Abstract We examined effects of central hypoxia on tracheal smooth muscle (TSM) tone, phrenic nerve activity (PNA) and blood pressure (BP) in decerebrated, paralysed, and artificially ventilated dogs. Central hypoxia was induced by injection of N 2-saturated saline (5 ml; P O 2 25–32 torr) through a catheter in the vertebral artery. The effects of central hypoxia were compared with the responses to central chemoreceptors stimulation, namely central hypercapnia induced by intravertebral injection of high CO 2 saline (5 ml; P CO2 90–100 torr, P O2 80–120 torr, pH 7.38–7.42) buffered by HCO 3 − Central hypoxia caused relaxation of TSM accompanied by depression of PNA and elevation of BP. In contrast, central hypercapnia evoked tracheal constriction along with respiratory excitation and pressor response. The tracheal relaxation in response to central hypoxia occurred with onset and peak latencies similar to those observed in PNA depression and BP elevation. This suggests a common source for the synaptic inputs to three distinct control systems involved in cardiovascular, respiratory and airway functions. Such neuronal substrate is considered to be activated by central hypoxia.