Cigarette smoking and hypertension influence nitric oxide release and plasma levels of adhesion molecules

Progression of atherosclerosis is currently believed to involve interaction s between leukocytes and vascular endothelium. Epidemiological risk factors for atherosclerosis such as hypertension and smoking are known to cause en dothelial dysfunction, which is an early event in the atherosclerotic proce ss; they also may be considered in the light of their effects on adhesion m olecule expression and release. Little is known about the additive effect b etween these two risk factors on endothelial adhesion molecule expression a nd nitric oxide release. Soluble adhesion molecules and the nitric oxide we re quantified in smoking hypertensive patients in comparison to those from patients with hypertension alone. Cotinine, a stable metabolite of nicotine , has been used to identify smokers. One hundred and three hypertensive pat ients were selected: 51 smokers (plasma cotinine levels > 25 ng/ml) and 52 non-smokers. Plasma concentrations of soluble intercellular cell adhesion m olecule-1 (sICAM-1), soluble endothelial leukocyte adhesion molecule-1 (sEL AM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) were quantifi ed with ELISA methods. Plasma concentration of nitric oxide metabolites was measured by HPLC, whilst plasma concentration of cotinine was measured by RIA. Significant increases of sICAM-1 and sVCAM-1 were demonstrated in smokers ( p < 0.001 and p < 0.05, respectively). In the same patients, a positive sig nificant correlation between sVCAM-1 and plasma cotinine levels was observe d (p < 0.002). Nitric oxide metabolites were reduced significantly (p < 0.0 4) in smokers. In conclusion, our data show that the two risk factors, smoking and hyperte nsion, are additive risk factors in generating endothelial dysfunction and vascular damage, which plays a key role in atherogenesis.