Baroreflex Control of Heart Rate in Mice Overexpressing Human SOD1: Functional Changes in Central and Vagal Efferent Components

作     者：Jin Chen He Gu Robert D.Wurster Zixi Cheng 

作者机构：Division of Neuroscience and Division of Metabolic and Cardiovascular SciencesBurnett School of Biomedical SciencesCollege of MedicineUniversity of Central FloridaOrlandoFL 32816USA Department of Cellular and Molecular PhysiologyStritch School of MedicineLoyola UniversityMaywoodIL 60153USA 

出 版 物：《Neuroscience Bulletin》 (神经科学通报（英文版）)

年 卷 期：2019年第35卷第1期

页      面：91-97页

核心收录：

学科分类：1002[医学-临床医学] 100201[医学-内科学(含：心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学] 

基　　金：supported by National Institutes of Health grant HL-75034 by Institutional Funds of the University of Central Florida 

主　　题：SOD1 Parasympathetic Baroreflex 

摘      要：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 C57 B6 SJL-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.