Endothelin in Renal Diseases and Cardiovascular Remodeling in Renal Failure.

DOI Web Site Web Site PubMed 101 References
  • ORTH Stephan R.
    the Department of Internal Medicine, Sections of Nephrology, Ruperto Carola University
  • VIEDT Christiane
    the Department of Internal Medicine, Sections of Cardiology, Ruperto Carola University
  • AMANN Kerstin
    the Department of Pathology, Friedrich-Alexander University of Erlangen-Nurnberg
  • RITZ Eberhard
    the Department of Internal Medicine, Sections of Nephrology, Ruperto Carola University

Search this article

Description

The pathogenetic mechanisms leading to progression of renal failure are only partly understood. Several studies in immune- and non-immune-mediated models of renal damage have recently implicated the endothelin (ET) system as a major player in these processes. In animal models, ET receptor antagonists have been shown to be highly effective in abrogating the progression of renal failure. Furthermore, cardiac structural alterations seen in hypertension and/or renal insufficiency, e.g. left ventricular hypertrophy, thickening of intramyocardial arterioles, and the increase in non-vascular interstitial tissue, are largely prevented by ET receptor antagonists. In this context it is of interest that these beneficial renal and cardiac effects are, at least in most studies, independent of systemic blood pressure. In addition to the specific pharmacological blockade of the renin-angiotensin system [ACE inhibitors, angiotensin II receptor (AT1) antagonists], blockade of ET receptors or ET converting enzyme (ECE) may be a new tool to interfere with progression of renal failure and cardiovascular remodeling in humans.<br>(Internal Medicine 40: 285-291, 2001)

Journal

  • Internal Medicine

    Internal Medicine 40 (4), 285-291, 2001

    The Japanese Society of Internal Medicine

References(101)*help

See more

Keywords

Details 詳細情報について

Report a problem

Back to top