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Journal of Renin-Angiotensin-Aldosterone System
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Losartan inhibits in vitro platelet activation: comparison with candesartan and valsartan

Antonio Núñez

Cardiovascular Research and Hypertension Laboratory, Fundación Jiménez Díaz, Madrid, Spain

Juan Gómez

Cardiovascular Research and Hypertension Laboratory, Fundación Jiménez Díaz, Madrid, Spain

Luis Rico Zalba

Cardiovascular Research and Hypertension Laboratory, Fundación Jiménez Díaz, Madrid, Spain

Mercedes Montón

Cardiovascular Research and Hypertension Laboratory, Fundación Jiménez Díaz, Madrid, Spain

Ana Jiménez

Cardiovascular Research and Hypertension Laboratory, Fundación Jiménez Díaz, Madrid, Spain

Sandra Velasco

Cardiovascular Research and Hypertension Laboratory, Fundación Jiménez Díaz, Madrid, Spain

Almudena López-Blaya

Cardiovascular Research and Hypertension Laboratory, Fundación Jiménez Díaz, Madrid, Spain

Angel Celdrán Uriarte

Cardiovascular Research and Hypertension Laboratory, Fundación Jiménez Díaz, Madrid, Spain

Santos Casado

Cardiovascular Research and Hypertension Laboratory, Fundación Jiménez Díaz, Madrid, Spain

Antonio López-Farré

Cardiovascular Research and Hypertension Laboratory, Fundación Jiménez Díaz, Madrid, Spain, alopeza{at}fjd.es

A recent study has shown that losartan, an AT1-receptor antagonist, interacts with thromboxane A2 (TxA2)/prostaglandin H2 (PGH2) receptors in human platelets. The aim of the present study was to analyse the ability of different angiotensin II (Ang II) AT1-receptor antagonists to inhibit TxA2-dependent human platelet activation. Platelets were obtained from healthy volunteers and were stimulated with the thromboxane A2 analogue, U46619 (10-6 mol/L). U46619-stimulated platelet activation was significantly reduced by losartan in a dose-dependent manner. Only maximal doses of valsartan (5x10-6 mol/L), reduced U46619-induced platelet activation. The active form of candesartan cilexetil, candesartan (CV-11974), failed to modify platelet activation. Losartan reduced the binding of [3H]-U46619 to platelets, an effect that was observed to a lesser extent with valsartan but not with CV-11974. These results suggest that, whilst some AT1-receptor antagonists reduce TxA2-dependent human platelet activation, it is not a feature common to all AT1 antagonists.

Key Words: platelets • AT1 antagonists • receptors • thromboxane A2

Journal of Renin-Angiotensin-Aldosterone System, Vol. 1, No. 2, 175-179 (2000)
DOI: 10.3317/jraas.2000.022
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