New insights into the renin-angiotensin system and hypertensive renal disease

被引：8

作者：

Fogo A.B. ^{[1
]}

机构：

[1] MCN C3310, Department of Pathology, Vanderbilt University, Nashville

来源：

Current Hypertension Reports | 1999年 / 1卷 / 2期

关键词：

Angiotensin Converting Enzyme; Losartan; Angiotensinogen; Angiotensin Converting Enzyme Genotype; Reninangiotensin System;

D O I：

10.1007/s11906-999-0017-6

中图分类号：

学科分类号：

摘要：

The role of the renin-angiotensin system in hypertension and end organ damage has long been recognized. Recent advances in genetic models and newly available pharmacologic tools have allowed dissection of the mechanisms of actions of the renin-angiotensin system in hypertensive kidney disease. The newly cloned AT2 receptor is now recognized to oppose many of the AT1 receptor's actions. The renin-angiotensin system is now recognized to be linked to induction of plasminogen activator inhibitor-1 (PAI-1), possibly via the AT4 receptor, thus promoting both thrombosis and fibrosis. Interactions of the reninangiotensin system with aldosterone and bradykinin may have impact on both blood pressure and tissue injury. The effects of angiotensin 1 converting enzyme inhibitors versus those of the newly available AT1 receptor antagonists on blood pressure and organ damage are undergoing evaluation in clinical trials. Finally, polymorphisms of genes relevant to the renin-angiotensin system appear to affect response to treatment, although this effect varies in different populations. Copyright © 1999 by Current Science Inc.

引用

页码：187 / 194

页数：7

共 59 条

[1]

Kasiske B.L., Kalil R.S., Ma J.Z., Et al., Effect of antihypertensive therapy on the kidney in patients with diabetes: A metaregression analysis, Ann Intern Med, 118, pp. 129-138, (1993)

[2]

Esther C.R., Marino E.M., Howard T.E., Et al., The critical role of tissue angiotensin-converting enzyme as revealed by gene targeting in mice, J Clin Invest, 99, pp. 2375-2385, (1997)

[3]

Kim H.S., Krege J.H., Kluckman K.D., Et al., Genetic control of blood pressure and the angiotensinogen locus, Proc Natl Acad Sci u S A, 92, pp. 2735-2739, (1995)

[4]

Niimura F., Labosky P.A., Kakuchi J., Et al., Gene targeting in mice reveals a requirement for angiotensin in the development and maintenance of kidney morphology and growth factor regulation, J Clin Invest, 96, pp. 2947-2954, (1995)

[5]

Hilgers K.F., Reddi V., Krege J.H., Et al., Aberrant renal vascular morphology and renin expression in mutant mice lacking angiotensin-converting enzyme, Hypertension, 29, pp. 216-221, (1997)

[6]

Esther Jr. C.R., Howard T.E., Marino E.M., Et al., Mice lacking angiotensinconverting enzyme have low blood pressure, renal pathology, and reduced male fertility, Lab Invest, 74, pp. 953-965, (1996)

[7]

Chen X., Li W., Yoshida H., Tsuchida S., Et al., Targeting deletion of angiotensin type 1B receptor gene in the mouse, Am J Physiol, 272, (1997)

[8]

Tsuchida S., Matsusaka T., Chen X., Et al., Murine double nullizygotes of the angiotensin type 1A and type 1B receptor genes duplicate severe abnormal phenotypes of angiotensinogen nullizygotes, J Clin Invest, 101, pp. 755-760, (1998)

[9]

Yamada T., Horiuchi M., Dzau V.J., Angiotensin type 2 receptor mediates programmed cell death, Proc Natl Acad Sci u S A, 93, pp. 156-160, (1996)

[10]

Ichiki T., Labosky P.A., Shiota C., Et al., Effects on blood pressure and exploratory behaviour of mice lacking angiotensin II type-2 receptor, Nature, 377, pp. 748-750, (1995)

← 1 2 3 4 5 6 →