In sleep apnea, recurrent obstruction of the upper airway leads to sleep fragmentation and intermittent hypoxia (IH). In animal studies, IH causes wake-time hypertension by elevating vascular resistance due in part to decreased production of the vasodilator, hydrogen sulfide (H2S). Inhibiting cystathionine γ-lyase (CSE) to prevent H2S synthesis augments constriction in isolated mesenteric arteries, but H2S regulation of resistance in this vascular bed in vivo is unknown. The goal of this study w