The present studies examined the involvement of the rostral ventral medulla (RVM) in modulating the visceromotor response (VMR) evoked by urinary bladder distension (UBD) in adult female rats. The VMR was indexed by electromyographic (EMG) responses of the abdominal external oblique muscle to UBD. Experiment 1 showed that the predominant effect of electrical stimulation of the RVM in normal rats was to produce intensity-dependent inhibition of the VMR (54% of sites sampled). Facilitatory, biphasic, or no effects were obtained at the remaining sites. Experiment 2 showed that RVM-induced inhibition of the VMR was significantly attenuated by intraperitoneal (i.p.) administration of naloxone but not saline vehicle. In experiment 3, we examined the effect of lesions of the RVM in rats with inflamed bladders because previous research has shown that an endogenous opioid inhibitory system is engaged by bladder inflammation. Electrolytic lesions of the RVM but not sham lesions of the RVM significantly increased the VMR to graded UBD in rats with augmented VMRs induced by prior inflammation of the bladder. The present data suggest that the RVM can inhibit the VMR to UBD, acting in part via an opioid-inhibitory system, and that bladder inflammation can recruit the RVM to produce a net inhibitory effect on the VMR to UBD. Perspective: Stimulation of the RVM resulted in inhibitory, facilitatory, and biphasic modulation of the visceromotor reflex to urinary bladder distension. Inhibitory effects of stimulation were attenuated by naloxone, and lesions of the RVM enhanced the VMR in rats with inflamed bladders. These data indicate an important role of the RVM in modulating bladder pain. © 2008 American Pain Society.