The apnoea, accompanied by bradycardia and hypotension caused by injection of 5-Hydroxytryptamine (5-HT) into the vascularly isolated nodose ganglion is characterised by intense electrical activity in the internal intercostal muscles. No such activity was recorded when apnoea was provoked by electrical stimulation of the central end of the superior laryngeal nerve. The cardiac slowing induced by 5-HT was less marked when the superior laryngeal nerve was concomitantly stimulated with an intensity sufficient to inhibit the internal intercostal activity. When central respiratory drive was depressed by hypocapnic ventilation nodose ganglion-induced bradycardia was comparable to that provoked during electrical stimulation of the superior laryngeal nerve in eupnoea. Unlike chemoreceptor-induced bradycardia the cardiac slowing caused by nodose ganglion stimulation was not reduced by "ramp" inflation of the lungs. The results were similar during hypocapnic depression of the "Respiratory Centre". These findings suggest that: (a) central expiratory activity contributes to the bradycardia induced by nodose ganglion stimulation, and (b) the inhibition of bradycardia by lung expansion occurs before the neural impulses reach the nucleus ambiguus but does not involve the central respiratory neurones.