2003
DOI: 10.1016/s0195-668x(03)95150-5
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P2156 Platelet inhibition by valsartan and valeryl 4-hydroxy valsartan: a possible missing link to explain benefits of angiotensin II receptor blockers in patients after acute vascular events

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Cited by 6 publications
(6 citation statements)
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“…With regard to CD42b (GPIb), the effects of ESC were less potent than those of clopidogrel or prasugrel, similar to those of aspirin, and stronger than sertraline or valsartan. 15,51 In a previous similar study, our group demonstrated that platelet aggregation and surface expression of platelet receptors were affected by another SSRI, sertraline, and its metabolite N-desmethylsertraline. 15 Lysosome integral membrane protein (CD63) is down-regulated to a similar extent by aspirin and ESC, whereas other antiplatelet agents show no effect on this receptor.…”
Section: Discussionmentioning
confidence: 88%
“…With regard to CD42b (GPIb), the effects of ESC were less potent than those of clopidogrel or prasugrel, similar to those of aspirin, and stronger than sertraline or valsartan. 15,51 In a previous similar study, our group demonstrated that platelet aggregation and surface expression of platelet receptors were affected by another SSRI, sertraline, and its metabolite N-desmethylsertraline. 15 Lysosome integral membrane protein (CD63) is down-regulated to a similar extent by aspirin and ESC, whereas other antiplatelet agents show no effect on this receptor.…”
Section: Discussionmentioning
confidence: 88%
“…The platelet angiotensin receptors were described a decade ago [100,101] and the platelet model has been extensively used in many in vitro and ex vivo studies [102,103]. Previous findings suggest that ARBs (including losartan and valsartan) exhibits potent antiplatelet properties [104][105][106][107][108][109]. In particular, it has been shown that, at 10 nM or below, Ang II promotes aggregability and PKC phosphorylation in human platelets through the AT1 receptor, which can be inhibited by AT1 receptor antagonists, but at higher concentrations, the promotion effects were lost through the opposing action of the AT2 receptor [108].…”
Section: The Pleiotropic Action Of Antihyperten-sive Drugs: Effects Omentioning
confidence: 99%
“…The antiplatelet profile of this agent, at least in vitro, is quite different from the established platelet inhibitors such as aspirin, dipyridamole, or glycoprotein IIb/IIIa inhibitors. In fact, niacin, targets specific combination of platelet indices which is not similar to the in vitro antiplatelet properties of the indirect platelet inhibitors done at the same laboratory with selective serotonin reuptake inhibitors (16), acid ester of probucol (AGI-1067) (17), astaxanthine (18), fibrin-derived peptide FX-06 (19) or angiotensin receptor blockers (20). Interestingly, the lowest used concentration of niacin was not sufficient to cause moderate inhibition of platelet aggregability; therefore, dose-dependency pattern suggests that there may be need for higher levels to achieve the sustained antiplatelet potency with this agent.…”
Section: Discussionmentioning
confidence: 99%