Partial bladder outlet obstruction induced by partial ligation of the urethra has widely been used as a model of obstructed bladder, although bladder dysfunction is caused by not always mechanical but functional obstruction. Previous studies have demonstrated that long-term deficiency of nitric oxide (NO) can produce detrusor overactivity. However, the pathophysiologic features of this model have not been well defined. The aim of this study was to examine the characteristics of chronic NO deficiency-induced urinary bladder dysfunction in vivo and in vitro. Rats were divided into two groups. L-NAME was given p.o. for 4 w. In L-NAME group, blood pressure rose, and plasma nitrite/nitrate levels decreased compared to control group. Chronic L-NAME treatment caused frequent bladder contractions, increased residual volume and rises in urethral pressure. In addition, L-NAME group exhibited diminished carbachol-induced contraction of isolated detrusor strips and upregulation of an ischemic marker and a gap junction protein in the bladder. These data suggest that chronic L-NAME treatment produces bladder hyperactivity with residual urine, and may be a useful approach to simulating functionally obstructed bladder.