title: Sodium, arterial stiffness, and cardiovascular mortality in hypertensive rats.
abstract: BACKGROUND
  We examined the effects of early high salt diet (HSD) and angiotensin II type 1 (AT1) receptor antagonist valsartan (Val) on mortality and carotid distensibility in surviving spontaneously hypertensive rats (SHRs).
  
  
  METHODS
  The HSD was initiated either early (week 4 after birth) or late (week 10), continued until 20 weeks of age, and compared to normal salt diet (NSD) groups. Valsartan was given from the fourth week after birth.
  
  
  RESULTS
  Eighty-six percent of the rats died in early HSD on placebo, 70% in early HSD on Val-3 mg, 35% in early HSD on Val-30 mg, and 13% in late HSD on placebo. Mean arterial pressure (MAP) was higher in the early HSD and late HSD groups on placebo compared with NSD. The Val-30 mg reduced MAP in all except early HSD groups. Distensibility at MAP (operational distensibility) was lower in late HSD on placebo than in NSD placebo groups. The Val-30 mg increased distensibility in NSD groups. There was no effect of Val in late HSD and early HSD groups. Operational distensibility was negatively correlated with MAP and salt and positively correlated with Val treatment. All animals receiving HSD showed a higher isobaric distensibility in early HSD than in late HSD groups and a smaller distensibility in rats treated with Val.
  
  
  CONCLUSIONS
  Our results showed that administration of early HSD in SHR was associated together with a high mortality, a protective action of Val that increased longevity, and an increased level of isobaric distensibility. Survival in HSD groups suggest a direct role of angiotensin II in salt-induced cardiovascular mortality. This role is associated with MAP independent of changes in carotid stiffness.
authors.affiliation: INSERM, U684, Nancy, France; Université Henri Poincaré, UFR Médecine, Nancy, France.
authors.forename: Nathalie
authors.initials: N
authors.lastname: Mercier
authors.forename: Carlos
authors.initials: C
authors.lastname: Labat
authors.forename: Huguette
authors.initials: H
authors.lastname: Louis
authors.forename: Valerie
authors.initials: V
authors.lastname: Cattan
authors.forename: Athanase
authors.initials: A
authors.lastname: Benetos
authors.forename: Michel E
authors.initials: ME
authors.lastname: Safar
authors.forename: Patrick
authors.initials: P
authors.lastname: Lacolley
mesh_terms: D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology* / Q000627:therapeutic use; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology* / Q000627:therapeutic use; D001794:Blood Pressure / Q000187:drug effects; D002318:Cardiovascular Diseases / Q000209:etiology / Q000517:prevention & control*; D002339:Carotid Arteries / Q000187:drug effects* / Q000503:physiopathology; D003187:Compliance / Q000187:drug effects; D004195:Disease Models, Animal; D006973:Hypertension / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D008297:Male; D051381:Rats; D011918:Rats, Inbred SHR; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage*; D013777:Tetrazoles / Q000494:pharmacology* / Q000627:therapeutic use; D013997:Time Factors; D014633:Valine / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000627:therapeutic use; D000068756:Valsartan
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D000959:Antihypertensive Agents; D017673:Sodium Chloride, Dietary; D013777:Tetrazoles; D000068756:Valsartan; D014633:Valine