Tracheal, circulatory, and respiratory responses to electrical stimulation of the afferent nerve from the hindlimb were analyzed in decerebrate, paralyzed, and mechanically ventilated dogs. Tension of the tracheal smooth muscle (TSM), arterial blood pressure, and phrenic nerve activity (PNA) were measured during stimulation of the proximal end of the transected femoral nerve (FNS) with train pulses (duration; 0.5 ms, frequency; 40 Hz). With low intensity (e.g., 0.62 V) FNS, TSM exhibited relaxation, arterial pressure decreased, and neural respiratory output (NRO) was reduced (3 of 8 dogs) or unchanged (5 of 8 dogs). With increases in stimulus intensity, TSM always exhibited relaxation while arterial pressure and NRO exhibited excitatory responses almost at the same thresholds (approximately 5 V). The TSM relaxation and the excitatory NRO and arterial responses augmented with increases in stimulus intensity up to 16 times of threshold of the excitatory NRO response. TSM response was blocked by intravenous atropine but pressor response and phrenic response were not. The arterial response disappeared after administration of a ganglionic blocker. These findings suggest that TSM, arterial pressure, and PNA may be controlled by one neuronal mechanism during high intensity FNS, but that arterial pressure and PNA may be modified by another mechanism in an inhibitory direction when the stimulus intensity is low. This study suggested the existence of a neural mechanism which controls the airway and cardiorespiratory systems properly to execute exercise. Physiological significance of the responses to low intensity femoral nerve stimulation was uncertain.