The Role of the Autonomic Nervous System in Cardiovascular Toxicity

Carll, Alex P.; Farraj, Aimen K.; Roberts, Andrew M.

doi:10.1016/b978-0-12-801238-3.64259-9

Cited by 5 publications

(12 citation statements)

References 539 publications

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“…Phosphorylation of the NaV1.5 channel results in the alteration of the voltage-dependent kinetics and whole-cell INa amplitude [48]. There is limited evidence for direct regulation of cardiac Na + currents by parasympathetic activity, but the reversal of the effects of β-adrenergic receptor stimulation by acetylcholine has been described [49], likely via pre-synaptic inhibition upon muscarinic receptor activation [50]. β-adrenergic receptor stimulation appears to alter the voltage-gated calcium current via a dual mechanism, perhaps similar to that demonstrated previously for sodium channels [51].…”

Section: Cardiac Autonomic Nervous Systemmentioning

confidence: 99%

“…β-adrenergic stimulation also accelerates repolarization by augmenting IKs via PKA-dependent phosphorylation of Kv7.1 (also termed KvLQT1, encoded by the Kcnq1 gene) [52][53][54], and β-blockers prolong transmural dispersion of repolarization and action potential duration [55]. However, there is a potential inhomogeneity of effects of β-adrenergic stimulation on potassium channels across different species, which also vary by stimulus and disease states [50]. Vagal stimulation produces the opposite effects.…”

Section: Cardiac Autonomic Nervous Systemmentioning

confidence: 99%

“…Thus, nicotine is a particularly plausible culprit of these effects. Nevertheless, particulate matter and aldehydes within tobacco smoke may be key constituents and irritant reflexes or ischemia may be critical pathways through which smoking disrupts electrophysiologic homeostasis [276] Limitations It has not escaped our attention that a single measurement of serum cotinine may not fully reflect chronic smoking intensity. Moreover, because cotinine only reflects nicotine exposure, and by an imperfect proxy, smoking intensity, we are unable to assess relationships between other cigarette smoke constituents and cardiac electrophysiology.…”

Section: Qtc Interval Jt Interval and Qrs Durationmentioning

confidence: 99%

“…Finally, smoking and nicotine can affect myocardial conduction velocity through induction of cardiac remodeling, oxidative stress, and/or ion channel dysfunction, which were not assessed in this study and may occur independent of sympathetic activation. Nevertheless, sympathetic activation can induce all three of these pathogenic processes [299] and may thereby indirectly mediate atrioventricular conduction defects.…”

Section: Limitationsmentioning

confidence: 99%

“…Interestingly, we also found that cigarette smoking caused significant albeit minimal shortening of QTc. The relationship between QTc and the ANS is particularly complex [299]. However, several studies have shown that acute adrenergic stimulation shortens QTc in humans [64,336], possibly by reducing transmural dispersion of repolarization [337].…”

Section: Ventriclesmentioning

confidence: 99%

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The effects of nicotine and cigarette smoking on cardiac electrophysiology.

Irfan¹

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collaboration, and contribution to projects related to this dissertation. This work would not have been possible without the administrative and financial support of Marshall University's Departments of Cardiology and Clinical Translational Services. I am especially grateful to research coordinators, Melissa Marcum and Scott Wiley, for their perseverance and unwavering commitment to this research study. I am greatly indebted to, and honored by, the encouragement and guidance from Dr. Christian Mueller, who introduced me to cardiovascular research and helped take the first steps of my scientific pursuits. Lastly, I thank my dear family, especially my mother, father, brother, sister, and wife for their enduring love, support, and sacrifice.

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Section: Cardiac Autonomic Nervous Systemmentioning

confidence: 99%

Section: Cardiac Autonomic Nervous Systemmentioning

confidence: 99%

Section: Qtc Interval Jt Interval and Qrs Durationmentioning

confidence: 99%

Section: Limitationsmentioning

confidence: 99%

Section: Ventriclesmentioning

confidence: 99%

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The effects of nicotine and cigarette smoking on cardiac electrophysiology.

Irfan¹

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Nicotine Formulation Influences the Autonomic and Arrhythmogenic Effects of Electronic Cigarettes

Kucera,

Ramalingam,

Srivastava

et al. 2023

Nicotine and Tobacco Research

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Introduction Evidence is mounting that electronic cigarette (e-cig) use induces cardiac sympathetic dominance and electrical dysfunction conducive to arrhythmias and dependent upon nicotine. A variety of nicotine types and concentrations are available in e-cigs, but their relative cardiovascular effects remain unclear. Here we examine how different nicotine forms (racemic, free base, and salt) and concentrations influence e-cig-evoked cardiac dysfunction and arrhythmogenesis and provide a mechanism for nicotine-salt-induced autonomic imbalance. Methods ECG-telemetered C57BL/6J mice were exposed to filtered air (FA) or e-cig aerosols from propylene glycol and vegetable glycerin solvents either without nicotine (vehicle) or with increasing nicotine concentrations (1%, 2.5%, and 5%) for three 9-minute puff sessions per concentration. Spontaneous ventricular premature beat (VPB) incidence rates, heart rate, and heart rate variability (HRV) were compared between treatments. Subsequently, to test the role of β1-adrenergic activation in e-cig-induced cardiac effects, mice were pretreated with atenolol and exposed to either FA or 2.5% nicotine salt. Results During puffing and washout phases, ≥2.5% racemic nicotine reduced heart rate and increased HRV relative to FA and vehicle controls, indicating parasympathetic dominance. Relative to both controls, 5% nicotine salt elevated heart rate and decreased HRV during washout, suggesting sympathetic dominance, and also increased VPB frequency. Atenolol abolished e-cig-induced elevations in heart rate and declines in HRV during washout, indicating e-cig-evoked sympathetic dominance is mediated by β1-adrenergic stimulation. Conclusions Our findings suggest that inhalation of e-cig aerosols from nicotine-salt-containing e-liquids could increase the cardiovascular risks of vaping by inducing sympathetic dominance and cardiac arrhythmias. Implications Exposure to e-cig aerosols containing commercially relevant concentrations of nicotine salts may increase nicotine delivery and impair cardiac function by eliciting β1-adrenoceptor-mediated sympathoexcitation and provoking ventricular arrhythmias. If confirmed in humans, our work suggests that regulatory targeting of nicotine salts through minimum pH standards or limits on acid additives in e-liquids may mitigate the public health risks of vaping.

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Cardiovascular injury induced by tobacco products: assessment of risk factors and biomarkers of harm. A Tobacco Centers of Regulatory Science compilation

Conklin

Schick

Blaha

et al. 2019

American Journal of Physiology-Heart and Circulatory Physiology

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Although substantial evidence shows that smoking is positively and robustly associated with cardiovascular disease (CVD), the CVD risk associated with the use of new and emerging tobacco products, such as electronic cigarettes, hookah, and heat-not-burn products, remains unclear. This uncertainty stems from lack of knowledge on how the use of these products affects cardiovascular health. Cardiovascular injury associated with the use of new tobacco products could be evaluated by measuring changes in biomarkers of cardiovascular harm that are sensitive to the use of combustible cigarettes. Such cardiovascular injury could be indexed at several levels. Preclinical changes contributing to the pathogenesis of disease could be monitored by measuring changes in systemic inflammation and oxidative stress, organ-specific dysfunctions could be gauged by measuring endothelial function (flow-mediated dilation), platelet aggregation, and arterial stiffness, and organ-specific injury could be evaluated by measuring endothelial microparticles and platelet-leukocyte aggregates. Classical risk factors, such as blood pressure, circulating lipoproteins, and insulin resistance, provide robust estimates of risk, and subclinical disease progression could be followed by measuring coronary artery Ca2+ and carotid intima-media thickness. Given that several of these biomarkers are well-established predictors of major cardiovascular events, the association of these biomarkers with the use of new and emerging tobacco products could be indicative of both individual and population-level CVD risk associated with the use of these products. Differential effects of tobacco products (conventional vs. new and emerging products) on different indexes of cardiovascular injury could also provide insights into mechanisms by which they induce cardiovascular harm.

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The Role of the Autonomic Nervous System in Cardiovascular Toxicity

Cited by 5 publications

References 539 publications

The effects of nicotine and cigarette smoking on cardiac electrophysiology.

The effects of nicotine and cigarette smoking on cardiac electrophysiology.

Nicotine Formulation Influences the Autonomic and Arrhythmogenic Effects of Electronic Cigarettes

Cardiovascular injury induced by tobacco products: assessment of risk factors and biomarkers of harm. A Tobacco Centers of Regulatory Science compilation

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