Perinatal Hypoxia Enhances Cyclic Adenosine Monophosphate-mediated BKCa Channel Activation in Adult Murine Pulmonary Artery.

Détails

ID Serval
serval:BIB_3D53DCC29083
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Perinatal Hypoxia Enhances Cyclic Adenosine Monophosphate-mediated BKCa Channel Activation in Adult Murine Pulmonary Artery.
Périodique
Journal of Cardiovascular Pharmacology
Auteur(s)
Marino M., Bény J.L., Peyter A.C., Diaceri G., Tolsa J.F.
ISSN
1533-4023 (Electronic)
ISSN-L
0160-2446
Statut éditorial
Publié
Date de publication
2011
Volume
57
Numéro
2
Pages
154-165
Langue
anglais
Résumé
Exposure to perinatal hypoxia results in alteration of the adult pulmonary circulation, which is linked among others to alterations in K channels in pulmonary artery (PA) smooth muscle cells. In particular, large conductance Ca-activated K (BKCa) channels protein expression and activity were increased in adult PA from mice born in hypoxia compared with controls. We evaluated long-term effects of perinatal hypoxia on the cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA) pathway-mediated activation of BKCa channels, using isoproterenol, forskolin, and dibutyryl-cAMP. Whole-cell outward current was higher in pulmonary artery smooth muscle cells from mice born in hypoxia compared with controls. Spontaneous transient outward currents, representative of BKCa activity, were present in a greater proportion in pulmonary artery smooth muscle cells of mice born in hypoxia than in controls. Agonists induced a greater relaxation in PA of mice born in hypoxia compared with controls, and BKCa channels contributed more to the cAMP/PKA-mediated relaxation in case of perinatal hypoxia. In summary, perinatal hypoxia enhanced cAMP-mediated BKCa channels activation in adult murine PA, suggesting that this pathway could be a potential target for modulating adult pulmonary vascular tone after perinatal hypoxia.
Pubmed
Web of science
Création de la notice
22/03/2011 12:21
Dernière modification de la notice
20/08/2019 14:33
Données d'usage