Enhanced vascular contractility in alpha1-adrenergic receptor-deficient mice.

Détails

ID Serval
serval:BIB_FDE2B7FACE6B
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Enhanced vascular contractility in alpha1-adrenergic receptor-deficient mice.
Périodique
Life Sciences
Auteur(s)
Sanbe A., Tanaka Y., Fujiwara Y., Miyauchi N., Mizutani R., Yamauchi J., Cotecchia S., Koike K., Tsujimoto G., Tanoue A.
ISSN
1879-0631 (Electronic)
ISSN-L
0024-3205
Statut éditorial
Publié
Date de publication
2009
Peer-reviewed
Oui
Volume
84
Numéro
21-22
Pages
713-718
Langue
anglais
Résumé
AIM: Alpha1-adrenergic receptors (alpha1-ARs) are classified into three subtypes: alpha1A-AR, alpha1B-AR, and alpha1D-AR. Triple disruption of alpha1A-AR, alpha1B-AR, and alpha1D-AR genes results in hypotension and produces no contractile response of the thoracic aorta to noradrenalin. Presently, we characterized vascular contractility against other vasoconstrictors, such as potassium, prostaglandin F2alpha (PGF(2alpha)) and 5-hydroxytryptamine (5-HT), in alpha1A-AR, alpha1B-AR, and alpha1D-AR triple knockout (alpha1-AR triple KO) mice.
MAIN METHODS: The contractile responses to the stimulation with vasoconstrictors were studied using isolated thoracic aorta.
KEY FINDINGS: As a result, the phasic and tonic contraction induced by a high concentration of potassium (20 mM) was enhanced in the isolated thoracic aorta of alpha1-AR triple KO mice compared with that of wild-type (WT) mice. In addition, vascular responses to PGF(2alpha) and 5-HT were also enhanced in the isolated thoracic aorta of alpha1-AR triple KO mice compared with WT mice. Similar to in vitro findings with isolated thoracic aorta, in vivo pressor responses to PGF(2alpha) were enhanced in alpha1-AR triple KO mice. Real-time reverse transcription-polymerase chain reaction analysis and western blot analysis indicate that gene expression of the 5-hydroxytryptamine 2A (5-HT(2A)) receptor was up-regulated in the thoracic aorta of alpha1-AR triple KO mice while the prostaglandin F2alpha receptor (FP) was unchanged.
SIGNIFICANCE: These results suggest that loss of alpha1-ARs can lead to enhancement of vascular responsiveness to the vasoconstrictors and may imply that alpha1-ARs and the subsequent signaling regulate the vascular responsiveness to other stimulations such as depolarization, 5-HT and PGF(2alpha).
Mots-clé
Animals, Aorta, Thoracic/drug effects, Blood Pressure/drug effects, Blotting, Western, Dinoprost/pharmacology, Dose-Response Relationship, Drug, Gene Expression/physiology, Gene Targeting, Heart Rate/drug effects, Mice, Mice, Inbred C57BL, Mice, Knockout, Muscle Contraction/genetics, Muscle Contraction/physiology, Muscle, Smooth, Vascular/physiology, Receptors, Adrenergic, alpha-1/genetics, Receptors, Adrenergic, alpha-1/physiology, Reverse Transcriptase Polymerase Chain Reaction, Serotonin/pharmacology, Vasoconstrictor Agents/pharmacology
Pubmed
Web of science
Création de la notice
07/12/2009 13:12
Dernière modification de la notice
20/08/2019 16:28
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