This study examined the relationship between tracheal slowly adapting stretch receptor discharge and smooth muscle activity in a preparation in which the efferent supply to the airway was essentially intact. In 7 anesthetized, paralyzed, artificially ventilated dogs, smooth muscle activity was assessed by measuring the pressure of a water-filled cuff placed in the extrathoracic trachea and action potentials originating from 19 extrathoracic tracheal stretch receptors were recorded from the superior laryngeal nerve. Challenges were: hypercapnia (FI = 0.05 and FI = 0.10), hypoxia (FI = 0.10 and FI = 0.05) and asphyxia. Concurrent increases in cuff pressure and receptor discharge were present in 18 of the endings studied in response to all the challenges presented. The remaining receptor increased its rate of discharge with 10% CO2 and asphyxia; neither receptor discharge or cuff pressure increased with 5% CO2 and hypoxia. Following block of the recurrent laryngeal nerves, baseline values of both cuff pressure and receptor discharge, as well as the responses to asphyxia, decreased; any residual response was eliminated by atropine. Of the 17 receptors whose location could be precisely ascertained, 14 were found in the proximal third of the extrathoracic trachea, and the remaining 3 in the middle third. The temperature at which the nervous conduction was blocked was determined for 3 slowly adapting receptors; it ranged from 4.5 to 12.5 degrees C. Of 5 extrathoracic tracheal rapidly adapting receptors encountered during the course of the experiments, 3 were tested with asphyxia and found to be unaffected. This study shows that tracheal slowly adapting stretch receptors are activated by smooth muscle contractions reflexly induced by chemoreceptor stimulation.