Key result
Intravenously-administered endothelin-1 and bradykinin significantly reduced ADP-induced platelet aggregation in a dose-dependent fashion through ETB and B2 receptor activation, respectively.
Population
C57BL/6 mice and B2 knockout mice
Design
Preclinical
Authors
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ETB/B2 activation inhibits platelet aggregation in mice; hypothesis-generating and should not yet change clinical practice.
Endothelin-1 and bradykinin inhibit platelet aggregation ex vivo in mice via ETB and B2 receptor activation, respectively, with endothelin-1 requiring COX-2/prostacyclin and bradykinin additionally requiring nitric oxide.
Labonté et al. (2001) studied this question. Endothelin-1 and bradykinin was evaluated on ADP-induced platelet aggregation ex vivo. Intravenously-administered endothelin-1 and bradykinin significantly reduced ADP-induced platelet aggregation in a dose-dependent fashion through ETB and B2 receptor activation, respectively.
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