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(Stroke. 1998;29:1031-1036.)
© 1998 American Heart Association, Inc.

Original Contributions

Effect of Chronic Nitric Oxide Deficiency on Angiotensin II–Induced Hypertrophy of Rat Basilar Artery

Pierre Moreau, PhD; Hiroyuki Takase, MD; Livius V. d'Uscio, PhD; Thomas F. Lüscher, MD

From the Division of Cardiology, Cardiovascular Research, University Hospital, Bern, and Division of Cardiology, University Hospital and Institute of Physiology, University Zürich (Switzerland) (P.M., H.T., L.V.d'U., T.F.L.), and Faculty of Pharmacy, Université de Montréal (Québec, Canada) (P.M.).

Correspondence to Thomas F. Lüscher, MD, FACC, FESC, Division of Cardiology, University Hospital, Rämistrasse 100, CH-8091 Zürich, Switzerland. E-mail 100771.1237{at}compuserve.com

Background and Purpose—Although in vitro studies suggest that nitric oxide has an inhibitory effect on cellular proliferation and migration, in vivo experiments failed to support this conclusion. The present study was designed to determine the effect of endogenous nitric oxide on angiotensin II–induced hypertrophy of small arteries in vivo.

Methods—Angiotensin II (200 ng/kg per minute), alone or in combination with N-nitro-L-arginine methyl ester (L-NAME) (60 mg/kg per day), was administered for 2 weeks in normotensive rats. Basilar arteries were harvested, and their geometry was determined in perfused and pressurized conditions.

Results—Angiotensin II increased media thickness, media-lumen ratio, and cross-sectional area of the arteries, confirming the presence of hypertrophic remodeling. The concomitant administration of L-NAME, an inhibitor of nitric oxide synthesis, prevented vascular hypertrophy. The remodeling of the basilar artery geometry in the combined treatment was of eutrophic nature, similar to that observed with the administration of L-NAME alone.

Conclusions—Our results suggest that endogenous nitric oxide does not inhibit angiotensin II–induced vascular hypertrophy in vivo. Nitric oxide may even be a necessary factor for hypertrophy to develop.

Editorial Comment

Gary L. Baumbach, , MD, Guest Editor

Department of Pathology and Cardiovascular Center, University of Iowa College of Medicine, Iowa City, Iowa

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