Bladder dysfunction

Detrusor overactivity

Loss of compliance

Structural or physiologic changes in smooth muscle


Shift in myosin isoform ratio Shift to anerobic metabolism Impaired calcium mobilization

Elevated PVR Recurrent UTI Urinary retention

Denervation supersensitivity NGF-mediated nerve growth Altered Na-K membrane pump Altered intercellular junctions

Frequency Urgency Urge incontinence

Increased collagen deposition Altered collagen subtype ratio

Elevated resting Pdet ? Diminished bladder capacity Potential renal damage

Figure 9 The effect of partial bladder outlet obstruction on bladder dysfunction: K, potassium; Na, sodium; NGF, nerve growth factor; Pdet, detrusor pressure; PVR, postvoid residue; UTI, urinary tract infection. (Reproduced with kind permission from Lemack, G. E.; McConnell, J. D. Textbook of Benign Prostatic Hyperplasia, 2nd ed.; Taylor & Francis: London, 2005, pp 113-115 © Taylor & Francis.) Impact on Lower Urinary Tract Symptoms

It has been established that LUTS usually occur as a result of BPH-related bladder outlet obstruction (BOO). More recently, there is evidence to suggest that once present, BOO can induce overexpression of epithelial sodium channels (ENaCs) in the bladder (as shown by immunofluorescent staining and real-time quantitative reverse transcriptase-polymerase chain reaction), which has been shown to be associated with urinary storage symptoms. It is also thought that overexpression of ENaCs by BOO could be associated with the detrusor instability observed in BPH possibly via an effect on the bladder afferent activity.28

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