Abnormal platelet function may contribute to the complications of essential hypertension. We have studied the kinetics of platelet aggregation induced by adenosine diphosphate (ADP) or epinephrine, plasma β-thromboglobulin, and basal, cytosolic, and free calcium, as correlates of platelet function. Fifteen untreated patients with essential hypertension and without detectable atherosclerosis, 18–40 years old, were compared with 30 matched normotensive control subjects. Maximal rates of platelet aggregation (Vmax) with ADP and epinephrine were significantly higher in patients than in control subjects (p< 0.03), as assessed by quenched-flow aggregometry. However, significance was lost when Vmaxwas corrected for the platelet count. Paradoxically, the activation constants (Ka) for ADP were higher in patients than in control subjects (p< 0.03). With ADP as the inducing agent, onset time (t) or lag period before aggregation begins was longer in patients than in control subjects (p< 0.02). β-thromboglobulin levels, an index of in vivo platelet activation, were not significantly different between the two groups (p= 0.13). The mean platelet cytosolic free calcium concentration was higher in patients (213±19 nM) than in control subjects (172±14 nM), but this difference was not statistically significant (p= 0.07). However, there was a close correlation between the free calcium level and systolic, diastolic, and mean blood pressure (p< 0.003,p< 0.04,p< 0.004, respectively). No difference in platelet volume between the two groups was found. Our data suggest that platelets in the early stages of essential hypertension display an overall increased aggregation potential but a diminished sensitivity to ADP. The tendency toward elevated calcium suggests that in hypertensive patients the platelets circulate in an already activated state; this occurrence could contribute to acceleration of atherosclerosis.