title: A reduction of 3 g/day from a usual 9 g/day salt diet improves endothelial function and decreases endothelin-1 in a randomised cross_over study in normotensive overweight and obese subjects.
abstract: OBJECTIVE
  It is unclear if a modest reduction in dietary salt intake has beneficial effects on vascular function. The aim was to compare the effects of 9 g salt/day with 6 g salt/day intake on measures of vascular function and explore mechanisms of effect in overweight and obese adults.
  
  
  METHODS
  Twenty-five overweight/obese subjects (BMI 27-40 kg/m(2)) completed a randomised cross-over study of 6 weeks each on a reduced salt (RS) (6 g/day) and usual salt diet (US) (9 g/day). Flow-mediated-dilatation (FMD), 24 h blood pressure (BP), augmentation index (AIx), pulse wave velocity (PWV), plasma and urinary nitrate/nitrite, asymmetric dimethylarginine (ADMA), renin, aldosterone and endothelin-1 and vascular adhesion molecules were measured after 2 days and 6 weeks. Adherence to the diets was determined from two 24 h urine collections.
  
  
  RESULTS
  Urinary sodium excretion was 155 ± 58 mmol/24 h US vs 113 ± 45 mmol/24 h RS (p = 0.002). Following the RS diet there was a significant improvement in FMD from 3.5 ± 2.8% to 5.6 ± 2.8% (P < 0.001) and decrease in serum endothelin-1 from 1.45 ± 0.38 pg/ml to 1.25 ± 0.39 pg/ml (P < 0.05). Endothelium-independent vasodilatation was also significantly different between treatments (P < 0.05). AIx, PWV, serum ADMA and plasma and urinary nitrate/nitrite concentrations were not different between treatments. Change in FMD was related to the urinary sodium: creatinine ratio (r = -0.47, P < 0.05) and was independent of blood pressure. Aldosterone and renin were unchanged.
  
  
  CONCLUSIONS
  A small reduction in dietary salt intake of 3 g/day improves endothelial function in normotensive overweight and obese subjects. This response may be mediated by serum endothelin-1. This small reduction in salt had no effect on aldosterone and renin concentrations. This trial was registered with the Australian and New Zealand Clinical Trials Registry Unique Identifier: ACTRN12609000321246 http://www.anzctr.org.au/ACTRN12609000321246.aspx.
authors: Commonwealth Scientific and Industrial Research Organisation, Animal, Food and Health Science, Adelaide, South Australia, Australia; Discipline of Physiology, Faculty of Health Science, University of Adelaide, South Australia, Australia; The National Health and Medical Research Council of Australia, Centre of Clinical Research Excellence in Nutritional Physiology, Interventions and Outcomes, Adelaide, South Australia, Australia.
authors: Kacie M
authors: KM
authors: Dickinson
authors: The National Health and Medical Research Council of Australia, Centre of Clinical Research Excellence in Nutritional Physiology, Interventions and Outcomes, Adelaide, South Australia, Australia; School of Pharmacy and Medical Sciences, Division of Health Sciences, University of South Australia, Adelaide, South Australia, Australia.
authors: Peter M
authors: PM
authors: Clifton
authors: School of Pharmacy and Medical Sciences, Division of Health Sciences, University of South Australia, Adelaide, South Australia, Australia. Electronic address: jennifer.keogh@unisa.edu.au.
authors: Jennifer B
authors: JB
authors: Keogh
mesh_terms: D000328:Adult; D000077300:Bosentan; D018592:Cross-Over Studies; D004039:Diet, Sodium-Restricted; D019332:Endothelin-1 / Q000097:blood*; D004730:Endothelium, Vascular / Q000502:physiology; D005260:Female; D006801:Humans; D008297:Male; D013449:Sulfonamides / Q000494:pharmacology; D014664:Vasodilation
chemical_list: D019332:Endothelin-1; D013449:Sulfonamides; D000077300:Bosentan
keywords: Aldosterone; Dietary salt; Dietary sodium; Endothelial function; Endothelin-1; Renin