Perinatal hypoxia triggers alterations in K+ channels of adult pulmonary artery smooth muscle cells.

Détails

ID Serval
serval:BIB_520D1B33E6B2
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Perinatal hypoxia triggers alterations in K+ channels of adult pulmonary artery smooth muscle cells.
Périodique
American Journal of Physiology. Lung Cellular and Molecular Physiology
Auteur(s)
Marino M., Bény J.L., Peyter A.C., Bychkov R., Diaceri G., Tolsa J.F.
ISSN
1040-0605
Statut éditorial
Publié
Date de publication
08/2007
Peer-reviewed
Oui
Volume
293
Numéro
5
Pages
L1171-1182
Langue
anglais
Notes
Publication types: Journal Article
Résumé
Adverse events during the perinatal period, like hypoxia, have been associated with adult diseases. In pulmonary vessels, K(+) channels play an important role in the regulation of vascular tone. In the fetus, Ca(2+)-activated K(+) channels (K(Ca)) are predominant, whereas from birth voltage-gated K(+) channels (K(V)) prevail in the adult. We postulated that perinatal hypoxia could alter this maturational shift and influence regulation of pulmonary vascular tone in relation to K(+) channels in adulthood. We evaluated the effects of perinatal hypoxia on K(V) and K(Ca) channels in the adult main pulmonary artery (PA) using a murine model. Electrophysiological measurements showed a greater outward current in PA smooth muscle cells of mice born in hypoxia than in controls. In controls, only K(V) channels contributed to this current, whereas in mice born in hypoxia both K(V) and K(Ca) channels were implicated. K(V) channel activity was even higher in mice born in hypoxia than in controls. Therefore, perinatal hypoxia results in increased K(Ca) and K(V) channel activity in adult PA. Moreover, PA of adults born in hypoxia displayed higher large-conductance K(Ca) alpha-subunit and K(V)1.5 alpha-subunit protein expression than controls. Interestingly, relaxation induced by nitric oxide (NO) donors [S-nitroso-N-acetyl-D,l-penicillamine, 2-(N,N-diethylamino)-diazenolate-2-oxide] in isolated PA of control mice was not mediated by K(Ca) channels and only slightly by K(V) channels, whereas following perinatal hypoxia both K(Ca) and K(V) channels contributed to this relaxation. Thus perinatal hypoxia results in altered expression and activity of different K(+) channels in the adult main PA, which could contribute to modifications of pulmonary vasoreactivity.
Mots-clé
Animals, Anoxia/metabolism, Blotting, Western, Female, Mice, Mice, Inbred C57BL, Muscle, Smooth, Vascular/metabolism, Nitric Oxide Donors/pharmacology, Potassium Channels/metabolism, Pulmonary Artery/cytology, Vasodilation
Pubmed
Web of science
Création de la notice
25/01/2008 14:18
Dernière modification de la notice
20/08/2019 15:07
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