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(Hypertension. 2001;38:439.)
© 2001 American Heart Association, Inc.

Scientific Contributions

Effects of Valsartan on Mechanical Properties of the Carotid Artery in Spontaneously Hypertensive Rats Under High-Salt Diet

Carlos Labat; Patrick Lacolley; Malika Lajemi; Marc de Gasparo; Michel E. Safar; Athanase Benetos

INSERM U337 (C.L., P.L., M.L., M.E.S., A.B.), Paris, France; and Research Department Novartis (M.d.G.), Basle, Switzerland.

Correspondence to Athanase Benetos, MD, PhD, INSERM U337, 15 Rue de l’Ecole de Médecine, Paris 75270, Cedex 06, France. E-mail benetos{at}ccr.jussieu.fr

Abstract—— The aim of this investigation was to evaluate the influence of a high-salt diet (HSD) on the effects of valsartan, an angiotensin II type 1 (AT₁) receptor antagonist, on carotid arterial stiffness and structure in spontaneous hypertensive rats (SHR). Carotid arterial stiffness was studied in SHR receiving a HSD or a normal-salt diet (NSD) from the 10th to 20th week of age. Within each of the 2 groups, the animals received treatment with either placebo or valsartan (30 mg · kg^-1 · d^-1) administered on the 4th to 20th week of age. Arterial pressure, wall stress, incremental elastic modulus (Einc), medial cross-sectional area, and EIIIA fibronectin isoform were significantly increased in placebo-HSD rats compared with placebo-NSD rats with no change in the ratio of collagen to elastin. Valsartan reduced mean arterial pressure in both NSD and HSD rats but reduced pulse pressure only in NSD rats. In NSD rats, valsartan reduced Einc and medial cross-sectional area. In HSD, valsartan increased Einc and did not modify medial cross-sectional area and fibronectin. In valsartan-treated rats, the ratio of collagen to elastin was greater in HSD than in NSD rats. In conclusion, the effects of AT₁ blockade are greatly influenced by salt intake in SHR. Despite a reduction in mean arterial pressure in HSD rats, AT₁ blockade was not able to prevent the effects of a HSD on pulse pressure, carotid artery stiffness, and hypertrophy.

Key Words: salt • angiotensin II • AT₁ blockade • large artery stiffness • carotid artery

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