Aim: Cardiovascular events associated with hypertension often involve thrombosis. Increased platelet activity is one of the risk factors of cardiovascular diseases. Antithrombotic properties of antihypertensive agents are not fully characterized. Angiotensin II type 1 receptor blockers (ARBs) are widely used for the treatment of hypertension. Some ARBs can provoke antiaggregatory effects on platelets in vitro. Whether ARBs can inhibit platelet aggregation was tested in hypertensive patients in vivo.
Methods: Platelet aggregation was assessed by the highly sensitive particle counting method using laser-light scattering.
Results: Large platelet aggregation induced by adenosine diphosphate (ADP, 3 µM) was 2.6±0.4 (×10&sup7;) (SE) in hypertensive patients treated with losartan (72±3 years old, n=10) while it was 3.9±0.6 in hypertensive patients treated with candesartan (70±5 years old, n=6; p=0.056). Large platelet aggregation induced by thromboxane A2 receptor agonist, U46619 (10 µM), was 2.8±0.5 (×10&sup7;) in hypertensive patients treated with losartan while it was 5.1±0.9 in hypertensive patients treated with candesartan (p=0.033). Clinical characteristics including the control of blood pressure did not differ between the two groups (losartan 136±5/73±3 mmHg vs. candesartan 135±4/76±5).
Conclusion: Thus, losartan may have the possibility to inhibit platelet activation in patients with hypertension independent of blood pressure reduction. Antiaggregatory properties may be independent of angiotensin II type 1 receptor or of antihypertensive actions. The favorable effects of losartan on reduction of adverse cardiovascular events among hypertensive patients may be at least partly mediated by inhibition of platelet activation.