Urinary continence is maintained through coordination of electrical (nervous) and mechanical (muscles, ligaments and other structures) systems in the body. During micturition, the central nervous system sends a signal to the detrusor and sphincter muscles to coordinate voiding. Pathological problems can undermine either of the two systems and result in urinary incontinence (UI). Thirteen million people in the United States live with UI. Clinical treatments to date are largely mechanical in nature, restoring function through surgical interventions. However, electrically-based treatments, such as electric stimulation, offer a promising alternative. Here we investigate the utility of electrical stimulation of the periurethral neuromusculature to reduce voiding contractions in well-controlled animal experiments. Female Sprague Dawley rats were anesthetized with a ketamine/xylazine/acepromazine cocktail and the bladder was catheterized through a small incision in the bladder dome and was infused with saline. Continuous filling of the bladder triggered related cycles of voiding which was identified through bladder pressure increases and visual urination. The pubic symphysis bone was cut to expose the urethra and a stimulating electrode was placed in the periurethral region. The electrical stimulation parameters were 2.8 mA of current, 200 us pluses, and 20 Hz. The electrical stimulation was done in fifteen minute intervals. Statistically, the rats without electrical stimulation have an average contraction period of 63.1 sec (+/– 31.3 sec) and the rats with electrical stimulation have an average contraction period of 97.2 sec (+/– 43.0 sec). The results showed that the electrical stimulation of the periurethral neuromusculature in the group revealed 54.0% increase in average contraction period and decrease in voiding frequency. Electrical stimulation of the periurethral neuromusculature increases the voiding interval and void volume for the rats. This suggests the existence of an external urinary sphincter to the bladder inhibitory pathway and supports periurethral neuromusculature stimulation as an alternative to spinal nerve stimulation for the treatment of bladder overactivity.