Abstract:
:Background Platelets play a role in promoting inflammatory responses under several disease conditions. Platelets are activated in hypertensive patients. However, the mechanisms responsible for platelet-mediating vascular inflammation are unknown. The present study investigated the role of platelets in promoting vascular inflammation following angiotensin II (Ang II ) stimulation, and the efficacy of antiplatelet intervention. Methods and Results Within a mouse model of Ang II infusion (490 ng/kg per min), we measured the portion of P-selectin-positive platelets and platelet-monocyte (P-M) binding in blood samples, and platelet accumulation and P-M binding in vessels under Ang II stimulation at days 1, 3, and 7. We tested the efficacy of clopidogrel (15 mg/kg per day, followed by 5 mg/kg per day) on Ang II -induced platelet activation, P-M binding, vascular platelet accumulation, as well as vascular inflammation and remodeling at day 7 or 14. Clopidogrel reduced platelet vascular deposition (28.7±2.4% versus 18.3±2.9%), suppressed inflammatory cell infiltration (3.6±0.8×104/vessel versus 2.3±1.2×104/vessel) and oxidative stress, and attenuated vascular remodeling and dysfunction (55.0±5.5% versus 84.0±6.0%) following Ang II stimulation at day 7 or 14. Clopidogrel suppressed Ang II -induced P-M binding both at circulating (13.4±3.3% versus 5.9±2.7%) and regional (33.4±4.3% versus 11.9±2.7%) levels. Conclusions Platelets play a critical role in vascular inflammation under Ang II stimulation, with a marked promotion of P-M binding as an important mechanism. Clopidogrel prevented vascular inflammation in Ang II -infused mice.
journal_name
J Am Heart Assocjournal_title
Journal of the American Heart Associationauthors
An X,Jiang G,Cheng C,Lv Z,Liu Y,Wang Fdoi
10.1161/JAHA.118.009600subject
Has Abstractpub_date
2018-11-06 00:00:00pages
e009600issue
21issn
2047-9980journal_volume
7pub_type
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