["Classical" apo B,E-receptor does not mediate the activating effect of low density lipoproteins on the second messenger system in human platelets and vascular smooth muscle cells].

The possible role of the "classical" LDL receptor (apo B,E-receptor) in activation of second messenger systems in human platelets and vascular smooth muscle cells (VSMC) has been investigated. The LDL-induced elevation of free cytoplasmic Ca2+ in platelets and VSMC was not inhibited by EGTA, which is known to block the LDL interaction with the apo B,E-receptor. Heparin abolished the binding of LDL to the apo B,E-receptor but did not influence the LDL-induced accumulation of inositol phosphates in VSMC. Acetylation or carbamylation of lysine residues, or modification of arginine residues of apo B by cyclohexanedione treatment did not influence the ability of LDL to activate the phosphoinositide turnover in VSMC. It was found also that LDL are capable of activating cell-signalling systems in platelets of homozygous hypercholesterolemic patients and in VSMC from Watanabe rabbits lacking functional apo B,E-receptors. These data indicate that the "classical" high affinity LDL receptor does not mediate the activating effects of LDL on platelets and VSMC.