Lack of effect of vitamin E administration on basal nitric oxide function in male smokers and non-smokers.
1. 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.
D000328:Adult; D001783:Blood Flow Velocity; D016022:Case-Control Studies; D005542:Forearm / Q000098:blood supply; D006801:Humans; D008297:Male; D009569:Nitric Oxide / Q000502:physiology*; D012039:Regional Blood Flow; D012907:Smoking; D014810:Vitamin E / Q000008:administration & dosage / Q000494:pharmacology*
D014810:Vitamin E; D009569:Nitric Oxide