Issues on Smoking and Cardiovascular Disease, Part IISmoking and endothelial function☆,☆☆
Section snippets
Normal endothelial function
The endothelium is able to detect and respond to changes in hemodynamic forces or blood-borne signals by membrane receptor mechanisms. A variety of vasoactive and growth factors are released in response to physical and chemical stimuli. The substances released include NO, endothelins, endothelial growth factors, thromboregulators, plasminogen inhibitors, and von Willebrand factor. In addition to these generalized systemic functions in the vasculature, the endothelium also may have
Assessment of endothelial function
Most methods developed to date for studying endothelium rely on the detection of endothelium-mediated vasodilatation and/or assessing the normal endothelium's ability to release NO in response to pharmacologic and physiologic stimuli. Indeed the release of NO is particularly important because it also can inhibit monocyte adhesion, platelet aggregation, and smooth muscle proliferation, as well as being a vasodilator. Thus in vivo testing for NO release via measuring endothelium-dependent
Early atherogenesis
Endothelial dysfunction, either through physical injury or more subtle cellular damage, is a key early event in atherogenesis.33, 34 More specifically in the presence of coronary risk factors, the endothelium may develop a phenotype that facilitates inflammation, thrombosis, vasoconstriction, and eventually atherosclerotic lesion formation. Such dysfunction becomes apparent before the development of advanced plaque formation and is associated with both traditional risk factors (such as
Smoking and the endothelium
Smoking represents one of the most important modifiable risk factors for atherosclerosis. It has been shown that even light smoking from an early age may damage the vascular endothelium. This development of endothelial dysfunction becomes an initiating event in athersosclerosis and potentially accelerates it, preceding the onset of occlusive vascular disease. It also is established that long-term cigarette smoking is associated with impaired endothelium-dependent peripheral and coronary
Conclusion
Endothelial dysfunction is an established marker of smoke-related arterial damage. Both active and passive smoking are associated with dose-related and (partially) reversible arterial endothelial damage. The majority of smokers attempting the goal of smoking cessation are unsuccessful, however, and even those who achieve cessation show only partial reversibility of endothelial dysfunction. It appears that antioxidant therapy is ineffective in delivering sustained improvement in smoking-related
References (96)
Endothelial dysfunction: Does it matter? Is it reversible?
J Am Coll Cardiol
(1997)- et al.
Non-invasive detection of endothelial dysfunction in children and adults at risk of atherosclerosis
Lancet
(1992) - et al.
Differential formation of prostacyclin (PGX or PGI2) by layers of the arterial wall: An explanation for the anti-thrombotic properties of the vascular endothelium
Thromb Res
(1977) - et al.
Close relationship of endothelial function in the human coronary and peripheral circulations
J Am Coll Cardiol
(1995) - et al.
Cigarette smoking is associated with increased monocyte adhesion to endothelial cells in humans: Reversibility with L-arginine but not vitamin C
J Am Coll Cardiol
(1997) - et al.
Endothelium-dependent dilation in the systemic arteries of asymptomatic subjects relates to coronary risk factors and their interaction
J Am Coll Cardiol
(1994) - et al.
Effects of acute cigarette smoking on endothelium-dependent arterial dilation in normal subjects
J Am Coll Cardiol
(1998) - et al.
Epidemiology of coronary arterial disease in the Chinese
Int J Cardiol
(1989) - et al.
The impact of heavy passive smoking on arterial endothelial function in modernized Chinese
J Am Coll Cardiol
(2000) - et al.
Does passive smoking impair endothelium-dependent coronary artery dilation in women
J Am Coll Cardiol
(1998)
Passive smoking increase experimental atherosclerosis in cholesterol-fed rabbits
J Am Coll Cardiol
Effects of smoking and vitamin E on blood antioxidant status
Am J Clin Nutr
A novel angiogenic pathway mediated by non-neuronal nicotinic acetylcholine receptors
J Am Coll Cardiol
Nicotine effects the eicosanoid formation and hemostatic function: Comparison of transdermal nicotine and cigarette smoking
J Am Coll Cardiol
Enhancement of monocyte adhesion to endothelial cells by modified low density lipoprotein is mediated via activation of CD 11b
Biochem Biophys Res Commun
Statistical analysis of clinical risk factors for coronary artery spasm: Identification of the most important determinant
Am Heart J
Oral vitamin C and endothelial function in smokers: Short-term improvement, but no sustained beneficial effect
J Am Coll Cardiol
Vitamin E ingestion does not improve endothelial dysfunction in older adults
Atherosclerosis
Tetrahydrobiopterin restores endothelial function in long-term smokers
J Am Coll Cardiol
Fine structure of blood capillaries
J Appl Physiol
Culture of vascular endothelium
Prog Hemost Thromb
Multiple pathways of capillary permeability
Circ Res
Paradoxical vasoconstriction induced by acetylcholine in atherosclerotic coronary arteries
N Engl J Med
Biological importance of prostacyclin
Br J Pharmacol
Fibrinolytic pathways and the endothelium
Semin Thromb Hemost
Endothelium and control of vascular function
Hypertension
Endothelium surface enzymes and the dynamic processing of plasma substrates
Int Rev Exp Pathol
The obligatory role of endothelial cells in the relaxation of arterial smooth muscle by acteylcholine
Nature
Vascular endothelial cells synthesize nitric oxide from L-arginine
Nature
Nitric oxide activates guanylate cyclase and increases guanosine 3:5-cyclic monophosphate levels in various tissue preparations
Proc Natl Acad Sci U S A
Endothelium derived relaxing factor alters calcium fluxes in rabbit aorta: A cyclic guanosine monophosphate-mediated effect
J Physiol (Lond)
Estimated rate of prostacyclin secretion into the circulation of normal man
J Clin Invest
A novel vasoconstrictor peptide produced by vascular endothelial cells
Nature
The discovery, the present state, the future prospects of endothelin
J Cardiovasc Pharmacol
The fate of radio-iodinated endothelin-1 and endothelin-3 in the rat
J Cardiovasc Pharmacol
Endothelin in renal failure
Nephrol Dial Transplant
The potential role for endothelin as a vasoconstrictor substrate in congestive heart failure
Eur Heart J
Paracrine coronary endothelium control of left ventricular function in humans
Circulation
Endothelial function in human coronary arteries in vivo
Hypertension
Modulation of coronary vasomotor tone in humans: Progressive endothelial dysfunction with different early stages of atherosclerosis
Circulation
Coronary vasomotor response to acetylcholine relates to risk factors for coronary artery disease
Circulation
the effect of cholesterol lowering and anti-oxidant therapy on endothelium-dependent coronary vasomotion
N Engl J Med
Beneficial effects of cholesterol-lowering therapy on the coronary endothelium in patients with coronary artery disease
N Engl J Med
Angiotensin-converting enzyme: Inhibition with quinapril improves endothelial vasomotor dysfunction in patients with coronary artery disease
Circulation
Oral L-arginine improves endothelium-dependent dilation in hypercholesterolemic young adults
J Clin Invest
Ascorbic acid reverses endothelial vasomotor dysfunction in patients with coronary artery disease
Circulation
the pathogenesis of atherosclerosis: A perspective for the 1990s
Nature
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2022, Nitric Oxide - Biology and ChemistryCigarette Smoking, Smoking Cessation, and Risk of Hearing Loss in Women
2020, American Journal of MedicineCitation Excerpt :Components of cigarette smoke, such as toluene, benzene, and carbon monoxide, have also been associated with hearing loss.11,12 Cigarette smoke exposure may also impair vascular endothelial function, increase the risk of atherosclerosis and increase blood viscosity, and compromise oxygen delivery to the cochlea.58-60 Nicotine from tobacco may induce vasoconstriction, impair tissue perfusion, and lead to cellular dysfunction.59-61
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2020, Microvascular ResearchCitation Excerpt :Patients with dyslipidemia apparently show normal capillaroscopic features, but only one article, and with limited population size, was identified. Interestingly, although tobacco exposure promotes endothelial damage (Puranik and Celermajer, 2003) and smoking cessation is generally advised to reduce the symptoms of both primary and secondary RP, literature about the impact of smoking on NC features is not extensive and the only retrieved study described an increased prevalence of microhaemorrhages and dilated capillaries in chronic smokers. Notably, NC has been studied also in less common diseases, as tetralogy of Fallot (Chang et al., 1996), chronic viral hepatitis (Pancar and Kaynar, 2020), coronary slow flow phenomenon (Yuksel et al., 2014), pseudoxanthoma elasticum (Stumpf et al., 2020), acromegaly (Schiavon et al., 1999), or occupational exposure to vinyl chloride monomer (Lopez et al., 2013), suggesting how interest in NC and applications of the technique might extend far beyond SSc and CTDs.
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Address reprint requests to David Celermajer, MB, BS, PhD, FRACP, Department of Cardiology, Royal Prince Alfred Hospital, Missenden Rd, Camperdown 2050, Sydney, Australia; e-mail: [email protected].
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