Abstract
The carotid bodies are the principal sensory organs for detecting changes in arterial blood oxygen concentration, and the carotid body chemoreflex is a major regulator of the sympathetic tone, blood pressure and breathing. Intermittent hypoxia is a hallmark manifestation of obstructive sleep apnea (OSA), which is a widespread respiratory disorder. The first part of this review discuss the role of carotid bodies in heightened sympathetic tone and hypertension in rodents treated with intermittent hypoxia, and the underlying cellular, molecular, and epigenetic mechanisms. We also present evidence for hitherto uncharacterized role of carotid body afferents in triggering cellular and molecular changes by intermittent hypoxia. The second part of the review presents evidence for contribution of hypersensitive carotid body to OSA and potential therapeutic intervention to mitigate OSA in a murine model. Abstract figure legend OSA = obstructive sleep apnea; IH = intermittent hypoxia; ROS = reactive oxygen species; CB = carotid body; SNA = sympathetic nerve activity; HO-2 = hemeoxygenase 2; CSE = cystathionine-ϒ-lyase. This article is protected by copyright. All rights reserved.
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