Obstructive sleep apnea (OSA) is a syndrome characterized by intermittent nocturnal hypoxia, sleep fragmentation, hypercapnia and respiratory effort, and it has been associated with several complications, such as diabetes, hypertension and obesity. Quantitative real-time PCR has been performed in previous OSA-related studies; however, these studies were not validated using proper reference genes. We have examined the effects of chronic intermittent hypoxia (CIH), which is an experimental model mainly of cardiovascular consequences of OSA, on reference genes, including beta-actin, beta-2-microglobulin, glyceraldehyde-3-phosphate dehydrogenase, hypoxanthine guanine phosphoribosyl transferase and eukaryotic 18S rRNA, in different areas of the brain. All stability analyses were performed using the geNorm, Normfinder and BestKeeper software programs. With exception of the 18S rRNA, all of the evaluated genes were shown to be stable following CIH exposure. However, gene stability rankings were dependent on the area of the brain that was analyzed and varied according to the software that was used. This study demonstrated that CIH affects various brain structures differently. With the exception of the 18S rRNA, all of the tested genes are suitable for use as housekeeping genes in expression analyses.

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Introduction: Recent investigations over the past decade have linked the development of hypertension to sleep loss, although the mechanisms underlying this association are still under scrutiny. To determine the relationship between sleep deprivation and cardiovascular dysfunction, we examined the effects of paradoxical sleep deprivation on heart rate, blood pressure, sympathetic nerve activity (SNA) and their consequences in the blood renin-angiotensin system. Materials and methods: Wistar-Hannover male rats were randomly assigned to three experimental groups: 1) control, 2) paradoxical sleep deprivation for 24 h and 3) paradoxical sleep deprivation for 96 h. Blood pressure and heart rate were recorded in awake, freely moving rats. Results: Heart rate was higher in the 96 h paradoxical sleep deprivation group compared with the control group. Renal SNA was increased in all deprived groups. However, no significant statistical differences were observed in blood pressure or splanchnic SNA among groups. Paradoxical sleep deprivation (24 and 96 h) reduced plasma angiotensin II (Ang II) concentrations. Conclusions:The results suggest that selective sleep deprivation produces an increase in SNA, preferentially in the kidney. Thus, alterations in the sympathetic system in response to sleep loss may be an important pathway through which hypertension develops.

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