The role of nicotine in the pathogenesis of atherosclerosis

Abstract

Smoking is a major preventable risk factor for atherosclerosis. xposure to cigarette smoke activates a number of mechanisms redisposing to atherosclerosis, including thrombosis, insulin esistance and dyslipidemia, vascular inflammation, abnormal vasular growth and angiogenesis, as well as loss of endothelial omeostatic and regenerative functions [1–3]. The pathophysioogic mechanisms by which tobacco smoke accelerates vascular isease are manifold and complex, in part because the smoke conains over 4000 different chemicals [4]. Of these, the polycyclic romatic hydrocarbons, oxidizing agents, particulate matter, and icotine, have been identified as potential contributing factors to therogenesis. In addition to its role as the habituating agent in obacco, nicotine also accelerates vascular disease. By inducing the elease of catecholamines, nicotine increases heart rate and blood ressure. These adverse hemodynamic effects are associated with rogression of atherosclerosis. Furthermore, nicotine-induced catcholamine release increases platelet aggregability [3]. Platelets ontribute to the growth of plaque through the accretion of thromus, aswell as through the releaseof growth factors (suchasplatelet erived relaxing factor) that induce vascular smooth muscle cell roliferation. In addition to these actionsmediated by activation of he sympathetic nervous system, nicotine has direct actions on the ellular elements participating in plaque formation.