Key result
Eprosartan therapy significantly reduced systolic blood pressure from 152.2 to 142.2 mm Hg (P<0.01) and normalized platelet microparticle formation in hypertensive patients.
Why the study?
Does eprosartan reduce blood pressure and improve platelet function in hypertensive patients?
Does eprosartan reduce blood pressure and improve platelet function in hypertensive patients?
Eprosartan effectively lowers blood pressure and mitigates undesirable platelet activation and microparticle formation in hypertensive patients.
May reduce platelet activation in hypertension; leaves open whether this affects outcomes in randomized trials.
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.
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Labiós et al. (2004) studied Hypertension (n=61). Eprosartan vs. Baseline / Normotensive individuals was evaluated on Systolic blood pressure at 2 months (p=<.01). Eprosartan therapy significantly reduced systolic blood pressure from 152.2 to 142.2 mm Hg (P<0.01) and normalized platelet microparticle formation in hypertensive patients.
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