Carbon monoxide inhibits endothelin-1 release by human pulmonary artery smooth muscle cells

被引：31

作者：

Stanford, SJ

Walters, MJ

Mitchell, JA

机构：

[1] Univ London Imperial Coll Sci Technol & Med, Royal Brompton & Harefield NHS Trust, Crit Care Unit, London SW3 6NP, England

[2] Inst Child Hlth, London WC1N 1EH, England

来源：

EUROPEAN JOURNAL OF PHARMACOLOGY | 2004年 / 486卷 / 03期

关键词：

biliverdin; carbon monoxide (CO); endothelin-1; herne oxygenase; pulmonary artery smooth muscle cell; human; pulmonary hypertension;

D O I：

10.1016/j.ejphar.2003.12.026

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Endothelin-1 is a potent vasoconstrictor with mitogenic properties. This 21-amino-acid protein, released in the vasculature by endothelial and smooth muscle cells, has been implicated in pulmonary hypertension. More recently, evidence has accumulated for a role of the heme oxygenase system in pulmonary hypertension. Heme oxygenase catalyses the breakdown of heme to produce carbon monoxide, biliverdin and free iron. Here we show that a carbon monoxide-releasing molecule, but not biliverdin, inhibits endothelin-1 release from serum-stimulated human pulmonary artery smooth muscle cells. Under certain conditions, carbon monoxide appears to act as an endogenous break on endothelin-1 release. (C) 2004 Elsevier B.V. All rights reserved.

引用

页码：349 / 352

页数：4

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