Noradrenergic A2 neurons in NTS respond to stressors such as hypoxia. We hypothesize that tyrosine hydroxylase (TH) knockdown in NTS reduces cardiovascular responses to chronic intermittent hypoxia (CIH), a model of the arterial hypoxemia observed during sleep apnea in humans. Adult male Sprague-Dawley rats were implanted with radio telemetry transmitters and adeno-associated viral constructs with a GFP reporter having either short hairpin RNA (shRNA) for TH or scrambled virus (scRNA) were injected into caudal NTS. Virus injected rats were exposed to 7 days of CIH (alternating 6 min periods of 10% O2 and 4 min of 21% O2 from 8am-4pm; from 4pm-8am rats were exposed to 21% O2). CIH increased MAP and HR during the day in both the scRNA (n= 14, P <.001 MAP and HR) and shRNA (n=13, P <.001 MAP and HR) groups. During the night MAP and HR remained elevated in the scRNA rats (P <0.001 MAP and HR) but not in the shRNA group. TH immunoreactivity and protein were reduced in shRNA group. FosB/FosB immunoreactivity was decreased in paraventricular nucleus (PVN) of shRNA group (P < 0.001). However, shRNA group did not show any change in the FosB/FosB immunoreactivity in the rostral ventro-lateral medulla. Exposure to CIH increased MAP which persisted beyond the period of exposure to CIH. Knockdown of TH in the NTS reduced this CIH-induced persistent increase in MAP and reduced the transcriptional activation of PVN. This indicates that NTS A2 neurons play a role in the cardiovascular responses to CIH.