Excitation of both slowly and rapidly adapting pulmonary stretch receptors attenuates tachypnea induced by ammonia.

To elucidate the mechanism of attenuating the ammonia-induced tachypnea, the present study examined the discharge patterns and rates of slowly adapting pulmonary stretch receptors (SARs) and rapidly adapting pulmonary stretch receptors (RARs) in relation to the change in respiration produced by ammonia inhalation in anesthetized, spontaneously breathing rabbits. Extracellular action potentials of these two receptors were recorded at the peripheral cut-end of the left vagus nerve. A prolongation of expiration following ammonia inhalation occurred during the discharge of receptors increased continuously, particularly when the level of the discharge rate during expiration reached to approximately 20-fold, and under such circumstances the respiratory response was regularly associated with gasps. On the other hand, RARs increased their activity during only inspiration; this increased activity correlated with augmentation of inspiration. Furthermore, the prolongating effect of expiration due to ammonia inhalation was not observed after surgical denervation of the remaining right vagus nerve. These results suggest that vigorous stimulation of the SAR activity induced by ammonia inhalation can elicit a prolongation of expiration possibly resulting from augmentation of the Hering-Breuer inflation reflex and that augmentation of the increased RAR activity after ammonia inhalation counteracts the Hering-Breuer inflation reflex to shorten inspiration. Therefore, it is conceivable that strong stimulation of the SAR activity after ammonia inhalation counteracts the ammonia-induced tachypnea.