Background: Hypertensive patients show greater platelet activation than do normotensive individuals. Platelet activation is characterized by increased phosphatidylserine (PS) exposure in the external hemilayer of the membrane, a larger number of platelet microparticles (PMP), and changes in intraplatelet-free calcium kinetics. This study evaluated whether eprosartan can protect against undesirable platelet activation.
Methods: A total of 30 hypertensive patients (systolic blood pressure [SBP] 140 to 189 mm Hg; diastolic blood pressure [DBP] 90 to 109 mm Hg) without renal, liver, or cardiac organic lesions and with a mean age of 47.6 +/- 9.4 years and mean body mass index (BMI) of 27.9 +/- 3.9 kg/m2 received eprosartan (600 mg/day). They were compared with 31 normotensive individuals with a mean age of 43.3 +/- 6.7 years and a mean BMI of 26.8 +/- 3.9 kg/m2. Blood pressure measurements and platelet function changes were assessed at baseline (control and hypertensive patients) and after 1 and 2 months of eprosartan monotherapy (hypertensive patients only).
Results: Significant baseline to endpoint (month 2) changes in SBP and DBP were noted in the eprosartan group (SBP: baseline 152.2 +/- 16.8 mm Hg, endpoint 142.2 +/- 16.9 mm Hg, P <.01; DBP: baseline 93.5 +/- 9.9 mm Hg, endpoint 85.8 +/- 11.9 mm Hg, P <.001). Native circulating activated platelets increased in both groups after shear stress or Ca2+ ionophore activation, and were reduced by eprosartan (after shear exposure from 104% at month 1 to 76% after 2 months of therapy). Eprosartan therapy normalized the number of microparticles after blood shear exposure (P <.01) and after exposure to Ca2+ ionophore activation (P <.05) and significantly reduced the trend for platelets to be more readily activated in hypertensive compared with normotensive subjects (baseline to endpoint change P <.001; increase/shear versus baseline P <.001). Eprosartan partially normalizes cytoplasmic-free calcium mobilization in platelets.
Conclusions: Eprosartan significantly reduces blood pressure and normalizes undesirable changes in platelet function.
Copyright 2004 American Journal of Hypertension, Ltd.