The aim of this research is the study of haemostasis of pregnant women suffering from various forms of hypertensive disorders in their III trimester of pregnancy. 165 women at 26-41 weeks of pregnancy were examined: 22 women had moderate preeclampsia, 31 had severe preeclampsia, 45 women suffered from chronic hypertension, 20 women have developed preeclampsia on the background of chronic hypertension and 47 women had no hypertensive disorders (control group). The hemostasis system has been assessed using the results of the following investigations: thromboelastography, induced platelet aggregation with ADP and adrenaline at a dosage of 1.25 and 2.5 μg/ml respectively and collagen at a dosage of 20 mg/ml, platelet ATP secretion and the average concentration of platelet components. Thromboelastography has been performed using TEG® 5000 thromboelastograph (Haemoscope Corporation, USA). The study of platelet aggregation and platelet ATP secretion has been performed at automatic aggregometer CHRONO-LOG® Model 700 (USA). The mean platelet component concentration has been measured using SIEMENS ADVIA 2120i automated hematology analyzer (Siemens Healthcare Diagnostics Inc., USA). Thromboelastogram analysis showed a decrease in the plasma hemostasis activity in all groups of women with hypertensive disorders. The functional activity of platelets of women with moderate preeclampsia and chronic arterial hypertension did not change in comparison with to the control group. The disorder of dense platelet granules degranulation and decrease in their aggregation ability have been detected in a cohort with severe preeclampsia. The decrease in adrenaline induced platelet aggregation has been noted in the group of women suffering from preeclampsia on the background of chronic arterial hypertension. Thromboelastography analysis (R, K, angle α, TMA, Cl, LY30) may be useful for the differential diagnosis of severe preeclampsia and chronic arterial hypertension. The results of the study led to the conclusion that it is advisable to use low doses of ADP and adrenaline as inducers of platelet aggregation, considering their granulocyticity and the ability to secrete ATP.