Propranolol decreases cholesteryl ester accumulation in mouse peritoneal macrophage in vitro.

Current evidence indicates that the non-selective beta-blocker propranolol reduces the severity of experimental atherosclerosis in animal model. We studied the effect of propranolol on cholesterol ester synthesis and storage in mouse peritoneal macrophages in vitro. Propranolol in concentrations found in the plasma of patients treated with it (150 ng/ml) decreased by 20-30% beta-VLDL-stimulated synthesis of cholesterol esters with (14C)-oleate. A similar effect was observed also on this synthesis stimulated by acetyl-LDL. In a similar degree the accumulation of cholesteryl esters in the cells was decreased during the 48-hour incubation with lipoproteins in the presence of propranolol. No effect of the drug was observed on the uptake and degradation of beta-VLDL or acetyl-LDL. These observations suggest that propranolol may inhibit cholesteryl ester accumulation in macrophages at the point subsequent to lipoprotein uptake. This may have an impact on the treatment or prevention of atherosclerosis.