The role of nicotine in smoking-related cardiovascular disease.
Nicotine activates the sympathetic nervous system and in this way could contribute to cardiovascular disease. Animal studies and mechanistic studies indicate that nicotine could play a role in accelerating atherosclerosis, but evidence among humans is too inadequate to be definitive about such an effect. Almost certainly, nicotine via its hemodynamic effects contributes to acute cardiovascular events, although current evidence suggests that the effects of nicotine are much less important than are the prothrombotic effects of cigarette smoking or the effects of carbon monoxide. Nicotine does not appear to enhance thrombosis among humans. Clinical studies of pipe smokers and people using transdermal nicotine support the idea that toxins other than nicotine are the most important causes of acute cardiovascular events. Finally, the dose response for cardiovascular events of nicotine appears to be flat, suggesting that if nicotine is involved, adverse effects might be seen with relatively low-level cigarette exposures.
Benowitz
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NL
Division of Clinical Pharmacology and Experimental Therapeutics, San Francisco General Hospital Medical Center, California 94110, USA. nbeno@itsa.ucsf.edu
D000208:Acute Disease; D000818:Animals; D001161:Arteriosclerosis / Q000209:etiology; D002318:Cardiovascular Diseases / Q000139:chemically induced / Q000453:epidemiology / Q000209:etiology* / Q000503:physiopathology; D004305:Dose-Response Relationship, Drug; D006801:Humans; D009538:Nicotine / Q000008:administration & dosage / Q000009:adverse effects*; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects* / Q000503:physiopathology; D013564:Sympathetic Nervous System / Q000187:drug effects
D009538:Nicotine