Sex influences blood pressure but not blood pressure variability in response to dietary sodium and potassium in salt-resistant adults.

Dietary sodium and potassium have been shown to affect blood pressure (BP) but their influence on BP variability (BPV) is less studied as is the influence of sex. The aim of this study was to compare 24 h BP and short-term BPV in response to varying dietary levels of sodium and potassium in healthy non-obese normotensive salt-resistant adults. We hypothesized that high sodium would increase short-term BP and BPV while the addition of high potassium would counteract this increase. Furthermore, we hypothesized that women would experience greater increases in BPV under high sodium conditions compared to men while potassium would attenuate this response. Thirty-seven participants (17 M/20 W; 27 ± 5 years old; BMI 24.3 ± 3 kg/m2) completed seven days each of the following randomized diets: moderate potassium/low sodium (MK/LS), moderate potassium/high sodium (MK/HS) and high potassium/high sodium (HK/HS). BP and short-term BPV were assessed using 24 h ambulatory BP monitoring starting on day 6. BPV was calculated using the average real variability (ARV) index. Twenty-four hour, daytime, and nighttime systolic BP (SBP) were lower in women compared to men regardless of diet. However, 24 h and daytime SBP were lowered in women on the HK/HS diet compared to the MK/HS diet. There were no significant effects of diet or sex for 24 h, daytime or nighttime SBP ARV. However, men exhibited a higher 24 hDBP ARV than women regardless of diet. In conclusion, a high potassium diet lowered BP under high sodium conditions in women alone while men exhibited higher short-term BPV that was not influenced by diet.

Melatonin supplementation does not alter vascular function or oxidative stress in healthy normotensive adults on a high sodium diet.

High sodium diets (HSD) can cause vascular dysfunction, in part due to increases in reactive oxygen species (ROS). Melatonin reduces ROS in healthy and clinical populations and may improve vascular function. The purpose was to determine the effect of melatonin supplementation on vascular function and ROS during 10 days of a HSD. We hypothesized that melatonin supplementation during a HSD would improve vascular function and decrease ROS levels compared to HSD alone. Twenty-seven participants (13 M/14 W, 26.7 ± 2.9 years, BMI: 23.6 ± 2.0 kg/m2 , BP: 110 ± 9/67 ± 7 mmHg) were randomized to a 10-day HSD (6900 mg sodium/d) supplemented with either 10 mg of melatonin (HSD + MEL) or a placebo (HSD + PL) daily. Brachial artery flow-mediated dilation, a measure of macrovascular function, (HSD + PL: 7.1 ± 3.8%; HSD + MEL: 6.7 ± 3.4%; p = 0.59) and tissue oxygenation index (TSI) reperfusion rate, a measure of microvascular reactivity, (HSD + PL: 0.21 ± 0.06%/s; HSD + MEL: 0.21 ± 0.08%/s; p = 0.97) and TSI area under the curve (HSD + PL: 199899 ± 10,863 a.u.; HSD + MEL: 20315 ± 11,348 a.u.; p = 0.17) were similar at the end of each condition. Neither nitroxide molarity (HSD + PL: 7.8 × 10-5 ± 4.1 × 10-5 mol/L; HSD + MEL: 8.7 × 10-5 ± 5.1 × 10-5 mol/L; p = 0.55) nor free radical number (HSD + PL: 8.0 × 1015 ± 4.4 × 1015 ; HSD + MEL: 9.0 × 1015 ± 4.9 × 1015 ; p = 0.51) were different between conditions. Melatonin supplementation did not alter vascular function or ROS levels while on a HSD in this sample of young healthy normotensive adults.

Melatonin supplementation reduces nighttime blood pressure but does not affect blood pressure reactivity in normotensive adults on a high-sodium diet.

High-sodium diets (HSDs) can cause exaggerated increases in blood pressure (BP) during physiological perturbations that cause sympathetic activation, which is related to cardiovascular risk. Melatonin supplementation has been shown to play a role in BP regulation. Our aim was to examine the effects of melatonin taken during an HSD on 24-h BP and BP reactivity during isometric handgrip (IHG) exercise, postexercise ischemia (PEI), and the cold pressor test (CPT). Twenty-two participants (11 men/11 women, 26.5 ± 3.1 yr, BMI: 24.1 ± 1.8 kg/m2, BP: 111 ± 9/67 ± 7 mmHg) were randomized to a 10-day HSD (6,900 mg sodium/day) that was supplemented with either 10 mg/day of melatonin (HSD + MEL) or placebo (HSD + PL). Twenty-four-hour ambulatory BP monitoring was assessed starting on day 9. Mean arterial pressure (MAP) was quantified during the last 30 s of IHG at 40% of maximal voluntary contraction and CPT, and during 3 min of PEI. Melatonin did not change 24-h MAP (HSD + PL: 83 ± 6 mmHg; HSD + MEL: 82 ± 5 mmHg; P = 0.23) but decreased nighttime peripheral (HSD + PL: 105 ± 10 mmHg; HSD + MEL: 100 ± 10 mmHg; P = 0.01) and central systolic BP (HSD + PL: 97 ± 9 mmHg; HSD + MEL: 93 ± 8 mmHg; P = 0.04) on the HSD compared with the HSD + PL. The absolute and percent change in MAP during IHG was not different between conditions (all P > 0.05). In conclusion, melatonin supplementation did not alter BP reactivity to the perturbations tested on an HSD but may be beneficial in lowering BP in young healthy normotensive adults.NEW & NOTEWORTHY BP reactivity was assessed during isometric handgrip (IHG) exercise, postexercise ischemia (PEI), and the cold pressor test (CPT) after 10 days of a high-sodium diet with and without melatonin supplementation. Melatonin did not alter BP reactivity in healthy normotensive men and women. However, melatonin did decrease nighttime peripheral and central systolic BP, suggesting it may be beneficial in lowering BP even in those with a normal BP.

Greater adherence to healthy dietary patterns is associated with lower diastolic blood pressure and augmentation index in healthy, young adults.

More than two-thirds of cardiovascular disease (CVD) deaths worldwide are attributable to dietary factors. Blood pressure variability (BPV), endothelial dysfunction, and arterial stiffness are important CVD risk factors. Although studies show a link between consuming a healthy diet and lower BPV and stiffness and improved endothelial function, research in young, healthy adults is scarce. We hypothesized that, in young, healthy adults, diet quality would be inversely associated with BPV and arterial stiffness and positively associated with endothelial function. This cross-sectional study included 56 healthy young adults (34 women/22 men, age 26.7 ± 0.8 years, body mass index 23.4 ± 0.4 kg/m2, blood pressure [BP] 113/69 mmHg). Three-day diet records were used to calculate two Dietary Approaches to Stop Hypertension (DASH) diet scores, the alternative Mediterranean Diet (aMED) score, and the Healthy Eating Index-2015 (HEI-2015) based on the 2015-2020 Dietary Guidelines for Americans. Twenty-four-hour ambulatory BP data were used to calculate average real variability of systolic and diastolic BP. Endothelial function was assessed by flow-mediated dilation, and arterial stiffness was assessed by pulse wave velocity and augmentation index (AIx). Overall, the HEI-2015 was inversely associated with 24-hour diastolic BP (DBP) and daytime DBP, and the aMED score was inversely associated with AIx. In our exploratory analyses, the Fung DASH score was inversely associated with 24-hour DBP and daytime DBP in women, but not men. These findings suggest that consuming a diet that aligns with the DASH diet, the Mediterranean diet, and/or the 2015-2020 Dietary Guidelines for Americans is associated with cardiovascular benefits in healthy, young adults.

Associations of Ultra-Processed and Unprocessed/Minimally Processed Food Consumption with Peripheral and Central Hemodynamics, and Arterial Stiffness in Young Healthy Adults.

Consumption of ultra-processed food (UPF) replaces the intake of freshly prepared unprocessed/minimally processed food (MPF) and is positively associated with hypertension and cardiovascular disease (CVD). The objective of this observational study was to investigate the relation between (1) UPF and (2) MPF with peripheral and central blood pressure (BP), wave reflection, and arterial stiffness. Habitual dietary intake, ambulatory BP, augmentation index (AIx), and pulse wave velocity (PWV) were assessed in 40 normotensive young adults (15 M/25 W; 27 ± 1 y; body mass index 23.6 ± 0.5 kg/m2). UPF consumption was positively associated with overall and daytime peripheral systolic BP (B = 0.25, 95% confidence interval (CI) 0.03, 0.46, p = 0.029; B = 0.32, 95% CI 0.09, 0.56, p = 0.008, respectively), daytime diastolic BP (B = 0.18, 95% CI 0.01, 0.36, p = 0.049) and daytime peripheral pulse pressure (PP; B = 0.22, 95% CI 0.03, 0.41, p = 0.027). MPF consumption was inversely associated with daytime peripheral PP (B = -0.27, 95% CI -0.47, -0.07, p = 0.011), overall and daytime central systolic BP (B = -0.27, 95% CI -0.51, -0.02, p = 0.035; B = -0.31, 95% CI -0.58, -0.04, p = 0.024, respectively), and nighttime central PP (B = -0.10, 95% CI -0.19, -0.01, p = 0.042). Both UPF and MPF were not associated with AIx nor PWV. These data suggest avoidance of UPF and consumption of more MPF may reduce CVD risk factors.

Antioxidant cocktail following a high-sodium meal does not affect vascular function in young, healthy adult humans: a randomized controlled crossover trial.

Chronic high sodium intake is a risk factor for cardiovascular disease as it impairs vascular function through an increase in oxidative stress. The objective of this study was to investigate the acute effects of a high-sodium meal (HSM) and antioxidant (AO) cocktail on vascular function. We hypothesized that a HSM would impair endothelial function, and increase arterial stiffness and wave reflection, while ingestion of the AO cocktail would mitigate this response. Healthy adults ingested either an AO cocktail (vitamin C, E, alpha-lipoic acid) or placebo (PLA) followed by a HSM (1500 mg) in a randomized crossover blinded design. Blood pressure (BP), endothelial function (flow-mediated dilation; FMD) and measures of arterial stiffness (pulse wave velocity; PWV) and wave reflection (augmentation index; AIx) were made at baseline and 30, 60, 90, and 120 min after meal consumption. Forty-one participants (20M/21W; 24 ± 1 years; BMI 23.4 ± 0.4 kg/m2) completed the study. Mean BP increased at 120 min relative to 60 min (60 min: 79 ± 1; 120 min: 81 ± 1 mmHg; time effect P = .01) but was not different between treatments (treatment × time interaction P = .32). AIx decreased from baseline (time effect P < .001) but was not different between treatments (treatment × time interaction P = .31). PWV (treatment × time interaction, P = .91) and FMD (treatment × time interaction P = .65) were also not different between treatments. In conclusion, a HSM does not acutely impair vascular function suggesting young healthy adults can withstand the acute impact of sodium on the vasculature and therefore, the AO cocktail is not necessary to mitigate the response.

Dietary Potassium Attenuates the Effects of Dietary Sodium on Vascular Function in Salt-Resistant Adults.

The influence of dietary sodium and potassium on blood pressure (BP) has been extensively studied, however their impact on endothelial function, particularly any interactive effects, has received less attention. The purpose of this study was to determine if dietary potassium can offset the deleterious effect of high dietary sodium on endothelial function independent of BP. Thirty-three adults with salt-resistant BP (16 M and 17 F; 27 ± 1 year) completed seven days each of the following diets in a random order: a moderate potassium/low sodium diet (65 mmol potassium/50 mmol sodium; MK/LS), a moderate potassium/high sodium diet (65mmol potassium/300 mmol sodium; MK/HS) and a high potassium/high sodium (120 mmol potassium/300 mmol sodium; HK/HS). On day seven of each diet, 24-h ambulatory BP and a urine collection were performed. Brachial artery flow-mediated dilation (FMD) was measured in response to reactive hyperemia. Between diets, 24-h BP was unchanged confirming salt resistance (p > 0.05). Sodium excretion increased on both HS diets compared to MK/LS (p < 0.05) and potassium excretion was increased on the HK diet compared to MK/LS and MK/HS (p < 0.05) confirming diet compliance. FMD was lower in MK/HS (5.4 ± 0.5%) compared to MK/LS (6.7 ± 0.5%; p < 0.05) and HK/HS (6.4 ± 0.5%), while there was no difference between the MK/LS and HK/HS diets (p > 0.05). These data suggest that dietary potassium provides vascular protection against the deleterious effects of high dietary sodium by restoring conduit artery function.