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

Yuki Sato, Satoshi Fujii, Shogo Imagawa, Kazue Ohmura, Yoshinori Ohmura, Yasuhiro Andoh, Jie Dong, Naoki Ishimori, Tomoo Furumoto, Hiroyuki Tsutsui

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

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 (ADR, 3 μM) was 2.6 ± 0.4 (x107) (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 (x107) 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.

Original languageEnglish
Pages (from-to)31-35
Number of pages5
JournalJournal of Atherosclerosis and Thrombosis
Volume14
Issue number1
DOIs
Publication statusPublished - Jan 1 2007
Externally publishedYes

Fingerprint

Angiotensin II Type 1 Receptor Blockers
Platelets
Losartan
Blood Platelets
Hypertension
Platelet Aggregation
Agglomeration
Platelet Activation
Blood pressure
Antihypertensive Agents
Prostaglandin H2 Receptors Thromboxane A2
Blood Pressure
Chemical activation
15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid
Angiotensin Type 1 Receptor
Adenosine Diphosphate
Light scattering
Lasers
Thrombosis
Cardiovascular Diseases

All Science Journal Classification (ASJC) codes

  • Internal Medicine
  • Cardiology and Cardiovascular Medicine
  • Biochemistry, medical

Cite this

Platelet aggregability in patients with hypertension treated with angiotensin II type 1 receptor blockers. / Sato, Yuki; Fujii, Satoshi; Imagawa, Shogo; Ohmura, Kazue; Ohmura, Yoshinori; Andoh, Yasuhiro; Dong, Jie; Ishimori, Naoki; Furumoto, Tomoo; Tsutsui, Hiroyuki.

In: Journal of Atherosclerosis and Thrombosis, Vol. 14, No. 1, 01.01.2007, p. 31-35.

Research output: Contribution to journalArticle

Sato, Y, Fujii, S, Imagawa, S, Ohmura, K, Ohmura, Y, Andoh, Y, Dong, J, Ishimori, N, Furumoto, T & Tsutsui, H 2007, 'Platelet aggregability in patients with hypertension treated with angiotensin II type 1 receptor blockers', Journal of Atherosclerosis and Thrombosis, vol. 14, no. 1, pp. 31-35. https://doi.org/10.5551/jat.14.31
Sato, Yuki ; Fujii, Satoshi ; Imagawa, Shogo ; Ohmura, Kazue ; Ohmura, Yoshinori ; Andoh, Yasuhiro ; Dong, Jie ; Ishimori, Naoki ; Furumoto, Tomoo ; Tsutsui, Hiroyuki. / Platelet aggregability in patients with hypertension treated with angiotensin II type 1 receptor blockers. In: Journal of Atherosclerosis and Thrombosis. 2007 ; Vol. 14, No. 1. pp. 31-35.
@article{78759c1b1b3e49e2804c2d229dc0edea,
title = "Platelet aggregability in patients with hypertension treated with angiotensin II type 1 receptor blockers",
abstract = "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 (ADR, 3 μM) was 2.6 ± 0.4 (x107) (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 (x107) 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.",
author = "Yuki Sato and Satoshi Fujii and Shogo Imagawa and Kazue Ohmura and Yoshinori Ohmura and Yasuhiro Andoh and Jie Dong and Naoki Ishimori and Tomoo Furumoto and Hiroyuki Tsutsui",
year = "2007",
month = "1",
day = "1",
doi = "10.5551/jat.14.31",
language = "English",
volume = "14",
pages = "31--35",
journal = "Journal of Atherosclerosis and Thrombosis",
issn = "1340-3478",
publisher = "Japan Atherosclerosis Society",
number = "1",

}

TY - JOUR

T1 - Platelet aggregability in patients with hypertension treated with angiotensin II type 1 receptor blockers

AU - Sato, Yuki

AU - Fujii, Satoshi

AU - Imagawa, Shogo

AU - Ohmura, Kazue

AU - Ohmura, Yoshinori

AU - Andoh, Yasuhiro

AU - Dong, Jie

AU - Ishimori, Naoki

AU - Furumoto, Tomoo

AU - Tsutsui, Hiroyuki

PY - 2007/1/1

Y1 - 2007/1/1

N2 - 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 (ADR, 3 μM) was 2.6 ± 0.4 (x107) (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 (x107) 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.

AB - 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 (ADR, 3 μM) was 2.6 ± 0.4 (x107) (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 (x107) 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.

UR - http://www.scopus.com/inward/record.url?scp=34249859312&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=34249859312&partnerID=8YFLogxK

U2 - 10.5551/jat.14.31

DO - 10.5551/jat.14.31

M3 - Article

C2 - 17332690

AN - SCOPUS:34249859312

VL - 14

SP - 31

EP - 35

JO - Journal of Atherosclerosis and Thrombosis

JF - Journal of Atherosclerosis and Thrombosis

SN - 1340-3478

IS - 1

ER -