Ticagrelor, but not clopidogrel and prasugrel, prevents ADP-induced vascular smooth muscle cell contraction: A placebo-controlled study in rats
Key result
Oral administration of ticagrelor, in contrast to clopidogrel and prasugrel, prevented adenosine diphosphate-induced contraction of vascular smooth muscle cells in a rat model.
Why the study?
Does ticagrelor prevent ADP-induced vascular smooth muscle cell contraction compared to clopidogrel, prasugrel, or placebo in Wistar rats?
Population
Wistar rats (n=30)
Comparison
Ticagrelor vs Clopidogrel, prasugrel, or placebo administered…
Design
Preclinical, placebo-controlled
Authors
Discussion
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Implication
Should not change antiplatelet choice in patients; leaves open whether ticagrelor offers unique vascular benefits in humans.
Study Design
Type
RCT (n=30)
Structured PICO
Does ticagrelor prevent ADP-induced vascular smooth muscle cell contraction compared to clopidogrel, prasugrel, or placebo in Wistar rats?
P
Population
30 Wistar rats pretreated with clopidogrel, prasugrel, ticagrelor, or placebo to assess effects on vascular smooth muscle cell reactivity.
I
Intervention
Ticagrelor (10mg/kg orally 12 and 2 hours before experiments, plus 1μM/L in perfusion solution)
C
Comparator
Clopidogrel (50mg/kg, n=7), prasugrel (10mg/kg, n=7), or placebo (n=9) administered orally 12 and 2 hours before experiments
O
Outcome
Constrictions of rat tail arteries induced with 2-MeS-ADP, phenylephrine and arginine vasopressin measured as an increase in perfusion pressuresurrogate
Ticagrelor, unlike clopidogrel and prasugrel, prevents ADP-induced vascular smooth muscle cell contraction in a rat model, suggesting potential off-target vascular benefits.
Cite This Study
Grześk et al. (2012) conducted an RCT in Vascular smooth muscle cell contraction (n=30). Ticagrelor, clopidogrel, and prasugrel vs. Placebo was evaluated on 2-MeS-ADP-induced contraction of vascular smooth muscle cells. Oral administration of ticagrelor, in contrast to clopidogrel and prasugrel, prevented adenosine diphosphate-induced contraction of vascular smooth muscle cells in a rat model.