The arterial pressure elevations that accompany sleep apneas may be ca
used by chemoreflex stimulation, negative intrathoracic pressure, and/
or arousal. To assess the neurocirculatory effects of arousal alone, w
e applied graded auditory stimuli during non-rapid-eye-movement (NREM)
sleep in eight healthy humans. We measured muscle sympathetic nerve a
ctivity (intraneural microelectrodes), electroencephalogram (EEG; C-4/
A(1) and O-1/A(2)), arterial pressure (photoelectric plethysmography),
heart rate (electrocardiogram), and stroke volume (impedance cardiogr
aphy). Auditory stimuli caused abrupt increases in systolic and diasto
lic pressures (21 +/- 2 and 15 +/- 1 mmHg) and heart rate (11 +/- 2 be
ats/min). Cardiac output decreased (-10%). Stimuli that produced EEG e
vidence of arousal evoked one to two large bursts of sympathetic activ
ity (316 +/- 46% of baseline amplitude). Stimuli that did not alter EE
G frequency produced smaller but consistent presser responses even tho
ugh no sympathetic activation was observed. We conclude that arousal f
rom NREM sleep evokes a presser response caused by increased periphera
l vascular resistance. Increased sympathetic outflow to skeletal muscl
e may contribute to, but is not required for, this vasoconstriction. T
he neurocirculatory effects of arousal may augment those caused by asp
hyxia during episodes of sleep-disordered breathing.