2022-07-052022-07-052013-04-12https://hdl.handle.net/20.500.12503/31319Purpose: Obstructive sleep apnea produces hypertension and increases sympathetic nerve activity during the hypoxic sleeping events as well as during the waking hours. This study examined a possible receptor contribution to the sustained component of hypertension. Methods: To model the hypoxemia experienced during sleep apnea, rodents are exposed to chronic intermittent hypoxia (CIH). The median preoptic nucleus (MnPO) is a forebrain region that contributes to this sustained increase in mean arterial pressure (MAP) from CIH. This region integrates information from forebrain circumventricular organs and projects to the paraventricular nucleus to influence sympathetic nerve activity. Our lab has previously shown that in response to CIH there is increased ΔFosB expression in the MnPO and that after a 7 day hypoxia protocol MnPO AT1a receptor mRNA is increased 7 fold whereas AT1b shows no change. In this study, we tested the hypothesis that MnPO AT1a receptors contribute to CIH hypertension using adult male Sprague Dawley rats injected with a neuron specific adenoviral vectors with either shRNA to knock down expression of AT1a receptors in the MnPO or a scrambled RNA sequence. Results: All rats showed an increase in MAP during the hypoxic light period, but rats receiving the AT1a knock down did not exhibit the sustained increase in MAP during the normoxic dark phase (P<.05). Conclusions: This data indicates that the AT1a receptors in the MnPO is necessary for the sustained component of hypertension resulting from CIH.AngiotensinHypertensionSleep Apneaposter