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Blockade of platelet alpha2B-adrenergic receptors: a novel antiaggregant mechanism.

Abstract：

BACKGROUND:Platelets play a vital role in hemostasis and thrombosis. Catecholamines have a profound effect on platelet aggregation and atherothrombosis but the exact mechanism involved is insufficiently understood. In this report, we demonstrate the existence and role of alpha2B-adrenergic receptors (α2B-ARs) in normal human platelets. METHODS:Sixteen healthy individuals were recruited as donors of normal blood from which platelets were isolated. The presence of α2B-ARs in platelets was proven by Western blot analysis. In order to investigate their function, we performed light transmittance aggregometry and platelet function activity tests by examining the inhibitory effects of specific α2B-AR antibodies and of the selective α2B-AR antagonist ARC 239. RESULTS:Pretreatment of human platelets with agents that selectively block α2B-ARs showed a substantial inhibition in platelet aggregation that had been induced by adenosine diphosphate (ADP), by epinephrine and by arachidonic acid. The percent aggregation decreased from 81.5 ± 1.7% to 35.8 ± 5% and to 24 ± 4.6% for ADP with α2B-Abs and ARC 239 respectively, from 72.2 ± 1.9% to 25.5 ± 4.3% and to 8.8 ± 1.7% for epinephrine with α2B-Abs and ARC 239 respectively, and from 87 ± 2.1% to 47.9 ± 6.2% and to 61.2 ± 5.7% for arachidonic acid with α2B-Abs and ARC 239 respectively, p<0.05 for all. Additionally, collagen/epinephrine closure time increased from 120.8 ± 6.1s to 189.5 ± 39.5s (p=0.001). CONCLUSIONS:Our results reveal that contrary to previous knowledge, the α2B-AR subtype does exist in platelets and is an important regulator of aggregation. Inhibition of α2B-ARs in platelets may offer a novel therapeutic opportunity in the prevention of atherothrombotic events.

journal_name

Int J Cardiol

journal_title

International journal of cardiology

authors

Marketou ME,Kintsurashvili E,Androulakis NE,Kontaraki J,Alexandrakis MG,Gavras I,Vardas PE,Gavras H

doi

10.1016/j.ijcard.2013.03.051

subject

Has Abstract

pub_date

2013-10-03 00:00:00

pages

2561-6

issue

3

eissn

0167-5273

issn

1874-1754

pii

S0167-5273(13)00470-1

journal_volume

168

pub_type

杂志文章

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