Clinical Chemistry
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Clinical Chemistry 43: 9-10, 1997;
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (1)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Mathew, V.
Right arrow Articles by Lerman, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Mathew, V.
Right arrow Articles by Lerman, A.
Related Collections
Right arrow Endocrinology and Metabolism
(Clinical Chemistry. 1997;43:9-10.)
© 1997 American Association for Clinical Chemistry, Inc.

Editorials

Clinical Implications of a Sandwich Enzyme Immunoassay for Big Endothelin-1

Verghese Mathew and Amir Lermana

Division of Cardiovascular Diseases, Mayo Clinic Rochester, 200 First St. SW, Rochester, MN 55905
a Author for correspondence.

Endothelin (ET) is an endothelial-derived peptide that exerts potent vasoconstrictive activity in vivo and in vitro. An increasing body of evidence suggests that ET may have a significant role in the pathophysiological processes leading to cardiovascular disease states. Although it is not certain at this point whether ET is primarily responsible for initiating these events, sufficient evidence exists to conclude that ET is involved as a mediator or cofactor in these disease states.

ET was first described by Yanagisawa et al. in 1988 (1). The pre-propeptide is cleaved to form big ET (39 amino acids) and then is further cleaved by an endothelin-converting enzyme (ECE) to form the 21-amino acid active peptide. Three pharmacologically distinct isopeptides (ET-1, ET-2, and ET-3) exist, derived from three different pre-propeptides that are encoded by separate genes (2). The ET-1 isopeptide is primarily responsible for the observed vasomotor effects. Two distinct ET receptors exist: ET-A and ET-B, the latter being associated with both vasoconstrictive and vasodilatory effects (3). In addition to its vasoactive effects, ET has been shown to affect cellular proliferation.

Endothelial cells form a single-cell-thick layer that lines the entire vasculature. The continuous production and release of endothelin from the endothelial cells underscores the significant role of this peptide in the regulation of vascular tone and growth in both physiological and pathophysiological states. ET-1 has been implicated in the pathogenesis of numerous disease processes, particularly cardiovascular diseases. Significant ongoing research efforts . . . [Full Text of this Article]


References




The following articles in journals at HighWire Press have cited this article:


Home page
 Am. J. Respir. Crit. Care Med.Home page
C. ODOUX, B. CRESTANI, G. LEBRUN, C. ROLLAND, P. AUBIN, N. SETA, M.-F. KAHN, J. FIET, and M. AUBIER
Endothelin-1 Secretion by Alveolar Macrophages in Systemic Sclerosis
Am. J. Respir. Crit. Care Med., November 1, 1997; 156(5): 1429 - 1435.
[Abstract] [Full Text]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1997 by the American Association for Clinical Chemistry.