The cardiovascular response to an arousal from sleep at the termination of an obstructive apnoea is more than double that to a spontaneous arousal. We investigated the hypothesis that stimulation of respiratory mechanoreceptors, by inspiring against an occluded airway during an arousal from sleep, augments the accompanying cardiovascular response. Arousals (>10 s) from Stage 2 sleep were induced by a 1 s auditory tone (85dB) during a concomitant 1 s inspiratory occlusion (O) and without an occlusion (i.e. control arousal, C) in 15 healthy males (mean ± SEM: Age, 25 ± 1 yrs). Arousals were associated with a significant increase in mean arterial blood pressure (MAP) at 4 s (p<0.001) and a significant decrease in RR interval at 3 s (p<0.001). However, the magnitude of the cardiovascular response was not different between C compared to O (MAP: C, 86 ± 3 to 104 ± 3 mmHg; O, 86 ± 3 to 105 ± 3 mmHg; p=0.99. RR interval: C, 1.12 ± 0.03 to 0.89 ± 0.04 s; O, 1.11 ± 0.02 to 0.87 ± 0.02 s, p=0.99). Ventilation significantly increased during arousals under both conditions at the 2nd breath (p<0.001); this increase was not different between the two conditions (C: 4.40 ± 0.29 to 6.76 ± 0.61 Lmin^-1, O: 4.35 ± 0.34 to 7.65 ± 0.73 Lmin^-1, p=0.31). We conclude that stimulation of the respiratory mechanoreceptors by transient upper airway occlusion is unlikely to interact with the arousal-related autonomic outflow to augment the cardiovascular response in healthy young males.