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Published on: February 14, 2021
SOD1 Overexpression Preserves Baroreflex Control of Heart Rate with an Increase of Aortic Depressor Nerve Function
Jeffrey Hatcher1, He Gu2, Zixi Jack Cheng1
1Biomolecular Science Center, Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, FL 32816, USA.
Abstract:
Overproduction of reactive oxygen species (ROS), such as the superoxide radical (O2 (∙-)), is associated with diseases which compromise cardiac autonomic function. Overexpression of SOD1 may offer protection against ROS damage to the cardiac autonomic nervous system, but reductions of O2 (∙-) may interfere with normal cellular functions. We have selected the C57B6SJL-Tg (SOD1)2 Gur/J mouse as a model to determine whether SOD1 overexpression alters cardiac autonomic function, as measured by baroreflex sensitivity (BRS) and aortic depressor nerve (ADN) recordings, as well as evaluation of baseline heart rate (HR) and mean arterial pressure (MAP). Under isoflurane anesthesia, C57 wild-type and SOD1 mice were catheterized with an arterial pressure transducer and measurements of HR and MAP were taken. After establishing a baseline, hypotension and hypertension were induced by injection of sodium nitroprusside (SNP) and phenylephrine (PE), respectively, and ΔHR versus ΔMAP were recorded as a measure of baroreflex sensitivity (BRS). SNP and PE treatment were administered sequentially after a recovery period to measure arterial baroreceptor activation by recording aortic depressor nerve activity. Our findings show that overexpression of SOD1 in C57B6SJL-Tg (SOD1)2 Gur/J mouse preserved the normal HR, MAP, and BRS but enhanced aortic depressor nerve function.
Insights
Overexpression of SOD1 in mice preserved normal cardiac autonomic function and hemodynamics. However, it enhanced aortic depressor nerve activity, suggesting a specific improvement in baroreceptor reflex.
Area of Science:
- Cardiovascular Physiology
- Autonomic Nervous System
- Oxidative Stress
Background:
- Overproduction of reactive oxygen species (ROS) impairs cardiac autonomic function.
- Superoxide dismutase 1 (SOD1) protects against ROS, but its reduction may affect cellular functions.
- Understanding SOD1's role in cardiac autonomic regulation is crucial for disease management.
Purpose of the Study:
- To investigate the impact of SOD1 overexpression on cardiac autonomic function in a mouse model.
- To assess changes in baroreflex sensitivity (BRS), heart rate (HR), mean arterial pressure (MAP), and aortic depressor nerve (ADN) activity.
Main Methods:
- Utilized C57B6SJL-Tg (SOD1)2 Gur/J mice and C57 wild-type littermates.
- Measured baseline HR and MAP under isoflurane anesthesia.
- Assessed BRS via induced hypotension/hypertension (SNP/PE) and recorded HR/MAP changes.
- Evaluated ADN activity during induced hypotension/hypertension to assess baroreceptor reflex.
Main Results:
- SOD1 overexpression maintained normal HR, MAP, and BRS in mice.
- Enhanced aortic depressor nerve (ADN) activity was observed in SOD1-overexpressing mice.
- These findings suggest SOD1 overexpression specifically augments arterial baroreceptor function.
Conclusions:
- Overexpression of SOD1 in the C57B6SJL-Tg (SOD1)2 Gur/J mouse model preserves cardiac autonomic function.
- Enhanced ADN function indicates a potential protective or modulatory role of SOD1 in the baroreflex pathway.
- Further research is warranted to explore therapeutic implications of SOD1 modulation in cardiovascular diseases.
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