Summary
Very low density lipoproteins (VLDL) and low density lipoproteins (LDL) were isolated
from serum of hypercholesterolemic guinea-pigs, and the effect of these lipoproteins
on guinea-pig platelets was studied. VLDL (>100 μg/ml) and LDL (>100 μg/ml) were found
to cause aggregation of gel-filtered platelets (GFP), although the extent of GFP aggregation
by LDL was smaller than that by VLDL. In platelet-rich plasma, however, lipoproteins
could not induce platelet aggregation. VLDL and LDL even at the low concentrations
at which lipoproteins alone could not induce aggregation potentiated ADP-induced aggregation
of GFP. VLDL-induced aggregation of GFP was inhibited by apyrase (0.2–1.0 mg/ml) in
a concentration-related manner. Prostaglandin E1, dipyridamole, potassium cyanide and ethylenediaminetetraacetic acid inhibited VLDL-
and ADP-induced aggregation of GFP in the almost same degree. Inhibitions of VLDL-induced
GFP aggregation by acetylsalicylic acid and albumin were slightly stronger than that
of ADP-induced aggregation. These findings suggest that lipoproteins modulate platelets
so that endogenous ADP can be released from platelets.
