Abstract
Smoking is a significant independent risk factor for cardiovascular disease and is a leading cause of structural and functional alterations of the cardiovascular system. Most clinical and experimental investigations of the pathophysiology of cigarette smoking have studied the effects of smoke as a whole, while a few studies focused on specific components of cigarette smoke, e.g. nicotine and carbon monoxide, which are only 2 of the more than 4,000 different chemicals present in cigarette smoke. The findings point to some discrepancies when the effects of whole smoke are compared to nicotine alone, while there is almost uniform agreement that both active and passive smoking have detrimental effects on the cardiovascular system, although a milder effect was suggested for the latter. This review focuses on findings from clinical and experimental studies on the vascular effects of active and passive cigarette smoking and nicotine exposure. The findings are discussed in terms of tissue (conduit vs. resistance arteries and veins), species, age, gender and dosage. Although the exact pathophysiology of cigarette smoking has not been unveiled, cigarette smoking causes injury to the vascular endothelium, produces superoxide anions, reduces production and bioavailability of nitric oxide (NO), increases production and release of endothelin, causes endothelial dysfunction, thrombosis, atherosclerosis, infarction, coronary artery disease (CAD), stroke and death.
Keywords: Cigarette smoking, blood vessels, endothelin, oxidative stress, endothelial dysfunction, atherosclerosis, matrix metalloproteinase, erectile dysfunction
Current Vascular Pharmacology
Title: Structural and Functional Alteration of Blood Vessels Caused by Cigarette Smoking: An Overview of Molecular Mechanisms
Volume: 5 Issue: 4
Author(s): Mohammad M. Rahman and Ismail Laher
Affiliation:
Keywords: Cigarette smoking, blood vessels, endothelin, oxidative stress, endothelial dysfunction, atherosclerosis, matrix metalloproteinase, erectile dysfunction
Abstract: Smoking is a significant independent risk factor for cardiovascular disease and is a leading cause of structural and functional alterations of the cardiovascular system. Most clinical and experimental investigations of the pathophysiology of cigarette smoking have studied the effects of smoke as a whole, while a few studies focused on specific components of cigarette smoke, e.g. nicotine and carbon monoxide, which are only 2 of the more than 4,000 different chemicals present in cigarette smoke. The findings point to some discrepancies when the effects of whole smoke are compared to nicotine alone, while there is almost uniform agreement that both active and passive smoking have detrimental effects on the cardiovascular system, although a milder effect was suggested for the latter. This review focuses on findings from clinical and experimental studies on the vascular effects of active and passive cigarette smoking and nicotine exposure. The findings are discussed in terms of tissue (conduit vs. resistance arteries and veins), species, age, gender and dosage. Although the exact pathophysiology of cigarette smoking has not been unveiled, cigarette smoking causes injury to the vascular endothelium, produces superoxide anions, reduces production and bioavailability of nitric oxide (NO), increases production and release of endothelin, causes endothelial dysfunction, thrombosis, atherosclerosis, infarction, coronary artery disease (CAD), stroke and death.
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Cite this article as:
Rahman M. Mohammad and Laher Ismail, Structural and Functional Alteration of Blood Vessels Caused by Cigarette Smoking: An Overview of Molecular Mechanisms, Current Vascular Pharmacology 2007; 5 (4) . https://dx.doi.org/10.2174/157016107782023406
DOI https://dx.doi.org/10.2174/157016107782023406 |
Print ISSN 1570-1611 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6212 |
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