The most marked conclusion is the establishment of the important role of non-parenchymal cells in the catabolism of the low density lipoproteins by the rat liver. Because the liver is responsible for 70-80% of the removal of LDL from blood this conclusion can be extended to total LDL turnover. The relatively important role of the non-parenchymal liver cells in LDL uptake might be due to the low interaction of rat hepatocytes with human LDL, both in vivo and in vitro. This is in contrast to results obtained with hepatocytes from pig (108) and rabbit (30, 109). The role of non-parenchymal cells from pig, rabbit or human liver in LDL catabolism is unknown at the moment. Beside the important role of the non-parenchymal cells in LDL catabolism, we also illustrate an important role of these cells in the uptake and degradation of the potentially atherogenic lipoproteins acetyl-LDL and lipoprotein{a). Just like acetyl-LDL and biologically modified LDL (110) 1 Lp( a) is taken up by the endothelial liver cells to a higher extent than LDL, probably due to its interaction with the acetyl-LDL receptor. The receptor-dependent uptake of acetyl-LDL and Lp(a) by the liver endothelial cells and LDL by the Kupffer cells can have important consequences for the cholesterol metabolism in liver, because specifically receptor-dependent uptake regulates cholesterol synthesis and esterification (30, 108, 111). The low temperature perfusion and cell isolation techniques have greatly improved the recoveries of the total liver-associated radioactivity in the isolated liver cell types. The applied method may be an important aid in future experiments on the role of parenchymal and non-parenchymal cells in lipoprotein catabolism, in which the consequence of the receptor-dependent and independent uptake of lipoproteins for cholesterol metabolism in the various liver cell types can be studied.