Role of membrane potential in endothelium-dependent relaxation of isolated mouse main pulmonary artery

Détails

ID Serval
serval:BIB_852A6006636E
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Role of membrane potential in endothelium-dependent relaxation of isolated mouse main pulmonary artery
Périodique
Journal of Cardiovascular Pharmacology
Auteur(s)
Tolsa  J. F., Marino  M., Peyter  A. C., Beny  J. L.
ISSN
0160-2446 (Print)
Statut éditorial
Publié
Date de publication
04/2006
Volume
47
Numéro
4
Pages
501-7
Notes
In Vitro
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Apr
Résumé
The physiology of smooth muscle and endothelial cells of a particular vascular bed and from different species differs from each other. Acetylcholine causes an endothelium-dependent relaxation of preconstricted pulmonary arteries from the rat. This relaxation is mediated by nitric oxide (NO) plus a yet-unidentified endothelium-derived hyperpolarizing factor, which relaxes the smooth muscles by hyperpolarizing them. Our aim is to test whether these observations could be generalized to the smooth muscle cells from the mouse pulmonary artery. Smooth muscle or endothelial cell membrane potential of strips of murine pulmonary artery were measured simultaneously with the force developed by the strip. Acetylcholine hyperpolarized the endothelial cells. However, acetylcholine did not induce an endothelium-dependent hyperpolarization of the smooth muscle, while it relaxed the strip in an endothelium-dependent manner. This relaxation was abolished by an inhibitor of NO synthesis, nitro-L-arginine. Moreover, nitroglycerin relaxed the strips without changing the membrane potential of the smooth muscle cells. Injection of Lucifer yellow into the endothelial cells and the smooth muscle cells did not show heterocellular dye coupling. Furthermore, electron microscopy did not show gap junction plate at the myoendothelial junctions. We conclude that in the mouse main pulmonary artery, NO alone is responsible for the acetylcholine-induced endothelium-dependent vasodilatation, whereas the phenomenon called endothelium-derived hyperpolizing factor is not present. Therefore, caution should be taken when comparing different animal models to study pulmonary circulation and its reactivity.
Mots-clé
Animals Endothelium, Vascular/*physiology/ultrastructure Isometric Contraction/physiology Male Membrane Potentials/*physiology Mice Mice, Inbred C57BL Microscopy, Electron Muscle Relaxation/physiology Muscle, Smooth, Vascular/*physiology/ultrastructure Pulmonary Artery/*physiology/ultrastructure Vasodilation/physiology
Pubmed
Web of science
Création de la notice
25/01/2008 14:18
Dernière modification de la notice
03/03/2018 18:56
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