Cardiac sympathetic afferent reflex and its implications for sympathetic activation in chronic heart failure and hypertension

2015 ◽  
Vol 213 (4) ◽  
pp. 778-794 ◽  
Author(s):  
W.-W. Chen ◽  
X.-Q. Xiong ◽  
Q. Chen ◽  
Y.-H. Li ◽  
Y.-M. Kang ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Sympathetic Activation ◽  
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.

AT1 receptor mRNA antisense normalizes enhanced cardiac sympathetic afferent reflex in rats with chronic heart failure

2004 ◽  
Vol 287 (4) ◽  
pp. H1828-H1835 ◽  
Author(s):  
Guo-Qing Zhu ◽  
Lie Gao ◽  
Yifan Li ◽  
Kaushik P. Patel ◽  
Irving H. Zucker ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Paraventricular Nucleus ◽  
Genetic Manipulation ◽  
Intracerebroventricular Administration ◽  
Renal Sympathetic Nerve Activity ◽  
Protein Levels ◽  
Coronary Ligation ◽  
Cardiac Sympathetic Afferent Reflex

Previous studies showed that the cardiac sympathetic afferent reflex (CSAR) is enhanced in dogs and rats with chronic heart failure (CHF) and that central ANG II type 1 receptors (AT1R) are involved in this augmented reflex. The aim of this study was to determine whether intracerebroventricular administration and microinjection of antisense oligodeoxynucleotides targeted to AT1R mRNA would attenuate the enhanced CSAR and decrease resting renal sympathetic nerve activity (RSNA) in rats with coronary ligation-induced CHF. The CSAR was elicited by application of bradykinin to the epicardial surface of the left ventricle. Reflex responses to epicardial administration of bradykinin were enhanced in rats with CHF. The response to bradykinin was determined every 50 min after intracerebroventricular administration (lateral ventricle) or microinjection (into paraventricular nucleus) of antisense or scrambled oligonucleotides to AT1R mRNA. AT1R mRNA and protein levels in the paraventricular nucleus were significantly reduced 5 h after administration of antisense. Antisense significantly decreased resting RSNA and normalized the enhanced CSAR responses to bradykinin in rats with CHF. Scrambled oligonucleotides did not alter resting RSNA or the enhanced responses to bradykinin in rats with CHF. No significant effects were found in sham-operated rats after administration of either antisense or scrambled oligonucleotides. These results strongly suggest that central AT1R mRNA antisense reduces expression of AT1R protein and normalizes the augmentation of this excitatory sympathetic reflex and that genetic manipulation of protein expression can be used to normalize the sympathetic enhancement in CHF.

Biventricular pacing in chronic heart failure acutely facilitates the arterial baroreflex

2008 ◽  
Vol 295 (2) ◽  
pp. H755-H760 ◽  
Author(s):  
Maaike G. J. Gademan ◽  
Rutger J. van Bommel ◽  
Claudia Ypenburg ◽  
Joris C. W. Haest ◽  
Martin J. Schalij ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Mechanical Response ◽  
Biventricular Pacing ◽  
Cardiac Resynchronization ◽  
Arterial Baroreflex ◽  
Acute Response ◽  
Cardiac Sympathetic Afferent Reflex ◽  
The Difference ◽  
Relative Change

Metabolic and mechanical stress in the failing heart activates the cardiac sympathetic afferent reflex (CSAR). It has been demonstrated that cardiac resynchronization therapy (CRT) acutely reduces MSNA in clinical responders. Mechanistically, this beneficial effect might be explained by acute deactivation of the CSAR. In addition to sympathoexcitation, CSAR inhibits the arterial baroreflex at the level of the nucleus tractus solitarii. Hence, in responders, CRT is likely to remove/reduce this inhibition. Therefore, we hypothesized that CRT acutely facilitates the arterial baroreflex. One day after implantation of a CRT device in 32 patients with chronic heart failure (LVEF; 27 ± 6%), we measured noninvasive baroreflex sensitivity (BRS) and heart rate variability (HRV) in two conditions: CRT device switched on and switched off (on/off order randomized). BRS changes were correlated with the difference in unpaced/paced LVEF, a measure of acute mechanical response to CRT. CRT increased BRS by 35% from 2.96 to 3.79 ms/mmHg ( P < 0.02) and increased HRV (standard deviation of the intervals between normal beats) from 18.5 to 24.0 ms ( P < 0.01). The CRT-induced relative change in BRS correlated with the change in LVEF ( r = 0.44; P < 0.01). In conclusion, CRT acutely increases BRS and HRV. This favorable response of the autonomic nervous system might be caused by CRT-induced CSAR deactivation. Follow-up studies should verify the mechanism of the acute response and the possible predictive value of an acute positive BRS response.

Sympathetic activation and outcomes in chronic heart failure: Does the neurohormonal hypothesis apply to mid-range and preserved ejection fraction patients?

2020 ◽  
Vol 81 ◽  
pp. 60-66 ◽  
Author(s):  
Santiago Jimenez-Marrero ◽  
Pedro Moliner ◽  
Iris Rodríguez-Costoya ◽  
Cristina Enjuanes ◽  
Lidia Alcoberro ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Ejection Fraction ◽  
Preserved Ejection Fraction ◽  
Sympathetic Activation
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