Answers are grounded in this paper and cite their sources.
The antioxidant properties of vitamin E (alpha-tocopherol) have been proposed to account for a possible protective effect in coronary artery disease. Coronary risk factors are associated with depressed endothelium-derived nitric oxide responses, and some evidence suggests increased quenching of the vasodilator effect of nitric oxide by oxygen free radicals. This study examined the possibility that vitamin E supplementation would improve basal function of the nitric oxide dilator system in long-term smokers and non-smokers. 2. Nine healthy male life-long non-smoking subjects and eight smokers (36 +/- 6 cigarettes per day, > 7 years) were given 1000 i.u. of vitamin E per day for a 4-week period, while five additional non-smokers received placebo. Forearm blood flow responses to intra-arterial infusion of noradrenaline (60, 120 and 240 rho mol/min) and the competitive inhibitor of nitric oxide synthesis, NG-monomethyl-L-arginine (1, 2 and 4 mumol/min) were measured before and after therapy. 3. No changes were evident in the constrictor responses to noradrenaline or NG-monomethyl-L-arginine in any group. These results indicate that vitamin E supplementation does not influence basal activity of the nitric oxide-dilator system in vivo.
No takes yet. Share an insight, caveat, or question.
Green et al. (1995) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: