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Enhancement of Endothelin Converting Enzyme and Endothelin Receptor Subtypes in Human Myocardium with Congestive Heart Failure

Published online by Cambridge University Press:  02 July 2020

J. Lin  and
C Wei
J. Lin
Affiliation:
Cardiovascular Molecular Research, Department of Surgery, University of Maryland School of Medicine, Baltimore, MD, 21201
C Wei
Affiliation:
Cardiovascular Molecular Research, Department of Surgery, University of Maryland School of Medicine, Baltimore, MD, 21201
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Extract

Endothelin-1 (ET-1) is a potent endothelial cell-drived vasoconstrictive peptide which is increased in congestive heart failure (CHF). ET-1 is converted from its precursor big ET-1 by activation of endothelin converting enzyme (ECE). ET-1 binding to ET-A receptor in vascular smooth muscle cells stimulates vasoconstriction and binding to ET-B receptor in vascular endothelial cells mediates vasodilation. In previous studies, we and others demonstrated that plasma ET-1 was significantly increased in congestive heart failure. However, the presentation and localization of endothelin converting enzyme and endothelin receptors (ET-A and ET-B) in human cardiac tissue with and without heart failure remain unclear. Therefore, the current study was designed to investigate the expression and localization of endothelin receptors and endothelin converting enzyme in human myocardium in the absence or presence of congestive heart failure.

Human atrial tissues (n=6) were obtained from normal subjects and end-stage CHF patients during cardiac transplantation. The expression of ECE, ET-A and ET-B were determined by immunohistochemical staining (IHCS).

Type
Pathology
Information
Microscopy and Microanalysis , Volume 6 , Issue S2: Proceedings: Microscopy & Microanalysis 2000, Microscopy Society of America 58th Annual Meeting, Microbeam Analysis Society 34th Annual Meeting, Microscopical Society of Canada/Societe de Microscopie de Canada 27th Annual Meeting, Philadelphia, Pennsylvania August 13-17, 2000 , August 2000 , pp. 608 - 609
Copyright
Copyright © Microscopy Society of America

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References

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5. This research was supported in part by grants from the N1H (HL03174 & HL61299, C. Wei), AHAMD, NKF and University of Maryland School of Medicine.Google Scholar