Changes in laryngeal resistance to airflow have been measured in cats during spontaneous breathing through the larynx, and while the larynx was isolated in 8itU with constant airflow. Intravenous injections of veratrine resulted in apnoea with a large increase in laryngeal resistance, followed by expiratory increases in laryngeal resistance. These responses were abolished by cutting the vagi in the chest and were absent on injection of veratrine into the left atrium, which established the pulmonary nerves as the main afferent pathway for the reflex. It is concluded that stimulation of pulmonary receptors constricts the larynx.Many papers deal with the veratrum alkaloids and their influence on the cardiovascular and respiratory systems [Dawes and Comroe, 1954] and the hypotension, bradycardia and arrest of breathing induced by intravenous injections of veratrum alkaloids, classically described by Bezold and Hirt [1867], are known to depend on vagal reflexes. The inhibition of respiration caused by veratrine -a mixture of veratrum alkaloids -was studied by Dawes, Mott and Widdicombe [1951] who showed that the apnoea observed in cats with small doses of veratridine (a pure alkaloid) is blocked by cooling the vagi to 10TC, and that the lung receptors responsible for this response are the pulmonary stretch endings. These investigations were complemented by recordings of the activity of single fibres from pulmonary stretch receptors, which showed after veratridine injection an increased frequency in the inspiratory volleys, and tonic, frequency modulated activity, coupled with slowing of breathing. This has been confirmed for rabbits [Meier, Bein and Helmich, 1949], cats [Paintal, 1953] and guinea pigs [Zipf and Marquardt, 1966]. Thus the vagal pathway for the inhibitory effects of veratrum alkaloids on breathing is well established [see also Herzog, 1958; Hapke, 1963a and b].The reflex cardiovascular actions of injections of veratrine are mediated mainly by stimulation of receptors in the muscle of the ventricles of the heart, probably with nonmyelinated vagal fibres [Sleight and Widdicombe, 1965].In previous experiments we have found increases in laryngeal resistance in expiration with induction of respiratory reflexes from the lungs and the upper airways [Stransky, Widdicombe, 1972, 1973] and have here tried to relate the respiratory changes induced by veratrine to quantitative measurements of laryngeal resistance to airflow.