Our studies with the animal model show that arterial stenosis and insufficiency--a common problem in the elderly--lead to marked changes in bladder structure and function. Moderate chronic ischemia leads to functional and structural changes quite different from those caused by severe chronic ischemia. The extent of histopathophysiologic changes in the chronically ischemic bladder depends on the degree of arterial stenotic disease and the severity of bladder ischemia. Histopathophysiologic changes in our animal model appear to be similar in many ways to those reported in clinical detrusor instability. This would suggest that vascular risk factors and ensuing arterial obstructive disease and bladder ischemia might play an important role in the development of bladder dysfunction. A better understanding of the involvement of vascular risk factors in voiding dysfunction may lead to more accurate assessment of LUTS, precise patient selection for prostatectomy, and the development of prophylactic strategies and newer treatment.