title: Platelet aggregability in patients with hypertension treated with angiotensin II type 1 receptor blockers.
abstract: OBJECTIVE
  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 microM) was 2.6+/-0.4 (x10(7)) (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 microM), was 2.8+/-0.5 (x10(7)) 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).
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Cardiovascular Medicine Hokkaido University Graduate School of Medicine, Japan.
authors.forename: Yuki
authors.initials: Y
authors.lastname: Sato
authors.forename: Satoshi
authors.initials: S
authors.lastname: Fujii
authors.forename: Shogo
authors.initials: S
authors.lastname: Imagawa
authors.forename: Kazue
authors.initials: K
authors.lastname: Ohmura
authors.forename: Yoshinori
authors.initials: Y
authors.lastname: Ohmura
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Andoh
authors.forename: Jie
authors.initials: J
authors.lastname: Dong
authors.forename: Naoki
authors.initials: N
authors.lastname: Ishimori
authors.forename: Tomoo
authors.initials: T
authors.lastname: Furumoto
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Tsutsui
mesh_terms: D019796:15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid / Q000627:therapeutic use; D000368:Aged; D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use*; D001562:Benzimidazoles / Q000627:therapeutic use; D001713:Biphenyl Compounds; D002318:Cardiovascular Diseases / Q000517:prevention & control; D005260:Female; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000188:drug therapy*; D008027:Light; D019808:Losartan / Q000627:therapeutic use; D008297:Male; D010974:Platelet Aggregation / Q000187:drug effects*; D010975:Platelet Aggregation Inhibitors; D010979:Platelet Function Tests; D012542:Scattering, Radiation; D013777:Tetrazoles / Q000627:therapeutic use; D013810:Therapeutic Equivalency
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D001562:Benzimidazoles; D001713:Biphenyl Compounds; D010975:Platelet Aggregation Inhibitors; D013777:Tetrazoles; D019796:15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid; D019808:Losartan; C081643:candesartan