Increased angiotensin-(1-7)-forming activity in failing human heart ventricles: Evidence for upregulation of the angiotensin-converting enzyme homologue ACE2

The formation of angiotensin-(1-7) from either angiotensin (Ang) I or Ang II in failing human hearts is not well understood. Angiotensinase activity in left and right ventricular membranes from 14 idiopathic dilated cardiomyopathy (IDC), 8 primary pulmonary hypertension (PPH), and 13 nonfailing huma...

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Bibliographic Details
Published in:Circulation (New York, N.Y.) N.Y.), 2003-10, Vol.108 (14), p.1707-1712
Main Authors: ZISMAN, Lawrence S, KELLER, Rebecca S, WEAVER, Barbara, QISHAN LIN, SPETH, Robert, BRISTOW, Michael R, CANVER, Charles C
Format: Article
Language:English
Subjects:
Adult
Angiotensin I - metabolism
Angiotensin II - metabolism
Biological and medical sciences
Carboxypeptidases - metabolism
Cardiac Output, Low - enzymology
Cardiac Output, Low - metabolism
Cardiology. Vascular system
Female
Heart
Heart failure, cardiogenic pulmonary edema, cardiac enlargement
Heart Ventricles - enzymology
Heart Ventricles - metabolism
Humans
Male
Medical sciences
Peptide Fragments - metabolism
Peptidyl-Dipeptidase A
Up-Regulation
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Summary:The formation of angiotensin-(1-7) from either angiotensin (Ang) I or Ang II in failing human hearts is not well understood. Angiotensinase activity in left and right ventricular membranes from 14 idiopathic dilated cardiomyopathy (IDC), 8 primary pulmonary hypertension (PPH), and 13 nonfailing human hearts was measured with either 125I-Ang I or 125I-Ang II as substrate. Ang-(1-7)-forming activity from 125I-Ang I was inhibited by thiorphan. With 125I-Ang II as substrate, Ang-(1-7) formation was inhibited by the ACE2-specific inhibitor C16. Western blotting with an anti-ACE2 antibody confirmed the presence of ACE2. Angiotensinase activity with 125I-Ang I as substrate was increased in failing IDC left ventricles (LVs) compared with nonfailing LVs (P
ISSN:0009-7322
1524-4539
DOI:10.1161/01.CIR.0000094734.67990.99