Aggregation of gel-filtered guinea-pig platelets by lipoproteins.

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 (greater than 100 microgram/ml) and LDL (greater than 400 microgram/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.