Issues on Smoking and Cardiovascular Disease, Part II
Smoking and endothelial function,☆☆

https://doi.org/10.1053/pcad.2003.YPCAD13Get rights and content

Abstract

The arterial endothelium is a vital homeostatic cell layer responsible for a variety of functions such as thromboresistance, control of vessel tone, and vessel growth. Recent evidence has indicated that both active and passive cigarette smoking are associated with dysfunction of normal endothelial physiology, in a dose dependent and potentially reversible way. Endothelial abnormalities may predispose to the atherogenic and thrombotic problems associated with cigarette smoking. Copyright 2003, Elsevier Science (USA). All rights reserved.

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)

  • BQ Zhu et al.

    Passive smoking increase experimental atherosclerosis in cholesterol-fed rabbits

    J Am Coll Cardiol

    (1993)
  • GG Duthie et al.

    Effects of smoking and vitamin E on blood antioxidant status

    Am J Clin Nutr

    (1991)
  • C Heeschen et al.

    A novel angiogenic pathway mediated by non-neuronal nicotinic acetylcholine receptors

    J Am Coll Cardiol

    (2003)
  • NL Benowitz et al.

    Nicotine effects the eicosanoid formation and hemostatic function: Comparison of transdermal nicotine and cigarette smoking

    J Am Coll Cardiol

    (1993)
  • C Weber et al.

    Enhancement of monocyte adhesion to endothelial cells by modified low density lipoprotein is mediated via activation of CD 11b

    Biochem Biophys Res Commun

    (1995)
  • M Nobuyoshi et al.

    Statistical analysis of clinical risk factors for coronary artery spasm: Identification of the most important determinant

    Am Heart J

    (1992)
  • OT Raitakari et al.

    Oral vitamin C and endothelial function in smokers: Short-term improvement, but no sustained beneficial effect

    J Am Coll Cardiol

    (2000)
  • LA Simons et al.

    Vitamin E ingestion does not improve endothelial dysfunction in older adults

    Atherosclerosis

    (1999)
  • S Ueda et al.

    Tetrahydrobiopterin restores endothelial function in long-term smokers

    J Am Coll Cardiol

    (2000)
  • GE Palade

    Fine structure of blood capillaries

    J Appl Physiol

    (1953)
  • MA Gimbrone

    Culture of vascular endothelium

    Prog Hemost Thromb

    (1976)
  • EM Renkin

    Multiple pathways of capillary permeability

    Circ Res

    (1997)
  • PL Ludmer et al.

    Paradoxical vasoconstriction induced by acetylcholine in atherosclerotic coronary arteries

    N Engl J Med

    (1986)
  • S Moncada

    Biological importance of prostacyclin

    Br J Pharmacol

    (1982)
  • CM Hekman et al.

    Fibrinolytic pathways and the endothelium

    Semin Thromb Hemost

    (1987)
  • PM Vanhoutte

    Endothelium and control of vascular function

    Hypertension

    (1989)
  • JW Ryan et al.

    Endothelium surface enzymes and the dynamic processing of plasma substrates

    Int Rev Exp Pathol

    (1984)
  • RF Furchgott et al.

    The obligatory role of endothelial cells in the relaxation of arterial smooth muscle by acteylcholine

    Nature

    (1980)
  • RMJ Palmer et al.

    Vascular endothelial cells synthesize nitric oxide from L-arginine

    Nature

    (1988)
  • WP Arnold et al.

    Nitric oxide activates guanylate cyclase and increases guanosine 3:5-cyclic monophosphate levels in various tissue preparations

    Proc Natl Acad Sci U S A

    (1977)
  • P Collins et al.

    Endothelium derived relaxing factor alters calcium fluxes in rabbit aorta: A cyclic guanosine monophosphate-mediated effect

    J Physiol (Lond)

    (1986)
  • GA Fitzgerald et al.

    Estimated rate of prostacyclin secretion into the circulation of normal man

    J Clin Invest

    (1981)
  • M Yanagisawa et al.

    A novel vasoconstrictor peptide produced by vascular endothelial cells

    Nature

    (1988)
  • T Masaki

    The discovery, the present state, the future prospects of endothelin

    J Cardiovasc Pharmacol

    (1989)
  • E Anngard et al.

    The fate of radio-iodinated endothelin-1 and endothelin-3 in the rat

    J Cardiovasc Pharmacol

    (1989)
  • AN Warrens et al.

    Endothelin in renal failure

    Nephrol Dial Transplant

    (1990)
  • RJ Cody

    The potential role for endothelin as a vasoconstrictor substrate in congestive heart failure

    Eur Heart J

    (1992)
  • WJ Paulus et al.

    Paracrine coronary endothelium control of left ventricular function in humans

    Circulation

    (1995)
  • H Drexler et al.

    Endothelial function in human coronary arteries in vivo

    Hypertension

    (1991)
  • AM Zeiher et al.

    Modulation of coronary vasomotor tone in humans: Progressive endothelial dysfunction with different early stages of atherosclerosis

    Circulation

    (1991)
  • JA Vita et al.

    Coronary vasomotor response to acetylcholine relates to risk factors for coronary artery disease

    Circulation

    (1990)
  • TJ Andeson et al.

    the effect of cholesterol lowering and anti-oxidant therapy on endothelium-dependent coronary vasomotion

    N Engl J Med

    (1995)
  • CB Treasure et al.

    Beneficial effects of cholesterol-lowering therapy on the coronary endothelium in patients with coronary artery disease

    N Engl J Med

    (1995)
  • GBJ Mancini et al.

    Angiotensin-converting enzyme: Inhibition with quinapril improves endothelial vasomotor dysfunction in patients with coronary artery disease

    Circulation

    (1996)
  • P Clarkson et al.

    Oral L-arginine improves endothelium-dependent dilation in hypercholesterolemic young adults

    J Clin Invest

    (1996)
  • GN Levine et al.

    Ascorbic acid reverses endothelial vasomotor dysfunction in patients with coronary artery disease

    Circulation

    (1996)
  • R Ross

    the pathogenesis of atherosclerosis: A perspective for the 1990s

    Nature

    (1993)
  • Cited by (132)

    • Cigarette Smoking, Smoking Cessation, and Risk of Hearing Loss in Women

      2020, American Journal of Medicine
      Citation 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

    • Nailfold capillaroscopy in common non-rheumatic conditions: A systematic review and applications for clinical practice

      2020, Microvascular Research
      Citation 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.

    View all citing articles on Scopus

    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].

    ☆☆

    0033-0620/03/4506-0001$30.00

    View full text