title: Glomerular filtration rate and blood pressure are unchanged by increased sodium intake in atorvastatin-treated healthy men.
abstract: OBJECTIVE
  Improved cardiovascular survival during statin treatment might be due to effects in addition to cholesterol lowering. We hypothesize that sodium intake affects renal function and vasoactive hormones in atorvastatin-treated healthy subjects.
  
  
  METHODS
  In a randomized, placebo-controlled, double-blind, crossover study we measured the effect of a moderate change in sodium intake on glomerular filtration rate (GFR), blood pressure (BP), renal tubular function, plasma concentrations of vasoactive hormones and urinary excretion of aquaporin-2 (u-AQP2) in 22 healthy subjects. The subjects were randomized to standardized fluid intake and diet corresponding to the need for calories in the 4 days before each of the 2 examination days. In one of the periods they were randomized to receive sodium chloride tablets (2 g) thrice daily for 4 days. Two doses of atorvastatin (80 mg) were given; one at 2200 h the evening before the study day, the other at 0830 h in the morning.
  
  
  RESULTS
  24-h urinary sodium excretion increased by 23%. GFR and BP were unchanged. Sodium clearance, fractional excretion of sodium and u-AQP2 increased, whereas free water clearance decreased during high sodium intake. PRC and aldosterone were suppressed during the high sodium diet.
  
  
  CONCLUSIONS
  A change in dietary sodium intake of approximately 100 mmol daily does not change GFR and BP in atorvastatin-treated healthy men. The lack of change in BP might reflect that the subjects studied were not sodium sensitive, or that atorvastatin treatment modified sodium sensitivity.
authors.affiliation: Department of Medical Research and Department of Medicine, Holstebro Hospital and Aarhus University, Holstebro, Denmark. 55@stofanet.dk
authors.forename: L
authors.initials: L
authors.lastname: Paulsen
authors.forename: L M
authors.initials: LM
authors.lastname: Holst
authors.forename: J N
authors.initials: JN
authors.lastname: Bech
authors.forename: J
authors.initials: J
authors.lastname: Starklint
authors.forename: E B
authors.initials: EB
authors.lastname: Pedersen
mesh_terms: D000328:Adult; D000450:Aldosterone / Q000097:blood; D000804:Angiotensin II / Q000097:blood; D051399:Aquaporin 2 / Q000652:urine; D000069059:Atorvastatin; D009320:Atrial Natriuretic Factor / Q000097:blood; D001794:Blood Pressure / Q000187:drug effects*; D005260:Female; D005919:Glomerular Filtration Rate / Q000187:drug effects*; D006538:Heptanoic Acids / Q000494:pharmacology*; D006801:Humans; D007677:Kidney Function Tests; D008094:Lithium / Q000493:pharmacokinetics; D008297:Male; D020097:Natriuretic Peptide, Brain / Q000097:blood; D011758:Pyrroles / Q000494:pharmacology*; D012083:Renin / Q000097:blood; D012964:Sodium / Q000493:pharmacokinetics / Q000494:pharmacology*; D014667:Vasopressins / Q000097:blood
chemical_list: C496023:AQP2 protein, human; D051399:Aquaporin 2; D006538:Heptanoic Acids; D011758:Pyrroles; D014667:Vasopressins; D000804:Angiotensin II; D020097:Natriuretic Peptide, Brain; D000450:Aldosterone; D009320:Atrial Natriuretic Factor; D008094:Lithium; D012964:Sodium; D000069059:Atorvastatin; D012083:Renin