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Platelet aggregability in patients with hypertension treated with angiotensin II type 1 receptor blockers

Yuki Sato1, Satoshi Fujii, Shogo Imagawa

  • 1Department of Cardiovascular Medicine Hokkaido University Graduate School of Medicine, Japan.

Journal of Atherosclerosis and Thrombosis
|March 3, 2007
PubMed

Insights

Losartan, an angiotensin II type 1 receptor blocker (ARB), demonstrated in vivo inhibition of platelet aggregation in hypertensive patients. This antiplatelet effect may contribute to reduced cardiovascular events, independent of blood pressure control.

Area of Science:

  • Cardiology
  • Pharmacology
  • Thrombosis Research

Background:

  • Hypertension-associated cardiovascular events frequently involve thrombosis.
  • Increased platelet activity is a significant risk factor for cardiovascular diseases.
  • The antithrombotic properties of antihypertensive agents, particularly Angiotensin II type 1 receptor blockers (ARBs), require further characterization in vivo.

Purpose of the Study:

  • To investigate the in vivo effects of ARBs on platelet aggregation in hypertensive patients.
  • To compare the antiplatelet activity of losartan versus candesartan in patients with hypertension.

Main Methods:

  • Platelet aggregation was assessed using a highly sensitive particle counting method with laser-light scattering.
  • Adenosine diphosphate (ADP) and a thromboxane A2 receptor agonist (U46619) were used to induce platelet aggregation.

Main Results:

  • Losartan significantly reduced platelet aggregation induced by ADP and U46619 compared to candesartan in hypertensive patients.
  • Platelet aggregation induced by ADP was 2.6±0.4 (x10^7) with losartan versus 3.9±0.6 (x10^7) with candesartan (p=0.056).
  • Platelet aggregation induced by U46619 was 2.8±0.5 (x10^7) with losartan versus 5.1±0.9 (x10^7) with candesartan (p=0.033).
  • Blood pressure control was similar between the losartan and candesartan groups.

Conclusions:

  • Losartan exhibits in vivo antiplatelet properties in hypertensive patients, independent of its blood pressure-lowering effects.
  • These antiaggregatory effects may be mediated through mechanisms distinct from Angiotensin II type 1 receptor blockade or general antihypertensive actions.
  • The observed inhibition of platelet activation by losartan may partially explain its favorable impact on reducing adverse cardiovascular events in hypertensive individuals.
Abstract

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