Recently, the effects of alpha-adrenergic and beta-adrenergic antagonists on plasma lipoprotein concentrations have been reported. Evidence from diverse lines of research has been brought together that suggests three potential mechanisms by which these antihypertensive agents affect lipoprotein metabolism. First, the known alterations in plasma triglyceride levels caused by adrenergic antagonists may be mediated through the activity of lipoprotein lipase. This enzyme, located on the capillary endothelium of adipose tissue and skeletal muscle, catabolizes chylomicrons and very-low-density lipoproteins. Catecholamine-induced changes in precapillary sphincter tone could affect the delivery of triglyceride-rich lipoproteins to endothelial lipase, cause changes in capillary endothelial surface area for lipase-binding sites, and/or modulate the synthesis of lipoprotein lipase by adipocytes and myocytes. Since high-density lipoprotein levels increase by taking up components of chylomicrons released by lipoprotein lipase, these pathways might explain the adrenergic-induced changes in high-density lipoprotein that are reciprocal to those in plasma triglycerides. Second, hepatic production of very-low-density lipoproteins might be affected by adrenergic-induced changes in insulin release. Decreased insulin release may direct glucose metabolites from adipocytes to hepatocytes for lipogenesis. Catecholamines and other glucoregulatory hormones are known to alter hepatic cholesterol synthesis and secretion of very-low-density lipoproteins. These observations also suggest that dietary carbohydrate and fat might modulate adrenergic influences on lipoprotein metabolism by other than classic means. Third, as suggested by studies of cultured fibroblasts, alpha-adrenergic antagonists may increase receptor-mediated catabolism of low-density lipoprotein.