Short‐Term Effects of Beta Blockers Atenolol, Nadolol, Pindolol, and Propranolol on Lipoprotein Metabolism in Normolipemic Subjects

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Abstract
The short‐term effect of the blockade of the beta‐adrenergic receptors on serum lipoproteins and the plasma activities of the enzymes involved in the metabolism of the serum lipoproteins: lipoprotein lipase (LPL), hepatic lipase (HL) and lecithin: cholesterol acyltransferase (LCAT) was evaluated in ten healthy normolipemic and normotensive subjects. In the first part of the study, the first three‐day period of placebo was followed by another three‐day period during which propranolol (120 mg/d) was given. In the second, third, and fourth part of the study, the same schedule was used but pindolol (15 mg/d), nadolol (160 mg/d), atenolol (100 mg/d) were given respectively instead of propranolol. The four drugs induced a significant blockade of the beta‐adrenergic receptors as evaluated by the measurement of the double two‐step test of Master (‐45%). Despite similar blockade, the effect on serum lipid concentrations depended on the type of drug: propranolol induced an increase in triglycerides and apoprotein B‐concentrations and a decrease in serum high density lipoprotein cholesterol (HDL‐C) and apoprotein AI‐concentrations. Pindolol provoked only a slight decrease of serum HDL‐C concentration. Nadolol and atenolol elicited a lowering of the same magnitude in HDL‐C. Except for a possible slight increase in plasma LCAT activity on propranolol, there was no significant change in the plasma activities of LPL, HL, and LCAT during the blockade of the beta‐adrenergic receptors with the drugs used. It is difficult to draw firm conclusions in regard to the mechanism by which beta blockers given to patients for much longer periods of time alter lipoprotein metabolism from results obtained in normolipemic subjects receiving beta blockers for only three days. It seems that pindolol modifies the serum lipoprotein pattern less likely than propranolol, nadolol, or atenolol. This difference could be attributed to the intrinsic sympathomimetic activity of pindolol of which the other beta blocking drugs that were used are devoid. The mechanism by which the serum lipid changes can be induced by beta blockade does not involve a lower activity of any of the plasma enzymes regulating the intravascular metabolism of lipoproteins.