Baroreflex Control of Heart Rate in Mice Overexpressing Human SOD1: Functional Changes in Central and Vagal Efferent
Jin Chen1, He Gu1, Robert D Wurster2
1Division of Neuroscience and Division of Metabolic and Cardiovascular Sciences, Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, FL, 32816, USA.
Abstract:
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.
Insights
Superoxide dismutase 1 (SOD1) overexpression preserves baroreflex function but alters autonomic control. While enhancing aortic depressor nerve activity, it reduces vagal efferent control of heart rate.
Area of Science:
- Cardiovascular physiology
- Autonomic nervous system function
- Oxidative stress and disease
Background:
- Excessive reactive oxygen species (ROS) are linked to cardiac autonomic dysfunction.
- Superoxide dismutase 1 (SOD1) overexpression may mitigate ROS damage.
- Previous studies showed hSOD1 overexpression impacts aortic depressor nerve activity without altering baroreflex heart rate responses.
Purpose of the Study:
- To investigate the effect of human SOD1 (hSOD1) overexpression on the central and vagal efferent pathways of heart rate (HR) regulation.
- To determine if hSOD1 alters the mediation of HR responses via central autonomic components and vagal efferents.
Main Methods:
- Utilized transgenic mice overexpressing human SOD1 (Tg).
- Measured HR responses to direct vagal efferent nerve stimulation.
- Assessed HR responses to aortic depressor nerve (ADN) stimulation.
Main Results:
- hSOD1 overexpression decreased HR responses to vagal efferent stimulation.
- HR responses to ADN stimulation remained unchanged in hSOD1 overexpressing mice.
- Data suggests differential effects on autonomic components.
Conclusions:
- SOD1 overexpression preserves overall baroreflex function.
- hSOD1 overexpression enhances aortic depressor nerve function and central bradycardia mediation.
- Conversely, SOD1 overexpression diminishes vagal efferent control of heart rate.
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