Urethral closure mechanisms during abrupt elevation of intravesical pressure (P(ves)) were investigated. During sneezing, the middle urethral closing response was observed and it still remained after opening the abdomen. The middle urethral response was almost completely abolished after bilateral transection of somatic nerves innervating the external urethral sphincter and the pelvic floor muscles, while bilateral transection of both pelvic nerves and hypogastric nerves had no effects. Somatic nerve transection resulted in fluid leakage from the urethral orifice during sneezing. Passive increments of P(ves) for 120 seconds by elevating a saline reservoir connected to the bladder also induced the middle urethral closing response in rats with spinal cord transection at T8-T9. The response was totally abolished by cutting pelvic nerves bilaterally, and partially reduced after bilateral transection of pudendal nerves, nerves to pelvic floor muscles or hypogastric nerves. Electrical stimulation of abdominal muscles (ESAM) for 1 second elevated P(ves) in a stimulus-dependent manner in the spinal cord-transected rats, and the P(ves) rise was almost lost when the abdomen was opened. The P(ves) inducing fluid leakage from the urethral orifice was lowered in rats when pelvic nerves or somatic nerves were cut bilaterally, while transection of bilateral hypogastric nerves showed smaller effects. These results indicate that at least two kinds of urinary continence reflexes close the middle urethra during abrupt elevation of P(ves); one reflex observed during sneeze is preprogrammed so as to close the urethra automatically irrespective of bladder afferent activity, and the other reflex is triggered by bladder afferent excitation. During momentary stress events such as sneezing (<0.15 seconds) and ESAM (1 second), the striated muscles mainly contribute to the urethral closure, while during events for a relatively long period like passive P(ves) elevation for 120 seconds, both striated and smooth muscles are involved in the prevention of stress urinary incontinence.