Cigarette smoking is the leading cause of death in the United States. The addictive component of tobacco is nicotine, which has been found to be responsible for many of the adverse cardiovascular effects normally associated with smoking. A number of studies have demonstrated that vascular tone can be increased or decreased in response to nicotine depending on the origin of the blood vessels examined, the concentration of nicotine used, and the method of administration. These effects can be a result of differential gene expression, abnormal growth and proliferation, endothelial damage, superoxide radical ion production, and altered cation permeability. Nicotine also affects hemostasis by increasing thrombogenesis and platelet aggregation. In addition, nicotine influences hematopoiesis by altering the hematocrit, the expression of adhesion molecules, the erythrocyte-leukocyte ratio, and the specific leukocyte composition in the blood. In this paper we review these implications of nicotine use and also examine the role of nicotine in the development of several cardiovascular diseases.