The effects of hypercapnia and isocapnic hypoxia on the respiratory movements of the vocal cords were assessed in anesthetized cats before and after bilateral vagotomy. In vagally intact animals, these stimuli lowered laryngeal airflow resistance by increasing both inspiratory and expiratory vocal cord abduction through activation of the posterior cricoarytenoid (PCA) muscle. Vagotomy had little effect on the laryngeal response to hypercapnia, but led to an increase in expiratory laryngeal resistance during hypoxia owing to a decrease in expiratory PCA activity. Carotid arterial NaCN injection caused a similar increase in expiratory laryngeal resistance after vagotomy, suggesting that the response to hypoxia was due to carotid chemoreceptor stimulation. The laryngeal responses to both hypoxia and NaCN were abolished by carotid sinus nerve section. The results indicate that afferents from central and peripheral chemoreceptors have different effects on the activity of motoneurons governing vocal cord movements during expiration. Vagal afferent feedback serves to maintain the patency of the laryngeal airway during hypoxia.