The pharynx is a very important region for eliciting reflex swallowing. The region is innervated by the pharyngeal branch of the glossopharyngeal nerve (GPN-ph). Nitric oxide (NO) plays an important role in various physiological functions. The purpose of this study is to investigate NO's contribution to reflex swallowing evoked by electrical stimulation of the GPN-ph. Urethane-anesthetized rats were used. To evoke swallowing, repetitive electrical stimulation (10-20 µA, 10-20 Hz, 1.0 ms) was applied to the central cut end of the GPN-ph or superior laryngeal nerve (SLN). Swallowing was identified by the electromyographic activity of the mylohyoid muscle. The latency to the first swallow and the time interval between swallows were measured. Intravenous administration of N^G-nitro-L-arginine (L-NNA, 0.6 mg/kg), a non-selective inhibitor of NO synthase (NOS), extremely prolonged both the latency to and the time interval between swallows evoked by the GPN-ph. Intraperitoneal administration of 7-nitroindazole (7-NI, 5.0 mg/kg), a selective inhibitor of neuronal NOS, significantly prolonged the latency to and the time interval of swallowing evoked by the GPN-ph. Furthermore, an additional administration of L-arginine (a NO donor, 500 mg/kg) and sodium nitroprusside (a NO releaser, 0.6 mg/kg) restored the suppression of swallowing induced by the NOS inhibitor. SLN-evoked swallowing was suppressed by the administration of a higher dose of L-NNA (6.0 mg/kg). Swallowing evoked by water stimulation of the pharynx was also suppressed by L-NNA (0.6 mg/kg). These results suggest that NO plays an important role in signal processing for the initiation of reflex swallowing from the pharynx.