title: Plasma volume and arterial stiffness in the cardiac alterations associated with long-term high sodium feeding in rats.
abstract: BACKGROUND
  Rats fed an early and long-term high-salt diet (HS, NaCl 8%) developed significant cardiovascular hypertrophy without major changes in blood pressure. The mechanism of this cardiac hypertrophy has not been yet elucidated.
  
  
  METHODS
  In the present work, we assessed the influence of volume overload and arterial stiffness on the structural and functional cardiac changes induced by a high salt feeding from weaning to 5 months of age in Sprague-Dawley rats.
  
  
  RESULTS
  Cardiac hypertrophy in HS rats was associated with clear augmentation in the size of left ventricular (LV) cardiomyocyte as compared with rats fed regular diet (NS). Echocardiography revealed a marked increase in relative wall thickness. Of note, no alteration of global and regional systolic and diastolic function was detected in HS rats. High sodium consumption was associated with a slight increase in aortic mean and pulse pressure (PP) without effect on pulse wave velocity (PWV) and elastic modulus. Plasma volume and central venous pressure were higher in HS than NS rats. Whereas plasma endothelin level was twofold higher in HS than in NS rats, LV endothelin level was similar in both groups. Treatment by the endothelin receptors blocker bosentan had no detectable effect on the changes induced by HS diet.
  
  
  CONCLUSIONS
  High sodium intake was associated with concentric cardiac hypertrophy without change of systolic and diastolic function. Aortic rigidity was not a determinant of cardiac hypertrophy. Beside a likely direct effect of sodium on cardiovascular system the slight increase in arterial pressure and plasma volume play a role.
authors.affiliation: Groupe Rein et Hypertension, Montpellier University, Montpellier, France.
authors.forename: Magali
authors.initials: M
authors.lastname: Cordaillat
authors.forename: Cyril
authors.initials: C
authors.lastname: Reboul
authors.forename: Virginie
authors.initials: V
authors.lastname: Gaillard
authors.forename: Isabelle
authors.initials: I
authors.lastname: Lartaud
authors.forename: Bernard
authors.initials: B
authors.lastname: Jover
authors.forename: Caroline
authors.initials: C
authors.lastname: Rugale
mesh_terms: D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects / Q000502:physiology; D001783:Blood Flow Velocity / Q000187:drug effects; D000077300:Bosentan; D006332:Cardiomegaly / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D015150:Echocardiography, Doppler; D065128:Endothelin Receptor Antagonists; D019332:Endothelin-1 / Q000097:blood; D008297:Male; D010953:Plasma Volume / Q000187:drug effects*; D011673:Pulsatile Flow / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage* / Q000009:adverse effects; D013449:Sulfonamides / Q000494:pharmacology; D014655:Vascular Resistance / Q000187:drug effects*
chemical_list: D065128:Endothelin Receptor Antagonists; D019332:Endothelin-1; D017673:Sodium Chloride, Dietary; D013449:Sulfonamides; D000077300:Bosentan