The present study stems from our recent demonstration that a progressive increase in nasal intermittent positive-pressure ventilation (nIPPV) leads to active glottal closure in non-sedated, newborn lambs. The aim of the study was to determine whether the mechanisms involved in this glottal narrowing during nIPPV originate from upper airway receptors and/or from bronchopulmonary receptors. Two groups of newborn lambs were chronically instrumented for polysomnographic recording: the first group of 5 lambs underwent a two-step bilateral thoracic vagotomy using video-assisted thoracoscopic surgery (bilateral vagotomy group) while the second group comprised of 6 lambs underwent chronic laryngo-tracheal separation (isolated upper airway group). A few days later, polysomnographic recordings were performed to assess glottal muscle EMG during step-increases in nIPPV (volume control mode). Results show that active glottal narrowing does not develop when nIPPV is applied on the upper airways only, and that this narrowing is prevented by bilateral vagotomy when nIPPV is applied on intact airways. In conclusion, active glottal narrowing in response to increasing nIPPV originates from bronchopulmonary receptors.