Summary
The amino sugars glucosamine, galactosamine and man- nosamine (30 mM) inhibited aggregation
of human or rabbit platelets induced by ADP, collagen, thrombin, PAF or high concentrations
of sodium arachidonate. 125I-fibrinogen binding during ADP-induced aggregation, and release of amine storage
granule contents were also inhibited. Increasing the calcium concentration of the
suspending medium to 5 mM did not overcome the inhibitory effect on the release reaction.
The amino sugars deaggregated rabbit platelets that had been aggregated by ADP, collagen
or thrombin, but deaggregated human platelets readily only when ADP was used as the
aggregating agent. Fibrinogen-induced aggregation of chymotrypsin-treated platelets
was blocked by the amino sugars. They did not inhibit platelet adherence to a collagen-coated
glass surface, nor affect release of granule contents from the adherent platelets.
Aggregation and release induced by low concentrations of sodium arachidonate or the
divalent cation ionophore A23187 were potentiated, indicating that the effects of
the amino sugars on platelets are more complex than simple inhibition of the lectinlike
activity that becomes available on the surface of platelets that have undergone the
release reaction. One of the effects of the amino sugars, however, is interference
with the binding of fibrinogen to platelets. The effects of the amino sugars are shared
by other primary amines.
Keywords
Platelet aggregation - Fibrinogen binding - Amino sugars
