Angiotensin-converting enzyme inhibitor therapy prevents upregulation of endothelin-converting enzyme-1 in failing human myocardium

Biochem Biophys Res Commun. 2002 Aug 2;295(5):1057-61. doi: 10.1016/s0006-291x(02)00799-4.

Abstract

In this study, we investigated the role of the renin-angiotensin system in expression of the endothelin system in atrial myocardium of patients with congestive heart failure. Atrial myocardium of control patients without angiotensin-converting enzyme (ACE) inhibitor therapy and heart failure patients without or with ACE inhibitor therapy undergoing aorto-coronary bypass surgery was studied. Endothelin-converting enzyme-1 (ECE-1) expression and endothelin-1 peptide level was upregulated in myocardium of heart failure patients without ACE inhibition. ACE inhibitor therapy prevented upregulation of ECE-1 and endothelin-1 in failing myocardium. Prepro-endothelin-1 and endothelin receptor A expression were not affected by heart failure. Endothelin receptor B was downregulated in heart failure patients. Our data demonstrate an upregulation of ECE-1 mRNA expression in failing human myocardium. Inhibition of the renin-angiotensin system by ACE inhibitor treatment prevents upregulation of ECE-1, suggesting that angiotensin II regulates ECE-1 expression in vivo.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Angiotensin-Converting Enzyme Inhibitors / pharmacology*
  • Aspartic Acid Endopeptidases / metabolism*
  • Down-Regulation
  • Endothelin-Converting Enzymes
  • Heart / drug effects*
  • Heart Failure / pathology*
  • Humans
  • Metalloendopeptidases
  • Myocardium / enzymology*
  • RNA, Messenger / metabolism
  • Receptor, Endothelin B
  • Receptors, Endothelin / metabolism
  • Up-Regulation

Substances

  • Angiotensin-Converting Enzyme Inhibitors
  • RNA, Messenger
  • Receptor, Endothelin B
  • Receptors, Endothelin
  • Aspartic Acid Endopeptidases
  • Metalloendopeptidases
  • ECE1 protein, human
  • Endothelin-Converting Enzymes