This study investigated the role of the hypogastric nerve and β-adrenergic mechanisms in the inhibition of nociceptive and non-nociceptive reflex bladder activity induced by pudendal nerve stimulation (PNS). In α-chloralose anesthetized cats the non-nociceptive reflex bladder activity was induced by slowly infusing saline into the bladder, while the nociceptive reflex bladder activity was induced by replacing saline with 0.25% acetic acid (AA) to irritate the bladder. PNS was applied at multiple threshold (T) intensities for inducing anal sphincter twitching. During saline infusion, PNS at 2T and 4T significantly (p<0.01) increased bladder capacity to 184.7±12.6% and 214.5±10.4% of the control capacity. Propranolol (3 mg/kg, i.v.) had no effect on PNS inhibition, but MTEP (1-3 mg/kg, i.v.) significantly (p<0.05) reduced the inhibition. During AA irritation, the control bladder capacity was significantly (p<0.05) reduced to about 22% of saline control capacity. PNS at 2T and 4T significantly (p<0.01) increased bladder capacity to 406.8±47% and 415.8±46% of the AA control capacity. Propranolol significantly (p<0.05) reduced the bladder capacity to 276.3%±53.2% (at 2T PNS) and 266.5±72.4% (at 4T PNS) of AA control capacity, while MTEP removed the residual PNS inhibition. Bilateral transection of the hypogastric nerves produced an effect similar to that produced by propranolol. This study indicates that the hypogastric nerve and a β-adrenergic mechanism in the detrusor play an important role in PNS inhibition of nociceptive but not non-nociceptive reflex bladder activity. In addition to this peripheral mechanism, a CNS mechanism involving metabotropic glutamate 5 receptors also has a role in PNS inhibition.