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* Evans Memorial Department of Medicine and Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, 02118, USA;
Cardiovascular Division, Brigham and Women's Hospital, Boston, Massachusetts 02114, USA; and
Departments of Medicine and Pharmacology, Georgetown University, Washington, D.C. 20007, USA
1Correspondence: Whitaker Cardiovascular Institute, Boston University School of Medicine, 715 Albany St., W507, Boston, MA 02118, USA. E-mail: jkeaney{at}bu edu
Considerable epidemiologic data suggest that dietary consumption of vitamin E reduces the incidence of cardiovascular disease. The precise mechanisms are not clear, but emerging data indicate that vitamin E has numerous activities that may, in part, explain its effect on vascular disease. In particular, vitamin E enhances the bioactivity of nitric oxide, inhibits smooth muscle proliferation, and limits platelet aggregation. One common mechanism to account for these effects of vitamin E is the inhibition of protein kinase C stimulation. In the setting of atherosclerosis, inhibition of protein kinase C by vitamin E would be expected to maintain normal vascular homeostasis and thus reduce the clinical incidence of cardiovascular disease.—Keaney, J. F., Jr., Simon, D. I., Freedman, J. E. Vitamin E and vascular homeostasis: implications for atherosclerosis.
Key Words: LDL • vascular homeostasis • 
-tocopherol • nitric oxide
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