Abstract
Chronic intermittent hypoxia (CIH), the hallmark of obstructive sleep apnea, is the main risk factor to develop systemic hypertension. Oxidative stress, inflammation, and sympathetic overflow have been proposed as possible mechanisms underlying the CIH-induced hypertension. CIH potentiates the carotid body (CB) chemosensory discharge leading to sympathetic overflow, autonomic dysfunction, and hypertension. Oxidative stress and pro-inflammatory molecules are involved in neurogenic models of hypertension, acting on brainstem and hypothalamic nuclei related to the cardiorespiratory control, such as the nucleus of the solitary tract, which is the primary site for the afferent inputs from the CB. Oxidative stress and pro-inflammatory molecules contribute to the activation of the CB chemoreflex pathway in CIH-induced hypertension. In this brief review, we will discuss new evidence for a critical role of oxidative stress and neuro-inflammation in development of the CIH-induced hypertension through activation of the CB chemoreflex pathway.
Highlights
Specialty section: This article was submitted to Autonomic Neuroscience, a section of the journal Frontiers in Physiology
Oxidative stress and pro-inflammatory molecules are involved in neurogenic models of hypertension, acting on brainstem and hypothalamic nuclei related to the cardiorespiratory control, such as the nucleus of the solitary tract, which is the primary site for the afferent inputs from the carotid body (CB)
Del Rio et al (2016) found that CBs ablation in hypertensive rats exposed to Chronic intermittent hypoxia (CIH) for 21 days, restores the autonomic balance, the cardiac baroreflex sensitivity and reduces the elevated arterial pressure (BP), even when the CIH stimuli was maintained for 7 days and systemic oxidative stress persisted after the elimination of the CBs
Summary
The CB chemoreceptor cells are innervated by sensory petrosal neurons that project to the nucleus of the tractus solitarius (NTS), which is the primary site of integration of gastrointestinal, respiratory and cardiovascular information in the brainstem (Berger, 1980; Finley and Katz, 1992; Grimes et al, 1995). Del Rio et al (2012) found that exposure to CIH for 21 days produced a progressive increase of the immunoreactivity levels of TNF-α, IL-1β and iNOS in the rat CB, while ET-1 showed a transient increase during the first week of CIH These results suggest that pro-inflammatory molecules may mediate the onset (ET-1) and the maintenance (proinflammatory cytokines) of the CB chemosensory potentiation. We found IL-1β, IL-6, and TNF-α mRNA levels were augmented in the NTS of hypertensive rats after 21 days of CIH (Oyarce and Iturriaga, 2018) These findings suggest that pro-inflammatory cytokines in the NTS may contribute to the maintenance of the hypertension, since CIH increases BP in 3–4 days in conscious rats, paralleling the time required to establish the enhanced CB chemosensory discharge (Del Rio et al, 2016)
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
