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Intermittent Hypoxia in Rats Increases expression of AP‐1 target genes in the median preoptic nucleus

Intermittent hypoxia (IH) is an animal model of hypoxemia similar to obstructive sleep apnea. In addition to hypertension and sympathoexcitation, IH increases FosB expression and angiotensin II signaling in several brain regions including the median preoptic nucleus (MnPO). Inhibition of FosB or angiotensin II reduces IH‐induced hypertension. Rats were subjected to one week of exposure to IH during the light phase. IH increased arterial pressure (Base: 103±4 IH: 108±4, mmHg). After IH, animals were anesthetized and the MnPO was dissected using stainless steel punches. MnPO total RNA was isolated, reverse transcribed, and PCR arrays were performed on a list of selected genes containing AP‐1 response elements because FosB is a component of the AP‐1 transcription factor complex. IH increased FosB expression by 75%. Further, both endothelial and neuronal nitric oxide synthases (NOS) were upregulated by 40–60%. Consistent with increased angiotensin signaling in IH, expression of both angiotensin converting enzyme types I and II were increased by approximately 50%. Lastly, the antioxidant enzyme peroxiredoxin 2, a putative response to increased oxidative stress, is increased by 62%. These data indicate that IH increases a host of genes that may be responsible for the increased blood pressure seen during IH and in downstream fashion to FosB/AP‐1 regulated gene expression. Supported by PO1 HL‐88052.