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J Hypertens. 2014 Feb;32(2):300-5. doi: 10.1097/HJH.0000000000000016.

Arterial hypertension in a murine model of sleep apnea: role of NADPH oxidase 2.

Author information

1
aUniversities of Giessen and Marburg Lung Center, Excellence Cluster Cardio-Pulmonary System, German Lung Research Center, Justus-Liebig-University Giessen, Giessen bDepartment of Internal Medicine, Infectious Diseases and Pulmonary Medicine, Charité-Universitätsmedizin Berlin, Berlin cDepartment of Lung Development and Remodeling, Max-Planck-Institute for Heart and Lung Research, Bad Nauheim, Germany.

Abstract

OBJECTIVES:

To investigate whether NADPH oxidase 2 (NOX2), a major source of reactive oxygen species (ROS), contributes to the emergence of arterial hypertension in a murine model of sleep apnea.

BACKGROUND:

Obstructive sleep apnea (OSA) is a risk factor for arterial hypertension and it is linked to oxidative stress.

METHODS:

C57BL/6J mice were exposed to chronic intermittent hypoxia (CIH) for 6 weeks (5 days/week, 8 h/day, alternating cycles of hypoxia and normoxia, each lasting 120 s, nadir FiO2: 7%). Blood pressure was monitored by telemetric catheters implanted into the abdominal aorta. Pharmacological inhibition of NOX by apocynin and NOX2-deficient mice were used to assess the role of NOX in CIH-induced arterial hypertension. NOX2 gene expression was measured by real-time PCR in different cardiovascular tissues.

RESULTS:

When compared with room air conditions, wild-type mice showed significant blood pressure elevations after exposure to CIH. This response was attenuated after treating animals with apocynin and in NOX2 (=gp91) knockout mice, whereas NOX2 was not upregulated in the heart, aorta, and femoral/carotid arteries of CIH mice.

CONCLUSION:

We suggest that the CIH-induced arterial hypertension is mediated by ROS derived from an activation of NOX2 within cells located outside the cardiovascular system.

PMID:
24270180
DOI:
10.1097/HJH.0000000000000016
[Indexed for MEDLINE]

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