Chronic nitric oxide synthase inhibition and carotid artery distensibility in renal hypertensive rats.

Détails

ID Serval
serval:BIB_4563109450B9
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Chronic nitric oxide synthase inhibition and carotid artery distensibility in renal hypertensive rats.
Périodique
Hypertension
Auteur(s)
Delacrétaz E., Zanchi A., Nussberger J., Hayoz D., Aubert J.F., Brunner H.R., Waeber B.
ISSN
0194-911X
Statut éditorial
Publié
Date de publication
1995
Peer-reviewed
Oui
Volume
26
Numéro
2
Pages
332-6
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't - Publication Status: ppublish
Résumé
The goal of the present study was to examine the viscoelastic properties of the carotid artery in genetically identical rats exposed to similar levels of blood pressure sustained by different mechanisms. Eight-week old male Wistar rats were examined 2 weeks after renal artery clipping (two-kidney, one clip [2K1C] Goldblatt rats, n = 53) or sham operation (n = 49). One half of the 2K1C and sham rats received the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME, 1.48 mmol/L) in their drinking water for 2 weeks after the surgical procedure. Mean blood pressure increased significantly in the 2K1C-water (182 mm Hg), 2K1C-L-NAME (197 mm Hg), and sham-L-NAME (170 mm Hg) rats compared with the sham-water rats (127 mm Hg). Plasma renin activity was not altered by L-NAME but significantly enhanced after renal artery clipping. A significant and similar increase in the cross-sectional area of the carotid artery was observed in L-NAME and vehicle-treated 2K1C rats. L-NAME per se did not modify cross-sectional area in the sham rats. There was a significant upward shift of the distensibility-pressure curve in the L-NAME- and vehicle-treated 2K1C rats compared with the sham-L-NAME rats. L-NAME treatment did not alter the distensibility-pressure curve in the 2K1C rats. These results demonstrate that the mechanisms responsible for artery wall hypertrophy in renovascular hypertension are accompanied by an increase in arterial distensibility that is not dependent on the synthesis of nitric oxide.
Mots-clé
Amino Acid Oxidoreductases, Animals, Arginine, Blood Pressure, Carotid Arteries, Heart Rate, Hypertension, Renovascular, Male, NG-Nitroarginine Methyl Ester, Nitric Oxide Synthase, Rats, Rats, Wistar, Vascular Resistance
Pubmed
Web of science
Création de la notice
17/01/2008 17:38
Dernière modification de la notice
20/08/2019 14:50
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