To test the hypothesis that platelet activation is present in hyperten
sion, we measured plasma markers beta thromboglobulin and soluble P-se
lectin in hypertensive patients and normotensive controls. Both marker
s were raised in the patients (P < 0.05), and in a subgroup of patient
s, beta thromboglobulin was reduced with successful treatment of hyper
tension with the ACE inhibitor quinapril. We suggest that reversible p
latelet activation is present in hypertension. This may be a contribut
ing factor to the link between this risk factor and the development of
thrombotic disease such as stroke.