Dietary sodium loading in normotensive healthy volunteers does not increase arterial vascular reactivity or blood pressure


  • Dr Alwyn Todd's current address: School of Pharmacy and Medical Sciences, Division of Health Sciences, P1-31 Playford Building, City East Campus, University of South Australia.

  • Dr Robert MacGinley's current address: The Deakin University Medical School, Deakin University, Geelong, Australia.

  • The authors have no reported conflicts of interest.

Professor Robert Walker, Department of Medicine, Dunedin School of Medicine, University of Otago, PO Box 913, Dunedin 9054, New Zealand. Email:


Background:  Studies of dietary sodium on vascular function and blood pressure in normotensive volunteers have shown conflicting results. There are very limited data available on the effect of chronic sodium loading from a low-sodium diet to a high-sodium diet on vascular function and blood pressure in normotensive volunteers.

Objective:  To assess the effect of modifying dietary sodium intake on arterial function and surrogate markers of arterial remodelling in normal healthy volunteers.

Design:  Twenty-three normotensive volunteers met the inclusion criteria. After a 2 week run-in with a low-sodium diet (60 mmol/day), the participants maintained their low-sodium diets and were randomly assigned to receive sequentially one of three interventions for 4 weeks, with a 2 week washout between interventions: sodium-free tomato juice (A), tomato juice containing 90 mmol Na (B) and tomato juice containing 140 mmol Na (C). The outcomes measured were changes in pulse wave velocity (PWV), systolic blood pressure and diastolic blood pressure.

Results:  There was no difference in PWV between interventions (B–A 0.00 m/s, 95% CI: −0.30, 0.31 m/s; C–A 0.01 m/s, 95% CI: −0.38, 0.40 m/s). There was also no change in pulse wave analysis, systolic or diastolic blood pressure between interventions. There was an appropriate increase in urinary sodium excretion in the added sodium interventions.

Conclusion:  Dietary salt loading did not produce significant increases in PWV and blood pressure in normotensive subjects with systolic blood pressure <130 mmHg. The lack of an observed effect supports Guyton's pressure–natriuresis hypothesis with appropriate renal excretion of the excess sodium load.