Endogenous hydrogen peroxide in paraventricular nucleus mediates sympathetic activation and enhanced cardiac sympathetic afferent reflex in renovascular hypertensive rats

2011 ◽  
Vol 96 (12) ◽  
pp. 1282-1292 ◽  
Author(s):  
Yao Xu ◽  
Qing Gao ◽  
Xian-Bing Gan ◽  
Lei Chen ◽  
Lei Zhang ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Paraventricular Nucleus ◽  
Sympathetic Activation ◽  
Hypertensive Rats ◽  
Cardiac Sympathetic Afferent Reflex

scholarly journals Angiotensin-(1-7) in Paraventricular Nucleus Contributes to the Enhanced Cardiac Sympathetic Afferent Reflex and Sympathetic Activity in Chronic Heart Failure Rats

2017 ◽  
Vol 42 (6) ◽  
pp. 2523-2539 ◽  
Author(s):  
Xingsheng Ren ◽  
Feng Zhang ◽  
Mingxia Zhao ◽  
Zhenzhen Zhao ◽  
Shuo Sun ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Signaling Pathway ◽  
Paraventricular Nucleus ◽  
Superoxide Anion ◽  
Coronary Artery Ligation ◽  
Ang Ii ◽  
Sympathetic Activation ◽  
Mas Receptor ◽  
Cardiac Sympathetic Afferent Reflex

Background/Aims: Cardiac sympathetic afferent reflex (CSAR) enhancement contributes to exaggerated sympathetic activation in chronic heart failure (CHF). The current study aimed to investigate the roles of angiotensin (Ang)-(1-7) in CSAR modulation and sympathetic activation and Ang-(1-7) signaling pathway in paraventricular nucleus of CHF rats. Methods: CHF was induced by coronary artery ligation. Responses of renal sympathetic nerve activity (RSNA) and mean arterial pressure (MAP) to epicardial application of capsaicin were used to evaluate CSAR in rats with anesthesia. Results: Ang-(1-7) increased RSNA, MAP, CSAR activity, cAMP level, NAD(P)H oxidase activity and superoxide anion level more significantly in CHF than in sham-operated rats, while Mas receptor antagonist A-779 had the opposite effects. Moreover, Ang-(1-7) augmented effects of Ang II in CHF rats. The effects of Ang-(1-7) were blocked by A-779, adenylyl cyclase inhibitor SQ22536, protein kinase A inhibitor Rp-cAMP, superoxide anion scavenger tempol and NAD(P)H oxidase inhibitor apocynin. Mas and AT1 receptor protein expressions, Ang-(1-7) and Ang II levels in CHF increased. Conclusions: These results indicate that Ang-(1-7) in paraventricular nucleus enhances CSAR and sympathetic output not only by exerting its own effects but also by augmenting the effects of Ang II through Mas receptor in CHF. Endogenous Ang-(1-7)/Mas receptor activity contributes to CSAR enhancement and sympathetic activation in CHF, and NAD(P)H oxidase-derived superoxide anions and the cAMP-PKA signaling pathway are involved in mediating the effects of Ang-(1-7) in CHF.

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