Administration of serotonin (5-HT) to pulmonary circulation elicits prompt apnoea, followed by subsequent tachypnoea. The present study was designed to ascertain whether 5-HT challenge into the laryngeal artery will evoke the full constellation of this chemoreflex and to examine the role of laryngeal sensory input and importance of vagal afferents in the respiratory sequelae. The experiments were done on 10 anaesthetized, spontaneously breathing cats. Laryngeal artery injections of 5-HT, similarly to intravenous challenge, caused apnoeas, which were significantly diminished by the section of cervical vagal trunks. Breathing frequency increased in all conditions on intravenous injection but only prior to vagotomy, when administered into laryngeal artery. With resumed breathing, the peak inspiratory airflows were significantly increased in the neurally intact, those treated by bilateral section of the superior laryngeal nerves (SLNs-cut) and vagotomized cats, with no difference between them and independent of the route of injection. The results show that serotonin chemoreflex could evolve from the laryngeal vascular bed and that laryngeal afferents do not contribute to the respiratory arrest.