As the bladder fills to between 150 and 300 cc, stretch receptors in the bladder walls are activated, creating the sensation of the need to void. Parasympathetic pelvic nerves transmit this signal to the detrusor muscle, initiating bladder contractions. The higher the amount of urine in the bladder, the stronger the impulse to micturate. Sympathetic nerve innervation of the detrusor muscle and internal sphincter prevent premature parasympathetic stimulation and maintain the muscle tone of the internal sphincter. Higher level motor impulses inhibit the voiding reflex by constricting the urethral sphincter and delaying voiding. Generally, ignoring the urge to void prevents release of the external sphincter and neuron fatigue delays further stimulation of the voiding reflex arc for a few minutes to 1 hour. If the urge to void continues to be ignored, eventually bladder reflex contractions take over and cause involuntary voiding. Although micturition is generally under voluntary control, an overfilled or irritated bladder results in incontinence or the involuntary passage of urine.

By age 9 most children no longer experience enuresis, a condition during which the child has either voluntary or involuntary wetting either at night or during the day. Primary nocturnal enuresis (PNE), the most common type of enuresis, affects 5-7 million children over age 5 and occurs during
deep sleep cycles with the child never having a sustained period of dryness at night. This type of enuresis is often due to a developmental lag, small bladder capacity, and possible sleep apnea and/or night time vasopressin deficiency. Three times more boys than girls experience PNE, which may have a familial link. The familial risk factor for developing PNE is as follows: a 77% risk if both parents had PNE, a 44% risk if one parent had PNE, and a 15% risk if neither parent had PNE.