Research article summary (published 30 Aug 2009):

Novel pathway of endothelin-1 and reactive oxygen species in coronary vasospasm with endothelial dysfunction.

Full Abstract

The role of endothelial dysfunction in coronary vasospasm is controversial. We hypothesized that reactive oxygen species (ROS) and endothelin-1 (ET-1) are plausible candidates as the mediator of vasospasm is linked to endothelial dysfunction. In a pig model with repetitive endothelial injury in coronary arteries, intracoronary administration of serotonin induced a vasospasm at the endothelial injury site. The level of endothelin-converting enzyme was upregulated at that site where, upon exposure to serotonin, there were also increases in p47(phox), ROS, and ET-1 fluorescence intensities, and myosin light chain phosphorylation and RhoA activation were detected. The nicotinamide adenine dinucleotide phosphate oxidase inhibitor, apocynin, had the effect of extinguishing not only ROS but also the appearance of ET-1. The chronic blockade of endothelin type-A receptor prevented a serotonin-triggered vasospasm along with the inhibition of ROS generation and myosin light chain phosphorylation. Under the coronary artery endothelial dysfunction, ET-1 is essential for an ROS-dependent coronary vasospasm. Our findings suggest that endothelial dysfunction plays a critical role in clinically defined human Prinzmetal angina.

Author information

Author/s: Saitoh, Shu-Ichi (S); Matsumoto, Ken (K); Kamioka, Masashi (M); Ohkawara, Hiroshi (H); Kaneshiro, Takashi (T); Ishibashi, Toshiyuki (T); Maruyama, Yukio (Y);

Affiliation: First Department of Internal Medicine, Fukushima Medical University, Hikarigaoka, Fukushima, Japan. sais(-atsign-)fmu.ac.jp

Journal and publication information

Publication Type: Journal Article; Research Support, Non-U.S. Gov't

Journal: Coronary artery disease (Coron Artery Dis), published in England. (Language: eng)

Reference: 2009-Sep; vol 20 (issue 6) : pp 400-8

Dates: Created 2009/08/21; Completed 2009/10/29;

PMID: 19623039, status: MEDLINE (last retrieval date: 10/29/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Acetophenones - pharmacology Angina Pectoris, Variant - metabolism; physiopathology Animals Aspartic Endopeptidases - metabolism Coronary Angiography Coronary Vasospasm - chemically induced; metabolism; physiopathology; radiography Disease Models, Animal Endothelin-1 - blood; metabolism Endothelium, Vascular - drug effects; metabolism; physiopathology Enzyme Inhibitors - pharmacology Metalloendopeptidases - metabolism Myosin Light Chains - metabolism

NADPH Oxidase - antagonists & inhibitors; metabolism Phosphorylation Pyrimidines - pharmacology Reactive Oxygen Species - metabolism Receptor, Endothelin A - antagonists & inhibitors; metabolism Serotonin Signal Transduction - drug effects Sulfonamides - pharmacology Swine Time Factors Vasoconstriction - drug effects rhoA GTP-Binding Protein - metabolism

Associated Chemicals: Acetophenones (0) ; Endothelin-1 (0) ; Enzyme Inhibitors (0) ; Myosin Light Chains (0) ; Pyrimidines (0) ; Reactive Oxygen Species (0) ; Receptor, Endothelin A (0) ; Sulfonamides (0) ; T 0201 (0) ; acetovanillone (498-02-2) ; Serotonin (50-67-9) ; NADPH Oxidase (EC 1.6.3.1) ; neutrophil cytosolic factor 1 (EC 1.6.3.1) ; Aspartic Endopeptidases (EC 3.4.23.-) ; Metalloendopeptidases (EC 3.4.24.-) ; endothelin-converting enzyme (EC 3.4.24.71) ; rhoA GTP-Binding Protein (EC 3.6.5.2)

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