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

A. Mazzone, C. Cusa, I. Mazzucchelli, M. Vezzoli, E. Ottini, S. Ghio, G. Tossini, R. Pacifici, P. Zuccaro

Research output: Contribution to journalArticlepeer-review


Progression of atherosclerosis is currently believed to involve interactions between leukocytes and vascular endothelium. Epidemiological risk factors for atherosclerosis such as hypertension and smoking are known to cause endothelial dysfunction, which is an early event in the atherosclerotic process; they also may be considered in the light of their effects on adhesion molecule expression and release. Little is known about the additive effect between these two risk factors on endothelial adhesion molecule expression and nitric oxide release. Soluble adhesion molecules and the nitric oxide were 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 patients were selected: 51 smokers (plasma cotinine levels >25 ng/ml) and 52 non-smokers. Plasma concentrations of soluble intercellular cell adhesion molecule-1 (sICAM-1), soluble endothelial leukocyte adhesion molecule-1 (sELAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-I) were quantified 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

Original languageEnglish
Pages (from-to)822-826
Number of pages5
JournalClinical Chemistry and Laboratory Medicine
Issue number9
Publication statusPublished - 2001


  • Cotinine
  • Hypertension
  • Nitric oxide
  • Smoking
  • Soluble adhesion molecules

ASJC Scopus subject areas

  • Clinical Biochemistry


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