ANTIHYPERTENSIVE AGENTS, SERUM-LIPOPROTEINS AND GLUCOSE-METABOLISM

Effective blood pressure control with traditional high-dose diuretic therapy has led to a distinct decrease in cerebrovascular morbidity and mortality, but failed to achieve a satisfactory reduction of coronary complications and sudden death. The same applies also for beta-blockers, although they have been shown to be effective in secondary prevention of myocardial infarction. It is suspected that conventional antihypertensive treatment has an unfavorable effect on coronary risk factors other than hypertension. For instance, thiazide-type diuretics can impair glucose tolerance and increase the potentially atherogenic serum low-density lipoprotein (LDL) cholesterol fraction and triglycerides. Beta-blockers without partial intrinsic sympathomimetic activity increase serum triglycerides and tend to lower the potentially antiatherogenic high-density lipoprotein (HDL) cholesterol. Certain beta-blockers may also impair glucose tolerance, particularly when they are combined with diuretics. Calcium channel blockers, angiotensin converting-enzyme inhibitors and alpha-1-receptor blockers do not adversely affect lipoprotein or carbohydrate profiles. The latter two drug classes may even increase insulin sensitivity, and alpha-1-blockers may also slightly improve lipid metabolism. The prognostic relevance of drug-induced dyslipidemia and/or glucose intolerance awaits further clarification. In the meantime, it is of clinical interest that several of the generally available antihypertensive drugs seem to be metabolically neutral or sometimes perhaps even potentially beneficial with regard to the lipoprotein and carbohydrate metabolism.