Baroreflex Control of Heart Rate in Mice Overexpressing Human SOD1: Functional Changes in Central and Vagal Efferent Components.
10.1007/s12264-018-0302-y
- Author:
Jin CHEN
1
;
He GU
1
;
Robert D WURSTER
2
;
Zixi CHENG
3
Author Information
1. Division 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.
2. Department of Cellular and Molecular Physiology, Stritch School of Medicine, Loyola University, Maywood, IL, 60153, USA.
3. Division 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. zixi.cheng@ucf.edu.
- Publication Type:Journal Article
- Keywords:
Baroreflex;
Parasympathetic;
SOD1
- MeSH:
Animals;
Baroreflex;
physiology;
Blood Pressure;
physiology;
Bradycardia;
metabolism;
Heart Rate;
physiology;
Humans;
Mice, Transgenic;
Superoxide Dismutase-1;
metabolism;
Vagus Nerve;
metabolism
- From:
Neuroscience Bulletin
2019;35(1):91-97
- CountryChina
- Language:English
-
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.
