Previous studies in healthy subjects have demonstrated a lack of response of platelets to epinephrine at a rate of 16-40% on an aggregometer. An association between the increased procoagulant factors during pregnancy and venous thromboembolism is known, and it has also been shown that prolactin levels increase platelet aggregation. We evaluated whether platelet functions in pregnant women and also assessed the lack of response to epinephrine during this period. We compared 27 healthy and volunteering pregnant women with 26 similar control subjects. Platelet functions were assessed with an aggregometer and a Platelet Function Analyzer (PFA-100). Less than 40% response to epinephrine on the aggregometer was defined as an impaired epinephrine response. The aggregation response of epinephrine was normal in 25 of the 27 pregnant women, while two of them showed a late-rising response. Eight of the 26 subject control group (30.8%) showed an impaired response to epinephrine. When we compared the 25 pregnant and 18 control subjects with normal aggregation responses, the maximum aggregation responses to ADP and epinephrine, and the Col/Epi and Col/ADP cartridge closure time values were significantly lower in pregnant women. There were no difference beetween second and third trimesters as regards platelet function parameters. The fact that no impaired response to epinephrine was detected in pregnant women while a 30% rate was observed in non-pregnant women indicates that the platelet malfunction caused by a disorder in the Gi protein and intracellular mechanisms is bypassed during pregnancy thanks to some physiological changes.