The centrally generated respiratory rhythm is under strong modulation by peripheral information, such as that from the slowly adapting pulmonary stretch receptors (SA-PSRs) conveyed via the vagus nerve. We have already demonstrated that vagal afferent stimulation at a low frequency (5-40 Hz), or holding the lung volume at the end-expiratory level (no-inflation test) prevents spontaneous termination of the inspiratory (I) phase or initiates I activity in anaesthetized rabbits in which the NMDA receptors (NMDA-Rs) are pharmacologically blocked. Here we show that this I-promoting vagal reflex also becomes manifest in animals where the pontine respiratory groups are ablated. Following lesions of the rostral dorsolateral pons, including the nucleus parabrachialis medialis and Kölliker-Fuse nucleus, with radio-frequency current or local injection of kainic acid, low-frequency stimulation of the vagus nerve and the no-inflation test significantly prolonged the I phase in a manner highly similar to that observed in rabbits with NMDA-R block. Brief stimuli at low frequency during the mid-expiratory (E) phase evoked I discharge with a latency significantly smaller and less variable than that before the lesions. It is concluded that low-frequency input from the SA-PSR suppresses I-to-E phase transition and promotes central I activity when the medullary respiratory network is released from pontine influence, which involves NMDA-R-mediated signalling.