[Antihypertensive therapy and lipid metabolism].
Hypertension, hyperlipidaemia and cigarette smoking are major risk factors in coronary heart disease. Since many antihypertensive drugs alter plasma lipid levels it is a subject of current discussion that these agents may increase associated coronary risk and therefore offset the beneficial effects of lowering blood pressure. The purpose of this paper is to review clinical and experimental data in the literature on the influence of data in the literature on the influence of antihypertensive drugs on lipid metabolism. The thiazides hydrochlorothiazide and chlorthalidone cause an elevation of plasma triglycerides and very low density lipoprotein (VLDL) but have little effect on total cholesterol, low density lipoprotein (LDL) and high density lipoprotein (HDL). The unspecific beta-blockers, e.g. propranolol, do not affect total cholesterol and LDL but increase total triglycerides and VLDL and decrease HDL. The changes of plasma lipids and lipoproteins caused by cardio-selective beta-blockers, e.g. atenolol and metoprolol, and unspecific beta-blockers with intrinsic sympathomimetic activity (ISA), e.g. oxprenolol and pindolol, appear to be qualitatively similar but less pronounced. The alpha 1-blocker prazosin reduces total triglycerides and slightly lowers total cholesterol. The concentration of VLDL plus LDL decreases while HDL may increase. Only very few studies have been reported on the effects of other antihypertensive drugs, e.g. clonidine, hydralazine, on plasma lipids. Several experimental studies reveal that antihypertensive agents exert direct effects on triglyceride and cholesterol metabolism. Although the pathophysiological mechanisms and the significance of the alterations of lipid metabolism induced by antihypertensive drugs are not yet clear, the following guidelines for the clinical use of these agents are recommended: (1) before initiating drug treatment in hypertensive patients, blood lipid levels should be measured to exclude a preexisting hyperlipidaemia, (2) during long-term therapy with antihypertensive agents, lipoprotein fractions should be controlled in order to reconsider the therapeutic regime if major alterations of blood lipid levels are observed.
D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000959:Antihypertensive Agents / Q000009:adverse effects / Q000494:pharmacology*; D001581:Benzothiadiazines; D002784:Cholesterol / Q000097:blood / Q000378:metabolism; D003327:Coronary Disease / Q000209:etiology; D004232:Diuretics / Q000494:pharmacology; D006801:Humans; D050356:Lipid Metabolism; D008055:Lipids / Q000097:blood; D008074:Lipoproteins / Q000378:metabolism; D012306:Risk; D049993:Sodium Chloride Symporter Inhibitors / Q000494:pharmacology; D014280:Triglycerides / Q000378:metabolism
D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D000959:Antihypertensive Agents; D001581:Benzothiadiazines; D004232:Diuretics; D008055:Lipids; D008074:Lipoproteins; D049993:Sodium Chloride Symporter Inhibitors; D014280:Triglycerides; D002784:Cholesterol
Antihypertensive Therapie und Fettstoffwechsel.