Cardiovascular influences of alpha1b-adrenergic receptor defect in mice.

Détails

ID Serval
serval:BIB_98B65B3B71EA
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Cardiovascular influences of alpha1b-adrenergic receptor defect in mice.
Périodique
Circulation
Auteur(s)
Vecchione C., Fratta L., Rizzoni D., Notte A., Poulet R., Porteri E., Frati G., Guelfi D., Trimarco V., Mulvany M.J., Agabiti-Rosei E., Trimarco B., Cotecchia S., Lembo G.
ISSN
1524-4539 (Electronic)
ISSN-L
0009-7322
Statut éditorial
Publié
Date de publication
2002
Volume
105
Numéro
14
Pages
1700-1707
Langue
anglais
Résumé
BACKGROUND: The alpha1-adrenergic receptors (alpha1-ARs) play a key role in cardiovascular homeostasis. However, the functional role of alpha1-AR subtypes in vivo is still unclear. The aim of this study was to evaluate the cardiovascular influences of alpha1b-AR.
METHODS AND RESULTS: In transgenic mice lacking alpha1-AR (KO) and their wild-type controls (WT), we evaluated blood pressure profile and cardiovascular remodeling induced by the chronic administration (18 days via osmotic pumps) of norepinephrine, angiotensin II, and subpressor doses of phenylephrine. Our results indicate that norepinephrine induced an increase in blood pressure levels only in WT mice. In contrast, the hypertensive state induced by angiotensin II was comparable between WT and KO mice. Phenylephrine did not modify blood pressure levels in either WT or KO mice. The cardiac hypertrophy and eutrophic vascular remodeling evoked by norepinephrine was observed only in WT mice, and this effect was independent of the hypertensive state because it was similar to that observed during subpressor phenylephrine infusion. Finally, the cardiac hypertrophy induced by thoracic aortic constriction was comparable between WT and KO mice.
CONCLUSIONS: Our data demonstrate that the lack of alpha1b-AR protects from the chronic increase of arterial blood pressure induced by norepinephrine and concomitantly prevents cardiovascular remodeling evoked by adrenergic activation independently of blood pressure levels.
Mots-clé
Angiotensin II/pharmacology, Animals, Aorta/physiology, Arterioles/drug effects, Arterioles/physiopathology, Atrial Natriuretic Factor/genetics, Atrial Natriuretic Factor/metabolism, Blood Pressure/drug effects, Blood Pressure/genetics, Cardiomegaly/chemically induced, Cardiomegaly/pathology, Cardiovascular System/drug effects, Cardiovascular System/pathology, Echocardiography, Heart Rate/drug effects, Heart Rate/genetics, Heart Ventricles/drug effects, Heart Ventricles/metabolism, Hypertension/chemically induced, Hypertension/pathology, Male, Mesentery/blood supply, Mice, Mice, Transgenic, Norepinephrine/pharmacology, Organ Size/drug effects, Organ Size/genetics, Phenylephrine/pharmacology, RNA, Messenger/metabolism, Receptors, Adrenergic, alpha-1/deficiency, Receptors, Adrenergic, alpha-1/genetics, Vasoconstrictor Agents/pharmacology, Ventricular Remodeling/drug effects, Ventricular Remodeling/genetics
Pubmed
Web of science
Open Access
Oui
Création de la notice
24/01/2008 11:06
Dernière modification de la notice
20/08/2019 15:00
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