Adrenergic mechanisms in the control of plasma lipids in man.
The effects on plasma lipids of beta-blocking antihypertensive agents with differing degrees of selectivity and intrinsic sympathomimetic activity were studied. The interrelationship between changes in lipid factors, lipoprotein lipase function, the degree of response, and pretreatment characteristics were examined. Beta-adrenergic blockade increased plasma triglycerides but decreased high-density lipoprotein cholesterol. Cardioselective drugs (atenolol and metoprolol) had less effect on triglyceride and very low-density lipoprotein cholesterol than the nonselective beta blockers (propranolol and oxprenolol). Inhibition of lipoprotein lipase was suggested by a reduction of the fractional removal rate of triglyceride in conjunction with increased total and very low-density lipoprotein cholesterol levels and reduced high-density lipoprotein cholesterol. Consistent decreases in free fatty acids lend argument against elevated triglyceride synthesis.
D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D002784:Cholesterol / Q000097:blood; D004311:Double-Blind Method; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D006801:Humans; D006973:Hypertension / Q000188:drug therapy*; D050356:Lipid Metabolism; D008297:Male; D014280:Triglycerides / Q000097:blood
D000319:Adrenergic beta-Antagonists; D005230:Fatty Acids, Nonesterified; D014280:Triglycerides; D002784:Cholesterol