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Abstract
There is consensus that the heart is innervated by both the parasympathetic and sympathetic nervous system. However, the role of the parasympathetic nervous system in controlling cardiac function has received significantly less attention than the sympathetic nervous system. New neuromodulatory strategies have renewed interest in the potential of parasympathetic (or vagal) motor output to treat cardiovascular disease and poor cardiac function. This renewed interest emphasizes a critical need to better understand how vagal motor output is generated and regulated. With clear clinical links between cardiovascular and metabolic diseases, addressing this gap in knowledge is undeniably critical to our understanding of the interaction between metabolic cues and vagal motor output, notwithstanding the classical role of the parasympathetic nervous system in regulating gastrointestinal function and energy homeostasis. For this reason, this review focuses on the central, vagal circuits involved in sensing metabolic state(s) and enacting vagal motor output to influence cardiac function. It will review our current understanding of brainstem vagal circuits and their unique position to integrate metabolic signaling into cardiac activity. This will include an overview of not only how metabolic cues alter vagal brainstem circuits, but also how vagal motor output might influence overall systemic concentrations of metabolic cues known to act on the cardiac tissue. Overall, this review proposes that the vagal brainstem circuits provide an integrative network capable of regulating and responding to metabolic cues to control cardiac function.
Highlights
While sympathoexcitation may be widely accepted as a hallmark of the pathogenesis of cardiovascular disease, decreased parasympathetic, or vagal, tone is linked to a broad spectrum of diseases, including cardiac arrhythmias, coronary heart disease, and heart failure, and is an accurate predictor of morbidity and mortality in humans and animals (Barkai and Madacsy, 1995; La Rovere et al, 1998; Nolan et al, 1998; Thayer and Lane, 2007; Franciosi et al, 2017)
Using techniques with improved specificity, like optogenetics, activation of dorsal motor nucleus of the vagus (DMV) motor neurons increased cardiac ventricular contractility and enhanced exercise endurance in rodents (Machhada et al, 2017), protected ventricular cardiomyocytes from ischemic/reperfusion injury (Mastitskaya et al, 2012), and altered the electrical properties of cardiac tissue (Machhada et al, 2015). These latter two results were independent of changes in heart rate, providing key experimental evidence that the DMV might be the source of vagal nerve-dependent coronary artery dilation (Reid et al, 1985; Kovach et al, 1995)
While metabolic disorders come with complex multisystem morbidities, longitudinal studies conducted in human patients have long indicated that vagal dysfunction is first in the autonomic dysfunction sequelae and occurs prior to overt cardiac complications (Ewing et al, 1980; Vinik et al, 2011) or induction of fasting hyperglycemia (Wu et al, 2007)
Summary
While sympathoexcitation may be widely accepted as a hallmark of the pathogenesis of cardiovascular disease, decreased parasympathetic, or vagal, tone is linked to a broad spectrum of diseases, including cardiac arrhythmias, coronary heart disease, and heart failure, and is an accurate predictor of morbidity and mortality in humans and animals (Barkai and Madacsy, 1995; La Rovere et al, 1998; Nolan et al, 1998; Thayer and Lane, 2007; Franciosi et al, 2017). Understanding the neuronal modulation of cardiac activity could provide novel mechanistic details into the pathogenesis and treatment of cardiovascular disease. This idea is further reinforced since advanced neural modulation techniques have proven effective treatments for other cardiovascular diseases, including cardiac arrhythmias (Kapa et al, 2010; Shen et al, 2011). It will aim to define basic brainstem circuits and the influence of metabolic signaling on plasticity within these circuits It will hopefully compel more investigations into how vagal motor output is both affected by and an effector of metabolic cues
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