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It has been shown that losartan inhibits vasoconstriction through binding to the thromboxane A 2 receptors. We investigated whether Thromboxane A 2 -induced platelet aggregation can be inhibited by losartan and if this effect is present in losartan treated hypertensive patients. Platelet aggregation was measured in platelet rich plasma from healthy volunteers and hypertensive patients, with the use of an aggregometer. Losartan inhibited the effect of Thomboxane A 2 agonist (U46619)-induced platelet aggregation, with a pA 2 value of 48.9 μM and inhibited both second and first phases of Adenosine diphosphate-induced aggregation, from 109 ± 9 to 65 ± 10 mm and from 62± 8 to 0 mm. U46619’s and Adenosine diphosphate's concentration required to produce half-maximal response were higher in normotensive volunteers (EC 50 2.01 ± .3 μM and 2.6 ± .4 μM) compared to the hypertensive patients without treatment (EC 50 0.6 ± .2 μM and 2.0 ± .3 μM). The concentration required to produce half-maximal response in losartan treated patients was similar to the healthy volunteers(EC 50 1.7 ± .2 μM and 1.4 ± .3 μM), whereas in the lisinopril hypertension treated patients the concentrations used, were lower (EC 50 1.4 ± .3 μM and 2.11 ± .5 μM). Losartan plasma concentration of hypertensive patients was 60.3 ± 18.7 ng/ml. Computer analysis showed that losartan, Thromboxane A 2 and the Thromboxane A 2 receptor antagonist, SQ29548 have equivalent functional groups and spatial distribution. Conclusion. We suggest that losartan inhibits platelet aggregation through Thromboxane A 2 dependent and independent mechanisms. [ABSTRACT FROM AUTHOR]