High-phosphorus diet controlled for sodium elevates blood pressure in healthy adults via volume expansion.
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ABSTRACT:
SUBMITTER: Zhang JY
PROVIDER: S-EPMC8678725 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundHigh sodium (Na+) intake augments blood pressure variability (BPV) in normotensive rodents, without changes in resting blood pressure (BP). Augmented BPV is associated with end-organ damage and cardiovascular morbidity. It is unknown if changes in dietary Na+ influence BPV in humans. We tested the hypothesis that high Na+ feeding would augment BPV in healthy adults.MethodsTwenty-one participants (10 F/11 M; 26 ± 5 years; BP: 113 ± 11/62 ± 7 mm Hg) underwent a randomized, controlled feeding study that consisted of 10 days of low (2.6 g/day), medium (6.0 g/day), and high (18.0 g/day) salt diets. On the ninth day of each diet, 24-h urine samples were collected and BPV was calculated from 24-h ambulatory BP monitoring. On the tenth day, in-laboratory beat-to-beat BPV was calculated during 10 min of rest. Serum electrolytes were assessed. We calculated average real variability (ARV) and standard deviation (SD) as metrics of BPV. As a secondary analysis, we calculated central BPV from the 24-h ambulatory BP monitoring.Results24-h urinary Na+ excretion (low = 41 ± 24, medium = 97 ± 43, high = 265 ± 92 mmol/24 h, P < 0.01) and serum Na+ (low = 140.0 ± 2.1, medium = 140.7 ± 2.7, high = 141.7 ± 2.5 mmol/l, P = 0.009) increased with greater salt intake. 24-h ambulatory ARV (systolic BP ARV: low = 9.5 ± 1.7, medium = 9.5 ± 1.2, high = 10.0 ± 1.9 mm Hg, P = 0.37) and beat-to-beat ARV (systolic BP ARV: low = 2.1 ± 0.6, medium = 2.0 ± 0.4, high = 2.2 ± 0.8 mm Hg, P = 0.46) were not different. 24-h ambulatory SD (systolic BP: P = 0.29) and beat-to-beat SD (systolic BP: P = 0.47) were not different. There was a trend for a main effect of the diet (P = 0.08) for 24-h ambulatory central systolic BPV.ConclusionsTen days of high sodium feeding does not augment peripheral BPV in healthy, adults.Clinical trials registrationNCT02881515.
| S-EPMC7188796 | biostudies-literature
Project description:The present study evaluated the response of blood pressure (BP) by dietary sodium in sodium resistant (SR) subjects. One hundred one subjects (mean age, 46.0 yr; 31 hypertensives) were admitted and given low sodium-dietary approaches to stop hypertension (DASH) diet (LSD, 100 mM NaCl/day) for 7 days and high sodium-DASH diet (HSD, 300 mM NaCl/day) for the following 7 days. On the last day of each diet, 24 hr ambulatory BP was measured. Morning systolic BP (SBP) and diastolic BP (DBP) were elevated after HSD in all subjects (P < 0.01), but daytime SBP and DBP were not changed (P > 0.05). In hypertensive subjects, morning DBP elevation was greater than daytime DBP elevation (P = 0.036), although both DBPs were significantly elevated after HSD. The augmented elevation of morning DBP in hypertensive subjects was contributed by the absolute elevation of morning DBP (P = 0.032) and relative elevation to daytime DBP (P = 0.005) in sodium resistant (SR) subjects, but not by sodium sensitive subjects. Although there was no absolute elevation, SR subjects with normotension showed a relative elevation of morning SBP compared to daytime SBP change after HSD (P = 0.009). The present study demonstrates an absolute and relative elevation of morning BP in SR subjects by HSD.
| S-EPMC3617308 | biostudies-literature
Project description:Little is known about prostaglandin F(2alpha) in cardiovascular homeostasis. Prostaglandin F(2alpha) dose-dependently elevates blood pressure in WT mice via activation of the F prostanoid (FP) receptor. The FP is expressed in preglomerular arterioles, renal collecting ducts, and the hypothalamus. Deletion of the FP reduces blood pressure, coincident with a reduction in plasma renin concentration, angiotensin, and aldosterone, despite a compensatory up-regulation of AT1 receptors and an augmented hypertensive response to infused angiotensin II. Plasma and urinary osmolality are decreased in FP KOs that exhibit mild polyuria and polydipsia. Atherogenesis is retarded by deletion of the FP, despite the absence of detectable receptor expression in aorta or in atherosclerotic lesions in Ldlr KOs. Although vascular TNF(alpha), inducible nitric oxide enzyme and TGF(beta) are reduced and lesional macrophages are depleted in the FP/Ldlr double KOs, this result reflects the reduction in lesion burden, as the FP is not expressed on macrophages and its deletion does not alter macrophage cytokine generation. Blockade of the FP offers an approach to the treatment of hypertension and its attendant systemic vascular disease.
| S-EPMC2673134 | biostudies-literature
Project description:Dietary salt intake has significant effects on arterial blood pressure and the development of hypertension. Mechanisms underlying salt-dependent changes in blood pressure remain poorly understood, and it is difficult to assess blood pressure salt-sensitivity clinically. Methods: We examined urinary levels of metabolites in 103 participants of the Dietary Approaches to Stop Hypertension (DASH)-Sodium trial after nearly 30 days on a defined diet containing high sodium (targeting 150 mmol sodium intake per day) or low sodium (50 mmol per day). Targeted chromatography/mass spectrometry analysis was performed in 24 h urine samples for 47 amino metabolites and 10 metabolites related to the tricarboxylic acid cycle. The effect of an identified metabolite on blood pressure was examined in Dahl salt-sensitive rats. Results: Urinary metabolite levels improved the prediction of classification of blood pressure salt-sensitivity based on race, age and sex. Random forest and generalized linear mixed model analyses identified significant (false discovery rate <0.05) associations of 24 h excretions of β-aminoisobutyric acid, cystine, citrulline, homocysteine and lysine with systolic blood pressure and cystine with diastolic blood pressure. The differences in homocysteine levels between low- and high-sodium intakes were significantly associated with the differences in diastolic blood pressure. These associations were significant with or without considering demographic factors. Treatment with β-aminoisobutyric acid significantly attenuated high-salt-induced hypertension in Dahl salt-sensitive rats. Conclusion: These findings support the presence of new mechanisms of blood pressure regulation involving metabolic intermediaries, which could be developed as markers or therapeutic targets for salt-sensitive hypertension.
| S-EPMC5858161 | biostudies-literature
Project description:BACKGROUND:Both sodium reduction and the DASH (Dietary Approaches to Stop Hypertension) diet, a diet rich in fruits, vegetables, and low-fat dairy products, and reduced in saturated fat and cholesterol, lower blood pressure. The separate and combined effects of these dietary interventions by baseline blood pressure (BP) has not been reported. OBJECTIVES:The authors compared the effects of low versus high sodium, DASH versus control, and both (low sodium-DASH vs. high sodium-control diets) on systolic blood pressure (SBP) by baseline BP. METHODS:In the DASH-Sodium (Dietary Patterns, Sodium Intake and Blood Pressure) trial, adults with pre- or stage 1 hypertension and not using antihypertensive medications, were randomized to either DASH or a control diet. On either diet, participants were fed each of 3 sodium levels (50, 100, and 150 mmol/day at 2,100 kcal) in random order over 4 weeks separated by 5-day breaks. Strata of baseline SBP were <130, 130 to 139, 140 to 149, and ?150 mm Hg. RESULTS:Of 412 participants, 57% were women, and 57% were black; mean age was 48 years, and mean SBP/diastolic BP was 135/86 mm Hg. In the context of the control diet, reducing sodium (from high to low) was associated with mean SBP differences of -3.20, -8.56, -8.99, and -7.04 mm Hg across the respective baseline SBP strata listed (p for trend = 0.004). In the context of high sodium, consuming the DASH compared with the control diet was associated with mean SBP differences of -4.5, -4.3, -4.7, and -10.6 mm Hg, respectively (p for trend = 0.66). The combined effects of the low sodium-DASH diet versus the high sodium-control diet on SBP were -5.3, -7.5, -9.7, and -20.8 mm Hg, respectively (p for trend <0.001). CONCLUSIONS:The combination of reduced sodium intake and the DASH diet lowered SBP throughout the range of pre- and stage 1 hypertension, with progressively greater reductions at higher levels of baseline SBP. SBP reductions in adults with the highest levels of SBP (?150 mm Hg) were striking and reinforce the importance of both sodium reduction and the DASH diet in this high-risk group. Further research is needed to determine the effects of these interventions among adults with SBP ?160 mm Hg. (Dietary Patterns, Sodium Intake and Blood Pressure [DASH-Sodium]; NCT00000608).
| S-EPMC5742671 | biostudies-literature
Project description:Both sodium reduction and the Dietary Approaches to Stop Hypertension (DASH) diet lower blood pressure (BP); however, the patterns of their effects on BP over time are unknown. In the DASH-Sodium trial, adults with pre-/stage 1 hypertension, not using antihypertensive medications, were randomly assigned to either a typical American diet (control) or DASH. Within their assigned diet, participants randomly ate each of 3 sodium levels (50, 100, and 150 mmol/d, at 2100 kcal) over 4-week periods. BP was measured weekly for 12 weeks; 412 participants enrolled (57% women; 57% black; mean age, 48 years; mean systolic BP [SBP]/diastolic BP [DBP], 135/86 mm Hg). For those assigned control, there was no change in SBP/DBP between weeks 1 and 4 on the high-sodium diet (weekly change, -0.04/0.06 mm Hg/week) versus a progressive decline in BP on the low-sodium diet (-0.94/-0.70 mm Hg/week; P interactions between time and sodium <0.001 for SBP and DBP). For those assigned DASH, SBP/DBP changed -0.60/-0.16 mm Hg/week on the high- versus -0.42/-0.54 mm Hg/week on the low-sodium diet (P interactions between time and sodium=0.56 for SBP and 0.10 for DBP). When comparing DASH to control, DASH changed SBP/DBP by -4.36/-1.07 mm Hg after 1 week, which accounted for most of the effect observed, with no significant difference in weekly rates of change for either SBP (P interaction=0.97) or DBP (P interaction=0.70). In the context of a typical American diet, a low-sodium diet reduced BP without plateau, suggesting that the full effects of sodium reduction are not completely achieved by 4 weeks. In contrast, compared with control, DASH lowers BP within a week without further effect thereafter.Clinical trial registrationURL: http://www.clinicaltrials.gov. Unique identifier: NCT00000608.
| S-EPMC5659740 | biostudies-literature
Project description:BackgroundMaternal overnutrition during pregnancy predisposes the offspring to cardiometabolic diseases.ObjectivesThis systematic review and meta-analysis aimed to investigate the association between maternal overnutrition and offspring's blood pressure (BP) and the effect of offspring's obesity on this association.Data sourcesPubMed, EMBASE, Clinicaltrials.gov, CENTRAL.Study selection and data extractionHuman studies published in English before October 2021 were identified that presented quantitative estimates of association between maternal overnutrition just before or during pregnancy and the offspring's BP.SynthesisRandom-effect model with the DerSimonian and Laird weighting method was used to analyse regression coefficients or mean differences.ResultsAfter selection, 17 observational studies (140,517 mother-offspring pairs) were included. Prepregnancy body mass index (ppBMI) showed positive correlation with BP in offspring (regression coefficient for systolic: 0.38 mmHg per kg/m2 , 95% confidence interval (CI) 0.17, 0.58; diastolic: 0.10 mmHg per kg/m2 , 95% CI 0.05, 0.14). These indicate 1.9 mmHg increase in systolic and 0.5 mmHg increase in diastolic BP of offspring with every 5 kg/m2 gain in maternal ppBMI. Results on coefficients adjusted for offspring's BMI also showed association (systolic: 0.08 mmHg per kg/m2 , 95% CI 0.04, 0.11; diastolic: 0.03 mmHg per kg/m2 , 95% CI 0.01, 0.04). Independent from ppBMI, gestational weight gain (GWG) showed positive correlation with systolic BP (systolic BP: 0.05 mmHg per kg, 95% CI 0.01, 0.09), but not after adjustment for offspring's BMI. Mean systolic BP was higher in children of mothers with excessive GWG than in those of mothers with optimal GWG (difference: 0.65 mmHg, 95% CI 0.25, 1.05).ConclusionsIndependent from offspring's BMI, higher prepregnancy BMI may increase the risk for hypertension in offspring. The positive association between GWG and offspring's systolic BP is indirect via offspring's obesity. Reduction in maternal obesity and treatment of obesity in children of obese mothers are needed to prevent hypertension.
| S-EPMC9305555 | biostudies-literature
Project description:Raised blood pressure is a leading cause of morbidity and mortality worldwide; improved nutritional approaches to population-wide prevention are required. Few data are available on dietary phosphorus and blood pressure and none are available on possible combined effects of phosphorus, magnesium, and calcium on blood pressure. The International Study of Macro- and Micro-Nutrients and Blood Pressure is a cross-sectional epidemiologic study of 4680 men and women ages 40 to 59 from 17 population samples in Japan, China, United Kingdom, and United States. Blood pressure was measured 8 times at 4 visits. Dietary intakes were obtained from four 24-hour recalls plus data on supplement use. Dietary phosphorus was inversely associated with blood pressure in a series of predefined multiple regression models, with the successive addition of potential confounders, both nondietary and dietary. Estimated blood pressure differences per 232 mg/1000 kcal (2 SD) of higher dietary phosphorus were -1.1 to -2.3 mm Hg systolic/-0.6 to -1.5 mm Hg diastolic (n=4680) and -1.6 to -3.5 mm Hg systolic/-0.8 to -1.8 mm Hg diastolic for 2238 "nonintervened" individuals, ie, those without special diet/nutritional supplements or diagnosis/treatment for cardiovascular disease or diabetes. Dietary calcium and magnesium, correlated with phosphorus (partial r=0.71 and r=0.68), were inversely associated with blood pressure. Blood pressures were lower by 1.9 to 4.2 mm Hg systolic/1.2 to 2.4 mm Hg diastolic for people with intakes above versus below country-specific medians for all 3 of the minerals. These results indicate the potential for increased phosphorus/mineral intake to lower blood pressure as part of the recommendations for healthier eating patterns for the prevention and control of prehypertension and hypertension.
| S-EPMC6556767 | biostudies-literature
Project description:IntroductionVitamin D insufficiency, defined as 25-hydroxyvitamin D (25(OH)D) levels < 75nmol/L is associated with cardio-metabolic dysfunction. Vitamin D insufficiency is associated with inflammation and fibrosis, but it remains uncertain whether these anomalies are readily reversible. Therefore, we aimed to determine the effects of vitamin D supplementation on markers of: 1) nitric oxide (NO) signaling, 2) inflammation, and 3) fibrosis, in healthy volunteers with mild hypovitaminosis.MethodsHealthy volunteers (n = 35) (mean age: 45 ± 11 years) with 25(OH)D levels <75nmol/L, received vitamin D supplementation (Ostelin ® capsules 2000IU) for 12 weeks. Resting systolic and diastolic blood pressures (BP) were assessed. Routine biochemistry was examined. Plasma concentrations of asymmetric dimethylarginine (ADMA), thrombospondin-1 (TSP-1), plasminogen activator inhibitor-1 (PAI-1), hs-CRP, activin-A, and follistatin-like 3 (FSTL3) were quantitated.ResultsVitamin D administration for 12 weeks significantly increased 25-(OH)D levels (48.8 ± 16 nmol/L to 100.8 ± 23.7 nmol/L, p<0.001). There was significant lowering of systolic and diastolic BP, while there was no significant change in lipid profiles, or fasting insulin. Plasma concentrations of ADMA, hs-CRP, PAI-1, activin A, and FSTL-3 did not change with vitamin D supplementation. However, there was a marked reduction of TSP-1 (522.7 ± 379.8 ng/mL vs 206.7 ± 204.5 ng/mL, p<0.001).ConclusionsVitamin D supplementation in vitamin D insufficient, but otherwise healthy individuals markedly decreased TSP-1 levels and blood pressure. Since TSP-1 suppresses signaling of NO, it is possible that the fall in BP is engendered by restoration of NO effect.
| S-EPMC5425007 | biostudies-literature
Project description:Our understanding of Na+ homeostasis has recently been reshaped by the notion of skin as a depot for Na+ accumulation in multiple cardiovascular diseases and risk factors. The proposed water-independent nature of tissue Na+ could induce local pathogenic changes, but lacks firm demonstration. Here, we show that tissue Na+ excess upon high Na+ intake is a systemic, rather than skin-specific, phenomenon reflecting architectural changes, i.e. a shift in the extracellular-to-intracellular compartments, due to a reduction of the intracellular or accumulation of water-paralleled Na+ in the extracellular space. We also demonstrate that this accumulation is unlikely to justify the observed development of experimental hypertension if it were water-independent. Finally, we show that this isotonic skin Na+ excess, reflecting subclinical oedema, occurs in hypertensive patients and in association with aging. The implications of our findings, questioning previous assumptions but also reinforcing the importance of tissue Na+ excess, are both mechanistic and clinical.
| S-EPMC7445299 | biostudies-literature