Arrêt de service programmé du vendredi 10 juin 16h jusqu’au lundi 13 juin 9h. Pour en savoir plus
Accéder directement au contenu Accéder directement à la navigation
Article dans une revue

Role of angiotensin II in the remodeling induced by a chronic increase in flow in rat mesenteric resistance arteries

Abstract :

Angiotensin II is a potent growth factor involved in arterial wall homeostasis. In resistance arteries, chronic increases in blood flow induce a rise in diameter associated with arterial wall hypertrophy. Nevertheless, the role of angiotensin II in this remodeling is unknown. We investigated the effect of blocking angiotensin II production or receptor activation on flow-induced remodeling of mesenteric resistance arteries. Arteries were ligated in vivo to generate high-flow arteries compared with normal flow (control) vessels located at a distance. Arteries were isolated after 1 week for in vitro analysis. Arterial diameter, media surface, endothelial NO synthase expression, superoxide production, and extracellular signal-regulated kinase 1/2 phosphorylation were higher in high-flow than in control arteries. Angiotensin-converting enzyme inhibition (perindopril) and angiotensin II type 1 receptor blockade (candesartan) prevented arterial wall hypertrophy without affecting diameter enlargement. The nonselective vasodilator hydralazine had no effect on remodeling. Although perindopril and candesartan increased endothelial NO synthase expression in high-flow arteries, hypertrophy remained in rats treated with N(G)-nitro-l-arginine methyl ester and mice lacking endothelial NO synthase. Perindopril and candesartan reduced oxidative stress in high-flow arteries, but superoxide scavenging did not prevent hypertrophy. Both Tempol and the absence of endothelial NO synthase prevented the rise in diameter in high-flow vessels. Extracellular signal-regulated kinase 1/2 activation in high-flow arteries was prevented by perindopril and candesartan and not by hydralazine. Extracellular signal-regulated kinase 1/2 inhibition in vivo (U0126) prevented hypertrophy in high-flow arteries. Thus, a chronic rise in blood flow in resistance arteries induces a diameter enlargement involving NO and superoxide, whereas hypertrophy was associated with extracellular signal-regulated kinase 1/2 activation by angiotensin II.

Type de document :
Article dans une revue
Liste complète des métadonnées
Contributeur : Okina Univ Angers Connectez-vous pour contacter le contributeur
Soumis le : mercredi 20 octobre 2021 - 10:44:55
Dernière modification le : mercredi 10 novembre 2021 - 15:32:04

Lien texte intégral




Maud Cousin, Marc-Antoine Custaud, Céline Baron-Menguy, Bertrand Toutain, O. Dumont, et al.. Role of angiotensin II in the remodeling induced by a chronic increase in flow in rat mesenteric resistance arteries. Hypertension (Dallas, Tex. : 1979), 2010, 55 (1), pp.109 - 15. ⟨10.1161/HYPERTENSIONAHA.108.127456⟩. ⟨hal-03388015⟩



Consultations de la notice