Inhibition of lecithin: cholesterol acyl transfer by propranolol treatment in man.
The changes in some parameters of plasma lipoprotein metabolism in 25 hypertensive men, caused by a two months lasting oral treatment with 120 mg propranolol/day, were compared to the changes that occur during the same time in the subjects (n = 9) of an untreated control group. Propranolol led to an increase of triglycerides and a decrease of HDL cholesterol in plasma, the latter consisting in a small increase of unesterified cholesterol and a larger decrease of cholesteryl esters. In parallel a decrease in the lecithin:cholesterol acyl transfer, measured as initial rate of cholesterol esterification, was observed. The extent of the plasma lipid and enzyme alterations was shown to be dependent on the patient's pretreatment situation. Changes in lecithin:cholesterol acyl transfer rate after oral treatment correlated significantly with similar changes after propranolol addition in comparable amounts to plasma in vitro. A similarity between propranolol induced alterations in the metabolism of plasma lipoproteins and the situation in hereditary LCAT deficiency is obvious and may be interpreted as a harmful component of propranolol action.
D002788:Cholesterol Esters / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D005990:Glycerol / Q000097:blood; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000188:drug therapy; D008074:Lipoproteins / Q000097:blood; D008297:Male; D007862:Phosphatidylcholine-Sterol O-Acyltransferase / Q000037:antagonists & inhibitors* / Q000097:blood; D011433:Propranolol / Q000009:adverse effects*; D014280:Triglycerides / Q000097:blood
D002788:Cholesterol Esters; D008076:Cholesterol, HDL; D008074:Lipoproteins; D014280:Triglycerides; D011433:Propranolol; D007862:Phosphatidylcholine-Sterol O-Acyltransferase; D005990:Glycerol