bladder function .
Various imbalances within this suburothelial complex have been identified as significant contributors to the generation of storage LUTS , along with potential abnormalities of central function
CONTEXT The focus of clinical underst and ing and management of male storage lower urinary tract symptoms ( LUTS ) has shifted from the prostate to the bladder .
This is mirrored by an increasing body of experimental evidence suggesting that the bladder is the central organ in the pathogenesis of LUTS .
OBJECTIVE A systematic review of the literature available on pathophysiologic aspects of storage LUTS .
Parallel changes in bladder suburothelial vanilloid receptor TRPV1 and pan‐neuronal marker PGP9.5 immunoreactivity in patients with neurogenic detrusor overactivity after intravesical resiniferatoxin treatment
To compare PGP9.5 and transient receptor potential vanilloid receptor ( TRPV1 ) suburothelial immunoreactivity between controls and patients with spinal neurogenic detrusor overactivity ( NDO ) before and after treatment with intravesical resiniferatoxin , as suburothelial PGP9.5‐staining nerve fibres decrease in patients with spinal NDO who respond to intravesical capsaicin , and TRPV1 is present on these suburothelial nerve fibres in normal and overactive human urinary bladder
Studies revealed both structural and functional alterations in bladders from patients with LUTS symptoms or animals with experimentally induced bladder dysfunction .
In particular , the urothelium and the suburothelial space , containing afferent nerve fibres and interstitial cells , have been found to form a functional unit that is essential in the process of bladder function .
Various imbalances within this suburothelial complex have been identified as significant contributors to the generation of storage LUTS , along with potential abnormalities of central function
CONTEXT The focus of clinical underst and ing and management of male storage lower urinary tract symptoms ( LUTS ) has shifted from the prostate to the bladder .
This is mirrored by an increasing body of experimental evidence suggesting that the bladder is the central organ in the pathogenesis of LUTS .
OBJECTIVE A systematic review of the literature available on pathophysiologic aspects of storage LUTS .