Summary
Aggregation and secretion of ATP induced by thrombin, collagen, the snake venom component
convulxin and platelet-activating factor (PAF-acether) were studied after the exposure
of rabbit platelets to 1 μM of PAF-acether. This concentration, which is around 6
orders of magnitude above the concentration needed to induce full aggregation, was
required to remove most of the releasable ATP from the platelets. The depleted platelets
aggregated to PAF-acether, to thrombin and to convulxin under conditions where only
very low amounts of ATP were secreted, confirming that these agents do not require
the release of dense body components to trigger aggregation. Furthermore, when exposure
to PAF-acether was associated to inactivation of platelet cyclooxygenase with aspirin,
aggregation to thrombin persisted, validating the claim that thrombin induces aggregation
by a third pathway unrelated to ADP and to thromboxane A2. Aggregation by collagen
was markedly reduced by exposure of the platelets to PAF-acether or to aspirin; when
both procedures were associated, aggregation was suppressed. Failure to desensitize
the rabbit platelets to PAF-acether upon exposure to high amounts of it indicates
the absence of irreversible membrane changes due to PAF-acether, and allows its use
as a depleting procedure for the dense body materials, which does not affect platelet
membrane components as is the case for thrombin.
Keywords
Aggregation - Aspirin - ATP - Collagen - Convulxin - Platelet-activating factor (PAF-acether)
- Thrombin
