Effects of tobacco and non-tobacco cigarette smoking on endothelium and platelets

Davis, James W.; Shelton, Loretta; Eigenberg, D A; Hignite, Charles E.; Watanabe, Itaru

doi:10.1038/clpt.1985.83

Cited by 148 publications

(52 citation statements)

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“…This is supported with the finding that, in the presence of L-NNA, there was no significant difference between the control and nicotine-treated uterine arteries. Previous studies have indicated that chronic cigarette smoking causes morphologic changes and functional alteration in endothelial cells (Davis et al, 1985;Powell, 1998). In addition, inhibition of eNOS with N G -monomethyl-L-arginine produced a significantly greater decrement in forearm blood flow in smokers versus nonsmokers (McVeigh et al, 1996), suggesting that cigarette smoking altered endothelial function and increased vascular tone.…”

Section: Discussionmentioning

confidence: 88%

Direct Effects of Nicotine on Contractility of the Uterine Artery in Pregnancy

Xiao¹,

Huang²,

Yang³

et al. 2007

J Pharmacol Exp Ther

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Recent studies indicate that smoking/nicotine increases maternal blood pressure and decrease in uterine blood flow in pregnancy. However, the mechanisms are not fully understood. The present study was designed to test the hypothesis that nicotine exposure decreases endothelium-dependent relaxation and increases vascular contractility of the uterine artery in pregnancy. Uterine arteries were isolated from near-term (ϳ140 days gestation) pregnant ewes. Arteries were subjected to acute (20 min) or chronic (48 h) nicotine treatment, and agonist-induced contractions and relaxations were measured in tissue bath. Endothelial eNOS was detected by immunohistochemistry in situ in arteries and by Western blotting in isolated endothelial cells. Chronic nicotine treatment produced a concentration-dependent increase in ␣ 1 -adrenoceptor agonist phenylephrine-induced contractions. In contrast, the acute treatment showed no effect. Inhibition of eNOS with N G -nitro-L-arginine (L-NNA) significantly increased phenylephrine-induced contractions, which was abolished in uterine arteries after chronic nicotine treatment. In the presence of L-NNA, there was no significant difference in phenylephrine-induced contractions between control and nicotine-treated vessels. Chronic, but not acute, nicotine treatment significantly attenuated the calcium ionophore A23187-induced relaxations. Unlike A23187, the endotheliumindependent relaxation mediated by sodium nitroprusside was not affected by nicotine. Endothelial eNOS protein levels and the phosphorylation levels of eNOS Ser1179 were significantly decreased in nicotine-treated uterine arteries. The results suggest that nicotine impairs uterine vascular function in pregnancy, which may lead to an increased vascular resistance and a decrease in uterine blood flow.

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Section: Discussionmentioning

confidence: 88%

Direct Effects of Nicotine on Contractility of the Uterine Artery in Pregnancy

Xiao¹,

Huang²,

Yang³

et al. 2007

J Pharmacol Exp Ther

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“…Smoking is associated with a direct toxic effect on human endothelial cells, reduces endothelial prostacyclin production and increases leukocyte adhesion to endothelial cells. [24][25][26][27] Cigarette smoke contains a large number of oxidants; the role of oxygen-derived free radicals in mediating endothelial dysfunction can be modulated by the potent antioxidant vitamin C. [28][29][30] Alternatively, smoking increases endothelial angiotensin II production, which reduces nitric oxide activity, and might contribute to endothelial damage in smokers. 31 Increased platelet and serum fibrinogen, as well as decreased serum plasminogen levels known to occur in smokers, might also impair endothelial function in smokers.…”

Section: Discussionmentioning

confidence: 99%

Effect of Smoking on Endothelial Function and Wall Thickness of Brachial Artery

Esen

Barutçu

Açar³

et al. 2004

Circ J

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igarette smoking is a well-known cardiovascular risk factor, and it affects both the coronary and peripheral circulation. [1][2][3][4] Because cigarette smoke contains a large number of oxidants, it has been hypothesized that the adverse effect of smoking could result in oxidative damage to vascular endothelium. 5 Indeed, endothelial dysfunction in brachial and coronary arteries has been demonstrated in long-term smokers and even in passive smokers. [6][7][8] However, it has also been found that acute cigarette smoking causes vasoconstriction of the epicardial coronary artery and increases the coronary resistance vessel tone. 9,10 Acute cigarette smoking has also been shown to cause a transient increase in pulse rate and blood pressure. 11 Although previous studies have apparently found that chronic cigarette smoking is associated with endothelial dysfunction, data regarding the dose-dependent effects of smoking on endothelial dependent vasodilatation are limited and inconclusive. 6-8, 12,13 Flow mediated dilatation in systemic as well as coronary arteries is mediated by the endothelium through the release of dilator substances that act on the underlying smooth muscle; these endothelium-derived relaxing factors have Circulation Journal Vol. 68, December 2004 been identified as nitric oxide. 14 Anderson et al 15 found that coronary artery endothelium dependent vasomotor responses to acetylcholine and flow-mediated vasodilatation in the brachial artery were similar. Thus, endothelial function in peripheral vessels such as the brachial artery can be measured noninvasively and inferentially correlated to responses within the coronary vasculature. In addition, Weideinger et al 16 recently showed that brachial artery wall thickness (BA-WT) is independently correlated with the presence of coronary artery disease (CAD) and that BA-WT can provide a novel noninvasive marker of atherosclerosis.Therefore, the purpose of this study was to determine chronic as well as instantaneous effects of smoking on brachial artery endothelial function in long-term smokers and non-smokers, and the effect of chronic smoking on BA-WT. Methods SubjectsTwenty healthy long-term heavy smokers (15 males, 5 females, mean age 27±9 years, smoking average of 25 cigarettes/day) and age-matched 20 healthy nonsmoking hospital staff (14 males, 6 females, mean age 25±7 years) were studied. A complete physical and echocardiographic examination was performed prior to the study. The participants were free from the other risk factors for CAD and none were taking any any medication during the study (Table 1). All participants gave their informed consent and the institutional review board approved the study protocol. Background Impaired flow mediated dilatation (FMD) and increased wall thickness (WT) of the brachial artery have been associated with atherosclerosis and its risk factors. In this study we sought to determine brachial artery wall thickness in chronic smokers and the instantaneous effect of smoking on brachial artery endothelium dependent vaso...

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“…For example, Kritz and Sinzinger (30) observed an increase in markers of platelet activation and a decrease in platelet sensitivity to PGI2 among 12 nonsmokers exposed for 20-min in an 18 m3 room in which 30 Gitanes had recently been smoked. The hypercoagulable state demonstrated among nonsmokers acutely exposed to ETS (30)(31)(32)(33)(34) resembles the acute changes in smokers who consume one or two cigarettes after a period of abstinence (35)(36)(37)(38)(39)(40)(41)(42)(43). Schmid et al (31) found that, prior to ETS exposure, the platelets of nonsmokers were significantly less activated than those of smokers, whereas after 20 min exposure to ETS, platelet activation increased among the nonsmokers exposed to ETS (p < 0.01) but remained constant among the active smokers (p > 0.05).…”

Section: Experimental Studies Ofets Exposurementioning

confidence: 99%

Why Is Environmental Tobacco Smoke More Strongly Associated with Coronary Heart Disease Than Expected? A Review of Potential Biases and Experimental Data

Howard¹,

Thun²

1999

Environmental Health Perspectives

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Despite exposure levels estimated to be equivalent to smoking only 0.1-1.0 cigarettes per day, exposure to environmental tobacco smoke (ETS) is estimated to increase the risk of death from coronary heart disease (CHD) between 25 and 35% above the risk of nonexposed persons. This surprisingly large risk associated with a seemingly small exposure has raised doubts about the validity of attributing the increased CHD risk to ETS exposure. This paper reviews various biases that have been hypothesized to account for the increased CHD risk associated with ETS in the epidemiologic studies and characterizes the adverse effects of ETS on thrombosis, vascular endothelium, and exercise tolerance observed in experimental studies of humans and laboratory animals. None of the identified factors that has been proposed to introduce a spurious association between ETS and heart disease seem to invalidate the epidemiologic findings, either separately or in combination. In addition, experimental studies of ETS and heart disease demonstrate that acute exposure of humans and other species to ETS affects platelet function, vascular endothelium, and myocardial exercise tolerance at exposure concentrations widely prevalent in the workplace. Because exposure to ETS affects multiple physiologic pathways, it appears biologically plausible that ETS could cause the substantial increase in CHD risk that has been observed in epidemiologic studies. Key words: atherosclerosis, cardiovascular disease, risk factor, smoking. -Environ Health Perspect 1 07(suppl 6): 853-858 (1999). http.//ehpnet 1. niehs. nih.gov/docs/1999/suppl-6/853-858howard/abstract. html

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Effects of tobacco and non-tobacco cigarette smoking on endothelium and platelets

Cited by 148 publications

References 0 publications

Direct Effects of Nicotine on Contractility of the Uterine Artery in Pregnancy

Direct Effects of Nicotine on Contractility of the Uterine Artery in Pregnancy

Effect of Smoking on Endothelial Function and Wall Thickness of Brachial Artery

Why Is Environmental Tobacco Smoke More Strongly Associated with Coronary Heart Disease Than Expected? A Review of Potential Biases and Experimental Data

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