Mechanism of differential effects of antihypertensive agents on serum lipids

被引：44

作者：

Brook R.D. ^{[1
]}

机构：

[1] Division of Hypertension, 3918 Taubman Center, University of Michigan, Ann Arbor, MI 48104

来源：

Current Hypertension Reports | 2000年 / 2卷 / 4期

关键词：

Insulin Sensitivity; Angiotensin Converting Enzyme Inhibitor; Antihypertensive Agent; Lipoprotein Lipase Activity; Postprandial Lipemia;

D O I：

10.1007/s11906-000-0040-0

中图分类号：

学科分类号：

摘要：

Essential hypertension is frequently associated with the metabolic abnormalities of insulin resistance and dyslipidemia. This prevalent clustering of multiple cardiovascular risk factors may help explain the less-than-expected improvement in coronary heart disease mortality provided by simple blood pressure reduction alone. Many antihypertensive medications effectively reduce blood pressure while providing no benefit or even causing a detrimental effect on the associated metabolic abnormalities. (3-Blockers and diuretics tend to negatively affect both glucose tolerance and plasma lipids. Calcium channel blockers, angiotensin converting enzyme inhibitors, and angiotensin II receptor blockers are most often found to be metabolically neutral. a-Blockers provide the most favorable metabolic effects of antihypertensive agents by improving both insulin sensitivity and dyslipidemia. The multiple physiologic mechanisms by which blood pressure medications alter plasma lipids are discussed in detail. The effects of antihypertensive medications on postprandial lipid metabolism and the associated postprandial lipemia-induced endothelial dysfunction deserve special attention. Copyright © 2000 by Current Science Inc.

引用

页码：370 / 377

页数：7

共 50 条

[31]

Lithell H., Pollare T., Berne C., Et al., The metabolic and circulatory response to beta-blockade in hypertensive men is correlated to muscle capillary density, Blood Pressure, 1, pp. 20-26, (1992)

[32]

DeFronzo R.A., Thorin D., Felber J.P., Et al., Effect of beta and alpha adrenergic blockade on glucose-induced thermogenesis, J Clin Invest, 73, pp. 633-639, (1984)

[33]

Toft I., Bonaa K.H., Jenssen T., Insulin resistance in hypertension is associated with body fat rather than blood pressure, Hypertension, 32, pp. 115-122, (1998)

[34]

Patsch J.R., Miesenbock G., Hopferwieser T., Et al., Relation of triglyceride metabolism and coronary artery disease, Aterioscler Thromb, 12, pp. 1336-1345, (1992)

[35]

Boquist S., Ruotolo G., Hellenius M.L., Et al., Effects of a cardi oselective 3 blocker on postprandial triglyceride rich lipoproteins, low density lipoprotein particle size and glucose insulin homeostasis in middle aged men with modestly increased cardiovascular risk, Atherosclerosis, 137, pp. 391-400, (1998)

[36]

Haenni A., Lithell H., Treatment with a 3 blocker that has 32 agonism improves glucose and lipid metabolism in essential hypertension, Metabolism, 43, pp. 455-461, (1994)

[37]

Tikkanen H.O., Naveri H., Harkonen M., Skeletal muscle fiber distribution influences serum high density lipoprotein cholesterol level, Atherosclerosis, 120, pp. 1-5, (1996)

[38]

Lithell H., Pollare T., Vessby B., Metabolic effects of pindolol and propranolol in a double blind cross over study in hypertensive patients, Blood Pressure, 1, pp. 92-101, (1992)

[39]

Jl D., Metcalfe J., Simpson C.N., Adrenergic mechanisms in control of plasma lipid concentrations, Br Med J, 284, pp. 1145-1148, (1982)

[40]

Campos H., Genest J.J., Blijlevens E., Et al., Low density lipoprotein particle size and coronary artery disease, Arterioscler Thromb, 12, pp. 187-195, (1992)

← 1 2 3 4 5 →