Vagal nerve modulation: A promising new therapeutic approach for cardiovascular diseases

Abstract

The physiological activities of the mammalian heart are regulated by the autonomic nervous system. An imbalanced autonomic nervous system with increased sympathetic tone and reduced vagal tone has been implicated in cardiovascular diseases. Experimental and clinical reports have demonstrated that vagal nerve activation is able to improve outcomes for multiple cardiovascular diseases, such as ischaemic heart disease, heart failure, arrhythmia and hypertension. In this paper, we mainly focus on the potential cardioprotective mechanisms of vagal nerve activation. Based on the knowledge gained from our experiments and other published reports, vagal activation results in cardioprotection is not only associated with heart rate, anti-adrenergic effect but also related to anti-inflammatory activity, regulation of cellular redox states and regulation of mitochondrial targets. In conclusion, vagal nerve activation may be a promising new therapeutic approach for the treatment of cardiovascular diseases.

Vagus nerve stimulation attenuates myocardial ischemia/reperfusion injury by inhibiting the expression of interleukin-17A

“…Previous studies have demonstrated that vagal activation is capable of exerting cardioprotective effects in various cardiovascular diseases, including ischemic heart disease, heart failure, arrhythmia and hypertension (7,15). In the present study, VS was initiated at 15 min following acute myocardial ischemia and maintained for 30 min, which is similar to a previous study (9).…”

“…Previous studies have demonstrated that vagal stimulation (VS) and acetylcholine (ACh) are capable of exerting cardioprotective effects in various cardiovascular diseases (7,8). Furthermore, the inhibition of inflammation has been demonstrated to be one of the major pathophysiological mechanisms by which VS induces cardioprotection (9,10).…”

Reduction of Mitochondria–Endoplasmic Reticulum Interactions by Acetylcholine Protects Human Umbilical Vein Endothelial Cells From Hypoxia/Reoxygenation Injury

“…More recently, the importance of elevating vagal activity has been discussed. [7][8][9]26 A growing body of evidence indicates that the vagal nerve and its neurotransmitter acetylcholine play defensive roles in the pathogenesis of cardiovascular diseases 27 ; however, few studies have explored the effects of acetylcholine treatment on Ca 2+ regulation in endothelial cells in the context of I/R. Importantly, this study demonstrated that acetylcholine reduced both mitochondrial and cytosolic Ca 2+ overload that inhibiting the Ca 2+ -related apoptotic pathway, leading to attenuation of cell death and preservation of endothelial structure.…”

Acetylcholine Promotes ROS Detoxification Against Hypoxia/reoxygenation-Induced Oxidative Stress Through FoxO3a/PGC-1a Dependent Superoxide Dismutase

“…Increased vagal activity reduces cardiovascular risk factors and improves prognosis [17,18,19]. Recently, vagal nerve stimulation (VNS) has been used as a promising therapeutic approach for chronic heart failure [20,21,22].…”