title: Salt sensitivity in genetically hypertensive rats of the Lyon strain.
abstract: BACKGROUND
  Genetically hypertensive (LH) rats of the Lyon strain exhibit a blunted pressure-natriuresis function when compared, in acute conditions, with their normotensive (LN) and low blood pressure (LL) controls. The present work was aimed to determine whether LH rats were salt sensitive in chronic conditions. In addition, a protocol was developed to determine the renal function curve in freely moving rats.
  
  
  METHODS
  Fourteen-week-old rats either untreated or orally treated since weaning with perindopril (3 mg/kg/24 h), an angiotensin-converting enzyme inhibitor, or with valsartan (15 mg/kg/24 h), an angiotensin II subtype 1 receptor antagonist, so as to eliminate the influence of endogenous changes in angiotensin formation were used. Blood pressure (BP) and urinary sodium excretion were measured before, during an oral salt load (2% NaCl in drinking water), and during a two-week aldosterone infusion (50 microg/kg/24 h subcutaneously).
  
  
  RESULTS
  NaCl induced a greater BP increase in untreated LH rats than in LN and LL controls. Perindopril normalized the BP of LH rats but not its elevation during a salt load. Aldosterone slightly increased BP in LH and LL rats either untreated or treated with valsartan. Finally, the combination of telemetric BP measurement with 24-hour urine collection when salt was added to drinking water allowed accurate determination of the slope of the chronic renal function curve in freely moving rats.
  
  
  CONCLUSIONS
  The present work demonstrates that LH rats are salt sensitive. This characteristic manifests despite the lack of an active renin-angiotensin system and is not explained by a hypersensitivity to aldosterone.
authors.affiliation: Département de Physiologie et Pharmacologie Clinique, CNRS UMR 5014, Institut Fédératif de Recherche Cardio-Vasculaire n 39, Faculté de Pharmacie, Université Claude Bernard, Lyon, France.
authors.forename: M
authors.initials: M
authors.lastname: Florin
authors.forename: M
authors.initials: M
authors.lastname: Lo
authors.forename: K L
authors.initials: KL
authors.lastname: Liu
authors.forename: J
authors.initials: J
authors.lastname: Sassard
mesh_terms: D000450:Aldosterone / Q000494:pharmacology; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000818:Animals; D000959:Antihypertensive Agents / Q000627:therapeutic use; D001794:Blood Pressure / Q000187:drug effects* / Q000502:physiology; D004351:Drug Resistance; D006973:Hypertension / Q000188:drug therapy / Q000235:genetics* / Q000503:physiopathology*; D007668:Kidney / Q000503:physiopathology; D008297:Male; D020913:Perindopril / Q000627:therapeutic use; D051381:Rats; D017673:Sodium Chloride, Dietary / Q000494:pharmacology*; D013777:Tetrazoles / Q000627:therapeutic use; D014633:Valine / Q000031:analogs & derivatives* / Q000627:therapeutic use; D000068756:Valsartan
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents; D017673:Sodium Chloride, Dietary; D013777:Tetrazoles; D000450:Aldosterone; D000068756:Valsartan; D014633:Valine; D020913:Perindopril