Aims: Smoking is a major risk factor for developing atherosclerosis. In order to understand the vascular abnormalities observed in smokers, we investigated vascular responsiveness in cigarette smokers. Methods: We performed two consecutive matched group comparative studies to investigate vascular responsiveness using venous occlusion plethysmography. The mean effects of three incremental doses of each vasoactive agent are presented. Both studies compared smokers with nonsmokers. Results: The first investigated 68 subjects (smokers = 29; mean ts.d. ages; 24 ± 6 vs 25 ± 5 years; P = NS) and found smoking was associated with a significant blunting of the flow ratio between treated and untreated arms to endothelium-dependent vasodilatation to acetylcholine (mean ± s.d., nonsmokers vs smokers) 4.07 ± 2.18 vs 3.42 ± 1.79 (P = 0.04, 95% CI 0.02, 1.12). By contrast, there was no significant difference in the responses to the endothelium-independent vasodilators sodium nitroprusside and verapamil. Smoking was also associated with a significant impairment in endothelium-dependent vasoconstriction induced by monomethyl-L-arginine (L-NMMA) 0.78 ± 0.22 vs 0.87 ± 0.21 (P = 0.006, 95% CI -0.14, -0.02) and a trend to blunted endothelium-independent vasoconstrictor responses to noradrenaline. In the second study we investigated the response to angiotensin I and II in 23 subjects (smokers = 12; mean ts.d. ages; 34 ± 10 vs 32 ± 11 years). There was significant impairment in smokers of the mean vasoconstrictor response to angiotensin I 0.51 ± 0.15 vs 0.59 ± 0.16 (nonsmokers vs smokers; P = 0.003, 95% CI -0.13, -0.03) and a nonsignificant trend towards impairment of the response to angiotensin II. Conclusions: Cigarette smoking in male volunteers is associated with blunted basal and stimulated nitric oxide bioactivity. Endothelial independent vasodilator responses (to nitroprusside and verapamil) were unaltered in smokers. A defect in the vasoconstrictor response to angiotensin I was also seen.
- Angiotensin I
- Nitric oxide