Chronic cigarette smoking is associated with impaired basal and stimulated nitric oxide release in young men

R. Butler*, A. D. Morris, A. D. Struthers

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

Abstract / Description of output

Smoking continues to be a major public health issue, in particular, the increase in smoking among younger age groups causes significant concern. We examine the effects of moderate smoking on endothelial function (EF) of young men, who are otherwise well. We performed a cross-sectional study comparing the EF of smokers and controls (mean ages 25±5 vs. 24±6 years). We assessed the impact of smoking on endothelial dependent and endothelial independent vasodilatation on one study day. This was followed by the assessment of endothelial dependent and independent vasoconstriction on a second study day, one week later. We found smoking was associated with a significant impairment in endothelial dependent vasodilatation; acetyl choline (mean ± standard deviation, non-smokers vs. smokers) ( 4.071±2.183 vs. 3.415±1.787 mls/100mls/min; p=0.02, 95% CI 0.09,1.22). There was no significant difference between endothelial independent vasodilators; sodium nitroprusside (2.61±1.19 vs. 2.43±1.32 mls/100mls/min; p=0.30, 95% CI -0.70, 1.00) and verapamil (4.87± 3.44 vs. 4.74± 3.56; p=0.79, 95% CI -0.80, 1.06). There was also a significant impairment in both endothelial dependent and independent vasoconstrictors; monomethyl-L-arginine (0.78±0.22 vs. 0.87±0.21 mls/100mls/min; p=0.005; 95% CI -0.15,-0.02) and noradrenaline (0.61±0.20 vs. 0.68±0.17 mls/100mls/min; p=0.008, 95% CI -0.16, - 0.05). These data demonstrates that cigarette smoking in a young population causes a significant impairment of both stimulated and basal nitric oxide release. There is an associated significant reduction in the response to noradrenaline.

Original languageEnglish
Issue numberSUPPL. 1
Publication statusPublished - 1 May 1998


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