Role of Angiogenesis in Bladder Response to Partial Outlet Obstruction

Benign prostatic hyperplasia (BPH) is a disease that has its etiology in the abnormal growth of the adult human prostate gland that accompanies the aging process in men. The symptomatic presentation of this disease, however, is related largely to degenerative changes in the bladder that occur as a result of the increasing urethral resistance and partial bladder outlet obstruction (PBOO) caused by the growing prostate gland. BPH is characterized by bladder hypertrophy, significant decreases in urinary flow and compliance, presence of residual urine after voiding, voiding urgency and incontinence (). Obstructed bladder dysfunction secondary to BPH is a slow, progressive disease that is so strongly associated with human aging that it is an expected occurrence of the male aging process. Although the symptoms of BPH are usually not life threatening, they effect an extremely negative quality of life for men who suffer from them. However, many men delay seeking medical treatment for early BPH since bladder function can remain relatively normal as the hypertrophying bladder initially compensates for the progressive increase in urethral resistance caused by prostatic obstruction. The limited changes in micturition pressure and flow characteristics that occur during compensated function are not usually disabling enough to motivate seeking medical attention, which, often, is not sought until the symptoms become typical of advanced disease. Recent advances in detection methods enable identification of patients with significant BPH during compensation before the bladder becomes dysfunctional (decompensated). A more complete understanding of the disease processes that underlie the loss of bladder function associated with BPH might enable the development of treatments that better protect these early-stage BPH patients from the more debilitating aspects of the disease. This review updates the understanding of obstructive bladder dysfunction via the use of animal models.