Elsevier

Thrombosis Research

Volume 23, Issue 6, 15 September 1981, Pages 521-532
Thrombosis Research

Paper
Thromboxane A2 and the endoperoxides mediate canine platelet activation

https://doi.org/10.1016/0049-3848(81)90175-4Get rights and content

Abstract

With canine platelets, arachidonate consistently induces a shape change and potentiates the response to a submaximal ADP stimulus even though it does not generally induce aggregation. We have determined that TXA2 and possibly the endoperoxides are responsible for these effects based on the following data: (i) indomethacin (14uM) blocks both actions of arachidonate, (ii) imidazole (5uM) partially blocks both, and (iii) the endoperoxide analog, U-46619, produces effects similar to arachidonate, whereas other stable metabolites of arachidonate (PGE2, PGF, PGD2, PGI2, 6-keto-PGF and TXB2) do not. Specifically, PGI2 and PGD2 inhibit ADP-induced aggregation; low concentrations of PGE2 and PGF2 facilitate secondary aggregation; and the other metabolites are relatively inactive. With the exception of PGF , these activities are qualitiatively identical to those observed with human platelets. A decreased sensitivity of canine platelets to TXA2 and the endoperoxides is advanced as the explanation of their diminished responsiveness to arachidonate relative to other species.

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