Smoking is considered to be one the of risk factors effecting atherosclerosis which is associated the physical forces, biological and chemical stimuli occuring in vessel wall. The aim of this study is analysis of the biomechanical (plasma viscosity) and biochemical effect (nitric oxide, NO x; asymmetric dimethylarginine, ADMA) of smoking on endothelial function. One hundred-twenty two individuals were divided into three groups according to their smoking status. Plasma viscosity was measured by Harkness Capillary Viscometer. Plasma NO x level was determined by enzymatic methods using commercial kits. ADMA concentration was determined by Elisa Plasma Assay and and physiologic spirometric and arterial gas parameters and pulmonary blood flow rate (PBFR) were measured. Viscosity variables of former smokers were significantly higher than those of non-smokers (p< 0.001). NO x levels were found to be statistically significantly higher when compared with current smokers and non-smokers (p< 0.001), and former smokers and non-smokers (p< 0.05). There was a higher fibrinogen levels in current smokers (p< 0.05) than smokers. Smoking increases the plasma viscosity that may lead endothelial damage. Plasma viscosity plays an important role as a biophysical mechanical marker on the behalf of hemodynamics. Biochemical markers, NO x and ADMA may show this damage, however, we observed that plasma viscosity can be consistent with biochemical markers. Thus, plasma viscosity may be useful for diagnosis, treatment and follow-up of the patients.