Is nicotine a key player or spectator in the induction and progression of cardiovascular disorders?

Abstract

Cigarette smoking is common in societies worldwide and a growing body of evidence suggests that chronic cigarette smoking may affect the structure and function of cardiovascular system. The chronic exposure to high levels of nicotine, a major component of cigarette smoking, has been observed to play a pathogenic role in the induction and progression of cardiovascular disorders including cardiomyopathy and peripheral vascular disease. Nicotine alters the function of vascular endothelium, initiates the adhesion cascade and stimulates the vascular inflammatory events to induce atherosclerosis and hypertension. Moreover, nicotine has been noted to induce direct coronary spasm and ischemia, which develop coronary artery disease and myocardial infarction. In addition, nicotine stimulates the excessive release of impulses from sinoatrial node that may account for the induction of cardiac arrhythmia. The present review critically discussed the possible detrimental role of chronic nicotine exposure in cardiac and vascular endothelial dysfunction. Moreover, the signaling mechanisms involved in the pathogenesis of nicotine exposure-induced cardiovascular dysfunction have been discussed. In addition, the pharmacological interventions to ameliorate chronic nicotine exposure-induced cardiovascular abnormalities have been delineated.