Prostacyclin potentiates 13-azaprostanoic acid-induced platelet deaggregation.

Abstract:

:The specific thromboxane A2/prostaglandin H2 (TXA2/PGH2) antagonist 13-azaprostanoic acid (13-APA) reverses platelet aggregation stimulated by TXA2/PGH2 and the prostaglandin endoperoxide analog U46619. The present report demonstrates that the deaggregatory properties of 13-APA are potentiated by prostacyclin (PGI2). Human platelet-rich plasma was aggregated with U46619. Deaggregation was induced 2 min subsequent to the addition of the aggregating agent. Concentrations of 13-APA or PGI2 which induced 20 percent deaggregation were determined. Simultaneous addition of half of these concentrations resulted in 60 percent deaggregation, demonstrating that the observed response was supraadditive. Measurement of cyclic adenosine 3':5' monophosphate (cAMP) in resting or deaggregating platelets demonstrated that 13-APA itself did not stimulate cAMP production nor did 13-APA facilitate PGI2-induced increases in cAMP. In separate studies PGI2 and 13-APA were added to PRP prior to the induction of aggregation by U46619. Under these conditions, additive inhibition of aggregation was observed. Thus, it is clear that the pharmacological interaction between PGI2 and 13-APA depends upon the relative state of platelet activation.

journal_name

Thromb Res

journal_title

Thrombosis research

authors

Parise LV,Venton DL,Le Breton GC

doi

10.1016/0049-3848(82)90097-4

subject

Has Abstract

pub_date

1982-12-15 00:00:00

pages

721-30

issue

6

eissn

0049-3848

issn

1879-2472

pii

0049-3848(82)90097-4

journal_volume

28

pub_type

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