In times of tobacco‐free nicotine consumption: The influence of nicotine on vascular calcification

Abstract

Background Smoking remains the most important avoidable cause of global mortality. Even though the number of cigarette smokers declines in first world countries, the uses of alternative nicotine delivery products increase and may even surpass the sells of cigarettes. In this light, the explicit role of nicotine in the development of cardiovascular diseases should be elucidated. Objectives This narrative review attempts to connect current literature about possible effects of nicotine on the environment of the vasculature to the pathogenesis of vascular calcification, focusing on the tunica media of the vessel wall. Methods For this review, papers found on Pubmed and Medline until December 2018 by searching for the keywords nicotine, vascular calcification, oxidative stress, osteoblastic transdifferentiation and matrix degradation were considered. Results Nicotine creates an environment that probably facilitates and maybe even induces osteogenic transdifferentiation of VSMC by inflammation, endothelial dysfunction and reactive oxygen species. This process is believed to be a key event in calcification of the tunica media of the vessel wall. Furthermore, nicotine could lead to the formation of nucleation sites for hydroxyapatite by facilitating matrix vesicles and extracellular matrix degradation. Conclusions There is a growing body of evidence implicating that nicotine alone could impair vascular function and lead to vascular calcification. Further research is necessary to elucidate the explicit influence of nicotine on arteriosclerosis.

What are the respiratory effects of e-cigarettes?

“…Whether chronic activation of nAChR to nicotine via e-cigarettes can cause lung cancer is unknown, but the role of nAChR α7 in contributing to non-small cell lung cancer by altering cell proliferation and apoptotic resistance has been reported 154155. Nicotine contributes to vascular endothelial dysfunction by increasing leakiness 156. Furthermore, exposure to nicotine, but not propylene glycol/vegetable glycerin, increased arterial stiffness and adversely affected the microcirculation,157 suggesting that nicotine delivered by e-cigarettes may be a risk factor for cardiovascular disease.…”

Impact of delivery rate on the acute response to intravenous nicotine: A human laboratory study with implications for regulatory science

“…Nicotine, as a stimulant drug, activates the sympathetic nervous system, resulting in increased heart rate, blood pressure and the circulating catecholamines epinephrine and norepinephrine 42 . Given the potentially harmful cardiovascular effects of nicotine, the present study highlights the delivery rate as an important factor in estimating the overall health effects of nicotine products 43 …”

The Biological Effects of Smoking on the Formation and Rupture of Intracranial Aneurysms: A Systematic Review and Meta-Analysis

“…Long-term smoking can impair vascular endothelial function ( 60 ), which may be also related to nicotine and oxidants in cigarette smoke. Nicotine promotes oxidative stress in VSMCs and endothelial cells by downregulating superoxide dismutase (SOD), catalase, and glutathione reductase ( 45 ). Together, smoking exposure could cause endothelial dysfunction, increase oxidative stress, and increase morbidity and mortality of cardiovascular diseases, which promotes the formation and rupture of IA.…”