Role of the natriuretic peptides in the cardiorenal and humoral actions of omapatrilat: Insights from experimental heart failure

被引：3
作者：
Chen H.H. [1 ]
Cataliotti A. [1 ]
Burnett Jr. J.C. [1 ]
机构：
[1] Cardiorenal Research Laboratory, Mayo Clinic and Foundation, Rochester, MN 55905, Guggenheim 915
来源：
Current Hypertension Reports | 2001年 / 3卷 / Suppl 2期
基金：
美国国家卫生研究院;
关键词：
Natriuretic Peptide; Brain Natriuretic Peptide; Atrial Natriuretic Peptide; Fosinoprilat; Natriuretic Peptide System;
D O I：
10.1007/s11906-001-0102-y
中图分类号：
学科分类号：
摘要：
Vasopeptidase (VP) inhibitors are novel molecules that coinhibit neutral endopeptidase 24.11 (NEP), which degrades natriuretic peptides and angiotensin-converting enzyme (ACE). We review the biology of the natriuretic peptide system and a recent study of the role for the natriuretic peptide system in the mechanism of action of omapatrilat (the most clinically advanced VP inhibitor). This study compared the cardiorenal and humoral actions of omapatrilat with those of ACE inhibition. The actions of omapatrilat were further defined in the presence and absence of a natriuretic peptide receptor antagonist. This investigation provided insight into a unique new pharmacologic agent that has beneficial renal actions in experimental mild heart failure that exceed those seen with ACE inhibition alone and that are linked to the natriuretic peptide system. Copyright © 2001 by Current Science Inc.
引用
收藏
页码：s15 / s21
页数：6
相关论文
共 21 条
  • [11] Lopez M.J., Wong S.K.F., Kishimoto I., Et al., Salt-resistant hypertension in mice lacking guanylyl cyclase-A receptor for atrial natriuretic peptide, Nature, 94, pp. 14730-14735, (1995)
  • [12] Kishimoto I., Rossi K., Garbers D.L., A genetic model provides evidence that the receptor for atrial natriuretic peptide (guanylyl cyclase-A) inhibits cardiac ventricular myocyte hypertrophy, Proceedings of the National Academy of Sciences of the United States of America, 98, 5, pp. 2703-2706, (2001)
  • [13] Rouleau J.L., Pfeffer M.A., Stewart D.J., Isaac D., Sestier F., Kerut E.K., Porter C.B., Proulx G., Qian C., Block A.J., Comparison of vasopeptidase inhibitor, omapatrilat, and lisinopril on exercise tolerance and morbidity in patients with heart failure: IMPRESS randomised trial, Lancet, 356, 9230, pp. 615-620, (2000)
  • [14] Dries D.L., Exner D.V., Domanski M.J., Greenberg B., Stevenson L.W., The prognostic implications of renal insufficiency in asymptomatic and symptomatic patients with left ventricular systolic dysfunction, Journal of the American College of Cardiology, 35, 3, pp. 681-689, (2000)
  • [15] Margulies K.B., Heublein D.M., Burnett Jr. J.C., ANF-mediated renal cyclic GMP generation in congestive heart failure, Am J Physiol, 260, (1991)
  • [16] Lisy O., Jougasaki M., Schirger J.A., Et al., Neutral endopeptidase inhibition potentiates the natriuretic actions of adrenomedullin, Am J Physiol, 275, pp. 410-414, (1998)
  • [17] Ura N., Carretero O.A., Erdos E.G., Role of renal endopeptidase 24.11 in kinin metabolism in vitro and in vivo, Kidney International, 32, 4, pp. 507-513, (1987)
  • [18] Hillege H.L., Girbes A.R.J., De Kam P.J., Boomsma F., De Zeeuw D., Charlesworth A., Hampton J.R., Van Veldhuisen D.J., Renal function, neurohormonal activation, and survival in patients with chronic heart failure, Circulation, 102, 2, pp. 203-210, (2000)
  • [19] Volpe M., Rao M.A.E., Tritto C., Et al., Transition from asymptomatic left ventricular dysfunction to congestive heart failure, J Cardiac Failure, 1, pp. 409-419, (1995)
  • [20] McDonagh T.A., Morrison C.E., Lawrence A., Ford I., Tunstall-Pedoe H., McMurray J.J.V., Dargie H.J., Symptomatic and asymptomatic left-ventricular systolic dysfunction in an urban population, Lancet, 350, 9081, pp. 829-833, (1997)
123