Background: Smoking increases plasma nicotine. Nicotine releases catecholamine s and alters arterial distensibility. The nicotine intake per cigarette is great er and serum cotinine levels, the proximate metabolite of nicotine, are higher i n Blacks than in Whites. We tested the hypothesis that cigarette smoking increas es the pulse wave velocity(PWV), a marker of arterial stiffness, and the augment ation index(AI), a measure of wave reflection, more in Blacks than in Whites. Me thods: We matched Black(n=30) and White(n=30) smokers for age, gender, body mass index and height. We determined carotid-femoral PWV(PWVCF) and carotid-radial PWV(PWVCR)(Complior), the AI derived from the aortic pressure waveform(applanat ion tonometry, Sphygmocor), blood pressure, heart rate(HR) and cotinine levels b efore and after cigarette smoking. We also performed measurements in 16 participants aft er sham smoking. Results: Smoking increased the AI, PWVCF and PWVCR in the whole population(all P< 0.05, n=60). Increases in the AI and PWV were positively rela ted to serum cotinine levels(all P< 0.05). Smoking increased serum cotinine(P=0. 01) and mean blood pressure(P=0.03) more,but raised the HR to a lesser extent, i n Blacks[+8±4 versus+13±6 beats/ min in Whites(mean±SD), P=0.01]. Blacks di sclosed larger increases in AI adjusted for HR(Blacks, +7.2±8 versus Whites, +4.4±8%; P=0.03), PWVCF(Blacks, +1.1±0.2 versus Whites, +0.6±0.3 m/s; P< 0.01) and PWVCR(Blacks, +1.4±0.1 versus Whites, +0.7±0.4 m/s; P< 0.01) norma lized for the mean blood pressure. No changes were observed with sham smoking. C onclusions: Smoking acutely increases the PWV and AI in Blacks more than in Whit es. Differences in nicotine metabolism and β-adrenergic sensitivity could expl ain these findings. Background: Smoking increases plasma nicotine. Nicotine releases catecholamine s and alters arterial distensibility. The nicotine intake per cigarette is great er and serum cotinine levels, the proximate metabolite of nicotine, are higher in Blacks than in Whites. We tested the hypothesis that cigarette smoking increas es the pulse wave velocity (PWV), a marker of arterial stiffness, and the augment index (AI), a measure of wave reflection, more in Blacks than in Whites. Me thods: We matched Black (n = 30) and We determined carotid-femoral PWV (PWVCF) and carotid-radial PWV (PWVCR) (Complior), the AI ​​derived from the aortic pressure waveform (applanat ion tonometry, Sphygmocor), blood pressure, heart rate (HR) and cotinine levels b efore and after cigarette smoking. We also performed measurements in 16 participants aft er sham smoking. Results: Smoking increased the AI, PWVCF and PWVCR in the whole population ( all P <0.05, n = 60). Increases in the AI ​​and PWV were positively rela ted to serum cotinine levels (all P <0.05). Smoking increased serum cotinine (P = 0.01) and mean blood pressure (P = 0.03) more, but raised the HR Blacks di sclosed larger increase in AI adjusted for HR (Blacks, +7.2 ± 8 vs. 8 ± 4 versus + 13 ± 6 beats / min in Whites (mean ± SD), P = 0.01] (Blacks, +1.4 ± 0.1 versus Whites, +4.4 ± 8%; P = 0.03), PWVCF (Blacks, +1.1 ± 0.2 versus Whites, +0.6 ± 0.3 m / No changes were observed with sham smoking. C onclusions: Smoking acutely increases the PWV and AI in Blacks more than in Whit es. Differences in nicotine metabolism and β-adrenergic sensitivity could expl ain these findings.