Abstract
This study was designed to investigate the effects of smoking on endothelial function in 88 healthy blood donors: 48 smokers and 40 non-smokers. Two markers of endothelial dysfunction, plasminogen activator inhibitor-1 (PAI-1) and nitric oxide (NO) levels, were measured at baseline and after phlebotomy. It has been proposed that phlebotomy acutely activates the renin–angiotensin–aldosterone system, thereby activating endothelial activity and increasing PAI-1 and NO expression. At baseline there were no significant differences between smokers and non-smokers in terms of PAI-1 expression and NO levels. After phlebotomy, both PAI-1 and NO levels were significantly increased in both groups. The increase in PAI-1 was more pronounced in smokers and the increase in NO was more pronounced in non-smokers. These findings suggest that smoking causes endothelial dysfunction, even in healthy smokers, which may remain silent until a clinically evident disorder develops.