Nitric Oxide Deficit Drives Intimal Hyperplasia in Mouse Models of Hypertension.

Détails

ID Serval
serval:BIB_C0A2446DFA5B
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Nitric Oxide Deficit Drives Intimal Hyperplasia in Mouse Models of Hypertension.
Périodique
European journal of vascular and endovascular surgery : the official journal of the European Society for Vascular Surgery
Auteur(s)
Allagnat F., Haefliger J.A., Lambelet M., Longchamp A., Bérard X., Mazzolai L., Corpataux J.M., Déglise S.
ISSN
1532-2165 (Electronic)
ISSN-L
1078-5884
Statut éditorial
Publié
Date de publication
05/2016
Peer-reviewed
Oui
Volume
51
Numéro
5
Pages
733-742
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Résumé
To evaluate the impact of different types of hypertension on the development of intimal hyperplasia (IH).
Genetic, surgical, and pharmacological models of hypertension were used to compare IH formation in a murine model of carotid artery ligation (CAL). CAL was performed in normotensive WT male mice and in three mouse models of hypertension: (1) L-NAME (Nω-nitro-l-arginine-methyl-ester) treatment for 2 weeks prior to CAL to instate renin-independent hypertension; (2) 2K1C (two kidneys, one clip) surgery 1 week prior to CAL to induce renin-dependent hypertension; (3) Cx40-/- mice, a genetic model of renin-dependent hypertension. Mice were sacrificed prior to CAL or 3, 14, or 28 days post CAL. Data collection included tail blood pressure measurements, and morphometric and histological assessment of the ligated carotids.
CAL triggered the formation of a VSMC-rich neointima layer after 14-28 days, which was increased in all hypertensive mice. Despite similarly increased blood pressure, L-NAME treated mice displayed more IH than all other hypertensive groups. In addition, L-NAME induced hypertension triggered more cell proliferation and recruitment of CD45 positive inflammatory cells to the ligated vessel wall compared with Cx40-/- or normotensive WT mice.
NO deficiency is a major aspect of vascular inflammation, VSMC proliferation, and IH in hypertensive conditions.

Mots-clé
Animals, Carotid Arteries/pathology, Disease Models, Animal, Hyperplasia/etiology, Hyperplasia/pathology, Hypertension/chemically induced, Hypertension/complications, Hypertension/pathology, Male, Mice, Mice, Inbred C57BL, Muscle, Smooth, Vascular/pathology, NG-Nitroarginine Methyl Ester/pharmacology, Nitric Oxide/deficiency
Pubmed
Open Access
Oui
Création de la notice
29/03/2016 12:50
Dernière modification de la notice
20/08/2019 16:35
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