Detection of Soluble Angiotensin-Converting Enzyme 2 in Heart FailureInsights Into the Endogenous Counter-Regulatory Pathway of the Renin-Angiotensin-Aldosterone System
Slava Epelman, MD, PhD*,
W.H. Wilson Tang, MD, FACC , ,
Stephen Y. Chen, MD*,
Frederick Van Lente, PhD,
Gary S. Francis, MD, FACC and
Subha Sen, PhD, DSc ,*
* Department of Internal Medicine, Heart and Vascular Institute, Cleveland, Ohio
Department of Cardiovascular Medicine, Heart and Vascular Institute, Cleveland, Ohio
Department of Cell Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio
Department of Molecular Cardiology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio.
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Figure 1 Plasma ACE2 Enzymatic Assay Specificity
(A) rACE2 (25 ng/ml) was mixed with 30% commercial human plasma in the presence of different concentrations of the specific ACE2 inhibitor DX600, and ACE2 activity was determined after incubation for 18 h. Data are expressed as the percentage of ACE2 activity of rACE2. (B) Thirty percent human plasma (patient sample) was pre-incubated with either DX600 (1 µmol/l), anti-human ACE2 polyclonal antibody, or isotype-matched control antibodies for 30 min and then ACE2 activity was determined at 4 and 18 h. One of 3 representative experiments is shown. ACE = angiotensin-converting enzyme; IgG = immunoglobulin G; rACE2 = recombinant angiotensin-converting enzyme 2 activity; SACE = soluble angiotensin-converting enzyme.
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Figure 2 sACE2 Activity Was Associated With Worsening NYHA Functional Class
Quartile plots are shown. One-way analysis of variance, p = 0.0067. Number of patients (n) is given for each group. HF = heart failure; NYHA = New York Heart Association; sACE2 = soluble angiotensin-converting enzyme 2 activity.
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