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 0-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 ( V J 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 V,., was corrected for the platelet count. Paradoxically, the activation constants (KJ for ADP were higher in patients than in control subjects (/7<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 (/><0.02). /3-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 (/?<0.003, /?<0.04, /?<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. (Hypertension 1989;13:558-566)