Cigarette smoking is a well established risk factor for cardiovascular disease, and it affects both the coronary and the peripheral circulation. Because cigarette smoke contains a large number of oxidants, it has been hypothesized that the adverse effects of smoking may result from oxidative damage to vascular endothelium. Indeed, endothe-lial dysfunction in brachial and coronary arteries has been demonstrated in long-term smokers and even in passive smokers.
Ascorbic acid, or vitamin C, is the main water-soluble antioxidant in human plasma; it protects lipids against peroxidative damage by scavenging superoxide and other reactive oxygen species. In smokers, plasma and tissue vitamin C levels are lower than in nonsmokers. In addition, vitamin C has been reported to improve endothelium-dependent vasodilation in the forearm of smokers. In hypertensives, vitamin C improved endothelium-dependent vasomotion of epicardial coronary arteries, providing evidence that their coronary dysfunction is at least in part caused by increased oxidative stress.