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.
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