Key result
Human SOD1 overexpression in mice significantly decreased the heart rate response to vagal efferent nerve stimulation (P < 0.05) while preserving the response to aortic depressor nerve stimulation.
Why the study?
Because the baroreflex arc includes afferent, central, and efferent components, it was unknown whether human SOD1 overexpression alters the central and vagal efferent mediation of heart rate responses.
Human SOD1 overexpression in mice preserves overall baroreflex function but differentially alters its components, enhancing central mediation of bradycardia while decreasing vagal efferent control of heart rate.
Answers are grounded in this paper and cite their sources.
Increases aortic depressor nerve activity without altering baroreflex responses; leaves open therapeutic role of SOD1 in autonomic dysfunction.
Excessive reactive oxygen species (ROS) (such as the superoxide radical) are commonly associated with cardiac autonomic dysfunctions. Though superoxide dismutase 1 (SOD1) overexpression may protect against ROS damage to the autonomic nervous system, superoxide radical reduction may change normal physiological functions. Previously, we demonstrated that human SOD1 (hSOD1) overexpression does not change baroreflex bradycardia and tachycardia but rather increases aortic depressor nerve activity in response to arterial pressure changes in C57B6SJL-Tg (SOD1)2 Gur/J mice. Since the baroreflex arc includes afferent, central, and efferent components, the objective of this study was to determine whether hSOD1 overexpression alters the central and vagal efferent mediation of heart rate (HR) responses. Our data indicate that SOD1 overexpression decreased the HR responses to vagal efferent nerve stimulation but did not change the HR responses to aortic depressor nerve (ADN) stimulation. Along with the previous study, we suggest that SOD1 overexpression preserves normal baroreflex function but may differentially alter the functions of the ADN, vagal efferents, and central components. While SOD1 overexpression likely enhanced ADN function and the central mediation of bradycardia, it decreased vagal efferent control of HR.
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Chen et al. (2018) studied Healthy (evaluating baroreflex control) (n=16). Human SOD1 overexpression vs. Wild-type C57BL/6 J mice was evaluated on Heart rate response to vagal efferent nerve stimulation (p=<0.05). Human SOD1 overexpression in mice significantly decreased the heart rate response to vagal efferent nerve stimulation (P < 0.05) while preserving the response to aortic depressor nerve stimulation.
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