The cardiovascular response to an arousal from sleep at the termination of an obstructive apnea 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 (Ͼ10 s) from stage 2 sleep were induced by a 1-s auditory tone (85 dB) during a concomitant 1-s inspiratory occlusion (O) and without an occlusion [i.e., control arousal (C)] in 15 healthy men (mean Ϯ SE: age, 25 Ϯ 1 yr). Arousals were associated with a significant increase in mean arterial blood pressure (MAP) at 4 s (P Ͻ 0.001) and a significant decrease in R-R interval at 3 s (P Ͻ 0.001). However, the magnitude of the cardiovascular response was not different during C compared with O (MAP: C, 86 Ϯ 3 to 104 Ϯ 3 mmHg; O, 86 Ϯ 3 to 105 Ϯ 3 mmHg; P ϭ 0.99. R-R interval: C, 1.12 Ϯ 0.03 to 0.89 Ϯ 0.04 s; O, 1.11 Ϯ 0.02 to 0.87 Ϯ 0.02 s, P ϭ 0.99). Ventilation significantly increased during arousals under both conditions at the second breath (P Ͻ 0.001); this increase was not different between the two conditions (C: 4.40 Ϯ 0.29 to 6.76 Ϯ 0.61 l/min, O: 4.35 Ϯ 0.34 to 7.65 Ϯ 0.73 l/min; P ϭ 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 men. blood pressure; heart rate SPONTANEOUS AROUSAL FROM SLEEP is associated with large surges in both heart rate and blood pressure (13,42,49). In patients with obstructive sleep apnea (OSA), the surges in sympathetic activity that occur during an arousal from sleep at the termination of an apnea are more than double in size compared with a spontaneous arousal (2,29,40). Frequent cardiovascular surges in OSA have been implicated in the increased prevalence of both nocturnal and diurnal hypertension associated with OSA (37, 41). The mechanisms responsible for the augmentation of the cardiovascular response to arousal at the termination of an apnea potentially include stimulation of the chemoreceptors (hypercapnia, hypoxia), stimulation of upper airway (UA) mechanoreceptors (occlusion), stimulation of the pulmonary stretch receptors (increasing negative intrathoracic pressure, lung inflation), or arousalrelated central activation of autonomic centers. Our laboratory has previously reported in this journal that combined stimulation of the central and peripheral chemoreceptors (using hypercapnic hypoxia) does not significantly augment the cardiovascular response to arousal from sleep in healthy human subjects (39).Brief inspiratory occlusion evokes cortical activity during wakefulness (12, 15) and sleep (1, 51). Additionally, during sleep, complete airway occlusion can rapidly induce arousal, most likely as a result of afferent activity from UA mechanoreceptors to the brain stem respiratory centers (24). Altering this afferent activity, by topical anesthes...