Key result
SOD1 overexpression in mice prevents intermittent hypoxia from blunting heart rate responses to nerve stimulation.
Why the study?
Chronic intermittent hypoxia impairs baroreflex control of heart rate via oxidative stress, but the effects across specific baroreflex components and the protective role of SOD1 overexpression were unclear.
Does SOD1 overexpression prevent chronic intermittent hypoxia-induced deficits in the baroreflex arc in mice?
Does SOD1 overexpression prevent chronic intermittent hypoxia-induced deficits in the baroreflex arc in mice?
SOD1 overexpression may prevent chronic intermittent hypoxia-induced central deficits in baroreflex mediation, highlighting the role of oxidative stress in OSA-related cardiovascular complications.
Answers are grounded in this paper and cite their sources.
Supports oxidative stress role in hypoxia-induced baroreflex attenuation; leaves open translation to human OSA therapy.
Obstructive sleep apnea (OSA) is a highly prevalent sleep disorder that is associated with many cardiovascular complications. Similar to OSA, chronic intermittent hypoxia (CIH) (a model for OSA) leads to oxidative stress and impairs baroreflex control of the heart rate (HR) in rodents. The baroreflex arc includes the aortic depressor nerve (ADN), vagal efferent, and central neurons. In this study, we used mice as a model to examine the effects of CIH on baroreflex sensitivity, aortic baroreceptor afferents, and central and vagal efferent components of the baroreflex circuitry. Furthermore, we tested whether human Cu/Zn Superoxide Dismutase (SOD1) overexpression in transgenic mice offers protection against CIH-induced deficit of the baroreflex arc. Wild-type C57BL/6J and SOD1 mice were exposed to room air (RA) or CIH and were then anesthetized, ventilated, and catheterized for measurement of mean arterial pressure (MAP) and HR. Compared with wild-type RA control, CIH impaired baroreflex sensitivity but increased maximum baroreceptor gain and bradycardic response to vagal efferent stimulation. Additionally, CIH reduced the bradycardic response to ADN stimulation, indicating a diminished central regulation of bradycardia. Interestingly, SOD1 overexpression prevented CIH-induced attenuation of HR responses to ADN stimulation and preserved HR responses to vagal efferent stimulation in transgenic mice. We suggest that CIH decreased central mediation of the baroreflex and SOD1 overexpression may prevent the CIH-induced central deficit.
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Chen et al. (2020) studied Chronic intermittent hypoxia (model for obstructive sleep apnea). SOD1 overexpression vs. Wild-type mice exposed to room air or chronic intermittent hypoxia was evaluated on Baroreflex sensitivity and heart rate responses to aortic depressor nerve and vagal efferent stimulation. SOD1 overexpression in transgenic mice prevented chronic intermittent hypoxia-induced attenuation of heart rate responses to aortic depressor nerve stimulation.
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