Cardiac autonomic nerve abnormalities in chronic heart failure are associated with presynaptic vagal nerve degeneration

Sanyal, Shamarendra; Wada, Tomoyuki; Yamabe, Motoko; Anai, Hirofumi; Miyamoto, Shinj̀i; Shimada, Toshio; Ono, Katsushige

doi:10.1016/j.pathophys.2012.07.004

Cited by 6 publications

(5 citation statements)

References 30 publications

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“…Cardiovascular diseases are accompanied by increased sympathetic and suppressed vagal activity, and therefore improvement of vagal activity appears to be a promising therapeutic strategy. 17 Previous studies have demonstrated that vagal stimulation significantly attenuated cardiac mtROS production, mitochondrial depolarization, and swelling during I/R. 18 In an in vitro study using primary-cultured cardiomyocytes, acetylcholine (ACh), the major neurotransmitter of the vagal nerve, prevented reoxygenation-induced collapse in the mitochondrial transmembrane potential by inhibiting permeability transition pore opening.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of the mitochondrial unfolded protein response by acetylcholine alleviated hypoxia/reoxygenation-induced apoptosis of endothelial cells

et al. 2016

Cell Cycle

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The mitochondrial unfolded protein response (UPR(mt)) is involved in numerous diseases that have the common feature of mitochondrial dysfunction. However, its pathophysiological relevance in the context of hypoxia/reoxygenation (H/R) in endothelial cells remains elusive. Previous studies have demonstrated that acetylcholine (ACh) protects against cardiomyocyte injury by suppressing generation of mitochondrial reactive oxygen species (mtROS). This study aimed to explore the role of UPR(mt) in endothelial cells during H/R and to clarify the beneficial effects of ACh. Our results demonstrated that H/R triggered UPR(mt) in endothelial cells, as evidenced by the elevation of heat shock protein 60 and LON protease 1 protein levels, and resulted in release of mitochondrial pro-apoptotic proteins, including cytochrome C, Omi/high temperature requirement protein A 2 and second mitochondrial activator of caspases/direct inhibitor of apoptosis-binding protein with low PI, from the mitochondria to cytosol. ACh administration markedly decreased UPR(mt) by inhibiting mtROS and alleviating the mitonuclear protein imbalance. Consequently, ACh alleviated the release of pro-apoptotic proteins and restored mitochondrial ultrastructure and function, thereby reducing the number of terminal deoxynucleotidyl transferase mediated dUTP-biotin nick end labeling (TUNEL)-positive cells. Intriguingly, 4-diphenylacetoxy-N-methylpiperidine methiodide, a type-3 muscarinic ACh receptor (M3AChR) inhibitor, abolished the ACh-elicited attenuation of UPR(mt) and TUNEL positive cells, indicating that the salutary effects of ACh were likely mediated by M3AChR in endothelial cells. In conclusion, our studies demonstrated that UPR(mt) might be essential for triggering the mitochondrion-associated apoptotic pathway during H/R. ACh markedly suppressed UPR(mt) by inhibiting mtROS and alleviating the mitonuclear protein imbalance, presumably through M3AChR.

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Section: Introductionmentioning

confidence: 99%

Inhibition of the mitochondrial unfolded protein response by acetylcholine alleviated hypoxia/reoxygenation-induced apoptosis of endothelial cells

et al. 2016

Cell Cycle

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“…These reductions in systemic blood pressures were associated with a temporary elevation of heart rate, which was observed in all RVF rats. Increased heart rate in PAH has been observed in human patients (Marcus et al, 2001 ; Gan et al, 2006 ; Hardziyenka et al, 2011 ; Manders et al, 2014 ) where it is seen to vary with the severity of hypertension (Wong et al, 2011 ), as well as in monocrotaline rats 4-week post-injection (Sanyal et al, 2012 ).…”

Section: Discussionmentioning

confidence: 97%

“…We interpret the increase in heart rate as a reflex response of the sympathetic nervous system (Sanyal et al, 2012 ). An increase in heart rate is necessary to compensate for the drop in LV stroke volume (Marcus et al, 2001 ; Gan et al, 2006 ; Hardziyenka et al, 2011 ; Manders et al, 2014 ) in order to maintain cardiac output (Stool et al, 1974 ).…”

Section: Discussionmentioning

confidence: 99%

Left-Ventricular Energetics in Pulmonary Arterial Hypertension-Induced Right-Ventricular Hypertrophic Failure

et al. 2018

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Pulmonary arterial hypertension (PAH) alters the geometries of both ventricles of the heart. While the right ventricle (RV) hypertrophies, the left ventricle (LV) atrophies. Multiple lines of clinical and experimental evidence lead us to hypothesize that the impaired stroke volume and systolic pressure of the LV are a direct consequence of the effect of pressure overload in the RV, and that atrophy in the LV plays only a minor role. In this study, we tested this hypothesis by examining the mechanoenergetic response of the atrophied LV to RV hypertrophy in rats treated with monocrotaline. Experiments were performed across multiple-scales: the whole-heart in vivo and ex vivo, and its trabeculae in vitro. Under the in vivo state where the RV was pressure-overloaded, we measured reduced systemic blood pressure and LV ventricular pressure. In contrast, under both ex vivo and in vitro conditions, where the effect of RV pressure overload was circumvented, we found that LV was capable of developing normal systolic pressure and stress. Nevertheless, LV atrophy played a minor role in that LV stroke volume remained lower, thereby contributing to lower LV mechanical work output. Concomitantly lower oxygen consumption and change of enthalpy were observed, and hence LV energy efficiency was unchanged. Our internally consistent findings between working-heart and trabecula experiments explain the rapid improvement of LV systolic function observed in patients with chronic pulmonary hypertension following surgical relief of RV pressure overload.

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“…No que se refere à captação do sinal de ECG em roedores, são utilizados sistemas cabeados, que apresentam algumas desvantagens de uso, como por exemplo: as medições realizadas em ratos conscientes e dentro de contensores plásticos gera um estresse ao animal, o uso de fármacos para anestesiar que geram mudanças na atividade cardíaca, ocorrência semelhante quando utilizado o método de congelamento por susto (frost), situações que afetam o resultado final da análise do eletrocardiograma (KONOPELSKI; UFNAL, 2016). O uso da comunicação sem fio tem se mostrado eficiente para a realização de pesquisas com roedores, como nos trabalhos realizados por Liang et al (2011) e Sanyal et al (2012). Neste último, os sinais de ECG de ratos Wistar foram obtidos por um transmissor de rádio que receberam monocrotalina (MCT) via injeção subcutânea.…”

Section: Introductionunclassified

Desenvolvimento De Um Hardware De Captação De Sinais De Ecg via Rede Wireless Para Uso Experimental

Lindoso¹,

Caetano²,

Quirino³

et al. 2019

Blucher Biophysics Proceedings

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Cardiac autonomic nerve abnormalities in chronic heart failure are associated with presynaptic vagal nerve degeneration

Cited by 6 publications

References 30 publications

Inhibition of the mitochondrial unfolded protein response by acetylcholine alleviated hypoxia/reoxygenation-induced apoptosis of endothelial cells

Inhibition of the mitochondrial unfolded protein response by acetylcholine alleviated hypoxia/reoxygenation-induced apoptosis of endothelial cells

Left-Ventricular Energetics in Pulmonary Arterial Hypertension-Induced Right-Ventricular Hypertrophic Failure

Desenvolvimento De Um Hardware De Captação De Sinais De Ecg via Rede Wireless Para Uso Experimental

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