Effects of alpha-adrenergic and beta-adrenergic receptor blockade on lipid metabolism

Abstract

The role of lipoprotein lipase in the pathophysiology of lipid changes during alpha-receptor or beta-receptor blockade was evaluated in this clinical trial. Thirty hypertensive patients were given 2 mg of prazosin twice daily or 100 mg of metoprolol twice daily for 10 weeks, according to an open, randomized protocol. Both drugs were effective in reducing arterial blood pressure (from 153 ± 16/102 ± 6 mm Hg to 146 ± 12/92 ± 8 mm Hg with prazosin and from 158 ± 17/103 ± 8 to 144 ± 14/94 ± 10 mm Hg with metoprolol). Prazosin significantly reduced total plasma cholesterol from 202 ± 39 to 188 ± 36 mg/dl and increased high-density lipoprotein cholesterol from 36 ± 8 to 40.5 ± 11 mg/dl. Prazosin did not affect plasma triglycerides levels, whereas patients taking metoprolol had a slight rise in these levels, from 122 ± 42 to 142 ± 57 mg/dl, along with a decrease in high-density lipoprotein cholesterol from 37 ± 10 to 31 ± 8 mg/dl. The concentration of apoprotein B did not change significantly with either treatment. Lipoprotein lipase activity increased in the prazosin group from 28.4 ± 16 to 37.7 ± 14 μmol/liter per minute (p <0.01), but did not change significantly (29.9 ± 12 versus 32.8 ± 8 μmol/liter per minute) in patients treated with the beta blocker. These data, which confirm previous reports of serum lipid changes during antihypertensive therapy, suggest that alpha 1 blockers may interfere with lipoprotein lipase, possibly by reducing its catecholamine-mediated inactivation.