New Insights Into the Sympathetic, Endothelial and Coronary Effects of Nicotine

Abstract

1. Nicotine is a well studied pleiotropic agent which occurs naturally in tobacco smoke and has been largely accused for many of the adverse effects of smoking on the cardiovascular system, including autonomic imbalance, endothelial dysfunction and coronary blood flow dysregulation. 2. The acute sympathoexcitatory effects of smoking on the cardiovascular system are partially mediated by catecholamine release, muscle sympathetic nerve excitation and peripheral chemoreceptor sensitivity increase, consecutive to nicotinic receptor stimulation in the autonomic nervous system. 3. Recent animal data suggest that nicotine promotes the oxidative and inflammatory stress to the endothelium and induces pathological angiogenesis, leading to the progression of the atherosclerotic lesions. 4. Nicotine increases myocardial work without impairing the physiological coronary vasodilatation. Consequently, nicotine per se cannot explain the sudden reduction in coronary flow reserve after exposure to both active and passive smoking. 5. Nicotine's biological effects are characterized by a rapid onset of tolerance, which can explain why nicotine administration does not elicit acute coronary and chemoreflex side-effect in smokers.

Autonomic Dysfunction in Current Cigarette Smokers Assessed by Time Series Analysis of Heart Rate Variability

“…As a major component of cigarette smoke, nicotine stimulates the nicotinic receptors of autonomic ganglia as well as adrenal medulla resulting in increased cardiac sympathetic activity and increased release of catecholamine. 12,[18][19] This effect is obviously attributed to the higher heart rate and the restriction of heart rate variability in the smokers of this study. This effect of nicotine may be further intensified by its action on peripheral chemoreceptors causing impaired baroreflex sensitivity.…”

“…This effect of nicotine may be further intensified by its action on peripheral chemoreceptors causing impaired baroreflex sensitivity. [18][19][20] In addition to nicotinic effect, the increased release of neuropeptide Y as a part of physiological adjustment for autonomic balance causing suppression of cardiac vagal tone also contribute to the reduced vagal modulation in smokers. 21 …”

Graves' Disease Complicated by Ventricular Fibrillation in Three Men Who Were Smokers

“…The constituents of inhaled tobacco are known to damage the cardiovascular system by numerous mechanisms, including endothelial dysfunction, platelet dysfunction, increased coagulation, increased heart rate, blood pressure, increased myocardial oxygen demand, and vasoconstriction. Further, nicotine has been shown to stimulate the sympathetic nerves and markedly elevate serum catecholamine concentration, which is potentially arrhythmogenic (18). Smoking is indeed a significant risk factor for appropriate ICD shocks among patients with heart failure with an ICD (19)(20)(21).…”

Changes in Sympathetic Nervous System Activity in Male Smokers After Moderate-Intensity Exercise

“…14 Nicotine activates sympathetic neurotransmission by inducing the release of ganglion catecholamine from postganglionic nerve endings. 32 In the present study, the lowfrequency/high-frequency value in the 5-10-min postexercise period was lower in the smokers, with an increase in the very-low-frequency/total value. The sympathetic nervous system activity (very-low-frequency/total and [verylow-frequency ϩ low-frequency]/high-frequency) of smokers remained elevated throughout the post-exercise period.…”