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

Todd, Alwyn; MacGinley, Robert; Schollum, John Bw; Williams, Sheila; Sutherland, W. H. F.; Mann, Jim; Walker, Robert

doi:10.1111/j.1440-1797.2011.01550.x

Cited by 41 publications

(43 citation statements)

References 41 publications

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“…Our study showed no change in PWV c-f between meals; however, we saw a small but significant trend for increased PWV c-f over time. Previous studies showed an improvement in fasting PWV c-f in hypertensive (10,33,34) but not normotensive (35) populations with reduced sodium intake. The influence of potassium on vascular function measures is unclear, with BP likely to influence any observed effect (14).…”

Section: Discussionmentioning

confidence: 99%

Effect of sodium and potassium supplementation on vascular and endothelial function: a randomized controlled trial

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Clifton

Petersen

et al. 2015

The American Journal of Clinical Nutrition

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Background: It is known that increased potassium and reduced sodium intakes can improve postprandial endothelial function. However, the effect of increasing potassium in the presence of high sodium in the postprandial state is not known. Objective: We aimed to determine the effect of high potassium and high sodium on postprandial endothelial function as assessed by using flow-mediated dilatation (FMD) and arterial compliance as assessed by using pulse wave velocity (PWV) and central augmentation index (AIx). Design: Thirty-nine healthy, normotensive volunteers [21 women and 18 men; mean 6 SD age: 37 6 15 y; BMI (in kg/m 2 ): 23.0 6 2.8] received a meal with 3 mmol K and 65 mmol Na (low-potassium, high-sodium meal (LKHN)], a meal with 38 mmol K and 65 mmol Na [high-potassium, high-sodium meal (HKHN)], and a control meal with 3 mmol K and 6 mmol Na (low-potassium, low-sodium meal) on 3 separate occasions in a randomized crossover trial. Brachial artery FMD, carotid-femoral PWV, central AIx, and blood pressure (BP) were measured while participants were fasting and at 30, 60, 90, and 120 min after meals. Results: Compared with the LKHN, the addition of potassium (HKHN) significantly attenuated the postmeal decrease in FMD (P-meal by time interaction , 0.05). FMD was significantly lower after the LKHN than after the HKHN at 30 min (P , 0.01). AIx decreased after all meals (P , 0.05). There were no significant differences in AIx, PWV, or BP between treatments over time. Conclusion: The addition of potassium to a high-sodium meal attenuates the sodium-induced postmeal reduction in endothelial function as assessed by FMD. This trial was registered at

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Section: Discussionmentioning

confidence: 99%

Effect of sodium and potassium supplementation on vascular and endothelial function: a randomized controlled trial

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Clifton

Petersen

et al. 2015

The American Journal of Clinical Nutrition

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“…17 Limited studies have examined the effects of sodium or potassium on measures of arterial stiffness, with inconclusive results both for sodium [18][19][20][21][22][23][24][25] and potassium. [26][27][28][29] We performed a randomised, placebo-controlled, crossover study to examine the effects of sodium and potassium supplementation on office BP, ambulatory BP and arterial stiffness in Dutch subjects with untreated elevated BP.…”

Section: Introductionmentioning

confidence: 97%

Effects of sodium and potassium supplementation on blood pressure and arterial stiffness: a fully controlled dietary intervention study

et al. 2015

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We performed a randomised, placebo-controlled, crossover study to examine the effects of sodium and potassium supplementation on blood pressure (BP) and arterial stiffness in untreated (pre)hypertensive individuals. During the study, subjects were on a fully controlled diet that was relatively low in sodium and potassium. After a 1-week run-in period, subjects received capsules with supplemental sodium (3 g d(-1), equals 7.6 g d(-1) of salt), supplemental potassium (3 g d(-1)) or placebo, for 4 weeks each, in random order. Fasting office BP, 24-h ambulatory BP and measures of arterial stiffness were assessed at baseline and every 4 weeks. Of 37 randomized subjects, 36 completed the study. They had a mean pre-treatment BP of 145/81 mm Hg and 69% had systolic BP ⩾140 mm Hg. Sodium excretion was increased by 98 mmol per 24 h and potassium excretion by 63 mmol per 24 h during active interventions, compared with placebo. During sodium supplementation, office BP was significantly increased by 7.5/3.3 mm Hg, 24-h BP by 7.5/2.7 mm Hg and central BP by 8.5/3.6 mm Hg. During potassium supplementation, 24-h BP was significantly reduced by 3.9/1.6 mm Hg and central pulse pressure by 2.9 mm Hg. Pulse wave velocity and augmentation index were not significantly affected by sodium or potassium supplementation. In conclusion, increasing the intake of sodium caused a substantial increase in BP in subjects with untreated elevated BP. Increased potassium intake, on top of a relatively low-sodium diet, had a beneficial effect on BP. Arterial stiffness did not materially change during 4-week interventions with sodium or potassium.

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“…Intervention studies looking at the effect of sodium on PWV have shown that in normotensive populations, sodium supplementation/a high-sodium diet for 2-6 weeks has no effect on PWV [29,30,31]. In hypertensive populations, a high-sodium diet (>90 mmol/24 h) compared to a lower sodium intake increases PWV [32,33,34].…”

Section: Dietary Intake and Pwvmentioning

confidence: 99%

Weight Loss, Dietary Intake and Pulse Wave Velocity

Petersen

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Keogh

et al. 2015

Pulse

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We have recently conducted a meta-analysis to determine the effect of weight loss achieved by an energy-restricted diet with or without exercise, anti-obesity drugs or bariatric surgery on pulse wave velocity (PWV) measured at all arterial segments. Twenty studies, including 1,259 participants, showed that modest weight loss (8% of the initial body weight) caused a reduction in PWV measured at all arterial segments. However, due to the poor methodological design of the included studies, the results of this meta-analysis can only be regarded as hypothesis generating and highlight the need for further research in this area. In the future, well-designed randomised controlled trials are required to determine the effect of diet-induced weight loss on PWV and the mechanisms involved. In addition, there is observational evidence that dietary components such as fruit, vegetables, dairy foods, sodium, potassium and fatty acids may be associated with PWV, although evidence from well-designed intervention trials is lacking. In the future, the effect of concurrently improving dietary quality and achieving weight loss should be assessed in randomised controlled trials.

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

Abstract: 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.

Cited by 41 publications

References 41 publications

Effect of sodium and potassium supplementation on vascular and endothelial function: a randomized controlled trial

Effect of sodium and potassium supplementation on vascular and endothelial function: a randomized controlled trial

Effects of sodium and potassium supplementation on blood pressure and arterial stiffness: a fully controlled dietary intervention study

Weight Loss, Dietary Intake and Pulse Wave Velocity

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