Deep breaths akin to sighs have been reported to cause peripheral vasoconstriction. Our previous simulation studies have shown that this phenomenon cannot be reproduced in existing circulatory control models without inclusion of a respiratory-vascular coupling mechanism. To better understand this "sigh-vasoconstriction reflex", we investigated the effect of spontaneous and passively induced sighs as well as spontaneous breathing on peripheral vasoconstriction during wakefulness and non-rapid eye movement sleep in human subjects. We found that both spontaneous and induced sighs caused vasoconstriction during wakefulness and sleep. The coupling between respiration and vasoconstriction is also present even in an absence of deep breaths. The coupling mechanism is largely linear with increased nonlinearity during induced sighs. Since peripheral vascular resistance modulation is known to be sympathetically mediated, investigation of this coupling could potentially allow us to assess sympathetic function through non-invasive measurements and simple interventions.