Chronic Administration of Nicotine-Free Cigarette Smoke Extract Impaired Endothelium-Dependent Vascular Relaxation in Rats via Increased Vascular Oxidative Stress

Abstract

CorrigendumCorrigendum to "Chronic administration of nicotine-free cigarette smoke extract impaired endothelium-dependent vascular relaxation in rats via increased vascular oxidative stress" [J Pharmacol Sci 118 (2012) 206Journal of Pharmacological Sciences © The Japanese Pharmacological Society J Pharmacol Sci 118, 206 -214 (2012) IntroductionEpidemiological studies indicate that cigarette smoking is one of the independent risk factors for hypertension, atherosclerosis, and ischemic heart diseases (1 -4). Endothelial dysfunction is thought to be an early sign of atherosclerosis (5) and that is observed in rodent models of cardiovascular diseases (6 -8). Impairment of vascular endothelial function has been reported in chronic smokers (9 -11). Nitric oxide (NO) is an intercellular signal-mediating molecule in the cardiovascular, immune, and nervous systems (12). In the cardiovascular system, NO plays a crucial role in the regulation of vascular tone (13,14) and in protecting against the development of atherosclerosis (15). NO bioavailability is decreased in cigarette smokers (16,17), but the underlying mechanism was not clarified. Physiological and pharmacological effects of nicotine, a major component of cigarette smoke, are well established, and it is reported that treatment with nicotine impairs endothelial function by decreasing NO bioavailability in the experimental animals (18,19). Cigarette smoke contains numerous vasoconstricting and vasorelaxing components other than nicotine (20, 21), and cigarette smoke extract (CSE) exposure affects vasomotor responses of isolated arteries (22,23). Recently nicotine-free CSE has attracted attention in the pathogenesis of vascular disorders caused by smoking (24 -26). However, the effect of cigarette smoke components other than nicotine on regulation of cardiovascular function is not sufficiently examined. Therefore, in the present study, acute and chronic effects of nicotine-free CSE on the vascular responsiveness were Science, Seta, Otsu, Shiga 520-2192, Japan Received October 7, 2011 Accepted December 12, 2011 Abstract. Cigarette smoking has been implicated in the initiation and progression of cardiovascular disorders and atherosclerosis. Here, we examined the effects of nicotine-free cigarette smoke extract (CSE) on the regulation of cardiovascular function. Rats were subcutaneously administered PBS or nicotine-free CSE at 0.05 to 1.5 mL/day per rat for 4 weeks. Blood pressure, cardiac function, and vascular responsiveness were measured at 4 weeks after administration. Furthermore, acute effects of nicotine-free CSE were also studied in the aorta isolated from normal rats. Blood pressure and left ventricular systolic pressure (LVSP) were significantly increased in the nicotinefree CSE-administered rats, but heart rate, dP/dt max , and dP/dt min were not affected. Endotheliumdependent relaxation by acetylcholine (ACh) in the nicotine-free CSE-treated rats was significantly attenuated compared to PBS-treated rats, but endothelium-independent relaxation ...

Smoking and Cardiovascular Disease

“…Cigarette smokemediated impairment of endothelium-dependent relaxation and the role of oxidants, radicals, and reduced NO in animals were previously described by studies in rats and rabbits. [41][42][43][44] As mentioned above, clinical data clearly show the pro-oxidative (and therefore proatherogenic) potential of smoking, which are further supported by a limited number of animal studies. In humans and in animals (mice and rabbits), smoking increases serum levels of oxidative stress markers, oxidative modification of LDL, lipid peroxidation, and lipid deposition in the vessel wall and causes plaque development and progression.…”

Recent updates on electronic cigarette aerosol and inhaled nicotine effects on periodontal and pulmonary tissues

“…Recent studies have indicated lung cellular toxicity by e-cig products (Cahn and Siegel, 2011;Shimosato et al, 2012;Cervellati et al, 2014;Wu et al, 2014). Lerner et al reported increased mitochondrial ROS, DNA nuclear fragmentation, and impaired stability of electron transport chain complex IV subunit on human lung fibroblasts exposed to e-cig and end products (copper nanoparticles) (Lerner et al, 2016).…”

Impacto do Tabagismo Passivo na Resposta Pressórica à Epinefrina e Felipressina em Ratos Hipertensos 1K1C Tratados ou não com Atenolol

“…Nicotine-free cigarette smoke extract administered by subcutaneous injection induced endothelial dysfunction, increased blood pressure values and reduced acetylcholineinduced vasodilatation. 18 Although the chemical component responsible for epithelial dysfunction is not clear, cigarettes smoke extract reduces vascular relaxation by increasing oxidative stress and reducing NO bioavailability. 19 Smokers also showed altered lipoprotein metabolism, increased levels of oxidized low density lipoprotein (LDL) which may contribute to vasoconstriction.…”