RESUMO
OBJECTIVES: We investigated the influence of angiotensin receptor blockade and angiotensin-converting enzyme inhibition on stress-induced platelet activation in hypertensive patients. Secondary aims were effects on inflammation, coagulation, and endothelial function. METHODS: Following a 4-week placebo period, 25 hypertensive patients entered a double-blind, crossover study comparing enalapril (20âmg once daily) and losartan (100âmg once daily) treatment (each for 8 weeks). Patients were studied at rest and after a standardized exercise test. RESULTS: Mean arterial pressure was reduced from 119â±â2 to 104â±â2 (enalapril) and 106â±â2 (losartan)âmmHg (both Pâ<0.001). Plasma angiotensin II decreased from 2.4â±â0.4 to 0.5â±â0.1âpmol/l with enalapril, and increased to 7.2â±â1.3âpmol/l with losartan (both Pâ<0.001). Exercise-evoked platelet activation, as evidenced by increased numbers of P-selectin-positive platelets (Pâ<0.01), elevated circulating platelet-platelet aggregates (Pâ<0.01) and soluble P-selectin levels (Pâ<0.001), and increased platelet responsiveness to adenosine diphosphate and thrombin (both Pâ<0.05). Neither drug influenced these markers of platelet activation at rest or following exercise. Markers of inflammation (high-sensitivity C reactive protein, interleukin-6, tissue necrosis factor-α), coagulation (tissue plasminogen activator antigen, prothrombin fragment F1+2), and endothelial function (von Willebrand factor, soluble vascular cellular adhesion molecule-1, and intercellular adhesion molecule-1) were also uninfluenced by treatment. CONCLUSION: Enalapril and losartan failed to reduce platelet activity both at rest and during exercise in hypertensive patients. Markers of inflammation, coagulation, and endothelial function were similarly unaffected. Inhibition of the renin-angiotensin system promotes its beneficial effects in hypertension through mechanisms other than platelet inhibition.
