Platelets from hypertensive patients show increased sensitivity to agonists and have high intracellular free Ca(2+) concentration. Furthermore, in hypertension, platelets show enhanced endogenous production of reactive oxygen species and a reduced antioxidant status which increases protein tyrosine phosphorylation, enhances Ca(2+) mobilization and attenuates NO bioavailability. The study of the abnormalities in platelet function in hypertensive patients can lead to the development of new pharmacological strategies to prevent and/or palliate hypertension-derived complications associated to platelet hyperactivity.