title: Effects of valsartan on mechanical properties of the carotid artery in spontaneously hypertensive rats under high-salt diet.
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 (AT(1)) 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 AT(1) blockade are greatly influenced by salt intake in SHR. Despite a reduction in mean arterial pressure in HSD rats, AT(1) blockade was not able to prevent the effects of a HSD on pulse pressure, carotid artery stiffness, and hypertrophy.
authors.affiliation: INSERM U337, Paris, France.
authors.forename: C
authors.initials: C
authors.lastname: Labat
authors.forename: P
authors.initials: P
authors.lastname: Lacolley
authors.forename: M
authors.initials: M
authors.lastname: Lajemi
authors.forename: M
authors.initials: M
authors.lastname: de Gasparo
authors.forename: M E
authors.initials: ME
authors.lastname: Safar
authors.forename: A
authors.initials: A
authors.lastname: Benetos
mesh_terms: D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology* / Q000627:therapeutic use; D001013:Aorta, Thoracic / Q000737:chemistry / Q000473:pathology; D001794:Blood Pressure / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D002339:Carotid Arteries / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology; D004305:Dose-Response Relationship, Drug; D005353:Fibronectins / Q000032:analysis; D006973:Hypertension / Q000188:drug therapy* / Q000503:physiopathology; D007150:Immunohistochemistry; D008297:Male; D020033:Protein Isoforms / Q000032:analysis; D051381:Rats; D011918:Rats, Inbred SHR; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage*; D013777:Tetrazoles / Q000494:pharmacology* / Q000627:therapeutic use; D014633:Valine / Q000031:analogs & derivatives / Q000494:pharmacology* / Q000627:therapeutic use; D000068756:Valsartan
chemical_list: D000959:Antihypertensive Agents; D005353:Fibronectins; D020033:Protein Isoforms; D017673:Sodium Chloride, Dietary; D013777:Tetrazoles; D000068756:Valsartan; D014633:Valine